THE PROGNOSIS OF 
INTERNAL DISEASES 
BY 
HENRY L. JELSNER, M.D., LL.D. 
PROFESSOR OF MEDICINE, COLLEGE 
OF MEDICINE, SYRACUSE UNIVERSITY 
NEW YORK AND LONDON 
D. APPLETON AND COMPANY 
1923 Copyright, 1916, 1923, by 
D. APPLETON AND COMPANY 
Printed in the United States erf America TO 
MY WIFE 
MY MOST CHARITABLE 
AND PATIENT CRITIC AND 
CONSTANT INSPIRATION “But the power of prognosis is at once the most complete and the most 
easily understood proof of the reality of knowledge. As soon as an eclipse 
could be correctly predicted, astronomy was proved to be a true science; 
and, particularly, we find that nothing so much secures the confidence of 
patients as a prediction which proves true” (Pye-Smith). Preface 
The prognosis of a disease presupposes a full knowledge of the disease 
in respect to its etiology, pathology and clinical manifestations. A review 
of the present edition reveals how logically the author has portrayed diseases 
from the viewpoint of prognosis. Ilis wide clinical experience and extensive 
knowledge of the literature made possible the creation of a work of this 
nature. Consciously or unconsciously the question of prognosis enters into 
the consideration of all disease. It was the desire of the author to place 
before his readers this phase of medicine for its guiding influence towards 
a broader horizon. 
Charles D. Post 
212 Physicians’ Bldg., 
Syracuse, N. Y. Preface 
The purpose of this book is to bring reassurance and comfort to the 
physician, and through him greater benefit to the patient. 
The study of prognosis begets confidence. 
“He heals best who is most certain of the course of disease.” This is 
an aphorism which is incontrovertible; hence the physician who would 
give a reliable forecast of disease is at once forced to a consideration of 
underlying conditions. He must think clearly, must have a fundamental 
knowledge of physiologic processes, must study the perversion of these— 
pathologic conditions—must be able to interpret the meaning of sub- 
jective and objective manifestations, must be able to determine the re- 
ciprocal relations of Constitution, Resistance and Heredity; he must view 
the body as a whole and he must recognize the fact that medical prog- 
nosis is exceedingly complex and therefore demands the consideration of 
multiple data. 
Medical 'prognosis includes the scientific survey of the entire field of 
Medicine. 
The author and the publishers hope that this work on “The Prog- 
nosis of Internal Disease,” the first systematic treatise on this subject 
to be presented to the medical profession, will stimulate the workers in 
the field of medicine to the acquisition of such fundamental knowledge 
as is needed for the reliable forecast of disease as it presents in practice. 
These facts, and the study of the meager literature of the subject of 
Prognosis, have encouraged the author during the many years of his pro- 
fessional activity to accumulate the material upon which his conclusions 
are based, and finally to launch this work. 
The author fully appreciates the fact that the study of medical prog- 
nosis must often forcibly impress the profession with the limitations of its 
art; on the other hand, it is made conscious of the possibilities of medicine 
by the association of pathologic knowledge with keen diagnostic and thera- 
peutic ability, tempered with tact and the humane spirit of the true 
physician. 
The enormous advances which have resulted from animal experimenta- 
tion, including vivisection, and the refinements of diagnosis aided by the 
newer sciences, particularly bacteriology, have completely changed our 
conception of many diseases. PREFACE 
The devotion of a band of unselfish and patient workers in the labor- 
atories and among the infected in far-off countries, many of whom wel- 
comed hardships and even sacrificed their lives that medical truths might 
be established, has led to the prevention of some diseases and favorably 
changed the forecast of others. 
The author has aimed to establish the urgent necessity in practice 
of correlating all available knowledge that safe conclusions for diagnosis, 
prognosis, and treatment may be reached, and he has sought to impress 
the further fact that the practical physician must brace himself against 
one-sided reasoning, and always place the greater reliance upon the 
subjective and objective features of the individual case, to which he 
should add (and aim to interpret correctly) the results of laboratory 
investigation. 
The author wishes to express his appreciation of the confidence which 
during more than a third of a century has been extended to him by his 
professional colleagues. Without their support this book would have been 
impossible. Their friendship and encouragement have been important 
factors in leading him to the completion of this monumental task. 
To the publishers, the author extends his thanks and his appreciation 
for their uniform courtesy and material assistance. 
To the reader, the author delivers the following pages with the hope 
that they will often reassure, comfort and stimulate him. 
If his friends and the readers find only a fraction of the pleasure in 
the study of “The Prognosis of Internal Disease” that the author has 
enjoyed during the years of its production, he will feel sufficiently re- 
warded. 
Henry L. Elsner. Contents 
Section I. Specific Infectious Diseases 
> 
PAGE 
A. Protozoan Infections 15 
1. Syphilis 16 
I. Acquired Syphilis 16 
Specific Diseases of the Cardiovascular System . . 26 
Arteritis 26 
Aortitis syphilitica 27 
Heart Syphilis 28 
Phlebitis syphilitica 29 
Syphilis of the Liver 30 
Syphilis of the Kidney 31 
Syphilis of the Testicle and Epididymis .... 32 
Syphilis of the Bones and Joints 32 
Syphilis of the Muscles (Myositis) 32 
Syphilis of the Respiratory Organs 32 
Kasai Syphilis 32 
Laryngeal Syphilis 33 
Bronchial and Tracheal Syphilis .... 33 
Syphilis of the Lung 33 
Syphilis of the Spleen 33 
Syphilis of the Digestive Tract 31 
Syphilis of the Rectum 34 
Syphilis of the Stomach 34 
Syphilis of the Esophagus 34 
Syphlis of the Intestines 34 
Syphilis of the Eervous System 35 
Syphilis of the Spinal Cord 35 
Syphilitic Peripheral Keuritis 37 
Cerebral Syphilis 38 
Late Tertiary Lesions—so-called “Metasyphilitic Dis- 
eases” ......... 44 
I. Tabes dorsalis—Locomotor ataxia ... 45 
II. Taboparesis 61 
III. General Paresis _ 02 CONTENTS 
PAGE 
2. Congenital Syphilis ........ 65 
•Syphilis and Marriage 68 
Syphilis and Life Insurance 68 
The Fate of Syphilitics and Their Children ... 69 
Carriers of Treponema pallidum 70 
> II. Malaria 72 
1. Intermittent Malarial Fever 73 
(a) Quotidian Type 73 
(b) Tertian Type 73 
(c) Quartan Type 73 
(d) Irregular Intermittent Fever . . . 73 
2. Remittent Malarial Fever 74 
(a) Aestivo-autumnal fever . . . . 74 
(b) Pernicious Malarial Disease . . . 74 
(c) Black Water Disease or Hemorrhagic Ma- 
larial Fever 76 
3. Chronic Malarial Cachexia 76 
4. Mixed Types of Malarial Fever .... 77 
5. Malarial Neuralgia 77 
6. Malarial Complications 77 
III. Amebic Dysentery—Amebiasis 78 
IV. Trypanosomiasis 81 
V. Relapsing Fever 82 
VI. Leishmaniasis 83 
B. Bacterial Diseases 84 
I. Typhoid Fever 84 
II. Typhus Fever 117 
III. Paratyphoid Disease 121 
IV. Influenza 124 
V. Pyogenic Infections—Septicemia—Pyemia . . .130 
VI. Diphtheria 134 
VII. Pneumococcus Infection 145 
1. Lobar Pneumonia ....... 145 
2. Bronchopneumonia 169 
VIII. Erysipelas 173 
IX. Epidemic Cerebrospinal Meningitis .... 177 
X. AVhooping-cough 186 
XI. Gonococcus Infections 189 
1. Gonococcus Endocarditis 190 
2. Gonococcus Arthritis ...... 192 
XII. Bacillary Dysentery ....... 193 
XIII. Malta F'ever 196 CONTEXTS 
PAGE 
XIV. Asiatic Cholera 197 
XV. Plague 201 
XVI. Tetanus 206 
XVII. Anthrax 209 
XVIII. Glanders 212 
XIX. Leprosy 214 
XX. Tuberculosis 216 
History 217 
1. Acute Miliary Tuberculosis .... 222 
I. Typhoid Form 223 
II. Pulmonary Form .... 224 
III. Meningeal Form 224 
2. Pulmonary Tuberculosis 226 
I. Acute Pneumonic Tuberculosis . . 227 
II. Chronic Pulmonary Tuberculosis . 229 
III. Fibroid Phthisis 244 
3. Tuberculous Pleurisy 247 
4. Parotid Tuberculosis 249 
5. Xasal Tuberculosis 250 
6. Laryngeal Tuberculosis 249 
7. Tuberculosis of the Digestive Tract . . 252 
8. Tuberculous Peritonitis 257 
9. Tuberculosis of the Pancreas . . . 262 
10. Tuberculosis of the Spleen . . . .262 
11. Tuberculosis of the Suprarenal Gland—Addi- 
son’s Disease 263 
12. Tuberculosis of the Lymphatic Glands . . 265 
13. Genito-urinary Tuberculosis .... 267 
14. Cardiovascular Tuberculosis . . . .274 
15. Tuberculosis of the Xervous System . . 277 
XXI. Rheumatic Fever (Acute Polyarthritis) .... 278 
XXII. Tonsillitis 292 
(a) The Influence of the Tonsil on Prophylaxis and 
Prognosis 292 
(b) Acute Follicular Tonsillitis .... 293 
(c) Phlegmonous Tonsillitis (Septic) . . . 297 
(d) Acute Suppurative Peritonsillitis (Quinsy) . 297 
(e) Vincent’s angina 298 
(f) Chronic Tonsillitis (Adenoids) .... 299 
XXIII. Metastatic Parotitis 300 
C. Non-Bacterial Fungus Infection 301 
Actinomvcosis 301 CONTEXTS 
PAGE 
D. Diseases Due to Metazoan Parasites 303 
1. Cestodes 304 
(a) Tenia solium 304 
(b) Tenia saginata or Mediocanellata .... 305 
(c) Bothriocephalus latus 305 
(d) Tenia echinococcus (Hydatid Disease) . . . 306 
2. Nematodes 309 
(a) Ascaris lumbricoides 309 
(b) Oxvuris vermicularis 309 
(c) Ankylostomiasis 310 
(d) Tricocephalus dispar 312 
(e) Trichinosis 312 
(f) Filiariasis 315 
3. Trematodes 316 
Bilharzia haematobia 316 
E. Infections of Unknown or Doubtful Origin .... 317 
I. Poliomyelitis 317 
1. Acute Poliomyelitis (Infantile Paralysis) . . 317 
2. Chronic Poliomyelitis 326 
II. Scarlet Fever 327 
III. Smallpox . . . , 333 
IV. Varicella 341 
V. Measles 342 
VI. German Measles 346 
VII. Yellow Fever 347 
VIII. Foot and Mouth Disease 349 
IX. Ephemeral Fever 350 
X. Infectious Jaundice (Weil’s Disease) .... 350 
XI. Sweating Sickness 351 
XII. Herpetic Fever 352 
XIII. Fourth Disease (Duke’s Disease) 352 
XIV. Epidemic Parotitis 352 
XV. Glandular Fever (Pfeiffer’s Disease) . . • . 353 
XVI. Hydrophobia 354 
XVII. Dengue 356 
Section II. Diseases of the Respiratory Apparatus 
A. Diseases of the Nose 357 
1. Acute Catarrhal Rhinitis (Coryza) ..... 357 
2. Hay Fever 353 
3. Epistaxis 359 CONTENTS 
PAGE 
B. Diseases of the Larynx 360 
1. Acute Laryngitis 360 
2. Chronic Laryngitis 361 
3. Edema of the Larynx 362 
4. Laryngismus stridulus 362 
5. Tuberculous Laryngitis 363 
6. Syphilitic Laryngitis 363 
C. Diseases of the Bronchi 363 
1. Acute Bronchitis 363 
2. Chronic Bronchitis 365 
3. Bronchiectasia 366 
4. Bronchial Asthma 368 
5. Fibrinous Bronchitis 373 
6. Whooping-cough 373 
D. Diseases of the Lung 373 
1. Circulatory Disturbances of the Lung . . . 373 
Congestion— 
(a) Active 373 
(b) Passive 374 
(c) Pulmonary Edema 375 
2. Pulmonary Hemorrhage 376 
(a) Hemoptysis 376 
(b) Pulmonary Infarct 378 
3. Chronic Eon-tuberculous Pneumonia 379 
(a) Chronic Pneumonia 379 
(b) Chronic Interstitial Pneumonia . . . .379 
(c) The Pneumonokonioses 380 
4. Emphysema 382 
5. Gangrene of the Lung 385 
6. Abscess of the Lung 386 
7. Heoplasm of the Lung 387 
E. Diseases of the Pleura 389 
1. Pleurisy 389 
(a) Fibrinous Pleurisy . 389 
(b) Serofibrinous Pleurisy 389 
(c) Purulent Pleurisy 392 
(d) Tuberculous Pleurisy 395 
(e) Chronic Pleurisy 395 CONTEXTS 
PAGE 
2. Hydrothorax 396 
3. Pneumothorax 396 
4. Mediastinal Disease 399 
Section III. Diseases of the Circulatory Apparatus 
A. Arteriosclerosis 402 
General Consideration: 
1. Age 404 
2. Heredity 405 
3. Syphilis 405 
4. Worry and Stress 405 
5. Alcohol 405 
6. Lead .......... 406 
7. Tobacco 407 
8. Infection ......... 407 
9. Occupation 407 
10. Overeating ......... 409 
11. Mechanical Factors 409 
12. Chemical and Toxic Factors 409 
13. Hypertension 410 
14. Kidney Invasion 411 
15. Coronary, Myocardial, Endocardial and Other Heart 
Lesions 411 
16. Vascular Crisis (Spasm) 414 
17. Cerebral, Spinal and Peripheral Changes . . .416 
18. Blood Pressure Study of Arteriosclerosis (after the 
stage of hypertension) 416 
19. Thrombosis 418 
20. Ocular Changes 418 
21. X-ray Examination 419 
B. Aneurism 420 
1. Aneurism of the Ascending Portion of the Arch of the 
Aorta 423 
2. Aneurism of the Transverse Portion of the Arch of the 
Aorta 423 
3. Aneurism of the Descending Portion of the Arch of the 
Aorta 424 
4. Aneurism of the Descending Thoracic and Abdominal 
Aorta 424 CONTENTS 
PAGE 
5. Aneurism of the Celiac Axis 425 
6. Aneurism of the Coronary Artery . . . . .425 
7. Aneurism of the Pulmonary Artery 425 
8. Aneurism of the Subclavian Artery . . . .425 
C. Diseases of the Pericardium 426 
1. Acute Pericarditis 426 
2. Adherent Pericardium 430 
3. Chronic Pericardioperitonitis 432 
4. Hydropericardium 433 
5. Hemopericardium ........ 433 
6. Pneumopericardium 434 
7. Neoplasms of the Pericardium 434 
D. Congenital Defects of the Heart 435 
1. Stenosis of the Pulmonary Orifice 435 
2. Defective Ventricular Septum 438 
3. Perforate Foramen ovale * 438 
4. Dextrocardia 438 
5. Stenosis of the Aortic Orifice 438 
6. Insufficiency and Stenosis of the Mitral and Tricuspid 
Valves 439 
7. Transposition of the Aortic and Pulmonary Artery: Per- 
forate ductus arteriosus and Premature Closure . . 439 
E. Myocardial Diseases 441 
1. Acute Purulent Myocarditis 442 
2. Acute Interstitial Myocarditis (Parenchymatous) . . 443 
(a) Simple Acute Interstitial Myocarditis . . . 443 
(b) Acute Septic Interstitial Myocarditis . . . 443 
3. Chronic Myocardial Insufficiency 443 
(a) Fibroid Degeneration (including the Arhythmias) 443 
(b) Fatty Heart 452 
(c) Fragmentation and Segmentation .... 454 
(d) Brown Atrophy 454 
(e) Coronary Sclerosis (Angina pectoris) . . . 454 
(f) Senile Heart . . * 460 
4. Hypertrophy and Dilatation 460 
(a) Overstrain ........ 460 
(b) Hypertension 461 CONTENTS 
PAGE 
(c) Hypertrophy — Secondary to Lung Disease, 
Asthma, Kyphosis, Fixed Thorax and Non-val- 
vular Heart Lesions 462 
(d) Hypertrophy—with Masturbation, Uterine Fi- 
broids and Hyperthyroidea . . . .462 
5. Stokes-Adams Disease 463 
6. Syphilis of the Heart . . . 464 
7. Heart Weakness Due to Insufficient Exercise . . . 464 
8. Inherent Muscular Weakness 465 
9. Insufficiency with the Anemias, Metabolic Faults and 
Toxic States 465 
10. Neoplasms 465 
11. Parasites of the Heart 466 
12. Rupture of the Heart 466 
13. Aneurism of the Heart . . . ... . . 467 
F. Endocarditis 468 
1. Acute Endocarditis . . 469 
(a) Simple Acute Endocarditis 469 
(b) Septic Endocarditis 471 
2. Chronic Endocarditis 477 
1. General Consideration of Chronic Cardiopathies . 477 
(a) Hypertrophy 478 
(b) Dilatation 480 
(c) Decompensation 482 
(d) Frequency of Valvular Lesions . . .483 
(e) Sex 483 
(f) Heredity and Family History . . . 483 
(g) Age 484 
(h) Occupation and Social Conditions . . 484 
(i) The Influence of Intercurrent Diseases . 485 
(j) The Influence of Marriage and Pregnancy 
on Valvular Diseases 486 
(k) The Influence of the Usual Complicating 
Diseases on the Course of the Chronic 
Cardiopathies 489 
(l) Blood 491 
(m) Skin 491 
(n) Nephritis 491 
(o) Liver 491 
(p) Nervous System 492 
(q) Dropsies 492 CONTENTS 
PAGE 
(r) Pulse 492 
(s) Blood Pressure 492 
(t) Rontgen Examination 492 
(u) Sudden Death and Valvular Anomalies . 493 
(v) Anatomic Cure of Valvular Lesions . . 493 
(w) Influence of Treatment 493 
(x) Influence of Physical Signs .... 494 
(v) Fate of the Chronic Cardiopaths . . . 494 
2. Localization of Valvular Lesions and Their Forms 495 
Mitral Insufficiency 495 
Mitral Stenosis 497 
Aortic Stenosis (Obstruction) .... 499 
Aortic Insufficiency 500 
Tricuspid Insufficiency 503 
Tricuspid Stenosis 503 
Defects of the Pulmonary Valve .... 503 
3. Arteriosclerotic and Syphilitic Endocarditis . . 504 
4. Combined Valvular Lesions 504 
G. Functional Diseases of the Heart 506 
1. Palpitation 507 
2. (a) Paroxysmal Tachycardia 508 
(b) Simple Tachycardia 510 
3. Bradycardia 511 
4. Arhythmia 512 
5. The Neurasthenic State 512 
Section IV. Diseases of the Blood and 
Hemopoietic Organs 
A. Anemia 514 
1. Symptomatic Secondary Anemia 514 
2. Primary or Essential 517 
(a) Chlorosis 517 
(b) Pernicious Anemia 519 
B. Leukemia . 530 
1. Leukocytic or Splenomyelogenous Leukemia . . . 530 
2. Lymphatic Leukemia 533 
3. Acute Leukemia 534 
4. Leukanemia 534 
5. Mixed Leukemia 535 CONTENTS 
PAGE 
C. Hodgkin’s Disease—Lymphoblastoma 536 
D. Purpura 542 
1. Secondary Purpura 542 
2. Primary Purpura 543 
(a) Purpura simplex 543 
(b) Purpura rheumatica (Schoenlein’s Disease) . 544 
(c) Purpura hemorrhagica (Werlhof’s Disease . . 545 
(d) Chronic Purpura 546 
(e) Henoch’s Purpura 547 
(f) Hemophilia 548 
E. Erythremia 549 
1. Primary .......... 549 
2. Secondary 551 
Section V. Diseases of the Digestive Apparatus 
A. Diseases of the Mouth (Stomatitis) 553 
B. Diseases of the Salivary Glands 557 
1. Mumps—Epidemic Parotitis 557 
2. Parotitis 557 
3. Mikulicz’s Disease ; . . . 557 
C. Diseases of the Pharynx 559 
1. Circulatory Anomalies 559 
2. , Pharyngitis 559 
(a) Acute Pharyngitis 559 
(b) Chronic Pharyngitis 560 
(c) Plcerative Pharyngitis 560 
(d) Phlegmonous Pharyngitis and Petropharyngeal 
Abscess 560 
(e) Ludwig’s Angina 560 
D. Diseases of the Tonsils 562 
E. Diseases of the Esophagus 562 
1. Acute Esophagitis 562 
2. Spasm and Paralysis of the Esophagus .... 565 CONTENTS 
PAGE 
3. Stricture of the Esophagus 566 
4. Cancer of the Esophagus 567 
5. Rupture of the Esophagus 568 
6. Dilatation—Diverticula 568 
F. Diseases of the Stomach 570 
1. Acute Gastritis 570 
2. Chronic Gastritis 572 
3. Dilatation of the Stomach—Gastrectasia . . . .576 
4. Gastroptosis—Enteroptosis 579 
5. Pyloric Obstruction . . . . . . . .581 
6. Gastric and Duodenal Ulcer 585 
7. Cancer of the Stomach 600 
8. Ilematemesis—Gastrorrhagia 613 
9. Gastric Neuroses 615 
G. Diseases of the Intestines 619 
1. Acute Enteritis—Acute Diarrhea 619 
2. Chronic Enteritis—Chronic Diarrhea .... 623 
3. Diarrheal Diseases of Early Childhood .... 627 
4. Celiac Disease—Diarrhea alba—Diarrhea chylosa . . 629 
5. Enteroptosis (Glenard’s Disease) 630 
6. Constipation—Obstipation 630 
7. Intestinal Obstruction 633 
8. Dilatation of the Colon 640 
9. Diverticulum of the Intestine 641 
10. Intestinal Cancer and Other Growths 642 
H. Diseases of the Appendix 644 
Appendicitis 644 
I. Diseases of the Peritoneum 659 
1. Acute Diffuse Peritonitis 659 
2. Chronic Peritonitis 662 
3. Tubercular Peritonitis 663 
4. New Growths of the Peritoneum 663 
J. Diseases of the Liver 664 
1. Jaundice 664 
(a) Hepatogenous (Obstructive) Jaundice . . . 664 
(b) Hemolytic (Toxic) Jaundice 668 CONTENTS 
PAGE 
(c) Hereditary Splenomegalic Jaundice . . .670 
(d) Icterus neonatorum 670 
2. Acute Yellow Atrophy of the Liver 673 
3. Circulatory Disturbances of the Liver . . . .676 
(a) Congestion of the Liver 676 
(b) Diseases of the Portal Vein 678 
(c) Diseases of the Hepatic Vein 679 
(d) Diseases of the Hepatic Artery .... 680 
4. Cirrhosis of the Liver 681 
5. Abscess of the Liver . . . . ; . . .704 
6. Neoplasm of the Liver—Cancer of the Liver . . .709 
7. Fatty Liver 712 
8. Amyloid Liver 712 
9. Echinococcus of the Liver 714 
10. Syphilis of the Liver 714 
11. Tuberculosis of the Liver 714 
K. Diseases of the Bile Passages and Gall-bladder . . . .714 
1. Acute Cholangitis 714 
2. Chronic Cholangitis 714 
3. Suppurative Cholangitis 715 
4. Acute Inflammation of the Gall-bladder . . . .715 
5. Chronic Cholecystitis 716 
6. Obliterative Cholecystitis and Cholangitis . . . .716 
7. Gangrene and Phlegmonous Cholecystitis . . . .717 
8. Cancer of the Gall-bladder 717 
9. Cholelithiasis 718 
L. Diseases of the Pancreas 734 
1. Pancreatitis 734 
2. Hemorrhage (Pancreatic Apoplexy) 737 
3. Necrosis of the Pancreas 738 
4. Pancreatic Calculi 738 
5. Pancreatic Cysts 738 
6. Pancreatic Neoplasms 739 
Section VI. Diseases of the Kidney 
Anomalies of the Urinary Secretion 741 
The Prognostic Significance of: 
(a) Albuminuria 741 
(b) Casts 749 CONTENTS 
PAGE 
(c) Hematuria 753 
(d) Uremia 762 
(e) Renal Sufficiency Tests 768 
(f) Bacilluria—Bacteriuria 774 
(g) Cliyluria 776 
(h) Phosphaturia 777 
(i) Oxaluria 779 
(j) Indicanuria 780 
(k) Urobilinuria 782 
(l) Other Substances . .785 
Diseases of the Renal System 788 
1. The Nephropathies 788 
(a) Acute Parenchymatous Nephritis . . . .788 
Nephritis of Pregnancy 794 
(b) Chronic Parenchymatous Nephritis . . .797 
(c) Chronic Interstitial Nephritis .... 804 
(d) Congested Kidney 811 
(e) Amyloid Kidney 814 
(f) Tuberculous Kidney—Tuberculous Nephritis . 815 
2. Surgical Diseases of the Kidney 815 
(g) Hydronephrosis 815 
(h) Nephrolithiasis 820 
(i) Neoplasms of the Kidney (including Hyperneph- 
roma) 825 
(j) Movable Kidney 828 
Suppurative Diseases of the Kidney . . 829 
(k) Pyelitis 829 
(l) Perinephric Abscess 834 
Section VII. Diseases of the Nervous System 
A. Diseases of the Peripheral Nerves 837 
I. Neuralgia 837 
(a) Trifacial Neuralgia (Tic douloureux) . . 841 
(b) Supra-orbital Neuralgia 841 
(c) Occipital Neuralgia 842 
(d) Intercostal Neuralgia 842 
(e) Mastodynia 843 
(f) Phrenic Neuralgia 843 
(g) Brachial Neuralgia 843 
(h) Lumbar Neuralgia 844 
(i) Sciatic Neuritis 844 CONTENTS 
PAGE 
II. Peripheral Neuritis 845 
1. Mononeuritis 846 
(a) Traumatic Neuritis 846 
(b) Postoperative Neuritis .... 846 
2. Multiple Neuritis (Polyneuritis) .... 848 
(a) Alcoholic Multiple Neuritis . . . 849 
(b) Postdiphtheritic Multiple Neuritis . . 850 
. (c) Lead Multiple Neuritis .... 850 
(d) Arsenical Multiple Neuritis . . . 852 
(e) Multiple Neuritis with Leprosy . . 853 
(f) Idiopathic Multiple Neuritis . . 853 
(g) Landry’s Ascending Paralysis . . . 854 
(h) Puerperal Multiple Neuritis . . . 854 
(i) Gonorrheal Multiple Neuritis . . . 855 
(j) Neuritis of Tuberculous Origin . . 855 
(k) Diabetic Neuritis 855 
III. Peripheral Paralysis 856 
Paralysis of the Cranial Nerves 856 
(a) Paralysis of Olfactory Nerve . . . 856 
(b) Paralysis of Optic Nerve 857 
Optic Neuritis 858 
Optic Atrophy 858 
Hemianopia 858 
Paralysis of Ocular Nerves 860 
(c) Paralysis of the Third Nerve .... 860 
(d) Paralysis of the Fourth Nerve . . . 861 
(e) Paralysis of the Sixth Nerve .... 861 
(f) Ophthalmoplegia 861 
(g) Paralysis of the Fifth Nerve .... 862 
Facial Hemiatrophy 863 
(h) Facial Paralysis 863 
Bell’s Palsy 864 
Pontine Facial Palsy 864 
(i) Facial or Mimic Spasm 866 
(Tic convulsive) 
(j) Paralysis of the Auditory Nerve . . . 868 
Tinnitus aurium 868 
Involvement of Vestibular Nerve . . 869 
Vertigo 869 
(k) Glossopharyngeal Paralysis .... 870 
(l) Pneumogastric Paralyis 871 
(m) Paralysis of the Spinal Accessory Nerve . 871 COVTEVTS 
PAGE 
(n) Spasm of the Trapezius and Sterno-cleido- 
mastoid 872 
(o) Paralysis of the Hypoglossal Nerve . . 873 
(p) Paralysis of the Phrenic Nerve . . .874 
(q) Hiccough—Spasm of the Diaphragm . . 875 
(r) Paralysis Due to Lesions of the Brachial 
Plexus 875 
(s) Paralysis Due to Cervical Rib . . .876 
(t) Paralysis of the Posterior Thoracic Nerve . 877 
(u) Paralysis of the Circumflex Nerve . .878 
(v) Paralysis of the Median Nerve . . .878 
(w) Paralysis of the Musculospiral Nerve . .878 
(x) Paralysis of the Ulnar Nerve . . .879 
(y) Lumbar and Sacral Plexus Paralysis . .879 
(z) Obturator Nerve Paralysis .... 880 
(aa) Paralysis of the Sciatic Nerve . . . 880 
(bb) Paralysis of the Gluteal Nerves . . .881 
(cc) Paralysis of the External Popliteal Nerve . 881 
(dd) Paralysis of the Internal Popliteal Nerve . 881 
(ee) Paralysis of the Sacral Plexus . . . 882 
(ff) Paralysis Due to Lesions of the Cauda equina 882 
IV. Tumors of the Peripheral Nerves 883 
Neuroma 883 
Disseminated Neurofibromata—von Recklinghausen’s 
Disease 883 
Elephantiasis neuromatosa 884 
B. Diseases of the Spinal Cord and Its Membranes . . . 885 
I. Diseases of the Afferent or Sensory System . . . 885 
1. Tabes dorsalis 885 
2. General Paralysis of the Insane .... 885 
3. Taboparesis 885 
4. Herpes zoster 885 
5. Hereditary Ataxia (Friedreich’s Disease) . . 887 
6. Marie’s Hereditary Ataxia 888 
II. Anterior Diseases—Diseases of the Efferent or Motor 
Tract 888 
1. Poliomyelitis Anterior—Infantile Paralysis . 888 
2. Landry’s Ascending Paralysis . . . .888 
3. Progressive Central Muscular Atrophy . . 888 
(a) Progressive (Central) Spinal Muscular 
Atrophy 889 CONTENTS 
PAGE 
(b) Amyotrophic Lateral Sclerosis . . 890 
(c) Bulbar Paralysis 891 
4. Progressive (Neural) Muscular Atrophy . . 894 
5. The Muscular Dystrophies 895 
I. The Muscular Dystrophies of Childhood 896 
1. Hypertrophic Muscular Atrophy. 896 
2. Atrophic Form .... 897 
II. Erb’s Juvenile Progressive Muscular 
Atrophy 897 
6. Myotonia or Amyotonia congenita (Oppen- 
heim’s Disease) 898 
III. Diseases of the Lateral Columns of the Cord . . . 899 
1. Primary Lateral Sclerosis 899 
2. Congenital Lateral Sclerosis (Little’s Disease) . 900 
3. Combined Lateral and Posterior Disease (Ataxic 
paraplegia) 901 
4. Amyotrophic Lateral Sclerosis (Charcot’s Disease) 902 
5. Erb’s Syphilitic Spinal Paralysis .... 902 
6. Secondary Spastic Paralysis 902 
7. Amaurotic Family Idiocy (Sachs’ Disease) . 903 
IV. Indiscriminate Lesions of the Spinal Cord . . . 904 
1. Myelitis 904 
2. Multiple Sclerosis of the Brain and Spinal Cord 908 
3. Pseudomultiple Sclerosis 913 
4. Abscess of the Spinal Cord 911 
5. Syringomyelia 915 
6. Tumors of the Spinal Cord 918 
7. Caisson Disease 927 
8. Affections of the Blood Vessels .... 927 
(a) Anemia of the Cord 927 
(b) Hyperemia of the Cord .... 928 
(c) Spinal Endarteritis—Arteriosclerosis . 928 
(d) Spinal Embolism and Thrombosis . . 928 
V. Diseases of the Spinal Membranes 930 
1. Hemorrhage into the Spinal Membranes and Cord 930 
2. Spinal Hematoma 931 
3. Spinal Meningitis 931 
(a) Spinal Pachymeningitis . . . . 932 
(b) Hypertrophic Cervical Pachymeningitis . 932 
(c) Acute Spinal Leptomeningitis . . . 933 
(d) Chronic Spinal Leptomeningitis . . 933 
(e) Postbasic Meningitis 934 CONTENTS 
XXV 
PAGE 
C. Diseases of the Brain and Its Membranes 934 
I. Diseases of the Membranes of the Brain . . . 934 
1. Pachymeningitis 934 
2. Leptomeningitis 937 
(a) Purulent Leptomeningitis. . . . 938 
(b) Serous Leptomeningitis .... 942 
I. Serous Meningitis . . . 943 
II. Acquired Hydrocephalus . . 943 
III. Congenital Hydrocephalus . . 944 
(c) Chronic Leptomeningitis . . . . 946 
3. Syphilitic Cerebral Meningitis .... 947 
4. Tuberculous Meningitis 947 
5. Cerebrospinal Meningitis (Epidemic) . . . 947 
II. Circulatory Disturbances of the Brain .... 947 
1. Anemia 947 
2. Hyperemia of the Brain 949 
3. Occlusion of the Cerebral Vessels . . . .953 
4. Cerebral Hemorrhage 957 
5. Encephalitis 973 
6. Cerebral Paralysis of Childhood . . . .977 
7. Abscess of the Brain—Suppurative Encephalitis 980 
8. Aneurism 987 
III. Tumors of the Brain 988 
IV. Parasites of the Brain 1002 
V. Cerebellar Diseases 1003 
D. Functional and General Diseases of the Nervous System . . 1005 
1. Hysteria 1005 
2. Traumatic Neurosis 1021 
3. Neurasthenia 1025 
4. Paralysis agitans 1033 
5. Chorea 1037 
6. Tetany 1046 
7. Epilepsy 1046 
8. Migraine 1059 
9. Occupational Paralyses and Neuroses 1064 
10. Infantile Convulsions 1065 
E. Diseases of the Sympathetic System 1066 
Vasomotor and Trophic Disorders 1066 
1. Erythromelalgia 1066 
2. Raynaud’s Disease . . 1069 CONTENTS 
PAGE 
3. Acroparesthesia 1074 
4. Angioneurotic Edema 1075 
5. Scleroderma 1077 
6. Adiposis dolorosa 1978 
7. Intermittent Dropsy of the Joints 1079 
8. Hereditary Edema of the Legs (Milroy’s Disease) . 1080 
9. Paralysis of the Cervical Sympathetic .... 1081 
10. Irritation of the Cervical Sympathetic . . . 1082 
11. Vagotonia 1082 
12. Sympathicotonia 1083 
Section VIII. Diseases of the Locomotor System 
A. Diseases of the Muscles 1084 
1. Myalgia—Myositis 1084 
2. Progressive Myositis ossificans 1085 
3. Thomsen’s Disease (Myotonia) 1085 
4. Paramyoclonus multiplex 1086 
5. Akinesia algera 1086 
B. Diseases of the Joints 1088 
Destructive Chronic Polyarthritis 1088 
(a) Arthritis deformans 1088 
(b) Chronic Articular Rheumatism ..... 1088 
C. Diseases of the Bones 1093 
1. Osteitis deformans (Paget’s Disease) 1093 
2. Leontiasis ossea 1095 
3. Hypertrophic Pulmonary Arthropathy .... 1096 
4. Eragilitas ossium 1097 
Section IX. Metabolic Faults 
1. Gout 1098 
2. Diabetes mellitus 1106 
3. Diabetes insipidus 1122 
4. Obesity .1124 
5. Rachitis 1129 
6. Achondroplasia 1131 
7. Osteomalacia 1131 
8. Scorbutus 1132 
9. Multiple Myeloma 1134 CONTENTS 
Section X. Diseases of the Ductless Glands 
PAGE 
A. Thyroid Diseases 1136 
1. Growths 1136 
(a) Tumors—Thyroiditis 1136 
(b) Goiter 1137 
2. Hyperthyroidea 1139 
(a) Exophthalmic Goiter ...... 1139 
(b) Myxedema, Cretinism 1153 
B. Diseases of the Pituitary Gland 1158 
1. Hypopituitarism 1158 
Infantilism 1158 
2. Hyperpituitarism 1158 
Acromegaly 1160 
C. Diseases of the Suprarenal Gland 1163 
Addison’s Disease 1163 
D. Diseases of the Thymus Gland . 1163 
1. Hypertrophy 1163 
2. Atrophy 1164 
3. Status thymo-lymphaticus 1164 
Lymphatism 1164 
E. Diseases of the Parathyroid Gland 1165 
Tetany 1165 
F. Diseases of the Spleen 1169 
1. Secondary Splenomegaly 1169 
(a) Passive Congestion 1170 
(b) Abscess 1170 
(c) Perforation 1170 
(d) Perisplenic Abscess 1170 
(e) Perisplenitis or Capsulitis 1170 
(f) Tuberculous Spleen 1170 
(g) Amyloid Spleen 1170 
(h) Syphilis 1170 
(i) Uncomplicated Enlargement in Otherwise Healthy 
Subjects 1170 CONTEXTS 
PAGE 
(j) Chronic Enlargement with Polycythemia . . 1170 
(k) Enlargement with Liver Cirrhosis . . . .1171 
(l) Rupture of the Spleen 1171 
(m) Cyst of Spleen 1171 
(n) Infarct 1171 
2. Primary Splenomegaly 1171 
(a) Gaucher’s Disease (Primary Endothelioma) . . 1171 
(b) Banti’s Disease—Splenic Anemia .... 1172 
3. Mobile Spleen 1173 
Section XI. Intoxications 
1. Alcoholism 1175 
(a) General Consideration of the Alcoholic Habit. . 1175 
(b) Acute Alcoholic Poisoning 1179 
(c) Chronic Alcoholism 1180 
(d) Delirium tremens 1183 
2. Morphinism 1185 
3. Cocainism 1187 
4. Lead Poisoning 1187 
5. Arsenical Poisoning 1193 
6. Mercurial Poisoning 1195 
7. Carbon Monoxid Poisoning 1196 
8. Pellagra 1197 
9. Beriberi 1201 
10. Food Poisoning (Ptomain and Leukomain Poisoning) . 1203 
Section XII. Diseases Due to Physical Agents 
1. Sunstroke (Heat Exhaustion) 1205 
2. Caisson Disease 1207 
3. Mountain Sickness 1209 
LNDEX 1211 THE PROGNOSIS OF 
INTERNAL DISEASE The Prognosis of Internal Disease 
General Considerations 
Medicine has not grown to its present advanced position in logical 
sequence. 
Prognosis is the 'prescience of disease, the art of foretelling the progress 
and termination of disease. The foreknowledge thus obtained is included 
in the term uprognosis.” 
Prognosis, therefore, includes a forecast of the patient’s future, not 
only whether the disease is curable, but how long under existing conditions 
life may be prolonged, what influence the disease is likely to have on his 
activities and the enjoyment of life, what factors may lead to its advance 
and what will influence its course favorably; hence it stimulates rational 
treatment. 
Leyden has truthfully said “Prognosis represents the very quint- 
essence of the physician’s knowledge.” 
The literature which has accumulated on the subject of the Prognostics 
of Disease, is comparatively meager. (See Bibliography appended, and 
full literature in Volumes XI, 1st Series, and XIII, 2nd Series, Index 
Catalogue of the Library of the Surgeon-General’s Office, United States 
Army). 
The history of medicine proves that the disciple of our art Hippocrates, 
was more concerned with the prognostics of disease than with any other 
question connected with its study. Prognosis became the first object of 
all Theory connected with Medicine. 
“A glimpse into ancient medical literature shows that more space was 
devoted to the Prognostics of Disease than is occupied for a similar 
purpose in the modern compendium” (Xeuburger). It is a fact that 
formerly, prognosis was made without accurate diagnosis, without patho- 
logic knowledge; today prognosis is based not only on subjective symp- 
toms but upon the results of thorough physical examination, the con- 
sideration of pathologic conditions, the revelations of the laboratory and 
a well digested previous history—a consideration of all of the features 
made clear by thorough investigation. This is not all as we shall see; 
the paramount facts are also offered by the picture which the patient 
1 2 
THE PROGNOSIS OF INTERNAL DISEASE 
presents. A projection upon the diagnostic screen is made, not from the 
study of text books or monographs, but as a result of years of experience, 
painstaking analysis and correct reasoning. 
Prognosis is often made without accurate diagnosis or positive knowl- 
edge of the anatomic lesions, and yet it proves fairly valuable for the 
immediate future in important cases, pending the acquisition of exact 
knowledge gained from further study of the individual case. 
Hippocrates3 rules of practice were based on experience; he was, as 
his critics have said “the physician of experience and common sense.” 
“What he appears to have studied with particular attention is the natural 
history of diseases, that is to say, their tendencies to a favorable or fatal 
issue; and without this knowledge, what can all medical practice be hut 
blind empiricism ?” . . . “The physician who cannot inform his patient 
what would be. the probable issue of his complaint, if allowed to follow 
its natural course, is not qualified to prescribe any rational plan of treat- 
ment for its cure” (Francis Adams). Hippocrates was fully conscious 
of the fallaciousness of experience and “therefore never exempts the ap- 
parent results of experience from the strict scrutiny of reason.” To prove 
this great truth he made the following, the first of his aphorisms:— 
Aphorisms of Hippocrates (I) :— 
“Life is short, and the Art long; the occasion fleeting; experience falla- 
cious, and judgment difficult. The physician must not only he prepared 
to do what is right himself, hut also to make the patient, the attendants, 
and externals co-operate.” 
Galen’s Commentary on this aphorism shows that he interpreted it as 
meaning “The occasion is fleeting, experiment is dangerous and decision is 
difficult.” 
Galen remarks that it is “hazardous to experiment in a case which 
involves the life of a human being, and that it is difficult to catch the 
truth in medicine, as is evident from the circumstances of the profession 
being divided into so many opposite sects” (Adams). 
Hippocrates was conscious of the power of Nature to cure disease. He 
upheld the principle that “Nature is the physician of diseases’’ (Hippo- 
crates). “Nature although untaught and uninstructed does what is 
properSydenham placed his stamp of approval upon these philosophical 
tenets by quoting them frequently, while Galen’s Commentary remains 
a classic, full of interesting and profitable data, “a fine specimen of the 
medical philosophy of the ancients.” 
. Herophilus (300 a. d.) was the first commentator on Hippocrates of 
whom we have any record; unfortunately his Commentaries were never 
preserved so far as we know. He was also the first to study the character 
of the pulse. GENERAL CONSIDERATIONS 
3 
It is of interest to note that no mention is made in the “Books of the 
Epidemics” on the characters of the arterial pulse and contagion. Hippo- 
crates, as well as his contemporary Thucydides, must have appreciated 
the contagiousness of the plague which the latter described clearly, and 
taught that the disease was contagious. 
Adams’ conclusions concerning the authenticity of the works of “The 
Father of Medicine” may be accepted as being as near the truth as we 
can ever hope to get: 
1. “All the authorities, ancient and modern, who have investigated the 
question regarding the genuineness of the works which have come down to 
us under the name of Hippocrates, are agreed that a considerable portion 
of them are not the production of the author himself.” 
2. “It is almost universally admitted that the following treatises are 
genuine, viz:— 
The Prognostics 
On Airs, et cetera 
On Regimen in Acute Disease 
Seven of the Books of Aphorisms 
Epidemics I and III 
On the Articulations 
On Fractures 
On the Instruments of Reduction 
The Oath” 
Adams further holds that it may be conceded with considerable cer- 
tainty that the following treatises are genuine though the “evidence in 
their favor is not so strong as it is with regard to the preceding list 
On Ancient Medicine 
On the Surgery 
The Hand 
On Ulcers 
On Fistulae 
On Hemorrhoids 
On the Sacred Diseases” 
The first “Prorrhetics” and the “Coacae probably ante- 
dated the time of Hippocrates. 
“It appears to me a most excellent thing for |(fljfcphysician to cultivate 
prognosis; for by foreseeing and foretelling i:r»T|(||eresence of the sick, 
the present, the past, and the future, and expMfl$®lhe omissions which 
patients may have been guilty of, he will be ,’e readily believed 4 
THE PROGNOSIS OF INTERNAL DISEASE 
to be acquainted with the circumstances of the sick, so that men will have 
confidence to entrust themselves to such a physician. And he will manage 
the case best who has foreseen what is to happen from the present state 
of matters” (Hippocrates). 
The Book of the Prognostics continues the most learned systematic 
consideration of the subject which was included in fragmentary references 
to but few individual diseases until 1G01 when Prosper Alpinus, Pro- 
fessor of Medicine at Padua, published a most remarkable dissertation on 
Prognostics “in confirmation of the Hippocratic method” with the title 
“De Praesagienda Vita et Morte Aegrotantium,” in seven volumes. The 
work was translated by R. James, M.D., and published in London in 
1746 with an introduction by the renowned Boerhaave, taken from an 
edition of Alpinus published in Leyden in 1709. Since that day there 
has been no attempt to present a systematic work by a single clinician 
dealing with the leading feature of all internal diseases which bear upon 
their prognosis. 
J. Harvey published his “Praesagium Medicum or the Prognostick 
Signs of Acute Diseases, Established by Antient Observation and Ex- 
plained by the Best modern Discoveries” in London in 1706; a work 
which created a sensation in the profession. 
The leading publications dealing with the separate consideration of the 
prognostics of disease during the nineteenth century were “Traite Ele- 
mentaire de Diagnostic de Prognostic, et cetera,” par Leon Rostan, Paris 
1830; Cyclopedia of Practical Medicine, Vol. III., article “Prognosis” 
by Edward Ash, London 1834; a unique article “On Prognosis,” by 
William Farr, in the British Medical Almanack, 1839; “Observations 
of Prognosis” Vol. XLIV, Guy’s Hospital Report 1887, P. H. Pye- 
Smith, and another article by Pye-Smith: “Observations upon Certain 
Elements in General Prognosis, upon the Particular Prognosis of 
Phthisis and of Enteric Fever.” An oration on Prognostics was deliv- 
ered before the Hunterian Society of London in 1858 by Doctor Munk, 
from which the following is quoted to add the valuable included his- 
toric data:— 
“Coincidently with the return from the polluted stream of Arabian Medi- 
cine to the pure fountain of Grecian physic, was the renewed cultivation of 
a rational and scientific prognosis. It was in connection with a humoral 
pathology that prognosis made the greatest progress and achieved its 
highest triumphs.” “The doctrines of solidism on the other hand 
have uniformly proved inimical to the study of prognosis” 
“Prognosis was but little regarded by Hoffman, and still less by Cullen. 
To the neglect it experienced from the luminary of the Edinburgh School, 
its decadence in this country (England) is to be attributed. The pupils 
of Boerhaave and of the school over which this name and example con- 
tinued to shed luster, were still cultivating prognosis in all its minutiae, GENERAL CONSIDERATIONS 
5 
and applying its rules with startling accuracy at the very time when 
Cullen’s genius blazed above the medical horizon; and it was not until 
these had died off, and Edinburgh had taken that place in public esti- 
mation as a medical school, which Leyden had previously enjoyed, that 
the regular minute and systematic study of a rational prognosis became 
extinct in this country.” 
Dyce Duckworth in the paragraph following the above which he also 
quotes, writes: “I think that just consideration of the prevailing doctrines 
of pathology at the present time may encourage us to hope that renewed 
attention and study may henceforth be directed to the subject of prog- 
nostics.” 
Reynolds in his System of Medicine in 1866 declared “the practical 
test of a true science is the power which it confers of ‘prevision’ or knowing 
what will follow hereafter.” “When we can prognosticate with 
certainty, medicine will have become a science” “Life is too subtle 
for us to know or measure all its possible contingencies.” 
The more recent English publications include the classic contributions 
of Sir Dyce Duckworth (London 1896)—from whom, for these General 
Considerations I have gained many facts; the oration of George Dock on 
“Prognosis, Its Theory and Practice” (The Journal of the American 
Medical Association, 1904). In German, Franke’s “Lehre von der Bedeu- 
tung des Pulses und die Respirations Frequenz fiir die Prognose acuter 
fieberhafter Krankheiten” (Beitr. z. Pathol, u. Physiol., Berlin, 1878, 
III., p. 303) remains a classic in medical literature. They also include 
C. Gerhardt’s “Leber Vorhersage am Krankenbette (Munch. Med. Woch- 
enschr., Hov. 24, 1896) ; the contribution of Moritz E., “Ueber Lebens 
Prognose,” 1905; an article by Neuburger, “Zur Entwicklungsgeschichte 
der Prognostik” (Wiener Med. Presse, 1907) ; and the brochure of Nor- 
bert Ortner on “Klinische Prognose,” Wien, 1908. Short, in England, 
with the assistance of over twenty clinicians has edited an Index of 
Prognosis which includes surgical affections (London and Hew York, 
1915). 
The eloquent Address in Medicine, on Medical Prognosis, delivered by 
Chauffard at the Seventeenth International Congress of Medicine (London 
1913) has awakened anew the interest in the Presage of Disease. Chauf- 
fard clearly demonstrated that the paths to prognosis are open by the study 
of morbid disturbances, and by the “analytical method with the help of 
a more and more penetrating technique.” 
For safe prognosis we assume that pathology is but perverted or, as 
Chauffard says, “deviated” physiology, and disease, a disturbance of nor- 
mal functions. We must associate with our knowledge of pathology a thor- 
ough acquaintance with the resulting functional disturbances. But while 
we gauge the result of disease on the various functions of disturbed organs 
there are innumerable factors which influence the prognosis of disease. 6 
THE PROGNOSIS OF INTERNAL DISEASE 
Exogenous and endogenous influences must be considered. 
The defensive reaction of the blood and the cellular elements to bac- 
terial contamination and mechanical insult, the prompt alignment of the 
protective forces against the invading army, become at once factors with 
which the prognostician must rechon. 
There are factors of which we are still uncertain which lead to the 
formation of antibodies, stimulate cellular elements to activity and increase, 
provide the blood with opsonins and other protective substances, produce 
protective exudates, stimulate Organs to compensatory action, promptly 
arouse the innumerable “factors of safety” which are present in almost all 
of our organs (Meltzer), and light to activity that innate, indefinable 
resistance which is so prominent in some and so feeble in others—all of 
which are potent factors for rational prognosis. 
The influence of age is always important. Experience teaches how 
variable this is in different diseases. Diseases which are well borne by the 
young are often promptly fatal in the adult and in the aged. Thus diabetes 
is uniformly fatal during early life, often without serious consequences 
after the thirtieth year; pneumonia and typhoid fever on the other hand 
show a reversal of this prognosis; endocarditis following or associated with 
rheumatism in the young is always ominous ; in the adult it is less serious ; 
arteriosclerosis is among the conditions which are fatal during early life; 
the aged may live on with advanced arterial change with but few or no 
symptoms. 
An element which often influences prognosis unfavorably is the toler- 
ance of organs to pathologic change during long periods, without revolt. 
Early diagnosis improves the prognosis of most diseases. 
The tolerance of the stomach, intestines and other organs during long 
periods to invading cancer or other organic diseases without subjective 
manifestations brings the victim to the physician long after the initial 
period of the disease. The gradual unobserved advance of arteriosclerosis 
with kidney invasion is another example of insidiously increasing and un- 
recognized, but serious, disease. 
The localization of lesions is another factor which influences prognosis 
materially. The same general pathologic change so localized as to allow 
continuance of function practically unchanged, offers a more favorable 
prognosis than does a similar deposit so localized as to interfere at once 
with the necessary productive power of the organ. 
The influence of occupation in inviting disease and in fighting it is 
among the important questions to be considered in connection with prog- 
nostics. 
The increase of cardiovascular lesions dependent upon changed social 
and business conditions, the alarming arterial breakdown in men and 
women in the professions, especially the medical, the increase of cancerous 
diseases with advancing civilization, are among the problems which demand GENERAL CONSIDERATIONS 
7 
serious thought and attention in the attitude of the clinician to the indi- 
vidual and to the public. 
The influences of “constitution” and the “diatheses” on prognosis, par- 
ticularly during early life, are paramount. The inherent endogenous fac- 
tors which so change the blood plasma of children burdened by diathesis 
remain unexplained; they exist and handicap the child in the race of life. 
The knowledge of the presence of such condition makes it possible for the 
parent, aided by the attendant, to supply the resistance which in many 
instances proves sufficient to bridge the child over critical periods. 
The resistance which the different races offer to disease is among the 
interesting studies connected with prognosis, as well as the immunity which 
certain sections enjoy. Thus there is a decided variation in the vulner- 
ability between the light and dark complexioned races. Dyce Duckworth 
says: “The vital resistance and invulnerability of the Hebrew race is, to 
my mind, very noteworthy. So much so is this the case, that I am wont to 
frame a better prognosis generally for Jewish patients under all circum- 
stances.” In spite of this fact diabetes mellitus is most prevalent among 
the Jewish race. 
The negro invites tubercidosis and smallpox, and in him, both diseases 
are surprisingly fatal. 
The influence of habits, alcohol and intemperance, early training, exer- 
cise, exposure, environment, social status and the innumerable factors 
which arise in individual cases under the many conditions of life, each 
demands special consideration and proves the complex nature of prognosis. 
The varying character of epidemics, malignant during one outbreak, 
benign in another; the milder character of the cases toward the end of epi- 
demics, the seasonal influences, the variation in the virulence of the sepa- 
rate strains of infecting organisms, the immunity to infection against cer- 
tain disease-producing germs which often exists in the individual, the dif- 
ferences in disease to leave permanent immunity after a single infection 
and the predisposition to repeated infections with a like offender, often 
remain without satisfactory explanation, but all have a direct bearing on 
prognosis. 
There are facts which influence the acute infections, with which it is 
always safest to remember the admonition of Hippocrates: “In acute 
disease it is not safe to prognosticate either death or recovery.” 
It is equally important for the conscientious clinician to consider the 
fate of the descendants of his patients as well as their antecedents (family 
history). The application in practice of the Laws of Heredity demon- 
strated by the teachings of Mendel and his followers will prevent untold 
misery to many, during many generations. The improving of the “racial 
qualities” as advocated by the modern science of Eugenics cannot be ac- 
complished without the cooperation of the clinician. 
The questions connected with prognosis include the after effects of dis- 8 
THE PROGNOSIS OE INTERNAL DISEASE 
ease as well as the relations of the infected individual to his surroundings. 
The prognostics of the infections teach the urgent need of long surveillance 
of the individual patient and the recognition of the dangers to vital organs 
after acute disease. This is particularly true of rheumatism, scarlet fever, 
pneumonia, typhoid fever, influenza and the exanthemata. 
The infected individual relieved of his acute symptoms may still he 
dangerous as a “carrier ’ and often becomes the starting point of far- 
reaching disease. 
The milder infections are as dangerous to their surroundings as are 
the more malignant and should he so considered by the proper authorities. 
The influence of neurophathic tendencies and the traumatic neuroses 
on prognosis is not to he lightly regarded. What Sir James Paget so 
happily named “the Mimicry of Disease” includes a chapter in medicine 
(Neuromimesis), which for its full interpretation and prognostic signifi- 
cance requires enormous knowledge, tact, and a judicial mind. The 
underlying anomalies leading to the complex of Neurasthenia may be 
said to include the same requirements for reliable prognosis and its rational 
treatment as the bJeuromimeses. 
Phagocytosis and extra cellular digestive processes are elements of 
enormous value in prognosis. The cure of bacterial disease results from 
the destruction of the micro-organism in the organ invaded and in the 
blood, by the aid of phagocytosis and the activity of extra cellular diges- 
tion. 
Iloekten has demonstrated in pneumonia—and this is probably true 
of other infectious disease—the general defensive reactions of leukocytes 
and the production of antibodies “of which the opsonins are the best 
known.” With inadequate destruction of pathogenic bacteria in indi- 
vidual disease and their proliferation, with the absence of antibodies from 
the blood the prognosis is bad; there is no army to meet the invadingf 
forces. 
The influence of acute infections on existing chronic diseases is often 
overlooked, faultily interpreted or not considered at all in framing the 
prognosis. The favorable influence of acute infection on the course of 
chronic disease at times has been fully appreciated, and the literature 
of the subject contains a number of striking examples taken from the 
experiences of acute clinical observers. In occasional cases chronic proc- 
esses of long duration have been so favorably influenced as to disappear 
entirely. In some the disease is held in abeyance only during a limited 
period, while in other cases the clinical picture of the disease may be 
materially changed by the added infection. 
Gerhardt reports: 
I. Trigeminal neuralgia relieved during acute pneumonia. 
II. Tuberculous ascites has after profuse diuresis been relieved during 
croupous pneumonia. GENERAL CONSIDERATIONS 
9 
III. Chronic arthritis—so-called rheumatism—has been without symp- 
toms during acute tonsillitis. 
IV. Acute psychosis is often controlled during erysipelas. 
V. Measles has relieved the pressure symptoms of brain tumor. 
VI. Chronic malignant tumors, facial carcinomata (epitheliomata) have 
often shown marked improvement, even cure, after erysipelatous 
infection. 
Kopff has seen subacute arthritis promptly cured spontaneously by 
erysipelatous complication. 
Measles has cured eczema capitis, chronic pemphigus, chorea, epilepsy 
and urinary incontinence. 
One infection grafted on another is likely to influence the primary 
infection. Splenic fever is prevented experimentally by inoculation with 
the erysipelatous streptococcus, prodigiosis, staphylococci or the Fried- 
lander germ. The influence of pneumothorax on the chronic tuberculous 
lung disease is thoroughly recognized. 
1STaunyn has observed the favorable influence on sugar loss, without 
increase of hyperglycemia with the intercurrent infections of diabetics. 
There are cases of pernicious anemia which with tuberculous infec- 
tion show an improved blood picture (Diabella). 
The influence of tuberculous disease on the leukemias, also other 
infections, is often striking and favorable (See Leukemia for Eisner and 
Groat, also Dock’s references). 
Collective investigation of disease has resulted in the accumulation of 
data which strengthen prognosis and make it more certain than ever 
before. Among the diseases thus studied are tuberculosis, typhoid fever, 
the results of inoculation against the latter and against smallpox and 
diphtheria. The collective data which prove the prognostic value of the 
recognition of the specific nature of many brain tumors and the dependence 
of many liver enlargements and diseases on syphilis, and their disappear- 
ance under specific treatment are noteworthy. The subject of Cretinism 
and its prognosis has been enormously advanced by the collective investiga- 
tion made in England. A basis for classification was given and the in- 
fluence of the organic extracts—the introduction of which is easily the 
most marvelous advance made in medicine during the past century. The 
prognostic significance of the general symptoms (pulse, respiration, fever, 
et cetera) will be considered with the separate diseases. 
Tact and humanity combined, with all that is complete and highest 
in our art, a full knowledge of all that makes the cause and recognition 
of disease possible, scientific methods of treatment with reasoning ability 
sharpened by well digested experience and a delicate poise, are among 
the requirements necessary for prognosis. 
The question often arises in the course of practice whether it is wise 10 
THE PROGNOSIS OF INTERNAL DISEASE 
to give an unfavorable prognosis in the individual case. The tactful 'phy- 
sician will rarely do harm to his patient by leading him to an appreciation 
of his condition without robbing him entirely of the hope to which he is 
entitled. The element of Hope in prognosis ought never to be disre- 
garded. It means much to be aided by a suggestion which stimulates hope. 
In cases of positively fatal diseases this will occasionally prolong life; 
if it does not do this, it certainly adds materially to the comfort of the 
individual and makes pain and mental pang more bearable. The power 
which the experienced physician holds over the patient for good or ill, 
by giving thoroughly considered and honest prognosis, is enormous. Much 
depends upon the method and tact of the attendant. 
Patients with acute infectious diseases rarely inquire themselves as 
to the outcome; those afflicted with sub-acute or chronic ailments unless 
they are deluded and fail to appreciate the seriousness of their maladies 
are eager for an honest prognosis. I have always contended that either 
the patient, some interested member of his family or close friend is en- 
titled to such information concerning the course of the disease as the 
physician can give with reasonable certainty. Distortion and misunder- 
standing cannot always be prevented. Where prognosis is impossible in 
the presence of a large element of uncertainty, the ignorant as well as 
the intelligent will respect the physician more for having candidly and 
without equivocation given expression to an opinion which proves his 
limitations than to a prognosis which finally proved to be incorrect. 
Patients when properly informed are led to a thorough appreciation of 
the gravity of their condition, but also understand that the physician is 
not infallible and that in the may come to the rescue. Further, 
the tactful physician, with patilfc even of ordinary intelligence, can so 
frame his prognosis without injurifgfcs to lead to the peace of mind which 
follows attention to the requiremeh®pf religion and to material affairs. 
In my experience I have invariab1|f|$imong our Catholic patients in 
hospital and in private practice given UlSkple time for the administration 
of the rites of the church in all cases where life seemed threatened by 
disease, usually with comfort resulting, without unfavorable influence 
on the course of the disease; in many cases the fight has been renewed 
and won. 
Cruel and heartless prognoses which rob the patient of all hope are 
never justified; one can be truthful without being barbarous. 
Thoughtless and unqualified prognoses have often led to sudden death 
and suicide. The blunt and inconsiderate prognosis of ultimate blindness 
in a case of locomotor ataxia in one of our patients made bv a busy, 
thoughtless ophthalmologist after a single examination of the background 
of the eye, without a knowledge of the previous history of the case of 
long continued eye symptoms, was followed by the suicide of the patient 
within the following twenty-four hours. GENERAL CONSIDERATIONS 
11 
The physician in many cases needs to he guarded lest he betray his 
feelings during the examination of the patient before he has thoroughly 
assimilated the facts in the case sufficient to lead to a diagnosis. 
Gardner says “Beware the unguarded word! Beware the unguarded 
hesitation! Beware even the unconscious sigh.” 
The setting of a time limit in framing prognosis is indiscreet, unsafe, 
unscientific. The physician may guess right and thus strengthen himself 
in the minds of the ignorant, but to the thinking layman and to the 
scientific, such a forecast is without value and weakens faith in the 
profession. 
Optimism in prognosis whenever honestly possible is justified. “It is 
1 ot only the privilege of the physician but his bounden duty” to continue 
hopeful, for it may turn the scale in favor of the patient and start him 
toward recovery. Unwarranted optimism, however well intended, may 
lead to embarrassment and should not be encouraged. 
Honest suggestion with prognosis is an asset which belongs to the 
physician’s armamentarium. Though we may not always be justified 
in giving hope of complete cure, partial relief in many cases may be pre- 
dicted. We are often certain that the underlying pathologic condition 
can never be removed, but life may be prolonged and usefulness con- 
tinued. Percival’s advice in this connection is wholesome. “A physician 
should not be forward to make gloomy prognostications, because they 
savor of empiricism, by magnifying the importance of his service in the 
treatment or cure of disease.” . . . He should “give to the friends of 
the patient timely warning of danger, wffien it really occurs and even to 
the patient himself, if absolutely necessary.” 
Hot infrequently we are for a time, unless on guard, misled to change 
an original diagnosis and discredit prognosis. This is often true in cases 
of pernicious anemia, when for a time the disease remains stationary or 
improvement continues during long periods; in cases of ulcer of the stomach 
and duodenum, when symptoms disappear, but finally recur; in leukemia, 
in which modern methods of treatment lead to surprising but temporary 
reduction of lymphocytosis; in cases of cancer, where during long periods 
of latency the clinical features are entirely changed. 
In early life, we know the baneful influence of tuberculous glands; long 
periods of health may follow their neglect but in the end the original 
prognosis must stand. 
So, too, we are justified in calling attention to the grave import of the 
neglect of treatment of many diseases, in spite of few or annoying sub- 
jective or objective symtoms. 
The early diagnosis correctly made must always remain the foundation 
of authentic prognosis. 
The physician as his experience grows reaches conclusions wffiich mod- 
ify prognosis from his general survey of the patient, exclusive often of 12 
THE PROGNOSIS OF INTERNAL DISEASE 
physical signs and subjective complaints. The physiognomy, the facies of 
the patient, the expression, the brilliancy or dullness of the eye, the way in 
which the patient lies or handles himself in the midst of serious disease, 
more particularly the infections; it is in short the picture which allows of 
no description, which cannot be defined, which impresses the clinician 
and materially influences the forecast. Dyce Duckworth has well said: 
“The organs may be found in detail free from structural disease, but there 
may be appearances and features indicative of progressive failure not yet 
registrable by the stethoscope or the test tube, of which the significance is 
of the last importance, and these may escape recognition and appraise- 
ment. ... A little more attention to the individual, his aspect, his gait, 
and his manner, would sometimes be well repaid in a sounder appreciation 
of his life value. ... I am constantly training students to begin by look- 
ing at their patients.” We often fail to take the time “for a meditative 
survey” of facts in order “adequately to apprehend the general laws 
which underly and govern them.” (Duckworth.) 
All of these facts prove that the art of prognosis can never be acquired 
from boohs. The clinician will rarely fail if he has the ability to read 
disease, if he correctly appreciates that added to his scientific knowledge, 
gained after painstaking examination and investigation, divorced from 
the test tube and the microscope, there is much which the ready eye sees 
which must influence him in treatment and in prognosis. Sir Jonathan 
Hutchinson was profoundly impressed by the lectures and clinical teach- 
ings of Laycock, afterwards Professor of Medicine in Edinburgh, for he 
taught the “value of the general appearance of physiognomy of the patient 
as an indication of his physical condition.” 
“An entirely modern idea—but one wdiich should imbue our minds 
nowadays—is that of defining in each particular case the mutual relation- 
ship between those three fundamental elements of medical judgment; to 
know, to foresee, to act.” (Chauffard.) 
“As observation becomes more accurate, as the number of observed 
cases increases, and as classes are better and better distinguished, the 
nearer will the physician be able to approach an accurate prognosis, though 
the time when any sufficient rule can be applied to individual cases must 
long be out of our sight and the application of any approximate rules must 
long be subordinate to the instinctive tact of the educated physician him- 
self, who alone can apprehend the sum of the peculiarities which must 
modify their application to individual instances” (Allbutt). 
With this statement before us, mindful of the many perplexing prob- 
lems included in Medical Prognostics, I hesitated to present any mate- 
rial to the profession until I had a long and broad experience in both 
private and hospital practice. 
I have sought in the consideration of the separate diseases to consider 
the cause and nature of the pathologic processes in connection with symp- GENERAL CONSIDERATIONS 
13 
toms and signs and to add to these my knowledge of the outcome of the 
combinations in the series of cases which served to supply the material. 
As I said in the preface, my desire is to bring comfort to the physi- 
cian, and through him benefit to the patient; this I expect to do hv 
stimulating the study of the forecast of disease through pathologic knowl- 
edge, diagnosis—as accurate as it can he made in the present state of our 
knowledge—with tact and humanity. 
“He who remains silent will not easily err. He will never shoot at a 
target, will therefore never miss it, but he will never he a thorough marks- 
man” (Gerhardt). 
We will often be disappointed and uncertain, “but since the science 
of prognosis is one of the loftiest summits of medicine” (Chauffard) we 
are never to slacken our pace. To make the supreme effort is our duty than 
which there is no greater stimulus to the active physician. 
References 
Adams (Francis). Preliminary discourse. In: Works of Hippocrates, 15. 
Allbutt. System of medicine. 1896, Introduction, i. 
Chauffard. Address on Medical Prognosis. In: Medicine. 17. Internal. Congress of 
Med., 1913. 
Duckworth (Dyce). The sequels of disease and prognosis, London, 1896. 
Gardner. Brit. Med. J., London, 1896, Feb. 10, 1912, 285. 
Gerhardt. Ueber Vorhersage am Krankenbette. Munch, med. Wch., Nov. 24, 1896. 
Hippocrates. Epidemics. Book i. 
Prognostics. 
Prognostics. 19, sect. ii. 
Hektoen. J. Am. M. Ass., Chicago, Jan. 24, 1914. 
Leyden. Ueber Prognose der Herzkrankheiten. Berlin, 1889. 
Meltzer. Harvey Lecture. 1907. 
Paget (James). Clinical lectures, etc. 
Percival. Manchester letter. 1803, 31. 
Pye-Smith. Sheffield Med. J., part ii., i. 
Neuburger Zur Entwickelungsgeschichte der Prognostik. Wien. med. Presse, 1907, 1. 
Reynolds. System of Medicine. 1866, Introduction, i, 21. 
Short. Index of prognosis. London, 1915. 
Note.—(See Text—General Considerations) 
Additional References to General Considerations 
Diabella. Ztschr. f. klin. Med., Bd. Ixxi, 284- 
Eisner & Groat, also Dock. See References—Leukemia. 
Gerhardt. Mitth. Grenzgeb. d. Med. u. Chirurg., xxv. 
Kopff. Berl. klin. Wchnschr., 1882, 290. 
Naunyn. Diabetes. 2 Aufl., 179 ff. / 14 
THE PROGNOSIS OE INTERNAL DISEASE 
For influence of artificially produced changes, see 
Donath. Injection of nuclein. Int. Med. Congress, 1909. 
Ref. Centralbl. f. Neurol., 1909, 1182. 
Fischer. Injection of nuclein. Prager med. Wchnschr., 1909. 
Pilcz. Tuberculin injection. Wien. med. Wchnschr., 1907. Section I 
Specific Infectious Diseases 
A« Protozoan Infections 
I. Syphilis 
Lues 
Syphilis is a specific disease due to the Treponema pallidum of Schau- 
dinn (1905), which invades the blood and all tissues of the body from the 
primary and local lesion—the latter characterized by ulceration and in- 
flammation at the seat of inoculation—with prompt lymphatic invasion, 
probably a rapid, possibly a single excursion of the Treponema through 
the blood-stream to the various organs of the body, in which, after longer 
or shorter periods local changes of a productive and destructive nature may 
follow, depending on many factors, the most important of which is the 
early and intensive treatment of the disease. 
Wassermann Reaction.—Syphilis is inoculable to the ape and offers 
a positive Wassermann reaction which includes the indirect recognition 
of a specific antibody by the fixation of complement test. In the carrying 
out of the test through its two stages in the tubes in which complement has 
been absorbed, hemolysis is absent, therefore the test is “positive”; in the 
tube in which there is hemolysis the complement has not been absorbed 
and therefore the test gives a “negative” result. 
The Wassermann reaction is so exceptionally present in nomsyphilitic 
diseases that its presence in suspected syphilis justifies a positive conclu- 
sion. 
The few diseases in which the Wassermann reaction is present offer 
such positive symptoms as to make differentiation easy. Included among 
these are leprosy, framhesia, scarlet fever, rarely; occasionally cancer, 
tuberculosis and pregnancy complicated with acute yellow atrophy of the 
liver (Scholtz). 
We consider the prognosis of syphilis based upon the following classi- 
fication : 
15 16 
SPECIFIC INFECTIOUS DISEASES 
1. Acquired Syphilis. 
(a) Early manifestations. 
(i) Primary and secondary stages. 
(b) Late manifestations. 
(i) Tertiary stage (including visceral syphilis. 
(ii) Late tertiary lesions — so-called metasyphilitic 
lesions. 
2. Congenital Syphilis. 
(i) Intra-uterine. 
(ii) Post embryonic. 
Acquired Syphilis 
With the introduction into medicine by Ehrlich of chemotherapeusis 
including salvarsan, neosalvarsan and its modifications, the prognosis of 
all forms of syphilis in all of its stages has been enormously influenced, 
though we must confess that long years of observation are needed before 
positive conclusions can be reached which justify a forecast of the syphi- 
litic’s future who to-day subjects himself to the modern and supposedly 
rational treatment of the disease. 
By modern diagnostic methods, i. e., the Wassermann reaction and the 
examination of the spinal fluid, we are able to reach positive conclusions 
with regard to the activity of the infection in all of its stages. 
Primary Stage 
During the primary stage of the disease the patient as well as the 
attendant should recognize in syphilis a serious infection, which, if a 
favorable forecast is to be given must include not the treatment of the 
palpable and visible symptoms alone, but the constitutional invasion by 
intensive methods. The prognosis of untreated cases of syphilis is unfa- 
vorable for the subject infected, his offspring, and for the nation. There 
is no spontaneous cure of syphilis; no subject is safe to his surroundings 
who has remained untreated. Symptoms may disappear during periods 
which vary in length, but in all there are recurrences which include de- 
tected or undetected lesions (mucous patches especially) from which in- 
fection may spread to the innocent. Bramwell has called attention to the 
fact, and his experience is corroborated by that of others, that those 
syphilitics are most likely to develop the serious late manifestations of the 
disease who are insufficiently treated during the primary and secondary 
stages; who, after the disappearance of visible lesions neglect themselves. 
The 'prognosis, therefore, of constitutional syphilis is enormously influr 
enced by the rational, scientific, and intensive treatment of the early mani- 
festations of the disease. 
Not all subjects react alike to syphilitic infection. In some, we find a PROTOZOAN INFECTIONS 
17 
tendency toward malignancy in the obstinacy of the initial lesion and in its 
early tendency to deep destructive changes with marked constitutional dis- 
turbances; and in some, the early invasion of the nervous system. Others, 
present features which at once brand the infection, so far as evident 
changes and reactions are concerned, as benign during the early days of 
the disease. Such behavior should not mislead, for mild and evidently 
benign cases during the early stage may offer late manifestations and so- 
called metasyphilitic lesions out of all proportion to the benign nature of 
the early symptoms. 
Syphilitics who are reduced by previous disease, constitutional anom- 
alies, who are inherently weak and nonresistant, are likely to show the 
effect of such handicap during the early stages of the disease. 
The influence of syphilis on tuberculous disease is considered sepa- 
rately (See Tuberculosis). 
Alcoholics and the dissipated are prone to show ulcerative and de- 
structive changes, with marked constitutional disturbance during the pri- 
mary stage of the disease. The phagedenic tendencies of syphilitic tissue 
in alcoholics is characteristic. 
The aged and overworked who contract syphilis show great tendency 
to destructive and constitutional symptoms, including wasting of tissues, 
anemia and asthenia. 
Blood Changes During the Early Stages.—Marked changes in the red 
corpuscles during the early stages are exceptional. There may be a slight 
reduction of erythrocytes, but this is not significant. 
In the exceptional case in which there is a material reduction of ery- 
throcytes—late during the primary and in the secondary stages—the infec- 
tion is severe, or there is lowered vitality of the patient, previous disease, or 
some one of the diatheses. 
The hemoglobin during the secondary stage in the average case which 
progresses favorably does not fall below 70 per cent, while as Haegeli has 
shown, the red blood-corpuscle reduction is insignficant. 
When during the. secondary stage hemoglobin falls to 30 per cent or 
only slightly higher, the infection is severe and the prognosis should be 
guardedly given. 
Several authors have claimed that there is a lymphocitic increase during 
the acute stage; this we have not been able to confirm. It is safe to con- 
clude that the lymphocytes are markedly increased only when the patient 
shows marked improvement after the early stages and as FTaegeli reports, 
this should be regarded as a ‘“post-infectious lymphocytosis.” High leuko- 
cytic counts are rare (24,000). Our average leukocytic count of the sec- 
ondary stage is between 9,000 and 11,000. With leukocytosis, if present, 
the large mononuclears are increased. Following the injection of salvar- 
san, with the improvement of symptoms, a slight increase of neutrophils is 
found without the disappearance of eosinophils. 18 
SPECIFIC INFECTIOUS DISEASES 
Constitutional Symptoms.—During the primary stage there are rarely 
threatening or even serious constitutional symptoms from which the subse- 
quent course of the disease can be foretold. 
The fever of invasion may be associated with constitutional distur- 
bances including malaise, rapid pulse, depression and myalgia; the fever 
may be markedly intermittent, remittent or during a limited period may 
remain continuous, thus clouding the diagnosis. 
With all syphilitic febrile anomalies, the prognosis is good and conval- 
escence rapid. 
Wassermann Reaction During the Primary Stage.—Positive Wasser- 
mann reactions are not present during the early days of the initial lesion. 
In 70 per cent of cases, the reaction is positive between the fourth and 
seventh week. 
The time of constitutional invasion corresponds with the appearance of 
the positive Wassermann reaction. Bayly says: “Primary cases in which 
the lesion has been present for less than a fortnight almost invariably give 
a negative reaction, while 75 per cent of positive reactions are obtained if 
the primary sore has been present for over a month.” 
Secondary Stage 
The secondary stage is reached in from four weeks to three months 
after the appearance of the initial lesion. 
While the lesions of the secondary stage may be numerous, there are 
rarely serious complications during this stage. 
Positive Wassermann reaction is present in practically all cases during 
the secondary stage of the disease, showing itself between the fourth and 
seventh week after the appearance of the initial lesion, as already men- 
tioned (95 to 98 per cent). The Wassermann reaction is also positive in 
90 to 95 per cent of cases during the tertiary stage (Scholtz). 
Skin Lesions During Secondary Stage.—The roseola eruption may be 
so slight as to escape detection; with modern treatment it is usually absent. 
It is not persistent, and fades entirely in from four to fourteen days. 
Papular and pustular eruptions are more persistent than is the roseola 
syphilitica. 
Early pustulation in our experience has been evidence of the most re- 
bellious type of the disease. Squamous syphilids, early, are also evidences 
of resistance to the treatment, and unless they yield after systematic and 
intensive treatment, may be considered expressive of the more malignant 
types of syphilis. 
But few cases escape mucous patches: in all cases they are likely to 
recur. Their presence is always positive evidence of active syphilis and 
we place great importance upon this lesion in framing the prognosis which 
includes indication for the future treatment, and in deciding the many PROTOZOAN INFECTIONS 
19 
questions associated with modern eugenics. We insist that the 'presence 
of the mucous patch, wherever found, should lead to further observation 
and intensive treatment and always argues against the advisability of 
marriage. 
The prognosis of syphilis during this and subsequent stages is un- 
favorably influenced by the neglect of treatment: to wait until secondary 
symptoms appear is unwarranted, and influences the case unfavorably. 
The negative Wassermann reaction during the early stages of syphilis 
does not justify the conclusion that the syphilitic is cured. The negative 
phase may be followed by a positive reaction and a return of symptoms. 
With lesions suspicious of the secondary stage, mild or incomplete reac- 
tions should not be accepted as conclusive evidence, and should lead to 
further tests. 
The fever of the secondary stage behaves much like that of the primary; 
there may be no fever during the latter stage, or as usually happens, the 
fever begins with the end of the primary and the beginning of the sec- 
ondary stage. In all of these the prognosis remains unaffected. The ma- 
jority of cases remain afebrile throughout the early stages, or if fever is 
present, patients fail to recognize it. 
Accompanying Manifestations.—The severity and localization of the 
lesions of the secondary stage depend upon the seat and extent of the de- 
posits of the Treponema. The excursion of the Treponema pallidum 
through the blood is immediately followed by its deposit in the various 
organs of the body. The skin receives the larger number of spirochetes; 
hence the multiplicity and preponderance of lesions in it. The treponemata 
are held in the contracted capillaries of the skin, where they proliferate 
and cause changes. 
Alopecia.—Pronounced alopecia is evident in many cases; few that 
are radically treated have more than insignificant loss of hair. It is 
relieved quicker than is leukoderma ; it rarely causes permanent bald spots 
(alopecia areata). Alopecia is, in most cases, favorably influenced by radi- 
cal treatment. 
The other skin lesions of the secondary stage including the small papu- 
lar syphilid, leukoderma, serpiginous and psoriatic syphilids, and condy- 
lomata are all amenable to treatment. 
Coxdylomata.—Condylomata are a source of infection and should 
be so regarded by the clinician. 
Nephritis.—Nephritis sometimes develops during the secondary 
stage. The prognosis will be considered with the visceral lesions of the 
tertiary stage of the disease. 
Arteritis.—Arteritis may be an early complication; it may invade 
the cerebral, renal, or coronary arteries or may be general: the prognosis is 
not bad if detected early. 
Early Myocarditis.—Early myocarditis may prove threatening; its 20 
SPECIFIC INFECTIOUS DISEASES 
rational treatment usually leads to recovery. It will be considered under 
Heart Complications with visceral syphilis. 
Joint Invasion of Secondary Stage.—The joint invasion of the 
secondary stage is not serious. There is improvement under treatment 
after a few days or weeks of ill-defined pain, which may resemble acute or 
subacute arthritis, occasionally gout—without recurrence in most cases. 
The Eye.—Inflammatory conditions of the eye are not uncommon; 
the most painful and threatening among these is iritis. This usually yields 
to treatment after several weeks; there is but small remnant of disease left. 
In some cases adhesions cause permanent damage, though sight is preserved 
and often somewhat reduced. 
The Ear.—Ear changes are rare, when present they yield slowly to 
treatment. 
Lues Maligna.—The evidences of malignant lues during the early 
stages include ulceration of the skin and mucous membranes which may be 
disseminated. 
Papular lesions may promptly ulcerate; ecthymatous lesions are also 
characteristic with the development of rupia syphilitica. 
These lesions of malignant lues during the secondary stage do not de- 
velop, as do the ulcerations of the tertiary stage from gummatous tissue, 
but from the small and rapidly ulcerating papule or pustule. The fate of 
these, in the malignant cases of secondary syphilis, is surprising rapidity 
of ulceration with the upbuilding of crusts and the characteristic lesions of 
ulceration, the edge of which is in direct contact with the normal skin. 
“Galloping syphilis,” “malignant” and “florid,” always gives a posh 
live Wassermann. Galloping syphilis is associated with marked constitu- 
tional'disturbances, high fever, rapid pulse, and early arterial degeneration 
of an amyloid character. The prognosis of these cases in spite of active 
treatment is often bad. Many of these malignant cases bear medication 
badly; and when they do improve relapses are frequent and threatening. 
Evidently the subjects of malignant lues, for some reason, have less 
resistance to syphilitic infection than is possessed by average normal indi- 
viduals (Scholtz). Finger believes that in the ancestors of these subjects 
syphilitic infection was absent during many generations and because of the 
lack of the average immunity caused by such infection, the malignancy cor- 
responds with that of the disease during the early years of its existence in 
Europe. The absence of marked enlargement of the lymphatic glands dur- 
ing the early days of syphilitic infection in malignant cases, and the con- 
sequent failure to get the protecting influence of these, is advanced by 
others as a cause for malignancy. 
In some of the malignant and galloping cases, cachexia, diatheses, pre- 
vious disease and dissipation, should be considered as provocative. Malig- 
nant lues, complicated with visceral lesions early, offers a very dubious 
prognosis. PROTOZOAN INFECTIONS 
21 
Period of Latency.—This period has been described by Browning and 
Mackenzie as “a state of equilibrium between the host and the parasite” 
(Bayly), while Ehrlich gave it the name of “non-sterilizing immunity.” 
In the majority of cases, following the symptoms of the secondary stage as 
shown by skin lesions, mucous patches, and the positive Wassermann reac- 
tions, all symptoms may disappear and to all appearances the subject is 
cured ; in 50 per cent the Wassermann reaction becomes negative. For safe 
prognosis, these cases should be considered to be in a latent stage, and a 
positive forecast should not he offered. Relapse from the latent stage is the 
rule in from three to nine months with either mucous patches—usually 
buccal or tonsillar—skin lesions, and the return to the positive.phase (Was- 
sermann) of all. 
The foregoing facts are of enormous prognostic significance and their 
correct interpretation means much to the patient and his surroundings. 
The great value of the Wassermann reaction for the indications which it 
offers for treatment and 'prognosis must he recognized during this stage; it 
discloses “these hidden or latent cases, and in this way to cure them and 
to protect against the much dreaded parasypliilitic complications” (Neis- 
ser): The lighting of the disease to activity, as is shown by the return of 
the positive Wassermann reaction, where before the blood gave a negative 
response and an increase in the depth of color of existing skin lesions, is 
known as the “Jarisch-IIerxheimer reaction 
The prognosis of these cases is enormously improved for the recrudes- 
cence of the infection, and further lesions are prevented by appropriate 
treatment and the following of the indications offered by repeated Was- 
sermann reactions. In some, the latent phase is promptly changed to a 
positive reaction by the treatment. We quote from Bayly: “A single 
negative reaction obtained with the serum of a patient undergoing treat- 
ment by mercury or salvarsan means little but that the patient is reacting 
to such treatment. A series of negative results taken at intervals of three 
to six months after all treatment has been given up is necessary before the 
patient can be regarded as cured, and even then, until twenty years have 
passed, we cannot be absolutely certain that the disease is completely and 
permanently obliterated and that no late manifestations will ever occur. 
It is most important to remember that about 10 per cent of untreated cases 
of syphilis fail to give a positive reaction at the first examination, and that 
therefore a negative reaction only gives a 90 per cent probability of free- 
dom from infection.” 
During the secondary stage of the disease, the influence of the treat- 
ment on the Wassermann reaction offers decided indications for prognosis 
and the modification of the further treatment. If with treatment the reac- 
tion continues strongly positive, the medication is insufficient and the dis- 
ease uncontrolled. If the Wassermann reaction (a smaller complement is 
fixed) shows decided change, feeble reaction or the negative phase, the 22 
SPECIFIC INFECTIOUS DISEASES 
treatment is efficacious—the disease is under control and the prognosis is 
correspondingly better. 
Length of Secondary Stage.—The length of the secondary stage is 
variable. It may cover a long period of years, rarely longer than 4 to 5 
years, though mucous patches and small and large papular syphilids are 
found long years after the clinician had considered the stage passed. 
Smokers may show mucous patches so long as twenty and thirty years after 
infection. It is impossible in the individual case to be positive that the 
secondary stage is ended, until symptoms of the tertiary stage develop. 
This is an important fact. The secondary stage continues to be dangerous 
because during its persistence, the disease continues communicable. 
The Cerebrospinal Fluid.—The lumbar fluid gives valuable data for 
prognosis in the advanced stages of syphilis and in the secondary stage. 
Dreyfus, who has now made over 1,500 lumbar punctures, finds a positive 
Wassermann reaction during the early stages of syphilis in over 80 per cent 
of all syphilitics. This proves the early dissemination of the Treponema 
to the central nervous system, and that this may exist without subjective 
symptoms. It is assumed that a persistence of the Wassermann reaction 
during and following the secondary stage—a condition which is usually 
due to faulty treatment or malignancy of the infection—makes the prog- 
nosis unfavorable; for such subjects will be likely to develop serious ner- 
vous lesions: they are candidates for late tertiary disease (paresis, tabes, 
etc.) Under improving conditions during the early stages—usually due to 
treatment and rational living—the previously increased intralumbar pres- 
sure is lowered, the Wassermann reaction becomes negative in the blood 
and in the lumbar fluid. 
The influence of treatment on prognosis during the secondary stage can 
be best interpreted by the results of the Wassermann test of the blood and 
the lumbar fluid. Positive Wassermann reaction of the lumbar fluid in 
the secondary as well as in all stages of syphilis must be interpreted as posi- 
tive evidence of specific infection of the nervous system, and until a nega- 
tive phase is reached the disease cannot be considered to be under control; 
hence the enormous influence on prognosis of these results. We will refer 
to the importance of the examination of the cerebrospinal fluid in connec- 
tion with late tertiary disease. The blood may give positive Wassermann 
reaction, but unless the nervous system is involved, the spinal fluid will 
continue to give negative results. Besides ■ increased pressure there is 
marked increase of albumin during the secondary stage; both disappear 
under proper treatment. During this stage there is marked lymphocytosis 
of the fluid, and with severe nervous symptoms this is decided with great 
increase of the albumin content. Lymphocytosis of the fluid attends over 
50 per cent of all secondary syphilis. Plant- claims that the cerebrospinal 
fluid shows leukocytosis in one-third of all secondary syphilis, one-third 
are on the border line, and the remnant shows no cellular increase.” PROTOZOAN INFECTIONS 
23 
Tertiary Stage 
The tertiary stage of syphilis begins the period of late manifestations, 
during which there is no danger of infection to others, in which there may 
be years of latency, and in which visceral lesions may develop in vital 
organs. Tertiary syphilis, when it attacks the skin, leaves the remnant of 
the lesion which caused tissue breakdown in a characteristic cicatrix—in 
contradistinction to the secondary lesion. The cutaneous lesions are not so 
extensive as during the earlier stages, but more destructive. They are often 
asymmetrical, and during this stage, the internal organs may be invaded. 
The tertiary stage is characterized by the deposition of gummata, true 
granulation tumors. 
The tendency of all gummata wherever found is to necrosis and cica- 
trization. Gummata vary from microscopic-sized to large orange-sized 
tumors—occasionally even larger. 
The fate of the gumma of the skin is necrosis with ulceration, unless 
promptly influenced by treatment whereby these changes may be modified. 
When thus influenced, resorption takes place with resulting stellate cica- 
trization. In the liver, healed gummata often leave large and deep cica- 
trices with sufficient remnant of normal tissue to lead to unchanged func- 
tion of the organ. We will refer to the behavior of multiple gummatous 
deposit and its prognostic importance in connection with a consideration 
of the separate organs involved. 
Cutaneous Lesions of Tertiary Stage.—The cutaneous lesions of the 
tertiary stage include: (a) Papular syphilids (b) Gummatous syphilids. 
(a) Papular Syphilids—Papular syphilids include tubercular, tu- 
berculo-serpiginous syphilids, ulcerative serpiginous syphilids, rupia syphi- 
litica and psoriasis syphilitica. In all of these, ulceration and cicatriza- 
tion of the invaded tissue follow as a rule. 
(b) Gummatous Syphilids.—It is difficult to draw a sharp line be- 
tween papular syphilids and skin gummata; both rest on the same patho- 
logic foundation. This is particularly true of the serpiginous syphilids 
which ulcerate (serpigino-ulcerative syphilids). Both forms of tertiary 
cutaneous syphilids offer a good prognosis in cases which are not malignant 
and which are subjected to rational treatment. 
Neglected gummata of the scalp which invade the periosteum may lead 
to deep tissue loss and ulcerative destruction of bone. 
Gummata of the nose, which are internal—invading bone and mucous 
membrane—lead to destruction of the septum and other changes. The 
result of bone destruction leads to the characteristic deformity known as 
“saddle nose.” It often happens that gummata invade the nasal periosteum 
without causing symptoms sufficient to bring the patient to the physician, 
until irreparable injury has resulted. The perforation in such cases is the 
first evidence of destruction. The septum is the seat of gummatous deposit 24 
SPECIFIC INFECTIOUS DISEASES 
by predilection. The syphilids of the alee nasi and other parts of the nose 
are often destructive in malignant and untreated cases: early prompt treat- 
ment, local and constitutional, usually leads to satisfactory results with 
little damage remaining. 
Gummata of the tongue, soft palate, tonsils, and buccal mucosa tend 
toward prompt breakdown of tissue and perforation. Cicatrices often lead 
to adhesions and consequent distortion. The hard palate is often included 
in ulcerative destruction and is perforated. 
The Blood during Tertiary Stage.—There is but slight, if any, change 
in the red blood corpuscle count; there may be slight anemia in the average 
case. Severe anemias are always an expression of malignancy—depleting 
conditions due to complications and cachexia. Almost all severe anemias 
occur during the tertiary stage of the disease; they may be of the chlorotic 
type without leukocytosis. With chlorosis there may be leukocytosis or 
an approach to the picture of pernicious anemia. It is very rare that death 
follows these severe anemias. The larger number are found in over-wor- 
ried and weak women: many of these, work and live in unfavorable sur- 
roundings. 
Hemolysis following the administration of mercury may be a cause of 
grave anemia and is unfavorable; it shows intolerance of specific medica- 
tion. 
The presence of many large mononuclear lymphocytes has been re- 
ported by several reliable observers (14.1 per cent) (Hauck). The leuko- 
cytic count, in favorable and in the average cases, is between 9,000 and 
13,000 (Sabrazes and Mathis). 
Cerebrospinal Fluid during the Tertiary Stage.—In severe cases of 
tertiary syphilis the albumin content is large. Leukocytosis is found in 
cases which have been neglected or insufficiently treated. Disappearance 
of leukocytosis, and decrease of albumin, with lowered pressure, are proofs 
of improvement; there are exceptions to this rule, for occasionally the 
change is insignificant. 
With involvement of the nervous system there is lymphocytosis. The 
cells are small mononuclear with a few larger kite-shaped lymphocytes; the 
nucleus is in the broadened protoplasm of the cell. 
The presence of leukocytosis in the withdrawn fluid is always proof of 
organic disease, in spite of the absence of subjective symptoms. Func- 
tional neuroses never show leukocytosis. Lymphocytosis is proportionate 
to the gravity and extent of the inflammatory changes—usually in the men- 
inges—and the prognosis can usually be favorably influenced by early 
rigorous treatment. Plaut, Bayly and others agree that a “negative cyto- 
logical examination, namely, the presence of less than six cells per c. mm., 
will exclude general paralysis, syphilitic meningitis and tabes.” 
Frequency of Tertiary Lesions.—The frequency of tertiary lesions is 
certainly decreasing under modern methods of treatment and the increased PROTOZOAN INFECTIONS 
25 
knowledge of the effects of syphilitic infection among the masses. It is 
unfair to reach conclusions from hospital material alone, for such cases 
are usually found among the neglected, insufficiently treated, and the in- 
temperate. Seholtz says that “the percentage may be placed between 15 
and 20 ; more accurate statistics are not available, for the lesions of tertiary 
syphilis may not appear for twenty to thirty, yes, forty years after infec- 
tion—periods so long that it is impossible to follow the cases and determine 
their fate.” 
Tertiary lesions are invited by depressing influences, alcoholism, faulty 
nourishment, diathesis, tuberculosis and lympliatism. Tertiary lesions are 
often present without the patient’s knowledge of syphilitic infection: hid- 
den, unobserved and untreated primary lesions account for these in over 50 
per cent of cases. But few, thoroughly treated during the initial and sec- 
ondary stages of syphilis, develop tertiary lesions. Early and apparently 
benign symptoms do not preclude later malignancy and deep tertiary 
lesions. Such cases are likely to be neglected; occasionally in spite of ra- 
tional treatment they lead to so-called metasyphilitic disease. Neissers 
statistics which follow, are of great value for our purposes: they show how 
rarely patients with tertiary symptoms are treated radically during the 
early stages of syphilis and how often patients with tertiary symptoms re- 
ceive no treatment at all. 
Neisser’s Statistics on Tertiary Syphilis. 
Tertiary 
Syphilitics 
Received. 
Private 
Material. 
Clinic and 
Policlinic, 
until end of 1893. 
Clinic and 
Policlinic, 
1894 and 1895. 
No treatment, or 
treated but once 
insufficiently. 
35.4 per cent, males 
66.6 per cent, females 
72.3 per cent males 
80.45 per cent, females 
68.8 per cent, males 
76.8 per cent, females 
But one cure. 
23.3 per cent, males 
16.5 per cent, females 
20.4 per cent, males 
14.25 per cent, females 
14.0 per cent, males 
16.0 per cent, females 
Two or three separ- 
ate cures. 
29.3 per cent, males 
8.5 per cent, females 
3.5 per cent, males 
2.4 per cent, females 
8.9 per cent, males 
5.8 per cent, females 
Four or more (some 
thorough, others 
indifferently car- 
ried out) cures. 
12.0 per cent, males 
8.4 per cent, females 
3.37 per cent, males 
2.85 per cent, females 
8.9 per cent, males 
1.4 per cent, females 
These statistics are corroborated by all experienced clinicians and 
syphilographers, including Fournier, Haslund, Eiders, Neumann and 
Seholtz. 
Visceral Syphilis in Tertiary Stage 
The incidence of tertiary and metasyphilitic disease of the internal 
organs now considered late tertiary syphilis, has been proved by the newer 26 
SPECIFIC INFECTIOUS DISEASES 
methods of diagnosis—the Wassermann reaction particularly—to be more 
frequent than has been heretofore suspected. When we include among 
these the many cardiovascular conditions, formerly unexplained, and the 
specific diseases of the nervous system now known to be of luetic origin, we 
add an enormous material, and increase the percentage accordingly. 
Visceral syphilis includes the diseases of the internal organs which 
develop during the tertiary stage of the infection. It must not be forgot- 
ten that occasionally vital organs are attacked during the secondary stage 
of the disease; these include the kidney, central nervous system, the osseous 
system, the vascular system and rarely the liver. The organs which are 
attacked during the tertiary stage include the arteries, veins, the heart, 
the liver, the kidney, the bones and joints, the rectum, the digestive tract, 
the spleen, the testicles, the bladder and genitalia, the respiratory organs, 
and the central and peripheral nervous system. 
Specific Diseases of the Cardiovascular System 
Arteritis.—The classic work of Heubner, in which he called attention 
to the importance of lesions of the smaller cerebral vessels, which are 
always characteristic of endarteritis, in which the intima is the seat of 
proliferative change—still serves as the basis of our knowledge of the 
subject. The disease does not limit its ravages to the intima, for in 
advanced specific arteritis all coats may be invaded. The student of 
medical literature is referred to Virchow’s comprehensive treatment of 
visceral syphilis, which is one of the most marvelous additions of the past 
century. 
It can bei easily understood how far-reaching the influence of specific 
arteritis may be, and how many organs may suffer at the same time. Such 
weakening as is caused by endarteritis specifica of the arterial walls may 
lead to miliary or large-sized aneurysmal dilatation, with the included 
secondary manifestations. (Aneurysm of the aorta and larger vessels are 
separately considered.) The changes wdiich follow in the cerebral vessels 
and their baneful results, with prognosis, are considered with Cerebral 
Syphilis. 
With practically all specific arteritis the Wassermann reaction is 
positive. Specific arteritis invading the coronaries gives rise to threaten- 
ing symptoms, including the complex of angina pectoris. It must be 
remembered that stenocardia is not always, even during early life, of 
specific origin. Heredity is an important factor in many; but in young 
subjects evidences of arteritis, including coronary invasion, should always 
lead to the strong suspicion of syphilis as a cause, to corroborative Was- 
sermann tests, and specific treatment. If the myocardium is not too far 
degenerated, and other vital organs are not invaded—kidney, brain, etc.— 
the prognosis is fairly good. PROTOZOAN INFECTIONS 
27 
No specific arteritis is so far advanced as not to justify specific treat- 
ment, for in extreme cases we are often unexpectedly successful. Results 
have often been encouraging in cases which suffered repeated anginoid 
attacks. 
Blood-pressure study of these cases needs to he correctly interpreted 
to give data of value. If the endarteritis has existed during a long period, 
has been extensive, has involved the renal and mesenteric vessels, there 
will probably be a high systolic pressure with a high pulse pressure, a 
tense and thickened radial pulse. These cases also have decided accentua- 
tion of the second aortic sound and often an aortic systolic murmur. The 
aorta is included in the process and shows the characteristic changes of 
specific aortitis. The result of blood pressure study alone in such at case 
is valueless, this must be added to all which the case presents before prog- 
nosis is justified. 
Such cases as we have above mentioned are of serious character, they 
demand a guarded prognosis and before it is positively given, the effect 
of treatment should be studied. With some of these cases, the blood- 
pressure may be normal or reduced; such reduction is then evidence of 
myocardial weakness, and the prognosis is thereby unfavorably influenced. 
Specific obliterating endarteritis may cause gangrene of an extremity 
or less striking trophic changes. We have found intermittent claudica- 
tion, erythromelalgia, and symmetrical gangrene of the finger tips (Ray- 
naud’s disease), in which the underlying arteritis proved to be specific and 
in which rigorous treatment led to the recovery of some, and the material 
improvement of others. 
Specific amyloid degeneration of small and large vessels is always' 
serious; it is usually associated with similar degenerative processes in 
other vital organs, and is not often relieved by treatment. When the kid- 
ney is involved in a similar process and there is anemia gravis, but little 
hope can be given. 
For the purposes of the prognostician, it is necessary to assume that 
all unexplained arteritides in young subjects should be suspected to be of 
syphilitic origin, and demand the refinements of diagnosis and therapeu- 
tic tests before final conclusions are reached. Naturally the prognosis of 
arteritis specifiea depends largely upon the importance of the organs 
directly involved, and the influence of the changed relations. 
Aortitis Syphilitica.—Specific aortitis may lead to aneurysm of the 
aorta; it may be associated with non-specific arteriosclerosis of the aorta, 
but its seat is characteristic in almost all cases during its early existence. 
Uncomplicated specific aortitis causes irregular thickening of the aortic 
wall (fibrous thickening), with patches of thinner tissue between these 
plaques. It invades the ascending aorta and the arch. There is a distinct 
line of demarkation which separates the changed aorta from the valve 
and tissues of the aorta directly above it. The prognosis is uncertain. 28 
SPECIFIC INFECTIOUS DISEASES 
Physical signs of aortitis and subjective symptoms often disappear under 
treatment. 
There are according to Grassmann accidental or functional murmurs 
in 40 per cent of cases during the secondary stage of syphilis. In occa- 
sional cases during this stage, there may be threatening incompetence of 
the heart with low blood-pressure and dilatation of the right heart. Fever 
and anemia may be present. The prognosis is good in almost all of these 
cases. One of the dangers occurs from suddenly arising pulmonary 
edema. 
Heart Syphilis.—There is no tissue of the heart in which specific dis- 
ease may not cause organic change. We have mentioned coronary and 
aortic disease; the endocardium may degenerate, the aortic valves partic- 
ularly may be the seat of specific deposit and change, the myocardium may 
be uniformly infiltrated and degenerated—it may hold one or more gum- 
mata—the pericardium may be involved; in all of these the Wassermann 
reaction is likely to be positive. 
The Wassermann test has given us positive information concerning an 
enormous material which was formerly unexplainable. We refer to those 
heart lesions, the pathogenesis of which Xve did not understand—includ- 
ing especially the degenerative rather than the inflammatory processes—- 
usually found during middle life when arteriosclerosis and disorganizing 
changes are unexpected. The larger number of these lesions are aortic, 
endocardial, myocardial and coronary. The aortic lesions are in the 
ascendency. In over 50 per cent of these unexplained cases the Wasser- 
mann reaction is positive, and the prognosis is accordingly improved. 
Aortic valvular lesions are found with positive Wassermann reactions in 
over 55 per cent of our cases. 
There are unquestionably many specific lesions of the heart which 
never give rise to symptoms, which remain undetected, and are cured by 
the treatment of the constitutional infections, just as the large proportion 
of positive Wassermann tests of the cerebrospinal fluid and its cellular 
elements prove that changes in the nervous system may exist without sub- 
jective symptoms, which also disappear under similar conditions. 
We have elsewhere called attention to the evanescence of physical 
signs, the disappearance of murmurs with positive organic disease. Re- 
cent additions to our knowledge, prove these cases to be of specific origin, 
and materially improve their prognosis (Eisner). 
The prognosis of specific myocarditis depends on the length of its 
existence, the associated lesions, and the effect of specific treatment. Cer- 
tainly the prognosis of the degenerative diseases of the myocardium due 
to syphilis is much better than non-specific disease. Harlow Brooks says: 
“Nearly all cases of syphilis are well treated at least for so long as mucous 
membrane or skin lesions present themselves; just as long as these show, 
the patient is willing to submit himself to treatment and to observation. PROTOZOAN INFECTIONS 
29 
Hence, it is that at least for a time, many or most cases of cardiac involve- 
ment are correctly treated even though unrecognized.” 
Lesions of the heart of specific origin, including degenerative myo- 
carditis, valvular lesions, arteritis of the heart vessels, may become latent; 
they may “heal and resorb under proper medication.” There are unques- 
tionably many heart lesions during the early stages of syphilis which give 
rise to no symptoms—which unchecked would prove fatal—but which are 
stayed and cured by specific treatment. Cardiac lesions of late syphilis 
may often be threatening, the heart may be insufficient and yet under treat- 
ment there may be recovery or marked improvement. The prognosis can- 
not be given until the treatment has been sufficiently tested. Brooks says: 
“It is also true that a cheerful prognosis is not permissible until it has 
been determined just how much may be achieved by proper treatment. So 
frequently have I been deceived in both directions, that I now refuse prog- 
nosis until the case has been under treatment at least for a time—after 
which from the degree and character of the improvement or its failure, 
one may quite accurately prognose what may be expected with a further 
prosecution.” 
The Stokes-Adams phenomenon has in a few cases been found with 
specific degeneration of the intraventricular septum (Ilis fibers) ; gumma 
have been found in several cases post mortem. Such cases offer a serious 
forecast, though improvement or recovery may follow; rigorous treatment. 
All cases of infiltrating specific myocarditis must be considered se- 
rious, and justify only a tentative prognosis until the horizon is cleared 
by treatment, including rest. Mracek gives the specific heart lesions 
wffiich he found in 60 cases: 
Gummatous myocarditis 10 
Fibrous myocarditis 9 
Gummatous and fibrous myocarditis 8 
Endocarditis 2 
Coronary arteries alone 3 
Pericardium alone 1 
Myocardium and pericardium 15 
Pericardium, myocardium and endocardium 1 
Myocardium and coronary arteries 1 
All parts of the heart 6 
Cardiac ganglia 4 
(For further information concerning the fuller pathologic data which 
influence prognosis, the reader is referred to the works of Virchow and 
Mracek, above cited; also Hirschfelder, Huchard, Isaac Adler, Aschoff, 
Gruber and Stadler.) 
Phlebitis syphilitica.—Changes in the veins may lead to phlebitis, 
phlegmasia alba dolens and erythematous nodes associated with fever* and 
exacerbation of constitutional symptoms. In all of these conditions the 
prognosis is favorable. 30 
SPECIFIC INFECTIOUS DISEASES 
Syphilis of the Liver 
Specific diseases of the liver are found with: (a) acquired syphilis, 
(b) congenital syphilis. Specific lesions of the liver are the most frequent 
of the visceral diseases found in the abdomen. 
(a) Acquired Syphilis of the Liver.—Jaundice is not unusual dur- 
ing the secondary stage of acquired syphilis. The bile passages and liver 
parenchyma are invaded. The organ may be slightly enlarged. These 
cases run a benign course and recovery is the rule after a short period of 
treatment. 
Acute Atrophy of the Liver.—Atrophy of the liver occasionally 
arises during the secondary stage of syphilis, and with all of the symptoms 
of rapid degeneration, jaundice, sepsis and heart weakness; these patients 
die within from forty-eight hours to three or four days. Rolleston has 
reported twenty-eight cases of postsyphilitic acute atrophy of the liver. 
Gummata.—The liver invasion of the tertiary stage is usually gum- 
matous. There may he interstitial infiltration and connective tissue 
proliferation with marked contraction resembling the atrophic form of 
cirrhosis of the liver. These are not so-called parasyphilitic lesions, but 
are due to the proliferation of the treponema in situ. 
Specific diseases of the liver are usually associated with more or less 
fever of an atypical type; and multiple gummata may lead to the sus- 
picion of liver cancer and abscess. With nodules situated anteriorly, the 
masses are palpable. There is wasting and progressive weakness with the 
fever. There is also pain and the enlarged liver is tender. With dissemi- 
nated nodules there is usually ascites, more or less perihepatitis, and 
occasionally jaundice. Perihepatitis is an attendant of almost all liver 
gummata. 
With lues maligna (malignant syphilis) amyloid degeneration of the 
liver with enlarged and waxy spleen and kidney invasion is frequent. 
Characteristic anemia accompanies these conditions. 
The prognosis of uncomplicated gummata of the liver or specific hepa- 
titis and perihepatitis is usually good. It is surprising to find how 
promptly these cases improve under modern treatment. Cases that have 
been neglected, with complications, particularly in those whose resistance 
is below par, are serious. Malignant lues above mentioned, with the asso- 
ciated liver complications, is always ominous; usually death is thei result 
of widespread amyloid degeneration. 
(b) Congenital Syphilis of the Liver.—Syphilis of the liver may be 
an early or a late complication of congenital syphilis (lues hereditaria 
tarda). The early manifestations are those of far-reaching hepatitis: 
the Treponema pallidum can be found in the liver tissue. There is at the 
same time invasion of the spleen and kidney: occasionally the pancreas 
shows marked fibroid change. These changes may be found in the still- PROTOZOAN INFECTIONS 
31 
horn syphilitic child, or death may follow during the first week. Cases 
of congenital liver syphilis which develop early may occasionally, under 
prompt and rigorous treatment, recover; a grave prognosis should however 
always be given. With jaundice and ascites there is but little hope. 
Lues Hereditaria Tarda.—The tardy form of liver lues is always 
an interesting condition which usually develops sometime between the 
tenth and twentieth year in subjects who have all of the earmarks of the 
constitutional infection well developed in the skin, teeth, hones, eyes, and 
in faulty growth. Arterial changes with marked narrowing of the vessels 
are usually present. 
The physical signs referable to the liver are much the same as with 
the acquired forms of gummatous and interstitial hepatitis. Amyloid 
degeneration is usually widespread. The spleen is enlarged. Perihepa- 
titis is almost constant. The majority of these cases are neglected; after 
long periods of indefinite symptoms. Death is the rule with symptoms of 
toxemia, uremia, etc. 
Cirrhosis of the liver is not caused by syphilis, but there are cases in 
which syphilis of the liver may complicate and materially influence the 
course of the cirrhotic process. With congenital syphilis, changes which 
are differentiated from cirrhosis with great difficulty, are found. They 
offer a grave prognosis. 
The prognosis of all forms of liver enlargement or of liver lesions will, 
in a surprising number of cases where serious non-specific disease is sus- 
pected or even diagnosticated, be favorably influenced by specific treat- 
ment. This is a dictum of great importance. 
Syphilis of the Kidney 
During the secondary stage of the disease as already 
nephritis may develop. It usually appears with the roseola eruption. 
The features are those of acute tubal nephritis (parenchymatous), with 
dropsies and abundant albuminuria and casts. These cases are usually 
amenable to treatment, and recover. Neglected cases die of uremia with 
myocardial invasion as a rule. Occasionally subacute and chronic nephri- 
tis originates during the secondary stage. 
Tertiary syphilis may lead to gummatous deposit in the kidney, when 
there may be physical and subjective manifestations of renal tumor. 
Chronic interstitial nephritis may he associated with specific arteritis and 
specific heart changes (myocarditis). There are mixed forms of nephritis, 
also amyloid degeneration, with similar changes in other organs of the 
body. Interstitial nephritis and waxy or amyloid kidney are the most 
frequent kidney changes of tertiary syphilis and are never to be lightly 
regarded; they offer a serious prognosis. The gumma of the kidney im- 
proves and its size reduces with return to normal, after a sufficient period 32 
SPECIFIC INFECTIOUS DISEASES 
of rigorous treatment. Scars are found in such kidneys—proving the 
possibility of cure. 
Syphilis of the Testicle and Epididymis 
Early swelling of the testicle and epididymis of specific origin are 
promptly influenced by treatment, and lead to full recovery without injury 
to the organs infiltrated. The late manifestations of syphilis usually 
limit themselves to the testicle; the epididymis escapes. The late processes 
may be either gummatous or there may be a diffuse interstitial infiltration 
of the organ, or both forms may be together (Scholtz). 
Scholtz calls attention to the fact that even with relatively early treat- 
ment the functions of the testicle may suffer; spermatozoa may disappear 
(azoospermia) or they are much reduced in number (oligospermia). If 
the disease is neglected, aspermia may result (Scholtz). In most cases 
the prognosis is good, and complete restoration of function results with a 
remnant of scar tissue in the testicle. 
The syphilitic diseases of the genitalia in both sexes—the bladder and 
the urethra are exceedingly rare—are surgical affections, and their con- 
sideration is therefore omitted. In passing, it may.be said that they offer 
favorable prognosis. 
Syphilis of the Bones and Joints 
Syphilis of the bones and joints belongs to the domain of surgery. 
Syphilis of the Muscles (Myositis) 
The> various forms of specific myositis all yield to treatment. When 
neglected, atrophy may result. 
Syphilis of the Respiratory Organs 
Nasal Syphilis.—We have already, in connection with the considera- 
tion of gummatous deposits, considered nasal syphilis. The remaining 
nasal lesions are surgical, and offer favorable prognoses only when treated 
early. The destruction of tissues goes on unobserved, insidiously, until 
there is irreparable injury and deformity. Labial and pharyngeal gunv- 
mata may cause tissue loss, and the deep ulcerations of the pharynx may 
lead to adhesions and consecutive symptoms. In smokers these lesions 
may heal slowly, and leukoplakia with mucous patches may be constantly 
present in such mouths during many years. 
There are occasional cases of malignant syphilis in which these lesions 
refuse to yield to any form of treatment: glandular enlargement increases, 
there is a hard infiltration of the glands (sublingual and submaxillary) PROTOZOAN INFECTIONS 
33 
with invasion of the surrounding tissue, ultimate breakdown of tissue, 
increasing anemia, and final cachexia—the patients dying with all of the 
symptoms of malignant disease absolutely uninfluenced by any treatment, 
as already mentioned. These cases are among the most rebellious which 
we have encountered in connection with syphilitic disease. 
Laryngeal Syphilis.—The appearance of syphilitic laryngeal lesions is 
at once associated with subjective symptoms, which in consequence, us- 
ually receive early and successful treatment. The larger number of 
lesions are of secondary origin. Gerber reports that laryngeal syphilis 
represents 4.5 per cent of syphilitic lesions and 3.6 per cent of all diseases 
of the larynx. 
The gummata of the larynx when neglected, as they are found in the 
tertiary stage, may lead to deep and irreparable ulceration, cicatrization 
and malformation, due to adhesions. 
Stenosis of the glottis and cartilaginous destruction may complicate 
and add to the dangers. Suddenly arising edema of the glottis in occa- 
sional cases, may prove life-threatening, and unless promptly relieved 
ends fatally. This may folloiv the injection of salvarsan and prove to he 
a true Ilerxheimer reaction; a fact of enormous importance. Relapses 
of laryngeal syphilis are frequent, though the ulcerative process usually 
yields to treatment promptly. 
Syphilis of the Bronchi and Trachea.—Bronchial and tracheal syphilis 
is rare. Occasionally there are secondary ulcerative lesions which yield 
promptly. Tertiary lesions of the bronchi and trachea may, if undetected, 
lead to ulceration and stricture with serious results. 
Syphilis of the Lung.—Syphilis of the lung is rare, and is an evidence 
of tertiary disease. It may be either gummatous—usually multiple—or 
it may be interstitial, and lead to chronic pneumonia. (See Interstitial 
Pneumonia; also the chapter on Tuberculosis showing the influence of 
syphilitic infection on the prognosis of pulmonary tuberculosis, where this 
subject is fully considered). Gummata of the lung are favorably in- 
fluenced by treatment and offer a fairly good prognosis. Widespread 
interstitial changes in the lung are but little influenced by treatment. 
Such cases offer the same prognosis as do the other chronic types of pneu- 
monia (See Chronic Interstitial Pneumonia). 
Syphilis of the Spleen 
The spleen may be enlarged during the secondary stage; there is 
usually fever and an exanthematous eruption. Hoffman claims to be able 
to demonstrate the Treponema in the spleen by puncture at this time 
(Scholtz). This enlargment is not significant prognostically. 
Gummata of the spleen accompany similar liver deposits, and offer 
the same prognosis as does liver syphilis. The spleen may be enlarged, or 34 
SPECIFIC INFECTIOUS DISEASES 
the gumma may be so located as to cause no great change in the form or 
size of the organ. With lues maligna, the spleen may undergo amyloid 
degeneration. This is a part of a general process in which liver, kidney 
and blood-vessels are involved. The prognosis is unfavorable. 
Most forms of syphilitic disease of the spleen are evanescent and offer 
good prognoses. 
With congenital lues there may be chronic enlargement of the spleen 
with characteristic anemia. This may develop early. The spleen may 
increase to ten times its normal weight (Aschoff). These cases are 
amenable to treatment: many make permanent recoveries. When enlarged 
spleen is coincident with hepatitis in the subject of congenital syphilis 
(syphilis hereditaria tarda), the prognosis is not good. 
Syphilis of the Digestive Tract 
Syphilis of the Rectum.—The rectum is more frequently the seat of 
specific lesions than any other part of the digestive tract, and these may 
be present during any stage. Primary lesions are occasionally found in 
the rectum which lead to ulceration, and make differentiation difficult; 
such lesions heal without leaving remnants. Secondary rectal lesions offer 
a good prognosis; the mucosa is not permanently damaged and heals 
promptly under treatment. Tertiary lesions may cause deep changes and 
stricture if neglected. 
There may he simple gummatous deposits with ulcerations, or a pro- 
ductive proctitis with considerable thickening and persistent subjective 
symptoms. The connective tissue proliferation with accompanying thick- 
ening and ulceration in the infiltrating form of specific proctitis is often 
rebellious to treatment; in some, the rectum is finally converted into a 
thickened, uneven, and narrowed tube with stricture formation periproc- 
titis, consecutive anemia and resulting chronic invalidism. 
Syphilis of the Stomach.—The dyspeptic symptoms of the secondary 
stage are evanescent. Tertiary lesions when present, rarely cause symp- 
toms which lead to their detection. Fournier has reported such cases, and 
recently Jerome Meyer has made an exhaustive review of this subject. 
We know of no serious results which have followed the stomach lesions of 
syphilis in our practice. Possibly an occasional gastric ulcer may be of 
syphilitic origin. 
Syphilis of the Esophagus.—Esophageal ulcers are rare and usually 
heal; in exceptional cases stricture of the esophagus has been found in 
syphilitics, without the history of previous ulceration. 
Syphilis of the Intestines.—Intestinal lesions of specific origin are 
also exceedingly rare. When suspected, without positive history, the 
Wassermann reaction and a therapeutic test may be needed. We have 
had no experience with intestinal syphilis. PROTOZOAN INFECTIONS 
35 
Syphilis of the Nervous System 
There are inviting factors which lead to syphilis of the nervous sys- 
tem ; among these are alcoholic excess, overwork, and the worry which is 
associated with the stress of modern life (Edinger). The influence of 
these factors is denied by some, but the weight of experience strengthens 
the contention that they do exert a powerful influence. 
The prime factor, as will be accented in considering cerebral syphilis, 
is insufficient or faulty treatment during the early stages of the infection. 
The mild early infections, because of their rapid relief and short treatment, 
are oftener followed by nerve syphilis than are those with the more serious 
initial lesions. The lesions of the nervous system (excluding paresis and 
locomotor ataxia) may appear early or late: the average time is between 
one and four years after the primary infection. With our present method 
of treatment it would appear that the early cases, radically treated, will 
prove to be the more tractable. 
At least 15 to 20 per cent of all syphilitics—until the introduction 
of salvarsan and the modern treatment of syphilis—developed specific dis- 
ease of the nervous system. It will require at least two decades of observa- 
tion to reach conclusions which justify figures based on the newer therapy 
of Ehrlich and mercury. The most encouraging statement which we 
can make at the present time is that the outlook seems encouraging. If 
the recently made observations of ISToguchi which seem to prove the pres- 
ence of the Treponema pallidum in the brain of paretics are corroborated, 
paresis and tabes must be included among the tertiary lesions of syphilis. 
Syphilis of the Spinal Cord.—The manifestations of syphilis of the 
cord are numerous, and it is exceedingly difficult to offer a single clinical 
picture which includes all of its possible manifestations. In considering 
the prognosis of the lesions of the nervous system, especially of the cord, 
it must be remembered that there is no proof that syphilis ever causes any 
of the functional diseases of the nervous system. 
Spinal syphilis tends to indiscriminate lesions with the inclusion of 
meningeal and cerebral changes. Spinal syphilis as shown by lumbar 
puncture is a frequent complication of tertiary syphilis; its diagnosis can 
be positively established by the Wassermann reaction of the blood and the 
examination of the cerebrospinal fluid. 
There are occasional cases of spinal syphilis which cause positive 
symptoms within one month of the initial infection; as a rule from three 
to five years lapse before the spinal lesions of syphilis develop subjective 
symptoms. 
Spinal syphilis during its course is characterized by remissions and 
exacerbations; for this reason threatening symptoms do not have the same 
prognostic significance as they do with non-syphilitic disease of the cord 
in which the prognosis is less favorable. With spinal syphilis, the multi- 36 
SPECIFIC INFECTIOUS DISEASES 
plicity and incompleteness of symptoms are characteristic. Oppenheim 
accents “the instability, the coming and going of symptoms.” Paresis of 
one or both legs may develop suddenly, and promptly increase to para- 
plegia, or paresis of one limb may remain. Spinal syphilis is a protean 
disease: its typical form includes sensory and motor symptoms—usually 
specific, partial paraplegia—with bladder invasion in some cases. Oppen- 
heim describes a “pseudotabes syphilitica,” in which the disease extends 
to the posterior roots and column. 
So far as life is concerned, the prognosis of the majority of these cases 
is good; complete restitutio ad integrum is not often reached, for there 
are secondary changes which result from compression and scar tissue, 
and in cases which mend, are likely to leave permanent weakness of the 
lower extremities. As a rule bladder function is restored in the favor- 
able cases. 
There is always danger in these cases of sudden and severe exacerba- 
tion of symptoms, associated meningo-myelitis; the brain symptoms may 
suddenly gain the ascendency, and death follows within a few days or 
weeks. The prognosis is always graver in those cases in which brain 
symptoms are present either from the beginning, or develop gradually 
or suddenly. Such cases may develop and lead to death during periods 
of latency. 
I feel that, with the positive results of cytological examinations;— 
the four reactions, i. e., (1) Honne reaction (globulin + Phase I (2) 
Wassermann reaction (within the blood) (3) Pleocytosis (lymphocy- 
tosis) (4) Wassermann reaction (in the spinal fluid)—cases will come 
under earlier treatment, and the prognosis will be accordingly improved; 
that there will in consequence he fewer advanced cases and less perma- 
nent damage. 
Cases in which there are far-reaching changes in the arteries (endar- 
teritis obliterans) and veins, lead to myelitic softening and permanent 
loss of function. 
Spinal syphilis may run its course with all of the symptoms of an 
acute dorsal or dorsocervical meningitis. In these cases the prognosis 
depends on the extent of the specific changes, the stage of the disease, 
the reaction to treatment and the strength of the patient. We have seen 
a number of cases in which recovery followed; some of our cases devel- 
oped cerebral symptoms and died. In one, the spinal symptoms yielded, 
the patient fell into a somnolent condition, in which she remained during 
a number of weeks, and under rigorous specific treatment (mercurial 
inunction), recovered completely. 
Spinal lesions which limit themselves to the nerve roots and meninges, 
without involving the substance of the cord, offer a good prognosis in a 
large proportion of cases. These are the more favorable cases of spinal 
lues. Whenever the cord substance has degenerated the prognosis for res- PKOTOZOAN INFECTIONS 
37 
toration of function is bad. Paraplegia of short duration, promptly 
subjected to treatment, offers a fair prognosis. 
The prognosis of specific spinal paralysis is materially influenced by 
its extent and the time of its existence. Spastic contractures with such 
paralysis, and exaggerated reflexes argue against relief by treatment. 
A large number of the cases of spinal syphilis included in our con- 
sideration, correspond exactly with the complex now known as “Erb’s 
syphilitic spinal paralysis” to which Erb called attention in 1892. The 
paralyses are always spastic; the tendon reflexes are exaggerated; the 
tension of the muscles themselves is not markedly increased. There are 
paresthesias and girdle sensation without pain, save in occasional cases. 
The bladder and rectum are involved in advanced cases. Erb’s syphilitic 
paralysis is chronic; it tends to improve; there are long periods of remis- 
sion and in many cases the process remains stationary—covering a period 
of many years. 
Relapse, years after improvement or cure, is not infrequent. 
There are cases of spinal syphilis which remain uninfluenced by any 
treatment, progress either insidiously or as may happen, run an acute 
course, ending in a few weeks. 
Acute tertiary lesions of the spine added to so-called metasyphilitic 
disease of the nervous system offer an unfavorable prognosis. 
Hereditary types of cerebrospinal syphilis may lead to indiscriminate 
and chronic lesions which are hut little influenced by treatment; occasion- 
ally Oppenheim claims to have seen satisfactory recoveries. 
Syphilitic Peripheral Neuritis.—There are occasional forms of syphi- 
litic peripheral neuritis ; the ulnar nerve is invaded by predilection. 
Syphilitic poison does not show marked affinity for the nerve trunks 
but we have met a number of cases which prove the possibility of such 
invasion, in all of which, the prognosis was good. 
Evidences of compression of separate nerves of the periphery, due 
either to the pressure of specific exostoses or to gummata, may yield to 
treatment. 
References 
Adler (Isaac). New York Med. J., 1898, Ixvii, 577. 
Aschoff. Path., Anat., etc. 1912. 
Jores Path. Wichtig Erkrank. 1913. 
Path., Anat. 2 Bd., 2 Aufl., 15J). 
Bayly. Clinical pathology of syphilis. 1912. 
Bramwell. Clinical studies. 
Brooks (Harlow). Interstate Med. J., June, 1913, 512-513. 
Dreyer. Medizin. Klinik, May 4 1913. 
Dreyfus. Munch, med. Wchnschr., 1912, Nos. S3 & 34- 
Edinger. Der Antheil von Function, etc. Wiesbaden, 1908. 
Eisner. Serious heart lesions without persisting physical signs. Arch. Diagnosis, 1909. 38 
SPECIFIC INFECTIOUS DISEASES 
Fournier. La syphilis. Paris. 
L’ her ed.-syphilis. Paris, 1907. 
Gerber. See Scholtz, [l. c.] 
Grassmann. Ueber aquirirte Syphilis des Herzens. Munch, med. Wchnschr., 1897; 
also Deutsch. Arch. f. klin. Med., Leipzig, 1900, Ixix, 58-264- 
Gruber (G. B.). Uber d. Doehle-Hellersche Aortitis. Jena, 1914. 
Hauck. Naegeli, Bluterk. u. Blutdiagn. 1912, 667 p. 
Hirschfelder. Diseases of the heart and aorta. 
Huchard. Malad de coeur and syphilis gommeuse de coeur. Rev. de Med., Paris, 1907. 
xxvii. 
Heubner. Die luctische Erkrank. der Hirnarterien. Leipzig, 1874. 
Hutchinson. Allbutt & Rolleston, System of Medicine, i, 100. 
Hyde. Handbuch d. Kinderkrarikh. (Pfandler & Schlossmann). 2. ed., ii. 
Kaufman-Wolf. Ztschr.f. klin. Med.,Bd. Ixxv, Hft. 3-8; also Bd. Ixxvi. 
Koplik. J. Am. M. -Ass , Jan. 3, 1914. 
Mracek. Die Syphilis des Herzens, etc. Arch. f. Dermatologie u. Syphilis, 1893, xxv 
[Ergenzungshefte), 279. 
Meyer {Jerome). New York State J. of Med., 1912. 
Naegeli. Bluterkrankk. u. Blutdiagnostik. Leipzig, 1912. 
Neisser. Cavendish Lecture, 1911, quoted by Scholtz [Z. c.]. 
Oppenheim. Lehrbuch der Nervenkrank. 6 Aufl., 400. 
Plaut, etc. Leitfaden zur Untersuch. der Zerebro-spinal-fliissigkeit. ■ 1913. 
Rolleston. Diseases of the liver, etc. 1912. 
Scholtz. Lehrbuch der Haul u. Geschlechtskrankh. Leipzig, 1913. 
Sabrazes & Mathis. Quoted by Naegeli [Z. c.]. 
Stadler (E.). Die klinik d. syphilit. Aortenkrank. Jena, 1912. 
Virchow (R.). Archiv. f. path. Anat. 1858, Bd. xv. 
Cerebral Syphilis.—The frequency and great importance of syphilitic 
infection as a cause of grave disease of the nervous system is promptly 
appreciated when we consider the results of lumbar puncture, which 
offer positive evidences in characteristic change in the fluid, of the 
existence of such complication. The results in over 1,400 lumbar punc- 
tures made and reported by Dreyfus at the Stadtisches Krankenhaus in 
Frankfurt a/M. are instructive. It was found that during the early 
period of syphilitic infection the lumbar fluid showed positive involve- 
ment of the nervous system (brain and spine) in 80 per cent of all such 
cases, and that 12 per cent of all latent syphilis showed positive syphilitic 
disease of the central nervous system in characteristic changes in the 
lumbar fluid withdrawn. By this method therefore—the appreciation 
of the significance of its revelations and the rigorous modern treatment 
of the disease—the prognosis of cerebral and all metaluetic infection is 
being favorably influenced. In a lecture which Ehrlich delivered (Jan- 
uary 16, 1914) on the difficulties which he Avas forced to overcome in 
bringing his remedy to its present usefulness and safety, he made the 
positive statement that, guided by the results of lumbar puncture, the PROTOZOAN INFECTIONS 
39 
clinician was now in position to positively prevent the development of 
paresis and tabes by the intensive treatment of the infection. 
General Consideration oe Cerebral Syphilis.—The separate 
types of cerebral syphilis offer a varying prognosis, yet it may be wise in 
a work of this character to follow the example of Xonne as set forth in 
his lectures on syphilis of the brain, to devote a short chapter to the gen- 
eral consideration of the subject. 
It may be assumed that all types of syphilitic disease, as it invades 
the brain, are of serious import and frequently lead to death; often, to 
a chronic state of complete or partial incapacity persisting during years; 
while in a number of cases the disease may be followed by complete 
restoration to health—physical and mental. It may be assumed further 
that syphilis of the brain offers a more favorable prognosis than most 
non-syphilitic diseases of that organ, including more particularly brain 
tumor, abscess, multiple sclerosis and degenerative changes associated 
with paralysis; this is true when the diagnosis is made early. 
Comparing the results of the operative treatment of brain tumors, 
we find, in the event of the prolongation of the life of the patient, that 
recovery is not likely to be complete; that as a rule the symptoms have 
not been materially relieved. Single abscess of the brain is rare; usu- 
ally there are multiple lesions; as Ronne emphasizes in his comparison 
of the prognosis of these conditions, there is likely to be secondary menin- 
gitis. Multiple sclerosis and secondary paralyses lead to death sooner 
or later, either directly or frequently indirectly, from distant invasion—- 
heart, lung, sepsis, etc. These facts justify the statement above made 
that specific brain lesions when recognized early offer a much better prog- 
nosis than do those of non-specific nature. 
Paresis is not included in our consideration of brain syphilis, this 
will receive separate treatment. We wish to include in this chapter, 
brain syphilis in which the symptoms are dependent upon specific menin- 
gitic invasion, gummatous infiltration and specific arteritis. Fournier 
reports that of his cases are cured, | are materially improved, and £ 
die. In Rumpfs analysis of 34 cases he found 31 justifying conclusions; 
of these latter, 5 died, 8 remained incapacitated and sick, improvement 
followed in 6 cases, and 12 made full recoveries. Hjelmman on the other 
hand holds that his experience justifies the conclusion that one-half of his 
cases proved fatal or fell into hopeless conditions, that the fully cured 
cases were not above 25 per cent, while in the remaining cases there was 
only partial improvement. 
My experience justifies the conclusions that have been advanced by 
Fournier and Rumpf. The time of recognition of the disease becomes 
an important factor; in no other disease of the nervous system is this 
more vital. Further, it must be agreed that our free recourse to modern 
methods of diagnosis, including blood tests (Wassermann) have influ- 40 
SPECIFIC INFECTIOUS DISEASES 
enced the prognosis of cerebral syphilis very favorably, and our statistics 
are therefore more encouraging than ever before. 
The examination of the spinal fluid shows that there is lymphocytosis, 
the globulin reaction, some leukocytosis and the positive Wassermann 
reaction. The albumin content is slightly increased. Pressure increased. 
Phase /, or the globulin reaction with the saturated ammonium sul- 
phate solution, is only present when there are symptoms of central nerv- 
ous disease. Decided change in the lumbar fluid after treatment and a 
return to a negative Wassermann may be interpreted as being favorable. 
From both hospital and private practice we are able to furnish many 
examples of cerebral syphilis in which there has been no return of symp- 
toms during many years—varying from two to twenty, and even longer. 
It must be further conceded that with increased diagnostic ability we 
have traced a large number of cerebral symptoms to syphilitic infection, 
have treated these rigorously, and have in consequence materially changed 
our statistics. 
Adopting, as does the modern clinician the two underlying pathologic 
conditions as the leading causes of symptoms in cerebral syphilis—the 
first so thoroughly described by Virchow in 1858, which includes those 
lesions of gummatous nature with meningeal invasion, and the second, 
which proves the presence of specific arteritis included in the classic de- 
scription of Ileuhner in 1874—it becomes possible to plant our diagnosis, 
prognosis and treatment, upon a safe foundation. 
The analysis made by Haunyn of his own 88 cases and 325 collected 
from medical literature (total of 413 cases), proves profitable and inter- 
esting. Haunyn considers cases “cured” which show no recurrence after 
five years of apparent health. He found seven such cases in Caspary’s 
material, 3 in Fournier’s; his own included 10 cases; while Oppenheim 
in his monograph reports seven cases of complete cure 5 and 10 years 
after the last attacks. Honne presents a material of 124 cases of cere- 
bral syphilis in which symptoms were limited absolutely to the brain. 
Of this number he was able to follow only 22 cases 5 years, 4 cases over 5 
years. Of this latter number two cases followed six years, one seven, 
one eight years—all remaining without recurrence of symptoms. 
It may be accepted as true that in the majority of cases supposedly 
cured, unless treatment continues to be rigorous and the patients are prop- 
erly led and safely guarded, they fall into the larger class of the partially 
cured. 
My experience justifies the conclusion, that cerebral syphilis which 
has remained uncontrolled or untreated during a period sufficient to lead 
to paralysis with associated degeneration of brain tissue, whatever the 
type, is never fully cured; and though treatment may improve existing 
symptoms in a measure, the damage is permanent and the patient often 
develops sudden exacerbation which may lead to death. PROTOZOAN INFECTIONS 
41 
Many cases live for years with symptoms of secondary degeneration. 
Some are tied to a mattress grave. Neurologists are agreed in considering 
the prognosis of cerebral syphilis, that in no cases apparently cured can 
we be certain of freedom from relapse. “Syphilis never dies, it only 
sleeps” (Nonne). Relapses may include acute endarteritic attacks, spe- 
cific meningitis, fresh gummatous deposits; and these may alternate with 
each other in a single case. 
I have seen long periods lapse between attacks; in malignant cases 
one type may follow the other with but short intermission, patients finally 
yielding in coma to specific meningitis. 
The study of our own material justifies a more serious prognosis in 
the cerebral syphilis of advanced, than during early life. Age has seemed 
to be without marked influence until about the 45th to 50th year, after 
which, because of greater tendency to arterial degeneration, resistance 
to treatment has increased and its effect has become less efficient and 
slower. (Ricord, Fournier and Mingazzini report similar experiences.) 
Malignant types of brain syphilis are not infrequent among young sub- 
jects; many of these are found with the added depressing effect of dissi- 
pation in venery and alcohol. 
Interval Following Specific Infection and the Development 
of Cerebral Syphilis.—Long postponed cerebral syphilis offers a less 
favorable prognosis than does the development of brain lesions before the 
end of ten years (Hjelmman, Naunyn, Nonne). Heredity does not seem 
to influence the prognosis of cerebral syphilis. Neuropathic tendencies 
have not invited or influenced the development of the brain complication. 
Tuberculous and anemic individuals, the cachectic and generally re- 
duced—particularly those who, weakened by alcoholic excess, are not 
good subjects—offer scant resistance to the advance of cerebral lues. 
It has seemed to us that the most malignant types of cerebral syphilis 
met in our practice have followed alcoholic meningitis or wet brain, which 
in turn complicated delirium tremens. Most of these were seen in hos- 
pital wards; were neglected and among the lower classes. Tarnowsky 
found in 100 cases of pronounced cerebral syphilis, 43 chronic alcoholics, 
many neurasthenics, some cases of skull injuries, and a good number of 
patients overtaxed mentally; and he believes that these factors are of 
paramount importance in the prognosis of the disease. This would also 
corroborate the theory of Edinger. My experience does not include a 
single case in which I have reason to believe that trauma was a provo- 
cative factor, or directly influenced prognosis. 
The author is in accord with Byron Bramwell who has demonstrated 
the fact that the graver forms of nerve and brain syphilis follow the 
milder types of the initial disease. This is simply due to the early disap- 
pearance of visible lesions and the resulting neglect of treatment of these 
milder cases. Fournier believes that there is a form of syphilis which by 42 
SPECIFIC INFECTIOUS DISEASES 
predilection attacks the nervous system: “syphilis a virus nerveux 
That there are such cases, there can be no doubt. They may appear early 
or late ; they are likely to remain unaffected by treatment. They may 
follow the so-called milder infections or cases which show malignant 
tendencies ah initio. The location of the initial lesion has not seemed to 
influence the prognosis of any specific complications in our experience. 
Rational and early modern treatment has during the last five years 
materially influenced the prognosis of cerebral syphilis and all nerve com- 
plications of syphilis, and unless I misinterpret my experiences, has 
already reduced the number of these cases. In this connection the state- 
ment of ITjelmman is of vital importance, if correct: “In from 82-88 per 
cent, patients with symptoms of cerebral syphilis have had either no 
treatment or insufficient treatment,” and he believes as we all have reason 
to do, that in the majority of these cases rational treatment would have 
prevented the serious condition. 
There will always be a remnant of cases in which, in spite of early and 
persistent treatment, syphilitic lesions whether cerebral or not, will re- 
main rebellious and refuse absolutely to yield. In the majority of these, 
careful search will reveal the cause, but the therapeutist will be unable 
to antagonize it successfully. RTonne, however, believes that cases of brain 
syphilis offer no better prognosis, in spite of the fact that’ they were 
scientifically treated—mercury, etc., administered during several years— 
than do those cases in which the early treatment was neglected or entirely 
omitted. Cases of specific localized meningitis associated with long pe- 
riods of somnolence, frequently remaining unrecognized—splendidly 
pictured by Buzzard—offer a very favorable prognosis. To the inexpe- 
rienced, the clinical picture may appear exceedingly alarming. Haunyn, 
TIjelmman and Oppenheim place basilar meningitis of specific origin in a 
class offering a good prognosis (71 per cent). These cases, it has been 
our experience, may relapse, but in the end they seem to make good 
recoveries. * 
Diffuse deposits do not as a rule offer an encouraging outlook. The 
changes are not limited to the brain; there are likely to be indiscriminate 
lesions in distant nerve tissue. The early diagnosis is not easily made; 
the cases are therefore misunderstood during considerable periods. 
Syphilitic epilepsy with focal symptoms is in the majority of cases 
favorably influenced by treatment, and recoveries are not infrequent. 
Early recognized single gumma will in most cases show marked im- 
provement under treatment, and while a complete anatomic cure may not 
be certain, clinically the large majority of these cases has yielded and has 
remained without serious complications, though in none does the prog- 
nosis justify cessation of eternal vigilance. 
I have already referred to the Huebner type of specific endarteritis. 
Gummata of the arteries are not of frequent occurrence. In the Huebner PROTOZOAN- INFECTIONS 
43 
type of arteritis, the inflammatory infiltration of the vessel wall may be 
absorbed, the narrowing of the lumen may not be materially reduced, but 
the extent of brain tissue involved is likely to be limited; and though it 
may net regain its power, there will as a rule be compensation sufficient 
in most cases to supply function. I have seen cases diagnosticated as 
arteritis specifica, with hemiplegia, which have yielded after several 
weeks of persistent symptoms. In the majority of these cases the patients 
recover with clear intellect and memories, are undisturbed, though there 
may in the severe cases, be some motor weakness with few sensory symp- 
toms left. Hemiplegia, however, with syphilis should never be lightly 
considered; it is always serious. 
In cases associated with renal changes, chronic nephritis and hyper- 
tension, the prognosis must of necessity be grave. 
Recurrences are not infrequent, if there are many or if there is con- 
tinuous progression of arteritis, the patient falls into a pitiful condition— 
paretic and hopeless. 
Cases of specific arteritis (Huebner) do not as a rule die suddenly or 
early. When the process invades the basilar vessels, the prognosis is most 
grave because of the invasion also of the higher psychic centers. 
It is occasionally difficult to differentiate paralysis of the motor oculi 
of arteritic and gummatous origin. The former offers a less favorable 
prognosis so far as complete restoration of function is concerned. Ordi- 
nary syphilitic paralysis of the motor oculi, usually gummatous, is likely 
to disappear completely under treatment. Optic neuritis (choked disk) 
does not argue against the possibility of recovery; advanced optic atrophy 
with cerebral syphilis is always evidence of serious disturbance, and the 
prognosis is consequently bad. 
Long continued paralysis of the cranial nerves, with syphilis of the 
brain, offers an unfavorable prognosis for restoration of health or function. 
References 
Bramwell (Byron). Clinical studies. 
Buzzard. Lectures of diseases of nervous system. 
Edinger. Der Aniheil von Function, etc. Wiesbaden, 1908. 
Erb. Neurologisch.es Centralblatt, 1892. 
Fournier. Lecons clinique sur la syphilis. Paris, 1881, etc. 
Hjelmman. Ref. neurol. Centralblatt, 1894, 342, etc. 
Heubner. Die luetische Erkrank. der Hirnarterien. Leipzig, 1874. 
Mingazzini. Rivista di pathol. nervosa mentale, xi, Fasc. 12. 
Montegazza. Gaz. hebdem de med., 1902, No. 55. 
Naunyn. (Koenigsberg) Klinik. 
(Koenigsberg) Pr. Leipzig, 1888. 
Berl. klin. Wchnschr., 1879. 
Nonne. Syphilis d. Nervensystems. Berlin, 1909. 44 
SPECIFIC INFECTIOUS DISEASES 
Oppenheim. Syph. Erkrank. des Gehirns. Nothnagel Handbuch, 1897. 
Ricord. Lectures & letters. 1851. 
Rumpf. Syph. Erk. des Nervensystems. Wiesbaden, 1887. 
Tarnowsky. Medicine. 1891, No. 4 (Russian). 
Virchow (Rudolph). Virch. Arch. f. path. Anatomie, 1858, Bd. xv. 
Late Manifestations of Tertiary Syphilis of the Cord and Brain—So-called Meta- 
syphilitic Disease 
The manifestations of the tertiary stage of syphilis which I include 
in my consideration, have until the present time been considered to be 
metasyphilitic—not dependent upon syphilis primarily—but the condi- 
tions were supposed to develop in syphilitic subjects in whom it was 
assumed that the brain and cord were possibly vulnerable, or that for 
some unknown cause degenerative and atrophic changes were invited. 
With increasing clinical experience and pathological study, a strong 
suspicion had arisen in the mind of experienced neurologists and syphilog- 
raphers that the relation of metasyphilitic diseases to specify syphilitic 
infection was one of dir.ec-t cause and effect, and during several decades 
the French school led by Fournier, and the German school of which Erl) 
was the Nestor among the neurologists, fought an active battle to establish 
the direct pathogenic relation of syphilis to tabes, paresis, and tabo- 
paresis. 
Statistics gathered from the authoritive medical centers of both 
continents strengthened the contentions of Erb and Fournier, that in over 
90 per cent of all so-called metasyphilitic disease, a clear history of 
syphilis could be established and that syphilis therefore was the prime 
factor to be considered in the prognosis and treatment of these diseases. 
Even the strong opposition of such authorities as Charcot, Westphal, von 
Leyden, and J. A. Glasser, did not influence Erb nor Fournier, who, 
persistently, by their writings and in their clinics, added material to 
strengthen their views. 
The profession had registered itself in favor of the syphilitic path- 
ogenesis of the metasyphilitic diseases and was fully prepared to receive 
the results of the epoch-producing experiments of Noguchi, which 
demonstrated the Treponema pallidum in the cord of tabetics and in the 
brain of paretics. 
With these positive proofs of the presence of the Treponema, and the 
results of inoculation experiments by which similar conditions have been 
produced, and the further overwhelming evidence offered by the positive 
Wassermann reaction of the blood and by the spinal fluid (withdrawn by 
lumbar puncture), I feel justified in placing the conditions formerly 
included among the metasyphilitic diseases in the section on Syphilis. 
I believe that such classification will do much to justify the intensive PROTOZOAN INFECTIONS 
45 
treatment of syphilis, and will consequently favorably influence the inci- 
dence of tabes and paresis; further, I am fully satisfied that the infected, 
when aware of the true cause of the most dreaded of all of the complica- 
tions of syphilis, will be more eager than ever before for such radical treat- 
ment as is demanded in the individual case. 
We consider: (1) tabes dorsalis (locomotor ataxia), (2) taboparesis, 
(3) paresis (progressive paralysis of the insane). 
Tabes dorsalis 
{Locomotor ataxia) 
The prognosis of locomotor ataxia has been powerfully influenced by 
the introduction of the newer methods of treating syphilis, the discovery 
of the Treponema in the cord and brain of tabetics and paretics, and the 
revelations of sero- and cytodiagnosis. Several years must lapse before 
positive conclusions can be justified. 
The characteristic and constant lesion of locomotor ataxia is the grey 
degeneration, probably developed after' a limited period of irritation— 
possibly inflammation, of the posterior columns of the cord. The disease 
is primarily a system disease of the cord, but its many manifestations 
soon prove its indiscriminate tendencies. 
There are occasional juvenile forms of the disease due to congenital 
syphilis. As a rule tabes is found in the male, three times as often as in 
the female, and between the thirtieth and fiftieth years, and from 5 to 20 
years after infection, with an average of 9 years. 
Tabes within one to five years after initial infection has in my 
experience developed rapidly, and has usually entered the ataxic stage 
early. These cases offer a less favorable prognosis than do those which 
follow infection after a longer time. 
In a fully developed case the following conditions may prevail: 
1. The membranes of the cord are thickened over the part involved—* 
more posteriorly. 
2. There is flattening of the cord. 
3. With degeneration, the posterior columns and nerves are shrunken 
and atrophied. 
4. Connective tissue proliferation in the postero-external columns 
and posterior horns. 
5. The disease attacks the dorsal and lumbar regions by preference. 
6. With the onward march of the disease, the postero-internal columns 
and the posterior horns may be involved. 
Y. There are likely to be degenerative changes in one or more of the 
cranial nerves—the optic and motor oculi are oftenest involved. These 
changes may be either early or late. 46 
SPECIFIC INFECTIOUS DISEASES 
8. During the terminal stage the anterior horns and the lateral 
columns may be invaded, leading to atrophy of muscles and contractures. 
9. There may be chronic arteritis invading the vessels of the cord 
and brain. 
10. The terminal stage may include paresis or other cerebral lesions 
•—hemorrhage, thrombosis, pachy—and leptomeningitis, and changes in 
the ependyma. 
11. Aortitis, arteriosclerosis or arteritis are frequent complications, 
depending upon the same initial cause. The rapid development of arterial 
degeneration in. tabetics of all ages is often surprising. The artery is uni- 
formly thickened—shows placque deposits, and aortitis in such cases is 
usual. 
The prognosis of locomotor ataxia must include the consideration of 
its (a) cause; (b) sex; (c) age; (d) possible prophylaxis; (e) location and 
extent of the degeneration; (f) the influence of the treatment on the symp- 
toms of the various stages of the disease—initial, ataxic and paralytic; 
(g) the prognostic significance of individual symptoms; (h) Wassermann 
reaction of the blood and spinal fluid; (i) the complications. 
(a) Causes.—In the light of our present knowledge, it is safe to 
assume that locomotor ataxia is always due to luetic infection. Basing 
the consideration of the disease upon this assumption strengthens the 
hope that with the dissemination of knowledge and the radical early 
treatment of those infected, the late manifestations referable to the 
nervous system will decrease in the future. 
Fournier reported that in one thousand cases of locomotor ataxia, he 
found 92.5 per cent syphilitic. Erb found in 1,100 cases of locomotor 
ataxia among men in good condition, 89.4 per cent syphilitic; and in 158 
workmen, 77.2 per cent syphilitic; 6,000 cases of nervous diseases, other 
than tabes, show 20 per cent of syphilitics. 
Congenital and unrecognized syphilis was considered the cause of 
tabes in the small and unexplained remnant by both authorities; and 
with our present methods of diagnosis this conclusion is justified. 
In Germany, Virchow in his Krankhaften Geschwiilsten—a work far 
in advance of its time—insisted, before either Fournier or Erb had offered 
their conclusions, that “there is no doubt of the fact that some cases of 
tabes are syphilitic.” For more complete statistics showing the relation 
of syphilis and tabes the reader is referred to Honne’s classic work; also 
Rumpf. The statistics of all large clinics gathered during the past 
decade fully corroborate the early conclusions of the French and German 
School. 
The so-called metaluetic diseases including locomotor ataxia—either 
by their history, when thoroughly considered, or as the result of cytosero- 
diagnostic methods—establish syphilis as the cause in most cases (92 to 
97 per cent). PROTOZOAN INFECTIONS 
47 
Predisposing Factors.—There are factors which predispose syphi- 
litics—acquired or congenital—to tabes; among these are improper treat- 
ment of the initial infection, hereditary tendencies and diathesis, ex- 
posure, excesses in alcohol and venery, traumatism, overwork, and worry. 
The theory of Edinger that the various parts of the nervous system yield 
to disease in proportion to the fatigue (exhaustion) resulting from over- 
work and the many other factors of life which, through the emotions and 
long continued wear and tear of an organ, prepare for surrender and ulti- 
mate pathologic degeneration—is plausible and deserves consideration. 
(b) Sex .—The influence of sex on prognosis is insignificant. Collins 
believes that the disease advances Avith greater rapidity in women; this is 
not the accepted view. I have found that women fall into the same 
chronic stages as men and are subject to the same complications. Our 
cases show a larger number of paralysis of the eye muscles in women. 
(c) The Influence of Age.—Pathologically juvenile tabes does not 
differ from the disease as found in the adult; both the symptoms and com- 
plications are identical though their development 'is different. 
Syphilis is the cause of juvenile tabes; girls are oftener affected than 
boys. In juvenile tabes, optic atrophy with consecutive blindness is an 
early symptom, Avhile lancinating pains are not as frequent as in the 
adult; the same is true of paresthesias and analgesias. Fully developed 
ataxia is exceptional; the course of the disease is protracted, but mild 
(Koester). Blind children are often found in public institutions with 
juvenile paresis: not an infrequent sequel. 
There are occasional acute cases which run a rapid course in patients 
between the ages of twenty and thirty. The younger the adult, the more 
likely is the process to show rapid progression. One-half of all cases be- 
tween 20 and 40 progress rapidly. After the fiftieth year, acute cases 
are unusual and chronicity is the rule. Tabetics often reach old age, as 
is shoAvn by the statistics offered in considering the duration of the 
disease. 
(d) Possible Prophylaxis.—For the future of the syphilitic, the possi- 
bility of the prevention of the late manifestations of disease of the brain 
and cord is of the utmost importance. The clinical experiences of the 
past prove that it is the rare exception for thoroughly treated cases of 
syphilis during the early and late stages to develop either tabes or paresis. 
It is the untreated, usually mild cases in which the initial lesions were 
either hidden, unrecognized, or evanescent, and which received practically 
no treatment during the secondary stage of the disease, which later develop 
the most serious complications; and when the nervous system is included, 
the progression of symptoms is as a rule so insidious as to remain unrecog- 
nized until grave and irreparable degeneration proves the presence of 
advanced disease. The further evidence offered by repeated examination 
of the lumbar fluid during the early stage of syphilis, proves that the 48 
SPECIFIC INFECTIOUS DISEASES 
intensive treatment at once overcomes the incipient invasion of the brain 
and cord. 
Dreyfus has demonstrated, after over 1,400 lumbar punctures, that 
the nervous system, i. e., the brain and cord, gives positive evidences of 
change in 80 per cent of all cases of early syphilis, and that in 12 per 
cent of syphilitics the reactions are positive during the late stages. It is 
the 12 per cent of uninfluenced cases which cloud the prognosis, and these 
are among the subjects who develop tabes and paresis when one or more 
of the exciting factors already mentioned prevail. 
The small proportion of syphilitics who develop tabes and paresis also 
argues in favor of the prophylactic influence of the radical and intensive 
treatment of the initial disease. In private practice, where there is an 
intelligent cooperation of the patient and the physician, I have less than 
one per cent of so-called metasyphilitic infections to report. The average 
reported by Scholtz is from 2 to 3 per cent; this includes the material of 
hospitals, etc. Reumont found 40 cases of tabes in 3,600 syphilitics—1.1 
per cent. 
It is, according to well-digested experience, fair to give almost positive 
assurance of escape from the late manifestations of the tertiary stage of 
the disease, provided that the treatment of the preceding stages has been 
intensive and appropriate. 
The profession is passing through a period in which positive conclu- 
sion with regard to the future of the syphilitic treated with salvarsan and 
mercury combined, cannot be given; the time for a safe forecast has been 
insufficient. To be certain that the late manifestations including tabes will 
be entirely prevented will require a period of observation, covering at 
least three decades. The indications, however, are favorable and those 
who have had the largest experience justify an encouraging outlook. 
Ehrlich believes “that the early intensive treatment of syphilis with sal- 
varsan and mercury will practically prevent the occurrence of tabes, 
taboparesis and paresis.” 
(e) The Location and Extent of the Degeneration.—The prognosis is 
worse in cases which are associated with multiple or disseminated cere- 
bral lesions; worse also so far as comfort and progression are concerned, 
the higher in the spine the degeneration spends its force; bad with cervical 
and bulbar invasion. 
The prognosis is absolutely bad when paresis complicates tabes; also 
with other psychoses. 
Reference to lesions of the peripheral nervous system, the brain and 
sympathetic system are found in the separate chapters dealing with these. 
(f) The Influence of the Treatment on the Symptoms of the Various 
Stages of the Disease.—We consider an (1) initial stage (neuralgic—pre- 
ataxic, (2) ataxic stage, (3) paralytic stage. 
1. The Initial or Neuralgic Stage.—Locomotor ataxia may re- PROTOZOAN INFECTIONS 
49 
main stationary in any stage of the disease—oftener in the first stage— 
with or without treatment. The increasing benign tendencies of certain 
types of the disease was recognized by Charcot and Brissaud because of 
the growing frequency of mild cases which show but little tendency to 
progress, and remain latent or stationary during several decades, in some 
instances. This fact has led to the conclusion that tabes is less serious 
to-day than in the past: a fact which unqustionably depends upon the 
more thorough and scientific treatment of the early stages of the disease. 
Oppenheim believes that there is in tabes, as in many other diseases, a 
lowering of the malignancy of the infection with succeding generations. 
The older neurologists including Duchenne, Romberg, Trousseau and 
Charcot during his early experiences, as well as Leyden as late as 1878, 
considered the disease to be always progressive, and rarely recognized the 
cases which have increased in frequency, with a duration often of 15 to 30 
years or even longer. It may be assumed that lack of the diagnostic ear- 
marks, which we now possess—Argyll-Robertson pupil, Westplial phe- 
nomenon—allowed some of these chronic cases to remain undetected. 
There are cases which show no tendency to progress but in which a 
single symptom remains in the ascendency. Such cases were prominent 
before the introduction of salvarsan and are still met, though the indi- 
vidual symptom is now often favorably influenced by treatment. Among 
the prominent single symptoms of these cases are the lightning pains, 
altered bladder function, or ocular paralysis. In occasional cases there 
may be improvement of a number of symptoms during the early period, 
while one or two symptoms remain unchanged but are not sufficiently 
severe to incapacitate the patient. In the cases with a single prominent 
symptom the progress of the disease may be so slow as to be unnoticed, or 
there may never be extension. Such a case I have had under observation 
in a banker who has during 30 years continued at his work with limited 
paralysis of the left motor oculi, loss of deep reflexes, but without pro- 
gression, and no evidences of incoordination. Another case with limited 
optic atrophy and Argyll-Robertson pupils has also been watched over 25 
years. The patient is now 70 years of age, has retired from his business, 
is still active in society and is president of a club, able to be about un- 
assisted with occasional lightning pains as his only troublesome symptom. 
It is interesting to note that these results w7ere obained before the days of 
salvarsan. 
Occasionally after a period of severe symptoms during the initial stage, 
with incoordination and sensory symptoms, improvement may follow suffi- 
cient to make it possible for the patient to return to his work without the 
advent of new symptoms during long periods. Such cases, unless they die 
of intercurrent disease, finally progress gradually and after 25 to 30 years 
pass through the ataxic to the paralytic stage. 
Cases in which gastric crises are the prominent feature of the incipient 50 
SPECIFIC INFECTIOUS DISEASES 
stage, with modern treatment are made comfortable during long periods. 
There are exceptions to this statement, but in the majority of such cases 
it is justified. 
In most cases it is difficult to determine the exact time of the advance 
from the initial to the second stage, for ataxic symptoms are not uncom- 
mon during the first year; and in a number of cases there are, as already 
suggested, cycles during which symptoms may increase followed by im- 
provement and stationary periods. As a rule, the return to the condition 
which existed before the exacerbation, with or without treatment, is m>t 
complete and there is a remnant of symptoms which shows progression of 
the lesion. 
In offering a forecast of the effect of treatment on the separate stages 
of the disease, I can give only general conclusions, but would refer the 
reader for detailed information to (d) the significance of the separate 
symptoms on prognosis. The initial stage varies in length and symptoms 
in different cases. There are tabetics who continue with but one or two 
symptoms during many years, without noticeable progression; the condi- 
tion is stationary, uninfluenced by any treatment. There are cases in 
which there is simply a loss of the patella tendon reflex without severe 
crises, occasional bearable pains, and some ocular paralysis. Such cases 
permit the patient to continue at his work without marked inconvenience. 
The reaction of the separate symptoms to treatment and the tendencies of 
such cases we consider in connection with the separate symiptoms; but the 
general statement is justified that these cases react favorably, so far as 
sensory symptoms are concerned. 
The cases in which the initial stage includes loss of patella tendon 
reflex, Argyll-Robertson pupil, lightning pains, analgesias, and paresthe- 
sias with girdle sensation, ocular paralysis, and early gastric crises may 
remain stationary during long periods, but as a rule are slowly pro- 
gressive. If during the initial stage urinary symptoms are superadded, 
the chances for control of symptoms or latency are reduced. 
Early ataxia during the incipient stage and sudden increase of symp- 
toms is always unfavorable; for it indicates deep involvement in a degen- 
erative process of the postero-external, possibly the cerebellar tract, and 
this condition is not easily influenced by treatment. 
ISTo treatment permanently influences advanced degeneration in any 
stage; inflammatory changes in the incipient stage may be improved. 
Improvement does not mean cure, and it is not as a rule held unless 
repeated injections and interval treatment is continued. 
The examination of the blood and spinal fluid for the Wassermann 
reaction and for other characteristic cellular conditions proves of inestim- 
able value for treatment and prognosis during the initial stage. 
The careful observation of the effect of the combined salvarsan and 
mercury treatment of the early stage of tabes proves the urgent need of PKOTOZOAN INFECTIOUS 
51 
prolonged treatment—repeated injections of sufficient size—before conclu- 
sions for prognosis are justified. So far as life is concerned the cautiously 
controlled treatment is practically without danger. 
During the incipient stage in a large experience, we have had not un- 
toward results. Herxheimer in a recent lecture reported 40,000 injections 
of salvarsan given to 11,000 patients in the Frankfurt Hospital under his 
supervision without a death, and Dreyfus reports 3,000 intravenous in- 
jections in 250 patients with hut one serious sequel and that was diagnos- 
ticated as meningo-encephalitis with recovery of the patient. Medical 
literature includes a number of deaths resulting from the use of salvarsan, 
hut these are exceedingly rare during the incipient stage of tabes. 
In occasional cases the patella tendon reflex, ocular paralysis, pains, 
and gastric crises are improved. The most encouraging feature of the 
treatment of the incipient stage of tabes is its favorable influence on the 
Wassermann reaction, which after one or two injections passes from the 
positive to the negative phase and often remains negative during long 
periods in most cases. Occasionally the treatment during the initial stage 
ct usss a positive reaction from a previously negative phase during a 
limited period. 
The most favor a Die cases are those in which the treatment leads from 
the positive phase to a persistence of the negative reaction. Less favorable 
cases are those in which after a limited period, there is a return from the 
negative to the positive reaction. Most unfavorable are those which in 
spite of treatment, continue to give a positive Wassermann reaction. 
My conclusions concerning the prognosis of the incipient or first stage 
of tabes based upon modern treatment prove the possibility of better con- 
trol of symptoms than by the previous methods, and in a number of cases 
the sensory symptoms and ocular paralyses have been so much improved as 
to encourage us to believe that they may be permanently relieved by several 
cycles of treatment. Marcus, Weber, McDonagh report the return of 
pupillary reflex after salvarsan with negative from a positive Wassermann 
reaction. 
In no single case, however, which I have observed thus far and treated 
according to modern mlethods, have I been able to banish the manifestations 
of the incipient stage sufficiently to justify the belief that the treatment 
did more than postpone longer than could be done by any previous treat- 
ment, the sensory disturbances with—as already suggested—improvement 
in other directions. It would seem that there is a strong likelihood of con- 
trol of symptoms during stationary periods by modern methods. Whether 
we shall be able to prevent the advance to the ataxic stage cannot be de- 
cided until our experience has grown and abundant time for observation 
has lapsed. 
Increase in weight and improvement of the general condition is the 
rule after treatment. 52 
SPECIFIC INFECTIOUS DISEASES 
2. Ataxic Stage.—Treatment has in individual cases improved some 
of the symptoms of the ataxic stage of the disease. As in the initial stage, 
so in the ataxic, sensory symptoms have been sufficiently improved to jus- 
tify the treatment. I have seen patients with both marked and insig- 
nificant ataxia, who had been incapacitated by severe crises so much im- 
proved by intensive treatment—salvarsan and mercury—as to return to 
and remain at their work. 
Occasionally the patella tendon reflex has been strengthened and with 
added mechanical treatment and resulting education, incoordination be- 
came less troublesome. All of these cases require repeated injections at 
varying intervals if the improvement is to be held. The sensory symptoms 
wdiile they recur, are less severe. Permanent results are not to be expected. 
3. The Paralytic Stage.—Treatment has absolutely no effect in per- 
manently controlling the symptoms of the advanced and final stage of tabes. 
Dreyfus claims that no tabetic is so far advanced as not to justify intra- 
venous injections of salvarsan. 
The treatment of tabes by means of the intraspinous injection of the 
salvarsanized serum taken from the patient according to the method of 
Swift and Ellis has been entirely without effect in our cases. My experi- 
ence with the method is limited, but the pains following were so severe and 
the results so unsatisfactory that I have no desire to continue the experi- 
ment, and do not believe that it offers promise of a favorable influence on 
the disease. Favorable results are recorded by others; the entire question 
is still sub judice. 
Dreyfus offers the following report of his experiences with the salvar- 
san treatment of tabes:— 
Leading Symptom. 
Number 
of 
Cases 
Treated. 
Materially 
Improved. 
Im- 
proved. 
Uninflu- 
enced. 
Symptoms 
Increased. 
Pains 
35 
20 
14 
1 
Headache, neurasthenia, 
perforating ulcer, blad- 
der symptoms 
9 
3 
4 
2 
Crises 
15 
7 
5 
3 
Ataxia 
18 
5 
7 
3 
3 
84 per 
cent. 
12 per cent. 
4 per cent. 
Dreyfus reports that some cases with advanced ataxia, which before 
treatment could neither walk nor stand for any length of time, were able 
after treatment to walk comfortably. Donath reports similar experiences. 
Donath’s material justified the following conclusions after the salvar- 
san treatment: PROTOZOAN INFECTIONS 
53 
Pupillary reaction returned in 3 of 28 cases 
Patella tendon reflex returned in 1 “ “ “ 
Walking was improved in 4 “ “ “ 
General improvement was manifest in 18 “ “ “ 
Marked gain of strength in 7 “ “ “ 
Improved mental state in 9 “ “ “ 
The reader is referred to the detailed rules given by Dreyfus for treat- 
ment in his full article (see references). 
(g) The Prognostic Significance of Separate Symptoms.—The rapid 
development of several symptoms at the same time during any stage of 
tabes is unfavorable. Cases in which there are but few symptoms offer a 
much better prognosis than do those in which there is a multiplicity of 
symptoms usually dependent upon indiscriminate lesions; these cases show 
rapid progression. 
Occasionally with many symptoms, the patient is advanced into the 
ataxic or from the ataxic to the paralytic stage and falls into a latent but 
helpless condition in which he may remain during a number of years; or 
there may be some improvement of one or more symptoms, but not sufficient 
in the presence of advanced ataxia to return the patient to usefulness. 
There are many cases which advance to the paralytic stage after steady 
progression of symptoms in which the ataxia is almost complete, in which 
the pains cease and the ocular paralyses remain. The mind is usually 
clear and active in these cases. I have one such case under observation 
of a man aged 60 who has been in the paralytic stage over 10 years and 
who is daily wheeled in his chair to his office, where he presides over a large 
institution as its president; there has been no apparent progression of the 
process during the past 5 years. In this case the bladder function has been 
paralyzed over 12 years; catheter life has been well borne. 
Multiplicity of symptoms does not always signify rapid progres- 
sion : there are occasional exceptions. Collins’ experience justifies the con- 
clusion that cases in which the sympathetic nervous system is involved— 
including crises, trophic disturbances, early troublesome bladder and rectal 
symptoms—offer the most unfavorable prognosis. With perforating ulcer, 
arthropathies, and other trophic changes, restitution to the former condi- 
tions is unusual. 
I have called attention to the cases in which gastric crises have 
yielded to modern treatment and there is a strong probability, basing our 
conclusions on the result of the experiences reported by Drefus and Herx- 
heimer and our own observations, that a favorable impression can be. made 
on many of these cases. 
Gastric crises do not of themselves shorten life. One of our cases is 
still living in the paralytic stage which has never during 30 years passed 
long periods without gastric crises; on the other hand, it is not impossible 
for crises which have continued during many years to cease and never 
recur. 54 
SPECIFIC INFECTIOUS DISEASES 
Benedikt says: “Gastric crises arc as favorable for prognosis as is the 
atrophy of the optic nerve.” This extreme statement is not justified, but as 
Malaise says, it should be accepted to prove that Benedikt saw cases in 
which early gastric crises were without unfavorable influence. 
The general condition of the patient is favorably influenced by the 
long intervals between gastric crises. I have seen surprising gain of 
weight during these prolonged intervals, produced in some cases by sal- 
varsan treatment. 
The development op THE morphin habit by patients with crises of 
all kinds has limited the usefulness and lowered the resistance of many 
tabetics in the past. It is a preventable factor and is usually chargeable to 
the attendant. Modern treatment will prove of inestimable value, reducing 
the number of morphinists and alcoholics. 
I have in connection with the prognosis of the initial stage and the 
subsequent general consideration, called attention to the unfavorable influ- 
ence of disturbed bladder function. 
Atrophy of the optic nerve has seemed to many to have an inhibit- 
ing influence on the advance of ataxia. This fact was accented by Bene- 
dikt, Gowers, Dejerne, and by Bayley and a host of others. Dejerne con- 
tended that a blind tabetic rarely developed the symptoms of the ataxic 
stage. Bayley found that among 12 tabetics who developed optic atrophy 
early, the onward march of the disease was inhibited in 9. Collins dis- 
agrees with the above conclusions. 
Malaise reports that in 73 per cent of the cases of optic atrophy ob- 
served at the Oppenheim clinic, it developed in the preataxic stage; and 
that three-quarters of these cases were followed by latency of the tabetic 
process after blindness; and that in many cases individual symptoms of 
ataxia were improved or relieved entirely, including urinary incontinence 
and lancinating pains. In 15 per cent of the cases the disease progressed 
pari passu with the optic atrophy entirely uninfluenced by the latter. The 
remnant of cases with optic atrophy advanced gradually to the late stages 
of tabes. I have seen a number of cases in which optic atrophy was a late 
development, in which the advanced symptoms of tabes remained entirely 
uninfluenced. 
It may be concluded that the fully developed symptoms of locomotor 
ataxia as a rule persist when once established; that the early development 
of optic atrophy is not likely to be associated with other severe tabetic 
symptoms; that in some cases improvement of these symptoms follows 
advancing optic degeneration; that the statistics offered by Malaise are 
approximately correct ; that the development of optic atrophy during the 
terminal stages of ataxia is without influence on the tabetic symptoms. 
Mott contends that when optic atrophy develops in advanced tabes, it is 
usually coincident with the progression of serious brain degeneration (pa- 
resis). Of his cases of optic atrophy which included 10 per cent of all PKOTOZOAN INFECTIONS 
55 
tabetics, 80 per cent developed symptoms of paresis. This conclusion is 
not generally accepted. In my experience I have found positive evi- 
dences of optic atrophy in 12 per cent of our cases of advanced tabes, 
but of these only few developed paresis. It must be remembered that 
Mott’s experience deals with hospital and asylum cases, and not with the 
cases which are met in every-day practice. 
Ataxia which develops before the end of the third or fourth year of 
tabes dorsalis indicates progressive tendencies, but is more favorable for 
life than when it is among the early symptoms of the initial stage or when 
it develops acutely. 
Schaffer called attention to tabes inversa in which the ataxia preceded 
all other symptoms. The prognosis of tabes inversa is more favorable than 
ataxia which is either acute or develops rapidly in the presence of the 
usual symptoms of the early stage. From 15 to 20 per cent of all tabetics 
never develop ataxia. 
The influence of scientifically directed and supervised exercises on the 
locomotion of chronic ataxia—Fraenkel and other exercises—is often en- 
couraging; the improvement is naturally greatest in cases where a suffi- 
cient remnant of muscles has escaped the loss of coordination, and by edu- 
cation a degree of compensation is obtained to permit of fair functional 
ability. 
Bladder and Rectum Symptoms.—The rule may be accepted that 
tabetics who are without bladder or rectum symptoms offer a better outlook 
than do those in whom there is retention, incontinence, or both. But few 
cases pass through to the paralytic stage without well marked bladder symp- 
toms. The continuous dribbling of urine may be evidence of retention 
from an overfilled bladder; in advanced cases it denotes sphincter paralysis 
as well. The dangers of infection from cystitis are increased by bladder 
paralyses. 
Rectal incontinence is rare without bladder paralysis, and occurs only 
with advanced tabes. Reference is made in this chapter to cases in which 
retention has not seemed to influence the disease unfavorably; but such 
cases to escape complications, demand the cautious use of aseptic methods 
during catheter life. 
Westphal Symptom.—Westphal symptom, or loss of patella tendon 
reflex, is one of the earliest of all symptoms and is likely to continue 
throughout the disease unless extension to the lateral columns finally causes 
return and exaggeration. In none of my cases has salvarsan treatment 
permanently changed the knee phenomenon. The same conclusions are 
justified in connection with the Romberg symptom (swaying with closed 
eyes) and the persistently present anesthesias, paresthesias and analgesias 
of the second and last stage. This has not been the experience of all—as 
has been demonstrated by the statistics of Dreyfus and Donath, quoted in 
another section of this chapter. 56 
SPECIFIC INFECTIOUS DISEASES 
The loss of the knee phenomenon should not alone be accepted as an 
indication of far advanced tabes; changed function does not always indi- 
cate destruction and degeneration. Many cases in which there is loss of 
this reflex, remain stationary or do not advance materially during many 
years. 
Ocular Paralysis.—It is often impossible to correctly determine the 
nature of the lesion which causes ocular paralysis. In our forecast it is 
safe to consider most cases of nuclear origin, i. e., central; muscular 
paralyses are more likely to depend upon central than upon peripheral 
lesions. 
The Argyll-Robertson pupil does not often disappear in advanced 
cases. A number of reliable observers have reported periods during which 
the light reflex returned after its positive disappearance. Donath found 
with salvarsan treatment, a return of pupillary reaction in 3 of 28 cases. 
This is possible in early tabes influenced by intensive treatment, but is not 
likely in the advanced stages. 
In considering the paralyses of the cranial nerves, I dilated on the 
prognosis of the paralyses of the eye muscles (See Paralysis of Ocular 
Muscles). 
Early paralysis of the ocular muscles in tabes is not often followed by 
the rapid progression to ataxia. Years (2 and 3 decades) may lapse, with 
progression so slow under these conditions, that it is almost unnoticed by 
the patient. Ophthalmoplegia may disappear under treatment as may the 
paralysis of separate muscles; this is true of the early stage only, as a rule. 
20 per cent of tabetics have ocular paralysis. Hypotonia is evidence of 
advanced tabes and is a symptom of the paralytic stage. 
Impotence.—Impotence, once present, is likely to continue. One- 
third of all tabetics are impotent by the end of the seventh year of the dis- 
ease. When impotence develops early in the disease it is evidence of rapid 
progression; such cases offer an unfavorable outlook. 
Incontinence of urine early in the disease, often late, is usually fol- 
lowed by impotence. 
In some cases sexual intercourse is impossible because of distortion of 
the penis, and occasionally hemorrhage into the corpus follows the act. 
Progression of the disease is likely to be rapid when the tabetic in vdiom 
the disease is fully developed is excessive in sexual indulgence. 
Emotion, long continued worry, any psychic disturbance which makes 
a profound impression or is continuous, react unfavorably on the tabetic; 
under these conditions the progression is often surprisingly rapid. Heavy 
manual labor always causes increase of symptoms denoting the unchecked 
advance of the disease. 
With some acute cases the progression is so rapid that the patient is 
promptly plunged into the paralytic stage, having skipped the initial and 
ataxic periods. If such rapidly advancing cases of acute tabes do become PROTOZOAN INFECTIONS 
57 
stationary, it is only after they enter the paralytic stage. This happens 
occasionally, but the paralytic stage under these conditions is as a rule 
shorter than in other cases—chronic ab initio. 
Perforating Ulcer.—In none of our cases have these trophic changes 
failed to recur after they were healed or partially healed, when the patient 
was on his feet much of the time. 
Perforating ulcers may not always recur in the same location but as a 
rule they do, or in the immediate neighborhood. They may form either in 
the ataxic or paralytic stage. Most of our cases were found in the ataxic 
stage and in men who were on their feet much of the time. They do not 
affect life directly, save as sepsis develops from their neglect. 
Arthropathies.—Arthropathies are trophic changes in which there 
are characteristic joint enlargements and destructive, usually non-suppura- 
tive changes. They develop during the advanced stages of the disease 
(oftener in the knee joint) and are beyond control by any known treat- 
ment. Our cases of Charcot arthropathies and spontaneous fracture have 
been far advanced and paralytic; other trophic changes add to make the 
prognosis bad. 
(h) The Wassermann Reaction of Blood and Spinal Fluid.—We have 
already mentioned the importance of the Wassermann reaction of the blood 
and the spinal fluid. It must be remembered that with progressive tabes 
the blood may give a negative reaction, while the lumbar fluid will be 
likely to give positive results. 
With tabes, which is active, there are 
1. Increased pressure in the subarachnoid space 
2. Phase 1 (Ronne), globulin reaction 90 to 95 per cent 
3. Lymphocytosis: 85 to 90 per cent 
4. Albumin presence: slight or normal. 
With Argyll-Robertson pupil and previous syphilitic infection, with- 
out syphilitic infection, without positive subjective symptoms of tabes, 
Phase 1 is present, albumin-(- (occasionally normal), lymphocytosis-f- (in 
most cases, though it may be absent). 
Plaut, Pehm and Sehottmiiller made the positive statement that with 
negative Wassermann reaction of the lumbar fluid and the Argyll-Robert- 
son pupil, without other symptoms, it may be assumed that the failure of 
the pupil to react to light (Argyll-Robertson) is the expression of a process 
which has run its course and is favorable. When with symptoms of loco- 
motor ataxia the four factors above mentioned are absent, this happens 
(according to Plaut, Rehm, etc.) in 7 per cent, 50 per cent of these cases 
may be considered to be stationary. 
The blood serum of tabetics offers positive reactions in over 70 per cent 
of cases. The lumbar fluid shows a positive Wassermann reaction in 
almost all cases of active tabes; with progressive paresis and taboparesis, 
the reaction is present in practically 100 per cent of all cases. 58 
SPECIFIC INFECTIOUS DISEASES 
The lumbar fluid and the blood therefore offer valuable data for the 
prognosis of tabes, and during the incipient stage demand repeated tests 
that the effect of treatment may be watched. 
(i) Complications.—The combination of independent specific disease 
of the nervous system during the existence of locomotor ataxia is possible. 
Gummata of the brain have been reported, specific and suddenly arising 
meningitides, and a variety of other lesions. Each deserves separate study, 
but all influence the forecast unfavorably. Naturally the rapid conversion 
of a system disease (locomotor ataxia) into one with far-reaching indis- 
criminate lesions (dissemination) in brain, cord and peripheral nerves 
influences the case unfavorably. 
Tabes complicated by trauma is usually progressive; its course is more 
rapid than is the average case, and bladder symptoms are often early and 
exceedingly troublesome (cystitis, etc.). 
Acute or chronic alcoholism always influences tabes unfavorably. 
These cases are usually neglected; they suffer from infected bladders, con- 
stitutional symptoms are numerous, and brain lesions (wet brain) often 
cause death. With chronic alcoholism it is safe to conclude that tabes is 
not stationary, but progression is certain and leads to the terminal stage if 
the patient does not die of intercurrent disease (pneumonia) sooner than 
do the non-alcoholic cases. 
Arteriosclerosis; Arteritis; Aortitis.—Among the most frequent 
complications of tabes is arteriosclerosis and specific aortitis. In some 
cases the process in the arteries is rapidly progressive, is associated with 
hypertension and nephritis. It may be safely concluded that arterioscle- 
rosis of the mesenteries with heightened blood pressure is a frequent factor 
in causing the vascular spasm which leads to gastric crises. 
Advanced evidences of arteritis are common in young tabetics. Aneu- 
rysmal dilatations are also a relatively frequent complication of locomotor 
ataxia. Osier reports 20 per cent of aneurysms in some series of tabes. 
Pneumonia.—Pneumonia (croupous bronchopneumonia and aspira- 
tion pneumonia) is among the more frequent causes of death of tabetics. 
Any form of pneumonia in the tabetic is serious: the majority die. 
Paralysis agitans.—My material includes two cases in which loco- 
motor ataxia was finally (ataxic stage) complicated by paralysis agitans, 
in which the former disease seemed uninfluenced. 
Basedow’s Disease.—Oppenheim mentions Basedow’s disease as a 
complication; we have no similar experience to report. 
Surgical Operations.-—Tabetics bear surgical operations badly; this 
is particularly true of those cases in which there is advanced arteritis. 
Infections and Tuberculosis.—Acute infections and tuberculosis 
are usually serious in tabetics. They offer little resistance to toxemia, par- 
ticularly when in the last stage. 
Acute invasion of the Medulla oblongata.—There are occasional PROTOZOAN INFECTIONS 
59 
cases of tabes in which the disease suddenly attacks the medulla oblongata, 
in which there are at once evidences of vague paralysis in rapid pulse and 
hyperpyrexia: the sensorium is promptly blunted; coma and death may 
result in the course of a few days. The pathologic conditions are either 
vascular, degenerative or both. Inflammatory lesions which cause these 
symptoms are infrequent. 
Epileptiform Seizures; Vertigo; Hysteria.—Cases of advanced 
tabes are occasionally complicated with epileptiform seizures or vertigo. 
Some have periodic outbreaks of hysteria. 
The epileptiform seizures are usually associated with transitory uncon- 
sciousness preceding mental disturbances and are followed by a period of 
memory lapse. The attacks are likely to recur, are depressing, often lead 
to melancholia, and are of grave import. 
Vertigo of the labyrinthine type is evidence of progression (See Me- 
niere’s disease). It may prove to be a persistent and recurring symptom, 
or it may never return after one or two attacks. 
The hysterical attacks are likely to recur and lead to all kinds of fears 
(phobia) and, at times, imperative conceptions in neurasthenic, over- 
wrought and weakened tabetics. 
The neurasthenic and hysterical element may predominate during any 
of the stages of tabes and influences the general condition unfavorably. 
Social Status.—The social status of the patient proves an enormous 
factor in the prognosis of tabes dorsalis. 
Poverty, with all of its baneful results, robs the patient of comforts 
including the necessary scientific nursing, which prevents septic infection 
in the terminal stages of the disease. 
The psychic element is a paramount factor: the depression of the para- 
lytic who lives in want exerts an unfavorable influence. Under these con- 
ditions there is often rapid progression, exhaustion, marasmus; and in 
same cases cerebral hemorrhage ends the scene. 
Septic conditions, including ascending infection from the bladder 
(pyelonephritis), are responsible for the death of some paralytics—espe- 
cially among those who are neglected. Cystitis is one of the leading causes 
of sepsis. 
Neglected cases of those markedly emaciated often develop bed-sores 
(decubitus) ; once formed they heal with great difficulty, and may also 
cause septic infection. 
Sepsis.—Sepsis may be either acute or chronic. Chronic cases are 
associated with progressive loss of weight, increasing anemia, albuminuria, 
irregular fever, and persistently rapid pulse. These symptoms may per- 
sist during a number of weeks or months, during which the patient gradu- 
ally wears out and usually dies in coma, with all of the symptoms of pro- 
found toxemia. 
The acute cases of sepsis are at times foudroyant, or they may lead to 60 
SPECIFIC INFECTIOUS DISEASES 
death after from 7 to 21 days, including delirium and most of the symp- 
toms of the chronic type. 
Hemorrhagic Conditions.—Purpura has been a terminal condition 
in some of our cases in which the patient gradually failed, was exhausted, 
and had been bedridden during varying periods. 
The forecast is always unfavorable when hemorrhagic symptoms, in- 
creasing marasmus, and bladder symptoms are associated in the ataxic or 
paralytic stages. 
Cerebral hemorrhage in patients with arteriosclerosis is a frequent 
cause of death; some remain hemiplegic during varying periods. 
The trophic changes including more particularly perforating ulcer and 
spontaneous fracture do not lead to death directly, but they often aggravate 
existing conditions: at times the ulcer causes septic infection; with frac- 
ture of the femur bed-sores form which, with persistent cystitis, are compli- 
cated with sepsis and death. 
Duration.—It is difficult in any case to foretell its duration. Ho fig- 
ures which we can give are absolutely reliable nor are they of great impor- 
tance. There are cases which cover 3 and 4 decades, others in which death 
follows after between 10 and 20 years, and still other cases in which the 
disease, because of complications, ends early. Each case demands separate 
consideration. 
Tabetics often reach old age. v. Malaise’s records prove that 51 per 
cent of his cases died after 60, and 83.3 per cent lived to reach 50 and 
longer. 
General Conclusions.—The degeneration which characterizes tabes 
provokes changes which do not permit the conclusion, with our present 
knowledge, that they can he overcome; in other words tabes dorsalis which 
presents symptoms sufficient to make its recognition positive, does not, in 
spite of statistics to the contrary, lead to restitutio ad integrum. Symp- 
toms may improve or during periods be entirely absent, hut the ravages 
of the disease continue. 
Chronicity is the rule. Long periods of latency are to be expected, ard 
often the relief of many sensory symptoms by modern treatment is posi- 
tively attainable; but persistent and almost continuous attention to the 
individual case, with scientific nursing, is necessary to hold the patient in 
the bettered condition. 
The outlook so far as the life of the patient is concerned is not so 
bad as is generally supposed by the lay world—a fact which we have ac- 
cented in this chapter. 
Statistics are materially influenced by many factors; foremost among 
these are heredity, diathesis, social status, occupation, and habits. The 
wide difference in the conclusions of different observers is demonstrated by 
the study of the following data taken from leading French and German 
sources. PROTOZOAN INFECTIONS 
61 
Pellugaud and Faure, Belugon and Faure, quoted by Oppenheim, 
report:— 
Tabes arrested in 19 per cent of cases 
Tabes with remissions in 40 “ “ “ “ 
Benign in 59 “ “ “ “ 
Tabes progressive in 30 “ “ “ “ 
Tabes acute in 6 “ “ “ “ 
Tabes grave in 36 “ “ “ “ 
Tabes regressive in 5 “ “ “ “ 
Tabes cured in 5 “ “ “ “ 
v. Malaise on the other hand is more conservative and does not speak 
of cured tabes. 
He reports of 76 cases: 
2 cases without symptoms. 
26 “ returned to work. 
30 “ show steady progression. 
18 “ rapid progression with bad general condition from the beginning. 
Syphilis of the spinal cord offers a less favorable prognosis than does 
cerebral syphilis. The latter is unquestionably always recognized in its 
incipiency, the former only after a period of progression. 
Taboparesis 
Taboparesis is a combination of disseminated changes in the spinal 
cord, brain, and peripheral nerves in which there has been, as a rule, a con- 
siderable period of tabes dorsalis with Argyll-Robertson pupil, character- 
istic behavior of the reflexes, ataxia in some cases, and lightning pains, to 
which the mental symptoms of paresis are added. 
Reverse conditions may prevail, and the symptoms of tabes are added 
to those of paresis; in rare cases the symptoms of both tabes and paresis 
are present together from the beginning. 
Optic atrophy with tabetic symptoms and even insignificant evidences 
of mental disease with the characteristic reactions of the lumbar fluid, 
including positive Wassermann reaction, with or without positive reaction 
of the blood serum, is strongly suggestive of approaching taboparesis. 
We know of no case in our practice in which any form of treatment has 
favorably influenced the disease. Whether the salvarsan-mercury treat- 
ment will ultimately prove of value in those cases in which the diagnosis 
can be made in the incipient stage of the disease, cannot be decided at the 62 
SPECIFIC INFECTIOUS DISEASES 
present time. Whether such treatment will prevent this late manifestation 
of tertiary syphilis entirely, cannot be determined until years of observa- 
tion have lapsed. 
General Paresis 
{Dementia paralytica, Progressive paresis) 
General paresis is always due to syphilitic infection: the presence in 
paretics of the Treponema in the brain, the positive Wassermann reaction 
of the blood and withdrawn cerebrospinal fluid, as well as the other char- 
acteristics—chemical and cellular—of the fluid, positively prove the patho- 
genesis of the disease. 
Five per cent of syphilitics develop paresis. While many paretics were 
insufficiently treated during the initial and secondary stage of the pri- 
mary infection, it may happen that thoroughly treated syphilis leads to 
paresis. Oppenheim and L. Meyer report cases which developed after the 
salvarsan-iodin and mercury treatment. 
The disease is most frequent between the thirtieth and fortieth year; 
rare before the twentieth and after the sixtieth; as tabes, it is also more fre- 
quent in men than in women. In over 20 per cent of paretics, symptoms of 
tabes dorsalis preceded the onset of mental deterioration. 
The same factors which predispose syphilitics to tabes are largely re- 
sponsible for the development of paresis. I am impressed by the fre- 
quency of paresis in syphilitics who are subjected to long mental strain 
and overwork, and lean strongly to the theory of Edinger, to which refer 
ence was also made in considering tabes. 
The average duration between the initial specific infection and the 
development of paresis is between 10 and 25 years. 
It does not matter what the psychic symptoms are, whether the disease 
is recognized early or late, what the behavior of the reflexes, however char- 
acteristic the pupillary reactions, what the changes in speech or penman- 
ship, whether tremor is present or not, whether paralytic conditions are 
complete or incomplete—we are absolutely powerless in positively diagnos- 
ticated cases to influence the disease itself favorably by any known treat- 
ment, though periods of apparent improvement and remission are not un- 
common. 
The foregoing statement is based on my own experience with the dis- 
ease, with the full knowledge of the cases of improvement and cure which 
have been reported by able authorities. Among these I refer to Dana and 
to the recently published statistics of Browning and Mackenzie and those 
cited by Oppenheim in considering the literature. 
Dana reported a number of recoveries and improvements in whom the 
diagnosis of paresis had been made. Browning and Mackenzie report 12 
of 58 paretics improved, of which number 6 returned to their occupations. PROTOZOAN INFECTIONS 
63 
There are a number of cerebral lesions of specific origin which are not 
true paresis, but in which the symptoms of paresis are simulated. In such 
cases improvement or cure is possible, and almost all of the cases reported 
as cured paresis belong to this class. 
It is not uncommon for the spinal fluid of paretics to show a reduction 
of lymphocytes after salvarsan injections and some have reported improve- 
ment of symptoms (Millian and Levy-Valensi). 
Remissions and long periods of latency are noted, but the disease finally 
proves to be progressive. It is these periods of latency or remission, some- 
times surprisingly long, which delude the enthusiastic advocates of a good 
prognosis to believe that the process is stayed or cured. 
Jacobsohn says that “the possibility of a cure has a more theoretical 
than practical value, and in offering the prognosis it need not be taken into 
account.” 
“In spite of this fact, it is not wise for the physician to give an abso- 
lutely bad prognosis at once; the withholding of the prognosis is wise until 
all doubt of the diagnosis has been overcome, for every neurologist has met 
cases in which the progress of the case has proved the possibility of error, 
and nothing is so humiliating to the diagnostician as to have delivered a 
death sentence in a case in which it was not justified.” 
The Wassermann reaction of the blood is positive in 100 per cent of 
paresis. The withdrawal of the cerebrospinal fluid shows 
1. Increased pressure in the subarachnoid space; besides this 
2. Globulin reaction (Phase 1, Nonne) positive in from 95 to 100 per cent 
3. Lymphocytosis in 95 per cent 
4. Wassermann reaction positive by the original method in 85 to 90 per cent, 
by the newer method in 100 per cent 
5. The total albumin content is increased, but varies materially without known 
cause. The average (Plaut, etc.) is 0.045 per cent, and is greatest in cases 
which have existed about 1 year. 
The cellular elements are greatest in cases which are in their second or 
third year, and may be reduced by salvarsan (Plaut). 
The stage of the disease does not influence the Wassermann reaction 
of the fluid. The weaker reactions (Wassermann) are found in cases 
which progress slowly or remain stationary during long periods. Negative 
reactions are found during stationary periods and remissions. In a few 
cases salvarsan weakens the Wassermann reaction of the spinal fluid; in 
rare cases it may become negative. 
Trophic changes may develop during the course of paresis, including 
perforating ulcer, spontaneous fracture, arthropathies and gangrene, and 
an atrophic condition of the nails; these conditions are but little influenced 
by treatment. 
The majority of our cases have died of cerebral hemorrhage after the 
usual apoplectic symptoms, which continue two or three days. 64 
SPECIFIC INFECTIOUS DISEASES 
Paretics may become hemiplegic or confirmed epileptics with distinct 
aurse—grand or petit mat. 
Transitory paralyses and aphasia characterize some of the cases in the 
last stage. These paralyses may disappear promptly or continue one or 
two days. Paretics with advancing paralysis or ataxia, finally become bed- 
ridden and helpless. They develop bed-sores, cystitis, and sepsis, unless 
well nursed. Death with septic symptoms in these cases is the rule with 
marked inanition. 
Dementia is prominent before the end of the second or third year in the 
average case, disturbance of speech is fully developed, the facies charac- 
teristic, locomotion usually much disturbed, and the sphincters are para- 
lyzed (incontinence of urine and feces). 
Death in the second or third year is the rule; acute cases may run a 
short course, ending within a few months—most of these are hemorrhagic. 
The cases which live during many years are usually women with marked 
dementia, senile patients, or taboparetics. 
Intercurrent infection has been followed by the remission of symptoms. 
Steiner reports erysipelas, and Foerster typhoid fever, Oppenheim pneu- 
monia and profuse suppuration closely related to remissions. 
Intercurrent pneumonia is often a cause of death in paretics with bul- 
bar symptoms (aspiration pneumonia). 
Salvarsan has been used long enough to prove that it does not cure nor 
materially influence paresis. The only hope lies in the possible prophylac- 
tic efficiency of the drug, by its intensive use during the early stages of 
syphilis. 
Ehrlich and his disciples have an abiding faith in the possibilities of 
prophylaxis from salvarsan; the reported development of paresis after its 
use by Oppenheim and L. Meyer is discouraging. Time and persistence 
will ultimately decide the question. 
Collins has recently placed himself on record as follows: 
“No matter how vigorous or drastic the antisyphilitic treatment, no 
one has ever been able to say that a case of tabes or general paresis has been 
cured by it; but, in making this “susceptibility to therapy” a distinguishing 
feature between the two classes of diseases (the syphilitic and so-called 
we have often lost sight of the fact that the former is a 
disease of the supporting or interstitial tissue and the latter of the paren- 
chyma, that is, of the nerve elements of the central nervous system. The 
parenchymatous cells have no more, and indeed no less, capacity of re- 
generation than the parenchymatous cells of any other organ of the body. 
Then, so far as we know, there is no substitution of function of the cells of 
the central nervous system. We are not in a position to say that if one cell 
in the central nervous system be destroyed, its function can be taken up by 
an adjacent cell.” 
“Since the introduction of salvarsan, and its utilization in the treat- PROTOZOAN INFECTIONS 
65 
ment of syphilis, there has been a great amount of reliable evidence—some 
of which I have furnished—tending to show that the parasyphilitic diseases 
can at least be brought to a cessation of activity by the appropriate use of 
this agency. It can no longer, therefore, be maintained that the so-called 
parasyphilitic diseases progress despite every treatment.” 
Juvenile Paresis.—Juvenile paresis is due to congenital syphilis and is 
more frequent in girls than boys. 
Rondonis and Strausslers have considered the developmental anomalies 
in cases of juvenile paresis, and Strausslers found these most prominent in 
the cerebellum. Strausslers in his work, claims that hereditary syphilis 
may cause paresis after the thirtieth year. 
Salvarsan improves the general condition of juvenile paretics; the Was- 
sermann reaction becomes negative, but soon returns to the positive phase; 
metabolism seems to be improved. The mental state is not changed. 
The reactions of the blood and cerebrospinal fluid of juvenile paretics 
run parallel with those of the adult. The prognosis is unfavorable. 
2. Congenital Syphilis 
Heredity in Syphilis.—Our views with regard to the heredity and 
mode of transmission of syphilis from parent to offspring have been ma- 
terially influenced by the newer methods of diagnosis. 
It may now be assumed with certainty that the disease is conveyed by 
the mother to the child through the placenta (maternal transmission), and 
whether the mother presents symptoms of syphilis or not, she offers a posi- 
tive Wassermann reaction. This disproves the contention of Sir Jonathan 
Hutchinson that “the father may infect his offspring (the mother never 
having suffered), and that this is by far the most frequent mode by which 
the disease is transmitted.” In the mother the disease may he latent—she 
may never develop active symptoms—hut she is nevertheless syphilitic. 
The mothers of congenitally syphilitic children are immune to syphilis; 
they cannot be infected through the syphilitic child nor in any other way 
(Colles-Baume law)—which is another proof of maternal and latent infec- 
tion; further the same syphilitic child can infect its nurse through the 
nipple, etc. 
For prognostic purposes it may be held that a father who has had 
syphilis need have but little fear for the safety of his children, so long as 
his wife shows a negative Wassermann reaction (Bayly). The rigorous 
treatment of the mother during pregnancy may result in the birth of an 
apparently healthy child. Most of these children give positive Wassermann 
reactions and are therefore latent syphilitics. Such children are as a rule 
immune to syphilitic infection {Profeta Law). Unquestionably a large 
number of these cases which with a positive Wassermann reaction are to he 
considered latent syphilitics, account for the late manifestations of the 66 
SPECIFIC INFECTIOUS DISEASES 
disease in the subjects of congenital lues which offer unfavorable forecasts 
(syphilis hereditaria tarda). 
Not all children of a syphilitic mother inherit syphilis. There are 
cases recorded in which with twins one was syphilitic, the other escaped 
infection. Bayly quotes the results of Wassermann reactions of congenital 
syphilis as follows:— 
In 20 cases he found 95 per cent positive. Noguchi and Kaplan in 37 
cases found 95 per cent positive. Hoehne found 88 per cent positive. 
Marcus in 29 cases found 90 per cent positive. Boas in 72 cases found 100 
per cent positive. 
A parent with tertiary syphilis may show active symptoms and objec- 
tive signs, and yet the children may be non-syphilitic. Hutchinson says: 
“a child may wholly escape under circumstances apparently full of risk.” 
The severity of the infection in the child is not in proportion to the 
severity of the symptoms in the parent. Mild symptoms or latency in the 
parent are often found with malignancy of infection in the child. 
The subject of congenital syphilis who lives beyond the dangers of the 
first few years of life offers a good prognosis so far as life, is concerned; 
but he is under par as a rule until he has gained his full growth and often 
after he is handicapped in the race, and to the expert presents stigmata 
which brand him. 
Characteristic Manifestations.—The syphilitic may come into the 
world with grave lesions of one or more vital organs: kidney, spleen, liver, 
pancreas, thymus, lung, etc. Specific change in one or more of these may 
cause death in utero. 
Early pemphigus syphiliticus is usually fatal; this may be present 
at birth, or develop within a few days. 
Changes in the nails and skin are characteristic of congenital syph- 
ilis (onychia syphilitica.) 
Coryza, persistent snuffles, with crusting in the nose and degenera- 
tive changes in the nasal septum, are among the earmarks of congenital 
syphilis and may persist during early childhood. 
Growth, nutrition and mental progress are materially influenced 
by congenital syphilis. “Fournier’s infantilism” characterizes many of 
these unfortunates. 
We have already considered the changes in the liver and spleen, to 
which we refer the reader. Most of these complications lead to early death. 
Nose and Ears.—Extension of disease through the nose to the ears is 
frequent and damaging, often leading to deafness. 
Enlargement of lymphatics, persisting during long periods with 
anemia and malnutrition, rob the child of resistance and make him ready 
to yield to acute infection. 
Anemia of Congenital Syphilis.—The anemia of congenital syph- 
ilis is of three types: (1) chloranemia with leukocytosis (2) pernicious PROTOZOAN INFECTIONS 
67 
type, (3) leukemic type (Bayly). Most forms resemble the usual secon- 
dary anemias of infancy and make satisfactory recoveries. Lymphocytosis 
is characteristic of all forms of syphilitic as well as the non-syphilitic ane- 
mias of early life. The leukemic type offers the most serious prognosis. 
There are many nucleated reds, and in some cases the combined count of 
lymphocytes may be high, reaching 50,000 to 60,000 (lymphocytes, mye- 
locytes, and polymorphonuclear leukocytes). 
Pneumonia is particularly fatal in the subjects of hereditary syphilis 
during the early years of life. 
Early and late purpura may be of specific origin. The hemorrhage of 
the newborn when specific is usually fatal (syphilis hemorrhagica neona- 
torum■). 
Hutchinsonian teeth (notched, malformed, undersized) are char- 
acteristic of congenital syphilis. We have never seen these teeth (per- 
manent teeth) in subjects who did not present other positive stigmata of 
hereditary lues. 
Eye lesions' may be either early or late. Keratitis (phlyctenular and 
interstitial) is frequent and often rebellious to treatment with great ten- 
dency to relapse. In many of these forms of corneal inflammation there 
are permanent though insignificant opacities of the cornea. 
Changes in the bones of hereditary luetics are frequent; during fetal 
life the epiphyses may be involved and loosened with cartilaginous prolif- 
eration. Most of these are stillborn (osteochondritis syphilitica). 
Hereditary lues is very likely to interfere with the growth of bone 
tissue and retards the closure of the fontanelles, or occasionally it happens 
that there is an abnormal overgrowth of bone which causes premature 
closure. Such skulls are often congenitally malformed. 
Most congenital hydrocephalus is of specific origin and offers an 
unfavorable prognosis. When these children live, as they sometimes do 
for several years, their development is exceedingly slow and their mental 
condition is always defective. 
Congenital lues predisposes to rachitis. 
With hereditary syphilis arteriosclerosis or arteritis is frequent 
during early life, and may lead to the same far-reaching organic changes 
which accompany non-specific arteritis. These luetics are constantly on 
the edge of a precipice: they rarely live beyond the thirtieth year. 
When syphilitic babes develop intestinal lesions they offer but little 
resistance and rarely recover. 
Destructive disease op the skin, nose and the soft palate is 
rarely found in cases which receive appropriate and early treatment. 
ISTervous System.—The ravages of hereditary syphilis as they are 
found in the nervous system often lead to irreparable damage. Paralysis, 
convulsions, epilepsy, blindness, deafness, idiocy are among the dreadful 
sequelae of the infection. Fournier includes amblyopia, myopia, nystag- 68 
SPECIFIC INFECTIOUS DISEASES 
mus, asymmetry of the face, congenital heart defects, harelip, spina bifida 
hydramnion hypospadias, abnormalities of the hands and feet. 
Congenital syphilis is uunquestionably responsible for a large number 
of so-called neuropathies. General paresis may develop in congenital 
syphilitics; also tabes and multiple sclerosis. 
There is scarcely an organ which may not show the ravages of heredi- 
tary syphilis; on the other hand it is encouraging to note that the perma- 
nent lesions of syphilis are in the majority of cases prevented by timely 
treatment. 
Syphilis can be transmitted to the third generation. This is the con- 
census of expert opinion, though there are able syphilographers who deny 
the possibility. Groups of such cases have been reported in medical litera- 
ture by reliable observers (Fournier). England’s greatest authority, the 
late Sir Jonathan Hutchinson, remained a strong opponent to the views of 
Fournier. 
Syphilis and Marriage 
The consideration of this subject requires but little time or space, if we 
divorce ourselves from sentiment and base our recommendations on scien- 
tific and clinical experience. 
I may be criticized for this arbitrary rule from which I claim there 
should be no exception, but in practice it offers the best prognosis. My 
rule is as follows: No syphilitic should marry unless he has been radically 
treated; has shown repeated negative Wassermann reactions during at least 
two years, and has been without mucous patches for at least twelve months. 
A' single negative Wassermann reaction after treatment is of no value in 
the matter of prognosis in connection with marriage, if considered apart 
from other features of the case, and will prove misleading and disastrous. 
Dreyer reports cases in which the Wassermann was negative for 3 or 
more years, with return to a positive phase and activity of the disease. 
Syphilis and Life Insurance 
No applicant who has had syphilis deserves to be considered a first- 
class risk. The dangers of late manifestations, metasyphilitic and cardio- 
vascular complications must be taken into account before giving a rating. 
In considering the problems connected with life insurance and syphil- 
itic subjects, it is well to remember that some luetics remain free from 
symptoms during many years, who suddenly develop active syphilis in its 
most malignant form. 
The average syphilitic will not live to his full expectancy. 
Mortuary records show that diseases of the circulatory organs are the 
cause of death in over 50 per cent of syphilitics. The involvement of the 
nervous system is among the frequent causes of death with which life 
insurance companies must reckon. PROTOZOAN INFECTIONS 
69 
Placing syphilitics in a class by themselves it is safe to conclude that 
with evidence of prolonged treatment, the period of freedom from symp- 
toms and the negative Wasserniann suggested in the rule given above, 
which justifies the marriage of the syphilitic subject, the risk may, with 
such added rates as are made by most companies, be accepted. 
The Fate of Syphilitics and their Children 
Kaufman has followed a large material which made it possible to offer 
valuable data concerning the fate of syphilitic couples and their children: 
It has been found that in 15 to 20 per cent the marriages of syphilitic 
couples are sterile; 32.9 to 40 per cent of tabetic wives are sterile. 
Following 10 couples, all syphilitic, and their children, the following 
facts were established by Kaufman-Wolf:— 
5 of the 10 men died, the causes of death and their ages were: 
1. Locomotor ataxia, aortic aneurysm; age 52 
2. Pulmonary tuberculosis with heart lesion; age 36 
3. Pneumonia with delirium tremens, arteriosclerosis and coronary 
disease; age 45 
4. Insane (suicide) ; age 36^ 
5. Paresis; age 57. 
Conjugal Nervous Lesions.—In 4 couples the following conditions 
were found: 
Husband Wife 
1. Paresis Locomotor ataxia 
2. Paresis Delirium tremens 
3. Psychosis Insane (psychosis) 
(manic depressive) 
4. Paresis Paresis 
In syphilitics the duration of married life was found between 6 and 25 
years. Among 9 syphilitic couples there were 66 pregnancies; these 
included 33 abortions or stillbirths and 33 living children. Of the 33 
living children, 20 died—14 during the first years of life: 3 suicided 
(12-|, 20, 28 years respectively), two were epileptics (both died in public 
institutions), and one aged 40 died as the result of an intestinal lesion 
requiring a surgical operation. Thirteen are still living of whom only 2 
are normal; all the others are mentally and morally defective. 4 children 
of the second generation are normal. 
All statistics 'prove the frightful mortality among the offspring of 
syphilitics during the first seven years of life. 
Fournier reports 18 syphilitic families with 161 pregnancies, of which 
137 were stillbirths—85 per cent. 
Hyde reports 1,121 syphilitic births, with 916 deaths during the first 70 
SPECIFIC INFECTIOUS DISEASES 
year of life. The Moscow Orphan Asylum presents 70 per cent of deaths 
during the first year of life, among 2,088 syphilitic children. Koplik 
reports 66,537 hirtlis, with 2,732 deaths from all diseases during the first 
four weeks of life in the Borough of Manhattan, of which but 47 are cred- 
ited to syphilis. 
Haskell gives the results of his observations as to syphilitic infection in 
the conjugal mate'and offspring in fifty-five cases of general paralysis in 
which the presence of syphilitic infection in the mate was tested, and in 
eighty-six cases of general paralysis in which there was a definite anam- 
nesis concerning pregnancies and offspring. Ilis conclusions are as fol- 
lows : 
“The large number of 38.18 per cent of conjugal mates of paretic 
patients is shown to be infected with syphilis. In most of these mates the 
condition courses unrecognized as lues latens. 
“A pitifully small number of them ever receive treatment. 
“The proportion of these infected mates who later develop paresis 
appears to be higher than those who receive their infection from non-ineta- 
syphiiitic sources. 
“The number of completely sterile marriages in syphilitic families in 
which one individual later develops paresis is abnormally high, constitut- 
ing 32.5 per cent. This percentage is higher when it is the female mate 
that later becomes a paretic. 
“The number of marriages in which repeated pregnancies result only 
in abortions is likewise abnormally high, constituting in our series 3 2.7 
per cent. 
“Of our series of eighty-six marriages 45.3 per cent were absolutely 
childless. 
“Among 167 pregnancies there were forty-two abortions, miscarriages 
and stillbirths. 
“Among 123 living-born children twenty had already died before their 
eleventh year. 
“The number of living children per family is abnormally small. 
“A large number, in some investigations reaching as high as 25 per 
cent, of these children are actively syphilitic. 
“An equally large additional number show signs of degenerative physi- 
cal conformation and psychopathic tendencies without a positive Wasser- 
mann reaction. 
“Much of all this is preventable.” 
Carriers of Treponema Pallidum 
There are “carriers” of spirochetes who never themselves know that 
they are syphilitic; thus a man may acquire syphilis during his first mar- 
riage or during illicit intercourse and infect his second wife or others, PROTOZOAN INFECTIONS 
71 
without having himself ever had any of the subjective manifestations of 
the disease. 
Bayley. Syphilis, etc. London, 1913. 
Benedikt. Prodromal. Wien. mcd. Pre.se, 1881, Hft. 1, 2, 45. 
Brissaud. Societe de Neurologic Peris, 1902. 
Browning and Mackenzie. Brit. Med. J., Sept. 23, 1911. 
Charcot. R port to Societe de Trologie. Paris, 1889-90. 
Collins. Prognosis of tabes. New York Med. News, Ixxxiii. 
Syphilis of the brain. J. Am. M. Ass., July 10,1915, Ixv, No. 2. 
Dana. New York Med. Rec.; also Diseases of the Nervous, System 1915. 
Dejeine. Neurol. Centralbl., 1890. 
Donath. Miinch. med. Wchnschr. 1912, 2274-2277 & 2342-2345. 
Dreyfus. Miinch. med. Wchnschr. 1913, No. 10, 525-530. 
Edinger. Der Antheil d. Funktion, etc. Wiesbaden, 1908. 
Ehrlich. Lecture delivered Jan. 16, 1914, Frankfurt a. M. 
Erb. Jahrb. f. Psych, u. Neurol. 1902, Bd. xxii. Berl. klin. Wchnschr. 1904, 9. 
Foerster. Monats. f. Psychiatrie, Bd. xvi. 
Fournier. Eliologic du tabes d’apre un milliers d’observation. Le bull, med., 1901. 
Gowers. Textbook diseases of the nervous system, 1883. 
Haskell (R. II.). Syphilitic infection in the conjugal mate. J. Am. M. Ass., March 13, 
1915, Ixiv, 890. 
Herxheimer. Lecture delivered, Frankfurt a. M. Winter, 1914. 
Jacobsohn. Klinilc. der Nervenkrankheiten, Berlin, 1913. 
Koester. Monatschr. f. Psychiatrie u. Neurologie 1905, Bd. xviii. 
Malaise. Monatschr. f. Psychiatrie u. Neurologie, 1905, Bd. xviii. 
Marcus. Miinch. med. Wchnschr., 1911, No. 20. 
McDonagh. Lancet, London, Oct. 22, 1910. 
Millian & Levy-Valensi. Miinch. med. Wchnschr., 1911, No. 30. 
Mott. Review of Neurol. & Psychiat., London, 1903. 
Morgan (William Gerry). Syphilis of the stomach. Am. J. Med. Sci., March, 1915, 
392. 
Noguchi. J. Exp. Med., New York, 1912, xv, 90-100. 
idem, xvi, 1912. 
Berl. klin. Wchnschr., 1912, 49. 
Nonne. Syphilis u. Nervensystem. Berlin, 1909. 
Oppenheim & Meyer (L.). Oppenheim, Lehrbuch der Nervenkrankheiten. Bd. it, 
1289. 
Osier. Practice of medicine, New York, 1913. 
Pellugaud & Faure, Belugon, Faure. Quoted by Oppenheim [Z. c.]. Ztschr. f. Nervenkr., 
Bd. xxodv. 
Plaut. Zerebrospinalfliissigkeit. Jena, 1913. 
Plaut, Rehm & Schottmiiller. Zerebrospinalfliissigkeit., Jena, 1913. 
Reumont. Syphilis & tabes dorsalis. Aachen, 1881. 
Rondonis. Archiv. f. Psychiatrie, Bd. xlv. 
Rumpf. Syphilis Erk. des Nervensystem. Wiesbaden, 1887. 
References 72 
SPECIFIC INFECTIOUS DISEASES 
Schaffer. Quoted by Malaise [l. c.]. 
Scholtz. Lehrbuch der Geschlechtskrank. Leipzig, 1913, i, 347. 
Steiner. Wien. klin. Rundschau, 1906. 
Strausslers. Ztschr. f. die gesammte Neurologie u. Psychiatrie. vii. 
Swift & Ellis. New York Med. J., July 13, 1912. 
Weber. Berl. klin. Wchnschr., 1911, No. 2. 
II. Malaria 
(Ague-Wechselfieber, Paludism, Intermittent Fever, Estivo- 
autumnal Fever) 
Malaria is a specific infectious disease of protozoan origin, due to the 
entrance into the blood of one of the Ilemosporidia or ITemocytozoa of 
Laveran attacking the red of man, in which the parasite 
undergoes a definite cycle of development. Its sexual phases take place 
in the mosquito—the Genus Anopheles—which has become infected by 
biting sufferers whose blood held the gametes of the Protozoa of malaria 
(.Plasmodium malaria). 
For our purpose we will consider the features of the disease as pre- 
sented by: 
1. Intermittent malarial fever. 
(a) Quotidian type (double infection with the tertian parasite). 
(b) Tertian type (Plasmodium vivax). 
(c) Quartan type (Plasmodium malaria?). 
(d) Irregular intermittent fever. 
2. Eemittent malarial fever (always due to the Plasmodium precox 
or falciparum). 
(a) Estivo-autumnal fever (or continued malarial fever). 
(b) Pernicious malarial disease. 
I. Cerebral. 
II. Algid (or gastro-intestinal). 
III. Pulmonary. 
(c) Black water disease (or hemorrhagic malarial fever). 
3. Chronic malaria (malarial cachexia). 
4. Mixed types of malarial fever. 
5. Malarial neuralgia. 
The general statement is justified that the lesions of; malaria are due 
to the destruction of blood-corpuscles by the individual parasites causing 
the special type of the disease, and the toxin produced when the organism 
divides (segmentation). 
The pigmentation in the various organs of the body is in proportion PROTOZOAN INFECTIONS 
73 
to the chronicity of the disease; is due to the plugging of capillaries by 
the organisms within them. 
The spleen is uniformly enlarged in all malarious diseases; its size 
and the organic changes are proportionate to the chronicity of the disease 
and the neglect of proper treatment. The same may be said of the liver 
and of the blood. The malignancy of all malarial disease depends upon 
the number of Protozoa and their resistance, the lack of strength and the 
endurance of the patient. As a rule, as will be emphasized in the consid- 
eration of the separate forms of the disease, even these factors are over- 
come in most cases by specific treatment. Whether the unqualified state- 
ment made by Osier: “Xo infection—except perhaps tuberculosis—com- 
pares with it (malaria) in the extent of its distribution or its importance 
as a killing and disabling disease” is still justified, is open to argument 
in the light of recent experiences. Immunity is by no means granted by 
one or more attacks of malarial infection. It has been shown in the 
tropics, however, that adults who suffered early in life have at times 
shown greater immunity than others. 
2. Intermittent Malarial Fever 
The quotidian type is more weakening than the tertian. When double 
(two cycles within 24 hours) it is depressing, may be associated with 
febrile albuminuria, but yields promptly to treatment. 
The larger number of cases are tertian—the cycle of symptoms recur- 
ring every other day at the same hour—observing the 'periodicity which 
is a family resemblance of all forms of. malaria. In an experience of 
over thirty-five years I have never known of a death due directly to inter- 
mittent malarial disease treated by quinin, and the deaths reported by 
others are so few that they offer only a negligible factor. 
(a) Quotidian Type 
(c) Quartan Type 
The quartan type is exceedingly rare (17 cases in 1613) (Thayer). 
Its prognosis is favorable; it is however more stubborn than the other 
forms of intermittent fever. 
(d) Irregular Intermittent Fever 
The merging of a tertian into a quotidian, or vice versa, or the 
development of double tertian from single tertian does not change the 
favorable prognosis. When the fever is “postponed,” i. e., the cycle 
begins later than in the previous attack, it is evidence of improvement, 
easy and early control. When the fever “anticipates,” it may be inter- 74 
SPECIFIC INFECTIOUS DISEASES 
preted as meaning that conditions are less favorable and demand active 
treatment, which will usually prove efficacious. 
Relapses will follow all forms of intermittent malarial disease unless 
rigorously treated or the patient is removed from the source of infection. 
Spontaneous recovery may follow change of abode. 
2, Remittent Malarial Fever 
(a) Aestivo-autumnal Fever 
(Continued Malarial Fever) 
This type of infection (Plasmodium falciparum) is rarer than the 
intermittent, and more resistant to specific treatment. The disease is 
less likely to observe the “family tendencies” in periodicity, is therefore 
given to irregularity, is likely to develop continuous fever, resembling 
typhoid—unjustly called by some typhomalarial fever—and if neglected 
or improperly treated, pernicious symptoms may prove threatening and 
serious. 
The paroxysms of the disease are longer than are those of the inter- 
mittent fevers In cases which are benign, there is, as a rule, a decided 
drop of temperature during the early morning hours. 
Patients may present with marked evidence of invasion of the nervous 
system, the typhoid condition becomes puzzling, the blood examination 
clinches the diagnosis and the prognosis at the same time. Unless the 
pernicious type of the disease develops, the prognosis continues good. 
The Estivo-autumnal infection may be complicated by the tertian or 
quotidian fever, both as a rule will yield to treatment, though the period 
of convalescence may be prolonged and anemia becomes striking. So- 
called “dumb chills” are among the more serious manifestations of the 
estivo-autumnal type of the disease. In the more severe types—those 
with pernicious tendencies—the nervous system is invaded, delirium— 
muttering or wild—is not uncommon. An average paroxsysm is between 
20 and 24 hours. In those cases where mixed infection with two Pro- 
tozoa modifies the temperature curve, there may be considerable difficulty 
in deciding upon the nature of the infection and typhoid may be strongly 
suspected. The prognosis should be guarded accordingly until treatment 
and blood examination clear the horizon. 
(b) Pernicious Malarial Disease 
This is always serious. As a rule the cases have become chronic; 
there are organic changes in the spleen and in the liver, the blood has 
been disorganized, and the patient has been robbed of resistance. In 
some cases there has been nephritis, occasionally hemorrhagic. 
Pernicious malarial complications offer the gravest of all prognoses PROTOZOAN INFECTIONS 
75 
in malarial infections. The symptoms are either, (I) cerebral, (II) gas- 
trointestinal (algid), or (III) pulmonary. 
Cerebral Pernicious Malaria.—Cerebral pernicious disease is always 
serious. 
Coma Type.—In some cases there is a sudden overwhelming of the 
nervous system, with final merging into deep coma after a period of 
exaltation, possibly delirium and few gastric symptoms. In the severe 
cases there may be irregular labored breathing (Cheyne-StoTces) or it is 
stertorous There is hyperpyrexia (106°-108° F.), which with rapid 
feeble pulse tells of the serious condition of the patient and clouds the 
outcome. In some of these cases improvement may lead to prompt 
recovery; in others it is soon followed by a repetition or deepening of 
symptoms, and death. Second paroxysms are almost always fatal. 
Quaife has called attention to cases of this type which have remained in 
coma during long periods, which finally recovered. One of Quaife’s 
cases (aet. 18) was unconscious during 48 hours—in deep coma—but 
finally made a full recovery. 
Cases of pernicious anemia of the cerebral type may suddenly 
develop active mania, convulsions, symptoms of active or passive cerebral 
congestion—usually the former—resembling meningitis; there may be 
paralysis (bulbar, aphasia, hemiplegia) with eye symptoms, amaurosis, 
cerebellar symptoms, or even tetanoid symptoms. An early prognosis in 
either of these pernicious types of cerebral pernicious invasion is impos- 
sible ; it will always require three days of active treatment to reach safe 
conclusions. In both these types of pernicious fever the end of the first 
period does not justify a positive forecast for there may be a repetition 
of all symptoms, with increased severity, and prompt death. In the 
majority of cases recovery follows the first paroxysm. 
Algid (or Gastro-Intestinal) Pernicious Malaria.—In this type of per- 
nicious disease the patient has many of the symptoms and the appearance 
of the cold or algid stage of Asiatic cholera; the condition is serious, and 
the outlook is often bad. The pulse in the grave forms is small, rapid, 
without character; the stools numerous, watery and large. The extremi- 
ties and the entire body are cold. Cyanosis with the symptoms mentioned 
makes the picture of the most severe cases complete. Death as a rule is 
not long postponed. In some of the suddenly depleting forms of algid 
disease death may follow in from 2 to 4 hours. 
A bilious type is occasionally met, in which vomiting, jaundice and 
other gastro-intestinal symptoms are in the ascendency. Many of these 
recover. 
Pulmonary Pernicious Malaria.—The pulmonary or pneumonic type 
of pernicious malaria is characterized by symptoms of edema, congestion, 
or pneumonic infiltration. Heart iveakness may seriously influence the 
outcome. In some, death follows promptly from edema of the lungs; in 76 
SPECIFIC INFECTIOUS DISEASES 
other cases prompt treatment—rigorous and persistent—leads to happy 
recoveries. 
In all types of the pernicious disease the prognosis is grave in direct 
proportion to the number of Protozoa in the blood in the interval follow- 
ing the attacks; though, to quote from Thayer: “the disappearance 
of the parasites from the blood under treatment of itself” “does 
not justify a favorable prognosis, for, despite this, the pernicious par- 
oxysm may continue to a fatal termination.” 
Purpuric complications (purpura hemorrhagica) with any form of 
pernicious malaria is evidence of malignancy. 
(c) Black Water Disease 
(Hemorrhagic Malarial Fever) 
This usually occurs in East and West Africa, the Southern States of 
America, and in Central America. Some have held that large doses of 
quinin given to malarial subjects have been responsible for the symp- 
tom complex. Those who have had most experience with the disease 
agree that this is not true, that as Stephens’ investigation shows in a 
study of 95 cases, Protozoa were present in 95.6 per cent of the cases 
before the onset of hemorrhagic symptoms, and in 61.9 per cent, on the 
day of the appearance of the disease. Thayer agrees that malarial 
hemoglobinuria, as found in the Southern States, is not due to quinin. 
The most reliable data dealing with prognosis are offered by the expe- 
riences of the employes along the Panama Canal zone. These prove that 
quinin as ordinarily administered is not efficacious but its intramuscular 
injection has proved specific in its effect in almost all cases of blackwater 
disease. The mortality of blackwater fever is between 5 and 10 per cent. 
Complete anuria may persist during long period (48 to 60 hours), and 
yet recovery follow. 
3. Chronic Malarial Cachexia 
ISTo thoroughly treated case of malaria develops the characteristic 
chronic cachexia. Whenever it is found it is evidence of neglect or 
repeated infection. 
The factors which influence prognosis with this condition are: the 
reduced state of the patient, the marked anemia, the condition of the 
spleen, associated kidney and liver complications, dropsies with circula- 
tory insufficiency. 
The anemia has the ear marks of the secondary type; color index is 
reduced with erythrocytes low, and leukocytes are also below the normal 
count. There is an increase of mononuclears—lymphocytes—with nucle- 
ated red blood corpuscles. The severity, or depth of these changes as shown 
by microscopic examination, are potent in giving a forecast. It must be PROTOZOAN INFECTIONS 
77 
remembered that in the presence of grave anemia with changes in spleen 
and other organs, the patient in a favorable environment with specific 
treatment may gradually lift himself back to health. Cases of malarial 
cachexia in which the blood picture of pernicious anemia developed have 
been found to lead to death within a short time. In these cases the meg- 
aloblastic evidences of the disease with a white count approaching leuko- 
penia, a large percentage of small mononuclear cells, and no nucleated 
red corpuscles were found (aplastic anemia) (Thayer, 1. c.; Bignami and 
Diosini; Ewing). Purpuric eruptions and hemorrhages are present with 
the more serious cachexias, but do not make the prognosis! absolutely bad 
if the patient can be controlled. The evidences of dropsy begin to dis- 
appear as the anemia is relieved and circulatory balance is restored. 
The chronic changes in the spleen, enormous “ague cake” and liver 
enlargement far advanced, may yield to treatment; and restoration to 
health with these complications is not unusual. 
In the majority of chronic malarial cachexias the patient holds his 
fate in his own hands, his recovery will depend entirely on his ability and 
willingness to remove himself from baneful surroundings and the relig- 
ious following of rational medical treatment. 
4. Mixed Types of Malarial Fever 
Reference has been made to the mixed types of the disease in the 
preceding pages—the merging of one type into another—the infection of 
the patient with the Protozoa of estivo-autumnal disease and one or more 
of the Ilemosporidia of the intermittent fevers. In all, the prognosis is 
good. Recovery may be delayed and convalescence interrupted by the 
development of the fresh outbreak, as a rule of tertian or quotidian fever. 
5. Malarial Neuralgia 
These types of neuralgia frequently met in the United States with 
or without febrile movements, as a rule observing characteristic period- 
icity, unquestionably of protozoan origin, yield very promptly to treat- 
ment. They recover with lowered resistance and evidences of anemia. 
There is slight enlargement of the spleen, which disappears with recovery. 
Complications 
Bronchitis, usually benign, is not infrequent and does not interfere 
with recovery. Pneumonia is not rare; its prognosis depends on many fac- 
tors which will be considered in connection with pneumococcus infection. 
Dysentery is a frequent complication of malaria, usually of the amebic 
type, oftener in the tropics than in the United States, though epidemics 
of dysentery in Central New York have been found with widespread in- 78 
SPECIFIC INFECTIOUS DISEASES 
termittent fever. In 1879 and 1880 as the Hew York Central Railroad 
built its freight tracks around the city of Syracuse, along the marsh, 
types of both diseases were found which yielded to antimalarial treat- 
ment only. 
Nephritis.—Both Thayer and B. Rosenstein call attention to the 
frequency of this complication. Thayer reports 1.7 per cent of 1832 
cases examined at the Johns Hopkins Hospital with acute nephritis. 
The complication is most frequent in the estivo-autumnal form. Most of 
these recovered. My experience runs parallel with this. I have traced 
several cases of chronic nephritis to malarial infection. 
The other complications, including orchitis, gastrointestinal disturb- 
ances, end in recovery. 
Miscarriages are not infrequent, during some seasons in malaria-ridden 
districts these have been as high as 50 per cent in the infected pregnant 
women. The influence of large doses of quinin in producing miscarriage 
should not be ignored. 
Tuberculosis and malaria are frequently associated; the association of 
these infections is likely to influence the former unfavorably. 
The few anomalies of the nervous system traceable directly to ma- 
larial infection are as a rule favorably and promptly influenced. 
In no other infection can a prognosis be given with greater certainty 
in the overwhelming majority of cases, than in malaria; the therapeutic 
test—the prompt use of the specific—not only allows early and easy prog- 
nosis, but at the same time it clinches the diagnosis. 
References 
Bignami & Diosini. Centralb. f. allgem. Path. u. pathol. Anat., 1894. 
Ewing. J. Exp. Med., N. Y., 1901 & 1902. 
Osier. Practice of medicine. 1913. 
Quaife. Lancet, London, Jan. 6, 1912, 20. 
Rosenstein (B.). Mohr & Staehelin, Handhuch der Inneren Med., Bd. i., 1911, 944- 
Stephens. Johnston Laboratory Reports, 1903. 
Thayer. Allbutt and Rolleston, System of medicine. Part i., ii, 245. 
III. Amebic Dysentery-Amebiasis 
Acute Form 
Amebic dysentery is endemic in the tropics and is caused by the 
Entameba histolytica and the Entameba tetragena; it is more likely to 
cause secondary changes of grave nature, including metastatic abscesses— 
liver oftenest. There is greater tendency to chronicity; there is greater 
tendency, as already suggested, to multiple ulcerations undermining of PKOTOZOAN INFECTIONS 
79 
the mucosa (liquefaction) (Councilman and Lafleur), than with the 
bacillary disease. The graver types show marked constitutional disturb- 
ance during the first 2 or 3 days of symptoms. The tongue is dry; abdo- 
men tender, at times tympanitic; great tenesmus; rapid, small pulse; 
stools numerous and small, at first fecal, then bloody, foul-odored, at 
times with slough. The frequent stools with tenesmus and rectal prolapse 
add greatly to the pitiful condition of the patient and provoke exhaus- 
tion. Cessation of pain in the last stage of the disease is often a 
precursor of death; the irritability of the expulsive muscles becomes 
exhausted so that painful efforts cease and are impossible. The urine 
decreases in amount in these cases; is heavily laden with indican; albu- 
minous; with hyaline and granular casts. In the acute period almost 
complete suppression adds an element of danger. 
Cases with many of the above symptoms may continue during weeks 
and months, emaciating until they look like the reconcentrados seen during 
the Spanish War, and yet they may recover. In these grave cases there is 
some enlargement of the spleen and liver. 
The most severe, usually the fatal cases, are of the gangrenous type. 
These patients are apathetic, have the appearance of deep sepsis, as a rule 
remain conscious, while stools are involuntary; there may be perforation, 
and if they recover, misshapen and strictured tissues result. Heart weak- 
ness, after a long period in which emaciation and exhaustion are extreme, 
ends the scene in most cases. 
Chronic Amebic Dysentery 
There is a strong tendency to chronicity in the amebic form of the 
disease. Subacute cases often continue to cause a modified symptom com- 
plex during 4 to 5, or even 6 months after the subsidence of the more 
painful accompaniments of the first month. With chronic amebic dysen- 
tery there is chronic invalidism, marked neurasthenia, or in some cases 
melancholia, irritable rectum, frequent stools; the patients are unable to 
return to the normal level of health, and in this state they live along for 
many years unless some of the usual complications terminate life. 
Periods of improvement, alternation of diarrhea and constipation, en- 
courage these patients to believe that recovery is complete, only to be 
discouraged by a return to the subacute or chronic state. 
Complications 
Abscess of the liver is one of the most frequent and serious complica- 
tions of amebiasis. Abscess may not form for weeks or even months after 
the initial symptoms. In one case, in ISTew York State, the patient who 
had a severe amebic dysentery, developed the abscess 6 months after sup- 
posed recovery, and was operated 2 months after its development. The 80 
SPECIFIC INFECTIOUS DISEASES 
symptoms which led to its recognition were chills—irregularly distrib- 
uted—fever and excessive sweating, with anemia and polymorphonuclear 
increase. Physical signs of limited enlargement of the liver were present. 
The abscess was single. Multiple abscesses of the liver are rare with 
amebic dysentery. 
Unless abscess is relieved by operative treatment—or as occasionally 
happens, perforation with protective adhesions prevents general peritonitis 
and escape of pus—death usually results directly as the result of the 
abscess; or perforation into the lung or pleura (empyema) prolongs the 
misery and usually causes death. Perforation into the peritoneal cavity 
with prompt peritonitis ends the scene in occasional cases. 
Brain and splenic abscesses may complicate suppurative hepatitis; in 
all, the prognosis is equally bad. 
Other complications which are occasional causes of sudden death are 
perforation of the intestine with secondary peritonitis, intestinal hemor- 
rhage, pyelothrombosis, and myocardial degeneration. 
The invasion of the nervous system includes the same complications as 
were mentioned in considering bacillary dysentery; myelitis is possibly 
more frequent with amebiasis. The outcome of these complications is the 
same in both forms of the disease. Joint complications offer the same 
symptoms and prognosis as with bacillary dysentery. 
It is difficult to give figures which are to be relied upon showing the 
approximate death rate to be expected in future epidemics of this form 
of the disease. Epidemics will be better controlled. 
The disease is always serious; its mortality varies enormously in dif- 
ferent countries with different epidemics, is necessarily influenced by com- 
plications and sequelae, as well as by the surroundings and resistance of 
the patient. 
Symptomatic Dysentery 
Dysenteric symptoms accompanying acute infections, typlioid fever, 
puerperal fever, diphtheria, malaria, scarlet fever, measles, and other 
diseases, always add an element of danger and receive consideration in 
the separate chapters dealing with the diseases mentioned. 
References 
Buchanan. Jochmann, Mohr & Staehelin Handb. der inneren Med. 1911, i. 
Councilman & Lafleur. Johns Hopkins Hospital Reports, 1891, ii. 
Hassler & Morgenroth. Jochmann, Mohr & Staehelin, etc. \l. c.]. 
Jochmann. Jochmann, Mohr & Staehelin, etc. [1. c.]. 
Macgregor. Quoted by Osier, Practice of medicine. 1913, 126. 
Mense. Tropenkrankheiten. 1905, etc.; also 1914. 
Woodward. Medical and surgical history of the War of the Rebellion. Medical, ii. PROTOZOAK IKEECTIOKS 
81 
IV. Trypanosomiasis 
(,Sleeping Sickness) 
Trypanosomiasis is a chronic disease, due to protozoan infection, Try- 
panosoma gambiense, which is introduced into the body by the bite of a 
fly—Glossina palpalis—characterized by malaise, fever, increasing weak- 
ness, loss of flesh, apathy, and somnolence. The Protozoon has been 
repeatedly demonstrated in the blood of the infected, also in the cerebro- 
spinal fluid. 
The disease has existed in equatorial Africa; now prevails to an alarm- 
ing extent in Siberia, Congo, Uganda, Rhodesia, along the Niger River 
and upper Nile. 
The infected may live many years, while in occasional cases death 
results during the first 12 months. In occasional cases there may be 
long periods of latency, with simple invasion of lymphatic glands and 
slight fever of remittent character. These periods may continue from 6 
to 12 months, and then follows the period of continuous symptoms with 
the characteristic apathetic and sleeping stage of the disease. In the 
severe types, involuntary discharge of stools and urine are unfavorable 
and presage early death. 
Drowsiness from which the patients are easily aroused, passing into 
coma or increasing slowly from day to day is unfavorable. When coma 
is deep, death promptly results. 
The hlood offers a few prognostic data. 
Suddenly arising cyanosis with polycythemia (6,200,000 per c. mm.) 
is promptly followed by death. 
Sudden increase of existing anemia, as shown by a fall to 2,000,000 
or under, is unfavorable. The hlood in average cases shows secondary 
anemia. Just before death the leukocytic count shows marked polymor- 
phonuclear increase, with large relative increase of mononuclear lympho- 
cytes. 
Anemia varies in accordance with the severity of the infection; it is a 
constant factor; the average count of erythrocytes is between 3,000,000 
and 3,500,000. 
The prognosis of trypanosomiasis has been considered by some to have 
been favorably influenced by the introduction of the newer arsenic prep- 
arations, atoxyl, arsenophenylglycin and salvarsan (Robert Koch and 
Ehrlich). It is doubtful whether the infected ever recover without the 
flooding of the blood with some one of the arsenic preparations, and the 
effect of these is still sub judice. No patient can be considered cured 
until it is established beyond peradventure by repeated blood examina- 
tions that trypanosomes have disappeared from the blood, and negative 
auto-agglutination as well as a negative inoculation of the suspected 82 
SPECIFIC INFECTIOUS DISEASES 
blood into susceptible animals has been fully proved. It is held by Low, 
that the prognosis is always grave, and the disease almost invariably fatal. 
Reference 
Low. Sleeping sickness. In: Allbutt & Rolleston’s System of medicine, ii, part ii., 224. 
V. Relapsing Fever 
(.Febris recurrens—Relapsing Typhus) 
Relapsing fever is due to infection with the Spirillum of Obermeier 
(1873) ; is sudden in its onset, the fever continuing during about one 
week, followed by an almost equal period of remission, with a renewal 
of the original syjnptoms. The first relapse is usually 1 or 2 days 
shorter than was the first attack; this may not always be the case. The 
average cases have hut two attacks, though exceptionally there may be 
as many as five or six. The disease is indigenous to Russia, Poland, some 
parts of Africa, and Egypt; is rare in America. High temperatures 
(105° to 106° F.) are not serious. 
The fever of the separate attacks ends by crisis and a fall of three 
degrees below normal, with profuse perspiration; sometimes considerable 
weakness follows: all of which need not alarm the attendant. Cases are 
reported in which the fall was as much as 10° F., ending favorably. The 
later relapses are shorter than those preceding, sometimes lasting only 
1 or 2 days. During the period of convalescence slight elevation of 
temperature may occur without giving rise to symptoms (subjective), 
and these do. not interfere with recovery. They are either due to weak- 
ness or to abortive or rudimentary attacks. 
The prognosis of relapsing fever is good; most epidemics show a low 
mortality (4 per cent) (Murchison). Fatal cases are always due to 
complications—either pneumonia, asthenia, weak heart, pi'eexisting dis- 
ease, or alcoholism. Striimpell insists that some of the fatal cases are 
due to “wretched nursing.” Deep jaundice has complicated serious 
cases. The diagnosis can be easily confirmed by blood examination. I 
have seen but one case, which was persistent: there were six relapses. The 
patient was an active priest who had traveled over a considerable dis- 
tance; the focus of infection could not be traced. His convalescence 
was slow hut complete; his health has been better since the attack; there 
never has been a return of symptoms. Vickery (Striimpell) reports one 
case found in Boston. 
One attack does not produce immunity; cleanliness, destruction of 
the body louse and bedbugs—the carriers of the Spirillum—will prevent 
the spread of the disease. PROTOZOAN INFECTIONS 
83 
References 
Murchison. Continued fevers. London, 1884. 
Striimpell. Textbook of medicine, i, 43. New York, 1912. 
Vickery. Striimpell Textbook of medicine, i. New York, 1912. 
VI. Leishmaniasis 
(Tropical Splenomegalia, Indian Kala-azar, Infantile Kala-azar, Tropical 
Sore or TJlcer) 
The protozoa which belong to the Leishman group and which are re- 
sponsible for leishmaniasis are of three forms, each differing from the 
other in morphological and cultural characteristics, each developed in 
flagellate form. These include the (a) Protozoon of Leishman or Leisli- 
mania infantum, the cause of (1) infantile kala-azar; (b) the Protozoon 
described by Donovan as the cause of the type of the disease in India 
(2) Indian kala-azar and (c) Leishmania tropica of Homer Wright, now 
considered the cause of (3) tropical sore or ulcer. 
The Protozoon to which Leishman called attention (1900-1902) is 
found in the blood, spleen and bone marrow. Rogers subsequently con- 
firmed Leishman’s find and developed the offender in flagellate form. 
For over three decades the disease has been recognized as a cause of fatal 
epidemics in India, where adults are mainly affected, while the infantile 
type of kala-azar has claimed its victims along the shores of the Mediter- 
ranean Sea, in Greece, Turkey, Italy, Malta, Sicily, Portugal, Algiers, 
Tunis and Tripoli. In India it attacks all ages, while the disease as it is 
found along the coast of the Mediterranean Sea is often of the infantile 
type, though adult cases are not uncommon. There are cultural differ- 
ences (Leishman) in these two forms of kala-azar parasites; the infantile 
type is easily grown on the Xovy-McFeal culture medium, while the 
Protozoon of the Indian type of the disease is not easily cultured on this 
medium. The Indian parasite is readily cultured in splenic blood with 
citric acid; not so the infantile form (Leishntan-Hicolle). The inocula- 
tion of dogs and monkeys with the infantile parasite produces the dis- 
ease (Leishmania infantum), while the parasite Leishmania donovani 
(Indian Protozoon) gives negative results. 
With all forms of leishmaniasis, the parasites infest the spleen, liver, 
bone-marrow; at times the kidney, lung, pancreas; mesenteric glands 
and lymphatics generally. The prognosis of the infantile form of the 
disease is said by Leishman to be better than the adult form or the type 
prevalent in India. The recognition of the bedbug and the flea in India 
and along the Mediterranean as the carriers of the Protozoon has led to 
prophylactic measures in some quarters, but no benefit to the masses has 
as yet been reported. 84 
SPECIFIC INFECTIOUS DISEASES 
The disease has raged in epidemic form in the colonies of India dur- 
ing many years and has at times claimed as high as 20 per cent of the 
entire population. The infection leads to secondary anemia, marked 
splenomegaly, emaciation, and atrophic changes in the internal organs 
(intestinal mucosa). 
The average duration is between 6 and 20 months. The period of in- 
cubation 20 to 30 days. Acute hemorrhagic conditions—profuse bleed- 
ing from mucous surfaces—nose, gums, stomach, intestines and meninges 
■—may lead to sudden death. The blood condition is advanced, and pro- 
gressive cases show a reduction of the red corpuscles to 1,500,000, to 
3,000,000, and the leukocytes to 700 to 1,000 per c. mm. with a marked 
polymorphonuclear decrease. Price placed the mortality of the epidemic 
in Assam at 73.6 per cent. 
Schilling contends that cases in which the fever becomes continuous 
offer the most unfavorable outlook. 
Rogers found that when the leukocytic count fell below 2,000 per 
c. mm. the rapid development of the disease was to be expected. Eo 
method of treatment used (including arsenophenylglycin and salvarsan) 
has proved of value to control the disease. 
Ricolle has seen but one case of the infantile disease recover. 
References 
Donovan. Quoted by Schilling [l. c.\. 
Leishman (Wm.). Meuse’s Handbuch der Tropenkrankheiten. Bd. Hi, 591. J. of the 
Royal Army Medical Corps 18,1912. 
Rogers. Quoted by Schilling, l. c. (below); also Osier, New York, 1913. 
Nicolle. Kala-azar. Archiv. de V Inst. Pasteur de Tunis, 1910 & 1911. 
Price. Mohr & Staehelin. 1911, i (See Schilling’s Tropische Spleno-megalia). 
Schilling. Tropenhygiene. Leipzig, 1909; also Mohr & Staehelin, 1911, i, 983. 
Wright (Homer). See Osier’s Practice of medicine. New York, 1913. 
B. Bacterial Diseases 
I. Typhoid Fever 
{Enteric Fever, Typhus abdominalis) 
Typhoid fever is a general infection dne to the Bacillus typhosus (Bac- 
terium typlii) of Eberth and Gaffky. 
Modern sanitation and the study of the life history of the infecting 
agent, have reduced the frequency of the disease, and promise, with the 
intelligent cooperation of the lay world and the medical profession, to 
efface it entirely. BACTERIAL DISEASES 
85 
Typhoid Immunity Through Vaccination 
The surprising results of inoculation with the antityphoid vaccine as 
reported by Firth, Major Russell of the United States Army, and many 
others in all parts pf the civilized world, are so convincing that it may be 
positively asserted that the scientific application of data which Russell and 
Firth have presented, prove conclusively that we possess in the antityphoid 
vaccine a prophylactic remedy, which in its results is as efficacious as is 
inoculation against small-pox. As the result of compulsory vaccination 
against typhoid in the United States Army, the disease has been practically 
removed. Personal communication from Major Russell and medical lit- 
erature give the information that during the year 1913 to July 14th, there 
was not a single case of typhoid reported in the United States Army, as 
against three cases for every 1,000 men per annum formerly. What this 
means to the nations of the earth can be readily understood when we con- 
sider the ravages of a single epidemic, or point with shame to the criminal 
loss of life from this disease during the Spanish-Ainerican War. Man- 
kind is under an everlasting debt to Major Russell and the pioneers who 
have worked in this field with such encouraging and profitable results. If 
prevention of typhoid fever is to be accomplished and its entire picture 
changed during the few years of education which will be needed to re- 
move sources of infection, there must be concert of action of those who are 
in charge of our departments of public health and the public—this means a 
campaign of education in which our profession must take a leading part. 
Typhoid immunity continues as a rule about 2-J years after inoculation. 
Firth shows that “even after 4 or 5 years—the maximum period of 
observation—the rate per thousand among the inoculated is, roughly speak- 
ing, only one-fourth that of the unprotected troops.” 
In 1911 among “80,000 persons vaccinated in the army,” there were 
twelve cases of typhoid with one death, due to intestinal hemorrhage; in 
1910, six cases appeared among the vaccinated, with no deaths. Without 
inoculation, there would have occurred “at the prevailing rates of inci- 
dence” 250 cases. 
We have now had sufficient experience with antityphoid vaccine to con- 
clude beyond peradventure that it modifies the severity of the disease, 
lowers the death rate and acts as a prophylactic. 
To lower the death rate, it will in the future be considered necessary to 
consider every convalescent from typhoid a “carrier”—a menace to the 
public—unless he is properly treated and Avatched. In all these cases inocu- 
lation with antityphoid vaccine should be obligatory. It is the best we 
have to offer in the present state of our knowledge. In all civilized coun- 
tries there has been a change in the lowering of the mortality due to 
typhoid infection which is most encouraging. Thus the following table 
tells its OAvn story: 86 
SPECIFIC INFECTIOUS DISEASES 
Mortality Due to Typhoid Fever per 100,000 Population 
1851-1860 
1861-1870 
1871-1880 
1881-1890 
1891-1900 
Berlin 
96 
83 
62 
20.5 
5.9 
Vienna 
221 
110 
64 
13. 
6. 
Paris 
67 
80 
65. 
25. 
London 
24 
19. 
14. . 
In Central Uew York, cases in which the surroundings are favorable, 
with rational modern treatment show an average mortality between 5 and 
7 per cent. Hospital statistics are less favorable but do not by any means 
equal the mortality of former years. In my service in a general hospital, 
the mortality has never during the past 10 years been higher than 10 per 
cent. In our own country, the United States, we must confess to our 
shame that in 1910 there were approximately 25,000 deaths due to typhoid 
fever. Germany lost but 2,856 lives during the same year and offers an 
apology for that mortality. A search would disclose criminal carelessness 
on the part of individuals and municipalities in the majority of these cases. 
In connection with the consideration of prophylaxis and prognosis, it 
might be wise for our lawmakers and departments of health to consider 
the monetary loss associated with these deaths. Such study and intelligent 
action would promptly change our statistics. Based upon the computation 
of Biggs, the loss due to typhoid deaths in the United States alone, during 
a single year, is in the neighborhood of one hundred million dollars. 
Factors Influencing Prognosis 
The prognosis of typhoid fever is often difficult, and at times it is 
impossible to offer a reliable forecast in the individual case because we 
have no gauge which tells of the depth of the lesions, nor their extent; 
nor can we be certain that the complexion of the mildest case may not 
suddenly change for the worse because of hemorrhage, perforation or other 
unexpected complication. We must therefore reason from the influence 
of separate symptoms, complications, etc., on the course of the disease. All 
forms of typhoid, however mild, should be considered serious. Yo acute 
infection is so likely to change the character of its symptoms as is typhoid. 
The severity of the third week of the disease may be out of all proportion 
to the benign character of the previous period. It is generally supposed 
that the prognosis of typhoid is more serious in hot than in cold weather. 
The disease is less serious toward the end of an epidemic than at its height. 
In some families there is a decided predisposition to the development 
of the infection. 
Enteric fever is unfavorably influenced by pregnancy, childbirth and 
the puerperal period. Pregnant women are likely to abort; The progno- BACTERIAL DISEASES 
87 
sis is not however absolutely bad in any of these conditions, though the 
lowered resistance and vitality must be considered. 
Morphinists, alcoholics and the subjects of chronic disease bear the 
infection badly. 
The prognosis of typhoid is materially influenced by: 
1. The resistance of the patient. 
2. The severity of the infection and 
3. The character of the complications. 
1 Resistance of the Patient 
I have already referred to the beneficent influence of antityphoid vac- 
cination. It is an established fact that resistance is heightened by previous 
typhoid infection, and Russell as well as Kutcher have proved this fact by 
incontrovertible evidence. 
Age.—Clinicians are all agreed that the prognosis of the disease dur- 
ing early life is more favorable than in adult life. My experiences show 
a mortality of 5 per cent in children; considering my statistics'of hos- 
pital and private cases I find the mortality between 10 and 12 per cent in 
the adult. The prognosis during the first year of life is unfavorable. Be- 
ginning with the sixtieth year the mortality is surprisingly high, but the 
disease is rare. The most dangerous period (Fornet) of the disease in 
women, who show a mortality of 12.7 per cent is between the fifteenth and 
nineteenth year of life. In men, the mortality in a large number of 
cases was 11.7 per cent, and the greater number of deaths between the 
thirtieth and thirty-fourth year. In a material including 11,000 cases of 
typhoid (Fornet), the mortality ranged between 10.8 and 11.4 per 
cent. Young, plethoric, obese, and mentally active adults (twentieth and 
fortieth years of life), offer a less favorable prognosis than do the thin 
and less active of the same age. 
2 The Severity of the Infection 
In a small proportion of typhoids the malignancy of the infection is 
early manifested. There are cases, fortunately rare, nevertheless suffi- 
ciently frequent and important to demand consideration, in which without 
a prodromal period the patient is at once found violently ill, usually after 
a single severe chill or repeated light chills, with hyperpyrexia and other 
symptoms of deep constitutional invasion. In some of these, meningismus 
typhosus is an early accompaniment. In children this type is less dan- 
gerous than in the adult; with the latter, this foudroyant type offers a 
very grave prognosis. Curschman has called attention to a class of cases 
in which the infection is so malignant as to present fully developed and 
severe symptoms during the period of incubation. In all of these type3 88 
SPECIFIC INFECTIOUS DISEASES 
in which the early symptoms are threatening, the prognosis is materially 
influenced by the rapidity of the pulse; and I am inclined to place consid- 
erable prognostic value on facial expression, and the mental state of the 
patient. Cases in which there is early hyperpyrexia, wdiich refuse to yield 
to treatment, in which there are no marked remissions, likely to be associ- 
ated with cerebral symptoms and rapid pulse, justify a very guarded prog- 
nosis; usually die early and are expressive of malignant infection. 
Experienced clinicians have repeatedly called attention to the decided 
variation in the malignancy and in the nature of different epidemics. In 
some of these, the cases are uniformly severe, in others the prognosis proves 
favorable and complications are either rare or if present, mild. These 
anomalies of behavior we cannot explain. There are epidemics in which 
the character of the eruption is hemorrhagic and the disease is likely to be 
severe. This does not, however, always follow, for in central and north- 
ern Hew York during mild epidemics and in isolated cases we have had 
hemorrhagic skin lesions which made uninterrupted recoveries. As a rule 
an epidemic in which the lesions are hemorrhagic offers a less favorable 
prognosis than does the usual roseola eruption. However, before reaching 
conclusions in these cases associated conditions should be thoroughly con- 
sidered. 
Malignant and severe infection is likely to show its effect on the myo- 
cardium early. Heart weakness, circulatory insufficiency early, is often 
attributable to the direct effect of typhoid toxemia on the heart muscle or 
to the paralyzing influence of toxins on the spinal centers and vasomotors. 
With these conditions there is lowering of arterial pressure, rapid and 
unsatisfactory systolic contraction, and often a lowering leukocytic count. 
With malignant infections the blood-stream is overcharged with typhoid 
bacilli, and Schottmiiller has demonstrated the persistence of typhoid ba- 
cilli in the blood in these cases in large numbers during long periods, while 
Liidke and Sturm have further demonstrated to the satisfaction of the 
German profession that the severity of the constitutional symptoms in 
typhoid fever is in direct proportion to the number of bacilli in the blood- 
stream, and that collapse is attended with enormous bacteremia. Hence a 
count of bacilli in the blood should prove of prognostic value. Schott- 
miiller’s highest count was 202 bacilli in 10 c. cm. of typhoid blood. 
This comparatively low count was made before the use of bile-agar, which 
gave Schiiffner (cited by Schottmiiller), a count of 872 bacilli in 1.5 
c. cm., and which may now be depended upon to give positive data in 
50 per cent of all cases. 
3. The Influence of the Complications of Typhoid 
The influence of the complications of typhoid deserves separate con- 
sideration, and this it will receive in the following pages. BACTERIAL DISEASES 
89 
In a large percentage of cases the height of the fever at the end of the 
first week of continuous symptoms offers a fair index of the severity of the 
disease in uncomplicated cases. Typical cases during the second week of 
symptoms, with temperature not higher than 103°F., pulse 100 to 110, 
and respiration not above 24 per minute, may be considered mild, and 
without complications offer a very good prognosis. In all cases of typhoid 
fever, a decided daily fall of temperature, making it possible for the heart 
to rest, and reducing the ravages of too rapid oxidation and consequent 
degeneration, influences the disease favorably. Such patients are able to 
bear the disease longer and better than do those whose temperature remains 
continuously high. It is a further fact that with a remission daily, higher 
temperatures are better borne than lower temperatures without decided 
fall; therefore I would formulate the following rule: A decided fall of 
temperature daily, during a period varying from 2 to 4 hours, associated 
with a corresponding lowering of the pulse, is of decided advantage to the 
typhoid patient. 
There are cases with indefinite symptoms during the first two and 
sometimes three weeks of the disease, with indefinite and irregular rises of 
temperature, often not above 102°F., occasionally from 100° to 101°F., 
in which the agglutination test is long postponed, and in which abdominal 
symptoms during this period are likely to be absent. These may, before 
the termination of the disease, present serious features, making the prog- 
nosis problematic for long periods. The foudroyant type already men- 
tioned in connection with malignant typhoid, plunges the patient into high 
fever at once, within 24 to 48 hours, without marked remission. 
The pulse is rapid, in some cases tense at first, becoming promptly 
dicrotic; there is early cerebral invasion, dry tongue, marked subsultus, 
occasional convulsions in children and young adults, and often opistho- 
tonos with other cerebrospinal symptoms. This type offers a very unfavor- 
able prognosis; the patients die as a rule within the. first week, or early 
in the second week of the disease. 
These cases present all of the features of deep toxemia. Most of the 
patients are robust adults, over twenty and below the 40th year of life. In 
some of these cases mixed infection has been considered as the cause of the 
foudroyant and malignant nature of the disease (Port). On the other 
hand Lenhartz has obtained pure cultures of typhoid bacilli from the 
blood in these cases without either ulceration or swelling of the intestinal 
glands. (See Typhoid, without intestinal lesions.) 
Temperature and Prognosis 
Prognosis in Various Forms of Typhoid 
Protracted Fever.—There are frequent cases—the majority of which 
are only moderately severe, though a few may he considered severe—in 90 
SPECIFIC INFECTIOUS DISEASES 
which the fever persists during unusually long periods. These may cover 
a febrile period varying from 4 to 6 or even 8 weeks. I have the notes of a 
case which terminated favorably, in which on the ninety-sixth day of the 
disease, without known complications and without preceding decided re- 
mission, the temperature still averaged 102 °F. As a rule it will be found 
that in these cases the fever is of an intermittent character and atypical. 
In the majority of these cases the prognosis is favorably influenced by the 
relatively short or even normal period of continuous fever, and the decided 
remissions during the longer period of intermittent fever. If in these 
cases of prolonged fever the digestive organs do not revolt, and there are no 
other serious complications; in spite of extreme weakness and muscular 
wasting, full recovery may slowly follow. These cases are likely, after 
the long postponed afebrile period is established, to have rises of tempera- 
ture on slight cause. An occasional case of this kind passes beyond the 
long period of fever, but fails to lift itself from the weakness which fol- 
lows ; wasting continues, the appetite does not improve, the organs of diges- 
tion become intolerant, vomiting is often an uncontrollable symptom, the 
abdomen is abnormally resistant and retracted, and death follows weeks or 
months after the initial symptoms of typhoid. There is another set of 
cases in which without knowm cause a slight fever persists long into the 
period when full convalescence is expected; which yields promptly, and 
offers a changed prognosis so soon as the patient is allowed to sit up and 
move about cautiously. Delafield called attention to these cases years ago. 
Abortive Typhoid and Mild Irregular Typhoid (Typhus abortivus, 
Typhus levissimus).—In America we meet but few cases of the abortive 
types of the disease ; that these are occasionally found in the midst of 
endemics or epidemics we cannot deny. Some of these correspond with 
the description given by the older writers of ephemeral fever (febricula). 
The majority of these cases offer a favorable prognosis. They are all char- 
acterized by a short febrile period. Liebermeister’s classification of these 
cases as 
1. Typhus levissimus 
2. Typhus abortivus 
is most satisfactory. 
1. Typhus levissimus. (Mild Typhoid).—In these cases the disease 
does not seem to be fully developed. The febrile period may be short and 
mild; one or more of the usual leading symptoms of the disease may also 
be of short duration, even in the presence of a slight continuous febrile 
movement. In occasional cases there is a remittent type of fever, in others 
the curve is irregular and erratic. The pulse in favorable cases is scarcely 
changed in character or in frequency. The general condition of the patient 
continues good. The disease ends in recovery as a rule between the four- 
teenth and twentieth day of the disease, without marked invasion of the 
sensorium. In occasional cases the early days of a mild typhoid may BACTERIAL DISEASES 
91 
include high fever with other transitory constitutional symptoms, but they 
soon prove to be benign because of the decided change in the nature of all 
attending conditions. In the United States cases of this kind such as 
Liebermeister has described, running their course in from 6 to 8 days, are 
among the clinical rarities. Mild typhoids may be followed by slow con- 
valescence. The enlarged spleen is in evidence early in most cases. 
2. Typhus abortivus (Liebermeister).—Occasionally a free out- 
spoken fever, early, with deep invasion of the sensorium at once—but with 
a reassuring pulse—runs a short course and may lead either to prompt or 
to slow convalescence. In these cases the severe headache during the first 
week, complete anorexia and apathy, occasionally a single heavy chill and 
early enlargement of the spleen, are not to he interpreted as arguing against 
a favorable prognosis. In these as in all cases of typhoid the pulse (myo- 
cardial condition), and the frequency of the respirations offer data which 
must be given great weight before safe conclusions are justified. In some 
of these abortive types the fever may return to normal within 9 to 14 days. 
Most of these cases, however, begin with a decided chill; after a short pro- 
dromal period, the temperature rises promptly; there is as a rule- some 
apathy with sleeplessness; there may be delirium; the roseola eruption is 
found early; but the pulse is likely to continue good. Complications and 
distant typhoid infections (liver, gall-bladder, lung, heart, etc.) occur, but 
are less serious and less frequent than with the usual types of the disease. 
The light form of typhoid (levissimus) differs from the abortive type 
in several particulars. In the former the constitutional symptoms are 
fewer; symptoms referable to separate organs are unusual; the tempera- 
ture is higher and associated with greater wear and tear in the abortive 
type; while albuminuria is more frequent, with casts (hyalin, granular, 
and blood). Roseolse are fewer and less constant in the abortive than in 
the typical disease. In both types of irregular fever considered, tympany 
and diarrhea are not as a rule disturbing. A full consideration of these 
earmarks will make it comparatively easy to prognosticate in these cases; 
but it must be remembered that none of these patients is immune to per- 
foration, peritonitis, hemorrhage or pulmonary complications. These 
added dangers are not frequent. Relapses are frequent after the milder 
types of fever and these may run a more typical course than did the origi- 
nal infection. The prognosis remains uncertain for days following the 
beginning of the relapse, but usually proves good. 
Ambulatory Typhoid (Walking Typhoid Fever.)—Most cases of am- 
bulatory typhoid may safely be considered to have been neglected. In 
these, patients have continued about, in spite of a prodromal stage and a 
train of continuous symptoms which, in all probability always include 
some elevation of temperature. The fever in these is not so high as in the 
usual cases ; there is less exhaustion and malaise attending it early; but the 
picture which is finally presented by these, cases is often serious and the 92 
SPECIFIC INFECTIOUS DISEASES 
outlook grave. This is particularly true of those typhoids who have been 
exposed to the hardships of travel. My experience justifies the conclusion 
that travel adds enormously to the dangers of every fully developed typhoid. 
While ambulatory typhoids may present with normal temperatures 
during the early hours of the day or during almost the entire morning, close 
observation will show some elevation later in the day. The pulse in spite 
of low temperature or afebrile state is rapid, as a rule, when these patients 
surrender, and there are often subjective complaints, including palpitation. 
In hospital cases I have often noticed more or less incoherence on admis- 
sion. I have learned to give a very guarded prognosis in these cases; they 
run an uncertain course, are likely to develop grave abdominal complica- 
tions—endocarditis, pulmonary infarct and infection, thrombosis, abscesses 
—and what I fear most, degeneration and dilatation of the heart muscle. 
There are on the other hand ambulatory cases so mild as to give no un- 
easiness, running a smooth and uneventful course to full recovery. 
Afebrile Typhoid.—Cases of feverless typhoid are not frequent; they 
do, however, occur. They are likely to be found in homes where several 
typical cases of the disease exist. In some of these the temperature has 
remained normal throughout, others have shown a slight elevation usually 
toward night of from -|0 to 1°F. In all the diagnosis has been confirmed 
either by a positive Widal reaction, or by blood cultures, or by both. With- 
out fever, the associated symptoms referable to the abdomen have per- 
sisted. Unquestionably a number of so-called “latent cases” to which Koch 
referred, belonged to this class. Tie held that these cases existed without 
marked symptoms, were not as a rule reported to the public health authori- 
ties, and that they continued to be a menace. The Trier Commission drew 
attention to the dangers to the public of these cases, and established the fact 
that the number of infected cases in Trier was nine times greater than the 
number “sufficiently ill to require treatment.” The majority of afebrile 
typhoids recover: death may follow, as has been reported by Strube and 
F rantzel. 
In the aged, afebrile typhoid, in the presence of chronic cardiovascular 
and renal disease, offers but little that is encouraging; in alcoholics and 
those reduced by previous disease the prognosis is correspondingly bad. 
Sudden fall of temperature is occasionally met when not of serious 
import. It should always be viewed with suspicion and the patient should 
be carefully observed, that its significance may not be misinterpreted. The 
fall may presage a favorable termination, for it has been my experience 
that in a majority of cases in which the true cause of the fall has not been 
made clear promptly by the development of positive symptoms, there 
has been a rise of temperature within 12 to 24 hours and then a gradual 
return after a varying period to normal or, if there are no added compli- 
cations, with a more or less irregular behavior the fever has gradually sub- 
sided In these cases the decided fall of temperature is not associated with BACTERIAL DISEASES 
93 
the symptoms of collapse due to profuse hemorrhage, nor the pain and 
physical signs referable to the abdomen which are characteristic of per- 
foration, nor the added evidences of circulatory embarrassment, which 
occasionally develop suddenly at the height of the typhoid infection. 
Sudden effacement of liver dulness with fall of temperature, abdominal 
pain, and collapse, is suspicious of perforation and justifies a serious prog- 
nosis. Blood pressure study will in the presence of perforation and begin- 
ning peritonitis show a slight, but easily demonstrable rise to promptly 
fall after a few hours, and may prove of prognostic as well as diagnostic 
value. 
Post-typhoid Pyrexia.—Transitory elevations of temperature which 
may last a short time during the period of convalescence are not of serious 
import. In some—particularly nervous subjects—excitement, worry, mus- 
cular effort, a hearty meal, or errors in diet during this period prove suf- 
ficient to cause these sudden rises. Long continued obstipation may also 
provoke insignificant exacerbations. Hypothermia, persisting for several 
days, mentioned by Osier, is also without unfavorable influence. In some 
of these cases the pulse has been erratic, occasionally slow and irregular, in 
others, abnormally rapid during limited periods. 
Circulatory Disturbances in Typhoid 
Pulse.—It is fortunate that the pulse of typhoid fever is in most cases 
slow in comparison with the temperature. In no other long continued 
acute infection does the heart behave so favorably. The pulse offers the 
safest indications for prognosis in typhoid fever. With a pulse, of good 
character, and average frequency of 100, in spite of an elevation of tem- 
perature of 103° to 104°F., the prognosis continues good. As has already 
been stated, remission of fever during the day with associated drop in heart 
frequency is favorable. When the pulse is persistently high, whatever the 
temperature—if above 120 to 130—there is serious complication, or heart 
weakness threatens. When the pulse, which during the first two weeks has 
been reassuring, begins to intermit in the third week, is irregular and 
rapid with feeble heart sounds, possible dilatation must be considered sug- 
gestive of myocardial insufficiency. When, with such a pulse there are 
evidences of pulmonary congestion or edema, consolidation, or bronchial 
catarrh, the prognosis is exceedingly grave. Cyanosis with evidences of 
myocardial insufficiency and correspondingly rapid pulse justifies an un- 
favorable prognosis. Rapid pulse with deep invasion of the sensorium is 
of serious import. Restlessness and insomnia with delirium add to the 
danger. With rapid pulse (120 to 140) and hurried respirations (30 to 
50) the patient must always be considered to be in a serious condition, and 
search will usually reveal pulmonary, renal, cerebral or other complication, 
though a tired heart with consecutive stasis may explain the symptom 94 
SPECIFIC INFECTIOUS DISEASES 
complex. Dicrotism at the height of the disease, if the heart is not abnor- 
mally rapid, is not as a rule unfavorable. There are but few cases of en- 
teric fever in which there is not more or less dicrotism at some time. 
Rapid pulse is the rule with infantile typhoid and does not argue against 
a favorable outcome of the disease. After the sixth or eighth year of life 
the character of the pulse and its frequency in children approaches that of 
the adult. 
As the disease advances, blood pressure is likely to be lowered and the 
pulse amplitude correspondingly changed. The pulse is softer and smaller: 
this is a natural result of toxemia and not unfavorable. Persistence of 
normal blood pressure is favorable. Increased frequency of the heart with 
sudden fall of blood pressure is unfavorable. Increase in the frequency 
of the pulse toward evening, with a reassuring condition during the day 
does not change the prognosis. In all cases there is likely to be a close rela- 
tion of temperature and pulse. With a rapid pulse early in the disease 
whatever the change of blood pressure, unless such condition depends on a 
neurotic state or the patient normally had a rapid, irritable heart, that 
organ is likely to prove insufficient. 
The heart itself is in most cases the seat of interstitial and degenerative 
changes (myocarditis). The extent of such changes is shown by the weak 
and muffled systolic sound, mitral systolic murmur—due to relative insuf- 
ficiency—accented II. pulmonary sound, distant heart sounds—embryonic 
in character—marked change in rhythm, and in severe cases decided dilata- 
tion of the ventricles. The early signs of cardiac weakness are due to 
vasomotor paralysis; the evidences of myocardial degeneration follow. 
Sudden Death.—Approximately 1.2 per cent of typhoids die suddenly 
from a variety of causes, among these myocardial invasion. Degeneration 
is the most frequent; thrombosis, embolism, cerebral apoplexy, pulmonary 
edema—due as a rule to circulatory insufficiency, and renal invasion, de- 
generative in character—are also to be considered. 
A distinct mitral systolic murmur with accented II. pulmonic sound 
is not of serious import unless there are other marked evidences of heart 
Aveakness in rapid pulse, etc. Diffuse apex-beat with rapid heart is 
deserving of careful consideration and is, if persistent, indicative of 
serious cardiovascular disturbance. In many patients, unless the nervous 
system, is profoundly involved, the pulse as counted by the physician is 
likely to be somewhat accelerated, hence the average count of the nurse 
must also be considered. Relatively sloiv pulse with dicrotism and normal 
arterial resistance, or only slightly lowered blood-pressure, is not of se- 
rious import. Sudden increase in the frequency of the pulse with or 
without evidences of collapse is ahvays ominous, and will be fully con- 
sidered in connection with intestinal hemorrhage, perforation and other 
complications. The crossing of the temperature curve by the pulse curve 
is suggestive of increasing danger. BACTERIAL DISEASES 
95 
Bradycardia following rapid pulse, particularly during the convales- 
cent period or in the terminal febrile stage, is not of serious import unless 
it is an evidence in young or in old subjects of heart block. Any change 
in the coronaries or disturbance of conduction {Stokes-Adams) adds a 
decided handicap, and materially lowers the chances of recovery. 
Accented aortic II. sound with increased ventricular effort and force- 
ful impulse, suggest a compensatory effort to overcome vasomotor paraly- 
sis in the periphery, usually in the domain of the splanchnics, and unless 
relieved overtaxes the cardiovascular system and leads to cardiac asthenia 
finally (Ortner). It not infrequently happens that the pulse rate is 
higher during periods of relapse than it was originally. Every case of 
typhoid fever during convalescence or after recovery may show some ab- 
normality of function or organic cardiovascular change. Of all modern 
clinicians, Thayer deserves the greatest credit for having demonstrated 
the fact that arteriosclerotic changes are unusually frequent in patients 
who have had typhoid, as well as other functional and organic heart 
lesions. 
Posttyphoid myocarditis may be the cause of symptoms during con- 
valescence in which the slightest excitement or muscular effort provokes 
palpitation or some subjective complaints referable to the heart. These 
types of myocarditis lead to complete recovery within a few months. 
If the pulse is persistently rapid during the period of convalescence 
with gradual improvement in the general condition of the patient, gain 
in weight, and good appetite, the heart will after a reasonable period of 
rest with moderate exercise, return to its normal state. Rapid pulse per- 
sisting during convalescence, without increase of weight, slight evening 
rise of temperature, general condition beloAV par, must lead to the sus- 
picion of some added infection—possibly tuberculosis, pus deposit, or 
other hidden complication. In severe cases, besides vasomotor paralysis 
already mentioned, there are anatomic arterial changes (Wiesel) in which 
the media is involved in a process of atrophy, connective tissue change, 
and lowered arterial resistance. This adds an element of danger which 
is overcome in the average case. 
Thrombosis.—Phlebitis cruralis.—Thrombosis of the anterior cru- 
ral is a frequent complication which fortunately as a rule follows either 
toward the end of the acute fever, or early during the period of convales- 
cence. While it is often exceedingly painful and causes in all cases more 
or less fever and acceleration of the pulse, it usually leads to full recovery 
after weeks or months. Occasionally double crural phlebitis postpones 
convalescence. I have never seen a case which led to gangrene, but 
rarely a detached bit of thrombus has led to fatal embolic infarct. 
Thrombosis or septic thrombophlebitis may invade any vein, and add a 
complication of serious import—pulmonary, portal or cerebral thrombosis 
—fortunately rarely encountered. 96 
SPECIFIC INFECTIOUS DISEASES 
Arteries.—Arteries may occasionally be occluded by either an 
embolus or thrombus. The complication is rare, not necessarily fatal; it 
may lead to gangrene. Holscher claims that 1 per cent of all typhoid 
deaths are due to embolism of the pulmonary artery. Limited superficial 
losses of tissue due to embolic infarct or arterial change heal slowly as a 
rule; their prognostic significance depends upon the cause and source of 
the embolus. If due to endocarditis, the latter may prove malignant or 
septic; then the prognosis is bad. 
Gangrene.—Gangrene due to thrombosis, embolism, or arteritis may 
prove serious when extensive. It is not a frequent complication; usually 
is unilateral, and involves one lower extremity. In all of these cases 
associated conditions, sepsis, and the extent and location of the process 
must be considered. Invasion of the iliac, femoral or posterior tibial is 
most frequent. In rare cases the prognosis becomes absolutely bad be- 
cause of double symmetrical and far-reaching gangrene (Trousseau, 
Potin, Mercier, Bachmayr and Dodd). The occurrence of double gan- 
grene is so rare that in an active hospital experience covering over thirty 
years, not a single case has presented. 
Pericarditis.—WThen positive symptoms, subjective and objective, of 
pericarditis present, these are due as a rule to septic infection, which is 
likely to be purulent and which adds a. factor of danger to an already 
serious condition. Holscher, in an analysis of 2,000 typhoids found 
this complication in .7 per cent of cases. 
Endocarditis.—Endocarditis arising during the course of the disease 
is not frequent. Occasionally with mixed infection the endocardium has 
been involved. It requires caution to eliminate in diagnosis the malignant 
endocarditis of typhoid type but not typhoid fever, in which the prognosis 
is always bad. In 2,000 typhoid autopsies (Holscher) there were 11 
cases showing acute endocarditis, i. e., .5 per cent. 
Disturbances in the Respiratory Organs 
Respiration.—The safest indications for the prognosis of a typhoid 
patient are offered by the pulse (heart) and the respiration (lungs). With 
a reassuring pulse and no evidences of serious pulmonary involvement or 
embarrassment of any kind, as shown by hurried or labored breathing, the 
outlook may in the overwhelming majority of cases be considered favor- 
able. Most serious complications will at once accelerate pulse and respi- 
ration. 
Rapid respiration without evidences of cardiac or pulmonary involve- 
ment, out of proportion to the height of temperature, unless of purely 
functional origin (hysteria, fear, neurosis) is always suggestive of a 
serious complication; its true significance can only be decided after its 
cause has been unearthed. Occasionally diabetes mellitus with acidosis BACTERIAL DISEASES 
97 
in a typhoid subject has been found to be the cause of hurried respira- 
tions. In other cases profound toxemia has proved to be the cause with- 
out high temperature but with great exhaustion; finally, with rapid heart 
such patients succumb to the disease. 
In the majority of typhoid cases pulse and respiration bear a close 
relation to the temperature; in a large number of cases however in which 
the temperature reaches a high degree, respiration is not markedly 
changed. These are favorable combinations. The cause of rapid res- 
pirations in any case determined, the prognostic significance is easily 
cleared. 
Considering pulse and respiration together, I would submit the fol- 
lowing: With acute typhoid infection a rapid pulse is always more omi- 
nous than a high temperature, hut with such complications as pneumonia 
or mixed infection, hurried, abnormally high respirations are more seri- 
ous than a rapid pulse. Where the two are present together, i. e., rapid 
pulse and abnormally frequent respirations, at the height of the acute 
disease unless one can be sure that the symptom complex rests on hysterical 
fundament, the prognosis is exceedingly grave. 
Most enteric fevers are associated with catarrhal changes in the upper 
respiratory tract and included bronchi. 
The ordinary nasal changes have no influence on the course of the 
disease, save as the dry mucosa, crusting, and at times ulceration with 
possible perforation, add to the discomfort of the patient. 
Epistaxis.—ISTosebleed is present at some time as a rule—usually 
early—and unless profuse is of no prognostic significance. Repeated 
profuse nosebleed with other evidences of hemorrhagic disease, usually 
with grave constitutional disturbances, often deep involvement of the sen- 
sorium, dry tongue, crusting, and sordes on teeth whenever present, is 
ominous—this symptom complex is not infrequent in chronic alcoholics 
with typhoid fever. 
Catarrhal Pharyngitis and Laryngitis.—Catarrhal pharyngitis and 
laryngitis do not influence prognosis materially. Deep ulceration of the 
larynx, with or without edematous swelling are usually found on the 
posterior laryngeal wall, and often with the more malignant types of the 
disease. The edema alone may threaten the life of the patient and de- 
mands) prompt relief, otherwise death follows. When ulceration leads to 
necrosis, perichondritis, cutaneous and deep emphysema, the outlook is 
bad. The mortality is as high as 40 to 50 per cent (Tiirck). In occasional 
cases, deep ulceration with destruction of tissue leads to stenosis if the 
patient recovers, demanding tracheotomy and the permanent or long wear- 
ing of the tube. Uncomplicated laryngeal ulcerations are not infrequent, 
as has been proved by post mortem study; they may be present without 
causing symptoms and in the majority of cases heal permanently, with- 
out deformity. 98 
SPECIFIC INFECTIOUS DISEASES 
Bronchitis.—Bronchitis, present in practically all cases of typhoid 
—when uncomplicated, does not lower resistance or influence prognosis. 
Extension to the finer bronchial tubes (bronchiolitis) is common in the 
severer cases, and is therefore of grave import. Consecutive ateleclasia 
adds another factor of danger, but unless bronchopneumonia (lobular 
pneumonia) follows, the prognosis, though grave, may yet hold hope of 
recovery. Disseminated islands (lobular) of pneumonia with atelectasia 
is a serious complication in all cases, and in all ages. 
Hypostatic Congestion.—Hypostatic congestion, usually found in the 
lower lobes, is serious in proportion to the added obstruction which it 
offers to the heart—always serious, when extensive—in the presence of 
a weak myocardium and deep infection. Pneumonic infection of the 
hypostatic lung, i. e., hypostatic pneumonia, is as a rule life-threatening, 
always a serious complication, and often ends in death (50 per cent). 
Children rarely develop more than transitory hypostatic congestion, and 
are not prone to have added pneumonia: this is due to the shorter dura- 
tion of the disease and relatively infrequent heart weakness. 
Pneumonia.—Pneumonia (lobar, i. e., croupous) is a serious compli- 
cation of typhoid fever. In the larger number of typhoids' this complica- 
tion (Fraenkel-Weichselbaum diplococcus) is developed during the height 
of the disease, near the end of the fever or during convalescence early— 
rarely late. As a rule there are early evidences of heart weakness, rapid 
pulse, and decided lowering of blood-pressure, with characteristic res- 
piration—all of which affect prognosis unfavorably. Cyanosis added to 
these conditions is serious. My experience with pneumonia in typhoid 
fever has been exceedingly unfortunate: over 50 per cent of these have 
died. It is exceedingly rare to find a favorable outcome after the fortieth 
year of life. Lobar pneumonia complicates typhoid in from 5 to 7 per 
cent of cases, the lobular form in 8 per cent. There are occasional cases 
of typhoid in which the early symptoms are clearly those of pneumonia, 
so-called pneumotyphoid, in which the lung may clear, and the patient 
falls into the continuous and characteristic symptoms of typhoid fever. 
Invasion of bronchial glands—suppuration—may prove serious, and occa- 
sionally leads to empyema. Strepto- and staphylococcus infection of the 
lung with typhoid, mixed infection, including the Bacillus typhosus, caus- 
ing either lobar or lobular pneumonia, always demands a guarded progno- 
sis. The pure pneumococcus infection offers a better prognosis than does 
the streptococcus. 
Lung Abscess.—Lung abscess is rare. If it follows pneumonia com- 
plicating typhoid, gangrene may finally develop, and death is the rule. 
Pulmonary Infarct.—Pulmonary infarct may cause hemoptysis; if 
small, it may lead to no serious condition, but if large or if it causes gan- 
grene and sepsis, or if caused by vegetating typhoid or septic endocarditis, 
the prognosis is bad. Gangrene has already been mentioned in connection BACTERIAL DISEASES 
99 
with lung abscess and pulmonary infarct. As a rule it is associated with 
or follows lobar pneumonia, develops late in the course of the disease. An 
idea of the frequency of gangrene can be obtained from the following 
figures: Liebermeister in 230 deaths from typhoid found 14 cases of 
gangrene; Griesinger in 118 found 7; Curschmann—Leipzig statistics— 
in 228 found 10 cases; Hdlscher in 2,000 autopsies of typhoids found 
40 cases, or 2 per cent. Murchison considered pulmonary gangrene 
exceedingly rare, having met the complication only twice. The prog- 
nosis is bad. 
Pulmonary Edema.—Pulmonary edema arising in the course of typhoid 
without other pulmonary or cardiac complication is rare, always serious, 
hut not necessarily fatal. Our experiences do not justify the high per- 
centage, i. e., 14 per cent, of this complication as reported by Holscher. 
Simple non-tuberculous serous pleurisy is not as a rule serious, but it re 
tards recovery if it arises late. It is naturally associated with the pneu- 
monias of typhoid, and as already stated, these offer a serious outloox, 
depending on conditions mentioned in the consideration of pneumonia as 
a complication. 
Purulent Pleurisy.—Purulent pleurisy, i. e., empyema, complicating 
typhoid, usually following pneumonia, may under some conditions prove 
serious. The prognosis depends on many factors: time of complication, 
resistance and general condition of patient, time of recognition, ability to 
relieve by prompt and thorough drainage. Bloody and foul effusions with, 
typhoid are always indicative of malignant infection. 
Pulmonary Tuberculosis.—It has been the experience of most clini- 
cians that associated tuberculosis of the lung with typhoid is due to the 
awakening of latent tuberculous disease which antedated, as a rule, the 
acute infection. If the process is of the acute miliary type it may be 
difficult, if an early complication, to differentiate without blood-culture 
and agglutination tests. In all cases of miliary tuberculosis complicating 
typhoid, the prognosis is unfavorable. 
Limited tuberculous deposits, i. e., infiltrating tubercle without disor- 
ganization, which have been lighted to activity by the typhoid process, 
under favorable conditions and environment, may yield to treatment and 
a return to latency. 
Pneumothorax.—Pneumothorax (pyopneumothorax) I have never met 
in connection with typhoid. It is an exceedingly rare complication. In 
the reported cases it wTas dependent on some one of the conditions (pneu- 
monia, tuberculosis, etc.) mentioned, and the outcome has been fatal. 
The Blood 
The blood offers some data which may serve in the prognosis of typhoid 
fever. The albumin and iron content of the blood are reduced in propor- 
tion to the severity of the disease. Fibrin is also below the normal unless 100 
SPECIFIC INFECTIOUS DISEASES 
it is increased by complications, such as disseminated bronchitis and pneu- 
monia. In most cases of typhoid a moderate anemia gradually increasing 
as the disease advances is the rule, and not unfavorable. Thayer, Win- 
ter, and Curschmann have shown that in the average. favorable cases 
there is during the first days slight reduction in the number of red cor- 
puscles; with young powerful men, this is less marked than in women or 
in the weak. The former give an average count of four million, the lat- 
ter three million. The reduction continues until the end of the febrile 
period and during the early days of convalescence. Then the rise begins 
in favorable cases, usually in 2 to 3 weeks. 
The clinician is not to be discouraged if the normal count is slowly 
reached; this is the rule. Ilelapses may give lower red counts than were 
found with the original fever, and yet the prognosis remains unaffected. 
Hemoglobin in the average favorable case does not sink far below 70 per 
cent. Sudden anemia is suggestive of intestinal hemorrhage. 
The leukocytic count is of considerable value. The tendency in typhoid 
fever is toward low leukocytic counts—possibly the first day of the disease 
and of relapses excepted—when it may reach 10,000. The average count 
in adults during the first stage is from 2,800 to 4,500. The more serious 
the infection the lower the count. Leukopenia must be expected in typhoid 
fever (85 per cent). The period of convalescence finds the patient with 
a normal count. 
Neutrophilic leukocytes are increased during the first days of the dis- 
ease, but as the symptoms increase in severity the count of these falls as 
low as 1,000 to 2,000. With improvement, when the patient is fever-free 
there is an increase, a gradual return to normal; often the count mounts 
above the normal (Schottmtiller). There is prompt disappearance of 
eosinophils from the typhoid blood. Return of eosinophils is an encour- 
aging feature; as a rule this indicates convalescence. 
There is a progressive decrease of lymphocytes during the active period 
of fever; their return, like the return of eosinophils, is favorable. 
If with complications such as pneumonia, intestinal hemorrhage, per- 
foration, diarrhea, pus accumulation, and nephritis (acute), marked leuko- 
cytosis is absent, particularly neutrophilic leukocytosis, prognosis is unfa- 
vorably influenced, because, as Schottmiiller has suggested, there is an in- 
ability of the bone marrow to react. The following are safe conclusions 
for prognosis: 
The persistence in typhoid blood of even a few eosinophils is a favorable 
feature. Relatively high neutrophilic values without complications are 
also favorable. Increase of lymphocytes argues in favor of a decline of 
fever. Marked leukopenia, particularly a low lymphocytic count, is unfa- 
vorable. With the complications already mentioned low leukocytic counts 
argue in favor of serious conditions. Blood counts alone should never 
lead to positive prognosis for there are cases in which in spite of severe BACTERIAL DISEASES 
101 
leukopenia, that is, low values, patients have made full recov- 
eries. 
In considering the malignancy of typhoid infection we called attention 
to the fact that the disease is severe in direct proportion to the number of 
bacilli found in the blood stream and that a count of bacilli in the blood 
was of great prognostic value (See references to Schottmuller’s and 
Schiiffner’s experiences). 
Disturbances of the Alimentary Canal 
The Mouth.—The organs of digestion offer valuable prognostic data. 
In serious cases the lips are abnormally dry, crusty, and often cracked 
and bleeding. In favorable cases, the lips are moister, with less evidence 
of change. In unfavorable cases, there is associated dryness of the mouth; 
the buccal mucosa is materially changed, ulcerated and bleeding, with 
sordes on teeth; gums incline to bleed. As a rule with these changes 
there is a dry tongue, covered with a thick brownish dirty coat, red at 
the tip and shining. The above picture, with marked fibrillary twitching 
of the tongue, is usually associated with cerebral invasion and is found 
in the more serious cases. Such conditions early, argue in favor of a 
severe course of the infection. 
The tongue is changed in practically all cases, and its study is often 
a valuable prognostic index. A dry cracked tongue, slowly protruded, 
long exposed, returned only after repeated suggestion, with apathy or mut- 
tering delirium, is characteristic of severe deep toxemia and is serious. 
Moderate f brillary twitching of the tongue is present in almost all cases 
and is not of serious import—less significant if the tongue continues 
moist and the patient is free from the symptoms of deep infection. The 
severer cases show the greatest fibrillary twitching of the tongue; in these 
the nervous system is profoundly invaded, as is shown by active subsultus 
tendinum and other symptoms. Moist tongue is found in the milder 
cases of typhoid with few mouth and lip lesions and with clean teeth or 
little sordes. 
There are cases in which changes in the tonsils are so evident as to 
cloud the diagnosis. Unless these are gangrenous or diphtheritic or are 
associated with noma, they are soon accompanied by the symptoms of 
general typhoid disease and do not influence prognosis. The more serious 
but rare complications are, as mentioned, diphtheria, deep ulceration, and 
noma. 
Parotitis.—Parotitis whether suppurative or not is always a serious 
complication. It is added as a rule when the patient is weakened by the 
toxemia and other complications; is always febrile; may occasionally be 
double. There is in these cases the added danger of thrombosis (jugular 
and cerebral), phlegmon, infiltration of surrounding muscular tissue, peri- 102 
SPECIFIC INFECTIOUS DISEASES 
chrondritis, and facial 'paralysis. Parotitis complicates from .3 per cent 
to 1 per cent of typhoids, and of this number one-half die. 
Stomach Disorders.—An intolerant stomach is always a decided handi- 
cap. Persistent vomiting from whatever cause lowers vitality and re- 
duces the patient’s chances. When this continues, and remains uncon- 
trolled in the third and fourth week, with anorexia, the wasting is enor- 
mous ; the pulse grows smaller; the tissues are dry; and death is the rule. 
Persistent vomiting is at times an early symptom of added meningitis; 
then it is “propulsive” and associated with other positive symptoms. 
Sudden severe vomiting with pain, not due to error of diet or transitory 
disturbance, is suggestive of perforation, peritonitis, latent hemorrhage, or 
involvement of the appendix. I have seen two cases in which after con- 
valescence was fully established, uncontrollable vomiting—the cause of 
which was never cleared—with increasing consecutive weakness, caused 
death. 
Tympany (Meteorismus).—Absence of tympany is always favorable. 
Severe cases at their height are likely to be burdened by intestinal disten- 
tion. It is a burden, for it increases the work of the heart, displaces or- 
gans—the liver more particularly—and adds to the patient’s discomfort. 
Suddenly arising tympany with evidences of collapse is significant, for it 
may mean serious complication, perforation, adynamic paralysis, hemor- 
rhage. Early meteorism is not usually significant. In many cases proper 
diet will prevent or control it, if not, then it must remain a factor in prog- 
nosis. 
Modern clinicians view tympany more as an expression of general in- 
fection (intestinal paralysis—adynamic) than an index of the extent of 
the intestinal lesions. 
Diarrhea.—In a moderately severe typhoid in which the bowels are 
loose the average number of stools is from 6 to 10, many of these are 
finally found with serious complications referable to the intestines. Move- 
ments above this average (ten) denote a serious condition. If most pas- 
sages are involuntary and other symptoms are correspondingly severe, a 
guarded prognosis is justified. Frequent involuntary passages are always 
of grave import. 
In my hospital and consultation practice I have found at least one- 
third of all cases free from diarrhea during the entire course of the dis- 
ease. Occasional frequency of evacuation is more favorable than persistent 
diarrhea. Constipation does not affect prognosis unfavorably. Those 
epidemics have seemed to be least malignant in which the intestinal symp- 
toms, more particularly diarrhea, are fewest. In some epidemics the num- 
ber of constipated patients outnumbered those with diarrhea. The depth 
and number of intestinal ulcers do not always bear a close relation to the 
severity of the typhoid toxemia. 
Intestinal Hemorrhage.—Intestinal hemorrhage complicates from 4 to BACTERIAL DISEASES 
103 
6 per cent of all typhoids. The frequency of this complication varies with 
different epidemics. Slight admixture of blood, during the second and 
third weeks of the disease, is not serious, and is not as a rule followed by 
larger losses of blood. Women are less likely to have severe and large 
hemorrhages than men. Curschmann reports the days of occurrence of 
hemorrhage in 148 cases observed by him as follows: 
6th to 9th day 12 
10th to 12th day 23 
13th to 15th day 23 
16th to 18th day 31 
19th to 21st day 17 
22d to 24th day 9 
25th to 27th day 11 
28th to 30th day 10 
31st to 33d day 3 
34th to 36th day 4 
After 36th day 5 
148 
The prognostic significance of intestinal hemorrhage with typhoid 
fever depends very largely upon the time of its occurrence, the condition 
of the patient, his resistance, the condition of his heart, and the quantity 
of blood lost. 
Different individuals react differently under similar conditions to the 
loss of blood. There are typhoids who may he thoroughly depleted, in 
whom the pulse becomes thready and exceedingly feeble, and blood pres- 
sure and pulse amplitude materially reduced, who for some unknown 
reason promptly regenerate sufficient blood to keep them alive during the 
critical period, the disease leading to full recovery. With high fever, 
previous rapid pulse, deep involvement of the sensorium, added intes- 
tinal hemorrhage, and marked tympany, a picture is presented as serious 
as any, save that of perforation, which we meet in the course of the dis- 
ease. Patients are better able to bear hemorrhage the nearer they are to 
the end of the febrile period. Hemorrhage during the early days of 
typhoid (ninth to the fourteenth day), if profuse or if repeated in the 
presence of other grave symptoms, is always serious—more serious if the 
patient is corpulent and in middle life. There are occasional cases which 
are influenced favorably by moderate intestinal hemorrhage (Graves, 
Trousseau). 
Relapses are not often complicated by intestinal hemorrhage. Chil- 
dren are not often found with this complication; this is due to the fact 
that the ulceration is not so deep as in the adult. Naturally, the more 104 
SPECIFIC INFECTIOUS DISEASES 
frequent the bloody stools, the'greater is the danger. Sudden death due 
to intestinal hemorrhage is rare; in most cases repeated bloody stools dur- 
ing several days deplete the patient. However, in occasional cases 
patients are carried safely over the critical period following large hemor- 
rhages with associated symptoms, only to die after relatively small losses 
of blood from the intestines later, when the attendant had reason to 
feel fairly secure. The prognosis in all cases of intestinal hemorrhage 
should be guardedly given; the most experienced clinician can offer no 
positive forecast; there are always days of anxiety and uncertainty in the 
presence of this complication. 
When death followed hemorrhage in cases which serve as the basis for 
conclusions in this chapter it was between the fourth and seventh day as a 
rule—in a few cases between the ninth and fifteen day. My percentage 
of deaths due directly to intestinal hemorrhage is not above 20 per cent, 
but as already hinted different epidemics offer a different mortality. 
There have been epidemics in which 50 per cent of the patients with intes- 
tinal hemorrhage died. Ilomolle gives 44 per cent, Griesinger 31.2 per 
cent, Liebermeister 38.6 per cent. In our own country Osier gives a 
series of 829 cases, with blood appearing in the stools in 50, or 6 per cent. 
Of these 5 cases died, or 10 per cent. The same author gives a series 
of 118 cases of hemorrhage with 12 deaths, or 10 per cent, and a series 
of 131 fatal cases with 12 deaths from hemorrhage. He states again (ref.) 
that hemorrhage occurs in 7 per cent of all cases. 
Peritonitis.—Peritonitis either circumscribed or diffuse, from what- 
ever cause, always secondary, is one of the most serious complications of 
typhoid fever. When due to perforation of an intestinal ulcer we con- 
sider it the most fatal of all complications (perforative peritonitis). 
Perforative Peritonitis.—Time of Occurrence of Perforation.— 
In 73 cases Curschmann found that perforation occurred as follows: 
On the 11th to 20th day 23 
21st to 30th day 31 
31st to 40th day 13 
After 40th day 6 
Perforative peritonitis among children is rare. It matters little 
which portion of the small intestine is the seat of perforation, or what the 
size of the opening, the dangers are the same and death is the rule. Per- 
foration is found in 3 per cent of typhoid fevers. Statistics vary between 
2 and 12 per cent. In men the complication is more frequent than in 
women. No case of typhoid, however mild or severe, is free from the 
possibility of perforation and consecutive perforative peritonitis until the 
ulcers have been fully healed, the cicatrices are strong, and the peritoneum BACTERIAL DISEASES 
105 
over the ulcer has been fully protected by nature’s reparative process. 
This means complete recovery. 
Prompt death with symptoms of perforation in collapse, with charac- 
teristic facies is the rule unless the condition is recognized within the 
first hour or two after its occurrence, and is relieved by immediate surgical 
interference. I am fully satisfied that in occasional and exceedingly 
rare cases, perforation takes place and general peritonitis is prevented by 
previous localized peritonitis and plastic organized protection. Such a 
case has been described in which death finally resulted from hemorrhage, 
and the autopsy clearly showed the earlier perforation (Eisner). The 
possibility of perforative appendicitis and peritonitis due to typhoid ulcer- 
ation of the appendix should not be forgotten. In these cases the early 
diagnosis with rational radical surgical treatment offers the only hope. 
Perforative peritonitis due to rupture of the spleen, gall-bladder, sup- 
purative mesenteric glands, or abscess of the liver is serious but offers a 
slightly better prognosis, if diagnosticated early, than does intestinal per- 
foration. 
Liver and Bile Passages 
Pathologic research has demonstrated the frequency of invasion of the 
liver, more particularly the bile passages, in typhoid fever. Jaundice is 
not a frequent symptom. Holscher found it in 1.1 per cent, 22 cases 
in 2,000 of those who died of typhoid. Previous diseases of the gall- 
bladder, cholelithiasis, typhoid cholecystitis or cholangitis, acute yellow 
atrophy of the liver, and abscess, are among the causes of jaundice with 
typhoid. 
Jaundice.—Jaundice may in occasional cases be dne to destructive 
blood changes—an evidence of malignancy when it is associated with hem- 
orrhages from various organs—hematuria, albuminuria, myocarditis, and 
coma; and death follows promptly as a rule. 
Typhoid infection of the bile passages and gall-bladder in individual 
cases is not to be ignored as a prognostic factor; its importance has in- 
creased during the past decade. 
Cholecystitis.—Cholecystitis may be present without causing symptoms 
or in any way influencing the immediate prognosis of the disease but 
there can be no doubt of the fact that it serves as a cause of subsequent 
disturbances, more particularly gall-stone formation; 30.9 per cent of 
Curschmann’s cases of typhoid fever followed during long periods, pre- 
sented symptoms of gall-stones after the original infection. 
Animal experimentation strengthens all conclusions which tend to 
demonstrate the importance of typhoid infection as a cause of gall-stones. 
It is a clinical and bacteriologic fact that the Bacillus typhosus finds a suit- 
able habitat in the gall-bladder and bile passages, and often remains there 
undisturbed during long periods. Thus, in considering the question of the 106 
SPECIFIC INFECTIOUS DISEASES 
prognosis of these cases, we are not to forget the dangers of these carriers 
(Futterer, Chiari, Flexner). 
The Skin in Typhoid 
Roseola.—The number and location of the roseola spots have no hear- 
ing on the prognosis, so far as I have been able to conclude from my ex- 
perience. The depth of color does hear a direct relation in many cases to 
the severity of the infection. Thus a mottled skin, with dark, at times 
hemorrhagic skin lesions is expressive of malignancy. 
Miliary Eruption.—Miliary eruption, sudaminous in character, is 
found in most cases and is not significant. Often the sudamince are most 
abundant after the profuse perspiration following a decided fall of tem- 
perature, and are therefore favorable. 
Bedsores.—Bedsores are not frequent and as a rule are evidences of 
faulty or insufficient nursing. In occasional cases their formation can- 
not be prevented; this* is true of those with deep invasion of the sen- 
sorium, frequent involuntary discharges of feces and urine, and at times 
myelitis. When bedsores are a late complication they heal as a rule but 
slowly, may cause some fever and other constitutional symptoms. When 
early they are usually an expression of deep infection or lack of resist- 
ance, and do not argue in favor of a mild typhoid. Bedsores with deep 
bone involvement are ominous. 
Abscesses.—Abscesses of the skin, superficial or deep in the subcu- 
taneous connective tissue, are late complications, and simply retard re- 
covery, without interfering with full recovery unless an expression of 
pyemia or other constitutional or mixed infection. When one of the lat- 
ter complications has caused multiple abscesses, the prognosis remains 
clouded for days at a time; in most cases recovery is slow, but many die 
for want of resistance and because of the deep infection. 
Alopecia and Atrophic Changes.—The lesions referable to the nails 
and hair are late manifestations without prognostic significance. Alo- 
pecia and atrophic changes are rarely permanent, and mend slowly after 
several months. 
Purpura Hemorrhagica.—Purpura hemorrhagica with skin lesions— 
macules or large ecchymoses—occasionally arises during the period of 
convalescence. Hemorrhages from one or many mucous surfaces may re- 
duce and deplete the patient. Hematuria, intestinal bleeding, severe epis- 
taxis, and bleeding through the external auditory canal are frequent ac- 
companiments of typhoid purpura. The prognosis in most of these cases 
is good in spite of extreme anemia and weakness. Recovery is very slow. 
Simple purpura hemorrhagica should not be mistaken for the bleeding and 
cutaneous lesions due to malignant endocarditis—hemorrhagic infarct— 
which offers a grave prognosis, as do those forms of cutaneous and other BACTERIAL DISEASES 
107 
internal hemorrhages complicating typhoid, due to deep blood changes, 
disorganization, septic conditions and pernicious toxemia. All hemor- 
rhagic lesions of the skin influence prognosis, and demand serious consid- 
eration. When purpura or any hemorrhagic cutaneous lesion is due to 
nephritis, either acute or chronic, the prognosis in most cases is bad. 
Erysipelas.—Erysipelas, an occasional early or late secondary infection 
of the skin is, when complicated with deep meningeal symptoms, serious— 
more serious when early. Limited erysipelatous blushes, without marked 
constitutional disturbances are not of great prognostic significance. 
Phlegmons depend, in their importance for prognosis, on location, ex- 
tent, the severity of the associated symptoms, time of occurrence, and other 
accompanying lesions. 
The Spleen 
Enlargement of the spleen, which is present in 90 per cent of typhoid 
cases, offers but few data which are of use in prognosis; its diagnostic 
value is much more important. 
The spleen often decreases in size after severe intestinal hemorrhages. 
Sudden decrease in the size of spleen after hemorrhage is evidence of 
marked depletion and is ominous. The size of the spleen hears no relation 
to the severity of the infection. The spleen recedes as the disease spends 
its force. So long as the spleen remains enlarged the disease has not run 
its course. Enlarged spleen persisting without fever, does not justify the 
conclusion that the patient is free from the possibility of relapse. 
I called attention to the serious nature of rupture of the spleen in con- 
nection with the. consideration of peritonitis as a complication. 
Complications causing changes in the enlarged spleen are compara- 
tively rare. In 577 autopsies of typhoid patients made by Curschmann at 
Hamburg and Leipzig, he found the following changes in the spleen:— 
Infarct and hemorrhage 25 times 
Abscess 4 “ 
Rupture 2 “ 
Perisplenitis 16 “ 
The Genito-Urinary Organs 
During the febrile period of typhoid fever the urine is reduced in 
quantity and concentrated, as in all acute infections. The increased intake 
of fluids is not likely to have a marked influence on the quantity secreted 
at the height of the disease. Typhoids who during the febrile period 
secrete satisfactory quantities of urine may be said to add a favorable fac- 
tor to the symptom complex. During convalescence there is often a de- 
cided increase in the quantity secreted, and this is favorable. 
Urea and uric acid loss, increased during the active period of the dis- 108 
SPECIFIC INFECTIOUS DISEASES 
ease, is lowered as the patient improves and returns to normal during con- 
valescence. Severe cases show the presence of leucin and tyrosin, though 
Frerichs and Stadler claim these are present in all cases. 
Return of normal chlorid excretion reduced during the height of the 
disease, is favorable and is found early during convalescence. 
Albuminuria.—The albuminuria of typhoid fever may be either: 
1. Febrile Albuminuria 
2. Albuminuria of Nephritis 
3. Albuminuria due to other complications 
1. Febrile Albuminuria.—If all cases are cautiously followed albu- 
minuria will be found in at least 50 per cent; in most of these it has no 
influence on the course of the disease. In some, however, it is of great 
importance. In all cases the presence of albumin demands scientific dif- 
ferentiation, that its prognostic significance may be fully determined. 
Those cases in which febrile albuminuria is of grave import show its 
presence early; in these it is likely to persist, and the quantity large. 
Almost 30 per cent of these die, as against 10 per cent—the average 
mortality of the disease. Cursclnnann places the mortality at 25 per 
cent. Mere traces of albumin without other symptoms are to be numbered 
among the benign febrile albuminurias. 
Febrile albuminuria which develops toward the end of the febrile 
period is serious and demands close inspection to determine its cause. 
Febrile albuminuria may disappear, to reappear later, and is likely to 
accompany exacerbation of other symptoms. The microscopic picture of 
febrile albuminuria ought to include only feiv hyaline casts—no others— 
uric acid crystals, urates, few squamous epithelia and white blood-corpus- 
cles. If there are many hyaline casts and other elements, i. e., renal epi- 
thelia are increased, the prognosis is influenced thereby, and in all likeli- 
hood there are organic changes in kidney substance. Urobilinuria with 
febrile albuminuria is suggestive of liver changes. 
There has been so far as we could find in our cases, no relation between 
indicanuria and the severity of these cases of febrile albuminuria; the 
presence of indican is not to be considered dangerous. 
2. The Albuminuria of Nephritis.—It is often impossible to dif- 
ferentiate febrile albuminuria from that of nephritis in typhoid fever. It 
has been my experience that acute nephritis is not a frequent complication 
of the disease. Curschmann reports its presence in 4.87 per cent. 
Gubler and Fobin originally described a symptom complex which is 
now characterized as nephrotyphoid, in which the symptoms, more particu- 
larly the urinary picture, of acute parenchymatous nephritis are in the 
ascendancy. 
These cases during their early history are often mistaken for uncom- 
plicated neph ritis, but they are not as a rule difficult of recognition. They BACTERIAL DISEASES 
109 
are not all serious, and most do not develop uremic symptoms, though occa- 
sionally patients have died of nephrotyphoid with profound uremia, but as 
a rule, without the usual edema of acute nephritis. My experience with 
typhoids in which the diagnosis of nephrotyphoid was justified, has been 
favorable. Four cases seen during the past 20 years all recovered. In 
most of these cases the urine is more or less bloody. There are a number 
of recorded cases (Immerman) in which death resulted with the full com- 
plement of symptoms of nephritis, hemorrhagic and non-hemorrhagic, at 
the height of the typhoid process. 
In the majority of such cases the urine is red, bloody, contains large 
quantities of albumin, many casts (granular, hyalin and blood), abundant 
red blood corpuscles, and epithelia. 
These cases are further characterized by deep involvement of the sen- 
sorium, and by the presence of but few or no abdominal symptoms of ty- 
phoid. It is not wise to consider these cases other than the usual typhoid 
infection, in which there is parenchymatous degeneration of kidney sub- 
stance, in which, however, the symptoms of such change for a time at least, 
are decidedly in the foreground. Whatever the symptoms, whenever 
typhoid fever is complicated by an acute parenchymatous nephritis, it adds 
an enormous element of danger, clouds the prognosis, and it may be as- 
sumed that the nephritis is a part of a profound toxemia; never an inde- 
pendent disease. Death follows in between 40 and 50 per cent of typhoid 
nephritides during the second week, with all of the symptoms of deep infec- 
tion. These patients do not as a rule become uremic. The larger number 
of fatal nephritides which I have seen complicating typhoid have been 
positively hemorrhagic. When they recover there is not likely to be any 
remnant of nephritis, as is customary after scarlatinal nephritis. 
Hemorrhagic infarct of the kidney associated with typhoid from what- 
ever cause (endocarditic, embolic, thrombotic), is always a grave disturb- 
ance. 
In children the result of painstaking examination of urines has demon- 
strated the fact that a limited number of red blood-corpuscles is normally 
present in the urine, and further, that albuminuria is not so frequent as in 
the adult—all of which adds to the factors which make the prognosis of 
typhoid in children favorable. 
Postfebrile nephritis is not frequent; most cases which I have seen 
finally recovered or became latent. Occasionally patients have developed, 
after several months of albuminuria with casts, general dropsy and heart 
complications, and have died either of uremia or with symptoms of dilated 
and worn-out heart. 
3. Albuminuria Due to Other Compeications.—Cystitis is a cause 
of albuminuria; it may prove annoying but does not of itself threaten life. 
Typhoid bacilli are present in the urines of all typhoid patients in 
large numbers (one hundred million in a single cubic centimeter) a fact 110 
SPECIFIC INFECTIOUS DISEASES 
which adds an element to be seriously considered in prophylaxis and in 
prognosis. 
Pyelitis is rare, though Schottmiiller calls attention to its occurrence, 
and in his case found typhoid bacilli in the urine months after full re- 
covery. 
Albuminuria may be present with many complications of typhoid, such 
as pneumonia, pleurisy, empyema, meningitis, otitis, erysipelas, kidney 
abscess and other conditions in which its prognostic significance must of 
necessity depend largely upon many factors, most of which have been con- 
sidered in this chapter. 
Neither the Elirlicli diazo-reaction nor the more recently considered 
Russo reaction to methylene blue have much bearing on prognosis. The 
former is found in 90 to 100 per cent of typhoids, the value of the latter 
is still sub judice; our figures are not yet sufficiently reliable to justify 
consideration. I am satisfied that for diagnostic purposes it will never 
displace the Ehrlich test. It would seem that serious cases as they im- 
prove, often lose the diazo-reaction. Genken holds that the reaction is coin- 
cident with the period of Eberth bacteremia, the appearance of the bacilli 
in the blood, and that it is lost as these disappear. With relapses the reac- 
tion returns if due to Eberth bacteremia, not if due to other complications; 
hence under these conditions it is of diagnostic and prognostic value. 
It must not be forgotten in considering the significance of the Ehrlich 
diazo-reaction that it is present with acute miliary tuberculosis, cerebro- 
spinal meningitis, lobar pneumonia and measles. 
Orchitis.—Orchitis, a late complication of but few cases, ends in full 
recovery and usually without suppuration. 
Menstruation.—-Menstruation during the course of the fever has been 
present in the majority of cases but once, and has occasionally been pre- 
mature, without influencing the symptoms so far as I could judge. Menses 
usually appear when due during the first 10 to 14 days of the disease, not 
as a rule, when due later, until some time after the period of convalescence 
has been fully established, and they are then without untoward results to 
the patient. Menstrual anomalies following typhoid need not disturb the 
patient; the flow will, after a reasonable, time, return to its previous regu- 
larity. Acute suppuration of the vulvovaginal gland, catarrhal conditions 
of the genitals, moderate local edema, decubitus, i. e., vaginal ulcers, only 
prolong convalescence, without threatening the patient. 
Gangrene of the Vulva.—Gangrene of the vulva I have never met in 
my practice. Spillman and others, Hoffman and Liebermeister included, 
have reported cases and consider the complication fatal as a rule. 
Pregnancy.—Pregnancy, as already mentioned early in the chapter, 
adds to the dangers of typhoid infection. A large proportion of pregnant 
women abort (46 to 56 per cent), usually during the second week of the 
disease, though this accident may happen later. Once beyond the febrile BACTERIAL DISEASES 
111 
period, the chances are against miscarriage. Murchison considered the 
prognosis of the pregnant woman with typhoid as very serious. Most 
authorities who have recorded their experiences place the mortality be- 
tween 8 and 16 per cent. 
The Nervous System 
There are hut few cases of typhoid which run their course without 
symptoms referable to either the 
1. Central nervous system, or 
2. Peripheral nervous system. 
1. Central Nervous System.—The hearing of symptoms referable to 
the central nervous system on prognosis is exceedingly important. The 
forecast is less favorable in direct proportion to the depth of cerebral inva- 
sion■, as shown by positive symptoms and by lumbar puncture. The prog- 
nosis is particularly had when in adults, full-blooded and previously 
healthy, these cerebral symptoms persist. Liebermeister places the mor- 
tality of these cases at 70 per cent. There is a class of cases which has 
been characterized as meningotyphoid, meningismus typhosus, in which 
the early symptoms are those of meningitis, the typhoid manifestations 
appearing later. These patients may present all of the appearances of 
fully developed meningitis, including the Kernig symptom, opisthotonos, 
vomiting, hyperesthesia, and wild delirium at times, sometimes low mutter- 
ing delirium. As a rule these symptoms clear with the appearance of a 
train of continuous typhoid manifestations. Persistence or increase of 
these evidences of deep cerebral (meningeal) invasion must be interpreted 
as signifying a serious condition. In children, meningismus typhosus is 
more frequent than in the adult and is less serious. 
Cerebral manifestations are most likely to be present and characteristic 
in moderately severe cases with the beginning of the second week. The so- 
called typhoid condition gives a clue to the severity of the individual case. 
Wild delirium at night beginning in the second week, repeated during 
the day at intervals, with more or less rigidity, exalted reflexes, dry tongue, 
sordes, high fever, correspondingly rapid pulse, retention of urine, Kernig 
symptom, mind clouded, with characteristics in the lumbar fluid of puru- 
lent meningitis, with or without typhoid bacilli, is a complex of symptoms 
of enormous gravity, but not absolutely hopeless. 
Alcoholics, with symptoms of wet brain, alcoholic meningitis, with 
active delirium, always justify a grave prognosis. Involuntary discharges 
of urine and feces are symptoms of the more serious typhoids. 
The temperature in cases of serious cerebral invasion is not necessarily 
high; in some it is but slightly elevated and these often drag a long and 
monotonous course during many weeks before the sensorium is entirely 
clear, while occasionally they lead to psychoses, which require attention 112 
SPECIFIC INFECTIOUS DISEASES 
during many months. More serious and permanent mental disturbance 
may finally develop. 
Active, persistent subsultus tendinum is an expression of the more 
serious types of the disease; as is picking at the bed-clothes and imaginary 
objects. 
Convulsions, in very young children, are occasionally an early symp- 
tom in cases with high temperature or in those of neuropathic habit, but 
are not of serious import as a rule. 
Improvement or moderate control of nervous symptoms by baths and 
other treatment is always a reassuring experience. Psychoses when pres- 
ent during the febrile period are likely to disappear early during convales- 
cence and as a rule do not return. In some cases delusions, hallucinations, 
illusions, or obsessions persist long after convalescence. In some there are 
finally developed a true circular insanity, manic depressive psychoses, 
while in others, fortunately not often, obstinate depression, from which 
after long periods most patients recover (65 per cent). The length of time 
during which these postpyrexial psychoses persist in favorable cases varies. 
It is impossible to set a time limit. My cases have averaged between 6 
and 9 months. An occasional case ends in permanent insanity ; here family 
history is of paramount importance. When hysteria develops after typhoid 
it is not to be regarded seriously—prompt treatment leads to satisfactory 
results. This is also true of all types of neurasthenia. I have seen several 
eases followed by multiple cerebrospinal sclerosis, in which the disease was 
progressive, following its typical course. 
Posttyphoid myelitis offers nothing favorable. 
Acute ascending paralysis, when complicating typhoid, will, as a rule, 
promptly lead to death because of respiratory involvement. 
Reflexes.—Curschmann reports the behavior of the reflexes as fol- 
lows: In severe typhoids, where the patients are much reduced, usually 
toward the end of the febrile period or during convalescence, there is de- 
cided increase of the patella tendon reflex, and marked ankle clonus. In 
cases of moderate severity the patella tendon reflex may be absent, normal, 
or oftener, feeble. Toward the end of the disease and during convalescence 
in these cases, he found moderate increase of the reflex. In children the 
reflex was more often absent or materially reduced. 
2. Peripheral Nervous System.—Multiple neuritis and peripheral pa- 
ralyses occasionally complicate typhoid fever. There are inflammatory 
changes in single nerves which may leave lasting symptoms—optic neuri- 
tis, auditory neuritis, and the so-called cerebral monoplegia, which is prob- 
ably peripheral neuritis. 
The prognosis of most peripheral neuritides is good; multiple neuritis 
leads to a protracted period of symptoms but, as a rule, to fair use of 
all of the extremities. 
The so-called typhoid spine, painful during long periods, as a rule leads BACTERIAL DISEASES 
113 
to a gradual full recovery, as does also typhoid spondylitis and perispondy- 
litis. 
The Muscular System 
The muscular system offers, aside from its enormous atrophy, nothing 
of prognostic value; time returns the skeletal muscles to their normal 
conditions. Grave atrophic and hypertrophic changes of organic origin 
are rare. 
The Osseous System 
The lesions referable to the osseous system are not infrequent. They 
belong to the. domain of surgery and as a rule, under proper treatment 
there is full recovery, even when many bones are involved in necrosis or 
caries. 
The Ear 
Complications referable to the auditory apparatus are frequent. 
Bezold found these in 4 per cent of typhoids. They include changes in the 
external ear, such as gangrene, superficial skin lesions, decubitus, periosti- 
tis and furunculosis, none of which are of themselves threatening. The 
affections of the inner ear may be functional or organic. But few cases 
of typhoid fever at the height of the disease, retain normal hearing; it is 
most blunted with the more serious cerebral complications, when it is a 
part of the general toxemia. Most cases in which the. changed hearing is 
due to functional disturbance, offer a good prognosis. 
Otitis media, when uncomplicated, is promptly relieved by puncture of 
the drum membrane, and as a rule makes an uninterrupted recovery. Neg- 
lected cases, those associated with deep infection and brain symptoms, 
periostitis, mastoid invasion, sinus thrombosis, and caries are often serious, 
though the more serious complications of otitis media suppurativa are not 
as frequent with typhoid as with scarlet fever, diphtheria and pyemic 
infections. For the good of all typhoid patients it is always wise to exam- 
ine the ears from time to time, that pus accumulations or otitis media may 
be promptly detected. This should be done by an expert: it may in occa- 
sional cases prevent serious complications, among these pyogenic meningi- 
tis. Labyrinthine disturbances are rare. When they persist they may 
lead to Meniere’s complex with defective hearing. 
Eye Complications 
There are but few cases in which eye symptoms or complications dur- 
ing the active period of the disease, cause anxiety or influence the course of 
the disease; these complications are less frequent than with other serious 114 
SPECIFIC INFECTIOUS DISEASES 
infections. The paralysis of the abducens or motor oculi, or optic neuritis, 
amaurosis, are late manifestations which belong in the field of ophthal- 
mology, and are not connected with the serious manifestations considered 
in the prognosis of the typhoid process itself. For their consideration and 
significance, it is always safest to consult the eye specialist. 
My experience with relapses—and these are veritable fresh infections 
—has been almost uniformly favorable. It is a rule that relapses are not 
so severe as the original infection. It is rare to lose a patient during an 
uncomplicated relapse, and these are less liable to complications than are 
initial infections. In my own experience I have found relapses in 8 per 
cent of all cases. 
Relapse 
The prognosis of those cases of typhoid without intestinal lesions which 
we meet occasionally, to which Eberth, Elexner, and Horton-Smith have 
called attention should be as cautiously made as that of typical typhoid. 
In the former we are dealing with a typhohacteremia, and it need not sur- 
prise the clinician to find some of these with profound septic symptoms, 
for they are due to mixed infection. Some were found with streptococcus, 
others with pneumococcus, and Lenhartz has reported a case of typhoid 
with staphylococcus aureus infection. All of these types make prognosis 
grave in accordance with the associated toxemia as expressed by heart, 
brain, lung and kidney symptoms. 
Typhoid Without Intestinal Lesions 
Causes of Death 
A thorough consideration of available and reliable post mortem find- 
ings proves that in 17.7 per cent of typhoid autopsies no complications were 
found, and death was due to toxemia. If we add to these the number of 
deaths (6.2 per cent) in which post mortem search showed but insignificant 
complications, the patients dying either in the first, second or third weeks 
of the disease, we find therefore 24 per cent (17.7 per cent and 6.2 per 
cent) in which typhoid toxemia may he considered to he the cause of death. 
Striimpell’s statement is therefore justified: “In only a relatively small 
proportion of cases have I found death due to general infection in typhoid 
fever. The majority (76 per cent) of deaths are due to complications 
uninfluenced by treatment, and not dependent directly upon the constitu- 
tional infection.” 
Complications which were the causes of death in 5 per cent and over 
of the autopsied cases (Holscher) may be classified as follows: BACTERIAL DISEASES 
115 
Pulmonary edema 15 per cent 
Myocardial degeneration (fatty and parenchymatous).. 13 “ “ 
Parenchymatous and fatty degeneration of the liver.. 10 “ u 
Bronchitis 10 11 “ 
Lobular pneumonia 8 “ “ 
Croupous pneumonia 7 “ “ 
Pulmonary infarct 6 “ “ 
Intestinal perforation with peritonitis 6 “ “ 
Intestinal hemorrhage 5 “ “ 
Edema of the brain 5 “ u 
Decubitus 5 “ “ 
The changes associated with typhoid fever are far-reaching and may 
invade any organ of the body. A study of the preceding pages will show 
that the alimentary tract from the tongue to the rectum, the parotid, pan- 
creas, liver, mesenteric glands, veins, arteries, heart, respiratory organs, 
the blood, the muscular system, the central and peripheral nervous sys- 
tems, the skin, and the connective and bone tissue may be the seat of 
pathologic change; in truth, no organ of the body is immune and many 
may be involved at the same time. For all of these reasons it may be posi- 
tively asserted that in no disease should the prognosis be more guardedly 
given and all that the individual case presents be more cautiously weighed. 
Deaths from the Sequelae of Typhoid Fever 
From the reports of the visiting nurse service of the Metropolitan Life 
Insurance Company as reported by Dublin, in a study of 1,936 cases of 
typhoid fever recorded in 1911, the following interesting features were 
established. 
The number of cases above mentioned include 362 which were finally 
eliminated from consideration because the diagnosis was not considered 
to be accurately established. The remaining 1,574 cases make clear the 
effect of typhoid fever on vitality during the first three years following 
recovery. 
It was found that 146 died while under treatment—a death rate of 
9.28 per hundred. The principal complications in fatal cases were intes- 
tinal perforation, hemorrhage, meningitis, pneumonia and heart involve- 
ment. 
“To determine the effect of the disease on vitality for the three years 
following the attack, it was necessary to compare the actual mortality of 
the 1,428 survivors with the expected mortality among the same class of 
persons. This was done by distributing the 1,428 cases by sex, color and 
10-year age period, and by comparing them with similar groups taken 
from the mortality tables of the company for the same years. In other 
words, the mortality was not an arbitrary measure, but gave the death 116 
SPECIFIC INFECTIOUS DISEASES 
rate which persons of the same age, sex and color among the policy holders 
had experienced for the same years. 
“From such comparisons, it was found that in the series of 1,428 per- 
sons the expected number of deaths was 26.45, whereas, the actual number 
that occurred was 54, the conclusion being that during the first three years 
after recovery from typhoid fever, the mortality is twice the normal. This 
increased rate, however, was not uniform for all three years, being greatest 
during the first year following recovery, less during the second year, and 
still less the third.” 
Of the 54 deaths, tuberculosis caused 39 per cent, and diseases of the 
heart 14.8 per cent. 
Dublin concludes that in the United States there are 8,000 deaths 
annually among those who have recovered from typhoid fever and who 
yield to disease because of their reduced resistance during two years fol- 
lowing recovery. 
References 
Bachmayr. Verhand. d. Wiirzburger med. Gesellsch., 1868. 
Bezold. Arch. f. Ohrenheilk., 1884. 
Curschmann. Der abdominal Typhus. Wien, 1913. 
Delafield. New York Med. Rec. 
Lectures on Typhoid. 1877. 
Dodd. British Med. J'., 1903, No. 14. 
Dublin (L. T.) Am. J. Public Health, Jan., 1915. 
Eberth. Fortschritte der Medizin, Bd. vii. 
Eisner. New York Med. J., 1892. 
Firth. J. Royal Army Med. Corps. 1911, 589. 
Flexner. Johns Hopkins Hospital Reports, 1900, No. 8. 
Fornet. Die Deutsche Klinik, 1913, xiv. 
Friantzel. Ztschr. f. klin. Med., Bd. ii. 
Fiitterer. Munch, med. Wchnschr, 1888, No. 19. 
Genken. Munch, med. Wchnschr., 1907, No. 18. 
Graves. Clinical Lectures. 1848. 
Gubler & Robin. J. de Therap., 1875. 
Holscher. Munch, med. Wchnschr., 1891-3. 
Horton (Smith). Lancet, London, 1900. 
Immerman. Jahresbuch der. Med. Abtheil. des Burgerspitales zu Basel, 1872. 
Koch. Die Bekampfung des Typhus, 1903. 
Kutcher. Lehrbuch der Militarhygiene, etc. 1912, Bd. iv. 
Lenhartz. Spedelle Pathol, u. Therapie, Nothnagel u. Hochwart, 2. ed. (quoted by Cursch- 
mann), 286. 
Special Pathol, u. Therapie, Nothnagel, 2. ed., Hi. 
Liebermeister. Vorlesungen iiber Infections Krankheiten. 1885. 
Ludke & Sturm. Deutsch. Archiv. f. klin. Med., Bd. c, Hft. 5. 1910. 
Mercier. Arch, de Mcdecine Experimental, 1878. BACTERIAL DISEASES 
117 
Murchinson. The continued fevers, etc. London, 1884. 
Ortner. Archiv. f. Heilkunde, 1905. 
Osier. Practice of medicine, 8. ed., 1914. 
Port. Deutsch. med. Wchnschr., 1908, No. 18. 
Potin. Quoted by Curschmann [/. c.]. 
Prinzing. Handbuch der medizinischen Statistik. Jena, 1906, Gustav Fischer. 
Russell (Major). J. Am. Med. Ass., Oct., 1912. 
Schottmuller. Mohr & Staehelin, Handbuch der Inneren Medizin, Bd. i. 
Schiiffner. Cited by Schottmuller [£. c.]. 
Spillman. Arch, de Mcdecin, 1881. 
Strube. Berl. klin. Wchnschr., 1871, No. 30. 
Strumpell. Congress f. Innere Med., 1885. 
Thayer. Am. J. M. Sci., 1904. 
Johns Hopkins Hospital Reports, 1900, viii. 
Trousseau. Clinical medicine. 2. ed. 
Clinical lectures, Philadelphia, 1873. 
T'urck. Laryngologie, Wien. 
Wiesel. Ztschr. f. Heilkunde, 1905, No. 9. 
Winter. Dublin Med. J., Oct., 1901. 
II. Typhus Fever 
{Spotted Fever, Typhus exanthem aticus, Famine Fever {of Ireland), Jail 
Fever, Camp Fever, Ship Fever, Brill’s Disease, Mexican tabardillo) 
History.—Typhus fever was first brought to America in 1812. The 
credit of having separated typhus from typhoid, thus making differentia- 
tion possible belongs to American Medicine, directly to Gerhardt of Phila- 
delphia in 1836. Jenner also insisted on typhus fever as a clinical entity 
separate from typhoid or enteric fever. 
Plotz, a young bacteriologist, has recently established the true cause 
of typhus fever. His investigations were made in the Pathological Labora- 
tory of Mt. Sinai Hospital in Hew York City, and the results were pres- 
ented to the profession in a “Preliminary Communication” on “The Eti- 
ology of Typhus fever (and Brill’s Disease)” which appeared in the Jour- 
nal of the American Medical Association May 16, 1914. In his original 
report he claims to have found the same organism in five of six cases of 
Brill’s disease by the use of anaerobic methods. A large number of con- 
trol cases were studied and the “organism was absent from each.” The 
bacillus is pleomorphic, “from 0.9 to 1.93 microns in length, the breadth 
being from one-fifth to three-fifths of the length.” It is Gram-positive, not 
acid-fast, has no capsule, “and polar bodies can be demonstrated with ap- 
propriate methods,” and it grows only anaerobically. 
In a private communication from Plotz (bearing date of May tenth, 118 
SPECIFIC INFECTIOUS DISEASES 
1915,) he says: “By means of an anaerobic method of blood culture, a 
bacillus was isolated in pure culture from seven cases of European epi- 
demic typhus fever, or one hundred per cent of the cases studied during 
the febrile period. With the same method the identical organism was 
recovered during the febrile period of the. local endemic form of the dis- 
ease in eighteen of thirty-four cases, or 53 per cent, and in two additional 
cases taken after the crisis similar blood cultures made in one-hundred and 
ninety-eight control cases yielded no such organism.” 
“Serological studies were carried on by Doctor Peter K. Olitsky, who 
has demonstrated the presence of immune bodies mostly in the apyrexial 
period” . . . “the same immune bodies have been demonstrated in mon- 
keys who recovered from the disease.” In guinea-pigs and monkeys who 
were inoculated and developed the disease the organism was recovered; the 
greatest bacteriemia has been found to occur early in the disease, when the 
temperature is highest. The pure culture of the organism can produce 
typical typhus fever in the guinea-pig.” Plotz has demonstrated that 
typhus blood without bacilli or but few, is non-infective for animals. “It 
seems that infectivity is absolutely dependent upon the presence of a suf- 
ficient number of these bacilli.” 
The discovery of the bacillus by Plotz and the elaboration of a vaccine 
promises to prove of enormous prognostic and prophylactic value, for it is 
reasonable to expect that with modern methods of cleanliness, the destruc- 
tion of the carrier—the body louse, from man to man—and compulsory 
vaccination against the disease among the belligerents, the same success 
will follow which we have had with the typhoid vaccine in our army. 
The recent consideration of the “Etiology of Typhus Fever and the 
Methods of its Prevention” by Anderson strengthens the conclusions given 
in the preceding paragraph. He insists that “the reduction of lice infesta- 
tion among the population in general,” “the destruction of all lice and their 
eggs found on the bodies, clothing, bedding and surroundings of all cases 
of typhus, typhus suspects and contacts” is absolutely necessary, and will 
eliminate the disease because the louse is unable to transfer itself to great 
distances.” 
“The history of typhus is written in those dark pages of the world’s 
history which tell of the grievous visitation of war, famine and misery of 
every kind” (Hirsch)—a frequent hut justified quotation. 
With positive bacteriologic data, we can more easily explain the ac- 
cepted conclusion that the disease reproduces itself “in the immediate sur- 
roundings of the patient sometimes before and after, as well as during, the 
febrile period” (Moore). 
The louse is carried on the body, clothing or other fabrics, furniture, 
more particularly woolly substances and furs. The contagium continues 
its vitality for months. 
With improved sanitary conditions in jails, in the army, on shipboard; BACTERIAL DISEASES 
119 
with better care of the masses in large cities, in tenements; with less filth, 
epidemic typhus fever, in civilized countries and sanitary communities has 
become exceedingly rare. In our own country we have had no alarming 
epidemic to report in over half a century, and the isolated cases which are 
occasionally brought to us are of a milder character than those seen over 
fifty years ago. In 1881 there was a small epidemic in ISTew York of 
which a large number (-|) were incorrectly diagnosed. There was a time 
when one-half of all physicians in Ireland attending cases of typhus, fell 
victims to the disease. In an epidemic about the middle of the nineteenth 
century, six of thirty-two (6 of 32) physicians at Bellevue Hospital in 
Hew York died of the disease. The number of physicians attacked during 
epidemics is larger than with any other single acute infection. The young, 
active, and mentally alert, are most likely to develop typhus during times 
of epidemics. One attack gives complete immunity. Typhus fever must 
always be considered a serious disease. The mortality ranges between 15 
and 20 per cent in times of epidemics. Hot so however in milder cases of 
so-called Brill's disease* which, if search is made and care in diagnosis is 
practiced, will be found to be comparatively frequent. In 500 uncompli- 
cated cases ending in recovery, the average duration was 13.43 days; of 
100 fatal cases, 14.6 days. Patients who live beyond the 20th day and 
die, yield to complications rather than to typhus itself (Murchison). 
Death is likely to follow during the second week. 
Foudroyant cases, beginning with fiery symptoms, so-called “sthenic 
fever” with full tense pulse which soon weakens, high fever, flushed ma- 
hogany-colored face, delirium, coma, Kernig symptom, great restlessness, 
opisthotonos, mottled skin, hemorrhagic eruption, involuntary stools, 
(though some patients may often be constipated), suppressed or materially 
reduced urine with evidences of nephritis or febrile albuminuria, are fatal 
usually during the first week. 
The Pulse.—The prognosis in those who have been previously reduced 
by illness or without resistance, is bad, and is the same in the aged. The 
pulse offers valuable data for prognosis. With persistent rapidity and high 
tfever, intermission or irregularity, pulsus alternans, with or without hur- 
ried respiration, the outlook is grave. When respiration is hurried, either 
due to myocardial weakness, secondary pulmonary engorgement, dissemi- 
nated bronchitis or pneumonia—catarrhal or lobar—the prognosis is cor- 
respondingly worse. Persistently slow pulse during limited periods after 
the fever has subsided is not unfavorable. 
The Blood.—The blood in unfavorable cases promptly shows a marked 
reduction of red blood corpuscles with a corresponding reduction of hemo- 
globin. 
Average cases of typhus show moderate leukocytosis—12,000 to 15,000 
* See last section of this article. 120 
SPECIFIC INFECTIOUS DISEASES 
though variations have been reported Hanging between 1,600 to 17,600 
(Krause). The low counts, i. e., marked leukopenia are unfavorable. Port 
in three cases on the third day found leukocytic counts of 7,900, 8,100, 
14,700, respectively. He found an increase of small lymphocytes, neutro- 
philic polymorphonuclears 60 per cent, small lymphocytes 30 per cent, 
large lymphocytes 3-7.5 per cent, eosinophils 1 per cent and mast-cells not 
above 0.5 per cent. According to Goldberg and Anderson satisfactory evi- 
dence has not yet been adduced that the blood of the monkeys infected with 
typhus is virulent in the prefebrile stage and, second, it is positive that the 
blood of the monkey may still be virulent 24 to 36 hours after the return of 
the temperature to normal. 
In favorable cases improvement should be apparent about the middle 
of the second week. 
The Urine.—Diazo-reaction is present in over 50 per cent of typhus 
urines and is of no prognostic value. Nephritis—parenchymatous, partic- 
ularly w?hen hemorrhagic—adds a serious complication. 
Alcoholics, early fall into a “typhoid condition” with deep invasion of 
the brain, marked evidences of such complication in delirium and lung 
invasion, when death is the usual result. 
Symptoms.—The gravest cases are those with symptoms of meningitis, 
“coma vigil” of Jenner, pin point pupils, hemorrhagic eruption, suppres- 
sion of urine with albumin and casts in the urine voided, myocardial weak- 
ness with feeble embryonic sounds, and pulmonary inflammation or con- 
gestion and meteorism. 
Persistent vomiting with hiccough is unfavorable. Vomiting early in 
most cases is controllable; 80 per cent of typhus patients are sufficiently 
nourished and are carried safely to recovery without serious incidents. 
Reduction in the size of the spleen—uniformly enlarged in typhus—is 
always favo7'able. 
Almost all cases have more or less catarrhal bronchitis, which does not, 
unless it leads to further infection, reduce the patient’s chances. 
The addition of bronchopneumonia, lobar pneumonia, empyema, endo- 
or pericarditis, hemorrhagic infarct or nephritis (hemorrhagic), the lat- 
ter, already mentioned, plunge the patient into a serious condition and 
naturally reduce the chances of recovery very materially. 
Profuse perspiration is mentioned as an unfavorable symptom by some 
when it persists after the tenth to the twelfth day. Peripheral neuritis, a 
painful and occasional sequel, usually yields after a long period. Relapses 
do not frequently follow typhus fever. 
Brill's Disease 
So-called Brill’s disease is now known to be a mild form of typhus 
fever. This type of the disease runs its course in from twelve to fourteen BACTEEIAL DISEASES 
121 
days, and terminates by crisis; convalescence is rapid. The mortality is 
below 1 per cent and it is most prevalent during the autumn months.. 
Anderson and Goklberger working in Mexico City have proved the identity 
of Brill’s disease and the typhus (tabardillo ) of Mexico. They inoculated 
monkeys successfully, and bel icve that the body louse carries the infection; 
indeed the monkeys were infected through the louse. The relationship of 
Brill’s disease in New York and typhus of Mexico was further established 
beyond peradventure by the experiments of these investigators, for they 
succeeded with the blood of Brill’s disease (three patients in New York 
furnishing this), in carrying the infection through eleven generations of 
monkeys. These results are in line with those of Plotz, Baehr and Olitsky. 
The prophylactic and prognostic value of these, positive conclusions is 
of inestimable value and is “far-reaching.” The experiments further 
proved that one attack produced lasting immunity. Sanitarians must rec- 
ognize the fact that these milder types of typhus may lead, through care- 
lessness and failure to recognize them, to endemics and epidemics of the 
disease, virulent or non-virulent. 
References 
Anderson (John F.). The etiology of typhus fever and the methods of its prevention. Pub. 
Health Report, April 30, 1915. 
Brill. An acute infectious disease of unknown origin. Am. J. of Med. Sci., 1910, m. 
Friedman. Arch. Int. Med., Oct. 15, 1911, 427. 
Goldberg & Anderson. J. Am. M. Ass., Aug. 17, 1912, 515. 
Hirsch. Handbuch der Histor. Geograph. Pathologie. 1881, 2. Aufl. 
Krause. Mohr & Staehlin, Handbuch der inneren Med. 1911, 296. 
Moore. Allbutt & Rolleston, System of medicine, ii, part i. 
Murchison. Continued fevers. London, 1884, 3. ed. 
Plotz. J. Am. M. Ass., May 16, 1914, Ixxii, 1556; also private communication 
Port. Deutsch. med. Wchnschr. 1908, No. 41 • 
III. Paratyphoid Disease 
Paratyphoid fever or disease includes all organic changes which are 
produced by infection with paratyphoid bacilli associated with bacteremia, 
occasionally wTith sepsis. The organic diseases which are thus produced 
may include enteritis, pyelitis, endometritis, cholecystitis, and meningitis 
( Schottmiiller). 
Achard and Bensaud called attention to the presence of bacilli in the 
pus of joints and in the urine of a typhoid patient which presented all of 
the characteristics of paratyphoid bacillus B. in culture media ; and named 
the infection paratyphoidique. To Schottmiiller belongs the credit of 
demonstrating in 1900 the existence of the clinical entity paratyphoid, and 122 
SPECIFIC INFECTIOUS DISEASES 
of tracing its origin to bacilli which admitted of positive differentiation. 
The clinician will continue anxious only until he has proved by bacterio- 
logical means the characteristics of the disease-producing bacilli, thus estab- 
lishing the positive diagnosis. The diagnosis may be strongly suspected 
without the more painstaking and exact methods, but it cannot be fully 
established. 
Once the diagnosis is made positive a favorable, prognosis may be given 
and full recovery expected after a period of varying symptoms with irregu- 
lar temperatures and convalescence, which is long and out of proportion to 
the benign nature of the disease. The mortality is not above 1 per cent, 
though Lorrain Smith reports 6 deaths in 162 cases. This mortality is 
much above that of our cases in New York State and those reported by 
continental observers. 
There are two types of paratyphoid bacilli which interest us—A and 
B. The latter is the cause of the disease in 80 per cent of cases. In con- 
sidering the conditions which may be produced by the introduction of the 
B bacillus, we include those cases of meat poisoning formerly considered 
to be due to the Bacillus enteritidis of Gartner, which we now know is 
identical with paratyphoid bacillus B. 
While it is not within the province of this work to consider bacterio- 
logic methods, I add the following that prognostic conclusions may rest on 
safe methods of diagnosis, and that errors in differentiation may be 
avoided:— 
Paratyphoid bacilli are actively motile, with side movements; the size of the 
typhoid bacillus; not colored by Gram. 
Grows as an anaerobic bacillus on all culture media. 
Bouillon is diffusely turbid, with a thin scum on its surface. On gelatin the 
growth causes a blue wl\ite opaque deposit. The isolated colonies are coarser 
than the typhoid culture, button-shaped and not fissured. 
On agar the deposit is thin, white, gray and translucent, with characteristic 
gas bubbles. 
On potato a grayish brown thick deposit, much like that produced by the coli 
communis bacillus. 
Milk is not curdled, finally becomes clear and translucent; is not fermented. 
In Drigalski, Conrad media (litmus milk-sugar, sodium bicarbonate, strong 
bouillon nutrose, and a small quantity of crystal violet B (Hoechst) deep blue 
colonies are grown. 
Indol formation is absent in cultures not older than 1 week. 
Milk- and cane-sugar are not fermented; grape-sugar is made to ferment in 
the presence of colonies of paratyphoid bacilli—one of the most important diag- 
nostic features. Typhoid bacilli do not form gas in the presence of grape-sugar; 
the coli group do ferment milk- and cane-sugar. Paratyphoid inoculation is highly 
fatal to small animals (mice, rats, etc.). 
In litmus whey, B produces an alkali, and type A an acid. 
Agglutination continues in much stronger dilution than do typhoid bacilli, 
when the latter are no longer influenced. Thus Libman reports a case in which 
the serum agglutinated the paratyphoid bacillus B at 1 to 50, and the typhoid BACTERIAL DISEASES 
123 
bacillus at 1 to 250. There is a diazo-reaction in 20 to 30 per cent of cases. 
Bacterial investigation of the blood and stools offers the safest method of reaching 
correct diagnostic conclusions. 
Pregnancy invites invasion of the genito-urinary tract in the presence 
of paratyphoid, infection. 
The disease is met oftener during the summer than winter; the epi- 
demics arise suddenly, many infected from the same source fall ill at the 
same time—transmission from patient direct is rare. Paratyphoid dis- 
ease differs from typhoid in the rarity of transmission from the patient* 
direct. 
Infections due to meat or other articles of food may present active and 
distressing symptoms early. The more severe cases are those in which 
there is obstinate nausea, vomiting, hiccough and weakening diarrhea. 
These cases begin to mend after a few days but recover strength slowly. 
The spleen offers no prognostic data; is uniformly enlarged. 
The blood picture is practically the same as in typhoid fever. There is 
an early leukocytosis, then the characteristic leukopenia, disappearance of 
eosinophils, to return as the patient improves. With far-reaching enteritis 
there may be persistent leukocytosis. These data are of some prognostic 
value. 
The skin lesions, urticaria, scarlatinal eruption, with desquamation are 
not unfavorable. Hemorrhagic lesions of the skin and mucous membranes 
are found among some of the few cases which end fatally. 
Loss of flesh is striking. 
Intestinal hemorrhage occasionally complicates paratyphoid (3 to 5 per 
cent), and is not as significant as in enteric fever. 
Albuminuria is present in most cases, is moderate, without the usual 
accompaniments of nephritis, though the latter has complicated some cases. 
The urine is markedly reduced in serious cases in which vomiting and 
diarrhea are excessive; complete anuria during limited periods has been 
alarming. High specific gravity with albumin, pus corpuscles, blood, casts 
and epithelia have been present in some of these cases. 
In unfavorable cases the temperature may, before death, drop to 1° to 
3° below normal. 
Furunculosis and distant infections, joint invasion, rarely osteitis, 
orchitis, otitis, liver inflammation, cholecystitis—all due to the paraty- 
phoid bacillus—have been met. 
Relapses may be expected in from 8 to 12 per cent of all cases. Most 
fatal cases die early, usually between the third and fifth days, with rapid 
small thready pulse, distant heart sounds, cold extremities, some cyanosis, 
great thirst, subnormal temperature, and respiratory paralysis. 
Schottm,filler calls attention to the fact that patients suffering from 
chronic ailments are prone to develop a chronic form of gastro-enteritis 124 
SPECIFIC INFECTIOUS DISEASES 
dependent on paratyphoid infection. Most deaths are due to the severity 
of the primary infection or to secondary lesions which the patients are 
unable to withstand because of reduced resistance. 
The prognosis of the abdominal type of the disease is almost uniformly 
favorable, as is also the invasion of the bladder and the kidney pelvis. 
Cases of puerperal paratyphoid which have been fatal, were of a mixed 
type with streptococcus infection. I have never seen a case in which the 
cholecystitic type of the disease has occurred—if I have, it has not been 
recognized. 
Schottmiiller has reported cases in children who died of paratyphoid 
meningitis. Complications may include many of those described in the 
chapter on Typhoid Fever and it is to he remembered that paratyphoid 
infection may follow or be associated with other acute and chronic infec- 
tions,, including pure typhoid bacteremia. 
References 
Achard & Bensaud. Infect 'paratyphoid. Soc. Med. desHosp. de Paris, 1897. 
Libman. J. Med. Research, viii. 
Schottmiiller. Mohr & Staehelin Handbuch der inneren Med. 1911, i. 
Smith (Lorrain). Allbutt’s System of medicine, i, 2. ed., 1158. 
IV. Influenza 
{Epidemic Catarrh, La Grippe, Febris epidemica) 
Influenza is a disease of protean character, panepidemic, acute, due tc 
the Bacillus of Pfeiffer (1892) which by predilection attacks the respira- 
tory mucous membranes, is characterized by fever, marked depression, 
exhaustion and weakness, and is prone to give a fresh impetus to latent 
diseases, particularly of tuberculous nature and circulatory disturbances, 
while it is often followed, particularly in those of neuropathic tendencies, 
by long periods of nervous symptoms. Epidemics may recur at intervals 
varying from a few (4 to 5) to one hundred years (100). 
There is an authentic account of an epidemic in Italy in 1173 A. D. 
In 1510 England was visited, and in 1627 the disease was brought to Mas- 
sachusetts. 
The disease travels as fast as travel itself, not faster. The last pan- 
epidemic which visited Europe and America was in 1889-90 when 
we were introduced to a disease unknown clinically to the profession of 
both continents. The students of medical history had only a vague concep- 
tion of influenza, but to none was its clinical history clear, nor were its 
after effects appreciated until the profession had been taught in the school 
of experience. BACTERIAL DISEASES 
125 
The disease is contagious and its period of incubation surprisingly 
short (2 to 4 days). The mortality of influenza does not exceed 1 per cent, 
including complications. The average mortality, including those given by 
continental and American clinicians, is 8 per cent. But few are immune 
to the disease though nurslings seem to escape, and the aged are attacked in 
smaller numbers than are the young and active. When the aged were 
attacked, the mortality usually due to complications, was higher than dur- 
ing early life. Thus in Prussia, statistics show the number of deaths and 
ages during years of limited epidemics as follows:— 
1904 3,Y96 cases 
1905 6,380 “ 
1906 2,516 “ 
190Y 5,516 “ 
Of these deaths 2,004 were over Y0 years of age 
4,109 between 60 to Y0 years of age 
1,190 “ 30 “ 60 “ “ “ 
206 “ 15 “ 30 “ “ “ 
The bacteriology of influenza is fully established. The Bacillus of Pfeiffer is 
very small, one-third the size of the tubercle bacillus, is dumb-bell shaped, usually 
single, occasionally in chains by end to end contact; it takes anilin dyes (carbo- 
fuchsin), is decolored by Gram, the ends stain more than the shaft; it is non- 
motile; is abundant in the sputum; is the cause of influenza pneumonia, and is 
often found with other bacteria, mainly pneumococci and streptococci. 
The leading types of Influenza are: 
1. Catarrhal (Respiratory) 
2. Gastro-intestinal influenza 
3. Influenza of the nervous system 
4. Influenzal fever 
1. Catarrhal or Respiratory Influenza 
This is by far the most common form of the disease during epidemics, 
and when uncomplicated and promptly treated yields within from 3 to 6 
days, leaving the patient weak out of all proportion to the duration 
of the symptoms. The bronchial and nasal catarrh, which is the usual 
accompaniment in over 90 per cent of all cases, disappears without leaving 
physical signs or permanent damage. In this as in all types of influenza 
the enlarged spleen, which is as a rule easily outlined by percussion is of 
no prognostic value. 
Moderate albuminuria at the height of the disease is not uncommon 
without ultimate serious complication, and is not of serious moment. SPECIFIC INFECTIOUS DISEASES 
126 
Albuminuria in catarrhal cases complicated by pneumonia, with evi- 
dences of nephritis is not to be ignored or lightly regarded. I have found 
abortion rare in pregnant women during influenza. 
The complications most to be feared in the catarrhal type of influenza 
are referable to the respiratory organs, more particularly the lung (pneu- 
monia), pleura (pleurisy, etc.) and also the heart. Mixed infection is the 
leading cause of secondary involvement of vital organs in catarrhal influ- 
enza, though a large number of pneumonias are due to direct infection with 
the Pfeiffer bacillus. In no disease does a good prognosis depend more 
upon rest than in catarrhal influenza, hence the necessity for cooperation 
of the patient with the physician. Serious complications are thereby re- 
duced to a minimum and the persistent anomalies referable to the heart 
are almost uniformly prevented even in the presence of previous weakness. 
Pneumonia most dreaded of all complications during times of influenza 
epidemics behaves peculiarly, and is often atypical. 
During a supposed period of convalescence I have found large areas of 
lung tissue consolidated with all of the physical signs of such a lesion, with- 
out marked change in respiration, with slight or no fever, pulse of fair 
quality, not above 110, and without cough or expectoration. These cases 
with rest and treatment make a slow but satisfactory recovery; in the aged 
this complication may be the cause of sudden death. 
The most serious cases of influenza pneumonia in the United States 
during the larger epidemic of 1889-90 were those which developed early— 
due to the Pfeiffer infection—or developed before the end of the first 
week. In active subjects this was of the lobar—in the old, in the young 
and in the feeble, of the lobular variety—while in occasional cases there 
was a mixed form in which both lungs were involved in good sized lobar 
deposit and islands of broncho-pneumonia. 
A serious type of pneumonia complicating influenza is the migratory 
type dependent on mixed (pneumococcus) or on streptococcus infection 
alone. These cases may lead the clinician to feel secure because of re- 
peated pseudocrises, when promptly there are evidences of fresh invasion 
and the disease drags a weary course through several weeks; the majority 
of such cases die of myocardial degeneration with more or less meningeal 
symptoms. 
The pure influenza pneumonia is usually catarrhal (bronchopneu- 
monia) and offers a good prognosis in children, a fair prognosis during 
early life (10 to 20 per cent mortality), a better prognosis during the active 
years of life (6 to 10 per cent in cases treated early), in the aged a very 
doubtful prognosis (20 to 50 per cent, varying in different epidemics and 
under varying conditions of health, resistance, etc.). With all pneumonic 
complications alcoholics are seriously handicapped. 
Pneumonia with Influenzal Meningitis.—If pneumonia is added 
to influenzal meningitis, the prognosis is exceedingly grave. In these cases BACTEKIAL DISEASES 
127 
as in the simple influenza pneumonia, the type is bronchial, in some cases 
lobar, in others we find the mixed type. In some epidemics the mortality 
from this combination has been as high as 50 per cent; in others lower, as 
low as 20 per cent. When meningitis is purulent with pneumonia, a high 
mortality must be expected (over 80 per cent). Pisek reported his mor- 
tality as 92 per cent. The majority of all deaths traceable to influenza 
are due to pneumonia of the catarrhal type (Bronchopneumonia). 118 
autopsies made by Hirschfeld on cases of influenza include: 
11 cases of croupous pneumonia 
8 “ “ mixed (croupons and lobular pneumonia) 
24 “ “ catarrhal (lobular) pneumonia 
Persistent cough, non-tuberculous, continues long after the acute symp- 
toms in a few cases. These are probably due to a chronic bronchitis or 
peribronchial change, at times to enlarged bronchial glands (nodes), the 
latter in children oftener than in the adult, a chronic tracheitis, and 
should always demand thorough differentiation, for in some tuberculosis 
is finally unearthed. These cases continue during relatively long periods 
to give negative reactions and physical signs. The majority of these coughs 
finally yield, and the patient recovers fully. 
dSTo acute epidemic disease lights so many latent processes into activity 
as does catarrhal influenza; among the most frequent of these is pulmonary 
tuberculosis; usually of infiltrating character, though acute miliary depos- 
its are not infrequent. The latter run the usual rapid course. This was 
particularly true of the panepidemic of 1889-90 in the central counties of 
New York State (For further data, see section on Pulmonary Tubercu- 
losis). 
Simple uncomplicated pleurisy, not a frequent accompaniment, offers a 
good prognosis, as do those cases of empyema which follow pneumonia. 
The early empyemata do not offer such a favorable prognosis, for they are 
only a part of acute and serious lung infection (pneumonia). 
When gangrene of the lung follows pneumonia, the majority die with 
symptoms of sepsis and exhaustion. 
Abscess of the lung if detected and relieved by operation, offers a fair 
chance of recovery. 
Bronchiectasis may result from one or both of the two preceding com- 
plications ; if the patients live, the condition continues to be chronic, more 
or less troublesome according to the size and location of the bronchial dila- 
tation. 
Pulse and Heart Changes.—With all the complications of catarrhal 
influenza the pulse offers the usual prognostic data as in other acute infec- 
tions. 
Persistent changes in the pulse and heart which are often more alarm- 128 
SPECIFIC INFECTIOUS DISEASES 
ing to the patient than to the physician, are likely to be late, and may 
follow any of the types of influenza. The number of cardiac anomalies 
and arhythmias following the infection is very large; they are dependent 
on either myocardial weakness or functional disturbances of the heart. 
Intermittence is present as a rule in these cases; occasionally tachy- 
cardia alternates with bradycardia or the latter is a postfebrile or post- 
pneumonic sequel; in all there is an enormous element of neurasthenia. 
Fear takes possession of the patient. In the larger proportion of cases the 
heart finally, after a long period, falls into better habits, and returns to 
normal. Early dicrotism need not be considered of serious nature. 
In rare cases, probably where the heart muscle was already the seat of 
some disease, fatty degeneration of the heart muscle with thrombosis in 
both ventricles has been found post mortem and occasionally gangrene of 
the lower extremities has developed in these cases (Eichhorst, Gerhardt). 
Relative mitral insufficiency is an expression of heart weakness which 
yields to rest in most cases with the disappearance of the systolic murmur. 
An occasional case develops fatal malignant endocarditis or the less 
serious type of the disease or, rarely pericarditis. 
Ear Complications.—With catarrhal influenza ear complications often 
retard recovery. Otitis media, either suppurative or non-suppurative, 
sinus disturbances, mastoiditis, all postpone convalescence or are early 
complications, all of which offer good prognoses if promptly treated. In 
only occasional cases which have been under treatment during reasonable 
periods, has meningitis developed from aural infections. 
Serious hemorrhagic diathesis with influenza, types of complicating 
purpura, have added depressing factors in occasional cases (Pick). In 
America we have seen but few of these. 
Other complications include disturbances of one or many organs in 
individual cases; many will be mentioned in connection with other forms 
of influenza in the following pages; the prognostic significance of all of 
these cannot be separately considered but will receive attention in connec- 
tion with the diseases of the separate organs. 
2. Gastro-intestinal Influenza 
As a rule the gastro-intestinal form runs a short course, during which 
the patient is uncomfortable for from 2 to 5 days because of the vomiting, 
at times obstinate watery diarrhea, abdominal paim, tender peritoneum 
and rarely ulceration in either the small or large intestines. 
In most of these cases there is enlargement of the spleen. The latter 
is proportionate to the severity of the infection. 
The prognosis of gastro-intestinal grip is good, though full recovery 
(return to normal resistance) is slow. Heart and other complications are 
not infrequent, the lungs are but rarely involved. BACTERIAL DISEASES 
129 
3. Influenza of the Nervous System 
The nervous system may be either (a) primarily or (b) secondarily 
involved by the Pfeiffer infection without catarrhal symptoms. 
(a) Primary invasion of the nervous system, leads to a train of posi- 
tive symptoms, varying according to the severity of the disease. 
In children there may, even in favorable cases be convulsions, early 
evidences of meningitis, the presence of the infecting agent in the with- 
drawn lumbar fluid, or there may be active delirium during a limited 
period. Most of these cases terminate favorably. In the adult the pri- 
mary symptoms are less severe, as a rule, and the outlook from the be- 
ginning is favorable, in spite of great prostration, severe headache, annoy- 
ing myalgias; in the severer cases there is delirium and at times somno- 
lence; occasionally insomnia. 
Primary peripheral limited neuritis, leading to severe neuralgia 
is favorably influenced by treatment. 
(b) The complications due to organic change in the nervous system 
at the height of the disease or manifested early, are of serious na- 
ture. 
With alcoholics “wet brain/’ alcoholic meningitis with all of the 
symptoms of delirium tremens may lead to death in deep coma from the 
sixth to the tenth day. 
Acute encephalitis simulating cerebral apoplexy, with or without 
motor paralysis or aphasia, occasionally monoplegia—usually of an arm 
—may promptly cause death. 
Meningitis with mastoiditis, venous thrombosis, or secondary 
meningitis to catarrhal infection of the nasopharynx is serious 
unless the condition is promptly recognized and surgical relief is obtained. 
Secondary multiple neuritis offers a good prognosis; recovery is 
slow but restoration of function is likely to be complete. 
Abscess of the brain is not frequent; it has occasionally been found 
post mortem. My records offer no well authenticated case diagnosticated 
ante mortem save those secondary to otitis media and mastoid invasion. 
The prognosis in reported cases has been very bad. 
The statistics of our state hospitals for the care of the insane gathered 
after the panepidemic of 1889-90, prove the enormous influence of influ- 
enzal infection in causing psychoses. Our hospitals were filled with all 
varieties of psychoses usually developed during convalescence. In some 
there were long periods of depression (melancholia), in others exhilaration 
and hallucinations. Those not seriously burdened by heredity ultimately 
returned to full health. 
Neurasthenia in all of its forms may develop; it yields slowly after 
months of patient waiting or the fully developed habit may persist, to 
make the victim wretched during years or forever. 130 
SPECIFIC INFECTIOUS DISEASES 
Myelitis and occasional ascending paralysis (Landry’s type) have 
been noted and are mentioned by Romberg and Osier. 
A study of the literature of these complications does not justify an 
encouraging forecast; no one man has a large material at his command, for 
the association of the myelitis of Landry's syndrome with influenza has 
been limited. 
4. Influenzal Fever 
Occasional cases without the usual catarrhal symptoms present with 
marked features; there is irregular fever, at times it is continuous and the 
patient falls into a typhoid condition; the fever may be remittent, with or 
without chills; there are no lung complications as a rule. 
These febrile types may present a variety of pictures, but the prognosis 
in the uncomplicated cases is good, though there may be great prostration, 
at times cardiac anomalies and psychoses long after the disappearance of 
acute symptoms. Any of the complications associated with the other forms 
of influenza may develop in exceptional cases. The respiratory organs 
rarely suffer. 
References 
Eichhorst & Gerhardt. Berl. klin. Wchnschr., 1890, No. 9. 
Osier. Practice of medicine. 1913, Appleton. 
Pick. Prager med. Wchnschr., 1890, No. 4- 
Romberg. Lehrbuch der inneren Medizin. 1913, Krehl. 
Satterthwaite. New York Med. J., May 24,1913, 1066. 
V. Pyogenic Infections—Septicemia—Pyemia 
(Sepsis, Blood Poisoning, Septicopyemia) 
Septicemia is a general disturbance due to the presence in the blood of 
septic, disease-producing bacteria or their products, i. e., toxins. Septice- 
mia may also be defined as a bacteremia or toxinemia (sapremia when 
products of decomposition are included). It is possible for sepsis to in- 
clude the presence in the blood of both bacteria (bacteremia) and toxins 
(toxinemia) at the same time. In contradistinction to pyemia (a surgi- 
cal affection), sepsis does not include suppurating metastatic foci. In all 
cases of sepsis, toxins finally become the cause of the general, i. e., con- 
stitutional symptoms, and are responsible for the consecutive degenerative 
changes in the vital organs of the body, i. e., heart, spleen, kidney, etc. 
Grave constitutional disturbances with degenerative changes may lead 
to death without evident bacteremia, as proved by blood cultural methods; 
these effects are always due to the overpowering toxinemia. 
Most constitutional infections are secondary to a primary local focue BACTERIAL DISEASES 
131 
through which, or from which bacteremia and toxinemia proceed (puer- 
peral sepsis, anthrax, pneumonia, gonorrhea, etc.). There are, on the 
other hand, grave forms of sepsis in which the constitutional disturbances 
are due to a prompt dissemination of disease-producing germs (streptococci 
usually) without known or evident local lesion from the blood stream to the 
vital organs, with the associated baneful and malignant results of toxic 
poisoning. These are the cases which offer the gravest forecast. There is 
always danger of septic deposits in organs which present changed or dis- 
eased surfaces to the blood and lymph stream. This is manifest in one of 
the gravest forms of septicemia—malignant endocarditis. In these cases, 
there is often grafted upon an old endocardial or valvular lesion an acute 
septic and malignant endocarditis from which, by the detaching of vegeta- 
tions to distant parts (emboli), grave complications (hemorrhagic infarcts) 
are added, which presage an absolutely unfavorable outcome. The septic 
type of endocarditis will be separately considered in connection with the 
diseases of the heart (See Septic Endocarditis). 
The search of the invading bacteria for a port of exit (elimination) 
leads to serious kidney change, i. e., septic nephritis in the graver forms of 
blood-poisoning, with the characteristic urinary evidences, which is never 
to be lightly regarded. Marked reduction in the quantity of the urine se- 
creted, lowered urea output, albuminuria, large numbers of casts with evi- 
dences of invasion of the nervous system, are among the symptoms which 
call for a guarded, usually a bad prognosis. 
The staphylococcus infections offer a more favorable prognosis than do 
the streptococcus. The latter infections, though grave do not always lead 
to death. (The staphylococcus does not enter the blood-stream so easily or 
readily as does the streptococcus, but when it does it has recently been held 
by pathologists that it is much more serious. This question is still sub 
judice.) 
The streptococcus is less likely to cause pyogenic processes (abscesses) 
than the staphylococcus. It enters the blood stream quicker and with 
greater ease than does the staphylococcus. Once the staphylococcus has 
caused bacteremia, it is a question whether it does not offer a less favorable 
prognosis than does streptococcemia. 
Many forms of septic and pyemic infections are likely to he mixed, 
complicating many other primary infections to which reference has been 
made in other chapters; these include, diphtheria, pneumonia, tuberculosis, 
typhoid fever, etc. Such mixed infection, as has been repeatedly demon- 
strated, adds a large element of danger. 
Organic diseases of the vital organs invite infections which are largely 
responsible for the death of the individual. These are considered “ter- 
minal infectionsOsier quotes Flexner, who analyzed 255 cases of chronic 
renal and cardiac disease in which full bacteriologic examinations were 
made at the autopsies “in which 213 gave positive, and 42 negative results.” 132 
SPECIFIC INFECTIOUS DISEASES 
The infections were local and general; the former were common “in a large 
proportion of all cases of Bright’s disease, arteriosclerosis, heart disease, 
cirrhosis of the liver, and other chronic disorders.” In these cases it was 
found that acute pleurisy, pericarditis, peritonitis, meningitis or endo- 
carditis were the usual seats of local infection. 
The most serious infection associated with previously existing organic 
disease is the streptococcus. 
General gonococcus infection, when associated with gonococcus endo- 
carditis—and it is very often—has in my experience been uniformly fatal. 
Flexner contends that “the blood serum of persons suffering from ad- 
vanced chronic disease was found by him to be less destructive to the sta- 
phylococcus aureus than normal human serum.” Lenhartz’s statistics show 
that 75 per cent of all general sepsis is dependent upon streptococcus infec- 
tion. Staphylococcus and pneumococcus infections are responsible for 8 to 
9 per cent. 
The female generative tract is the most frequent source of general 
infection, due to unclean hands, instruments, clothing, usually to prevent- 
able factors for which the physician is not always responsible. Surgical 
operations with consecutive infections are also a fruitful source of septic 
poisonings. 
Phlebitis with or without septic thrombosis must always be considered a 
menace, and when due to streptococcus infection is a serious complication. 
Septic thrombosis, with single or multiple thrombi, is a serious complica- 
tion with any form of sepsis; the prognosis is grave, depending largely on 
the depth of the toxinemia, the pathologic changes in vital organs (heart 
and kidney mainly) and the location of the thrombus. 
Apparently innocent local infections without grave initial symptoms 
may lead to grave constitutional disturbances due to bacteremia and toxi- 
nemia, or to changes in vital organs, with pus-producing organisms 
(pyemia), to multiple abscesses in the various organs of the body. Thus 
simple follicular (streptococcus) tonsillitis offers innumerable examples 
of the truth of this possibility. Other examples are otitis media, bone 
invasion, suppurating hemorrhoids, superficial or deep skin infections, 
prostatitis, urethral abscess, gonorrhea and trivial injuries. The prog- 
nosis is always clouded when there are multiple abscesses associated with 
pyemia in the lung or liver, or in both at the same time. 
The height and behavior of the temperature serves as a valuable guide 
in connection with the pulse for prognosis. 
With pyemia, multiple abscesses, purulent phlebitis and thrombosis, the 
character of the fever is likely to be intermittent, and profuse sweats fol- 
low with a fall of temperature. Severe chills in these cases are the rule. 
When with pus-producing infections there are long periods of apyrexia 
between the chills, the prognosis is more favorable than in cases with con- 
tinuous elevation of temperature—barring, however, those cases of malig- BACTERIAL DISEASES 
133 
nant endocarditis of the intermittent type, which always offer a grave fore- 
cast. 
Chronic cases due to the streptococcus viridwns may remain afebrile 
during several days, or the temperature may be but slightly elevated with 
or without the chronic form of endocarditis, for which this strain is re- 
sponsible ; the prognosis remains bad and the attendant is not to be deluded 
by the apparent improvement. 
Cases in which the temperature gradually falls to normal or below, 
with improvement of pulse and other constitutional symptoms offer a good 
prognosis, but in these, it requires more than a few days of the afebrile 
state before a positive opinion as to the outcome is justified. 
The effect of the toxinemia on the vasomotor system through the spinal 
centers is of paramount importance. If the heart, though rapid, shows no 
evidences of insufficiency, its separate sounds remain clear and fairly 
strong, and endocarditis does not develop, there is at least a powerful staff 
upon which we may continue to lean. 
Dilatation of the heart with relative mitral insufficiency, with or with- 
out accentuation of the second pulmonic sound and rapid pulse, persistence 
of fever, nephritis, and evidences of cerebral invasion, offer a bad prognosis. 
Patients developing sepsis from whatever source, with pre-existing 
endocarditis are handicapped, and in these the prognosis is always doubtful. 
The influence of hemorrhagic infarcts is always bad; to these we again 
refer in the chapter on Malignant Endocarditis. 
The blood shows marked leukocytosis in most cases of sepsis with reduc- 
tion in the number of red blood corpuscles. There are cases of fully devel- 
oped sepsis in which the blood picture is not materially changed. Limbeck 
has reported cases of puerperal sepsis without leukocytosis. The blood 
offers no data so far as the count or appearance of its corpuscular elemeids 
are concerned which influence prognosis. 
The degree of bacteremia in occasional cases does influence prognosis 
-—favorable in accordance with the number of bacteria in the blood stream. 
Pneumonia as a complication of sepsis or pyemia is always serious. 
Frequent respirations are not always due to pneumonic consolidation, hut. 
to a number of factors including heart weakness, muscular enfeeblement, 
hemorrhagic infarct, etc. 
The spleen is always more or less enlarged with all forms of blood- 
poisoning. It offers no prognostic data. 
The grave forms of sepsis are complicated with cerebral and meningeal 
symptoms. 
Septic meningitis is usually a fatal complication; with erysipelatous 
inflammation, it always proves serious (See Erysipelas). 
Duration.—The duration of all forms of blood-poisoning depends upon 
the source and extent of the primary lesion, the life history of the infecting 
germ, and many other factors. Acute sepsis may kill in a few days. 134 
SPECIFIC INFECTIOUS DISEASES 
Atypical cases, particularly streptococcus viridans infection with endocar- 
ditis, runs a chronic course covering many months. We recently saw a 
case which died at the end of the fourteenth month, of cerebral infarct. 
The average duration of septic processes may be safely placed between 5 
to 8 weeks. Pyemia is often chronic. Sudden death in acute or chronic 
cases may be due to thrombosis or embolism, cardiac insufficiency, pneu- 
monia or a variety of complications considered in connection with the spe- 
cial diseases. Pneumococceinia is separately considered. 
References 
Lenhartz. Die septischen Erkrankungen. In: Nothnagel’s Handbuch, etc. 1903, Bd. Hi. 
Limbeck. Klin. Pathol, des Blvtes. 1896. 
Osier. Practice of medicine. 8. ed., 1915. 
VI. Diphtheria 
General Considerations 
Bacteriology.—Diphtheria is an acute infectious disease, due to the 
Klebs-Loeffler Bacillus (1883-1884) (a short rod-shaped microorganism, 
which may be curved or club-shaped at one end. Gram-positive, it shows 
polar granules when stained with methylene-blue, with characteristic ar- 
rangement in groups like Chinese figures) contagious, attacking by predi- 
lection the tonsils, uvula, soft palate, postnasal space and larynx, extending 
into the trachea and bronchi and invading the lung in the graver infections, 
with evidences of general toxemia. The disease is sporadic and epi- 
demic. Uncontrolled, the infection is always serious and associated will 
a high death rate, hut is favorably influenced by the Behring a?ititoxin 
(1892) in almost all cases, if treated on the first day. 
History.—The disease is now prevalent in all parts of the civilized 
world, attacks the young especially, rarely the aged, though it is not infre- 
quent in adults during middle life. In 70,000 cases collected (London 
Lancet, 1878) the cases were distributed as follows, according to ages: 
Under 12 months 9 per cent 
1 to 5 years 45 
5 to 10 “ 26 “ “ 
10 to 15 “ 9 “ “ 
15 to 25 “ 5 “ “ 
25 to 45 “ 3.5 “ “ 
45 years and over 2.5 “ “ 
Jacobi’s case is tbe youngest on record and was 9 days old. The sta- 
tistics of the New York Health Department (1891-1900) show that 80.8 BACTERIAL DISEASES 
135 
per cent of deaths occurred under 5, and 17 per cent between 5 and 10 
years. The disease was known before the Christian Era (angina maligna, 
angina gangrsenosa) ; in Spain, where there were epidemics at short inter- 
vals between 1553 and 1618; in Italy, from 1610 to 1650; in France as 
early as 1736; 1744 in England; 1752 in Germany, and the same year it 
appeared in America. 
Bretonneau’s description of the disease remains among the classics of 
medicine, as well as that of Trousseau (1821-1828). There can be no 
doubt of the fact which clinical experience and a study of medical litera- 
ture prove, that the character of the disease, its virulence and mortality, 
are influenced by unknown factors, and vary materially with fresh epi- 
demics and during different years. The various seasons of the year do not 
influence the mortality of diphtheria, though the disease is more frequent 
during the winter months. 
In Germany the mortality reached its climax in 1886 with 122,000 
deaths. In 1900 there were 45,000 deaths. In 1885 the number of deaths 
due to the disease in Germany was 122.7 per 100,000; in 1895, 54; and 
in 1905 only 22.4. Huttall and Smith offer the following figures, showing 
the maximum and minimum death rate due to diphtheria in 100,000 of 
inhabitants in Boston, Providence, Hew York and St. Louis: 
Maximum. 
Minimum. 
Period 
of 
Observation. 
Boston 
163 in 1881 
51 in 1891 
1861-1895 
Providence 
314 in 1877 
8 in 1868 
1868-1895 
New York 
208 in 1877 
23 in 1873 
1868-1893 
St. Louis 
314 in 1877 
8 in 1868 
1868-1895 
Factors Influencing Growth of Disease.—The body, including the blood 
and mucous membrane particularly, offers marked resistance to the disease. 
There are factors, as Trumpf has demonstrated, which are necessary for 
the development of the disease. 
They are: 
1. A high degree of virulence of the infecting agent. 
2. The deposit of large numbers of bacilli on the mucous membrane. 
3. The membrane must be in a suitable condition to offer a habitat 
for the proliferation of the bacillus. 
4. The infected individual must be susceptible; hence this factor and 
the others are variable, protect or expose the same subject to the disease at 
different times. 
Mixed infection with pneumococci, staphylo- and streptococci, influen- 
ces the prognosis of diphtheria materially. 136 
SPECIFIC INFECTIOUS DISEASES 
A degree of immunity is developed by a single diphtheria infection. 
Diphtheria infection added to already existing scarlet fever is not asso- 
ciated with the same danger as is the addition of scarlet fever to diphtheria 
(Uppenheimer). 
Zucker’s statistics show second attacks in only 0.9 per cent, and third 
attacks in 0.13 per cent of cases. 
Carriers.—Malignant as well as benign diphtheria may be conveyed by 
“carriers” who may or may not have had the disease. The mildest type 
of the disease in one individual may transmit the most malignant form to 
others. 
Pharyngeal Diphtheria 
The following is the classification of pharyngeal diphtheria, nnder 
which the subject will be treated: 
1. Mild infection of the fauces, tonsils, without severe general toxemia. 
2. Pharygeal infection with severe general toxemia. 
(a) ISTon-gangrenous 
(b) Gangrenous . 
I. Mild Infection Without Several General Toxemia.—With mild in- 
fection of the tonsils and surrounding tissues, there are generally no evi- 
dences of severe constitutional toxemia, and if the case is recognized on the 
first or during the second day of the disease and promptly injected with a 
sufficient number of antitoxin units, improvement is prompt as a rule, the 
membrane begins to disappear, fever and pulse improve, glandular enlarge- 
ments recede, and between the sixth and tenth day convalescence has com- 
menced and in the majority of cases is uninterrupted. Cases which begin 
with laryngeal invasion so limited as to cause but few symptoms, with 
croupy cough, but without other evidences of laryngeal stenosis, may later 
“ascend” with invasion of tonsils and but few constitutional symptoms, 
when the prognosis is less favorable than in the first mentioned cases— 
because time has been lost before active treatment was commenced. 
If laryngeal diphtheria in these cases does progress in spite of the fail- 
ure to make an accurate bacteriological diagnosis early, the prompt treat- 
ment of the disease after the appearance of pharyngeal diphtheria will lead 
to recovery in over 85 per cent of such cases. If from these apparently 
mild cases there is progression to the posterior nares, and greater invasion 
of the cervical glands there will, as the process advances, be evidences of 
increasing toxemia. Fever may not be high, but the heart and kidney may 
suffer most, and the prognosis is accordingly influenced unfavorably. 
Leukocytosis is present in all of .these cases. Its influence on prognosis 
will also be studied in connection with the administration of antitoxin—to 
which reference will be made later in this chapter. The prognostic value 
of leukocytosis, has been epitomized by Kautback and Andrews as follows: BACTERIAL DISEASES 
137 
“1. A high leukocytosis signifies a good reaction and is present in 
those cases which recover. 
“2. A low leukocytosis at the height of the disease, before antitoxin 
has been injected, accompanies most, if not all fatal cases. 
“3. The high leukocytosis of well reacting cases after and during 
antitoxin treatment steadily diminishes, the number of cells decreasing by 
50 per cent in 3 or 4 days.” 
Cases which begin in the nose with descending disease, i. e., final de- 
position on tonsils and soft palate, even without constitutional symptoms at 
first, are usually complicated with painful enlargement of the lymphatics, 
increasing anemia, and before the fifth or sixth day there are in many cases 
evidences of toxemia, albuminuria, normal or subnormal or slightly ele- 
vated temperature, and with increasing heart weakness the patient’s con- 
dition becomes grave. These complications with beginning nasal diph- 
theria are as a rule prevented if the disease is promptly recognized, and 
the patient injected. Albuminuria without other symptoms or microscopic 
elements denoting nephritis, is present at sometime in the majority of these 
eases, and does not cloud the prognosis. 
II. Pharyngeal Infection with Severe Toxemia. 
(a) Hon-gangrenous Pharyngeal Diphtheria with Severe Tox- 
emia.—The majority of pharyngeal infections which are associated with 
severe toxemia are found among the poorer classes, in tenements and homes 
where there are many children, where the physician is rarely called early 
and the process with its overpowering toxemia is far advanced before treat- 
ment is instituted. In these cases, as a rule, there is some nasal invasion 
also; the general appearance of the patient is unfavorable, color pale, face 
puffy, at times ashen; breathing rapid; pulse accelerated, small and with- 
out character; urine is reduced in quantity and albuminous, with hyaline 
and granular casts; temperature behaves irregularly, at times is high, in 
some cases subnormal or only slightly elevated, the odor foul. In these 
non-gangrenous cases, there is less sloughing of tissues, but the membrane 
presents a greyish brown or dirty yellow appearance; the discharge from 
the nares is at times watery, almost continuous, ichorous, causes ulceration 
of the skin; and in spite of large doses of antitoxin there is a large mor- 
tality, ranging between 15 and 50 per cent, depending upon the day of 
injection, the extent and character of the associated lesions and the depth 
of toxemia. Albuminuria with casts, when an expression of acute non-sup- 
purative nephropathy (Councilman pathology), or glomerular or tubular 
invasion, adds an element of danger. 
(b) Gangrenous Pharyngeal Diphtheria.—The gangrenous form 
is always serious. These cases may arise sporadically or during epidemics; 
they show the character of the infection. Trousseau in 1846 called atten- 
tion to these cases. They have become less frequent during the past 20 
years. In gangrenous diphtheria we have the picture of deep sepsis with 138 
SPECIFIC INFECTIOUS DISEASES 
all of its classic constitutional symptoms to make the prognosis exceedingly 
grave. There are in the worst cases dark brown, blackish, foul-odored 
sloughs, with other local manifestations and swelling of glands; foul dry 
brown tongue; cracked ulcerated lips, almost continuous dark or bloody 
nasal discharge; increasing weakness; great thirst; thready pulse; albu- 
minuria, usually some form of nephritis. In occasional cases death fol- 
lows a number of hours of urinary suppression after coma or disturbed sen- 
sorium, including delirium and great unrest. In these cases there is likely 
to be hypoleukocytosis which is unaffected by serum injection. Acetonuria 
and acetonemia with glycosuria may be present in the gravest cases. 
Gangrenous cases developing laryngeal stenosis offer most unfavorable 
prognoses. 
Hoarseness, gradually increasing with this and most forms of diph- 
theria, is an ominous symptom and usually leads to stenosis, if the patient 
lives long enough. Cyanosis, rapid pulse, delirium, noisy respiration 
showing extreme stenosis, with air hunger—a pitiful picture of suffering 
—usually end the scene (carbonic acid poisoning). 
Nasal Diphtheria and Laryngeal Diphtheria 
Nasal and laryngeal invasion (stenosis), as has been emphasized in 
connection with all forms of the disease, are always of serious significance 
whether primary or secondary. 
Skin Diphtheria 
There are in some cases diphtheritic ulcerations of the shin. The inva- 
sion of the skin alone is rarely met without pharyngeal deposit. Its prog- 
nosis is relatively favorable when primary, depending on the degree of 
virulence and the time of injection. 
Conjunctival Diphtheria 
Conjunctival diphtheria is not often seen in hospital or private prac- 
tice. Occasionally during epidemics a case arises, in which with naso- 
pharyngeal disease the conjunctiva is infected. Unless improvement is 
prompt and the case has received early treatment, the danger to the eye is 
great and destructive ulceration may result. 
Diphtheria of the Vulva 
My experience includes 4 cases of vulvar diphtheria, all seen during 
the 'puerperal period. All had been treated for puerperal sepsis; in 3 for- 
tunately the antitoxin and local treatment saved the patients. 1 case seen 
during the preantitoxin period died with all the symptoms of puerperal 
peritonitis. BACTERIAL DISEASES 
139 
The amount of glandular invasion is as a rule proportionate to the 
extent of the nasopharyngeal involvement, and is an expression of the 
malignancy of the process in most, but not in all cases. There is but slight 
swelling of the glands in occasional cases of great virulence; on the other 
hand I have seen a goodly number of cases in which benign diphtheria was 
associated with glandular enlargement out of all proportion to the deposit, 
or to the extent of the disease. 
Complications of Diphtheria 
Nephritis complicates 50 per cent of all diphtherias. Councilman 
considers this a true non-suppurative interstitial nephropathy; in some 
cases there is hemorrhagic nephritis, at times atypical forms resembling 
parenchymatous disease of the kidney. The albumin loss is moderate, 
less than with scarlatinal nephritis; there is also less dropsy—often none. 
Albuminuria may in the milder cases prove to be transitory; the 
amount of albumin otfers no prognostic data. In the severe and malignant 
types, nephritis may show but slight albuminuria in the presence of the 
gravest possible conditions. It may be concluded that cases which are 
albumin-free offer a better prognosis than do those in which it is present, 
from whatever cause. 
If albuminuria is transitory, the prognosis is as a rule good in the 
absence of heart weakness or other depressing conditions. 
With nephritis and scanty urine, abundant casts, (hyalin, granular and 
blood) the prognosis is unfavorable. Uremia may end life within a limited 
period. This is not frequent. 
Diphtheritic nephritis does not cause dropsy. When the latter is pres- 
ent, it is due to circulatory embarrassment and is a serious complication. 
Chronic nephritis may develop after the acute symptoms have dis- 
appeared. This may be overlooked unless the cases are followed. The 
prognosis will be further considered in the chapter on nephritis. 
Heart Complications.—The heart is subject to myocardial change in all 
cases of diphtheria, the extent depending entirely upon the malignancy of 
the toxemia; its muscle may undergo either interstitial change (myocardi- 
tis interstitialis), fatty, or parenchymatous degeneration. 
The interstitial type of myocarditis is the most frequent cause of heart 
weakness in diphtheria (Jores, Romberg and others). The prognosis as 
influenced by the heart, depends on the extent of the degeneration or myo- 
carditis. In the milder cases this is limited, in the gangrenous toxemias 
it is far-reaching. With dilatation, weak heart sounds, rapid small pulse, 
with or without murmurs, the prognosis is bad. 
Irregularity of the pulse during the acute and toxic period of the 
disease is always serious; later however, during convalescence with or with- 
out paralyses, it is less serious, and great rapidity of heart action and 140 
SPECIFIC INFECTIOUS DISEASES 
erratic hearts are often well borne during long periods, leading ultimately 
to recovery. 
Endocarditis and Pericarditis if present are due to secondary infec- 
tion. They are likely to prove malignant and offer a grave prognosis (ma- 
lignant diphtheritic streptococcus endocarditis). 
Sudden Death.—There is in the profession a fixed belief that diph- 
theria often leads to sudden death. This is not based upon clinical obser- 
vation, and is unjustified by experience. 
Patients rarely die suddenly during the period of convalescence or at 
the height of the disease. I am in full accord with Harris, who says: 
“there have always been timely warnings of danger.” Experience proves 
that the heart weakness or other cardiac anomalies offer positive symptoms 
and physical signs, during a period of sufficient length to make their pres- 
ence recognized. Careful examination of the heart, repeated daily during 
convalescence, will give sufficient warning of a failing degenerated heart 
muscle; the same is true of all periods of the disease. 
It will be necessary in adding to other prognostic signs, the data offered 
by the heart, to consider as Harris has suggested: 
1. The heart sounds 
2. The position of the cardiac impulse 
3. The pulse 
4. The outline of cardiac dullness. 
Irregularity with reduplication of the second sound and gal- 
loping rhythm are always serious. 
Relative mitral insufficiency may persist for an indefinite period; 
in the absence of other grave symptoms, without extreme dilatation, these 
patients recover and the murmur ultimately disappears. 
Tachycardia due to paralysis of the pneumogastric, is often well borne 
by most children during long periods. To this I will again refer when 
considering diphtheritic paralysis. 
Embolic Infarcts are rare; if present they are an expression as a rule of 
malignant endocarditis or septic processes, and are therefore serious com- 
plications. 
Purpura, petechise, hemorrhages from mucous membranes are asso- 
ciated with heart weakness in malignant cases and are of grave import. 
Diphtheritic Paralysis.—Paralysis is a complication or sequel of diph- 
theria in about 12 per cent of all cases, and is by no means an expression 
of the severity of the diphtheritic infection. I have seen a number of 
cases which were so mild that no physician had been called, which were 
treated by mothers for mumps, in which paralysis developed. Often the 
gravest infections are entirely without this complication. 
Paralysis as a rule is a sequel of the disease, developing from 3 to 10 
weeks after infection. BACTERIAL DISEASES 
141 
In severe cases glossopharyngeal paralysis becomes a serious com- 
plication as early as the fifth to the eighth day. In these, the chances for 
the patient are unfavorable. 
Simple uncomplicated paralysis of tiie soft palate when it fol- 
lows the acute stage, offers a favorable prognosis; recovery may be ex- 
pected in from 3 to 10 weeks. 
Paralysis which interferes with deglutition, (glossopharyngeal) with 
choking cough, is always more serious than paralysis of the soft palate 
alone. It may lead to “Schluck pneumonia” or sudden asphyxia. Paraly- 
sis associated with changes in the voice, an unsatisfactory and inefficient 
cough, without a normally closing glottis, is always to be feared because 
of the danger of pneumonia from the entrance of food etc. into the air 
passages. Many of these cases,, under close watching and feeding, recover 
slowly. 
Paralysis of the extremities, usually most developed in the legs, 
if not associated with severe glossopharyngeal or pneumogastric paralysis, 
tends to full but slow recovery, requiring from 5 to 10 months. 
I have never in my own practice seen a case of hemiplegia with diph- 
theria. A number have been reported; probably these were embolic, 
thrombotic, or due to cerebral hemorrhage. The prognosis must of neces- 
sity be grave, but recovery is not impossible. Polleston, in 9,075 cases 
of diphtheria included 6 of hemiplegia, of which 4 died. In 1 of 
these there was an embolus in the cerebral vessels. When the respiratory 
muscles are involved (pneumogastric paralysis), the prognosis will be 
grave in proportion to the extent of the respiratory embarrassment. In 
these cases there is, as a rule, associated tachycardia. While the complica- 
tion will always cause the attendant great anxiety, and is serious, let him 
remember that in extreme cases recovery may follow. Long continued 
pneumogastric paralysis with fully developed symptoms have in my experi- 
ence finally yielded, and full restoration to health has followed with nor- 
mal pulse and respiration, in a number of cases. ]STo positive prognosis 
can be given; the patient until fully restored stands on the edge of a 
precipice, and may fall at any moment. Ocular paralyses may be the 
only evidence of diphtheritic palsy, or these may be a part of multiple 
neuritis and far-reaching paralysis. The prognosis is as a rule favorable 
when limited to the eye muscles. Nasal diphtheria is likely to be followed 
by paralysis of the lower extremities, at times by quadriplegia. The 
prognosis, if this is a late complication, is good. Fully developed paraly- 
sis which develops at the height of infection offers a very had prognosis. 
TIave the number of diphtheritic paralyses been increased by the use 
of the von Behring antitoxin? This question can be ansivered without 
qualification in the negative. There are a larger number of diphtheritic 
paralyses, it is true, but not because of antitoxin. There are fortunately 
a larger number saved, hence the increase of paralyses; our observation 142 
SPECIFIC INFECTIOUS DISEASES 
of cases is closer, a larger number are recorded by health authorities than 
formerly. Neither the close study of this subject by Rolleston, nor 
the statistics of Fibigan prove that the Behring serum has “altered the 
incidence to any appreciable extent.” 
Persistent vomiting during the acute period of infection is either due 
to diphtheria of the stomach, nephritis, cardiac insufficiency or other seri- 
ous conditions; if unrelieved, there is cardiac incompetence, and death 
follows. 
Pneumonia.—Pneumonia (lobular) is found in at least 50 per cent of 
autopsied diphtherias. When developed early it is among the complica- 
tions least amenable to treatment, and death is likely to follow. The 
unfavorable symptoms are increasing dyspnea, cyanosis, rapid small er- 
ratic and irregular pulse, physical signs of collapsed lung, and inability 
to cough, with hurried respiration and evidences of toxic nephritis. 
Pleurisy—serous and purulent—are not frequent; when late, less seri- 
ous than early. 
Otitis media suppurativa may be an early or late complication. Recov- 
ery follows unless it is present during the height of malignant infection, 
when it is simply one of many conditions which cloud the prognosis. 
Liver and spleen offer nothing of importance for our purposes. 
Parotitis is not frequent, but if present is likely to be an expression of 
profound toxemia and always secondary. 
Relapse 
Relapse occurs occasionally. In some cases the habit of reproducing 
membranous deposit is formed and is encouraged by the use of local treat- 
ment ; such cases if left untreated, promptly recover as a rule. 
Relapse immediately after acute infection or as the membrane is cast 
off, aggravates all symptoms, retards recovery, but offers a good prognosis if 
the patient is not exhausted and the disease is non-malignant. Associated 
complications (nephritis, myocarditis, etc.) naturally modify the prog- 
nosis. 
Diphtheria and Antitoxin 
Blood Counts after the Injection of Antitoxin.—Prognostic data may 
be furnished by blood-counts before and after the use of the serum. 
Hypoleukocytosis follows the injection of the serum; if after 3 or 4 
hours the leukocytic count present before injection is not reached, the 
prognosis is unfavorable. A return to a higher leukocytic count after 
injection than was primarily present is favorable. In unfavorable cases 
the hypoleukocytosis continues after injection; there is no effort to in- 
crease phagocytosis (Simon). 
Serum Sickness.—Methods have been and are being devised which have BACTERIAL DISEASES 
143 
reduced serum sickness materially. The use of calcium chlorid has been 
efficacious (Netter-Consin-Gervin). 
Serum sickness is present where horse serum was used: 
In cases where 1,500 units were injected in 8.6 per cent 
In cases where 1,500 to 4,500 units were injected in 13.13 per cent 
In cases where 4,500 units and upward were injected in 18.91 per cent. 
While painful arthritides and eruptions have followed the use of the 
serum in my practice, I have never recorded a death traceable to it. The 
use of lamb serum (Ascoli) offers encouragement, for by it, serum sickness 
becomes an infrequent complication. It will however prove more difficult 
to obtain a sufficient supply of this than horse serum. Behring’s newer 
methods will reduce this complication, it is hoped. 
It requires no extensive argument in considering the prognosis of diph- 
theria to prove to the clinician as well as to the lay world the fact that the 
addition by von Behring (1892) of his antitoxin to our armamentarium 
at once added a remedy which promptly changed the prognosis of the dis- 
ease. 
Within 3 years after its introduction, von Behring proved that in Ber- 
lin at the Charite in cases where antitoxin was used the mortality was 
reduced to 8 per cent against 32.1 per cent in the Berlin Bethany Hospital, 
where it had not yet been introduced. These and the figures which are to 
follow, with the experiences easily obtained from those who practiced dur- 
ing the pre-antitoxin period and have been privileged to continue their ob- 
servations since, are sufficiently convincing. We now enter the treatment 
of the disease with reasonable certainty of success, formerly it was with 
fear and a painful appreciation of the limitations of our art to combat the 
monster. 
Baginski has demonstrated a mortality of 15.8 in 10,000 inhabitants 
before the use of antitoxin; since its use a reduction to 2.4 in 10,000 in 
1908, and as low as 3. in 10,000 in 1907—the year of a severe epidemic 
in Germany. 
Further, I offer the following collective statistics: 
Name of 
Investigator. 
No. of 
Cases. 
Mortality, 
Per Cent. 
Mortality when Serum was injected on 
1st 
Day. 
2nd 
Day. 
3rd 
Day. 
4th 
Day. 
5th 
Day. 
6th 
Day. 
Welch 
1,489 
5,794 
9,581 
14.2 
2.3 
8.1 
13.3 
19.0 
29.3 
34.1 
American Pediatric So- 
ciety (Collective In- 
vestigations) 
12.3 
4.9 
7.4 
8.8 
20.7 
35 3 
Kaiserl. Gesundh. Amt. 
(Collective Invest.).... 
15.5 
6.6 
8.3 
12.9 
17. 
23. 144 
SPECIFIC INFECTIOUS DISEASES 
Mortality of diphtheria as shown by day of injection of serum, showing 
number injected each day: 
Cohn’s Statistics. Mortality Percentage. 
Injected 78 on first day 1.3 
Injected 361 on second day 11.1 
Injected 284 on third day 16.5 
Injected 101 on 4th day 24.7 
Injected 176 after 22.7 
Rolleston’s Statistics. Mortality Percentage. 
Injected 62 on first day 0 
Injected 324 on second day 3.1 
Injected 391 on third day 6.1 
Injected 309 on fourth day 10.6 
Injected 203 on fifth day 12.8 
Injected 211 on sixth day or after 10.9 
Kosel’s Statistics. Mortality Percentage. 
Injected on first day 0 
Injected on second day 4 
Injected on third day 13 
Injected on sixth day 53 
Ganghofner’s Statistics. Mortality Percentage. 
Injected on first day 0 
Injected on second day 8.4 
Injected on third day 14.2 
Injected on fourth day 17. 
At Heubner’s clinic in Berlin there were 40 deaths due to diphtheria 
between 1900 and 1910: 
Heubner’s Statistics. Mortality. 
Injected on the first day 0 
Injected on the second day 3 deaths. 
Injected on the third day 9 deaths. 
It is safe to conclude that: 
1. The prognosis of diphtheria is favorably influenced by antitoxin. 
2. Antitoxin influences local diphtheritic deposits favorably, the ear- 
lier it is used. 
3. If used early there are no advances of the disease to the larynx. 
4. The energetic and early use of antitoxin will save many lives in 
the presence of laryngeal stenosis, unless the cases are malignant. - 
5. The use of antitoxin adds materially to the chances of intubated 
and tracheotomized children and adults. 
6. Antitoxin cures the croup of measles. BACTEKIAL DISEASES 
145 
References 
Ascoli. Deutsch. med. Wchnschr., 1912. 
Baginski. Berl. med. Wchnschr., 1910. 
von Behring. Versammlung Naturforscher u. Arzte, Lubeck. 
Bretonneau. Angina maligna diphth. 1821. 
Councilman. Pathology. Boston, 1912. 
Fibigan. Compt. rend, of XII. Intern. Congress of Med., Moscow, 1898. 
Gervin, Munch, med. Wchnschr., 1908. 
Harris. Practitioner. June, 1912. 
Jores, Romberg & others. Anatom. Grundlagen wichtiger Krankh. 1913. 
Jacobi. Treatise on diphtheria. 
Kautback & Andrews. Allbutt & Rolleston, System of medicine. 2. ed., i, 999. 
Nuttal & Smith. Bacteriology of diphtheria. Cambridge, 1908. 
Netter-Cousin. Semaine medicale, 1905. 355. 
Simon. Arch. d. malad. des enf. 
Rolleston. Allbutt & Rolleston, System of medicine (Kautback & Andrews). 
Trumpf. Pfanndler & Schlossman, Handbuch der Kinderheilkunde, ii, 269. 
Trousseau. Clinical medicine. 
Uppenheimer. Jahrbuch der Kinderheilk. 1904, Bd. x. 
Zucker. P. Krause, Mohr & Staehelin, Handb. der inneren Medizin, i, 246. 
VII. Pneumococcus Infection 
Lobar Pneumonia 
(.Pleuropneumonia, Lung Fever, Croupous Pneumonia, Fibrinous 
Pneumonia, Lungenentziindung) 
The most frequent expression of the systemic infection due to the 
pneumococcus is lung fever—lobar pneumonia. It is a general infec- 
tion usually associated with febrile disturbances, in which large portions 
of one or both lungs are involved in a croupous inflammation, due as a rule 
to the pneumococcus of Sternberg and Fraenkel, though croupous pneu- 
monia may be the local expression of other general bacterial contamina- 
tion. Bacteremia, toxemia, pulmonary consolidation with consecutive 
obstruction and cardiac asthenia, form the complex which demands atten- 
tion and influences the prognosis of the disease. The prognosis is mate- 
rially influenced by the occurrences of double or multiple infections, and 
the further fact that the bacteriology of many of the acute infections 
which often complicate pneumonia is unknown or uncertain (Pye-Smith). 
As soon as it was fully understood that pneumonia is only the local ex- 
pression of a general disease, a step forward was taken which has had a 
powerful influence on prognosis, more particularly the prophylaxis of the 
disease. Sir Herman Weber in England (1869), Juergensen in Germany 146 
SPECIFIC INFECTIOUS DISEASES 
(1876), and Austin Flint, Sr. (1877), in the United States, were pio- 
neers in establishing our modern conception of pneumonia. 
Pneumococcemia 
With modern bacteriologic methods the presence of pneumococcemia is 
established in over 70 per cent of all cases of croupous pneumonia. The 
other and leading local manifestations of general pneumococcus infection 
are tonsillitis, otitis media suppurativa, meningitis, cholecystitis, endocar- 
ditis and arthritis. 
Among the most valuable data showing the influence of pneumococ- 
cemia on the prognosis of croupous pneumonia are those furnished by 
Dochez, from which we quote. The bacteriologic studies of the blood were 
made in 37 cases of lobar pneumonia. “The pneumococcus v7as isolated 
from the blood in approximately 50 per cent of the cases studied. The 
course of the infection in individuals with pneumococcus in the blood 
was more severe than in those in which no organism could be cultivated 
from the blood; 77 per cent of the patients with positive blood-cultures 
died, and 79 per cent of the patients with negative blood-cultures recov- 
ered. In fatal instances of pneumonia, where the pneumococcus was 
found in the blood, the number of organisms per cubic centimeter of blood 
was very high in the last stage of the disease. In individuals dying of 
pneumonia without evident blood infection, the disease w?as charac- 
terized by a rapid spread of the local process in the lungs!” It is believed 
by Dochez as the result of his observations, that the “symptoms of col- 
lapse developing on the fifth or sixth day of lobar pneumonia, are often 
the expression of serious invasion of the blood by the pneumococcus.” 
The virulence of the strain in the individual case as shown by animal 
experimentation and clinical experience has a direct influence on the 
prognosis of the disease. Rosenberger and Dorworth found that 54 per 
cent of their patients in whom blood-cultures showed organisms died; and 
50 per cent of the patients who died showed no blood contamination. Melt- 
zer and Lamar found that by intrabronchial insufflation of cultures of a 
very virulent pneumococcus, typical pneumonia lesions were invariably pro- 
duced. These experiments gave a mortality of 16 per cent and bacteremia 
was present only in fatal cases. Wallstein and Meltzer experimented 
with non-vimdent pneumococcus; they obtained typical consolidation of 
the lungs, with no mortality and no bacteremia. These views according 
to Meltzer, justify the conclusion which is by no means new, that the 
anatomic changes in pneumonia are not the immediate cause of death, and 
they do not present the essential features of the disease; “on the contrary 
they are manifestations of the body’s fight against the disease.” We 
would add that improvement and the favorable termination after crisis 
occur without material change in the structures involved in pneumonia; BACTERIAL DISEASES 
147 
the heart is relieved of its burden in spite of the practically unchanged 
area of consolidation through which it must, for a few days at least, con- 
tinue to force the blood. There is very likely in some way, at the time 
of crisis, a change in the character of the toxins of the pneumococcus.' 
Cole says, that there is “a neutralization of the intoxication rather than 
a destruction of the bacteria existing within the body.” Lees’ epigram- 
matic remark is applicable in the consideration of our subject. “Let it he 
remembered that every case of pneumonia is a fight for life” to which we 
add, no case is so severe that it may not recover; none so mild that it! 
may not become serious. 
In considering the prognosis of pneumonia the factors which concern 
us most are: 
1. The malignancy of the infecting organism. 
2. The effect of the toxemia and the associated local lung lesion on the 
cardiovascular system. 
3. The resistance offered by the patient. 
4. The extent of the pulmonary and associated lesions. 
1. The Malignancy of the Infecting Organism.—The malignancy of 
the infecting organism requires no further consideration. The foregoing 
paragraphs have proved that the prognosis depends very largely upon the 
virulence of the infecting strain, the result of the bacteremia and the 
toxemia. 
2. The Effect of the Toxemia and the Associated Local Lung Lesion 
on the Cardiovascular System.—This is the paramount issue in the prog- 
nosis of pneumococcus infection. We are not dealing with the heart alone; 
we must consider the vasomotors, and the effect of the toxemia on both. 
Passler and Romberg reported a series of experiments which served to 
prove the relative importance in the production of the so-called heart 
weakness of pneumonia, of the heart itself, and of the vasomotor system. 
Experiments made with the pneumococcus and the Bacillus pyocyaneus, 
in which rabbits were inoculated, proved conclusively that the vasomotors 
were weakened and showed evidences of paralysis. 
The prognosis of pneumonia depends largely upon the baneful influ- 
ences which the toxins exert upon the vasomotor centers in the cord. 
Primarily the toxemia leads to cardiac asthenia and vasomotor paral- 
ysis, to which must be added the changes in the right half of the heart, 
the far-reaching degenerative changes in the myocardium, the heart clots, 
and the mechanical obstruction in the pulmonary circuit. 
The effect of pneumococcus toxemia on heart and vessels is malignant; 
but fortunately for the prognosis, it is short lived. The heart and vaso- 
motors therefore are to be cautiously observed for prognostic data. 
Blood-pressure Study.—Associated with the influence on the heart and 
peripheral vessels we find in blood-pressure study a prognostic index of 148 
SPECIFIC INFECTIOUS DISEASES 
great value. For reliable conclusions it is necessary to have full daily 
records, including frequent measurements, which positively lead to the 
early recognition of circulatory embarrassment. 
A systolic blood-pressure much below normal in pneumonia is unfavor- 
able; any great fall is ominous. “When the arterial pressure expressed in 
millimeters of mercury does not fall below the pulse rate expressed in 
beats per minute, the fact may be taken as an excellent augury; while 
the converse is equally true” (Gibson’s rule). 
It does not appear to us that the conclusions of Newburgh and Minot 
are to be accepted as proving that there is no failure of the vasomotor cen- 
ters in pneumonia. Low blood pressure may not “invariably” be “of evil 
omen” but clinical experiences prove that with falling blood pressure, 
loivering pulse amplitude and increasing pulse rate, the prognosis in all 
pneumonics is unfavorably influenced. 
To reach safe conclusions on this subject the pulse pressure data cover- 
ing many cases and a series of years are needed, and these we have secured 
before framing our conclusions. Data from a small material do not 
justify conclusions. 
Cases of pneumonia complicated by arteriosclerosis and chronic nephri- 
tis in which the blood-pressure remains abnormally high during a day or 
two, prove exceptions to the Gibson rule, and offer an unfavorable prog- 
nosis in most cases. The heart tires because of the added burden to force 
the blood through the consolidated lung and the obstructed arterioles. 
An abnormally high blood-pressure with a slow, tense thick pulse early, 
is always of serious significance. 
When considering the prognostic significance of some of the separate 
symptoms we will again refer to the pulse and heart. 
3. The Resistance Offered by the Patient.—“The real predisposing 
moment in the case of pneumonia is to be found, not in those incidental 
and temporary impairments of resisting power which may occur in con- 
nection with mining work (speaking of the Rand) but in that abiding 
defect of resisting power which is normal to the native” (Sir Almroth 
Wright). 
The ability of children to resist all forms of pneumonia is surprising; 
the prognosis during early life is usually good. The mortality of pneu- 
monia during the first year of life is high, from the second year to 
puberty it is comparatively low, from thirty-five to forty it is high, from 
sixty to seventy, three-fourths of all pneumonics die. In old age, on the 
other hand, the disease is in many hospitals and during many seasons the 
principal cause of death. In old age the organs become more independent 
of one another than during early life; “they suffer separately, and the 
various lesions to which they may become subjected are scarcely echoed 
by the economy as a whole.” In old age latency of the disease is fre- 
quent and death may be sudden and unexpected in those who were about, BACTERIAL DISEASES 
149 
as if nothing were wrong with them. In the old as well as in the young, 
the association of diseases of the heart, lungs, kidney or other separate 
systems, which handicap the functions of organs in any way, add enor- 
mously to the danger of pneumococcus infection; this is particularly true 
of metabolic disturbances and arteriosclerosis (Eisner). The obese have 
a reduced resistance to pneumococcus infection, and melt away rapidly 
with symptoms of cardiac asthenia and nervous manifestations. Usually 
coma is a terminal symptom. 
Diabetics when infected with the pneumococcus offer an exceedingly 
grave prognosis. The majority of these cases are atypical and present 
complications which add to the dangers. 
The negro is more subject to the infection than is the white man. The 
inhabitants of the tropics when in their own habitations or in other cli- 
mates show a decided tendency to lung inflammation and have a lowered 
resistance. The report to the Rand Native Labor Association recently 
published is intensely interesting in connection with the fatality of pneu- 
monia among the African native, and especially the tropical native. “It 
was discovered that the blood-serum of whites and tropical natives has 
no immediate power to destroy the germ of pneumonia and that the blood 
of the natives does not acquire this power through either natural infec- 
tion, i. e., an attack of the disease, or artificial infection, i. e., inoculation. 
Power to resist the growth of the pneumococci in the system is acquired, 
however, in some degree by inoculation.” The blood of the African na- 
tive, and especially the tropical native, differs from that of the European 
in being incapable of developing a so-called bactericidal power toward 
pneumonic germs, and is inferior to it in respect of its “immunizing re- 
sponse” or ability to produce antibodies which shall prevent the hostile 
germs from becoming established in the body.” 
Pneumonia has caused a large mortality among the African natives 
working on the Panama Canal; kills large numbers of laborers and sol- 
diers (Wright) in Rhodesia, the African colonies and the Egyptian 
Sudan. 
Pneumococcus infections represent from 3 to 1 per cent of the diseases 
of the civilized races. Those who live in the open air are less disposed to 
pneumonia than are those who live in poorly ventilated or close quarters, 
and they offer greater resistance when infected. The disease is more fre- 
quent among workers who are exposed to storm and wet; among these the 
number of victims claimed is large. 
The excessive use of alcohol is a factor of enormous weight in invit- 
ing pneumococcus infection, and powerfully influences the prognosis. In 
our hospital we have found pneumonia in alcoholics among the most 
fatal of all diseases; the average mortality has rarely been below 50 per 
cent against a mortality of 10.3 per cent among the non-alcoholic patients. 
Alcoholics are usually neglected; they enter the hospitals or call for treat- 150 
SPECIFIC INFECTIOUS DISEASES 
ment when the disease is far advanced and are often nephritics or other- 
wise diseased. 
Traumatism invites pneumococcus infection. Contusions of the thorax 
or perforation of the wall are frequently followed by traumatic pneumonia. 
There are cases in which there seems to be a predisposition, in which 
pneumonia is repeatedly developed. It is surprising to note how well 
the disease is borne by these patients, often the type proves to be abortive, 
but not infrequently the patient succumbs to a second or third infection. 
This is particularly true of children, many of whom develop either catar- 
rhal or croupous pneumonia with every bronchial catarrh contracted or 
with the ordinary infections of early life. 
All experiences prove the greater frequency of the disease among men 
than among women. This is unquestionably due to the greater exposure 
of the former to the hardships of life and inclemencies of the weather. 
The disease shows a large mortality among the mentally defective; 
the higher the grade of these, the lower the death rate. 
Ziemssen many years ago called attention to the fact that the perma- 
nent inhabitants of any locality offer less resistance to pneumococcus in- 
fection than do strangers or new settlers. 
We have found from a study of our material that the prognosis is 
more unfavorable in endemic cases where several members of a family 
are stricken at the same time, than in homes where but one patient is in- 
fected. In the first mentioned there is apparently greater virulence of 
the infecting strain. 
It was formerly held that the robust were subject to the disease; this 
is not true, for we very often find pneumonia the terminal infection of 
many diseases, either infectious, of metabolic origin, associated with, 
cachexias or malignant. 
Pregnant women offer a strong resistance to pneumococcemia but when 
infected the prognosis is grave and abortion is likely to result. 
Immunity following pneumonia is short-lived. One pneumococcus in- 
fection in old and young alike does not cause immunity, but tends to lower 
the resistance against future infection and invites subsequent attacks. 
Unfavorable surroundings, dust, the inhalation of gases, poor ventilation, 
continuous dampness, faulty nutrition, lower resistance, invite the dis- 
ease, and the infected offer a more unfavorable prognosis than do those 
whose environment has been more favorable. 
There are seasonal influences which influence resistance and prognosis. 
The disease is most prevalent during the winter months, the first four 
months of the year particularly, and it is during these months that the 
prognosis is least favorable. 
IV. The Extent of the Pulmonary and Associated Lesions.—It may 
be safely concluded that in the majority of cases the extent of the lung 
consolidation influences the prognosis very materially; this is particularly BACTERIAL DISEASES 
151 
true of double pneumonia. On the other hand there are many cases in 
which the area of infiltrated lung tissue bears no relation to the gravity 
of the disease. There are malignant infections which offer the gravest 
prognosis, in which only a limited part of one lung is involved. It is 
never in any case safe to offer a prognosis from the extent of the consolidcv- 
tion alone. There are always other data, which, when considered, justify 
a forecast of the individual case. Associated lesions, particularly throm- 
bosis, endocarditis, pericarditis nephritis, and many others to all of 
which separate reference are made are powerful factors and influence our 
conclusions. 
Temperature 
Chill.—The graver infections are associated with the most severe in- 
itial chill. Two or more chills are unusual; if these recur at short in- 
tervals during the first day of symptoms a malignant infection may he 
suspected. 
Chills are absent as a rule in children, but convulsions are not infre- 
quent; they are not always an expression of the gravity of the pneumonia. 
Severe, often repeated chills in the adult, with rapid development of 
the local lesion, rapid pulse, increasing evidences of heart weakness, mut- 
tering or active delirium, unfavorable facies and early evidences of pul- 
monary edema, are included in a symptom complex of foudroyant cases, in 
which there is prompt paralysis of the vasomotor centers and death within 
24 to 36 hours. These cases are not frequent. In 14 per cent of our 
cases in adults the initial chill was absent. This was commonly observed 
in alcoholics, or in the aged and in enfeebled subjects. In the aged, with- 
out chill, the disease was of the asthenic type, to which reference will 
again be made. The mortality in these cases is very high. 
In 70 per cent of our influenza-pneumonias there was a severe initial 
chill. When this occurred the disease was of much shorter duration than 
in those cases in which there was no chill. In some of the latter cases 
there were large areas of consolidation, at times remnants of recent pneu- 
monia, without marked subjective symptoms, but in which there were 
positive physical signs. Most of these patients recovered completely. 
In many we found mixed infection, usually pneumococcus and strepto- 
coccus. 
Fever.—Early high temperature in pneumonia without evidences of 
heart weakness is by no means unfavorable. Such cases are often of 
short duration and terminate by crisis on the fifth to the seventh day of 
the disease. The frank fever is an expression of a good reaction. It is 
more favorable to have a high temperature early than after the third to 
the sixth day, unless at that time, it is transitory and is followed by a de- 
cided fall and profuse sweat. 
Sudden rise of temperature after the fifth day, after lysis has com- 152 
SPECIFIC INFECTIOUS DISEASES 
menced or after crisis which persists, is an indication of added complica- 
tion requiring close investigation. 
Under no conditions is the 'prognosis of pneumonia to he dependent 
upon the revelations of the thermometer. Such, reasoning must lead to 
frequent error. I have seen malignant cases in which the temperature 
has been continuously low (101° to 102°) with, marked asthenia and 
limited consolidation. Many of these cases ran atypical courses, were 
uninfluenced by treatment, the heart showing increasing weakness from 
day to day; some proved to be of the migratory type in which there were 
fresh exacerbations with marked adynamia, and most of these died in the 
course of 2 to 3 weeks (subacute types). 
In connection with the study of the temperature, we are never to 
divorce ourselves from the consideration of the pulse (i. e., the heart, etc.), 
the character and frequency of the respirations, the mental state of the 
patient, the character of the sputum, to which the experienced clinician 
will add the general impressions which he receives from his survey, in- 
cluding facies and much which no teacher can specify, but which neverthe- 
less becomes a factor of great value in reaching safe conclusions in many 
cases. 
In the majority of cases in which the temperature remains continuously 
high, uninfluenced by any treatment, there are other symptoms proving 
the malignancy of the infection; in some of these before the end of the 
third or fourth day there are meningeal symptoms with possible hyper- 
pyrexia which promptly increase, and death may follow in from 12 to 24 
hours. 
Fall of temperature to normal or slightly above with increase of respi- 
ratory embarrassment, cyanosis, and feeble pulse, with lowering blood- 
pressure and thin pink watery and profuse sputum, large and small moist 
rales generally distributed, is fatal in over 90 per cent of cases. In 
many cases there is a decided rise of temperature shortly before the crisis 
and in occasional cases there may be one or two exacerbations of tem- 
perature following but it is always of short duration, and convalescence is 
not disturbed. 
Subnormal temperature continuing after crisis for from 24 to 60 
hours is favorable, providing other conditions are equally encouraging. 
A sudden fall of temperature, hut a continuously rapid and unchanged 
weak pulse without a true crisis is not to be interpreted as favorable. 
Prompt and complete crisis is always more favorable than is a slow 
lysis, for with the latter there is greater likelihood of complications. 
So-called unresolved pneumonia, diagnosticated because of the persist- 
ence of fever and other symptoms beyond the reasonable period for crisis 
and lysis, is as a rule due to some discoverable complication; empyema, 
abscess, thrombosis or tuberculosis should be suspected. 
Afebrile pneumonia in the aged is always serious; it is often of grippal BACTERIAL DISEASES 
153 
origin, and may be associated with arteriosclerosis or renal complications. 
In these patients the blood is likely to be surcharged with urea and waste 
products; there is great danger of sudden heart weakness and overpower- 
ing toxemia. 
There seems to be an antagonism between pneumococcemia and uremic 
conditions; when both are present, the temperature is not likely to be 
high, but death is usual between the tenth and fourteenth day, without 
marked respiratory embarrassment, but with great loss of strength and 
nerve force, and vasomotor paralysis. 
The Circulation 
I have already referred to the influence of pneumococcus toxemia on 
the heart and vasomotors in this chapter; the fight for life is successful or 
fails in accordance with our ability to favorably influence the circulation 
during the active stages of the disease. The tendency as the disease ad- 
vances is toward lowering of the blood pressure, weakening of the heart 
muscle, paralysis of the vasomotor centers in the cord, and is often mate- 
rially influenced by the mechanical obstruction in the pulmonary circuit 
and thrombosis of the pulmonary artery. 
The paramount factor in the prognosis of all forms of pneumonia is 
the circulation, i. e., the heart; upon its ability to resist the effect of the 
pneumococcemia largely depends the fate of the patient. The association 
of an enfeebled heart with dilated peripheral vessels is always a serious 
feature. The right heart weakness depends upon the extra burden thrown 
upon the right ventricle by the mechanical obstruction within the pulmo- 
nary circuit and the effects of toxemia; hence the prognosis is worse when 
the consolidation is extensive in the presence of dilatation of the right 
heart and its subjective symptoms. When such symptoms develop shortly 
before crisis, the heart may be bridged over the critical period. 
When with weakness of the right heart, the liver and spleen are en- 
larged and there is marked meteorism with albuminuria} casts and reduced 
quantity of urine, the outlook is bad. 
Cyanosis at any stage of the disease with air hunger, hurried respira- 
tions, rapid feeble pulse, and lowering systolic blood-pressure is among 
the most dreaded of all symptoms. 
Previous disease of the heart handicaps the pneumonic and always 
proves to be a factor with which we must reason in prognosis. The valvu- 
lar lesions, more particularly mitral insufficiency, are more favorable than 
are the degenerative processes as they affect the aorta and the myocardium. 
Mitral stenosis and aortic insufficiency are the least favorable of the 
valvular lesions with pneumonia. I have piloted many pneumonics to 
safe convalescence and complete recovery whom I had previously treated 
for organic diseases of the heart including valvular, arteriosclerotic and 154 
SPECIFIC INFECTIOUS DISEASES 
myocardial changes. Much naturally depends in these cases on the asso- 
ciated conditions. The rule is, that the diseased heart offers less resist- 
ance to the infection than does the normal organ. 
Persistently rapid and small pulse from the beginning, with pro- 
gressively decreasing blood-pressure in the presence of constitutional and 
local symptoms is an expression of heart weakness. Such hearts, if crisis 
is early, may prove sufficient to serve through the infection but they always 
justify the greatest anxiety. 
Increasing rapidity of the heart on the third or fourth day, with at the 
same time evidences of fresh invasion, hurried and unimproved respira- 
tion with scanty albuminous urine, and deep involvement of the sensorium, 
is a serious symptom. 
Irregularity of a previously normal heart, arhythmia or intermissions 
before the crisis and during the first two stages of the. disease, are all to be 
interpreted as indicating the weakening of the circulatory apparatus; with 
or without an alternating pulse these conditions are alarming; they are 
evidences of myocardial involvement. 
The irregularities, intermissions, arhythmias and the erratic behavior 
of the heart during the period of convalescence, with a normal tempera- 
ture, and relief of the inflammatory process, usually with bradycardia, 
while they alarm the patient and the inexperienced attendant, yield after 
rest and without damage. These disturbances are frequent. 
Collapse during the acute stages of pneumonia is one of the dangers 
to be dreaded. This may be due to the sudden flooding of the blood with 
toxins or endotoxins, to sudden acute dilatation of the heart, pulmonary 
thrombosis, or embolism. Not all conditions of collapse in pneumonia 
prove fatal. Timely stimulation and absolute rest saves many lives. 
Often at the crisis there are associated symptoms of heart insufficiency, 
which in most cases are transitory. 
The Respiratory System 
Respiratory Symptoms.—It has been our experience that severe pain 
referable to the pleura of the inflamed lung which persists after the first 
24 hours, with rapid pulse and thin bloody sputum, is evidence of a severe 
pneumonia. The pain is wearing, prevents sleep, robs the patient of re- 
sistance, and interferes with an already obstructed respiration. 
Dyspnea per se is dangerous when it depends upon diffuse bronchioli- 
tis, edema of the lungs, the consolidation of unusually large areas of lung 
tissue or myocardial weakness or degeneration, with dilatation of the right 
heart. 
Frequency of Respirations.—With dyspnea there is always increased 
frequency of respiration. Marked disproportion of the pulse and respira- 
tion is always unfavorable. With a pulse of 110 to 120 and respiration of BACTERIAL DISEASES 
155 
30 to 40 per minute without complications, and no other grave constitu- 
tional disturbances at the height of the disease, the prognosis is good. 
Respirations of 40 to 50 per minute with corresponding increase of 
the pulse and fall of blood-pressure, offer a doubtful forecast. 
Respirations above 50—from 50 to 70—with other symptoms of cor- 
responding severity, are found only in malignant cases which offer but 
slight hope. 
Rapid respirations early, and large moist and crepitant rales, and pro- 
fuse watery pinkish sputum, are all evidences of pulmonary edema and 
promptly lead to death. 
Evidences of obstruction and respiratory insufficiency which include 
with very rapid respiration the active playing of all accessory muscles of 
respiration, are always of grave import. Pye-Smith says “The bearing of 
the respiratory rate on diagnosis and prognosis may be summarized as fol- 
lows : An increased rate due to causes local in the lungs is important in 
diagnosis and unimportant in prognosis; and when it is caused by toxemia,, 
exactly the opposite is true.” 
Cheyne-Stokes breathing is always serious. It is evidence of deep 
poisoning and heart incompetence. 
Hypostatic congestion of the dependent lung is an almost constant 
accompaniment of pneumonia. In severe and fatal cases it is fully devel- 
oped, an expression of heart weakness and in turn throws an extra burden 
on the overtaxed organ. 
Sputum.—The usual appearance and average quantity of sputum are 
found in the favorable cases. 
Persistence of bloody sputum without improvement of constitutional 
symptoms, including fever and rapid pulse, demands a cautious prognosis. 
Excessive and thin sputum with marked dyspnea, hurried respirations 
and cyanosis, is proof of respiratory embarrassment and edema, making 
the outlook exceedingly grave. 
Orthopnea and superficial irregular respiratory movements, without 
ability to expectorate, large rales, noisy breathing, are evidences of the 
terminal stage of heart incompetence. 
Cough.—The most dangerous period of pneumonia includes besides, 
increasing heart weakness, the inability to cough with the accumulation of 
exudate and secretion in the bronchi. With unrelieved pulmonary edema 
these patients literally drown themselves. Free expectoration shows the 
strength of the patient and is of great assistance. We have referred to the 
sputum in previous paragraphs, especially to the significance of the thin 
prune juice pinkish sputum with evidences of edema and again repeat that 
it is always a dangerous symptom. 156 
SPECIFIC INFECTIOUS DISEASES 
The Blood 
Carbon Dioxid.—It has been found that “in pneumonia the diminu- 
tion in the carbon dioxid content of the blood is a constant feature.” “Oc- 
casional cases, however, may fail to show low carbon dioxid” (Peabody). 
This observer further claims: “The carbon dioxid in the blood bears little 
definite relation to the severity of the disease, except that it tends to be 
lowest in severe cases and in the terminal stages of the disease. There is 
less deviation from the normal in short or mild cases.” 
Bacteremia.—We have already considered the significance of bac- 
teremia (pneumococcemia) on prognosis in this chapter and need not there- 
fore repeat at this point. 
Leukocytosis.—In no acute infection does prognosis depend more 
largely than in pneumonia on the protective powers of the blood. The 
assistance, of the leukocytes to combat the invading army of bacteria and 
nullify their toxins is demanded early (phagocytosis'). 
Hekton says: 
“The cure of pneumonia results from the destruction of the pneumo- 
cocci in the lungs and in the blood. This is accomplished by phagocytosis 
and also by extra cellular digestive processes. 
“The predominating general defensive reactions in pneumonia are 
leukocytosis and the production of antibodies for pneumococci, of which 
the opsonins are best known; and these appear to be specific for the group 
to which the infecting pneumococcus belongs.” 
In rapidly fatal cases Ilekton says the defensive reactions are inade- 
quate to destroy the pneumococci which persist and multiply in the lung 
and in the blood, while the free antibodies are absent from the blood. 
In cases which offer a good prognosis the pneumococci are destroyed 
when “antipneumococcal reactions reach a certain height.” 
With lysis there is a gradual, with crisis a prompt destruction of the 
pneumococci in the lungs and in the blood. “In both cases, but demon- 
strated more clearly in crises, there is an excess of antibodies in the blood.” 
The leukocytic count in pneumonia offers valuable prognostic data. 
With severe constitutional symptoms early and a high leukocytic count, 
the outlook for a favorable course is materially strengthened. Counts 
above 25,000 are under such circumstances encouraging. 
High leukocytic counts during the entire first week are favorable. In 
mild infections in which there are moderate constitutional symptoms, 
favorable facies and physical signs, the leukocytic count of 18,000 to 
25,000 considered with all that the case offers, usually justifies a favorable 
prognosis. 
Severe infections which include marked evidences of cardiac toxemia 
with a low leukocytic count, possible tendency to leukopenia, offer only 
the gravest prognosis. BACTERIAL DISEASES 
157 
Severe constitutional symptoms with fair heart strength, often delirium 
with high leukocytic count (40,000 to 50,000) offer encouragement, but 
the prognosis should be guardedly given. 
Decrease of leukocytes with positive crisis is favorable. 
Unchanged leukocytic count with pseudocrisis does not influence the 
course of the disease. 
Rise in the number of polymorphonuclear leukocytes after crisis with 
febrile, movement or other symptoms, is always suggestive of some com- 
plication, usually empyema, plebitis, thrombosis, abscess or other non-tu- 
berculous process. 
Suspicion of a tuberculous complication is justified with fever or per- 
sistence of physical signs, failure to convalesce satisfactorily, and a low 
white count. Such cases may require a number of days before positive 
conclusions are reached. 
Conclusions.—Conclusions from the foregoing statements justify a bad 
prognosis in pneumonia in cases with a low leukocytic count or leukopenia. 
The average mortality in cases without leukocytosis is over 50 per 
cent; often higher. 
Cabot in 329 pneumonics found 32 with white counts of 10,000 or 
less; 30 of these died. The author’s experiences run parallel with these 
figures. 
The leukocytic count bears no relation to the extent of the consolida- 
tion, so far as clinicians have been able to observe. 
High leukocytic counts during the first day or two with rapid decided 
fall following is always grave. This proved to be true experimentally by 
Rosenow, Williamson and others. Pneumonics showing high leukocytic 
counts who die, do not yield to pneumococcus toxemia directly, but to some 
complication such as myocarditis, meningitis, septic or pyemic disease, 
pulmonary thrombosis, or some other secondary disturbance. 
Neutrophilic leukocytosis predominates in pneumonia; this begins 
with the initial chill and continues until crisis. With, or shortly before 
crisis, there is a decided fall in the number of the neutrophilic leukocytes. 
Pseudocrises do not as a rule show marked change in the leukocytic count. 
Complications of inflammatory and pyogenic nature are associated 
with high leukocytic counts; these include abscess, empyema, endocarditis, 
pericarditis, phlebitis, as well as metastatic parotitis, and a variety of less 
frequent complications. 
Eosinophilia is not present until the beginning of crisis; its appear- 
ance one or two days before crisis presages a favorable outcome (Raegeli). 
Lymphocytes are relatively increased before the crisis though there is 
an absolute reduction of these in the blood. 
The complication of ankylostomiasis by pneumonia at once reduces the 
existing eosinophilia. Leichtenstern found a drop of eosinophils to 6 to 7 
per cent from 72 per cent. Warburg from 65 per cent to 0, and a return 158 
SPECIFIC INFECTIOUS DISEASES 
of the eosinophilia with the recovery of the patient. Acute sepsis has the 
same effect. 
Myelocytes are found in moderately severe and grave pneumonia; they 
practically follow crisis (Haegeli, Tiirck, Schindler). 
The blood-plates are always increased in numbers. The French hema- 
tologists have proved an enormous increase of platelets following crisis 
(Crise hematoblastique). 
Fibrin is increased in the blood. Maegeli calls attention to the reduc- 
tion of the fibrin content of the blood in the absence of leukocytosis. 
Miller and Reed (J. A. Miller and M. A. Reed), in a study of the 
leukocytes in pneumonia, found in their series of 40 cases leukocyte 
counts varying from 15,000 to 20,000 in all cases excepting the 10 which 
proved fatal, in which the average of 27 counts was 21,040, while an 
analysis of the records of the leukocyte count in the 514 cases occurring in 
the 5 years—1904-1908—in the First Medical Division of Bellevue Hos- 
pital showed average counts of 20,444 for the patients who recovered, and 
18,827 for those who died. From this the authors conclude that leukocy- 
tosis is as high in the fatal cases as in those which recover, a high leuko- 
cytosis indicating a very severe infection. They found also that the neu- 
trophils vary from 72 to 77 per cent in all classes of cases excepting in the 
very severe infections, where they averaged 81.8 per cent. (Their study 
of the Arneth differential neutrophil count, in which the neutrophils are 
classified according to the lobulation of the nucleus, showed an increase 
in the fewer lobed forms. Ho conclusions of clinical value are drawn from 
this finding.) 
Urobilin in the blood is probably evidence of interference with the liver 
function and the destruction of red blood-corpuscles; its appearance in the 
blood of pneumonics is unfavorable. Connor and Roper found that in 
fatal cases of pneumonia the bilirubin disappeared from the blood within 
8 days of death and that urobilin appeared. 
The coagulation time of the blood is prolonged during the acute stage 
of pneumonia. A return of the time to normal is favorable, and is coinci- 
dent with convalescence. Dochez says, “There seems to be a simultaneous 
increase in the quantity of circulating fibrinogen. The lengthening of the 
coagulation time is probably due to an increased formation of anti throm- 
bin.” Tin's comes from the liver, and it is further held that “the stimulus 
to increased production of these two substances (fibrinogen and antithrom- 
bin) is due to the nature of the infecting agent.” 
The Nervous System 
The gravest pneumococcus infections are likely to cause severe symp- 
toms referable to the nervous system; there are exceptions to this rule. 
But few cases of pneumonia pass through the acute stages without some 
evidences of toxemia of the nervous system. BACTERIAL DISEASES 
159 
The headache of the early stage may often be very severe; its severity 
is in no way related to the gravity of the disease. 
Early delirium is not of serious import. Muttering during sleep is 
usually present, and bears no relation to the nature of the infection in most 
cases. Wild, active delirium with failing pulse, is often evidence of deep 
infection; it may continue until shortly before death and in many such 
cases there is a large and organized thrombus in the pulmonary artery. 
In alcoholics, there are almost always delirium and other evidences of 
alcoholic meningitis, with rapid respiration, albuminuria with casts, and 
death with irregular breathing in coma, after several days of the active 
manifestations mentioned. 
Convulsions in children during the first or second days of pneumonia 
are not often serious; they are of grave import when they occur late and 
are then due to toxic nephritis or to malignancy of the infection. In the 
adult, convulsions during any stage of pneumonia are of serious import. 
Pneumococcus Meningitis.—With convulsions and the Kernig symp- 
tom with or without positive information from examination of the lumbar 
fluid, pneumococcus meningitis must be suspected and an unfavorable 
prognosis should be given. 
We have no record of recovery in which the diagnosis of 'pneumococcus 
meningitis was positively established. 
Spinal Fluid (Lumbar Puncture).—In connection with the prognostic 
significance of the-symptoms of meningitis with pneumonia, we consider 
(a) meningismus and (b) meningitis. 
(a) Meningismus.—Meningismus is also known as meningitis sine 
meningitide, pseudomeningitis, and circumscribed infectious meningitis. 
The study of the spinal fluid and pathologic observations, prove that 
there is no “universal meningitis” in these cases but that the brain, cord 
and membranes are hyperemic and succulent. Here and there are small 
deposits of pneumococci. The spinal fluid contains. an occasional poly- 
morphonuclear leukocyte but no pneumococci. With meningismus the 
prognosis is comparatively good; meningitis may finally develop and 
change the complexion of the case. The condition is frequent in children, 
and at times causes the leading symptoms of brain fever in both children 
and adults during 24 to 48 hours before pneumonia is diagnosed. 
(b) Pneumococcus Meningitis.—The pneumococcus is the most 
frequent cause of pyogenic meningitis. The. diplococcus rapidly multiplies 
in the membranes of the brain and in the spinal fluid. The development 
of symptoms is prompt and the clinical picture clear. As already inti- 
mated the prognosis is absolutely bad. 
The spinal fluid withdrawn through lumbar puncture early (first 12 to 
24 hours) may show no marked change, but soon (within 18 to 36 hours) 
there is increase of fluid, increased pressure (250 to 400 mm. and over), 
and albumin is found. The fluid is cloudy, it may be slightly purulent in 160 
SPECIFIC INFECTIOUS DISEASES 
occasional cases; there are many polymorphonuclear leukocytes and an 
abundance of pneumococci. Culture experiments prove corroborative. 
Cerebral symptoms, including delirium, great unrest with mutterings 
in the pneumonia of the aged, is almost uniformly fatal. 
Postpyrexial Delirium.—The prognosis of the delirium following 
crisis, either during convalescence, or several weeks after recovery, which 
we have called, postpyrexial delirium is good as a rule. In some cases 
there were no mental symptoms during the acute periods of the disease in 
spite of hyperpyrexia, and postpyrexial delirium followed before the end 
of the first week of convalescence. 
The duration of the delirium varied. In children it continued in our 
cases from 2 to 5 days, in adults, aged between 30 and 45 years, from 3 to 
6 weeks; in a few, with bad family histories, subacute or chronic mental 
disturbances developed. The latter sequel was found in our series to yield 
in almost all cases. 
The Urinary System 
Quantity of Urine.—In favorable cases the quantity of urine secreted 
continues considerably reduced, but there is not the great reduction found 
in the most malignant forms of the infection. In the most serious and 
malignant infections the quantity of the urine is reduced to but a few 
ounces. 
Albuminuria is an almost constant attendant of pneumonia; it is not 
always of serious significance. Unless careful and repeated examinations 
are made the foregoing statement will not be verified. 
Toxic nephritis shows abundant casts, marked reduction of the urine 
secreted, large albumin loss and the other characteristics of parenchyma- 
tous nephritis without many blood-cells. Nephritis adds to the dangers 
materially. Overpowering septic nephritis is more serious than are the 
other forms of kidney involvement. In all chronic nepliritides develop- 
ing pneumonia conditions of extreme gravity are presented; these include 
besides the cardiac toxemia, arteriosclerosis and the many associated 
lesions previously mentioned, upon all of which added infection can pro- 
duce only baneful results. 
Chlorid Excretion.—In most cases the chlorids are reduced, and re- 
turn at the end of the acute stage of the disease. Increase of the chlorid 
content may be interpreted as being favorable. 
Urea and uric acid offer no prognostic data. They are increased 
early, are often materially diminished before crisis, and increase within 
the early hours of the crisis or shortly after. 
Sugar.—Glycosuria may appear during any stage of pneumonia; in 
cases which were normal before infection it is usually transitory and does 
not recur after convalescence, neither does it interfere with the progress 
of the case. BACTERIAL DISEASES 
161 
With diabetes mellitus or diabetes insipidus the prognosis of pneu- 
monia is exceedingly grave. Most of these cases are atypical and present 
serious complications. Recovery is among the possibilities. 
The Skin 
The prognostic significance of herpes labialis is debatable. There are 
many who interpret the vesicular eruption favorably, others offer the 
opposite view or claim that it is without marked significance. The weight 
of authority is in favor of a favorable prognosis in the presence of herpes. 
Our conclusion from a study of pneumonias seen during the last 7 years 
proves that the majority of patients with herpes recovered. This subject 
is still sub judice. ISTo reliable clinician will ever offer prognosis based 
on the presence or absence of herpes vesicles. 
Free sweating with decided fall of temperature at crisis is always 
favorable. Excessive stveating with cyanosis and cold extremities, pinched 
facies, small pulse, rapid breathing, often associated with edema of the 
lung is almost always fatal. 
Gastro-intestinal System 
Vomiting' in children, occasionally in adults, does not persist as a 
rule and rarely interferes with the course of the disease: the same may 
be said of diarrhea. 
Membranous colitis is an infrequent complication but is always seri- 
ous. 
Meteorism which persists is of considerable importance; it interferes 
with respiration, throws added work on the heart, causes great discomfort 
by displacing the diaphragm and frequently prevents sleep. 
Hiccough is also wearing and unless controlled may increase the dan- 
gers of the infection. With alcoholics and with the asthenic types of the 
disease it is always ominous. 
Acute Dilatation of the Stomach.—Acute dilatation of the stomach 
due as has been demonstrated (Fussell) to constriction of the duodenum 
at the root of the mesentery, with probable primary involvement of the 
innervation, is one of the gravest complications of pneumonia. When it 
arises suddenly during the height of the disease it may promptly lead to 
death unless relieved. Sudden dilatation of the stomach with chronic 
valvular disease and pneumonia is almost always fatal. Prompt recog- 
nition of the acute dilatation of the stomach and the use of the stomach 
tube will remove the dangers due to this complication. 
Slight jaundice is not serious; deep jaundice with marked nervous 
symptoms is always grave (See Bilious Pneumonia). 162 
SPECIFIC INFECTIOUS DISEASES 
Spleen 
The spleen offers no data of significance in the prognosis of the disease. 
It is not much enlarged; in only 35 of 100 cases was the weight above 200 
grams (Osier). 
Hemorrhagic infarcts of the spleen with pneumococcus endocarditis 
or abscess, add to dangers already grave. 
Physical Signs 
The prognostic significance of the physical signs referable to the con- 
solidation must be interpreted in connection with the associated symptoms 
referable to the heart and vascular system separately. They offer but 
insignificant evidence of existing danger save in those cases where there 
is respiratory insufficiency with pulmonary edema and with far-reaching 
consolidation and atelectasis. The dangers of pneumonia are often out 
of all proportion to the extent of the physical signs. 
With central pneumonia there may be overpowering toxemia before 
the disease can be localized by the objective and positive manifestations 
of consolidation. 
Clinical Varieties of Croupous Pneumonia 
Afebrile Pneumonia.—We have already referred to the possibility of 
serious pneumonia without rise of temperature. These cases may lead 
to crisis just as do the febrile types of the disease. The association of 
nephritis with such infection and the influence of uremic poisoning we 
have already considered in this chapter. In old patients there is reason 
to fear for the outcome in these cases. 
Bilious Pneumonia.—In the grave cases there is deep jaundice, albu- 
minuria with casts, reduced and concentrated urine, cerebral disturb- 
ances ; these often include active delirium. There is, in most, infection 
of the bile passages; this may be of the mixed type (pneumococcus with 
either streptococcus, staphylococcus or other contamination). The added 
complication is a handicap. The mortality of our cases was about 35 per 
cent (this includes only those with deep jaundice and the clinical picture 
given in this paragraph). 
Pneumonia of the Alcoholic.—We have repeatedly referred to the 
pneumonia of the alcoholic and need not repeat. 
In our hospital experiences we have found that the majority of alco- 
holics who die with symptoms of meningitis, delirium tremens or other 
acute manifestations, show on post mortem examination the presence of 
pulmonary consolidation. 
Asthenic Pneumonia.—Friedrich Miiller has given a very clear clin- 
ical picture of asthenic pneumonia. In these asthenic types of the disease 
we find the subject reduced as a rule by previous disease; the pulse is BACTERIAL DISEASES 
163 
weak and small; the consolidation is usually limited; there is great unrest, 
marked delirium and many evidences of an atypical course. There may 
be no initial chill, and the sputum may never be rusty. The spleen is 
enlarged, pericarditis and endocarditis are frequent complications. En- 
demic influences are paramount. These cases, because of the adynamia 
and the multiplicity of complications offer an uncertain, often unfavor- 
able prognosis. 
Migratory Pneumonia.—The prognosis of migratory pneumonia con- 
tinues uncertain during long periods; the disease is exceedingly dangerous. 
There are repeated fresh invasions of lung tissue and in most there 
is added streptococcus infection. The duration of these cases varies. It 
may be 3 weeks, often longer, and occasionally the patient dies after 
several months of mixed infection. In some of these there is also malig- 
nant endocarditis; all with this complication die. 
Embolic Pneumonia.—Embolic pneumonia is often an expression of 
malignant endocarditis (pneumococcus or other infection). There are 
wedge-shaped infarcts; the symptoms are atypical, and the prognosis is 
grave. 
Influenza Pneumonia.—Influenza pneumonia has been fully consid- 
ered in the chapter on Influenza. 
Hypostatic Pneumonia.—Hypostatic pneumonia accompanies acute 
and chronic infections or disease in which there has been preceding hypo- 
static congestion. It always adds a large element of danger, and is often 
an expression of an insufficient myocardium. It is often a sequel of 
chronic disease in old people who have been bedridden during long pe- 
riods; often ends life after fracture of the hip, after operations in the 
decrepit, and in chronic brain and spinal lesions. 
Aspiration Pneumonia.—Aspiration pneumonia, due to the entrance 
of foreign substances into the lung, following ether anesthesia, or asso- 
ciated with paralyses—bulbar, glossopharyngeal—diphtheria, and other 
acute and chronic diseases, is serious if the associated condition is grave. 
The close study of the clinical history with the influence of the symptoms 
separately considered is needed to clear the horizon for prognosis. 
Pneumonia and Tuberculosis.—Pneumonia complicating tuberculosis 
is partially considered in connection with pulmonary tuberculosis. 
These cases include: 
I. Acute croupous pneumonia, in which the disease attacks an area of 
lung tissue, the greater part of which is the seat of infiltrating but latent 
tuberculosis. The prognosis is not necessarily bad; many under favorable 
conditions recover. 
II. Cases in which there is (a) an acute croupous or catarrhal pneu- 
monia in the immediate vicinity of tuberculous areas. The disease may 
run its course, terminate by crisis or lysis. There is usually no hemop- 
tysis. 164 
SPECIFIC INFECTIOUS DISEASES 
(b) Chronic or subacute pulmonary tuberculosis in which pneumonia 
attacks distant parts of the diseased or previously healthy lung, in which 
there is no early hemoptysis, but in which the tuberculous process is 
actively progressive. The prognosis of these cases is bad. 
III. Cases in which there is mixed infection (pneumococcus and 
streptococcus) in which the acute pneumonic consolidation is added either 
to a latent or an active pulmonary tuberculosis. Hemoptysis is an early 
symptom of the acute exacerbation, or immediately precedes the pneu- 
monia, the latter depending on the aspiration of infecting agents from 
the seat of the original tuberculous infiltration, which is usually disor- 
ganized. The prognosis of this type is bad. 
I\r. Cases of acute croupous or catarrhal pneumonia with concurrent 
tuberculous infection. This complex is usually found in patients with 
lowered vitality resulting from childbearing, alcoholism, or unfavorable 
environment. In these patients there is in a short time disorganization 
of lung tissue, cheesy infiltration, coagulation necrosis, hectic fever, and 
death. 
The complications which influence the prognosis of pneumococcus in- 
fection not previously fully considered in this chapter are: (1) Pulmo- 
nary edema, (2) Gangrene of the lung, (3) Empyema, (4) Pleurisy 
(serous), (5) Bronchitis, (6) Bronchorrhea, (7) Abscess of the lung, 
(8) Emphysema, (9) Purulent infiltration of the lung, (10) Fibrosis 
of the lung, (11) Pericarditis, (12) Endocarditis, (malignant and be- 
nign), (13) Arthritis (suppurative and non-suppurative), (14) Suppu- 
rative peritonitis, (15) Otitis media suppurativa, (16) Purpura, (17) 
Neuritis (peripheral), (18) Metastatic parotitis. 
1. Pulmonary Edema.—Pulmonary edema may develop early, when 
it literally drowns the patient in his own serum. Such cases are of the 
foudroyant type and die within the first 2 or 3 days of the disease. When 
pulmonary edema develops after the first stage of the disease, and is not 
promptly controlled it is amolng1 the most serious complications of pneu- 
monia. 
Pulmonary edema is always a life threatening complication. Re- 
peated reference has been made to its association with the clinical types 
in the previous pages. 
2. Gangrene of the Lung.—Gangrene of the lung is not a frequent 
complication. Pye-Smith reports 37 cases in 7,868 pneumonics. When 
extensive it is usually fatal. When circumscribed, recovery followed in 
several of my cases; such recoveries are always slow. Some cases lead 
to long periods of sepsis; loss of strength and flesh is progressive, and 
death occurs after several months. 
3. Empyema.—Pneumococcus empyema offers a more favorable prog- 
nosis than do any of the other infections which may cause it. 
Complications BACTERIAL DISEASES 
165 
Children develop empyema oftener than do adults. The incidence of 
this complication varies with different years and with different epidemics; 
the statistics are therefore unreliable unless the average covers several 
years. Such statistics of our cases show an average of 6 per cent in our 
pneumonias of the past 7 years. 
The early recognition of empyema and its prompt and radical treat- 
ment in all ages offers an excellent prognosis in the absence of other com- 
plications. This subject is fully treated in another chapter (See Purulent 
Pleurisy). 
4. Pleurisy (Serous and Fibrinous).—Pleurisy following pneumonia 
is usually promptly relieved, if detected early. But few cases of lung 
inflammation pass to convalescence without more or less inflammation of 
the overlying pleura during the second or third stage of the disease. The 
prognosis in uncomplicated cases is good. In the fatal cases of pneumonia" 
pleurisy is found in over nine-tenths of all cases, but is not the cause of 
death. 
Unrecognized pleurcd effusion, which displaces the lung and surround- 
ing organs during long periods in which spontaneous recovery follows, 
may cause permanent damage because of adhesions and consecutive inter- 
ference with the functions of separate organs (See Serous Pleurisy). 
When pleurisy becomes chronic, there is always danger of fibrosis of 
the lung, i. e., final chronic interstitial pneumonia (See Chronic Inter- 
stitial Pneumonia). 
5. Bronchitis and Bronchiolitis.—In old people and very young chil- 
dren bronchitis of the smaller tubes is often a serious complication. 
In adults, complicating bronchitis has less influence on prognosis than 
in other forms of the disease, more particularly bronchopneumonia. Most 
cases of croupous pneumonia have more or less bronchitis as a complica- 
tion. 
6. Bronchorrhea.—Bronchorrhea may either precede or follow pneu- 
monia. Bronchial dilatations may harbor disease-producing organisms 
and lead to further complications. Many patients who have bronchor- 
rhea seem predisposed to repeated but limited croupous or catarrhal pneu- 
monic processes. 
Chronic bronchitis with bronchorrhea may, in the presence of acute 
pneumonia, particularly when there is associated emphysema, interfere 
with the overburdened organs of respiration and throw added work on 
the right heart. 
7. Abscess of the Lung.—All of our cases of superficial lung abscess 
in which we made early diagnosis and treated radically, made satisfactory 
recoveries. Deep seated abscess of the lung is not frequent and is usually 
fatal; many of these cases are discovered post mortem. Multiple abscesses 
are found with mixed (pyogenic and pneumococcus) infection, are a part 
of an existing pyemia and are fatal (metastatic abscesses). Abscess of 166 
SPECIFIC INFECTIOUS DISEASES 
the lung may lead to or may be associated with gangrene, and the outcome 
is grave. Superficial abscess may break into the pleural cavity, into a 
bronchus, into the mediastinum or pericardium. Rupture into the pleural 
cavity leads to pyopneumothorax. All of these accidents are serious. Ab- 
scess of the lung with empyema offers a less favorable prognosis than does 
the latter alone (See Empyema). 
8. Emphysema.—We referred to emphysema in considering bronchor- 
rhea with chronic bronchitis. Emphysema may complicate acute pneu- 
monia involving healthy lung tissue, and is largely a compensatory hyper- 
trophy; it is physiological and does not influence the progress of the 
primary infection. 
9. Purulent Infiltration of the Lung.—Purulent infiltration of the 
lung may occur during the stage of grey hepatization. It is held by some 
authors to be identical patholigically with abscess (Beitzke), and by many 
is considered to be uniformly fatal. Pye-Smith expresses the belief “that 
purulent infiltration need not be fatal, but may end in complete recovery’’ 
and holds further “that it is nothing more than an acute edema of the 
lung in a stage of grey hepatization, and that it marks the complete arrest 
of the process of resolution for the time being.” We have reason to be- 
lieve from our experience with conditions diagnosed as purulent infiltra- 
tion complicating pneumonia that the contentions of Pye-Smith are 
correct—that while the condition is serious, it is not necessarily fatal. 
10. Fibrosis of the Lung.—Fibrosis of the lung following pneumonia 
is not frequent. The pathologic changes are identical with chronic inter- 
stitial pneumonia which is separately considered (See Chronic Pneu- 
monia). Probably deep pleural changes which become chronic are 
responsible for the connective tissue overgrowth. The condition is always 
chronic; patients may live during many years and usually die of intercur- 
rent disease, or tuberculization may follow. 
11. Pericarditis.—Inflammation of the pericardium may with pneu- 
monia be either serous or purulent. The serous effusion is less serious 
than is the purulent. The latter is more likely to run an acute course, the 
former is often subacute or may merge into a chronic state. 
Pericarditis may be an early or a late complication; it is more fre- 
quent with inflammation of the right lung. 
Post mortem statistics prove the presence of pericarditis in 10 to 12 
per cent of the pneumonias examined. Chatard found 35 cases of peri- 
carditis in 658 pneumonias at Johns Hopkins Hospital of which 31 died. 
These figures prove the great danger of the complication. 
Purulent pericarditis complicating the early stages of pneumonia is 
almost uniformly fatal. Pneumonics who live beyond the acute stage 
with pericarditis and effusion offer encouragement for radical surgical 
treatment. 
Myocarditis or myocardial degeneration is an almost constant accom- BACTERIAL DISEASES 
167 
paniment of pericarditis adding to its dangers. Acute dilatation of the 
ventricles with myocarditis and pericarditis is a frequent cause of sudden 
death. 
12. Endocarditis.—Endocarditis may be either (a) malignant or (b) 
benign. Preexisting endocarditis always adds to the danger of pneu- 
monia. It is at once a serious handicap for the heart; it is unfavorably 
influenced by the toxemia and the mechanical obstructions—conditions 
with which it is less able to cope than is the normal heart. 
(a) Malignant Endocarditis.—The diseased heart valves invite 
the deposit of pneumococci, acute exacerbations of endocarditis result, 
'pneumococcus endocarditis develops which may run an acute or exceed- 
ingly chronic course with multiple infarcts in the various organs of the 
body and which in the end kills the patient. We have not a single case 
of recovery of pneumococcus endocarditis to report in which the diag- 
nosis was positively confirmed by blood cultural methods (See Malignant 
Endocarditis). 
(b) Benign Endocarditis.—Endocarditis complicates between 6 
and 10 per cent' of pneumonias, but a small per cent of these are of the 
malignant type, and the majority therefore yield to treatment. There are 
many associated conditions which influence the prognosis of all forms of 
endocarditis complicating pneumonia; among these are, as with pericardi- 
tis, the associated myocardial degeneration and vasomotor paralyses. 
All features must receive careful consideration before the clinician com- 
mits himself. It will always be wise to give guarded prognosis with all 
heart complications in pneumonia. 
13. Arthritis.—In our experience suppurative arthritis has been 
so rare as to require but casual mention. The complication is more fre- 
quent in children than in adults. One large joint is usually involved 
which finally suppurates. The condition is grave and leads to death in 
one-half of the cases, or to permanent damage to the joint. When the 
complication is early it is most serious. Eon-suppurative polyar- 
thritis only occasionally complicates pneumonia; it may interfere with 
convalescence, rarely materially influences prognosis. 
14. Suppurative Peritonitis.—Suppurative peritonitis is mentioned 
by Pye-Smith as having occurred in 22 of his 7,868 cases of pneumonia 
—0.3 per cent. We have never, in our experience met with a case. 
15. Otitis media suppurativa.—Uncomplicated middle ear inflamma- 
tion is a frequent complication of the pneumonia of children; but few 
adults suffer. When radically treated early otitis does not influence the 
prognosis of the primary infection. Neglected cases or those overlooked 
may lead to sequeke; among thees are meningitis, septic or pyemic con- 
ditions, cerebral thrombosis, abscess of the brain and other distant 
disturbances. 
16. Purpura.—Purpuric conditions which develop during the active 168 
SPECIFIC INFECTIOUS DISEASES 
stages of pneumonia are always serious. In such cases the prognosis is 
exceedingly grave. 
Purpuric conditions which develop after the acute stages are either 
due to the malignant pneumococcus endocarditis (petechise, infarcts, etc.), 
or they may be an expression of a depraved blood state. If the latter con- 
dition is the cause of the symptoms, there are likely to he hemorrhages 
from mucous membranes and skin lesions; the prognosis is good, but 
convalescence is slow. When purpuric symptoms are due to septic emboli 
(malignant endocarditis) there are as a rule no hemorrhages from the 
mucous membranes, but infarcts into vital organs, including brain, kid- 
ney, spleen and lung, with characteristic symptoms. The prognosis is 
unfavorable. 
17. Neuritis (Peripheral).—Multiple neuritis may complicate con- 
valescence; it was found in few! of our cases. Recovery is slow but cer- 
tain. In the few cases we have seen the four extremities have been 
involved. 
18. Metastatic Parotitis.—Metastatic parotitis is considered in a sepa- 
rate chapter (See Metastatic Parotitis). 
With pneumonia it is always serious and is often associated with the 
more malignant infections, especially malignant endocarditis. 
There are no organs of the body which may not be involved during 
an acute pneumonia and complicate it. To consider all of the possible 
complications would lead us into an exhaustive study of the entire field 
of pathology (Jurgensen). With the data given in this chapter the lead- 
ing factors which influence prognosis are brought within the reach of the 
reader. 
Statistics and the Results of Treatment 
We quote from our article (Eisner): “Hospital statistics, which it 
may be assumed offer the only collective information available which 
shows the results of treatment, are misleading and often unjust. Neg- 
lected cases are found in all services and are numerous; many alcoholics 
are brought to our -wards moribund; not a few cases treated from the be- 
ginning of the infection in private homes without adequate nursing 
finally enter the hospital wards to die. All of these cases showing a high 
mortality are included in published statistics, and are received by the pro- 
fession and the lay world as representing the actual results of our fight 
against the disease. 
In my recent service at St. Joseph’s Hospital in Syracuse, we received 
into our wards 34 cases of pneumonia, of which 8 died; of this number 5 
died within the first 24 hours following admission. Our published mor- 
tality was 23.5 per cent, whereas the results of treatment, or more prop- 
erly, the mortality of cases receiving hospital care during more than 24 
hours, presented a more hopeful picture. Of the remaining 29 cases only BACTERIAL DISEASES 
169 
3 died, and of these, 2 were chronic alcoholics—a mortality of only 10.3 
per cent. These statistics are repeated in the wards of all general hospi- 
tals year after year, and lead the thoughtful to the conclusion that the 
truth concerning the effect of treatment can be reached only after a 
thorough analysis of statistics and the grouping of cases.” 
It may be concluded that the rational modern treatment of pneumonia, 
including careful nursing, materially influence the prognosis of the 
disease. It is a mistake to subscribe to the ancient dictum that the healthy 
and active offer a less favorable prognosis than do the weak and sickly. 
The Influence of Prophylactic Vaccination 
It would seem that with pneumonia as with typhoid fever, we may 
hope that prophylactic inoculation will finally influence the frequency 
and, the course of the disease. The observations of Sir Almroth Wright 
definitely proved that preventive inoculation in the Premier diamond 
mine only 5 per cent of the inoculated natives contracted pneumonia as 
against 10 per cent of the uninoculated, and that the percentage of deaths 
was: inoculated 1 per cent, uninoculated 3 per cent. 
There are at the present time no evidences which prove that vaccine 
therapy influences the prognosis of actual pneumonia. 
2. Bronchopneumonia 
(Insular Pneumonia, Catarrhal Pneumonia, Lobular Pneumonia, Desqua- 
mating Pneumonia, Secondary Pneumonia, Capillary Bronchitis) 
Bronchopneumonia is almost always secondary to preexisting bronchial 
catarrh; it is a catarrhal inflammation of the bronchioles with characteris- 
tic changes in the parenchyma of the lung, including exudation into the 
air cells which is highly albuminous, usually non-coagulable, containing 
desquamated epithelial alveolar cells, leukocytes and few erythrocytes. 
The desquamated epithelium undergoes fatty and cellular degeneration as 
the disease progresses. The exudate fills the air cells invaded. The 
alveolar walls are hyperemic and are infiltrated with round cells. The 
fibrin content varies. In cases following measles and diphtheria in chil- 
dren, fibrin is often present in large amounts wfith the cellular elements 
which justify the diagnosis of fibrinous bronchopneumonia. 
Primary bronchopneumonia is not frequent. Less than one-fourth of 
all cases are primary. This is probably a higher figure than would be 
justified if full histories were always obtainable. In children after the 
second year the prognosis of primary bronchopneumonia is relatively 
good. Younger babes show less resistance, but the prognosis cannot be 
considered absolutely bad (25 to 40 per cent). 170 
SPECIFIC INFECTIOUS DISEASES 
The lesions, in contradistinction to the lobar form of pneumonia, are 
lobular, multiple, and invade both lungs. Confluence of islands of disease 
is frequent. 
Bronchopneumonia is a disease of early and of late life. 
The catarrhal inflammation of the bronchioles of influenzal origin is 
frequently followed by lobular pneumonia, and has been considered in the 
chapter on influenza (See Influenza). 
Lobular pneumonia is the characteristic inflammation of the lung 
which complicates diphtheria, scarlet fever, measles, whooping cough, 
typhoid and typhus fever, plague, bronchitis, bronchiolitis and other acute 
infections. 
Clinical data which are fully discussed in connection with pneumo- 
coccemia and lobar pneumonia are largely applicable in reaching conclu- 
sions for prognosis in bronchopneumonia, and to these the reader is re- 
ferred (See Pneumococcemia). 
Complications of Bronchopneumonia 
Bronchopneumonia is oftener complicated by atelectasis than is lobar 
pneumonia, and when large areas of lung tissue are collapsed, the prog- 
nosis is correspondingly bad. 
The prognosis must of necessity depend very largely upon the nature 
of the primary disease and the other factors to which full reference was 
made in the Section on Croupous Pneumonia, including: 
I. The malignancy of the infecting agent. 
II. The effect of the toxemia and the associated local lung lesions on 
the cardiovascular system. 
III. The resistance offered by the patient. 
IV. The extent of the pulmonary and associated lesions. (For full 
consideration see Pneumococcemia). 
Bronchopneumonia is in many cases an expression of pneumococcus 
infection; it may be of streptococcus, staphylococcus, meningococcus, mi- 
crococcus catarrhalis, influenza bacillus, diphtheritic, bacillus coli or other 
bacterial origin. Mixed infection is frequent; usually the pneumococcus 
is found with some one of the infecting agents mentioned in the preceding 
paragraph. 
Pneumonic plague has been separately considered (See Plague). 
The prognosis of bronchopneumonia must always depend upon the 
character and cause of the preceding disease or accompanying bronchitis, 
the virulence of the specific associated microorganism, and the nature of 
the inspired or aspirated substances which were paramount in causing 
extension of the disease. 
The cases of aspiration bronchopneumonia are included in a separate 
class, and the prognosis also depends upon the cause of the entrance of the 
foreign and the infecting substances. BACTERIAL DISEASES 
171 
Aspiration pneumonia with cerebral apoplexy, bulbar paralysis, diph- 
theritic paralysis, uremia, associated with tracheotomy or other operative 
measures, cancer of the upper air passages, is almost always fatal. 
Bronchial hemorrhage may lead to catarrhal pneumonia; the prognosis 
is usually favorable. 
Cases in which the exudate is hemorrhagic are associated with the most 
malignant infections and are always serious. 
The ability of children to resist bronchopneumonia is often surprising: 
better after the second year than before. Obese children, those with ra- 
chitis, the syphilitic, and the tuberculous, offer reduced resistance and 
cloud the prognosis. Conditions in children may be extreme, the picture 
may appear hopeless and yet full restoration to health may follow. Cya- 
nosis and extensive atelectasis are unfavorable features. 
Special symptoms offer the same relative prognostic significance in 
bronchopneumonia as in lobar pneumonia (See Lobar Pneumonia: Pneu- 
mococcemia). 
It may be added to what has been said that early high temperatures are 
not to be interpreted as necessarily serious, but late hyperpyrexia is always 
an expression of uncontrolled disease and makes positive prognosis impos- 
sible. 
Low temperatures, i. e., to 101° F. or lower, are often an ex- 
pression of weakness; are found at times in cachetic children, those who 
are exhausted and without resistance. 
The disease in young children is of longer duration than is lobar pneu- 
monia: it may last from 7 to 21 days. Protracted cases usually die. 
Relapse is frequent. 
The Significance of the Complications 
There are fewer remnants of disease and complications than in lobar 
pneumonia. The significance of the few which are found may be studied 
in the chapter on lobar pneumonia. 
Septic lesions are rare after bronchopneumonia. 
The bronchial nodes are often enlarged; they may become tuberculous 
or they may, as has been repeatedly suggested in the consideration of pul- 
monary tuberculosis (See Tuberculosis), hold a latent focus during many 
years which may finally lead to active disease. 
The prognosis of pneumonia is less favorable in children with measles, 
whooping cough, diphtheria and scarlet fever than in those who had simple 
bronchitis of the larger bronchi before the lung infection. 
Our mortality in private practice in children is not above 10 per cent. 
In hospital practice it is much higher, 12 to 30 per cent. 
Aspiration, ether pneumonia and pneumonia in children following the 
entrance of foreign substances into the lung are all exceedingly grave dis- 
eases. 172 
SPECIFIC INFECTIOUS DISEASES 
The approach of bronchopneumonia may be expected in children when 
in the midst of an acute infection associated with bronchitis the respira- 
tions are suddenly increased, there is increased movement of the respira- 
tory and accessory muscles, the temperature shows a decided rise, and the 
pulse is correspondingly accelerated. 
In the aged bronchopneumonia is one of the most frequent causes of 
death. Statistics are of but little value because the primary conditions are 
often so serious that it is difficult to determine accurately their relative 
importance in the prognosis of separate conditions. It may be assumed, 
however, that in the aged, the secondary bronchopneumonia is the terminal 
complication which hastens death (See Influence of Age, etc.; chapter 
Pneumococcemia. 
With typhoid fever, long continued hypostatic congestion, adynamia, 
and often atelectasis, the prognosis continues grave, and the forecast un- 
certain during several days. 
Chronic pneumonia, bronchiectasis and emphysema are occasional se- 
quel of bronchopneumonia. 
Catarrhal pneumonia is more fatal than lobar pneumonia. 
The more acute the course, both in children and in adults, the better is 
the prognosis. 
The more extensive the inflammatory process, the greater is the danger 
to the patient. 
The combination of meningitis and catarrhal pneumonia offers only 
the most dismal prognosis. 
In reaching conclusions concerning the influence of the heart and vas- 
cular system the data given in connection with pneumococcemia should be 
studied. 
Marled leukocytosis is favorable, but blood pictures are less reliable 
than in lobar pneumonia because of the influence of the primary infections 
in most cases. 
The further considerations of the prognosis of bronchopneumonia is 
considered in connection with the many diseases which it may complicate 
in the separate chapters dealing with such diseases. 
References 
Beitzke. Aschofj Path. Anatomie. Jena, 1913, 2. Aufl. 
Cabot (R.). Clinical examination of the blood. 
Chatard. Osier’s Practice of medicine. 1912, 96. 
Cole. Report Path. Sect. Am. med. Ass., 1912, 39. 
Connor & Roper. Arch. Int. Med., Chicago, 1909. 
Dochez. J. Exper. Med., Nov. 1, 1912. 
Eisner (H. L.). Treatment of Pneumonia, Forchheimer System, etc. Appleton, 1913, ii. 
Fussell. Am. J. Med. Sci., Dec., 1911, 794. BACTERIAL DISEASES 
173 
Hekton. J. Am. M. A.ss., Jan. 24, 1914. 
Jurgensen. Handbuch der Krankheiten des resp. Apparat. Leipzig, 1877, ii. 
Lees. The Practitioner, London, Apr., 1908. 
Meltzer & Lamar. Report Path. Sec., Am. M. .Ass., 1912, 44. 
Miller (J. A.) & Reed (M. A.). Arch. Int. Med., May, 1912, ix. 
Muller (Friedrich). von Mehring u. Krehl, 8. ed., Jena, 1913. 
Naegeli. Blutdiagnost., etc., 1912, 2. Aufl. 
Newburgh & Minot. Arch. Int. Med., July, 1914. 
Osier. Practice of medicine, 8. ed., 1913. 
Passler & Romberg. Deutsch. Arch. f. klin. Med., 1905. 
Berl. klin. Wchnschr., 1896. 
Deutsch. Arch. f. klin. Med., Bd. Icxxii. 
Peabody. J. Exper. Med., Nov. 1, 1912. 
Plaut, Rehm, & Schottmiiller. Cerebrospinalfliissigkeit. 1913. 
Pye-Smith. Allbutt & Rolleston, System of medicine. 2. ed., v. 
Rosenberger & Dorworth. New York Med. J., March 15, 1913. 
Rosenow. Ref. fol. haem., 1904, 651. 
Schindler. Ztschr. f. klin. Med., 1904. 
Tiirck. Blut b. akut. infect. Krank. Wien, 1898. 
Wallstein & Meltzer. Report Path. Sec. Am. Med. Ass., 1912. 
Warburg. Naegeli, Blutkrank. u. Blutdiagnostik. 1912, 2 Aufl., 679. 
Williamson. Ziegler’s Beitrdge. 1901, Bd. xxix. 
Wright (Sir Almroth). Report, Rand Native Labour Ass., Jan. 2, 1914. 
Ziemssen. (quoted) Handbuch der Krankheiten des resp. Appar. {Jurgensen). 1877. 
VIII. Erysipelas 
(Die Rose, Rotlauf) 
Etiology 
The Streptococcus Erysipelatis.—Erysipelas is an infectious, con- 
tagious disease caused by the Streptococcus erysipelatis, a strain of the 
streptococcus longus, also known as Streptococcus erysipelatos hemolyticus 
(Schottmiiller), which gains entrance to the lymphatic spaces of the skin 
through an abrasion and causes local inflammatory changes, sometimes 
suppuration, often general sepsis and other complications. The disease is 
likely to recur; there is in some people a remarkable susceptibility and 
vulnerability which makes them ready to develop erysipelatous inflamma- 
tions at short intervals, on slight cause, not infrequently when the standard 
of health is lowered. 
Port of Entry.—Excoriations of the shin about the nose, and an eroded 
nasal mucosa are the most frequent ports of entry of the streptococcus; 
hence facial erysipelas is the most frequent form of the disease. 174 
SPECIFIC INFECTIOUS DISEASES 
Traumatism (surgical and non-surgical) causes'fewer cases at present 
than before the days of antisepsis when erysipelas was feared not only by 
the physician but more by the surgeon and obstetrician. Hospital wards, 
maternity and surgical, were at times of epidemics decimated by the infec- 
tion following operations and labor. The mortality in hospitals and public 
institutions at times of peace and during war in the past, has been alarm- 
ing, reaching from 7 to 25 per cent and higher, until at present owing to 
modern precautions the presence of erysipelatous infection in a hospital 
ward creates a strong suspicion of carelessness, which cannot always be 
charged to the attendants but should always be recognized as a preventable 
complication. 
Period of Incubation.—The period of incubation is short—not longer 
than from 3 to 4 days as a rule—though in the rapidly spreading and 
sthenic types of the disease it may be but 24 hours. 
Complications Influencing Growth of the Infection 
The more virulent and malignant cases, running a rapid course, are 
found in alcoholics and those debilitated by dissipation and chronic dis- 
ease. 
With cirrhosis of the liver and chronic nephritis, erysipelas is always 
a serious complication; also in the obese and those suffering from chronic 
heart lesions. 
Puerperal erysipelas is among the most serious complications of child- 
birth. The mortality varies in accordance with the virulence of the infect- 
ing strain, the resistance and age of the patient, the extent of the disease 
and the trauma, and the ability of the vasomotors and myocardium to with- 
stand the toxemia. It is never to be lightly regarded. 
Erysipelas of the newborn (umbilical) involving the skin and umbil- 
ical cord is often associated with phlebitis and offers a grave prognosis; 
most babes thus infected die. 
Erysipelas of the aged is always associated with great danger, greater 
when there is cardiovascular or renal disease coexistent. With diabetes 
and erysipelas the prognosis is almost always unfavorable. 
Local Manifestations 
The more extensive the local manifestations of infection, the more out- 
spoken are the constitutional symptoms. Tendency to migration of skin 
lesions is found in the less acute cases; the course of these is often tedious 
and convalescence, slow. Such cases often offer a serious outlook, they may 
complicate streptococcus tonsillitis due to milk infection or epidemics of 
streptococcus infection of unknown origin. Such a case we recently saw 
during an epidemic which spread over several townships in which the ini- BACTERIAL DISEASES 
175 
tial infection was tonsillar; later there were from 6 to 8 weeks of migra- 
tory erysipelas, in which the entire surface of the body was involved at 
various times, with final meningitis and death. 
Bloody vesicles with petechice and limited sloughs with other evidences 
of purpura or malignant endocarditis and infarcts, are unfavorable and 
present only in the gravest cases. 
Extension to the mucous membranes of the disease with edema of the 
glottis may lead to sudden death. 
Glandular enlargements in the neighborhood of the infected skin need 
cause no alarm. 
General Manifestations 
Circulatory Disturbances.—In the active and robust with a clean 'pre- 
vious history, the hyperpyrexia of the third and fourth days in the 
absence of other alarming symptoms such as heart weakness, need not dis- 
courage the attendant. In these cases there may be active delirium and a 
rapid pulse, and yet the prognosis in over 95 per cent of cases proves to be 
favorable. 
The height of the temperature may mislead the clinician in occasional 
£ases, for he may fail to recognize the danger in the aged or feeble, in 
which there is but slight fever but characteristic asthenia. Such patients 
bear erysipelas badly. 
The pulse is rapid according to the height of the fever and may be 
arhythmic at times during the first week. 
Arhythmia and dicrotism with hyperpyrexia and meningeal symptoms 
present a complex which should cause anxiety during several days. Unless 
there be purulent meningitis or other serious complication and the disease 
is limited, over 90 per cent of these patients finally recover. 
A small, rapid, soft and thready irregular pulse, with other evidences 
of malignancy or complications, is always alarming and should lead to a 
guarded forecast. 
Whenever in the course of erysipelas there are evidences of endocarditis 
the possibility of the malignancy of the latter must be considered. Com- 
plicating streptococcus endocarditis offers an unfavorable outlook. 
Dry pericarditis is not of itself fatal. Purulent pericarditis is a part 
of an existing pyemia or general sepsis, and is found only in the gravest 
cases. 
Systolic mitral murmur due to relative muscular insufficiency, with or 
without accentuation of the second pulmonic sound, disappears during or 
shortly after convalescence and is followed by normal heart function in 
almost all cases. 
Non-malignant endocarditis as a rule, when a complication, leads to 
the recovery of the patient, though there may be some evidences later of 176 
SPECIFIC INFECTIOUS DISEASES 
its previous existence in deformed valves (murmurs) and compensatory 
change (hypertrophy). 
Respiratory System.—Hurried respiration, with or without evidences 
of lung involvement (pneumonia, bronchitis, etc.) has in our experience 
been a symptom found with malignancy and is exceedingly grave. Rapid 
respiration does not always indicate the presence of pneumonia. 
Pneumonia, particularly with alcoholism, is likely to prove fatal in the 
presence of erysipelas. 
Purulent pleurisy, associated with migratory erysipelas, has proved to 
be a serious complication, though not all cases are fatal. 
Albuminuria is not of serious import, it is present in most cases at the 
height of the infection. In 10 per cent of our cases there were evidences 
of nephritis; among these the mortality was low. Occasionally bloody 
urine was found without interfering with a favorable issue. 
Purulent meningitis is an occasional cause of death in erysipelas. 
Metastatic parotitis (see Metastatic Parotitis), is evidence of sepsis 
and malignancy. 
Blood.—There is, in the severest cases, enormous albumin loss from 
the blood which is in direct proportion to the gravity of the disease. 
In severe cases there is enormous destruction of red blood-corpuscles. 
A count of 3,000,000 in a previously normal blood is of grave significance. 
Poikilocytosis in these unfavorable cases is striking. 
Large hemoglobin loss is also an early evidence of the gravity of the 
disease. 
Leukocytosis is usually present in cases of erysipelas, is largely de- 
pendent upon complications, mixed infections, etc.; alone it is of small 
prognostic value. 
Conclusions 
The prognosis of the average case of erysipelas is good; the mortality 
varies from 3 to 5 per cent. 
The leading causes of death in our experience have been cardiac tox- 
emia, purulent meningitis, general sepsis, malignant endocarditis (strepto- 
coccus), mixed infection, alcoholic meningitis and delirium tremens, sinus 
thrombosis, exhaustion due to repeated re-infection at short intervals. 
When erysipelas develops in the midst of other acute infections, as with 
typhoid and with surgical diseases, or after surgical operations, the prog- 
nosis is grave. 
Our experience with non-altoholic patients predisposed to the disease, 
who have been repeatedly infected at long intervals, has been uniformly 
favorable. In spite of repeated fiery attacks they have recovered. One of 
these is now alive, over 80 years of age, after 50 years of recurring erysip- 
elas. BACTERIAL DISEASES 
177 
IX. Epidemic Cerebrospinal Meningitis 
(Ubertragbare Genickstarre) 
Epidemic cerebrospinal meningitis is an epidemic or sporadic inflam- 
mation of the. cerebrospinal membranes due' to the Meningococcus of 
Weichselbaum (1887) ; characterized by symptoms referable to the brain 
and cord, in which the diagnosis can be positively vei'ified by the presence 
of the Meningococcus of Weichselbaum in the withdrawn lumbar fluid. 
Mortality 
There is scarcely a year when the disease fails to claim its victims in 
most cities and countries of the civilized world. The mortality is greatest 
during April and May, the number increasing during years of endemics 
and epidemics. Thus in a period of ten years before the introduction of 
the Flexner serum, there were in the city of Syracuse 175 deaths due to 
cerebrospinal meningitis, and 499 deaths due to non-epidemic meningitis. 
Cerebrospinal Non-epidemic 
Years. Meningitis. Meningitis. 
1893 * 11 55 
1894 4 61 
1895 17 61 
1896 18 51 
1897 12 51 
1898 19 71 
1899 45 43 
1900 13 29 
1901 9 23 
1902 19 32 
1903 8 22 
175 499 
In the city of Hew York the number of deaths from cerebrospinal 
meningitis from January 1894 to November 1904 was 3,189—the highest 
mortality was due to the prevalence of the disease in epidemic form during 
1904 and 1905. 
Year. Deaths, Cases. 
1894 213 
1895 204 
1896 178 
1897 232 
1898 258 
1899 287 
1900 201 
1901 201 
1902 210 
1903 195 
1904 (January 1 to November 1, 1904) 1,010 
3,189 178 
SPECIFIC INFECTIOUS DISEASES 
Statistics of the City of New York Since 1904. 
Year. Cases Reported. Deaths. 
*1904 482 1,403 
1905 2,755 2,025 
1906 1,032 812 
1907 828 642 
1908 380 316 
1909 346 326 
1910 242 191 
1911 266 224 
1912 250 196 
1913 232 202 
* 1,010 cases included in previous table would leave 393 deaths of the 482 
reported. 
The disease claims the larger number of its victims from the homes of 
the poor, though the disease may exist under favorable conditions and in 
sanitary homes. During epidemics, the limited number of cases and the 
absence of continuous extension are often surprising, as was also the high 
mortality, before the introduction of the present method of treating the 
disease. The disease is often held within a narrow precinct of a city or a 
corner of a township. 
When epidemic meningitis visits country districts the same remark- 
able limitation of its ravages is noticed in the small number attacked. 
These facts are well illustrated by an experience on board the U. S. re- 
ceiving ship Minneapolis, as reported by Surgeon Stokes. The ship was 
overcrowded with 1,450 men on board at the time of the outbreak, yet only 
23 cases developed; of these 6 died—an unusually low mortality of 26 per 
cent. 
Clinically and experimentally it has been demonstrated that pneumo- 
coccus, influenzal and other forms of cerebrospinal meningitis are more 
virulent than are those of epidemic origin due to the meningococcus. 
Pneumococcus meningitis is almost uniformly fatal. Of 68 cases, 61 died 
during the first day of the disease, while Netter who reports these figures, 
says that only one-third of his meningococcus cases died. Huebner says 
uthe benign nature of the meningococcus as compared with the virulence 
of other meningitis-producing germs, accounts for the comparatively few 
cases during epidemics, their ready control with the subjugation of the 
germ.” 
Occurrence 
Flatten’s statistics corroborate tbe data which I collected in New 
York State (Eisner), and prove that the disease is rare after the for- 
tieth year. Flatten's statistics, gathered during 1905-1907 in Kattowitz, 
showing ages of patients, are as follows: BACTEKIAL DISEASES 
179 
0 to 5 years 559 eases 
5 to 10 “ 248 “ 
10 to 15 “ 72 “ 
15 to 20 “ 47 “ 
20 to 25 “ 15 “ 
25 to 30 “ 14 “ 
30 to 35 “ 7 “ 
35 to 40 “ 3 “ 
40 to 45 “ 2 “ 
45 to 50 “ 2 “ 
50 to 55 " 5 “ 
55 to 60 “ 1 “ 
60 years and above 0 “ 
I found that when the disease did occur in adults, it was often invited by 
long continued worry and mental strain. 
Sporadic cases run much the same course as do those of epidemic 
origin; there are no differential features. 
Bacterial and cultural tests only, give the information which insure' 
safety and the protection to which the public is entitled. 
Second attacks of the disease are not likely to occur. Councilman 
(quoted by Eisner), found but five cases in which the disease did repeat 
itself in the same patient. Oppenheim does not believe that one attack 
gives immunity. 
Factors Influencing the Severity 
General Symptoms.—There are unexplainable factors which modify 
the severity of both the epidemic and sporadic disease during different 
years and influence its course. All degrees of severity are found with both. 
For purposes of prophylaxis and prognosis it cannot be repeated too 
often that the same bacteriologic cause is paramount in both epidemic and 
sporadic cases. 
Early coma or its persistence after the end of the first week is an 
unfavorable symptom. 
Early glycosuria with coma or with marked delirium is unfavorable. 
Deafness is not to be considered among the ominous symptoms so far 
as life is concerned. It is present in a large proportion of cases and leads 
to permanent deafness in from 15 to 25 per cent of cases. 
Suppurative ophthalmia, panophthalmitis with perforation, is found 
in severe cases with mixed infection (4 to 5 per cent). 
Optic neuritis is a serious complication, present in 17 per cent of 
Jochmann’s cases, and in those who recover often leads to blindness. 
Unfavorable conditions are persistence of coma, involuntary discharge 
of urine and feces, rapid emaciation, increasing tympany, hyperpyrexia, 
rapid small pulse, sudden heart weakness with subnormal temperature. 
The facies of the patient, unlike any other disease, not easily described, 180 
SPECIFIC INFECTIOUS DISEASES 
offer a picture which impresses the clinician at once and from which he 
can promptly reach conlusions for prognosis. 
The pulse and temperature offer nothing characteristic other than the 
acceleration of the former and the elevation of the latter. As death ap- 
proaches the pulse becomes exceedingly rapid—due to vagus paralysis. 
Hyperpyrexia with rapid pulse is usually a fatal combination. 
The. urine, usually secreted in good quantities, may be albuminous, and 
glycosuria is not uncommon. The former is not serious; the latter with 
high fever and deep invasion of the sensorium does not justify a favorable 
forecast. Not all cases with glycosuria die. 
The knee jerk is absent in one-sixtli of all cases. In one-tenth this 
phenomenon is absent to return as convalescence approaches. The varia- 
tion in the behavior of the reflexes in different cases proves that these 
follow no rule and offer little for prognosis; the sensorium is often so pro- 
foundly involved as to make the tests valueless. 
Striking, extreme opisthotonos with marked muscular rigidity is 
always an evidence of active and serious meningitis. The relief of muscu- 
lar rigidity and included opisthotonos, with brightening of the mind are 
always encouraging. 
Marked cutaneous hyperesthesia with or without the Kernig symptom, 
is always suggestive and is most pronounced in serious cases. 
Herpes facialis unusually frequent and profuse in Germany, is less 
frequent in the United States than are the erythemas and purpuric erup- 
tions (petecliise, etc.). Herpes is of no prognostic value. Petecliise are 
more ominous. 
Large cutaneous hemorrhages and bleeding from mucous membranes 
are evidences of malignancy. 
Early convulsions in children are not always of serious import; their 
persistence however is always grave. 
Tonic spasm limited, without full convulsions, is characteristic of the 
early stage of “postbasic meningitis.” (Lees and Barlow). These should 
all be considered cases of cerebrospinal meningitis and offer a bad prog- 
nosis. 
Trousseau s macule is neither of great diagnostic nor prognostic value. 
There are but few data referable to other organs, including kidney and 
spleen, which stand out as prognostic aids. Albuminuria is frequent, not 
significant; nephritis is rare, the spleen is not materially enlarged. 
The Kernig symptom is an early manifestation; it is as early as opis- 
thotonos and is late to disappear. It is present in between 90 and 95 per 
cent of all cases of epidemic cerebrospinal meningitis. The persistence of 
the Kernig phenomenon is of considerable value in diagnosis and prog- 
nosis in cases where the correct diagnosis was not suspected during the first 
week of the disease. As a rule, it is not needed to make the diagnosis; it 
is found with all forms of meningitis. If it persists, it should always lead BACTERIAL DISEASES 
181 
to the suspicion of cerebrospinal meningitis and for safety, the spinal fluid 
should he examined bacteriologically. 
Foudroyant Cases.—There are foudroyant cases in which the victim 
is suddenly overpowered; coma and malignant toxemia are prompt; and 
death may follow in the course of from 12 to 48 hours before the diagnosis 
can be made. We see fewer of these cases now than formerly, but occa- 
sionally they are encountered, usually early, or at the height of the epi- 
demic. Hyperpyrexia has been a bad feature of some of these cases. 
Sudden death in the midst of cases in which the prognosis has been 
held sub judice, is not infrequent. Such cases we have all met in the past 
and it is unjust now to charge these to the use of the serum or to any form 
of treatment. We have no definite cause to assign for some of these deaths, 
but would in explanation, quote Tourdes: “The disease is distinguished by 
the slowness of its cure and the rapidity of its fatal issue.” This dictum 
was advanced during the period preceding the introduction of the Flexner 
serum. 
Cases also foudroyant, meningitis siderans, are among the more fatal, 
and run their course unless controlled by treatment in from 4 to 6 days. 
If these patients finally recover, there are positive evidences of improve- 
ment after the second or third day. The sensorium gradually clears; tem- 
perature which is usually high shows decided remission; the cutaneous 
hyperesthesia is less; and the pulse shows increasing tone. With these 
changes, the blood picture and character of the lumbar fluid is also 
changed. Opisthotonus and rigidity, as already mentioned, are materially 
relieved also. 
In all cases of the disease the prognosis is not encouraging if improve- 
ment is not decided before the end of the second or early in the third week. 
The addition of other acute infections is always unfavorable, more par- 
ticularly pneumonia, scarletina, endocarditis, pericarditis and pleuritis. 
The interstitial myocarditis (toxic) of foudroyant cases adds enor- 
mously to the danger. The tonsils harbor meningococci, and from this 
port of entry the infection is often spread. The normal nasopharynx is 
antagonistic to the onward march of the Weichselbaum diplococcus. 
Chronic Cases.—Chronic cases with purulent deposit in the ventricles 
of the brain, bathing the cord also may persist during from 4 to 6 weeks— 
even longer—with marked symptoms, including rigidity, Kernig symptom; 
the sensorium may clear; some symptoms including fever may also im- 
prove, but with persistently high pulse, increasing weakness, final return 
of fever, and aggravation of all conditions, (mental and physical) these 
patients, usually neglected from the beginning, die. 
It is not at all unusual to find so-called chronic and subacute cases 
gradually mend, and in the end make full recoveries. Some of these how- 
ever escape with sequelae which handicap them throughout life. The 
chronic cases may end in hydrocephalus. 182 
SPECIFIC INFECTIOUS DISEASES 
Progressive hydrocephalus dependent on epidemic meningitis is among 
the most unfortunate and fatal sequelae of the disease. In these cases the 
disease may continue during weeks—not infrequently months. Changes 
are found in the ependyma; there is a persistence of meningococci in the 
ventricles of the brain, “in much diminished numbers and of reduced viru- 
lence” (Koplik). As already stated the chronic cases, i. e., hydrocephalus, 
may present a clear lumbar fluid; meningococci may appear to be absent, 
but cultural tests show their presence. 
The marked emaciation of these patients is characteristic and has 
claimed the attention of all clinicians; they look like reconcentrados 
when next to each other in the hospital wards. The prognosis of these 
cases is bad, and when they do recover a variety of sequeloe may follow 
besides those already mentioned, including permanent mental alienation, 
persistent cephalalgia, vertigo, loss of memory, ataxia, contractures, etc. 
Abortive Cases.—Abortive cases end in the course of a few days fa- 
vorably, after but few symptoms and without sequelae. Most of these 
cases are found late in epidemics of the disease. 
Blood Picture.—The blood picture of epidemic cerebrospinal menin- 
gitis offers valuable data for diagnosis and prognosis. Rusca has made a 
very extensive study of this subject. During the early stage in all cases, 
there is marked leukocytosis (10,000 to 45,000) ; polymorphonuclear 
increase is greatest, while the behavior of the lymphocytes is not always 
the same; in some cases there is increase, in others a reduction. 
As the disease advances and where the condition is serious, there is at 
once an increase of neutrophilic leukocytes; improvement of acute condi- 
tions is at once followed by a decided fall. 
There is lymphocytic increase with each improvement or favorable 
turn of the infection, whereas a decided fall is promptly noted with added 
complication of serious moment. 
Curtius and Rusca agree that the blood picture of cases with measle- 
like eruption proves the contention of the former, that such cases offer 
a favorable prognosis. 
Hemorrhagic exanthemata offer an unfavorable blood picture and are 
often foudroyant. 
Returning eosinophilia is always favorable and is found during con- 
valescence. Eosinophilia is usually absent in serious and malignant cases, 
and is never present during the terminal stage of cerebrospinal menin- 
gitis ; the latter statement is true also of mast cells. 
The blood picture of cerebrospinal meningitis is of greater prognostic 
than diagnostic value; for the latter, we must always rely upon lumbar 
puncture. 
Lumbar Puncture.—Lumbar puncture gives positive diagnostic infor- 
mation as well as valuable prognostic hints. 
The fluid in average cases is cloudy, and escapes under abnormally BACTERIAL DISEASES 
183 
high pressure. Where there is purulent and thick effusion, the first few 
drops may be thick—“pussy”—after which the fluid is thinner, but re- 
mains milky or clouded. If there is acquired hydrocephalus and the 
condition is advanced to the subacute or chronic stage the fluid may be 
clear, but still the pressure is high (180 to 220 mm.). The fluid usually 
offers positive bacteriologic and cytologic evidence. The centrifugalized 
fluid shows abundant polymorphonuclear leukocytes and lymphocytes. 
With a negative result (bacteriologically) and the absence of meningo- 
cocci with positive symptoms of cerebrospinal meningitis, repeated exam- 
inations of the fluid are necessary, and will lead to the correct diagnosis. 
It is not uncommon to find the first examination negative, the second 
positive. 
Herter placed himself with those who believed that “lumbar puncture, 
more particularly the appearance of the cellular exudate in the early 
stages of acute cerebrospinal meningitis” is of prognostic significance. 
“The presence of degenerated leukocytes, containing few microorganisms 
while many cocci are seen to be extracellular, points to feeble powers of 
resistance on the part of the leukocytes and hence to a bad prognosis.” It 
is further held that the persistence of well preserved leukocytes, showing 
many intracellular diplococci (indicating active phagocytosis) and the 
absence of many extra cellular microorganisms, indicate good powers of 
resistance and a better prognosis (other conditions being comparable) than 
in the former case.” Jochmann makes a suggestion, which seems 
important: that in suspected cases in which the first lumbar puncture 
fails, bacteriologic examination of the pharyngeal content will be likely 
to show the presence of the meningococcus. 
The presence of sugar in the cerebrospinal fluid may prove of some 
diagnostic and prognostic value in both cerebrospinal meningitis and 
tuberculous meningitis. This subject has received considerable attention 
of late, more particularly from Jacob and Connall. The latter gives the 
results of the examination of the cerebrospinal fluid for sugar in 133 cases 
of cerebrospinal meningitis, all stages of the disease included. ITe con- 
cludes that sugar is absent from the fluid during the acute stages of the 
disease. During1 the chronic periods sugar is present. “It may be said, 
however, with certain reservations, that the reappearance of the sugar is 
an indication that the disease is in process of cure.” Jacoh agrees 
with Connall that “in cerebrospinal meningitis sugar is absent (from the 
fluid) in the acute stage, but may return in some degree as the infection 
recedes.” 
Complications.—Mixed infection with either sporadic or epidemic 
cases is frequent; the meningococcus may have abundant companionship 
before death or recovery. This is always serious. 
Cases of cerebro-spinal meningitis with pneumonia offer only the most 
doleful forecast. SPECIFIC INFECTIOUS DISEASES 
184 
Meningococcus pneumonia may complicate cerebrospinal meningitis. 
In the presence of both of these conditions, i. e., pneumonia and cerebro- 
spinal meningitis, the meningococcus is present in 80 per cent and the 
pneumococcus in 20 per cent of cases (Eisner quotes Councilman, 
Mallory and Wright). 
Metastatic joint changes were found in a number of our cases, and 
when present early aroused suspicion of arthritis and pyemia. In one of 
our cases a woman, age 24, presented with arthritis limited to both ankles 
and profound meningococcus infection; she died in the second week of the 
disease. These cases are usually of mixed origin and demand a cautious 
forecast. 
Deafness often follows otitis media suppurativa, though the labyrinth 
may be involved without a single auditory symptom, until the patient 
awakens, or days after the beginning of convalescence it is noticed that the 
hearing is growing gradually less acute. In some cases patients lift them- 
selves from the acute delirium or period of unconsciousness with defective 
hearing, from which they may never recover. A large number of deaf 
mutes are found to have had epidemic cerebrospinal meningitis. Moos, 
quoted by Ormerod, found of 64 convalescents from cerebrospinal menin- 
gitis that 38 were deaf mutes; 20 were absolutely deaf, and 32 had a 
staggering gait. 
Both blindness and deafness offer a bad prognosis for return of func- 
tion if improvement is not prompt. Persistence beyond 3 moiiths of 
symptoms without improvement argues strongly against restoration later. 
The Influence of the Flexner Serum on the Prognosis of Meningococ- 
cus Cerebrospinal Meningitis 
There never will be a time when the prognosis of the disease will fail 
to be influenced by the virulence of line infecting agent. In spite of this 
fact, which has been discounted in the impartial consideration of the re- 
sults obtained, the profession is agreed that the Flexner serum is a 
remedy of undoubted value and that it has reduced the mortality of the 
disease, from 70 to 25 per cent. Indeed in some epidemics before the 
use of the serum, the death rate was 80, and it has been above 90 per cent. 
In some epidemics in which foudroyant cases were common 95 per 
cent died. Oppenheiin reports in one epidemic (Silesia) 3,102 cases 
with 1,789 deaths. Koplik says “the Flexner serum has given the disease 
a prognosis in epidemic periods equal to that of lobar pneumonia, and in 
sporadic cases even a better prognosis than the pulmonary affections.” 
He says further: “In sets of sporadic cases the outlook is not worse than 
in any of the ordinary affections of an infectious nature in childhood.” 
The prognosis during early life will continue to be influenced by the 
difficulties of early diagnosis and respiratory complications. BACTERIAL DISEASES 
185 
The delay of a single day or even 12 hours in very young children 
is often fatal (Koplik). Koplik in a series of 400 cases collected by 
him found a mortality of 50 per cent in 22 patients of 1 year and below, 
42 per cent between 1 and 2 years. In Koplik’s service at Mt. Sinai 
Hospital, of 15 patients below 1 year, 10 died—66 per cent; of these 15, 
2 injected on the fifteenth day recovered and 1 injected the seventeenth 
day was discharged improved, 1 on the twenty-first day was cured, as was 
1 injected on the twenty-ninth day. 1 injected on the third day died. 
Of 12 patients between 1 and 2 years of age injected, 6 recovered (50 
per cent) ; 1 of these injected on the second day of the disease died after 
an illness of 14 days. 
Among the causes of failure, virulence of the infecting strains, closure 
of the foramen of Magendie, adhesions preventing the entrance of the 
serum from the cord to the subarachnoid space above, late lumbar punc- 
ture (diagnosis), are included. 
Flexner’s statements are always concise and are accepted as absolutely 
reliable. We find in his report of 1,295 cases in which intraspinal injec- 
tions of his serum were given, 70 per cent of recoveries. In those in- 
jected within the first 3 days of the disease the mortality was but 18 per 
cent; injected between the fourth and seventh day, the mortality was 27 
per cent, and those injected later 36 per cent. 125 children less than 12 
months’ old were injected, and 50 per cent were saved. Of these, 5 were 
injected early and all were saved. “Reduction in mortality of cerebro- 
spinal meningitis due to the serum is from two-thirds to three-quarters of 
the average percentages, occurring in the same periods and places among 
patients not subjected to the specific treatment” (Flexner). These fig- 
ures tell their own story. Besides the enormous saving of life by the 
serum, we must add that by its use, the course of the disease is shortened 
and its sequelae are limited. 
References 
Connall. Quarterly J. of Med., January, 1910. 
Curtius. Med. Klinik, 1905, 80J+. 
Eisner (H. L.). Med. News, New York, Apr. 8,1905. 
Flatten. Klin. Jahrbuch, 1909, Bd. xv & xix. 
Flexner. J. Am. Med. 4ss., lx, 1937. 
The local specific treatment of infections, etc. Edinburg J., May, 1912. 
Herter. Diagnosis of organic nervous disease, 2. ed., 1907. 
Heubner. Eisner, The medical news. New York, April 8, 1905. 
Jacob. British Med. J., Oct. 26, 1912. 
Jochmann. Mohr & Staehelin. i, 768. 
Koplik. J. Am. Med. .Ass., lx, 1755. 
Lees & Barlow. Allbutt’s System of medicine, 1. & 2. ed., London. 186 
SPECIFIC INFECTIOUS DISEASES 
Moos. (Quoted by Ormerod, Allbutt & Rolleston) System of medicine, 2. ed., 982. 
Netter. Bull, de Vacad. de Med. Sci., and 'previous reports, 1909. 
Oppenheim. Lehrbuch der Nervenkrankheiten. 6. ed., 1913, ii, 1007. 
Rusca. Blulbild Meningitis Cerebrospinalis epidemica. Deulsch. Arch. f. klin. Med., 
1911, Bd. ciii. 
Stokes. Report of the Surgeon General, United States Navy, 1903. 
X. Whooping-cough 
(Pertussis, Keuchhusten, Coqueluche) 
Whooping-cough is an infectious contagious disease of early life, due 
probably to the Bordet-Gengou bacillus; it is characterized by catarrhal 
inflammation of the respiratory tract, a paroxysmal cough, and a “whoop” 
which is a long-drawn inspiratory movement coming at the end of several 
separate convulsive coughs. The disease occurs in epidemics usually, but 
is also sporadic; such unexplained infections are not infrequent and occur 
in all communities. 
Most children have had pertussis when they reach their tenth year. 
One attach usually produces immunity. Female children are always at- 
tacked in larger numbers than are males. Cold weather seems to invite 
the disease; complications are then more frequent than during warm 
weather. Negro children show a much larger fatality when infected than 
do whites. 
Uncomplicated whooping-cough leads to recovery after passing 
through three stages, unless as rarely happens, the case is of the abortive 
type: 
1. Catarrhal stage. 
2. Spasmodic stage. 
3. Stage of recession (decrementi). 
Pertussis is the cause of many serious complications and deaths. 
While the disease, per se, as already suggested offers an almost uni- 
formly good prognosis, its sequela; make it an infection to he feared, and 
one which stands out in bold relief as a leading cause of death in early 
life. “It exceeds diphtheria and scarlet fever in gross mortality” (Osier). 
The average duration of whooping-cough is between 6 and 8 weeks. 
In children less than 2 years of age the prognosis is exceedingly grave, 
because of the complications. Infants suffering from rachitis and syph- 
ilis, or other constitutional disturbances, are prone to develop serious 
complications with whooping-cough because they offer but little resistance. 
The average mortality of whooping-cough is between 5 and 6 per cent. 
Voit reports a mortality of 25 per cent during the first year of life in BACTERIAL DISEASES 
187 
whooping-cough; from 1 to 5 years, 4.8 per cent; and from 6 to 15 years, 
1.1 per cent. 
Complications 
Unfavorable surroundings invite complications and add enormously 
to the dangers of young children. 
Convulsions at any time during the course of whooping-cough are of 
serious import and unless due to errors of digestion, trivial or transitory 
causes, are ominous. When convulsions are due to sudden cerebral lesions 
(cerebral hemorrhage, tuberculosis, thrombosis), the prognosis is as a 
rule unfavorable. To these latter complications, we will again refer. 
Children who have enlarged lymph nodes need to be protected against 
all fresh infections, particularly pertussis and measles; for with these 
added diseases, there is always danger of complications, and with lowered 
vitality, tuberculization is to be feared. 
The most serious and numerous complications of whooping-cough are 
the catarrhal inflammations of the respiratory tract, the invasion of the 
bronchioles and air cells, causing bronchopneumonia. One-seventh of all 
cases of bronchopneumonia of early life are secondary to whooping-cough. 
It is often surprising to note the enormous resistance of children in 
the presence of far-reaching bronchopneumonia. During several days no 
forecast of value can be offered in the individual case. During this pe- 
riod children may continue desperately ill, and in spite of a complex of 
symptoms, which in the adult would warrant an unfavorable prognosis, 
they make happy recoveries. We have learned never to give up a child 
with bronchopneumonia for we have been agreeably surprised in cases 
where there seemed to be but the faintest glimmer of hope. These cases 
of bronchopneumonia are always secondary and are due to mixed infec- 
tion as a rule (pneumococcus and streptococcus). 
Hyperpyrexia with rapid heart action and symptoms referable to the 
nervous system in the presence of bronchopneumonia are always grave, 
and demand the greatest circumspection before a prognosis of any value 
can be offered. 
The youngest children are most likely to contract pneumonia and other 
complications. Nurslings offer a high mortality with pneumonia (95 per 
cent), and when attacked promptly die. When in the midst of whooping- 
cough fever develops, with increased respiration and the pulse correspond- 
ingly rapid, respiratory complications are to be expected; with such 
symptoms bronchopneumonia is most frequent. Rachitic children, those 
who have tuberculous (“scrofula”) tendencies in the presence of second- 
ary pneumonia, as in uncomplicated whooping-cough are non-resistant; in 
these, the mortality is very high. 
The duration of bronchopneumonia depends on the frequency of re- 
lapses, which are common and are due to fresh insular invasion. 188 
SPECIFIC INFECTIOUS DISEASES 
Tuberculous complications with pertussis are surprisingly frequent, 
as has been proved by post mortem examinations; the bronchial nodes are 
the most frequent seat of deposit. In these cases there are often long 
periods of fever and relapsing bronchopneumonia; or in occasional cases 
children recover with latent deposits. 
Pulmonary tuberculosis is also frequent in those who die of whooping- 
cough. Neuroth makes the unqualified statement, that “tuberculous 
disease of the lung is practically never absent in children who have died 
of whooping-cough.” Latent deposits following whooping-cough may be- 
come active years after the acute stage and may lead to death (See 
Tuberculosis). 
Chronic cough, due to bronchiectasia, may continue during many 
years; may or may not be complicated with tuberculosis—making prog- 
nosis doubtful. 
Emphysema which may be present during the stage of spasm usually 
disappears without causing damage to lung tissue. 
Lobar or croupous pneumonia is not sufficiently frequent to demand 
consideration. 
Increased intravenous pressure and associated nutritive changes in the 
walls of the blood-vessels may cause hemorrhages into the conjunctiva, 
from the nose, mouth, bronchi, ear, or into the skin during the paroxysmal 
stage—all of which are transitory and do not often influence the prognosis 
unfavorably. 
Influenza complicating wdiooping-cough adds an element of danger; 
complications are more likely to follow, and pneumonia is foremost among 
these. The same is true of the influence of other added infections 
(measles, diphtheria and varicella). 
Dilatation of the heart with moderate hypertrophy of the left ventricle 
may result in cases where paroxysms are severe and frequent; but these 
conditions yield after convalescence and sufficient rest. Only rarely have 
heart lesions in the previously healthy been the cause of sudden death. 
Convulsions due to trivial or transitory factors in uncomplicated cases 
have already been mentioned; when convulsions are due to complications 
leading to organic and central changes, the prognosis is exceedingly grave. 
Cerebral hemorrhage offers an unfavorable prognosis; it may lead to 
death or to permanent paralysis. 
Hemiplegia may improve but does not as a rule disappear entirely. 
Paralyses of central origin lead to permanently reduced function in 
most cases; though marked improvement may follow, life itself is unin- 
fluenced. When paralyses are associated with bulbar symptoms the prog- 
nosis so far as life is concerned is bad. 
Ocular hemorrhages usually yield, only rarely is sight permanently 
affected. 
In occasional cases, spinal complications include symptoms of mye- BACTERIAL DISEASES 
189 
litis, poliomyelitis, Landry’s paralysis; in all the prognosis is the same as 
in the uncomplicated diseases of the nervous system. Constitutional 
disturbances, anemia, chlorosis, asthenia, chorea and faulty digestion fol- 
lowing pertussis all yield under rest and rational treatment. 
Blood 
Cima found whooping-cough, as the result of his investigations of the 
blood, associated with leukocytosis very early in the disease (18,000 to 
22,000). The higher the leukocytic count the more severe the disease. 
The youngest children show the greatest increase of leukocytes and those 
cases in which there are mixed infections and complications. Other data 
offered by the blood are of no value for prognosis. 
Conclusions 
A history of whooping-cough is more frequent in choreic than in other 
children. 
In considering the prognosis of whooping-cough we are conscious of 
the fact that there are with this, as with all other infections, marked dif- 
ferences in the virulence and character of separate epidemics; that chil- 
dren react differently to the infection, that seasonal influences are of 
paramount importance, and finally that environment, as already suggested 
in this chapter, is a factor of the greatest prognostic significance. Trous- 
seau believed that the prognosis of whooping-cough was enormously in- 
fluenced by the numoer of paroxysms and concluded that more than 60 
daily, justified a bad prognosis. 
References 
Cima. Petraria (quoted by Neuroth). 
Pfaundler & Schlossmann. 2. ed., ii. 
Neuroth. Pfaundler & Schlossmann. 2. ed., ii, 378. 
Osier. Practice of medicine. 8. ed., 1913. 
Trousseau. Clinical medicine, etc. 
XI. Gonococcus Infections 
( Gonococcemia, Gonorrheal Sepsis) 
It is not within the province of this work to consider the prognosis of 
local changes in the urethra, vagina, or in the eye, caused by gonococcus 
infection. 
There are occasional septic conditions which are dependent upon the 
entrance of gonococci into the blood, in which there are prompt evidences 190 
SPECIFIC INFECTIOUS DISEASES 
of constitutional disturbance, and to these we refer in considering the 
prognosis of gonococcemia. The most frequent clinical pictures include 
1. Gonococcus endocarditis. 
2. Gonococcus arthritis (gonorrheal rheumatism). 
1. Gonococcus Endocarditis 
Ahmann, Thayer and Lazear were among the first to isolate gonococci 
from the blood in gonorrheal endocarditis. 
The clinical manifestations of gonococcus endocarditis are variable. 
We have referred to this subject in our consideration of septic conditions, 
also with malignant endocarditis (See Septic Endocarditis). 
There are cases which are not associated with joint symptoms; these 
are in the minority. 
As a rule there is monarthritis; there may be 'polyarthritis. Soon the 
physical signs of endocarditis are added. 
The disease may be either of the (a) typhoid, (b) pyemia (intermit- 
tent), or (c) irregular type. 
(a) The Typhoid Type.—In the typhoid type the fever is continuous 
with slight morning remissions. The appearance of the patient is charac- 
teristic of the typhoid condition. 
Physical signs are positive, both sides of the heart are often involved; 
the right side oftener than with rheumatic or non-malignant endocarditis. 
The pulse is rapid and feeble, the sensorium is more or less disturbed; 
in some cases there is wild, in others, low muttering delirium; albu- 
minuria is almost constantly present, which often denotes septic nephritis. 
(b) Intermittent or Pyemic Type.—Occasionally the typhoid type 
merges into the intermittent after a day or two; sometimes there is a 
longer afebrile period; after a period of intermittent fever following, 
there may be a return to the typhoid state. 
Gonorrheal endocarditis of the intermittent or pyemic type is likely 
to be of longer duration than is the typhoid type. With intermittent fever 
the periods of remission vary. 
In some cases the periodicity of an intermittent malarial fever is 
observed; in other cases the chills and fever recur at irregular intervals 
during a long period—every 3, 4 or 5 days—always with profuse and 
weakening sweats following, and often with delirium. The other attend- 
ing conditions, including albuminuria mentioned in connection with the 
typhoid type, are in evidence. 
There are cases in which we have been deluded by long periods of 
freedom from fever and other symptoms; in such cases from 7 to 10 days 
have intervened without any subjective complaints, sometimes longer, 
when without prodromal symptoms the patient suddenly had a chill and 
the typical cycle followed. BACTERIAL DISEASES 
191 
The intermittent may merge into the typhoid or irregular type of the 
disease. Under these conditions the usual course of the disease includes 
rapid exhaustion and the typical picture of septic fever, from which the 
patient rarely rallies. 
(c) Irregular Types.—Irregular types are not infrequent with endo- 
cardial invasion. Gonococcus endocarditis may begin with irregular 
symptoms; the temperature may continue erratic during several days, 
after which the patient may fall into a typhoid condition; or the pyemic 
intermittent type may continue in the ascendency. 
The behavior of the irregular type of gonococcus endocarditis may 
mislead the clinician and the gravity of the disease may not be appreciated. 
Cases with irregular fever and other anomalies may include periods 
of varying length during which the intermittent type predominates, from 
which the patients fall into a typhoid condition, or there is return to an 
erratic and irregular behavior. 
In some irregular types there is hyperpyrexia following a single chill 
which invites degenerative myocarditis, and death is not long postponed. 
Petechiae are found in most cases of gonococcus endocarditis and are 
of great diagnostic and prognostic value. Their presence with the pre- 
vious history of gonorrheal infection and physical signs of endocarditis 
clinches the diagnosis and justifies only the gravest prognosis. 
Hemorrhagic infarcts into lung, brain, spleen or kidney complicate 
many cases. Once the diagnosis of hemorrhagic- infarct is positive, an 
unfavorable forecast may be given. 
The Blood.—Leukocytosis is a constant attendant of gonococcus endo- 
carditis; we have failed to gain any facts from blood-counts which influ- 
ence prognosis. In the more chronic and subacute cases there is increas- 
ing anemia. Our average leukocytic count was between 18,000 and 
25,000. Blood cultural methods give positive results in over 70 per cent 
of endocardial infection. 
Gonococcus endocarditis may follow at any time while gonococci are 
present anywhere in the body. In occasional cases gonococcemia follows 
shortly after infection; in other cases 4 weeks or even a longer time may 
intervene. As we have already intimated our clinical material includes 
no case of recovery where the diagnosis was confirmed by blood cultural 
methods (See Septic Endocarditis). 
Recoveries have been reported by others and Jochmann contends that 
the prognosis of gonococcus endocarditis is the most favorable of all of the 
malignant endocarditis, and that recovery has followed in a few cases in 
which gonococcemia was positively proved by blood-cultures. The other 
prognostic data given in connection with our consideration of malignant 
endocarditis (See Septic or Malignant Endocarditis) are applicable also to 
gonococcus endocarditis. 
Complications.—With gonococcus endocarditis, pericarditis and myo- 192 
SPECIFIC INFECTIOUS DISEASES 
carditis often occur. Pericarditis has complicated one-fourth of all cases; 
myocarditis many more. 
Sudden and overwhelming symptoms of toxemia in cases following 
within 7 to 14 days after gonorrheal infection are always promptly fatal. 
These cases may show no endocarditis. Pneumonia, pleurisy or abscess 
of gonococcus origin are found post mortem in some of these. 
Mixed infection complicates one-fifth of all cases. 
2. Gonococcus Arthritis 
(Gonorrheal Rheumatism) 
So-called gonorrheal rheumatism when uncomplicated, in the absence 
of endocardial infection, offers a good prognosis for life; slow return of 
the involved joint to normal is the rule. Permanent damage to the joint 
often results, the swelling and stiffness may remain during many months, 
while anchylosis is a frequent sequel. Pains and swellings recur after 
exposure, or with the changes of the season. Cold and wet weather is 
unfavorable and increases all symptoms, often during months and years. 
Gonococcus arthritis is always rebellious to treatment. 
Most cases are monarticular, the knee and ankle are the seats of predi- 
lection. Polyarthritis usually causes constitutional disturbances, includ- 
ing fever, delirium and at times albuminuria. Suppuration may follow 
but is relatively rare. Relapses are frequent, provoked by insignificant 
factors and recurring acute gonorrheal infection. 
Most cases are chronic, even the mildest gonococcus arthritis shows 
remnants of invasion during months, often years, in either subjective or 
objective symptoms or both. 
Modern vaccine treatment has seemed to modify the course of gonor- 
rheal joint infection in some cases, but cannot be said to be a specific 
against the disease. 
Arthritis complicates from 2 to 4 per cent of gonococcus infections. 
References 
Ahmann, Thayer & Lazear. Mohr & Staeh liv. 1911, i, 697. 
J. Exper. Med., New York, 1899, iv, 81-116. 
Eisner (H. L.). Malignant endocarditis. 
Jacobi Festschrift. 
Jochmann. Mohr & Staehelin. i., 1911. 
Thayer (W. S.). Gonorrheal endocarditis and septicemia. 
Internat. Med. Congress, Moscow, 1899, Hi, 5. Sec., 360-367. 
Thayer & Blumer. Bull., Johns Hopkins Hospital, Baltimore, 1896, vii, 57-63. BACTERIAL DISEASES 
193 
XII. Bacillary Dysentery 
Dysentery is an infectious disease showing inflammatory and ulcera- 
tive (necrotic) lesions of the large intestine; usually endemic or epi- 
demic; characterized by frequent bloody and mucus stools, more or less 
tenesmus, constitutional disturbance, and in some forms, a strong tend- 
ency to secondary suppurative hepatitis (liver abscess). 
There are two varieties of dysentery: 
1. Bacillary dysentery due to any one or more of three strains of the 
bacillus dysentericus: 
(a) Shiga-Kruse bacillus. 
(b) Flexner bacillus. 
(c) Y bacillus. 
2. Amebic dysentery (Amebiasis) due to the Entameba histolytica 
(Loesch 1875, Koch 1883, Schaudinn). Amebiasis is considered in an- 
other chapter (q. v.). 
General Considerations 
BACILLARY DYSENTERY 
The Bacillus.—The Bacillus dysentericus (Shiga) resembles typhoid 
and colon bacilli very closely, is easily cultivated, there is no sporulation, 
and it is negative to Gram stain. 
The several species (Flexner, Y, and Shiga) all cause the same 
lesions, are morphologically similar, and all grow alike in culture media. 
The Flexner and Y bacilli produce indol in bouillon culture in a few 
days, the Shiga-Kruse does not. There are other differences which need 
not concern us in our special task of prognosis, included in differences of 
agglutinations, etc. 
Occurrence and Mortality.—Convalescents, patients and the appar- 
ently well, may he carriers and spread the disease. It is spread by man; 
his stools are the most important factor. The future clinician will prob- 
ably never have the experiences with dysentery that some who are active 
to-day had in the past. Modern sanitation, if practiced, can never again 
lead to such ravages as this epidemic disease has caused. Let the student 
of medical history familiarize himself with the data collected by Wood- 
ward which stands to-day, with clinical and pathological records as one 
of the most complete and painstaking medical works of the past century. 
Macgregor says: “In the tropics dysentery is a destructive giant com- 
pared to which strong drink is a mere phantom.” 
Wherever there is overcrowding, in camps, prisons, hospitals, asylums, 
during times of endemics large numbers are afflicted and in the past the 
mortality has been alarmingly high. 194 
SPECIFIC INFECTIOUS DISEASES 
Woodward’s statistics show that during our Civil War there were 
259,071 cases of acute, and 28,451 cases of chronic dysentery. To the 
latter number, the increasing pension rolls during the past 40 years would 
unquestionably add many. 
Dysentery in Japan shows a mortality of 26.5 per cent. 
Epidemics of dysentery in Hew York State (central) mentioned in 
this chapter in connection with malarial infection of bacillary origin, 
claimed less than 10 per cent of those infected. 
Symptoms 
The lesions which concern the clinician are an inflammation of the 
mucous membrane of the large intestine with strong tendency to ulcera- 
tion and destruction of tissue. In some cases, there is superficial loss of 
the mucosa with diphtheritic deposit (diphtheritic dysentery). Ulcers, 
according to the severity of the case, may he single or multiple. Entire 
areas of mucous membrane in grave cases may slough; in the milder cases 
the lesions are more limited. 
The incubation period of bacillary dysentery is from 2 to 7 days. 
During this period there are usually no alarming symptoms unless pa- 
tients have been weakened by previous disease, and if there are no anoma- 
lies the second stage is safely reached. 
Between the third and fifth days of the disease the character of the 
stool changes. In severe cases the stools are small, bloody; mucus may be 
mixed with blood; they are less fecal than earlier. Tenesmus and tor- 
mina, with the enormous frequency of movements, weaken the patient. 
In grave cases there is marked reduction in the quantity of urine 
secreted, albuminuria and casts, and there may be complete suppression. 
In the most serious infections the thirst is distressing, muscular 
exhaustion extreme, there may be vomiting of small amounts of mucus, 
intolerant stomach, hiccough with sunken abdomen. Hiccough is not 
favorable; with subnormal temperature it is ominous. 
As a rule the mind remains clear even in fatal cases; there are but 
few nervous symptoms save great unrest and inability to sleep because of 
the frequent stools and tenesmus. Frequent small bloody or blood-mucous 
stools with tenesmus, great thirst, suppression of urine, tormina, small 
rapid pulse, drawn and pinched expression, sunken eyes, cyanosis, sub- 
normal temperature, cold extremities, include the leading features of ■’.he 
most serious dysenteries. Temperature does not offer data for prognosis; 
in serious cases there may be subnormal or normal temperature while 
slight rise is of no value. Favorable cases may show several degrees of 
fever. Bacillary dysentery requires from 2 to 4 weeks before convales- 
cence is reached. 
Children, the aged, the feeble, the underfed, and the dissipated, offer BACTERIAL DISEASES 
195 
less resistance to bacillary dysentery than do the active during mature 
years, and those who have a good resistance. 
The tendency of bacillary dysentery is to recover. Convalescence is 
slow, and relapse promptly follows errors of diet. Relapses may last 
several weeks and merge into chronicity. 
Gangrenous dysenteric colitis is a grave complication and with symp- 
toms of sepsis, albuminuria or suppression, extreme exhaustion or collapse 
leads to death in most cases. 
Bacillary dysentery is less likely to produce the numerous irregularly 
shaped and undermining ulcerations, the deep submucous invasion so 
characteristic of the amebic type. The prognosis is naturally more favor- 
able in bacillary dysentery after the disappearance of acute symptoms 
than in the amebic form, because of fewer complications, more particu- 
larly the absence of suppurative hepatitis. 
Complications 
The dreaded abscess of the liver is not a complication of bacillary- 
dysentery. Buchanan reports 1,130 cases with but one abscess of the 
liver, and Hassler and Morgenroth assert that if present the abscesses are 
multiple, unquestionably septic metastases. (Coli bacilli and streptococci 
were found in the pus.) 
We had no experience with liver abscess in connection with the epi- 
demics of dysentery in New York State. So far as we know we have 
met but one case of abscess of the liver following dysentery and that came 
from the south and was clearly amebic. 
Rheumatic pains and joint swellings follow or are associated with 
acute dysentery in about 3 to 5 per cent of all cases These yield to 
treatment without leaving any permanent disability in most cases. 
An occasional complication referable to the heart may prolong the 
period of convalescence; these are very largely cardiac neuroses. 
Endocarditis, valvular defects and myocardial weakness have in 
isolated cases influenced the progress of patients. 
Bradycardia and tachycardia may persist during several weeks, 
but usually yield without recurring if the patient rests sufficiently. 
Those who have had the largest experience with dysentery report an 
occasional neuritis, paraplegia, hemiplegia, monoplegia, paralysis of a 
single group of muscles, in occasional cases a prolonged period of neuras- 
thenia. 
The peripheral neuritides offer a favorable prognosis; the outcome 
of the other paralyses must depend upon the underlying cause. Neuras- 
thenia yields slowly to treatment. 
Suppurative parotitis is a complication of the graver form of dysen- 
tery as is also empyema; both complications add to the dangers of an al- 
ready alarming infection. 196 
SPECIFIC INFECTIOUS DISEASES 
Chronic nephritis occasionally follows acute dysentery. 
Chronic bacillary dysentery follows only in a small proportion of 
acute bacillary infections. Following the cases which developed during 
the Civil War there were a larger number of so-called “chronic diarrheas.” 
Some of these were mild and easily controlled by diet, some were less 
tractable, and many veterans are still living who developed the opium 
habit from the taking of the “black drop” to control their symptoms. 
These patients may live for years and die of the disease, or after long 
periods of drain they die of exhaustion. 
As with most epidemic diseases the severity of dysentery epidemics 
is variable. The Shiga-Kruse strain causes more severe symptoms than 
do the Flexner or Y bacilli. The first mentioned strain seems to cause 
more profound constitutional disturbances than either of the other two— 
the prostration is greater and the number of movements more frequent; 
hence the mortality is also larger with Shiga infection. 
Jochmann claims that with Shiga-Kruse infection the death rate is 
10 to 15 per cent, with the other strains from 0 to .5 per cent. 
Sporadic cases as met in hospital and private practice in the United 
States offer a good prognosis. 
Reference 
See Amebic Dysentery. 
XIII. Malta Fever 
(TJndulant Fever, Mediterranean Fever, Neapolitan Fever) 
Etiology 
Malta fever is a specific infection closely resembling septicemia, due to 
the Micrococcus melitensis of Bruce (1886) which rages on the islands of 
the Mediterranean and along its coast; it is characterized by undulatory 
febrile relapses, excessive sweating, symptoms of arthritis, marked rheu- 
matic pains and enlarged spleen. The disease has at various times been 
found in Texas. The disease is now known to be due to the drinkinc of 
vncoolced goat milk which is charged with the organism of Bruce. The 
tendency of the disease is toward chronicity or a subacute course, the aver- 
age. duration being 120 days. There are occasional malignant infections 
in which the disease runs a rapid course to a fatal termination; these at 
present are exceedingly rare. The statistics of the Malta garrison show 
2,229 cases, with a mortality of 77. 
The discovery of the cause has reduced the number of cases, so that its 
occurrence is now comparatively rare; boiling the infected milk prevents 
the spread of the disease. The period of incubation is from 6 to 10 days. BACTERIAL DISEASES 
197 
The diagnosis is easily corroborated by modern blood cultural methods 
and characteristic agglutination. 
Symptoms 
The fully developed picture of the disease resembles the typhoid condi- 
tion very closely; in severe cases the heart muscle shows weakness, pulse 
may be small and intermittent, there may be edema of the lungs; pneu- 
monia is an occasional complication. The temperature which follows a short 
period of malaise may mount to 105° F., but after a few days there is 
decided remission, evident improvement of all symptoms, after which 
evening exacerbations become persistent with progressive anemia, malaise, 
asthenia and enlarged tender spleen. Basset Smith called attention to the 
reduction of the leukocytes and their phagocytic power. 
There is painful swelling of the joints and often swelling of the testes. 
Patients grow progressively weaker during these periods which continue 
2 or 3 weeks and which are followed by profuse sweating, but they bear the 
depression well; they then fall into an afebrile period which is soon fol- 
lowed by evening rise of temperature, and may continue with characteristic 
zigzagging of the curve during long periods. 
Bruce contends that one attack produces immunity. Manson and Bas- 
set-Smith deny this contention. 
The tendency is toward recovery. The mortality is not above 2 per 
cent. 
In exceptional cases early heart weakness may cause collapse and death; 
there is no stage of the disease which may not he complicated by sudden 
cardiac asthenia, edema of the lungs, or pneumonia. 
The. agglutinating power of the hlood is of great prognostic signifi- 
cance. Values above 1 to 300 are favorable; decided fall indicates earl} 
relapse. 
Prognosis 
References 
Bassett-Smith. Quoted by Mohr & Staehelin. 
Schilling. Idem. Handbuch der inneren Medizin. Bd. i, Berlin, 1911. 
XIV. Asiatic Cholera 
(Cholera asiatica) 
History 
Asiatic cholera is an epidemic disease due to the comma bacillus 
(Koch 1883), and is always spread by an infected water supply. The 
disease was first authentically described by Jessor in 1817, who probably 198 
SPECIFIC INFECTIOUS DISEASES 
observed it during the preceding year in Bengal; it has been endemic and 
epidemic for ages in India, the delta of the Ganges never being entirely 
free. Tscharaka, the Esculapius of India, and his pupil Sucrata who 
lived long before Christ and recorded their observations in northwestern 
India, gave a classic description of the disease. The first large outbreak 
of the disease on the European continent was early in the nineteenth cen- 
tury. 
There have been six large cycles of the disease recorded in modern 
medical literature: 
I. 1817 to 1823 in Asia and Africa. 
II. 1826 to 1837 in Asia, Africa, Europe, and America. 
III. 1846 to 1862 in Asia, Africa, Europe, and America. 
IV. 1864 to 1875 in Asia, Africa, Europe, and America. 
Y. 1883 to 1896 in Asia, Africa, Europe. 
VI. 1902—mild—Asia and Africa only 
As can be seen from the foregoing data, the United States has suffered 
several times, and its last experience with the disease was in 1893 when 
it was brought to the port of Yew York on several transatlantic steamers; 
but owing to the perspicacity of the health authorities with the concerted 
action of an intelligent and well organized profession, it failed to gain a 
foothold on American soil. 
Symptoms 
Infection of the alimentary canal of animals can be produced by neu- 
tralizing the gastric juice with sodium carbonate and the use of opium to 
prevent intestinal peristalsis. 
The disease presents severe symptoms of gastro-intestinal disturbance, 
watery discharges, associated weakness due to depletion and endotoxemia, 
with, in the severe cases, suppression of urine and other secretions, shrink- 
ing of tissues, great prostration, collapse and other symptoms resembling 
acute arsenical poisoning. 
The blood in the severe cases becomes viscid because of the sudden and 
great loss of serum, while in severe cases the specific gravity may reach 
1,070 or higher. 
In considering the prophylaxis and prognosis of cholera it is unsafe to 
ignore the influence of the carriers of comma bacilli in producing the dis- 
ease. 
There is a surprising difference in the virulence of comma bacilliJ 
hence during an epidemic, rapidly fatal, serious and mild cases may be 
found at the same time and bacilli may be present in the intestines of nor- 
mal individuals, without causing symptoms. Cholera causes greatest havoc 
in districts where sanitation is faulty and masses are crowded together 
under unfavorable conditions. BACTERIAL DISEASES 
199 
In offering a prognosis three stages must be considered: 
1. The stage of diarrhea 
2. The cold or algid stage 
3. The stage of reaction 
1. The Stage of Diarrhea.—Diarrhea may begin toward the end of 
incubation in some cases in which patients previously had gastro-intestinal 
disturbances, but usually during the period of invasion. This stage may 
continue from a few hours (12) to 2 days. 
In severe cases the movements are frequent, large and watery, asso- 
ciated with marked muscular enfeeblement, small thready pulse, and at 
once the evidences of depletion with evident loss of weight, pinched facial 
appearance, pointed prominent nose, sunken eyes, dry skin, great thirst 
and reduced secretion of urine. The persistent vomiting with these symp- 
toms adds to the danger. There is no way of stimulating or nourishing the 
patient except through the skin—the large intestine is also intolerant. The 
pulse grows weaker and smaller; there is feeble systolic force with decided 
fall of blood pressure to 60 to TO mm., mercury: At times there is delir- 
ium. During this stage, however, the mind may remain clear, and death 
is likely to result. 
In the more favorable cases the stools become less frequent, the vomit- 
ing is more easily controlled, and the urine secretion is increased. Cyano- 
sis, cold extremities, rapid pulse and sudden urinary suppression, usually 
lead to death. 
Decided fall of temperature (3 to 5°F.) with any of the above men- 
tioned alarming symptoms during the first stage is dangerous. 
The dryness of the tongue and throat which leads to the vox cholerica 
is not necessarily of grave import; though present in serious cases. 
The small amount of albuminous urine in the more serious cases is 
loaded with hyalin and granular casts. In this and all stages of the dis- 
ease, the urine offers valuable indications for prognosis. 
The prognosis is good, in proportion to the ability of the kidneys to 
withstand the ravages of the disease; hence the quantity of urine secreted 
becomes a paramount factor in prognosis. 
2. The Cold or Algid Stage.—If the prognosis is grave, the patient 
grows worse, urine scant, albuminous, or entirely suppressed; the appear- 
ance is cadaverous; the stools continue watery, large and frequent; the 
body is cold ; the skin is greyish-colored, in most severe cases cyanosed; the 
eyes sunken, uncovered and fixed; the pulse small and scarcely perceptible; 
coma is deep; almost complete analgesia exists; death usually ends the 
scene between the second and fifth day. 
If the case is likely to terminate favorably, the patient slowly bright- 
ens ; the temperature gradually rises from the low mark to which it fell; 
the pulse is fuller and perceptible; and the urinary secretion—the. import- 200 
SPECIFIC INFECTIOUS DISEASES 
ant factor—is increased, clears itself; and the tongue is moister; the stools 
less frequent; and vomiting is relieved. 
In cases with a severe first stage, the patients often die early in the 
algid stage. 
The cramping of muscles is a painful and weakening symptom in 
many cases. 
With nephritis uremia is supposed to be a cause of many symptoms, 
including convulsions, also a serious complication. 
Relapses in cases progressing favorably are not infrequent; this is often 
true where dietetic errors have been made. 
Cholerine, a mild form of the disease, may develop from a preceding 
diarrhea; the symptoms may include many of the more severe forms of the 
disease, but the prognosis is usually good. These cases are recognized by 
their more benign course, less collapse, though they may show cardiac 
weakness, marked renal invasion with less albumin loss than in the severe 
cholera. Occasional cases of cholerine may develop true Asiatic cholera. 
In the Hamburg epidemic this proved to be true in 50 per cent of cases. 
Cholerine is also caused by comma infection. 
3. The Stage of Reaction.—In occasional cases sudden death early in 
the third stage follows a severe case which may have improved slightly in 
the algid stage. 
Great weakness and apathy with cyanosis and cold extremities are 
unfavorable. 
Fall of temperature after rise in the second stage, early in the period 
of reaction with the symptoms above mentioned, is unfavorable. 
Patients falling into a typhoid condition with elevation of tempera- 
ture, without marked coma, abundant urinary secretion, and sufficient 
heart strength to give a fair systolic contraction, offer a more favorable 
prognosis than do those, with the symptoms mentioned in the two preceding 
paragraphs. 
Convalescence may begin suddenly with the appearance of an erythe- 
matous eruption and febrile movement. 
Coma in the third stage of the disease is always unfavorable, and likely 
to be due to uremia and endotoxemia. 
The Blood Picture.—Enormous relative increase of red blood corpus- 
cles is unfavorable; this may reach one to two millions per c. mm. (polycy- 
themia). Leukocytes are markedly increased in unfavorable cases— 
50,000 and over (Biernatzki). 
In unfavorable cases the alkalinity of the blood is reduced because of 
the loss of sodium. 
The height of the specific gravity is of some prognostic value. 
Patients infected toward the end of epidemics usually develop anoma- 
lous types of cholera, but in all of these the prognosis is relatively good. BACTERIAL DISEASES 
201 
Complications 
Complications are always of serious moment. 
Among the complications are gangrene, croupous pneumonia—rarely 
the catarrhal form—hypostatic congestion and edema of the lungs, paroti- 
tis, intestinal ulceration, diphtheritic infection of the intestines, uterus, 
bladder and vagina. 
Abortion which causes prompt death of the fetus offers an unfavorable 
prognosis for the mother. 
Secondary enteritis—chronic catarrh—may follow recovery from the 
acute symptoms. 
Following recovery, there are as a rule no permanent kidney lesions. 
The following general conclusions may be accepted in connection with 
the data already offered: 
Conclusions 
Cholera infection without outspoken symptoms offers a favorable, prog- 
nosis. These patients are, however, subject to the sudden development of 
severe symptoms on slight cause. 
Patients between 6 and 25 have the best chance for restoration to 
health. 
Individual resistance as an important factor in prognosis. 
Fever at any stage of the disease is more favorable than subnormal 
temperature. 
Brightening of the intellect with a good skin reaction, and erythema- 
tous eruption is favorable. 
Past experiences justify placing the mortality of epidemics between 
30 and 80 per cent. 
Alcoholics offer a grave prognosis. 
The period of immunity produced by the disease is exceptionally short. 
References 
Biernatzki. Deutsch med. Wchnschr., 1892 & 1896. 
Jessor. Handb. der Tropenkrankh. (Mense). ii, 294- 
XV. Plague 
{Bubonic Plague, Pest) 
Plague is an epidemic disease due to the Bacillus pestis (1894, Yersin 
and Kitasato), a non-motile, Gram-negative microorganism, showing well 
marked polar staining which may cause either 
1. Bubonic plague 
2. Septicemic plague 
3. Pneumonic plague 
4. Pestis minor 202 
SPECIFIC INFECTIOUS DISEASES 
History 
Plague has been known since the third century of the Christian era; 
there are references in medical history which create a strong suspicion that 
the disease raged before that time, hut information is not authentic. The 
Orient was the original home of the plague, which, during the centuries 
has invaded the continent of Europe repeatedly and has claimed thou- 
sands of victims. 
The plague which visited Europe during the reign of Justinian in the 
Second half of the sixth century was unquestionably due to the same infec- 
tion which caused the plague of Milan in the seventeenth century, which 
has been graphically discussed and illustrated by Fletcher, proving igno- 
rance of the cause of the disease, save as Pare positively declared that an 
invisible agent produced it, thus foreshadowing its bacterial origin. 
The “Black Death” of the fourteenth century invaded all of the then 
known world, destroying twenty-five million souls, and it is held by Ilecker 
that one-quarter of the earth’s population fell victims to the disease. Dur- 
ing the fifteenth and sixteenth centuries bubonic plague never entirely 
disappeared from the continent of Europe—there were epidemics of vary- 
ing severity. With the end of the seventeenth century the disease limited 
its ravages on the continent to Southeastern Europe until 1878 to 1879, 
when Astrakhan (Russia) was infested. During the early nineteenth cen- 
tury Europe continued free from plague. The epidemics of Hong Kong 
(1894), Bombay (1896), and Manchuria (1910 to 1911) include our 
latest experiences with the disease. It spread to many countries, includ- 
ing the West Indies and the United States; San Francisco and California 
suffered most. The virulence of plague is demonstrated by the experience 
of Toulon in 1721 when of its 26,000 inhabitants 20,000 were stricken 
and 16,000 died. 
Infected rats and rabbits introduce the disease indirectly through fleas 
which serve to inoculate man by their bites. Fifty per cent of the rat fleas 
belong to the variety pulex clieopis, which rarely bite man—hence the com- 
parative immunity of the human race; neither does the ceratopliyllus fas- 
ciatus bite man freely. “The common brown rat is not a house resident to 
any extent, so that conditions in England are not very favorable for epi- 
demic prevalence” (Osier). The same is true of the United States and of 
a large part of the European Continent. In the United States and Eng- 
land we have no conception of the terrors of plague without recalling the 
frightful mortality of the disease in India where in 5 years there have 
been, in three provinces almost 54 million deaths attributable to the dis- 
ease. In the remaining provinces of India, numbering 200 million souls, 
there have been 2 million deaths (Osier). At present, plague is endemic 
along the slopes of the Himalayas, in Bombay and its surroundings, in 
East African Uganda and the southeast of Russia. BACTERIAL DISEASES 
203 
Mode of Entry 
It is easy to understand how the unfortunate barber of Milan con- 
veyed the disease from person to person by his infected unguent, which 
must have carried the pus directly from the ulcers; for it requires only a 
slight abrasion or microscopic break of the skin to furnish the point of 
entry for the bacillus—possibly friction alone is sufficient. The lymphat- 
ics promptly transmit the infection and the destructive effect follows. 
The bacillus may also be. inhaled through the respiratory organs and 
provoke pneumonia. Whether through the lymphatics to the blood-stream 
or the lung, the blood is soon surcharged and a condition of profound and 
fatal sepsis develops. It is well to remember for prophylactic purposes 
that pus, urine, feces and the expectoration, may all hold pest bacilli, also 
clothing and dishes, and that they thrive during long periods in damp and 
moderately warm surroundings. Abundant sunlight and weak (1 to 2 
per cent) solutions of bichlorid of mercury promptly destroy the offender. 
Therefore unfavorable surroundings invite the disease. 
1. Bubonic Plague 
After a period of incubation of about 10 days, severe symptoms become 
continuous after a violent chill and high fever. 
The local manifestations of infection of the shin are redness, swelling, 
painful enlargement of the surrounding lymphatics, inflammatory reac- 
tion in the surrounding tissues, evidences of mixed infection, suppuration 
and free discharge of pus. 
Infection to surrounding lymphatics is prompt with furunculosis, char- 
acteristic carbuncles with central necrosis, and often extensive gangrene. 
The more favorable cases suppurate, without necrosis or gangrene. The 
presence of a necrotic or gangrenous center is always ominous. 
So-called “plague spots” are of hemorrhagic nature, and are associated 
with other evidences of purpura. Hemorrhages from the mucous mem- 
branes occur (black death, including hematuria) and are among the most 
unfavorable of all cases. 
The development of sepsis is associated with bacteremia; the bacillus 
is found in the blood; there is diarrhea, albuminuria, high fever of remit- 
tent character, delirium—often wild and uncontrollable—(pestis siderans) 
leading to prompt death in from 70 to 80 per cent of bubonic cases. 
In Egypt Gottschlich found (1899 to 1902) that there was a decided 
difference in the character of the epidemics during the winter and summer 
months. He found that during the summer the disease was widespread 
over entire villages and almost without exception bubonic, in which the 
infection spread from rats, while during the winter the pneumonic type 
was in the ascendency. The infection was “from man to man provoked by 204 
SPECIFIC INFECTIOUS DISEASES 
the massing of the victims in narrowed quarters.” The ravages of bubonic 
plague are naturally reduced as the diseased rats are exterminated by dis- 
ease or by man. 
To prevent the spread of all types of plague must of necessity include 
early diagnosis, prompt quarantine, destruction of infected rats and mice, 
care of the cadaver, proper screening and the use of all modern methods in 
the care of the sick and the protection of those exposed, including the 
immunization with the sera—now easily obtained either from the Pas- 
teur Institute (Roux and Dujardin-Beaumetz) or the Institute at Berne 
(Lustig and Markl). Unfortunately the period of immunization is short 
(3 to 4 weeks). 
Haffkin and Gaffky have done yeoman’s service in this field and both 
agree that the use of the sera is of enormous value in reducing the mor- 
tality of plague. Ilaffkin believes that the death rate among the injected 
is “four times less than those unprotected.” Gaffky, who represented the 
German Pest Commission, unreservedly recommends the use of the Ilaff- 
kin protective vaccination. 
2. Septicemic Plague 
Septicemic plague runs a rapid course with marked hyperpyrexia, deep 
involvement of the nervous system, delirium, coma, rapidly developing 
heart weakness (myocardial degeneration) ; often patients are suddenly 
overpowered and may die within a few hours or during the first day (pes- 
tis siderans). When there are purpuric symptoms (with hemorrhages 
from mucous surfaces), death usually promptly follows. 
3. Pneumonic Plague 
Pneumonia may lead to death without external evidences of lymphatic 
invasion. In many of these cases the bronchial glands show characteristic 
infection. Thorough search often reveals glandular swellings in distant 
parts of the body. The blood is infected and shows the presence of the 
bacillus. 
Pneumonic plague may he secondary to the clearly established bubonic 
picture, or the involvement of the lung follows a severe chill without a pro- 
dromal period. The evidences of grave toxemia are fever, headache, 
vomiting, with or without delirium. 
There may be either characteristic pneumonic sputum or hemoptysis. 
The latter with the hemorrhagic cases is always most ominous, for pul- 
monary edema is likely to be present. 
The unfavorable features which are usually present, besides the 
symptoms mentioned, are hurried respiration, marked dyspnea, cyanosis 
and often besides evidences of vasomotor paralysis, marked degeneration 
of the myocardium. BACTERIAL DISEASES 
205 
The pneumonic process may be either catarrhal (bronchopneumonic) 
or croupous. 
The prognosis of primary pneumonic plague is uniformly unfavorable, 
death ending the scene in from 2 to 5 days—as a rule on the third day. 
Secondary bronchopneumonia offers but slight encouragement for prog- 
nosis ; an occasional case has been saved. 
4. Pestis Minor 
These mild, almost symptomless cases are found at the end of epidemics 
or during periods when there is a lull. Patients are only slightly indis- 
posed ; there may be some tenderness and little swelling of the lymphatics, 
but insignificant febrile movement and recovery is prompt. 
General Considerations 
As we have already stated, the heart muscle is the point of attack which 
yields and promptly ends the life of the plague victims. There are prompt 
degenerative changes in the myocardium and the vasomotor paralysis which 
always accompanies profound toxic states. 
Dicrotism is usually present, blood-pressure reduced, the heart action 
enormously accelerated. 
Rapid pulse (tachycardia) with characteristic toxemia, final sudden 
fall of the pulse to 80 to 90 often precedes death. 
Fall of temperature with persistence of rapid heart action is unfavor- 
able. Arhythmia is less frequent than the pulsus paradoxus which is often 
present with pneumonic plague. 
If an occasional pneumonic recovers, there may he (as is often found 
with ordinary pneumococcus infection) during a considerable period, either 
persistent tachycardia, or what is often found in cases which demanded 
long stimulation, intermission and bradycardia. 
The spleen is usually slightly enlarged but offers no prognostic data, 
neither does the tongue which is uniformly dry, brown and coated. Neph- 
ritis is an accompaniment of the severe cases—hence is frequent. 
The blood shows moderate leukocytosis, and in the majority of cases, 
the presence of the Bacillus pestis. The greater the blood infection the 
more virulent is the disease. Reduction in the number of bacilli in the 
blood, and their disappearance is always of favorable, significance. 
Jochmann, whom I have consulted liberally in the preparation of this 
chapter, places the average duration of plague between 6 and 8 days and 
the average mortality as 70 to 90 per cent. As already stated pneumonic 
and septicemic plague offer the most unfavorable prognoses. The most 
dangerous cases to their surroundings, according to Jochmann, are those 
of the pneumonic type, in which the sputum and microscopic droplets 206 
SPECIFIC INFECTIOUS DISEASES 
exhaled hold the bacilli, and as they are released, spread the infection, 
either directly to the lung or to the tonsils, from which, through the lym- 
phatics, the lungs and distant organs are invaded. 
Complicating meningitis is uniformly fatal. 
The prognosis is always more unfavorable during the early days of an 
epidemic than later. 
Alcoholism, chronic metabolic faults, previously existing and depress- 
ing infections, all influence plague unfavorably. 
References 
Fletcher. A tragedy of the great plague of Milan in 1630. Johns Hopkins Hospital Bull., 
ix, 175. 
Gottschlich. Jochmann, mentioned by Mohr & Staehelin. In: IIandbuch inner. Med. 
1911, i. 
Hecker. Jochmann. Mohr & Staehelin [Z. c.]. 
Jochmann. Mohr & Staehelin Handb. 1911, i. 
Osier. Practice of medicine. 8. ed., 1913. 
XVI. Tetanus 
(Lockjaw) 
The Infection 
Tetanus is a disease caused by the tetanus bacillus (Hicolaier and 
Kitasato), anaerobic, Gram-positive with one swollen end holding a spore, 
characterized by recurring spasms, always painful, stiffness of the neck 
and jaw muscles, with final rigidity of the muscles of the trunk and 
extremities. When fully developed there is marked opisthotonos in most 
cases, the body may be inclined forward (emprosthotonos) or to one side 
(pleurosthotonos). In some cases at times during the course of the dis- 
ease the limbs may continue extended straight and stiff. 
The spore of the tetanus bacillus is resistent to external influence, 
which accounts for the persistence of the germ in earth and manure during 
unlimited periods, from which, through wounds, it enters the skin. The 
bacillus remains localized, and under favorable conditions sporulation 
follows. The toxin produced by the bacilli finds its way into the circula- 
tion, is promptly appropriated by the peripheral nerves, and through these 
is passed to the central nervous system (Meyer). The toxin acts as an 
excitant to the ganglionic motor cells of the cord; hence the spasms and 
tetanic state of the muscles, characteristic of the disease. 
Tetanus may be conveyed through any objects (such as slivers, utensils, 
fireworks) which hold the spores. 
Puerperal tetanus, tetanus or trismus neonatorum and tetanus rheu- 
maticus, are all due to the same microorganism. BACTEKIAL DISEASES 
207 
Tetanus is a widely spread disease over the temperate zones of the 
earth, but is by no means frequent. In the last consecutive 6,000 
cases of internal disease we failed to find a single case of lockjaw. Sur- 
geons report increasing fatalities following burns and injuries from fire- 
crackers and fireworks, many of which are manufactured in buildings 
wdiere they are easily contaminated. 
Factors Influencing Prognosis 
There are a number of facts closely related to the life history of the 
germ which materially influence the course and prognosis of the disease. 
The virulence of the bacillus is naturally an important factor. 
The shorter the period of incubation, the more virulent is the bacillus 
and the less favorable the prognosis. There are cases, usually foudroyaut, 
in which the symptoms follow within 3 or 4 days after injury. 
With the less virulent bacilli the period of incubation is long, varying 
from 2 to 4 weeks, and in these cases the picture of the disease is likely to 
be benign and the prognosis is correspondingly better. This statement 
ought not to lead the clinician to the conclusion that tetanus is ever a dis- 
ease without danger. 
The prognosis is always unfavorable in those cases in which the entire 
symptom complex of the disease develops suddenly or rapidly after the ini- 
tial rigidity. Such cases may show the gravest conditions within a few 
hours, during which there have been repeated tetanic convulsions at short 
intervals. 
In the less serious cases the development of symptoms may occupy a 
number of days, and the convulsions are infrequent. The patient gathers 
strength to resist the painful convulsions during the longer intervals and 
in favorable cases gets a fair amount of sleep. 
The frequency of the spasms is in direct proportion to the gravity of 
the disease. In the more serious cases the spasms may recur several times 
during a single hour. In the milder cases an entire day may pass with hut 
one or two attacks. 
In the more serious cases spasms are provoked by the slightest touch or 
movement of the body and in these, death may suddenly follow during■ 
respiratory spasm. 
Persistent sleeplessness with frequently recurring spasms is always 
grave. 
Foudroyaut cases may end in from 1 to 3 days. In these, the spasms 
are frequent, the pain severe, the pulse rapid and small, respirations hur- 
ried (20 to 80), and before death there is hyperpyrexia, the temperature 
reaching as high as 106° to 107° F. The urine is retained and likely to be 
albuminous. With hyperpyrexia the patient may fall into a comatose 
state. 208 
SPECIFIC INFECTIOUS DISEASES 
Retention of urine is frequent and is not of itself to be interpreted as 
a serious symptom. 
The pulse is rapid in serious, but little accelerated in mild cases. 
Sudden tachycardia which persists during one or more hours with 
frequent spasms almost always presages an early death. 
Cyanosis is always unfavorable. 
The temperature is not materially elevated and offers nothing of value 
for prognosis, save in those foudroyant cases already mentioned, and 
in some cases before death it suddenly rises to 105°-107° F. when the 
patient is likely to fall into coma. With hyperpyrexia there is marked 
myocardial insufficiency and cyanosis before the end. 
The wound itself offers nothing which serves to guide the clinician in 
offering a forecast of the disease. 
If at the height of the disease there is a decided increase in the fre- 
quency of the tetanic spasms the prognosis is bad. 
In favorable cases improvement includes the lengthening of the in- 
terval between the attacks, decrease of muscular rigidity and pain, ability 
to swallow without spasm, improvement of the pulse, return of the tem- 
perature to normal, and decided change in the facies of the patient. 
Before a favorable prognosis is justified in any case of tetanus all 
symptoms must continue favorable during several days, for relapse can- 
not be excluded until convalescence has been fully and permanently estab- 
lished. 
The duration of the disease is variable; death may follow only a few 
hours or a few days (2 to 6) or there may be from 6 to 10 weeks of un- 
certainty. The long drawn out cases usually recover. 
Convalescence is usually prompt, and it is surprising to note how 
rapidly, as a rule, the patient regains his health and strength without 
sequelae. 
Myocardial weakness may persist during several weeks with some 
cardiac dilatation. Full recovery from this sequel is the rule as well as 
from arhythmia, which occasionally follows the acute period. 
Puerperal tetanus may develop in from 3 to 15 days after confinement, 
is fortunately rare, but almost always leads to death. 
Trismus neonatorum usually develops from 4 to 10 days after birth 
and is almost uniformly fatal. There are cases on record which were 
also fatal in which the periods of incubation of both puerperal tetanus 
and that of the newborn were as long as 3 weeks. 
The mortality of tetanus is high in cases untreated by modern meth- 
ods. Of the cases with a short period of incubation, less than 10 days, 
Rose reported 96.7 per cent of deaths, against an average mortality of 80 
to 90 per cent. 
The prognosis of tetanus is unquestionably favorably influenced by 
the routine use of prophylactic injections of the tetanus antitoxin after BACTERIAL DISEASES 
209 
injuries. Already there are sufficient evidences at hand to justify the 
foregoing unqualified statement. So far as the influence of tetanus anti- 
toxin on the course of the disease after its full development is concerned, 
we have few favorable results to offer. 
There are a number of cases recorded in medical literature in which 
the injections of magnesium sulphate (intraspinous) after the method of 
Meltzer, with the free use of the tetanus antitoxin have been followed by 
recovery. There are also cases in which the hypodermic use of mag- 
nesium sulphate has seemed to influence the spasms favorably (Meltzer). 
Kocher found the prognosis bad and the magnesium sulphate contra- 
indicated when the cerebrospinal fluid failed to flow. 
References 
Henry. Magnesium sulphate & tetanus treatment. Internal. Clinic, 17 Series, iv. 
Kocher. Correspondenzblatt f. Schweitzer Aerzte, Basel, Sept. 10, 1912, No. 26. 
Meltzer. The literature on the use of intraspinous injections of magnesium sulphate has 
grown since the experiments of Meltzer and can easily and with great 
profit be followed by consulting the Index Medicus. Lancet, London, June 
26, 1915 (most recent resume). 
Meyer (H.). (Quoted by von Mehring &Krehl) Innere Medizin, 1913. 
Rose. Der Starrkrampf beim Menschen. Stuttgart, 1897. 
Stadler. Meltzer Injection, etc. Berl. klin. Wchnschr., 1914, No. 3. 
XVII. Anthrax 
(Woolsorters’ Disease, Malignant Pustule, Milzhrandj 
The Infection 
Anthrax is a disease of sheep and cattle, caused by the Bacillus 
anthracis, a large, Gram-positive bacillus, which spores outside the body 
and is conveyed to man either through the skin directly, the lungs, or 
the alimentary canal, occasionally through the nose and mouth. Pol- 
lender in 1855, and Brauell in 1857, described the bacilli now known 
to cause the disease after a period of incubation averaging 7 days. The 
most frequent source of the infection in man is through the skin from 
hides, wool and pelts of the infected animals; there are some who con- 
tend that insects through their sting may also convey the disease from 
infected animals to man. 
Anthrax may be either (1) external or (2) internal, and is classified 
as follows: 
1. External anthrax. 
(a) Malignant pustule. 
(b) Malignant anthrax edema. 210 
SPECIFIC INFECTIOUS DISEASES 
2. Internal anthrax. 
(a) Gastro-intestinal (alimentary mycosis intestinalis) 
(b) Respiratory. 
(c) Splenic. 
External Anthrax 
(a) Malignant Pustule.—Malignant pustule is the most frequent va- 
riety of anthrax found in man. Its early recognition and rational surgical 
and serum treatment save many patients. The fact that with anthrax 
there is less pain than with the ordinary furuncle, leads to delay in treat- 
ment and to consequent serious constitutional invasion. Rapid extension 
of the pustule with spreading and deep central gangrene, hemorrhagic 
vesicles in the periphery, extensive infiltration, erysipelatous blush with 
marked constitutional symptoms, are evidences of malignancy and demand 
a guarded prognosis. Marked lymphatic extension and tenderness with 
glandular enlargements are not always of serious moment; their 
ment without increase of constitutional manifestations after radical treat- 
ment is always encouraging. 
If the pustule is neglected, the prognosis is accordingly influenced un- 
favorably, for before the end of the first week there are symptoms of 
sepsis, including fever, delirium, diarrhea, vomiting, hematemesis, foul 
coated tongue, anorexia, enormous prostration, wasting, enlarged spleen, 
and after a period of collapse in many cases with myocardial weakness 
and continuation of the septic symptoms for from 2 to 4 days, death 
ends the scene. 
There are foudroyant cases in which evidences of sepsis are early and 
the development of grave symptoms is rapid in which death may follow 
within 2 days after the appearance of the skin lesion. 
Two-thirds of skin infections recover. 
(b) Malignant Anthrax Edema.—This variety of external anthrax is 
fortunately less frequent than is the malignant pustule. It is more fre- 
quently found with invasion of the face, i. e., eyelids, head, hands or arm. 
The pustule is absent, but the edema is rapidly formed and is diffuse. 
Sepsis is promptly developed and is severe; heart weakness and deep 
invasion of the nervous system are at once alarming. The prognosis of 
the edematous variety of external anthrax is almost uniformly fatal. 
2. Internal Anthrax 
The diagnosis of all types of internal anthrax is exceedingly difficult 
and in most cases impossible, as a rule it is made post mortem only. 
(a) Gastro-intestinal Anthrax (Mycosis Intestinalis).—The progno- 
sis is almost uniformly bad. There are. early evidences of grave infec- BACTERIAL DISEASES 
211 
tion with symptoms of severe gastritis, including vomiting, often hema- 
temesis, bloody diarrhea, prompt evidences of sepsis, including fever and 
weak heart, tympany and abdominal tenderness with other symptoms of 
peritonitis and enlargement of the spleen. In some of these cases there 
are evidences of cutaneous malignant purpura with bloody vesicles. Cases 
of alimentary anthrax rarely live beyond the third day of the disease. The 
mortality varies between 50 and 87 per cent. (The post mortem appear- 
ances are characteristic and show changes in the mucosa of the stomach 
and intestines, including elevations varying in number (20 to 50) with 
central necrobiotic patches, black sloughs and consequent ulcerations, be- 
sides the enlarged spleen already mentioned.) 
(b) Respiratory Anthrax.—There are occasional cases of respiratory 
anthrax which show less tendency to pulmonary edema than does the 
malignant type, which run a subacute course varying from 2 to 5 weeks, 
ending in recovery. These cases are exceptional. 
The majority of pulmonary invasions offer but scant hope of recovery. 
The mortality may he as high as 50 to 90 per cent. They begin with many 
of the symptoms of a severe pneumonia, promptly develop pulmonary 
edema, and the victim drowns in his own serum. Pleurisy is frequent. 
There is in the severe cases a violent initial chill with high fever, and early 
manifestations of cardiac toxemia. The extensive transudate into the 
alveoli causes distressing dyspnea, cyanosis, and evidences of carbonic acid 
poisoning. In these malignant cases, the sputum is promptly bloody after 
a short period during which it may be serous. Hemoptysis is not infre- 
quent within the first 24 hours, or it may precede death on the second or 
third day of the disease. The heart is rapid from the beginning and soon 
shows the strain due to toxemia and possible secondary pulmonary obstruc- 
tion (edema, etc.). Diarrhea, delirium and coma are always alarming 
symptoms. 
Infection of the nasal passages, larynx, treachea or larger bronchi, with 
or without pulmonary anthrax, adds an enormous element of danger and 
usually causes death. 
The majority of cases of the respiratory type are found among rag- 
pickers or woolsorters, and as all other forms of internal anthrax, are 
usually fatal. Death follows after 2 or 3 days of symptoms from cardiac 
asthenia or because of the reduced respiratory surface due to infiltration 
and edema. 
(c) Splenic Anthrax.—Cases of splenic anthrax run a fatal course 
without pustule or other evidences of local disturbance, but with all of 
the symptoms of the more virulent and malignant types of the infection, 
including brain symptoms due to embolic infarcts causing hemorrhages 
into the cerebral cortex and the usual evidences of sepsis, characteristic of 
all fatal cases. 
Encouraging reports which prove the value of the antianthrax serum 212 
SPECIFIC INFECTIOUS DISEASES 
are multiplying and justify a more hopeful view of the outcome of those 
cases of anthrax which are recognized early and which are promptly 
injected and treated, than has been offered in the past. 
Pasteur’s prophylactic vaccination of cattle and sheep has reduced the 
mortality among these in France to one-twelfth the former number, while 
the production of active immunization by means of the Sobernheim serum, 
now largely used on the continent of Europe, seems to be more certain 
and lasting in its effect—all of which argues favorably for the protection 
of mankind against the disease and the consequent limitation of its 
ravages. 
XVIII. Glanders 
{Farcy, Malleus, Die Rotz) 
The Infection 
Glanders is a highly contagious disease, due to the Bacillus Mallei 
(Loeffler-Schiitz Bouchard, 1882), a Gram-negative germ, which after a 
period of incubation, varying from 3 days to as many weeks (usually from 
3 to 4 days) is followed by symptoms of sepsis, suppurating and granulat- 
ing ulcerations, either of the nose or skin, with a tendency to spread over 
the body rather than to remain localized. 
The tissues around the ulcers are infiltrated. The ulcers are crater- 
shaped after a period of pustulation when the skin is involved. 
The disease is contracted from infected horses, mules, donkeys, rarely 
from other animals; the secretion of the ulcer in the nose, occasionally 
of the skin, holds the disease-producing bacillus. Those working in 
stables and on ranches are oftenest infected. The disease is either: (1) 
Acute glanders, or (2) Chronic glanders. 
1. Acute Glanders 
Acute glanders rum a rapid course to a fatal termination as a rule 
in from 7 to 14 days. The serious nature of the infection is recognized 
by the weakness and wasting during the period of incubation after which 
the severe chill, immediate constitutional symptoms and the facies of the 
patient with local manifestations, promptly prove the presence of grave 
disease. 
The spleen is usually palpable and enlarged. 
The site of infection shows changes early; there is redness, swelling 
and great pain when the skin is involved with the development of vesicles, 
pustules and ulcers. 
Nasal infection is associated with early symptoms of dry catarrh, soon 
followed by ulceration and abundant secretion which becomes foul-smell- 
ing and purulent. Nodes form on the mucous membrane of the nose, are BACTERIAL DISEASES 
213 
often found on the conjunctiva, in the mouth, pharynx, larynx, bronchi, 
lungs, intestines, and after 7 to 10 days appear in the muscles, usually 
those of the arm (biceps) the chest and calves. 
In occasional and rapidly fatal cases the disease begins with symptoms 
of transitory facial erysipelas or marked redness of the face after which 
the true nature of the disease is manifested in the development of the 
nasal and cutaneous changes. 
In all cases the lymphatics in the neighborhood of the lesion are swollen 
and tender. 
There are acute and rapidly fatal cases in which the early symptoms 
are those of general sepsis, which latter antedate all local manifestations 
and obscure the diagnosis. There may be periarticular swellings with pus 
formation and infiltration. 
Far-reaching invasion of the lung is uniformly fatal. 
The usual changes found with general sepsis in vital organs, heart 
and Jcidney particularly, increasing weakness of the former, insufficiency 
of the latter, are prominent before death. 
The character of the fever varies, but as a rule, it is intermittent; the 
sweats are often profuse and weakening, and with a rapid small pulse, 
such cases die during the second or third week. 
The onset of delirium or other symptoms of deep involvement of the 
nervous system, including coma is always ominous, usually fatal. 
2. Chronic Glanders 
This form of the disease may persist during a number of months or 
several years with exacerbations of all of the symptoms and multiple 
lesions of the acute cases already considered, including ulcerations, many 
abscesses, muscle nodes and lymphatic enlargements. Bollinger reports 
a case which lasted 11 years, while Romberg mentions cases which con- 
tinued with irregular fever 1 and 2 years. 
Recovery from chronic glanders is not exceptional and may follow in 
50 per cent of cases. Bristow reported a case which he persistently treated 
with an autogenous vaccine in which the patient made a full recovery. 
Prophylactic measures which include the prompt killing of all infected 
animals and the thorough disinfection of stables, cleanliness and the use 
of antiseptics by those who are exposed, with the early injection of mal- 
lein (a filtrate a dead glycerin and boullion culture of the Bacillus mal- 
lei) offer the only methods of controlling the ravages of the disease. 
Bollinger, (iQuoted by Romberg) von Mehring. 8. ed. 
Bristow. New York State J. of Med., May, 1910. 
Romberg, von Mehring-Krehl. 8. ed. 
References 214 
SPECIFIC INFECTIOUS DISEASES 
XIX. Leprosy 
{Lepra; Miselsucht (German); Meltzei (German); la Lepre (French); 
la Lebbra (Italian); Spedalsklied (Norwegian); Melaascheid 
(Dutch) ; Elephantiasis graecorum) 
The Infection 
Leprosy is a chronic infectious disease due to the lepra bacillus of 
Hansen (1871) (Bacillus leprae), which has been known for ages, is 
mentioned in the hible, in the old literature of India, was prevalent among 
the Egyptians, the ancient Jews and Greeks, many centuries before the 
Christian era. The history of leprosy includes one of the most interest- 
ing and important chapters of medicine, and should be studied by the 
student, that he may gain an idea of the importance of the infection 
during all of the ages, the sufferings of its victims, who were always 
feared, and usually banished to exile, too often neglected. Even Moses 
banished the afflicted from the camps of the Children of Israel. Since 
time immemorial the civilized and semi-civilized nations have all treated 
the leper with the same fear and have left him to his fate. It is a strange 
fact that in and in Portugal, leprosy has continued endemic to 
the present day, also in the West India Islands. 
With the introduction of syphilis in the fourteenth century leprosy 
seemed to recede. The disease was introduced into America by the African 
negro slaves. Indians seem to resist the infection while the European, the 
mixed races and negroes are most susceptible (Krause). 
Leprosy is not hereditary; it may be transmitted just as is tuberculosis. 
The new born babe has not been found infected, and the youngest leper 
children are not older than from 3 to 5 years. All persons above the third 
year may be attacked. 
Leprosy has a period of incubation which may extend over many years 
(3 to 32). The disease is rarely conveyed to the attending physician or 
to the nurses. For over 25 years we have been interested in the fate of a 
number of noble Sisters of Charity who went from St. Joseph’s Hospital, 
with which we have been connected, to Molokai in the Sandwich Islands; 
they have been in close contact with the lepers of the colony and all have 
continued free from infection. 
The disease is characterized by symptoms of three types: 
1. Tubercular type. 
2. The anesthetic type. 
3. Mixed type. 
1. The Tubercular Type 
This type includes skin changes in which, during varying periods, 
there are hyperesthetic and reddened macules usually on the face and BACTERIAL DISEASES 
215 
hands, later on the legs (elpra maculosa) in which nodules (tubercles) 
finally develop w7hich undergo retrograde change (necrobiosis), ulcerate, 
often involving the underlying tissues including the tendons, the bones 
and the adjacent soft parts. In some cases there are but few or no tuber- 
cles or nodules; the skin continues anesthetic, becomes pigmented, and 
shows other trophic changes; the spots of original erythema may bleach, 
becoming strikingly white (lepra alba). Sensory changes may develop 
very slowly; when once present they persist. 
Fever may precede the development of pigmentation or other visible 
trophic changes (lepra alba). 
The hair is usually diseased or lost; mucous membranes may show 
marked changes (including the conjunctiva and nasal mucosa) ; ulcerative 
keratitis and deep ocular changes may lead to far-reaching destruction and 
blindness. 
Many lepers of the tubercular type die of laryngeal invasion or pneu- 
monia. The prognosis is absolutely bad. The tubercular type of leprosy 
is more contagious than is the anesthetic. The nasal secretion according 
to Sticker holds the infecting bacillus, and he believes that the disease is 
spread from this course. Meier has proved that 70 per cent of tubercu- 
lous lepers offer a positive Wassermann reaction. 
Sexual intercourse is not an important factor in transmitting the 
disease; its influence is greater when the victims live under unsanitary 
conditions. Munch found that with marriage of short duration of a leper 
and non-leper, the disease was transmitted in 2.5 per cent of cases; while 
with those wTho lived together in matrimony during long periods of time 
the statistics showed 11 per cent of transmissions. 
Early invasion of the mucous membranes particularly the larynx is 
unfavorable so far as the duration of the disease is concerned. 
2. The Anesthetic Type 
The anesthetic type of leprosy is characterized by anesthesias and 
hyperesthesias. There are severe pains in the extremities (usually the 
legs) with hyperesthetic areas or there may be anesthesias. In some cases 
there are both anesthesic and hyperesthetic patches. As the disease 
develops, the nodules may easily be felt along the nerve trunks, and the 
trophic changes are marked. These include the formation of blebs with 
final ulceration which is deep and extensive, changes in the extremities, 
usually the toes and fingers, in which there are contractures, destruction 
of tissue and gangrene of terminal phalanges. 
The prognosis so far as life is concerned with anesthetic leprosy is not 
bad, for the patients may live and continue useful during many years; as 
a rule they die of inter current disease. 
The deformities due to loss of tissue and contractures prove a serious 
handicap, as do the anesthesias and paresthesias. 216 
SPECIFIC INFECTIOUS DISEASES 
3. The Mixed Type 
The possibility of the mixing of the two types in the same patient 
must be remembered. The tubercular type is very likely to develop periph- 
eral anesthesia and the patient dies with “mixed leprosy.” The anesthetic 
type is not likely to develop the characteristic “tubers” of type 1. 
Leprosy predisposes to tuberculosis; about 30 per cent of lepers were 
found tuberculous at the Trinidad Asylum. 
Nephritis is a frequent and serious complication; Abraham’s statistics 
showed that 32 per cent of 109 lepers autopsied had kidney disease. 
“There was no specific leprous invasion” of the kidney. 
Death may follow 1 or 2 years of infection in rare cases; there are on 
the other hand cases in which the disease has appeared to be arrested— 
even cured—while a period of 40 years has been recorded in some in- 
stances. Abrahams reports 18 years as the average duration of cases in 
Trinidad, 6| years for the nodular; 10 years for the anesthetic types, and 
9f years for the “mixed” cases. 
In young subjects the disease progresses more rapidly than during the 
active years of life, this is true of the anesthetic type particularly. 
Invasion of the internal organs always shortens life. 
With far-reaching infiltration of the skin the progress is slower than 
with multiple tubercle deposit. 
The number of cases is being rapidly reduced by the segregation of 
lepers and their proper hygienic care. 
Relapse 
The majority of cases which have been watched in which recovery was 
suspected, relapse after long or short periods, finally running an exceed- 
ingly chronic course. 
It may he safely assumed that “once a leper, always a leper.” 
References 
Abraham. Allbutt & Rolleston, 2. ed., ii, 665. 
Krause. Mohr & Staehelin, Handbuch der Medizin. i, 876. 
Meier. Lepra. Biblioth. Internat., Bd. II, 3J+0. 
Munch. Mohr & Staehelin [l. c.]. 
Sticker. Handbuch der Tropenkrankh. Mense, 1905 & 1914. 
XX. Tuberculosis 
Tuberculosis includes all diseases caused by the Bacillus tuberculosis 
of Robert Koch (1882), which latter causes the formation of nodular de- 
posits (tubercle), or diffuse infiltrating masses, showing tendency to be- BACTERIAL DISEASES 
217 
come caseated, causing ulceration and breakdown of included tissue, with 
an effort on the part of nature to heal by the formation of new connective 
tissue, calcification, the enclosure of deposits and the walling off of cavities. 
The disease is infectious, contagious, preventable and curable. 
History 
There have been epoch-producing periods and events in the history of 
tuberculosis which have cleared the horizon, proved the cause and pathol- 
ogy of all tubercular processes, extended our knowledge, made diagnosis 
positive, established rational methods of treatment and prophylaxis, and 
have further entirely changed the prognosis of all forms of the disease. 
Medical history includes references to tuberculosis, centuries before 
the Christian Era. Hippocrates understood and described the manifesta- 
tions of the disease 400 years before Christ; Celsus, Aretaeus, and Galen 
were also familiar with the disease but added little to the work of Hip- 
pocrates. The first advance was made when Sylvius (seventeenth century) 
demonstrated the association of nodular deposits with consumption. He 
considered these enlarged lymphatic glands. The next advance was made 
when Morton, a contemporary of Sydenham, in 1689 contributed a work 
in which he gave a classic description of the clinical history of the disease. 
Morgagni and Baillie followed, denying the identity of the tubercle 
nodules and demonstrated that they are not enlarged lymphatic glands. 
Their gross anatomic structure was recognized. The two most important 
advances of the early nineteenth century were: (1) the recognition by 
Bayle of the anatomic structure of the miliary tubercle with the recogni- 
tion of its general distribution, and its importance in causing constitu- 
tional disturbances, and (2) the establishing by Laennec (himself a 
victim of the disease) in 1819 of the most valuable of all knowledge con- 
nected with tuberculosis, save the discovery of its cause, the unity of all 
tuberculous lesions. At first his dictum was controverted; even Virchow 
remained unconvinced and differentiated cheesy pneumonia and other 
tuberculous processes. Fortunately Virchow lived long enough to change 
his views and subscribed willingly to the established conclusions of the 
French clinician. 
Valsalva and Morgagni understood the contagious nature of tubercu- 
losis. 
It remained for Villemin by experiment in 1865 to offer the next great 
advance in the history of tuberculosis and to lay the foundation of all 
advances which have followed since his day in connection with this disease. 
He proved the communicability and the infectious nature of all forms of 
tuberculosis, pointing the way to the search for its cause. Villemin’s work 
has failed to receive the attention and the praise from the profession which 
its enormous importance deserves. His name will live in history so long 218 
SPECIFIC INFECTIOUS DISEASES 
as our science and art sliall endure. Cohnheim, the leading pathologist of 
Germany, ridiculed the conclusions of Villemin; but he too lived to 
acknowledge his error and subscribed fully to knowledge which is now 
universally understood by the professional and lay world. 
In 1882 Robert Koch, a quiet, modest, almost unknown observer, 
working patiently away from the large medical centers, gave the world the 
results of his investigations and demonstrated the Bacillus tuberculosis as 
the real cause of all forms of tuberculosis, wherever located. 
Then followed in rapid succession the appreciation of the needs of the 
tuberculous sick by such men as Brehmer in Germany, and our own 
Trudeau, the underlying basis of their success including the full apprecia- 
tion of the life history of the infecting agent, the resistance which the 
patient offered when placed in a favorable environment reinforced by the 
strength which resulted from pure air, a flood of sunlight on the body and 
on the germ as well, with the pabulum so much needed to lift the resisting 
power of the patient to par or above. Alonzo Clark, my revered teacher in 
1877 and before, repeatedly insisted that “tuberculosis can never advance 
in normal tissue or when the patient’s health is at par,” to which we add 
to-day: the tubercle bacillus does not readily proliferate or find a suitable 
habitat in normal tissue. The germ lies ready to attach, and the disease 
progresses when vitality is lowered and tissues are changed from the 
normal. 
The final factors which have influenced the prognosis of tuberculosis 
have been the education of the people, and the growth of professional 
hnowledge which makes the early recognition of the disease possible. The 
tuberculous subject to-day enters upon the early treatment of his condition 
fully instructed, with hope and the belief that by natural methods he will 
either be cured or his disease will become latent. The factors previously 
mentioned have influenced prognosis favorably in all civilized countries 
during the past 30 years. The data collected by statisticians, particularly 
those of Hoffman, deserve recognition and wide publication. 
In the United States, statistical evidence proves that the mortality 
from pulmonary tuberculosis has actually and relatively diminished; 
“that on the basis of rates for the registration area, the saving of lives due 
to the campaign against this disease during the decade ending 1910 alone, 
has amounted to nearly 200,000.” The death rate during the past decade 
has been reduced from 174.5 per hundred thousand of population to 139.7. 
Hoffman s study of the combined mortality from tuberculosis of the cities 
of Hew York, Philadelphia and Boston for 100 years, commencing with 
1812, shows a persistent reduction of the death rate from 418.6 per hun- 
dred thousand population in the first decade of this period to 213.9 in the 
last decade. This tabulation of Hoffman’s is the first ever made for any 
group of large cities and establishes the fact that the greatest reduction 
commenced with the discovery of the tubercle bacillus in 1882 and the BACTERIAL DISEASES 
219 
education of tlie masses. The death rate in 1881 was 389.1, in 1912 it had 
declined to 180.1 per 100,000. A study of 50 large American cities for 
the 40 year period beginning 1871 shows a fall from 335 per hundred 
thousand in 1881 to 166 in 1911. 
In the northern and western cities the decline was from 325 to 160 
per hundred thousand, or 50.8 per cent. 
Among the whites of the southern cities the fall was from 301 to 150 
or 50.2 per cent; the colored population showed a reduction from 668 to 
423 or 36.7 per cent. 
Massachusetts, Rhode Island and Connecticut show a decrease from 
276 per 100,000 population in 1881 to 146 in 1911—47.1 per cent. 
The reduction in the death rate for women is greater than the decrease 
for men. 
The statistics as collected by Hoffman—a work for which the profes- 
sion owes this layman an everlasting debt of gratitude—prove that the 
reduction “in the tuberculosis death rate in the United States during the 
last 40 years has not been less, but in many cases more than in other civil- 
ized countries throughout the world.” 
In England the drop in the death rate during the past 40 years is 
almost 50 per cent. 
In London from 1901 to 1910 (Osier) the death rate from con- 
sumption has dropped 33 per cent; all other forms of tuberculosis have 
been favorably influenced. 
In Germany there has been a like and encouraging reduction. 
For the clinician, in the light of our present knowledge, it is safest to 
recognize two pathogenic types of bacilli as the cause of human tubercu- 
losis: 
I. Typus humanus (Koch). 
II. Typus bovinus (Theobald Smith). 
The overwhelming number of cases are due to the typus humanus of 
Koch. A bitter war has been waged in connection with the part played by 
the bovine tubercle bacillus in causing human tuberculosis, von Behring 
is a strong advocate of the theory of bovine tuberculosis, introduced by 
milk (enterogenic infection) as the main cause of pulmonary tuberculosis, 
assuming that the bacilli remain latent in the lymphatics during many 
years; to which Calmette vigorously subscribes. Robert Koch in London 
at the Congress for Tuberculosis (1902), and often after that memorable 
occasion, held opposite views. Koch did not believe that the bovine 
bacillus was pathogenic for man, and advanced strong arguments to prove 
his contentions. The conclusions of Kossel are as follows: 
1. Pulmonary tuberculosis with few exceptions depends upon infec- 
tion with the typus humanus. 220 
SPECIFIC INFECTIOUS DISEASES 
2. Tuberculosis is conveyed from man to man by means of the Koch 
bacillus. 
3. Bovine transmissions of tuberculosis to the human subject through 
milk or meat (typus bovinus) is rare and of minor importance. 
It will be noted that Kossel, an ardent disciple of Koch, does not com- 
mit himself against the possibility of bovine infection, but concludes that 
“to control tuberculosis, contagion from man to man must be prevented.” 
Orth contends that 10 per cent of all forms of tuberculosis of early life 
are of the bovine type and cites Kossel’s own statistics to prove the truth 
of his contentions. These show the bovine type in 4.3 per cent of bone 
tuberculosis, 10.1 per cent of tuberculous meningitis, 23.8 per cent of 
general tuberculosis, 40 per cent of tuberculosis of the neck glands, and 
49 per cent of all forms of abdominal tuberculosis. Orth’s conclusion 
for our purpose is significant: “tuberculosis cannot be effaced so long 
as bovine tubercle bacilli are conveyed from infected animals to man.” 
Heredity as a Factor in Prognosis 
Does heredity, by the transmission of tuberculosis from parent direct 
to the offspring, influence prognosis ? This question has been vigorously 
debated during the centuries. We are agreed that both in man and in the 
calf congenital tubercle is so rare as to be a curiosity. 
The child is not born with tuberculosis, the disease is acquired, Bande- 
lier and Roepke contend that medical literature includes but 120 cases 
of congenital tubercle, of which only 20 bear close scrutiny. Tubercu- 
losis during the first months of life is exceedingly rare. 
I have repeatedly used the von Pirquet test in babes, the offspring 
of tuberculous mothers or fathers, with negative result until the time of 
infection. One of the great advantages of the von Pirquet test for diag- 
nosis and prognosis is the fact that the time of infection can be established 
by it. If in a child, the offspring of a tuberculous parent there are no 
symptoms and the test is negative, later symptoms develop and another test 
is positive, it may be concluded that tuberculosis wherever located has not 
existed long. 
What the offspring of the tuberculous parent inherits, is a vulnerabil- 
ity, a predisposition, ivhich makes the child ready to develop tuberculosis 
on slight cause. The susceptibility in other words is greater in the off- 
spring of the tuberculous than in the child coming into the world without 
handicap. Every clinician of experience numbers “tuberculous families” 
among his clients. The following quotation is clear and to the point: 
“Dr. Horder says that the existence of tuberculous families is one of 
the cardinal facts in clinical medicine, and I agree with him; but on this 
point I am disposed to make one or two remarks. I would oppose the 
too frequent assumption—not by the present writers—that the victims BACTERIAL DISEASES 
221 
of tuberculosis are after all weaklings whose weeding out is painful to 
their friends, is on the whole, good for the stamina of the race. It is 
true that by inheritance or by privation, a person may be so debilitated as 
to offer a lessened resistance to any injurious influence from without; but, 
on the other hand, in respect of tubercle, such a lack may mark a family 
from generation to generation, as a peculiarity rather than a frailty, or 
at worst, as a flaw which is open to one kind of stress only.” “Such a 
constitution is as a lock, which may be shut to every key but one. Bar 
the tubercle, and such a one may continue strong and beautiful” (All- 
butt). Brehmer found that the youngest children of tuberculous parents 
and their children in turn were most disposed to tuberculosis. 
Children of the tuberculous show a higher mortality than do those of 
non-tuberculous parents, the death rate decreasing as these children grow 
older. The death rate is greatest among these children, the nearer their 
birth to the time of the parents’ death. We have found under improved 
environment that the removal of these children from the danger of infec- 
tion is a most important factor, for thereby their lives can often be saved. 
Congenital stenosis of the pulmonary valve invites tuberculosis. It is 
the exception to find a child with this defect without tuberculous infection 
after the fifteenth year; often earlier. 
Alcoholics wflth inherited susceptibility are ready victims. 
The habitus phthisicus predisposes to pulmonary and other forms of 
tuberculosis. The misshapen chest, the small heart, the tendency to 
glandular enlargements (lymphatism) and the habitus asthenicus (Kraus, 
F.) including faulty growth and development, are among the factors which 
invite in the vulnerable, the non-resistant, and predisposed, the develop- 
ment of tubercular phthisis. 
Acquired and Inviting Factors 
Acquired and inviting factors are of paramount importance in the 
development and progress of tuberculosis. 
All diseases which lower vitality increase susceptibility to tuberculosis. 
Improper diet, bad air, insufficient ventilation, crowded cities, tenements, 
impurities of all kinds, inhalation of dust, poor clothing, prolonged damp- 
ness, sedentary occupations, pernicious habits, alcoholism, worry, want, 
the crowded prison and workshop, all lower resistance and invite tuber- 
culosis. All acute and chronic respiratory diseases which are associated 
with changes in the bronchial nodes or respiratory mucous membrane, 
unless controlled by treatment or placed in favorable general condition, 
offer a ready culture medium for the tubercle bacillus. 
A large number of children are infected from tuberculous invasion of 
the bronchial lymph nodes which has remained latent during months at 
times, following measles, whooping cough, pneumonia (lobular and lobar), 
acute bronchitis, scarlet fever (less often), and other infections. 222 
SPECIFIC INFECTIOUS DISEASES 
In the adult, typhoid fever, malarial, and influenzal diseases, as well 
as syphilis, also prepare the individual for further infection by the tuber- 
cle bacillus. Usually they kindle a latent process into activity. Dia- 
betes and pregnancy are among the inviting conditions. When tubercu- 
losis follows pleurisy, the latter was in all probability of tuberculous origin 
also. 
There are diseases which seem to offer resistance to the progress of 
tuberculosis; these include gout, nephritis, asthma, emphysema, and mitral 
stenosis. The consecutive hyperemia associated with mitral stenosis is 
held to be antagonistic to the development of tuberculosis. The infection 
with tubercle bacilli of the majority of mankind at some time during life, 
usually before the twelfth or fifteenth year, unquestionably produces a 
degree of immunity and proves an important factor in prognosis later in 
life, von Behring believes that the favorable course of chronic tubercu- 
losis in the adult is due to this acquired and relative immunity. 
Tuberculosis is a disease of all ages. By predilection it chooses the 
lymph nodes, bones, and the meninges in early life. The importance of 
latent tuberculosis at all ages deserves serious consideration as a factor 
in the sudden dissemination of acute miliary disease. 
The prognosis of any form of tuberculosis presents serious difficulties 
owing to the variety of anomalies with which the disease may be associ- 
ated, the inherent tendencies of all tuberculous deposit, the inability to 
measure at any stage of the disease the resistance of the infected individ- 
ual and the intensity of the infection. 
It is not always possible to estimate the extent and location of the 
disease. There is scarcely an organ of the body which may not harbor 
one or more tuberculous deposits for years without revolt and without 
subjective or objective symptoms. Prognosis therefore must rest upon 
the clinical manifestations of the individual case and their association 
with such pathologic changes as are made clear by physical examination 
and the refinements of diagnosis. !No man can safely pierce the future 
of any form of the disease who has not a thorough understanding of the 
characteristics of the tubercle, its inherent tendencies including its easy 
breakdown, ulceration and caseation, the possibility of reparative and 
protective processes, its frequent latency as well as the enormous variations 
in the resistance of those infected. 
1. Acute Miliary (General) Tuberculosis 
Acute general miliary tuberculosis, in contradistinction to acute pul- 
monary miliary tuberculosis, is a far-reaching general infection, secondary 
to an existing focus, which is spread by the bloodstream, characterized by 
the formation of milletseedsized tubercles in large numbers, in many 
organs at the same time. Acute miliary tuberculosis is always proof of 
initial invasion of either a blood-vessel or lymphatic (thoracic duct), from BACTERIAL DISEASES 
223 
which bacilli are distributed to distant organs (Weigert). Experiences 
with acute miliary tuberculosis prove the importance of cautious observa- 
tion of all children and adults who have periods of indefinite symptoms in 
which positive diagnosis cannot be made and those who have had other 
acute or chronic infections which are likely to leave foci which invite 
tuberculous deposit. This is true of all acute diseases of the lung and 
bronchi which may be associated with latent deposits in lymph nodes, 
from which, as the general health of the host is reduced, bacilli find their 
way into the blood-stream (vein, artery, or lymphatics). There is often 
direct dissemination through the lymphatic channels from the thoracic 
duct into the right heart. Neglected pleurisy may supply the infection. 
Otitis media, the suprarenals, the genito-urinary tract or any of its 
separate organs, bone, or joints serve in different infections as the primary 
focus. 
Infection through the aorta and heart wall, the pulmonary artery, the 
carotid, may spread miliary disease. With miliary as in all forms of 
tuberculosis the vulnerability and susceptibility of the carrier of a latent 
focus become important prognostic factors. Ribbert called attention to the 
conservative processes which in the resistant prevents the entrance into 
and the invasion of the blood. In these there is a strong tendency to pre- 
vent contamination by protective local hyperemia, marked dilatation of 
vessels, acceleration of the local circulation, etc. The depressing and weak- 
ening effect of pregnancy and childbirth become important factors in low- 
ering the resistance of the patient and spreading infection. 
There are three clinical forms of acute miliary tuberculosis, each of 
which is characterized by the presence of leading symptoms: 
I. The typhoid form. 
II. The pulmonary form. 
III. The meningeal form. 
I. Typhoid Form 
The typhoid form of miliary tuberculosis resembles enteric (typhoid) 
fever, in so many ways, that but few men of large experience will deny 
having made errors of diagnosis. There may he and usually is enlarged 
spleen, albuminuria and irregular fever, which may assume the typhoid 
curve! Diazo (Ehrlich) reaction is positive; heart sounds rapid; systolic 
murmur distinct in many cases. Unless there is complicating tuberculous 
meningitis, the pulse may he dicrotic and rapid. If there is meningitis, 
during its early stage the pulse is slow. 
The symptoms which are unfavorable include: rapid pulse, low blood- 
pressure, marked apathy, involuntary discharges of urine and feces, and 
albuminuria. 
Leukopenia and reduced hemaglobin, in some cases, and relative reduc- 224 
SPECIFIC INFECTIOUS DISEASES 
tion of lymphocytes have characterized the graver and more acute forms of 
miliary infection. Leukocytosis of moderate degree is occasionally pres- 
ent. Hurried and irregular respiration with or without cough, Cheyne- 
/SHokes breathing, are all unfavorable and are soon followed by death. 
II. Pulmonary Form 
With evidences of acute infection, but without the marked and positive 
physical signs of acute pneumonic tuberculosis, there is a progressive loss 
of strength, with lung symptoms in the ascendency. These include dry 
cough, but little or no expectoration, at times rusty sputum, mucopurulent, 
rarely hemoptysis. It is difficult to make the accurate anatomic localiza- 
tion of lung changes, for the percussion note may not be changed and in 
many cases there are but few rales. In children the pulmonary form of 
acute miliary tuberculosis may promptly follow measles, whooping-cough, 
typhoid or other infections; or the bronchial nodes infected during these 
diseases may later, after long periods of latency, without symptoms and in 
apparent health, erode vessels or lymphatics and lead to general and fatal 
miliary tuberculosis. When any of the forms of miliary tuberculosis fol- 
low immediately on the acute infections the prognosis is absolutely bad, 
progression is rapid. The physical signs depend upon the size of the 
deposit, the amount of bronchitis and the associated acute and chronic 
changes. In some cases there are evidences of old and latent disease, there 
may be general infection with all of the symptoms of sepsis and no evident 
change in old deposits long recognized, which are the direct cause of 
miliary dissemination. 
With associated broncho-pneumonia the lung symptoms are most prom- 
inent. I have seen both lungs studded with miliary tuberculosis at the 
autopsy in cases which presented no positive physical signs during life. 
In such cases x-ray examinations will strengthen diagnosis and prognosis. 
The pulmonary form of acute miliary tuberculosis may be associated 
with the typhoid condition and to this may be superadded tuberculous 
meningitis. These cases are found both in children and adults. 
III. Meningeal Form 
(Tuberculous Meningitis, Basilar Meningitis) 
These cases have a well-defined prodromal stage during which the diag- 
nosis can he made and the prognosis given. The symptoms of this stage 
include irritability of the child, sudden vomiting, hydrocephalic cry, 
paralyses within the domain of the motor oculi, the facial or other cranial 
nerves, later opisthotonos, increasing apathy, at times early convulsions. 
The cerebral macule (dermography) is present, and as I determined from 
an analysis of a large number of cases, death followed in seventeen days BACTERIAL DISEASES 
225 
from the beginning of the continuous train of symptoms. The Kernig 
symptom is usually but not always present. My experience has been uni- 
formly unfavorable with tuberculous meningitis. My preceptor, Didama, 
believed that he had one recovery in his large experience. While I was 
writing this chapter I saw a case which Treupel presented at a post grad- 
uate clinic in Frankfort on the Main (Oct. 25th, 1913) of a boy in whom 
the spinal fluid contained tubercle bacilli, and all other elements, including 
ophthalmoscopic find, satisfied him, that the case was one of tuberculous 
meningitis, and fully recovered. 
The statement has been recently made (London Lancet), that one 
in 200 cases of tuberculous meningitis recovers. Pitfield reports 29 
cases (one of his own) from medical literature which recovered. In 
10, necropsies confirmed the diagnosis, in 18 tubercle bacilli were found. 
McCarthy in several reports of the Phipps Institute states that he fre- 
quently found evidences of healed tuberculosis of the nervous system in 
persons who ultimately died of phthisis pulmonalis. Others hold that 
the prognosis of tuberculous meningitis is not absolutely bad and base 
their conclusions upon the post mortem evidences of healed meningeal 
tuberculosis. The incidence of cure among the thousands of reported cases 
is so slight that in offering a prognosis it deserves but insignificant consid- 
eration. 
Tests 
Tuberculin Tests.—In all forms of positively diagnosticated acute 
miliary tuberculosis the tuberculin tests, preferably von Pirquet, Calmette 
and Moro, will in the overwhelming majority of cases give negative results. 
Tuberculous meningitis rarely reacts to these tests; my experiences prove 
them negative in over 90 per cent of all cases. The typhoid type is almost 
uniformly negative to the skin and ocular tests; injections of tuberculin 
are contraindicated. Negative tuberculin tests above mentioned, in cases 
positively tuberculous (acute miliary tuberculosis), argue in favor of un- 
favorable prognosis. 
The ophthalmoscope offers positive information in over 75 per cent 
of cases of miliary tuberculosis and should therefore be used for diagnostic 
and prognostic purposes, in this and in all forms of miliary disease. 
The study of the opsonic index is of indifferent or slight value for 
prognosis of any form of tuberculosis, and is unavailable for general use. 
(Bandelier in Roepke, 1. c.) 
Lumbar puncture is of positive prognostic value, for it clinches the 
diagnosis in doubtful cases very often, when tubercle bacilli are found in 
clear fluid as a rule under high pressure, with the presence of lymphocytes. 
It must be remembered that the latter may be present with congenital 
syphilis also. 
Sugar in the Cerebrospinal Fluid.—Connall, who has given this sub- 226 
SPECIFIC INFECTIOUS DISEASES 
ject great consideration, has examined 122 specimens from §9 cases of 
tuberculous meningitis and reports his results as follows: 
“In tuberculous meningitis sugar was found to be present in the great 
majority of the cases, and at all stages of the disease; 122 specimens were 
examined. An active reduction on boiling of the Fehling’s solution oc- 
curred in 15, a partial but decided reduction in 102, and no reduction at 
all in only 4 instances. Complete absence of sugar was observed in only 
2 cases. It was noted in the last week of illness, three times in one case 
and once in the other, and in each case at other times there was a slight 
reduction of Fehling’s solution.” Jacob concludes that “In tuberculous 
meningitis sugar is present, except in very rare cases shortly before 
death, in which stage difficulty of diagnosis rarely exists.” While the 
presence or absence of sugar is of some prognostic value, it is not of the 
same significance as in cerebrospinal meningitis. 
The majority of children who die of tuberculous disease between the 
first and fourth year fall victims to tuberculous meningitis; 40 per cent 
of these die during the first year of life and 60 per cent after. This high 
mortality is reduced with advancing years. In 70 per cent there is an 
hereditary predisposition. Koch (Bandelier and Roepke) reports 355 
cases of tuberculous meningitis in which 130 had measles and 67 whoop- 
ing cough preceding the tuberculous infection. The proportion of adult 
tuberculous meningitis to the infantile is 1 to 7.5 (8 to 60 cases). 
(Pulmonary Consumption, Phthisis pulmonalis, Phthisis tuberculosa, 
Schwindsucht [Lungen]) 
2. Pulmonary Tuberculosis 
All lung diseases due to the Bacillus tuberculosis are included in the 
group of pulmonary diseases known as consumption or phthisis pulmonalis. 
We will consider the prognosis of the disease basing our conclusions on the 
following classification: 
I. Acute pneumonic tuberculosis (lobar or lobular). 
II. Chronic pulmonary tuberculosis (ulcerative and caseating). 
III. Chronic fibroid phthisis (chronic tuberculous pneumonia) (tuber- 
cularized pneumonokoniosis). 
In all forms of lung tuberculosis we are dealing with complex problems 
and changing elements which must of necessity influence prognosis. It 
may be said that the extent and location of the tuberculous process, the 
virulence of the infecting agent, the many general factors already consid- 
ered, including predisposition (acquired and inherited), associated clinical 
manifestations which show the resisting power of the infected, the stage 
of the disease, the ability of the patient to take advantage of conditions 
which offer an obstruction to the onward march of the disease and stimu- BACTERIAL DISEASES 
227 
late the reparative and protective processes, with many other factors, to- 
gether and alone, influence the forecast decidedly. 
I. Acute Pneumonic Tuberculosis 
There are unquestionably cases of acute tuberculosis in which the 
deposit is limited, where there are indefinite symptoms during a short 
period, slight febrile movement, insufficient physical signs to make locali- 
zation possible, languor and anorexia which yield. Nature comes to the 
rescue. Calcification or fibroid change in these limited areas are re- 
sponsible for many healed and circumscribed lesions which are included in 
the post mortem findings in many who finally die of non-tuberculous 
disease and also for many positive tuberculin reactions. In these cases, 
which Sir A. E. Wright might include among the local infections, it is 
possible to raise the resistance of the patient sufficiently ato cause the in- 
fection to disappear” and present fresh infection. Wright contends that 
“the method of following the progress of an anti-tuberculous immuniza- 
tion lies in the observation of the opsonic capacities of the serum.” Pa- 
tients in whom the deposit is limited show a low opsonic index; when the 
process is active, it is occasionally high and irregular. 
(a) Lobular Pneumonic Tuberculosis.—Acute pneumonic tuberculo- 
sis in which there are physical signs of tuberculous bronchopneumonia is a 
virulent infection, most frequent in children, and usually associated with 
rapid loss of strength, cyanosis, hurried respiration and cough. There 
may be hemoptysis, and but few or no tubercle bacilli, depending upon the 
stage of the disease, evidences of constitutional disturbances and death in 
from two weeks to several months. It is surprising to note how long some 
of these patients tolerate the high temperature and the rapid pulse. A 
chronic stage follows, and months of fever, with extreme wasting, dry un- 
satisfactory cough, with night sweats, may precede death. In some there is 
laryngeal invasion finally, which makes the end painful. A reversal of 
the usual type of hectic fever in acute tuberculosis, high morning tempera- 
ture and nocturnal fall, is indicative of rapid failure and early death. 
The acute galloping consumption which may be either lobar or lobular 
(often of the mixed type, with far-reaching miliary deposit, infiltrating 
tubercle and in some cases coalescence of the smaller miliary deposits) 
offers an unfavorable prognosis and is likely to be of short duration. It is 
also frequent in children following respiratory infections, measles, whoop- 
ing cough or a long period of latency, in which the bronchial nodes were 
primarily infected. Hemoptysis is occasionally the first symptom of the 
disease; acute symptoms of pneumonia may follow and progression may be 
rapid. With this history it may be safely concluded that there existed for 
sometime, "without symptoms, a latent or partially healed but limited focus 
which was “opened” and the spread of the disease followed. A large num- 228 
SPECIFIC INFECTIOUS DISEASES 
ber of these acute cases are hurried to the end by the intolerance of the 
stomach and intestines. Tuberculous dyspepsia makes impossible the 
nourishing of some of these cases which become sub-acute, emaciation is 
rapid, heart insufficiency prompt, fever high—all conditions which invite 
early death. 
The duration of the galloping cases (acute pulmonary miliary tubercu- 
losis) is between 12 to 15 days and two to three months, averaging about 
seven weeks. 
(b) Lobar or Pneumonic.—In these cases there may suddenly de- 
velop all of the symptoms of an acute pneumonia (lobar) ; unless there 
are evidences of previously existing tubercular foci, the true pathologic 
conditions may not be suspected. There may be, as I found in one case 
Avhich I reported (Eisner) a sudden chill, high fever and suspicion of an 
apex pneumonia. There were pneumococci in abundance in the rusty 
sputum, the time for crisis passed without a change of symptoms, the hope 
for lysis was abandoned after ten days of unchanging conditions. The 
sputum continued free, there were evidences, after the twelfth day, of 
mixed infection, tubercle bacilli and the Fraenkel cocci were abundant. 
Close questioning proved that several years before his present illness the 
patient had an ischio-rectal abscess and this was the source of infection. 
Death resulted several months after the initial pneumonic tuberculosis, 
with cavity formation and other evidences of general tuberculous in- 
fection. There is in most of these cases an old focus which has been 
lighted into activity; infiltrating tubercle results; large areas are in- 
cluded or one lobe only is involved. With this there may also be miliary 
deposit. In the article which I mention above (Eisner), reference is 
made to pneumonic tuberculosis following aspiration of blood from germ 
laden cavities, after hemopytsis, as originally suggested by Baumler, to 
distant parts of the lung. Either pneumonic or bronchopneumonic tuber- 
culosis may be thus spread, and an acute process developed in the midst of 
chronic phthisis. It is possible for pneumonic herds to be produced solely 
by tubercle bacilli, without mixed infection. It occasionally happens that 
these types of acute pneumonic phthisis heal or fall into long periods of 
latency. One must not conclude that the prognosis is absolutely bad. A 
recent experience (1911) has been encouraging. A priest, age 45, de- 
veloped all of the classic symptoms of pneumonic tuberculosis (lobar) with 
positive bacteriologic find, with irregular fever and progressive emaciation 
and rapid pulse. To all who saw him the case seemed hopeless. In this 
condition he was transferred to St. Gabriel Sanitorium in the Adirondacks 
and there made, so far as we can judge from present indications and physi- 
cal examination, a full recovery with a gain in weight of over fifty pounds. 
What the future has in store for such patients we are not able to tell, but 
with the experience of the past already forewarned, early attention to 
symptoms, if any recur, may lead to satisfactory results. BACTEKIAL DISEASES 
229 
In all cases of pneumonic tuberculosis a guarded prognosis must be 
given, the fiery and acute cases will most of them fall victims to the vir- 
ulent toxemia, a number may live for a long time and ultimately die of 
chronic or subacute phthisis, others will enjoy long periods of latency, 
while the happier outcome of cure is a possibility and should encourage the 
therapeutist to take advantage of modern methods even in desperate cases. 
My clerical friend has remained without symptoms to the present time, 
the picture of health. 
II. Chronic Pulmonary Tuberculosis 
(Ulcerative and Caseous) 
The chronic type of pulmonary consumption is the most frequent of all 
lung invasions. With this, as in all diseases, as I am continually endeavor- 
ing to impress upon my readers, prognosis is nothing more than the con- 
clusions which we reach from thorough detailed and refined diagnosis. A 
large number of these cases are curable, many become latent; the vital fact 
which interests us in considering their future is that they can only be 
saved by early diagnosis and prompt treatment. Put in the resistance, 
bring the condition of the patient to par or above, and the disease, if in 
its incipiency, will be stayed and cured in over 80 per cent of all cases, 
while 20 per cent of all forms of the disease are saved. To wait for defi- 
nite physical signs before making the diagnosis darkens prognosis, for the 
patient’s chances are reduced thereby. To anticipate the final development 
in cases which are strongly suggestive, adds to the patient’s chances. Posi- 
tive physical signs are never early evidences of lung invasion; they mean 
that the case is advanced. 
Symptoms and their Prognostic Value 
The prognostic significance of symptoms may he summarized as fol- 
lows : 
Cough.—Cough, which is not promptly controlled by the usual methods 
of treatment, particularly if dry and hacking, which during the early 
morning hours may he followed by the expectoration of only a small pellet 
of sputum, which on examination gives negative results, which may or 
may not be accompanied by slight rise of temperature, usually some lassi- 
tude, is always strongly suspicious of tuberculosis. Cough with increas- 
ing muco-purulent expectoration is evidence of advanced disease and as a 
rule tubercle bacilli are present. 
In all cases of cough having no other symptoms to make diagnosis posi- 
tive, the sooner such cough is considered to he due to tuberculous deposits, 
the more the prognosis is improved. To wait for the appearance of tuber- 
cle bacilli reduces the chances of the patient. Some of these patients at 230 
SPECIFIC INFECTIOUS DISEASES 
first cough only once or twice during the early morning hours; the cough 
is due to the irritation of a focus still “closed.” 
Each day of cough with changing sputum, increasing evidences of 
bronchial irritation, robs the patient of resistance and lowers his chances 
of recovery. Cough may continue during weeks with no sputum, even in 
rapidly advancing cases in which miliary deposit predominates, but in 
these cases there are usually other evidences—fever, emaciation and accele- 
rated pulse—which are strongly suggestive. These cases offer a less favor- 
able prognosis than do those in which, from the beginning, there are none 
of the symptoms of miliary deposit, though these are by no means hope- 
less. Cough with nummular expectoration is always evidence of advanced 
disease. Tubercle bacilli will be found in such expectoration without long 
search. 
Cough with increasing infiltrating deposit of tubercle may in some 
cases be slight, as a rule it is troublesome. Large areas of lung tissue may 
be infiltrated without cough. This is not a frequent anomaly but it does 
present; failure to recognize the true pathologic condition, postpones diag- 
nosis and materially influences the outcome. 
With cavity formation there is usually abundant purulent and num- 
mular sputum, likely to be periodical, most abundant in the morning. 
Such sputum and cough are unfavorable. Besides tubercle bacilli, there 
are evidences of mixed infection. If the sputum shows besides, benign 
saprophytes, other bacteria wrhich are pathologic, the prognosis is accord- 
ingly influenced. The presence of the tubercle bacillus in the sputum is 
proof positive of a disorganizing process; there has been breaking down 
of tissue, the disease has become “open” and is beyond the incipient stage. 
The prognosis is therefore less favorable, for in those cases (barring acute 
miliary tuberculosis) which are “closed,” where there are no physical signs 
of disorganization or tubercle bacilli in the sputum, recovery follows ra- 
tional treatment in between 85 and 90 per cent of cases; the time required 
for a cure is materially shorter than in the more advanced cases. Large 
numbers of bacilli are unfavorable when found in single fields. The beaded 
appearance of bacilli has been variously interpreted by clinicians. Many 
hold the beading to be favorable. My experience does not j ustify that con- 
clusion, as I have found this oftenest with acute or rapidly advancing 
disease. This may ultimately prove to have been mere accident. Elastic 
fibers are evidences of disorganization. 
Shortness of Breath.—Shortness of breath wTith uncontrolled cough, 
few or no physical signs, no evidences of existing lesion in any organ ac- 
counting for the symptom, should be interpreted as due to tuberculosis. If 
there is no emaciation, a good family history, but little or no fever, fair 
circulatory condition, such cases offer a fair prognosis if treated early. 
Shortness of breath is not always evidence of the extent of the tuberculous 
process. With existing anemia, weak heart muscle, particularly in young BACTERIAL DISEASES 
231 
girls, or in some cases of mixed tuberculosis (i. e., miliary and infiltrat- 
ing), shortness of breath on slight exertion may be out of proportion to the 
extent of the disease. Shortness of breath with increasing loss of weight, 
rapid pulse and persistent elevation of temperature is unfavorable. 
Bronchial Hemorrhage.—The occasional admixture of a “streak of 
blood” should always lead to the suspicion of possible ulceration, erosion 
of a capillary, or disorganization of limited extent. The “streak” may be 
the fore-runner of a large or small hemoptysis. It may in some cases mean 
nothing at all. 
Hemoptysis, large or small, is always proof of an open focus, hence an 
active process. It is by no means always followed by an increase of symp- 
toms or progression of the disease. In many cases it is the first evidence 
of existing tuberculosis, has been the signal which the clinician and patient 
heeded which proved fortunate, for it may lead to full recovery. Even 
cases with positive evidences Of deposit in one or both apices, in which 
hemorrhage was the first expression of existing disease, have been cured 
or halted by timely intervention. There is no stage of tuberculosis in 
which hemoptysis may not occur. 
Death, the direct result of hemoptysis, is exceptional. The erosion of 
a large vessel, usually an artery in the advanced stage of the disease, has 
occasionally caused sudden death. 
Hemorrhage may in some cases lead to anemia by recurring at short 
intervals or because of its profusion. 
The immediate effect of hemoptysis is to frighten and depress; unless 
the loss of blood is considerable, reassurance promptly suffices to return the 
patient to his previous condition. Large hemorrhages repeated at short 
intervals, usually in the advanced stage of the disease, naturally rob the 
patient of resistance, weaken the heart and, if aspiration bronchopneu- 
monia of mixed type or tuberculous pneumonia results in distant parts of 
the lung, the condition may become serious and threatening. In occasional 
cases there is a depressing fever following hemoptysis which may continue 
for several days. 
There are cases in which for some reason the tuberculous process ad- 
vances rapidly after hemorrhage and disorganization promptly follows, 
causing cavity formation with high fever, rapid pulse, mixed infection and 
death in a few months. If the changes are limited to the dependent por- 
tions of the lung, we assume, as already suggested, that infection was 
spread by aspiration. 
It is safe to conclude that hemoptysis not otherwise explained is of 
tuberculous origin, that it does not lead to tuberculosis, but is evidence of 
an existing focus. Franz Strieker’s statistics prove 86 per cent of hemop- 
tvses tuberculous where the bleeding came on without known cause. 
Fever.—Fever is a symptom of enormous prognostic values. Rise of 
temperature which is not modified or controlled by rest and suitable sur- SPECIFIC INFECTIOUS DISEASES 
232 
roundings argues in favor of overpowering toxemia and insufficient resist- 
ance, and is always unfavorable. Slight evening rise of temperature in 
incipient cases deserves prompt consideration, whether associated with 
positive physical signs or not. Its disregard as a symptom of early 
tuberculosis, leading to procrastination, is always against the interest of 
the patient. 
The effect of short but repeated febrile attacks without positive symp- 
toms, usually diagnosticated as influenza or malaria, often burden the his- 
tory of the tuberculous subject when he presents with continuous and posi- 
tive symptoms. Latham adds to these the history in many cases of 
“feeling tired,” “not really fit,” without having consulted the doctor. 
These short periods of fever of doubtful significance originally prove to 
be of tuberculous origin and most of these subjects present with reduced 
resistance and positive physical signs of advanced disease. 
When such cases develop continuous fever, sweating, with accelerated 
pulse, the prognosis is accordingly influenced. 
The temperature curve is an expression of the behavior of the tubercu- 
lous process; it must always be thoroughly considered in offering a forecast 
in the individual case. If fever persists the process is not under control 
or there is some wearing complication. 
Early morning rise of temperatures is always ominous; if in cases 
where it is present there is gradual increase during the day, with accele- 
rated pulse, unless controllable, it is also of serious import; such cases fail 
rapidly. Intermittent fever, usually a decided chill, or chilly sensation 
during the afternoon followed by fever and later night sweat, is evidence 
of mixed infection, pyogenic as a rule, and does not complicate incipient 
chronic tuberculosis. It may in some cases prove expressive of associated 
miliary and spreading infection. Night sweats, unless due to some lion- 
tuberculous complication, unfavorably influence prognosis. There are 
cases of chronic tuberculosis which yield after the appearance of night 
sweats, an experience which justifies persistence in the treatment of 
chronic phthisis. 
Frequent daily measurements are absolutely necessary in all cases of 
chronic tuberculosis, that valuable deductions as to the true condition of 
the patient may be obtained. 
Hectic fever wears the patient, weakens and depresses, and is always 
evidence of failing resistance; the reparative powers have been exhausted. 
Anorexia during prolonged periods with slight fever and loss of weight is 
unfavorable. In these cases, with intolerant stomach, powerful and help- 
ful factors are withdrawn and the patient’s chances reduced. 
Diarrhea.—Early or late diarrhea is unfavorable. When early, if 
controllable, it is not significant of intestinal invasion; if not controllable, 
it remains a weakening factor. Late colliquative diarrhea depletes and 
hastens the end. The presence of tubercle bacilli in the stool of tubercu- BACTERIAL DISEASES 
233 
lous subjects is not positive proof of intestinal tuberculosis. Sputum is 
easily swallowed or bacilli may be washed into the stomach with food and 
drink. With 'persistent diarrhea, tubercle bacilli and characteristic stool, 
ulcerative tuberculous enteritis may be diagnosticated and offers an un- 
favorable prognosis. 
Pain.—Pain is usually an expression of plewritis sicca; if more seri- 
ous forms of pleurisy (effusion, chronic pleurisy, empyema, hydro and 
pyothorax pneumothorax) are not among the complications, it is of no 
great significance and is transitory. 
The misshapen or retracted thorax, with a previous history of pleurisy 
or pneumonia or suspected latent tuberculosis, with adhesions or retrac- 
tions due to the formation of fibrous tissue formed in the process of healing 
and positive evidences of fresh infection or exacerbation of existing dis- 
ease, require consideration and deserve to be weighed in offering prognoses. 
Limited expansion of the thorax in cases not too far advanced may be ma- 
terially increased by pulmonary gymnastics in a favorable climate, thus 
adding to the patient’s chances. 
The Heart.—The small heart of the tuberculous subject has been 
previously mentioned. Abnormal irritability of the heart, erratic behavior 
under stress, is not uncommon even in favorable cases. Hearts remaining 
rapid under rest and favorable conditions, with or without fever, suggest 
advance of the process. If there is fever with rapid heart which is not 
controllable, at the same time gradual loss of weight, the disease is not 
under stress, is not uncommon even in favorable cases. Hearts remaining 
is unfavorable. 
Blood pressure study proves chronic tuberculosis to be a hypotensine 
disease (80-90 mm. Hg.). Sudden or gradual fall of blood-pressure, 
with or without evidences of advancing disease in physical signs, needs to 
be watched and is not encouraging. 
Emaciation; Weight.—Chronic tuberculous subjects, when brought 
under favorable conditions, if they are doing well, should show a gain in 
weight. In no subject who is losing weight has the disease been brought 
under control. Weekly or semi-weekly weighing offers valuable indica- 
tions for prognosis. 
Pye-Smith says: “To put the matter briefly, I would say that, beside 
family history, the less important facts for prognosis in phthisis are those 
which concern the lungs, and the more important those which concern the 
whole body. While a patient puts on flesh and is free from feyer, he is 
doing well, whatever takes place in his chest; while he is losing weight, 
and suffers from anorexia, sweating, diarrhea and hectic, he is going down 
hill, however little sign of disease auscultation of his chest may show.” 
Muscular weakness, atrophy, exalted superficial reflexes are likely to 
indicate advancing diseases, though by no means dependable prognostic 
factors. 234 
SPECIFIC INFECTIOUS DISEASES 
Hoarseness, persisting, means either paralysis of the vocal cords or 
invasion of the larynx, usually ulceration of the anterior surface of the 
posterior laryngeal wall. Tuberculous laryngitis as a complication of 
chronic phthisis is always of the gravest import, decreases the patient’s 
chances of recovery and leads to weeks of suffering which is uncontrollable, 
and usually a painful death. No other condition is more likely to 
impress the physician with the limitations of his art. 
The subject of Tuberculous Laryngitis will be given special consid- 
eration. 
The Urinary Organs.—Albuminuria is not, when transitory, of seri- 
ous moment. In the later stages of the disease, with casts, and occasion- 
ally hematuria it may be an expression of either amyloid degeneration or 
tuberculous nephritis, when it is a symptom of serious and widespread dis- 
turbances. The addition of general dropsy is evidence of the terminal 
stage of the disease. 
Blood-pressure with degenerative changes in the kidney is low in pro- 
portion to the weakness of the heart muscle and the associated amyloid 
changes in the arterial walls. 
(Renal tuberculosis will receive separate consideration.) 
The Diazo-reaction (Ehrlich) is of positive prognostic value. Often 
present in chronic tuberculosis, if found early, it is likely to disappear as 
the process is brought under control and the patient improves. Persistence 
of the reaction after once found in severe cases (not all cases react) is 
with but rare exception an indication of an uncontrollable and progressive 
tuberculosis. 
There is a rheumatoid form of tuberculosis associated with chronic 
lung invasion, fully described in an exhaustive monograph by Poncet and 
Leriche which is obstinate, usually becomes chronic, and adds to the suffer- 
ings of the patient besides lowering vitality. 
Liver and Spleen.—Invasion of the liver and spleen, tuberculous de- 
posits of amyloid degenerations do not argue favorably for the future of 
the tuberculous patient. These are usually terminal complications and are 
not limited to the organs mentioned, but are likely to involve bone and, as 
already mentioned, the kidney. The usual changes in blood-vessels, 
characteristic of amyloid disease, with other factors lead to anemia, drop- 
sies and diarrhea. 
The Digestive Organs.—The influence of purulent discharges on the 
prognosis of chronic tuberculosis has been a source of controversy and dis- 
agreement in the past. Many of the older writers believed that the dis- 
charge from an ischiorectal abscess, usually a tuberculous process, had a 
wholesome and a restraining effect on pulmonary tuberculosis. That 
chronic phthisis may be complicated with chronic ischiorectal infection 
during many years without evident influence is true. The safest conclu- 
sion for us, in the light of modern knowledge, is that any tuberculous focus BACTERIAL DISEASES 
235 
within reach should be promptly removed; the patients’ chances are not 
prejudiced thereby, but rather improved. 
Tuberculous peritonitis complicating phthisis pulmonalis is always se- 
rious, but with abundant ascites is not always fatal. I number such cases 
among my tuberculous patients who made satisfactory progress ip whom 
abdominal section led to cure of the peritonitis and the lung process was 
either uninfluenced or in an encouraging number became latent. 
The Nervous System.—The nervous system, barring tuberculous men- 
ingitis, considered in connection with acute miliary tuberculosis, and occa- 
sional cerebrospinal meningitis, offers but few indications which mate- 
rially influence prognosis. I have met a number of peripheral neuritides, 
neuralgias, some suddenly arising hyperthyroideas, paresthesias, anes- 
thesias and finally mental disturbances, insanities, including melancholias. 
With the dissemination of knowledge concerning tuberculosis, the 
natural hopeful tendency of the consumptive has been encouraged and 
there is no longer in the incipient stage the depression which formerly fol- 
lowed immediately after the diagnosis became known; on the other hand, 
most patients to-day begin to make arrangements which they fully expect 
will lead to a happy termination. 
There is a wholesome autosuggestion which, if encouraged by every 
possible means (environment, etc.) proves an important factor in leading 
the patient toward recovery. 
The Blood.—Chlorosis and anemia invite tuberculosis. Increasing 
chlorosis and anemia are indicative of extension of disease or some asso- 
ciated depressing factor which is retarding the progress of the patient. 
Anemia with edema or other dropsies is always unfavorable. 
The blood condition may be considered favorable when the number of 
red corpuscles is not materially reduced, leukocytes unchanged and hemo- 
globin but slightly diminished. This is the blood condition which is 
found in the incipient stage of the disease. Grawitz, as the result of his 
observations found, with advance to the second stage, without fever, eryth- 
rocytes unchanged, slight increase of leukocytes with hemoglobin, as in the 
first stage. In the third stage, with fever, less favorable, there is a marked 
reduction of red corpuscles, decided increase of leukocytes with marked 
reduction of hemoglobin. 
The blood platelets are materially increased in number in tuberculosis. 
The rapid rise of the leukocytic count is always unfavorable, for it is 
indicative of advancing disease with mixed infection, such as is found in 
the terminal stages of the disease. 
In women, early chlorosis must be expected in many cases. A rise of 
color index is favorable. 
Increase of eosinophilia in the blood and sputum has been found by 
many to be coincident with improvement and their absence or decrease 
marked, when there are exacerbations or the disease progresses. 236 
SPECIFIC INFECTIOUS DISEASES 
Arenth believes that the simple counting of white blood corpuscles is 
of no value for diagnostic or prognostic purposes and has made exhaustive 
studies of the blood picture, more particularly the differential count of the 
polymorphonuclear neutrophils with regard to the number of their nuclei. 
Six classes are recognized according to the number of contained nuclei. 
With infectious disease Arenth found, in tuberculosis particularly, that 
the number of nuclei in the cells is decidedly reduced in unfavorable cases; 
in those without resistance there is a preponderance of cells with one or 
two nuclei only. In the favorable cases, the percentage of leukocytes hold- 
ing three and more nuclei is increased. In bad cases Arenth therefore 
contends, and clinical experiences strengthen his contentions, that “there 
is a shifting of the blood picture on the left, i. e., one or two nuclei.” 
(“ Verschiebung nach Links.”) The blood picture, therefore, shows, “as 
against the normal (25 per cent mononuclear, 75 per cent polynuclear 
leukocytes) an enormous disproportion in unfavorable cases; increase of 
mononuclears and decrease of polymorphonuclear cells.” 
Ringer and Minor have given some interesting data including their 
experiences with the “Arenth leucocytic picture in pulmonary tuberculosis 
and its prognostic value.” The first mentioned made 729 counts in 475 
patients. They divided their cases according to the extent of the lung 
invasion into four groups. 
1 Good. 2 Medium. 3 Bad. 4 Very bad. Going over their counts 
they found that the one and two nuclei cells were most frequent in the 
“bad” and “very bad” groups and decreased in the “good” and “medium” 
groups. In a small number of cases they found with a good clinical symp- 
tom complex, a very bad blood picture and “noted that shortly there- 
after the patient took a turn for the worse.” Ringer concludes that the 
Arenth count “is of a certain value, should not be abandoned and it will, 
in certain apparently favorable cases, correctly presage an unfortunate 
outcome, or vice versa.” The Arenth blood picture gives no indication of 
the extent of lung invasion nor of the stage of the disease; it is, hoivever, 
an index of the resisting power of the patient. 
Solis Cohen and Strickler conclude (quoted by Ringer) : “While 
the average index showed little change, in most of our individual cases the 
proportion of cells in the first two classes of Arenth seemed to be increased 
as the patient improved, and in a number of cases to be decreased as the 
patient grew worse.” Of 27 improving patients whose blood was exam- 
ined more than once, an increase in cells with one and two nuclei was ob- 
served in 22, and a decrease in 4. Among advancing cases there was an 
increase in 3, a decrease in 4, and no change in 2.” The figures of these 
observers are opposed to those of others. Differences in methods of count- 
ing the nuclei, a difficult process, must naturally be considerable. Miller 
and Reed, after considering the subject and making a large number of 
counts, believe that “the Arenth blood picture is of real value in prog- BACTERIAL DISEASES 
237 
nosis.” Miller and Reed report further that cases of pulmonary tubercu- 
losis which are doing badly, progressive or exacerbating, show the follow- 
ing blood changes: 
(a) Leukocytosis. 
(b) An increased percentage of neutrophils. 
(c) A diminished percentage of small lymphocytes. 
(d) A diminished percentage of eosinophils. 
(e) A marked shifting to the left of the Arenth blood-picture con- 
versely, changes in the opposite direction if any of the above factors are 
favorable. 
I fully agree with Ringer, that those who use the Arenth method 
will continue to use it, that it is simply one link in a chain which strength- 
ens prognosis, that blood pictures will never displace bedside findings in- 
cluding physical signs, that “he who places implicit confidence in its read- 
ings and bases his prognostic opinions chiefly thereon, will not infrequently 
be led into error.” 
The 'persistence of tubercle bacilli in the blood is always ominous. 
The more severe the infection, the nearer its termination, the more certain 
are we to find bacilli in the current. We do, however, find tubercle bacilli 
in the blood stream in incipient cases; but this is transitory as a rule. 
Liebermeister’s far-reaching study of this subject justifies conservatism 
before we conclude positively that the bacilli are true tubercle bacilli, for 
acid-fast bacilli were found by him in many non-tuberculous diseases in 
the blood, in children who did not react to tuberculin and in those appar- 
ently healthy. The fault lies in technique. Bandelier-Roepke conclude: 
“The significance of bacillemia in tuberculosis is not yet settled and 
positive conclusions are not justified.” 
The value of the opsonic index in the prognosis of tuberculosis has 
been considered in this chapter; as already suggested, the busy clinician 
will be unable to take advantage of it; in acute cases it may prove to be 
more valuable than in the chronic. 
Physical Signs 
Physical signs and stage of the disease must of necessity influence 
prognosis. It has been my object throughout this chapter to keep before 
the mental vision of the physician and student the enormous value of early 
recognition and its influence on prognosis. In the United States we con- 
sider “incipient cases” those with hut slight or “no constitutional symp- 
toms (including particularly gastric or intestinal disturbance or rapid loss 
of weight) ; slight or no elevation of temperature or acceleration of pulse 
at any time during the twenty-four hours.” 
“Expectoration usually small in amount or absent.” 
“Tubercle bacilli may be present or absent.” 238 
SPECIFIC INFECTIOUS DISEASES 
“8Ught infiltration limited to the apex of one or both lungs or a small 
part of one lobe.” 
“No tuberculous complications.” 
Every fresh extension sufficient to make its presence manifest by posi- 
tive physical signs is a menace. 
The increase of moist rales, sputum, bronchial breathing, with increase 
in rapidity of heart, with or without decided rise of temperature, with or 
without tubercle bacilli, are proof of advancing disease. Dullness over 
large areas, with bronchial or broncho-vesicxdar breathing, with moist, 
large, or small rales, indicate activity of the tuberculous process. 
Cavernous and amphoric breathing, metallic tinkling, marked tym- 
pany, large and coarse rales, abundant tubercle bacilli and negative reac- 
tion to all tuberculin tests, are proof positive of the third and last stage of 
the disease. 
Many patients recover after fully developed pleurisy, effusion or even 
empyema. There is no stage save the terminal of the disease, in which a 
reparative process may not be stimulated; post mortems show healing 
processes fully established, fibrous bands, enclosing walls, the encircling 
and closure of cavities, the lining of pus pockets and their side-tracking, 
the formation of protective adhesions and a variety of processes by which 
nature seeks to arrest the disease, establish latency or cure it. 
Every deposit which persists at the apex of one or both lungs should 
be considered tuberculous from the beginning, and this conclusion should 
not be changed until there is proof positive of error. Deposits in the de- 
pendent parts of the lung are less likely to be tuberculous than those at the 
apex, but these too must be viewed with suspicion until a correct pathologic 
diagnosis can be made. 
All complications and depressing factors influence prognosis unfavor- 
ably. 
Age is a factor to be considered in the prognosis of tuberculosis. In 
children the course of the disease is rapid, as a rule, and offers a less favor- 
able prognosis than in the adult. Disseminated tuberculous disease, acute 
miliary, including brain invasion, is more frequent in early life than later. 
Prognosis is more favorable as we advance in life; after the 60th to 
65th year we again approach the mortality and tendencies of early life. 
There is no time limit in tuberculosis. There are subjects who have been 
tuberculous during almost their entire lives and die of intercurrent disease 
late in life. 
Age 
Tuberculin Tests 
Tt will never be safe to consider the tuberculin tests too enthusiastic- 
ally, as some have done in offering the prognosis of pulmonary tubercu- 
losis. We do know that the reaction represents a phenomenon of sensitiza- BACTEKIAL DISEASES 
239 
tion; we know further that the majority of apparently healthy adults react 
to the Calmette, the Moro and the von Pirquet tests. The subcutaneous 
injection of tuberculin remains the very best method in use to-day for the 
detection of hidden tubercle deposit in the body. It is not without its 
dangers and is now used more for treatment than for diagnosis and prog- 
nosis. The conjunctival test (Calmette, Wolff-Eisner) demonstrates by 
positive reaction the presence of early tuberculosis in between 60 and 70 
per cent of cases. Vaughn, Jr., in 160 cases of early tuberculosis, found 
positive reaction in 72 per cent. My figures with a large clinical material 
are not so high; they are in the neighborhood of 55-60 per cent. Bald- 
win’s 67 per cent; Wolff-Eisner 75 per cent. In my practice most favor- 
able cases of incipient disease and those in the second stage have given 
positive reactions to all tuberculin tests. I am using preferably the von 
Pirquet and Moro tests in private practice, though in a large experience 
with the ophthalmic test I never had an untoward experience. Others 
have been less fortunate. The tuberculin injection is not available in 
cases with fever and wasting. 
Active miliary tuberculosis rarely reacts to the tests. Positive tubercu- 
losis of any organ in which the tuberculin tests remain negative is less 
likely to progress favorably than those in which the reactions were active 
and positive. My experience with tuberculous meningitis, acute 'pneu- 
monic tuberculosis, tuberculous peritonitis without ascites and often with- 
out elevation of temperature, show only a small proportion of positive 
reactions; the protective principles have been exhausted, the prognosis is 
correspondingly bad. In my tuberculous wards at St. Joseph’s Hospital, 
where advanced and neglected pulmonary tuberculosis are received, it has 
been the rarest exception to find positive reactions. 
The von Pirquet test for prognosis in the adult is valueless, the ma- 
jority of healthy adults give prompt reactions. In children the von 
Pirquet shows the time of infection in cases held under observation, but is 
of indifferent prognostic significance. 
There are patients who fail to react during the early stage of pul- 
monary tuberculosis and whom it is impossible to sensitize. 
In the presence of clinical symptoms of tuberculosis with suspicion 
that the case is advancing and a negative tuberculin reaction, the prognosis 
is likely to be doubtful, usually unfavorable. I have never in my experi- 
ence found positive von Pirquet, Moro or Calmette in the midst of rapidly 
advancing tuberculosis. Latent pulmonary tuberculosis in the adult is 
likely to give positive reaction to the tuberculin tests, particularly von 
Pirquet. 
Rontgenoscopy 
The x-ray in the diagnosis and prognosis of tuberculosis has become 
indispensable, but a word of warning against hasty conclusions by the 240 
SPECIFIC INFECTIOUS DISEASES 
inexperienced who have not learned to interpret pictures is not out of 
place. To be of any practical value the picture must always be interpreted 
by the expert who has trained himself by long practice for the work, aud 
who has had abundant opportunity to compare his conclusions with post 
mortem finds. So many errors have been made, that many are becoming 
skeptical and require but little discouragement to surrender this valuable 
method of diagnosis and prognosis. 
The more valuable results are obtained in chronic tuberculous phthisis 
and its associated changes. Solitary nodules and calcified deposits and 
glands are usually easily demonstrated. Unfortunately the Rontgen pic- 
ture is not absolutely dependable for early diagnosis, and negative results 
or suggestive shadows deserve less consideration than clinical data, includ- 
ing physical signs, with a thorough consideration of all that the case 
offers. 
Valuable data concerning the condition of the bronchial nodes for diag- 
nostic and prognostic use are given by x-ray examination. This area 
(hilus-bifurcation of trachea) is often suspected in cases where indefinite 
symptoms have followed the infections of early life, including measles, 
pertussis, pleurisy, lymphatic enlargements of the neck, and the true con- 
dition, if revealed early, may prove life-saving. 
Pleural effusion and nodular deposit, displacement of thoracic vis- 
cera, the size and position of the heart and diaphragm, all important, are 
frequently corroborated by x-ray examination. These conditions, wuth 
their influence on the progress of the individual case, can as a rule be 
studied and recognized without x-ray examination. There never will be a 
time when the well-balanced physician will surrender the results of pains- 
taking physical examination in favor of the revelations obtained from the 
Rontgenologist. The Rontgenologist demonstrates shadows only; what 
these are, what they mean to the pathologist and diagnostician, what their 
value for prognosis, is not easily determined and once more I must 
insist that the cautiously taken history, with a full consideration of the 
subjective and objective manifestations in the individual case, are needed 
to obtain rational and valuable data for prognosis. 
The Tuberculosis of Early Life 
The tuberculosis of children as it invades the lung is more likely to be 
disseminated, less likely to limit itself to the apices, is therefore often 
characterized by the more serious features of miliary deposit. The active 
disease in many is preceded by glandular enlargements and caseation, par- 
ticularly of the cervical glands, and we ought never to forget the enormous 
etiologic importance of the bronchial lymph-nodes. These may have been 
previously infected or the deposit of bacilli may take place during or fol- 
low any of the acute infections of early life. Changes in the mesenteric BACTERIAL DISEASES 
241 
glands with peritoneal invasion are not infrequent. These cases are always 
serious. Invasion of the bones and joints is more frequent than in the 
adult and precedes pulmonary tuberculosis in most cases. 
The development of amyloid disease, dropsies, and enlarged spleen is, 
in children with bone and pulmonary tuberculosis, characteristic of the 
last stage of the disease. The prognosis in children is materially in- 
fluenced by contact with, tuberculous parents. The mortality of early life 
has been changed by the improvement of social conditions; statistics will 
be still more favorable when there is a concerted effort which will make it 
possible to place the children of the active tuberculous in normal surround- 
ings. This not only influences the mortality of childhood, but will prevent 
latent deposit which may become active during the mature years of life. 
Other features of prognostic value influencing the tuberculous disease of 
the lung in children have been considered in the preceding pages. Atten- 
tion has been called to the frequency of tuberculous meningitis. 
Marriage 
As already shown, contact with tuberculous parents increases at once 
the chances of infection. Mothers who are tuberculous are a menace to 
their offspring; their children are more likely to be infected than are those 
of tuberculous fathers. The suckling of the tuberculous mother in whom 
the process is active is likely to develop some form of infection. I have 
been surprised to note the frequency of tuberculous meningitis under such 
conditions. The infection of the child is usually early. Latent tubercu- 
losis in the mother is often lighted to activity by pregnancy and childbirth. 
The extension or activity is greatest during the last half of pregnancy. 
My experience does not justify the nursing of a babe by a mother in 
whom the process has recently been arrested. Both will be likely to develop 
active tuberculosis. One of the most serious complications during preg- 
nancy or lactation is tuberculous laryngitis; this may develop in the 
mother in the presence of only limited lung disease. The prognosis is 
absolutely bad; the progress is rapid, with disorganization, painful ulcera- 
tion, and edema of the larynx. Dubois says: “If a woman threatened with 
phthisis marries, she may bear the first accouchement well; a second with 
difficulty, a third never.” Weinberg has shown that still births are in- 
creased 50 per cent in tuberculous mothers. Abortion, miscarriage, either 
criminal or spontaneous, increase the risk to the mother and invite the on- 
ward march of the disease. 
Subjects who have healed tuberculosis are likely to beget children who 
are ultimately burdened with some form of tuberculosis. Environment 
and social condition must of necessity remain important factors in the 
consideration of the influence of the tuberculous parent on offspring. 242 
SPECIFIC INFECTIOUS DISEASES 
Diabetes complicating tuberculosis, whether acquired after or before 
infection, is always serious and finally leads to death; usually the diabetes 
is pre-existent. The association of chronic alcoholism and tuberculosis 
is always unfavorable, the latter process seeming to advance with unusual 
rapidity, tissues are non-resistant and are ready to break down on slight 
cause. Tuberculous or non-tuberculous meningitis is often the cause of 
death. 
Exophthalmic goiter, typical and atypical, may materially influence 
the prognosis. Brandenstein found in his clinical material in Hamburg 
that 20 per cent of the male tuberculous and 33 per cent of women had 
enlarged thyroids and 20 per cent of the men and 28.5 per cent of women 
showed positive evidences of exophthalmic goiter. 
Gangrene of the lung is always of serious significance. It is a late 
complication, usually appearing when the disease has advanced to cavity 
formation and, with added symptoms of sepsis, often delirium and a 
typhoid condition, the patient dies. 
The obese who develop tuberculosis offer little resistance as a rule. 
They are inclined to be anemic, the myocardium is promptly weakened 
and the disease usually advances rapidly with increasing evidences of 
cardiac insufficiency. 
Gouty conditions do not influence tuberculosis unfavorably; with 
these there is greater tendency to fibroid change in the lung and chronicity. 
Syphilis, particularly neglected cases with lowered resistance, offers a 
favorable medium for the advance of tuberculous disease. Tuberculosis is 
never favorably influenced by the addition of syphilis. It is not unusual to 
find acute tuberculosis shortly after syphilitic infection, and to see the 
rapid advance of the chronic form of the disease as well as the kindling 
of latent deposit to activity. If, on the other hand, tertiary syphilis is 
present and tuberculosis is acquired, the course of the latter may be unin- 
fluenced by the previous specific infection. The French have claimed a 
favorable influence on the tuberculous disease by the exhaustion of the 
syphilitic poison and the ultimate tendency of the tuberculous process to 
fibrosis and chronicity. 
That there are many cases of tuberculous disease of the lung and 
syphilis combined, in which we find not only positive bacteriologic evi- 
dence of the former, but establish the certainty of the latter by sero-diag- 
nosis, in which the mixed treatment (salvarsan and anti-specific drugs) 
gives satisfactory results which cannot be denied. The clinician is fre- 
quently surprised to find his prognosis favorably influenced in such cases 
by systematic and specific treatment. 
In the presence of tuberculous invasion of the lung, specific treatment 
and the Wassermann test are often justified, and should be used for their 
diagnostic and prognostic value. 
Complications BACTERIAL DISEASES 
243 
Tuberculous pleurisy will be separately considered; it is rarely absent 
where lung deposit is superficial. 
Pneumothorax due to the perforation of the lung, because of super- 
ficial cavity formation, is a frequent complication and may lead to sudden 
death. It may occasionally arise from the rupture of a superficial em- 
physematous patch. If pyopneumothorax follows, there may be a period 
of acute symptoms, exacerbation with high fever, rapid pulse and death, or 
the patient may rally and fall into a chronic condition in which all physi- 
cal evidences of pus and air in the pleural cavity continue, or he may add 
to his weight and live for a number of months. In a proportion of cases, 
if the disease is limited to one lung, the occurrence of pneumothorax may 
stimulate reparative processes, particularly fibrous growth, and prove 
salutary. Those cases in which the lung process shows early tendency to 
disorganization with acquired pneumothorax are not among the favorably 
influenced by the accident. One-half of all pneumothoraces are tubercu- 
lous. 
Atelectasis may, if widespread, seriously interfere with the condition 
of the patient. It is caused by the occlusion, of one or more bronchi, 
usually by cheesy masses, either formed in situ or transported from another 
part of the lung. Naturally the area supplied by the included bronchus 
collapses and the patient is robbed of the breathing surface. If there is 
much associated consolidation, the condition proves promptly serious; 
otherwise compensatory efforts are sufficient to relieve the embarrassment. 
Emphysema may result from the expansion of the lung in the neighbor- 
hood of tuberculous infiltration; its importance depends on the extent of 
the primary disease, its stage and the ability of the heart to come to the 
rescue. As a rule limited emphysema need cause but slight concern. 
Purpura with pulmonary tuberculosis is always a grave symptom; it 
is likely to be associated with the end or cachectic stage of the disease. In 
some, it is an evidence of acute exacerbation and is not infrequently asso- 
ciated with active febrile movement and with rapid loss of strength. 
Death may follow in a short time or, as Cruice has reported, the patient 
may recover. 
Thrombosis is an occasional complication which may, within a few 
hours or days, end life. Thrombi may be multiple and extensive. Large 
numbers of pulmonary vessels may be plugged; at the same time one or 
more of the larger vessels (renal, branches of the portal or iliacs) may 
also be occluded. The complication is always grave. 
Healed and latent tuberculosis may without known cause suddenly 
become active. Fresh infection is not among the impossibilities. It must 
be assumed that the patient in whom the tuberculous process has been 
halted is less resistant than the previously uninfected, and, if he is to re- 
main free from relapse or fresh infection, he must guard himself with 
greater caution than is needed by the perfectly normal subject. 244 
SPECIFIC INFECTIOUS DISEASES 
III. Fibroid Phthisis 
Fibroid phthisis is a tuberculous disease .of the lung characterized by 
the development of new connective tissue. Such a process is rarely acute, 
almost always chronic and continues without marked constitutional symp- 
toms during many years with consecutive change in the heart, veins, and 
distant organs. I will discuss the subject under the following classifi- 
cation : 
A. Acute Fibroid Phthisis. 
B. Chronic Fibroid Phthisis. 
(a) Tuberculous ab initio. 
(b) Ffin-tuberculous with final tuberculization. 
(c) Chronic interstitial pneumonia sine tubercle. 
A. Acute Fibroid Phthisis 
Cases of acute fibroid phthisis, in contradistinction to the chronic and 
usual form of the disease, run a virulent and rapid course. Friedrich 
Muller has directed attention to cases of this nature which are 
not usually recognized during life. They begin with outspoken symptoms, 
including fever and malaise and rapid loss of strength. The tuberculous 
infiltrate is not encapsuled by the connective tissue proliferation, but there 
is prompt dissemination and increase of consolidation, tuberculous bron- 
chitis and bronchopneumonia, or there may be prompt development through 
the lymph channels of miliary invasion of both lungs. The characteristic 
features of the disease are the disseminated growth of connective tissue 
and the failure to encapsulate tuberculous herds with rapid deposit finally 
in both lungs, in most cases. These patients die in from 6 to 12 months 
and are, as a rule, between 20 and 30 years of age. Muller calls attention 
to the frequency of these cases, in those inherently weak, with inherited 
predisposition, deformed chests, after typhoid, measles, influenza, with 
alcoholism, diabetes, and after pregnancy. 
Chronic fibroid phthisis may have acute exacerbations of serious im- 
port lighted by influenza, bronchitis or other added infections, which in 
many respects resemble the acute type just described with a simliar out- 
come. 
B. Chronic Fibroid Phthisis 
(Chronic Fibroid Phthisis, Chronic Tuberculous Pneumonia, Tubercu- 
larized Pneumonohoniosis, Chronic Interstitial Pneumonia-tuber- 
culous) 
(a) Tuberculous ab Initio.—These cases are of long duration; patients 
usually present a history of acute disease of the pleura, bronchopneumonia, 
bronchitis or measles, whooping cough, influenza or other infection, which BACTERIAL DISEASES 
245 
has been followed by persistent cough, scant expectoration as a rule, during 
many years. 
During this long period the lung process, has advanced insidiously, the 
fibrous growth has gradually increased, cavities which may have existed, 
resulting from chronic ulcerative phthisis, have become encapsuled, the 
pleura is enormously thickened and, as the disease advances, one or both 
lungs show cirrhotic changes in various parts, and the lower lobes may be 
converted into masses of connective tissue. In some cases bacilli are long 
absent and the true condition can only be surmised; ultimately bacilli 
appear. 
Chronic fibroid phthisis leads to secondary changes materially influenc- 
ing the comfort of the patient during years before the end, which may be 
due to intercurrent disease. Among the changes are enlarged lymph nodes, 
bronchial dilatation {bronchiectasis), atelectasis and the evidences of an 
overworked right heart in dilatation of the right ventricle, often dilatation 
and hypertrophy of the entire heart; in the terminal stages evidences of 
engorged portal circulation, enlarged liver, with or without ascites, cya- 
nosed kidney, chronic gastritis, enlarged spleen and hemorrhoids. These 
patients as already suggested may, under changed or favorable, surround- 
ings, live to old age. Many live 20 and 30 years after the onset, and few 
die before the 10th year of symptoms. 
When the disease follows measles, whooping cough or rachitis in early 
life, it is difficult, as Miller has said, to tell what becomes of these chil- 
dren, for the majority are hospital inmates. If they are followed in pri- 
vate practice, as many are, with “chronic cough,” it will be found that in 
middle life and later some develop or have developed chronic fibroid 
phthisis with dilated hearts, and the other and usual consecutive changes. 
(b) Non-tuberculous Fibrosis with Final Tuberculization.—These 
forms, as also chronic interstitial pneumonia sine tubercle, are 
intimately associated with conditions which continue to serve as irritants 
during many years and will receive fuller consideration in the chapters on 
Chronic Interstitial Pneumonia and Zenker’s disease or the pneumono- 
konioses. 
In considering the prognosis of non-tuberculous fibrosis with 
final tuberculization, we must include those cases of fibroid change in 
the lung, either local or general, which follow healed tuberculosis, or are a 
part of the reparative process, diffuse interstitial pneumonia, chronic 
broncho-pneumonia, chronic pleurisy with adhesions and ultimate connect- 
ive tissue overgrowth in the lung, in which tuberculization follows. These 
cases usually offer a good prognosis so far as life is concerned; they con- 
tinue during many years before there are evidences of tuberculous 
infection, with all symptoms aggravated during the winter months, are 
materially relieved during warm weather and under favorable climatic 
conditions. The secondary changes mentioned under tuberculous ab 246 
SPECIFIC INFECTIOUS DISEASES 
initio, occurring in late stages, are likely to develop with this form of 
chronic phthisis. The addition of the tuberculous element influences the 
prognosis as a rule, duration depending upon many conditions. If there 
are acute exacerbations with fever, evidences of tuberculous broncho- 
pneumonia, or if large areas of consolidation with rapid pulse and dissemi- 
nation or associated miliary deposits are present, life is threatened and is 
usually shortened. In some cases with tubeculization there is only 
gradual progression; there seems to be a tolerance which prevents rapid or 
far-reaching deposit; the tuberculous herd is limited, may become encap- 
suled by the interstitial growth, and life is not materially shortened. 
If the disease is complicated by hemoptysis, and this in turn by fever 
—an indication of bronchopneumonia—the process is likely in most cases 
to advance and undermine the strength of the patient. Even after such 
complications and symptoms I have seen patients fall into their previous 
condition of chronic invalidism and live comfortably during many years. 
When there are evidences of cardiac insufficiency with dropsies, or 
marked changes in the portal system with jaundice (occasional), but little 
improvement is to he expected; death will not be long postponed. 
(c) Chronic Interstitial Pneumonia (Sine Tubercle).—This condition 
is non-tuberculous and will be considered with the Diseases of the Lung. 
(Chronic pneumonia, cirrhosis of the lung.) 
In no other disease is the physician more directly responsible for the 
outcome than in pulmonary tuberculosis. He must he willing to assume 
responsibility. Superficial examination, procrastination, failure to give 
the patient every advantage of existing doubt, in the incipient stage of the 
disease, apathy in the study of the social conditions of the sick, the lethargy 
of the public because of failure of the physician to educate and arouse it, 
remain among the leading causes of defeat. 
References 
Allbutt. Practitioner, Jan., 1913. 
Arenth. Die neutrophilenweisen Blutkorper bei infectidse Krankheiten. 1904. 
Brehmer. Die Aetiologie der chronischen Lungen Schwindsucht. Berlin, 1885. 
Brandenstein. Bandelier & Roepke [l. c.]. 
Bandelier-Roepke. Die Klinik der Tuberkulose. 2. ed., 1914, 13. 
Cohen & Strickler. (Quoted by Ringer) Am. J. Med. Sci., Oct., 1912. 
Connall. Quart. J. Med., London, 1910. 
Cruice. Am. J. Med. Sci., Dec., 1912. 
Eisner (Henry L.) On the clinical and bacteriological aspect of mixed infection, etc., in 
pulmonary tuberculosis. Buffalo Med. J., 1911. 
Grawitz. Die klin. Pathol, des Blutes. Berlin, 1906. 
Hoffman. J. Am. Med. ilss., May 17, 1913, 1571. 
Jacob. Brit. Med. J., Oct. 26, 1912, 1097. 
Kraus (F.). Ztschr. f. Tuberkulose, Bd. xix. BACTERIAL DISEASES 
247 
Latham. Practitioner, January, 1913. 
McCarthy-Phipps. Institute Reports. London Lancet, Oct. 25, 1913, 1183. 
Miller (Chas.). Practitioner, London, Nov., 1912, 619. 
Miller & Reed. Arch. Int. Med., May, 1912. 
Muller, von Mehring-Krehl. 8. ed., i, 275. 
Orth. Berl. Min. Wchnschr., 1904, No. 11-13. 
Pitfield. Amer. J. Med. Sd., July, 1913. 
Poncet & Leriche. La rheumatisme tuberculeux. Paris, 1909. 
Pye-Smith. Sheffield Med. J., Jan., 1893. 
Ribbert. Deutsch. med. Wchnschr., 1906, No. 1. 
Ringer. Am. J. Med. Sci., Oct., 1912. 
Ringer & Minor. Am. J. Med. Sd., May, 1911. 
Strickers {Franz). Osier’s Practice of medicine. 1913. 
Vaughn, Jr. J. Am. Med. Ass., Nov. 1, 1913, 1580. 
Weigert. Die miliar TuberJculose. 1877-1897. Deutsch. med. Wchenschr.,. 1897, No. 48. 
Wright. Proc. Royal Soc., London, Ixxiv, 147-378. 
3. Tuberculous Pleurisy 
It may be assumed that at least 50 per cent of all pleurisies after the 
fifth year of life are tuberculous. Physical signs of dry pleurisy with 
associated pain at the apex argue in favor of pulmonary tuberculosis and 
tuberculous pleurisy. 
Vincent Bowditch found that, of 90 patients treated for pleurisy by the 
elder Bowditch, 32 and one-tliird finally died of tuberculosis. Barrs of 
Leeds reported 57 cases of pleurisy in which 21 developed tuberculosis. 
Salonove-Ipin had 301 pleurisies of which 84 became tuberculous. Of 88 
cases treated at the Johns Hopkins Hospital, 30 later developed tubercu- 
losis. Of 131 cases, Osier found 32 to be tuberculous (24.4 per cent) at 
post mortem. Landouzy claims that 98 per cent of all so-called pleurisies 
“due to cold” are tuberculous. Stinzing believes that over 50 per cent of 
all pleurisies are tuberculous. Extreme figures are given by Jakob and 
Pannwitz, who claim 10 per cent, and v. Sokolowski, who found only 2.8 
per cent to be tuberculous. The safe figures according to an estimate made 
from an analysis of cases in private and hospital practice by the author, 
places the percentage of pleurisies positively shown to be tuberculous at 
30-35. 
Tuberculosis, if it follows initial (?), supposedly uncomplicated 
pleurisy, develops in an active form within five years in 50 per cent of the 
cases. R. C. Cabot in 300 cases at the Massachusetts General Hospital 
found 117 to have died within 5 years of tuberculosis. Hedges followed 
130 cases of pleurisy treated at St. Bartholomew’s Hospital and found 40 
per cent with fully developed tuberculosis in seven years. As a rule, the 
immediate prognosis of tuberculous pleurisy is good; in many cases, how- 
ever, the remote prospect becomes a source of anxiety during many years. 248 
SPECIFIC INFECTIOUS DISEASES 
The frequency of effusion with tuberculous pleuritis is shown by an 
analysis of Allard and Koester’s material. There were 514 pleurisies with 
effusion among 2133 cases of pulmonary tuberculosis. Pleurisy of early 
life (before the fifth year) is not often tuberculous. Allbutt gives the in- 
cidence as 1 in 10 and “even of these the pleurisy may be only incidentally 
associated with a tuberculous focus, or the tubercle may be a secondary 
consequence of a protracted empyema.” 
The larger number of tuberculous pleurisies are secondary to existing 
puliponary tuberculosis or are a part of general miliary infection. In 
cases which have etfery appearance of being primary the chances are that 
the pleural infection followed superficial lung tuberculosis which was in- 
active. 
Men develop tuberculous pleurisy oftener women (65-35, Bande- 
lier and Roepke, 1. c.). 
Adhesions which follow dry pleurisy may have a salutary effect on the 
progress of existing tuberculosis; indeed, many with truth consider it “al- 
ways a conservative and useful process” (Osier). 
The formation of dense adhesions may protect against pneumothorax, 
may also stimulate interstitial growth and encourage chronicity. 
Dry pleurisy with but few exceptions runs a favorable course. A 
limited patch of dry pleurisy over a consolidated area, with persistence of 
fever, occasional chills and sweats, must always be considered evidence of 
activity. Latham makes this unqualified statement: “The great majority 
of attacks of pleurisy in young adult life are tuberculous in nature. If this 
fact were appreciated sufficiently, and, still more, if all cases of pleurisy 
which cannot be shown to be non-tuberculous, were regarded as tuberculosis, 
a large number of cases of pulmonary disease would be prevented.” Cases 
of tuberculous pleurisy, in which the condition is early recognized and 
rationally treated (sanatorium, etc.) rarely develop active tuberculosis in 
later life. Latham and others believe that “a greater degree of immunity 
is produced, and that these patients are less liable to consumption subse- 
quently than the other members of the community.” Failure to recognize 
the significance of tuberculous pleurisy, on the other hand, increases subse- 
quent dangers, including further lung invasion. 
The French report pulmonary consumption widespread in later life in 
not less than 75 per cent of tuberculous pleurisies. 
In some cases tuberculous pleurisy may not finally be associated with 
more than limited and superficial pulmonary invasion, but tuberculosis of 
the spine or joints may develop or other distant infection may prove to be 
a serious complication. Invasion of the bronchial glands and pleurisy may 
be followed by periods of latency of the tuberculous process but remains a 
menace. 
Tuberculous empyema, unless treated early, may include persisting 
sinuses and, as mentioned in the chapter on Purulent Pleurisy, may lead BACTERIAL DISEASES 
249 
to amyloid disease. Tuberculous pleurisy does not often lead to empyema 
when modern methods of treatment are used. 
Pneumothorax and pyopneumothorax may result from the breaking of 
adhesions over cheesy herds or cavities or the separation of an adherent 
pleura. The significance of this complication is always serious in ad- 
vanced cases and has been considered in connection with Chronic Pul- 
monary Tuberculosis. 
Retractions and deformities of the chest are not as frequent as form- 
erly, because of early radical treatment and pulmonary gymnastics; in 
some cases pulmonary fibrosis follows and with bronchiectasis, the patient 
falls into a condition of chronic invalidism which may continue during 
many years. 
In acute miliary tuberculosis, the pleura may be studded with deposit, 
a part of the disseminated disease, in which the prognosis is always bad. 
References 
Allard & Koester. Hygiea. Oct., 1911. 
Allbutt. Lancet, London, Nov. 80, 1912. 
Bowditch (Vincent). Progressive medicine. 1911. 
International Clinics. 1912. 22. series, i. 
Barrs. Progressive Medicine. 1911. 
Cabot (R. C.). Amer. Medicine. 1902. 
Hedges. St. Batholomew’s Hospital Reports, 1895. 
Jakob & Pannowitz. Bandelier & Roepke [l. c.]. 
Landouzy. Bandelier & Roepke klin. Tuberculos., 1904. 
Latham. Practitioner, Jan., 1913. 
Osier. Practice of medicine. 1913. 
Salonove-Ipin. French Navy Reports. 
Stinzing. Handb. d. spez. Therapie, etc. 1909. 
v. Sokolowski. Brustkrankhtiten, 1906. 
4. Parotid and Thyroid Tuberculosis 
The prognosis of tuberculosis of the parotid is good. The disease is 
usually primary, superficial and amenable to surgical and early treatment. 
Tuberculosis of the Thyroid 
Tuberculosis of tlie thyroid is rarely primary, it is usually acute and 
part of a general miliary infection. In children, with acute infection the 
thyroid rarely escapes tuberculous deposit. There may be no subjective 
or objective evidences of thyroid disease. 
Secondary nodules isolated in the thyroid may calcify or heal without 
causing symptoms. 
Hector Mackenzie found but one case of Graves’s disease in a tubercu- 250 
SPECIFIC INFECTIOUS DISEASES 
lous subject, while on the other hand he cites L. Levy who had “13 cases 
of Graves’s disease among 170 tuberculous patients ; such an experience 
must be quite exceptional.” My experience is in accord with Hector Mac- 
kenzie, for in a large experience with typical and atypical exophthalmic 
goiter and tuberculosis, I have rarely found these complicating each other. 
References 
Levy (L.). Quoted by Allbutt & Rolleston. 2. ed., iv, part i, 361. 
Mackenzie {Hector). Idem., 361. 
5. Nasal Tuberculosis 
Nasal and oral catarrh, non-tuberculous, are frequently annoying and 
aggravate cough during all stages of pulmonary or laryngeal tuberculosis. 
The “dry catarrh” of the consumptive interferes materially with his com- 
fort, though it is at no time threatening to life. 
Ozena opens the avenues to tuberculous infection and may finally be- 
come tuberculous. 
Single tuberculous ulcers settle by predilection on the cartilaginous 
septum low down and are amenable to treatment. Tuberculoma and dif- 
fuse tuberculous infiltration of the nasal mucosa with final ulceration, may 
prove destructive, leading to perforation and loss of bone. 
If the lesions are limited, radical treatment will overcome them; if, 
however, infiltrating or multiple, single lesions may heal, but relapse and 
fresh ulcerations are the rule. Naturally the prognosis must depend upon 
the associated conditions, particularly upon the extent of the primary 
disease, and the general condition and social status of the patient. 
Post nasal, pharyngeal tuberculosis is not prominent during life; there 
are but a few symptoms which lead to its discovery. The condition is a 
part of the general infection. Post mortem ulcers of the pharynx are not 
infrequently found. During life their presence has no material bearing 
on the course of the disease. 
6. Laryngeal Tuberculosis 
For the purpose of the internist it may be concluded that: 
(a) Primary laryngeal tuberculosis is exceedingly rare, but is among 
the possibilities. It may be associated with perichondritis or may limit 
itself to the mucosa and submucous tissue. 
(b) Laryngeal tuberculosis is as a rule a secondary process. Its 
favorite seat is on the anterior surface of the posterior laryngeal wall and 
the arytenoid cartilages. 
(c) Laryngeal tuberculosis shows prompt tendency to infiltration of 
the underlying tissues and to ulceration. BACTERIAL DISEASES 
251 
(d) Miliary deposit in the larynx is not exceptional. 
(e) Ulcerations may be single or multiple, and “tuberculous tumors” 
(“tuberculoma”) may form with associated edema of the glottis. 
(f) The tuberculous laryngitis of the terminal stage of pulmonary 
tuberculosis is a potent factor in hastening the end. 
(g) Laryngeal tuberculosis with pulmonary phthisis is rapidly ag- 
gravated by pregnancy and childbirth, and offers an unfavorable prog- 
nosis, so bad, that laryngologists have often considered the advisability of 
inducing abortion to save the life of the mother. 
Robert Levy makes the following statement: 
“I know of no disease into the prognosis of which so many items enter 
as into that of laryngeal tuberculosis. The stage of the affection, the 
nature of the lesion, the situation of the lesion, the complication, the asso- 
ciated general or pulmonary involvement, the environment of the patient, 
the social position, all and more must enter into a consideration of the 
possible termination.” The spontaneous healing of laryngeal tuberculosis 
is so rare as to deserve but little consideration in offering a prognosis; a 
view which most modern laryngologists entertain. At the meeting of the 
Verein Deutscher Laryngologen in 1911, Dreyfuss, Kummel and Rumpf, 
held opposite views. Killian contended that these cures were found in 
those who lived in the open air, the patients had practically received the 
modern treatment for the primary disease. 
Where laryngeal tuberculosis exists with pulmonary consumption, the 
leading data for prognosis must always be given by the latter, i. e., the 
primary disease. Moderate pulmonary invasion with limited laryngeal 
infiltration or ulceration offers a good prognosis. Fever, anorexia, dys- 
phagia, edema of the glottis, with pulmonary and laryngeal tuberculosis 
are all unfavorable and hasten the end. 
Early recognition of laryngeal tuberculosis and prompt treatment, 
local and climatic offer great encouragement. Levy quotes Briill who 
“found 58 per cent of his cases clinically cured when they left the sani- 
torium, and that of these, 31 per cent remained cured.” 
Men show greater tendency to cure than women, 30 per cent against 
26 per cent. 
There are many chronic cases in which there is, as the result of local 
and climatic treatment, cicatricial repair of laryngeal lesions with result- 
ing deformity, consecutive hoarseness and noisy breathing. Patients may 
live many years in this condition. Ko case of pulmonary tuberculosis is 
favorably influenced by the advent of laryngeal invasion; the danger is 
greater when the disease is active; tubercle deposits are numerous and 
there is ulceration with edematous swelling. With infiltration only, the 
progress of the lung disease is not materially hastened. I know of no case 
of cure in my practice in which laryngeal and advanced pulmonary tuber- 
culosis were coincident. 252 
SPECIFIC INFECTIOUS DISEASES 
We ought never to divorce ourselves from the consideration of the in> 
fluence of predisposition and the social status of the patient in reaching 
safe conclusions for prognosis. 
Advanced larnygeal lupus offers an unfavorable prognosis; limited in- 
filtration may yield to radium or mesothorium. 
Tracheal and Bronchial Tuberculosis 
Ulceration of the trachea and larger bronchi are usually associated with 
advanced laryngo-pulmonary tuberculosis, associated with enlargement 
and caseation of the bronchial glands, always (practically) secondary and 
terminal manifestations, in which the end is not long postponed. 
Dreyfus, Killian, Rumpf, & Kummel. Verhandlung. Verein Deutscher Laryngologen, 
Levy (Robert). J. Am. Med. .Ass., May 17, 1913. 
References 
7. Tuberculosis of the Digestive Tract 
The Lips.—Labial ulcers are rare; they are occasionally found in the 
advanced stage of laryngeal or pulmonary tuberculosis, and, barring the 
pain which they cause, have no bearing on prognosis. When they are 
present early, the diagnosis may prove difficult without inoculation or bac- 
teriologic tests. 
The Tongue.—Tuberculous ulcerations of the tongue may be present 
with or without lip ulceration. These lesions show characteristic tubercle 
deposit, and ulceration soon follows with uneven edges, without the 
“punched out” appearance of the specific ulcer. Lupus of the tongue and 
lips is less likely to ulcerate than is the usual form of tuberculous deposit. 
Tuberculosis of the lips, tongue or tonsils, may be either primary or 
secondary and is usually caused by the human type of tubercle bacillus, 
though there are occasionally positive evidences of bovine infection. 
Tuberculosis of the tongue with invasion of the surrounding glands, often 
extensive, is not infrequent and is usually a part of a widespread process 
which is destructive and fatal. 
The Tonsils.—The tonsils are important organs in conveying tuber- 
culous disease. They harbor bacilli of tuberculosis, transmit them to the 
surrounding glands and thus become directly responsible for the dissemi- 
nation of the disease. During active tuberculosis the tonsils are always 
found to hold bacilli and often show remnants in chalky deposits of healed 
tuberculosis. Tonsils may hold tubercle bacilli during long periods with- 
out recognizable pathologic change in their structure. There can be no 
doubt of the fact that the tonsils of children often than adults furnish a BACTERIAL DISEASES 
253 
focus for general tuberculous infection through the cervical lymphatics; 
these facts have been fully corroborated by Latham and Schlenker. 
To prevent descending infection, all suspected tonsils should he excised 
early. 
The tonsils are often invaded during pulmonary and general miliary 
tuberculosis without much enlargement or disagreeable symptoms or ulcer- 
ation. In occasional cases, where there is marked tendency to breakdown 
of tissues, small or large ulcers form in the tonsils and soft palate. With 
laryngeal tuberculosis in the terminal stage of the disease, ulceration, 
edema and swelling of the tonsils and of the mucosa of the upper air 
passages add to the discomfort of the dying patient. 
The prognosis of primary tonsillar invasion is good. With tonsillar 
and pharyngeal invasion, as with nasal tuberculosis, the larger elements 
which influence prognosis are the extent of the primary disease, the resist- 
ance of the patient and the many other factors to which I have referred in 
the general consideration of tuberculous disease. It must be remembered 
that primary, labial or oral tuberculosis may promptly lead to infection of 
the intestinal and respiratory tract. 
The Esophagus.—Esophageal tuberculous ulcers occasionally compli- 
cate distant, usually pulmonary or intestinal tuberculosis, offer few or no 
symptoms, and are usually overlooked during life. If symptoms are 
present, the general process is usually advanced and the prognosis is corre- 
spondingly bad. 
The Stomach.—Reference to the dyspepsias of tuberculosis has been 
frequent in considering the subject generally, and their association with 
the acute and chronic forms of pulmonary tuberculosis. Intolerant stom- 
achs are always a source of anxiety, particularly when during the incipient 
stage of pulmonary tuberculosis all other factors, including environment, 
are favorable and the patient is handicapped because of the revolting 
stomach. 
True tuberculous lesions are so rarely found in the stomach (tubercu- 
lous ulceration, etc.), that they demand no consideration in this work. 
(See statistics of Melchior, Fredrichs, Diirck, Simmonds, Glaubitt and 
others in Bandelier and Roepke, 1914, p. 414). Chronic gastritis, due to 
stasis, may add an element of depression during the advanced stages of 
pulmonary tuberculosis with insufficient heart strength. Acute gastritis 
reduces the strength of the consumptive; it may recur at intervals. 
With miliary tuberculosis (general), the stomach is frequently the 
source of uncontrollable symptoms; malnutrition with associated anemia, 
high temperatures often, rapid pulse, with advancing evidences later of 
intestinal involvement, lead to death. 
In many cases the prognosis is still further influenced by persistent 
lack of free hydrochloric acid in the gastric juice. 
Intestinal Tuberculosis (Tuberculous Enteritis).—(a) Primary. 254 
SPECIFIC INFECTIOUS DISEASES 
Most primary tuberculous infections of the intestine are found among chil- 
dren and are due to tuberculous milk, meat, or contamination of food with 
other tuberculous material. In primary intestinal tuberculosis in children 
there may be no symptoms of pulmonary disease; the child presents the 
symptoms of acute or subacute gastro-enteritis, the wasting is usually rapid, 
loss of strength prompt, fever and increasing anemia striking; the weak- 
ness is often out of proportion to the diarrhea. Enlargements of the 
mesenteric glands are often palpable as the disease advances. In children 
there is rarely intestinal perforation and there is no tendency toward 
spontaneous repair. There is in some cases associated tuberculous lymph- 
angitis with deposit of small tubercles on the serosa over the intestinal 
ulcers. Primary tuberculosis of the intestine is associated with greater in- 
vasion of the intestinal glands than is secondary enteritis, which shows but 
little tendency to more than slight swelling of the mesenteric glands, rarely 
nodules or caseation. The prognosis of the primary intestinal tuberculosis 
of early life is absolutely bad. The duration of life varies from 6 to 8 
weeks to as many months after the onset of symptoms. 
(b) Secondary tuberculous enteritis is present in all cases of 
advanced pulmonary tuberculosis, according to Albrecht, in which there is 
cavity formation. In these cases isolated and characteristic ulcers are 
found, or there may be multiple ulcerations throughout the small and large 
intestines. As already mentioned in connection with the primary tubercu- 
lous ulcers, the secondary enteritis is not associated with more than slight 
enlargement of the mesenteric glands; there are but few or no nodules and 
there is rarely caseation. There may be far-reaching intestinal tubercu- 
losis with but slight deposit at one or both apices, which may run a rapid 
course with all of the symptoms of general infection (Piissler). 
Secondary enteritis is probably due to the swallowing of tuberculous 
sputum. Unquestionably intestinal infection is promptly associated with 
tubercle bacilli in the lymph of the thoracic duct and the blood of the 
portal system, and hence leads to flooding of the organism with tubercle 
bacilli which may have some influence on immunization or, what is more 
probable, causes metastases in the already infected lungs and other organs 
of the body (Fischer). Intestinal tuberculosis through the blood and 
lymph stream causes the deposit of masses of grayish tubercle nodules in 
the spleen, kidney and adrenals. 
Hot all ulcers found in tuberculous subjects are tuberculous; some 
may be due to associated mixed infection; the influence on the course of 
the disease is not materially different, for with the tuberculous as well as 
pyococcous ulcerations the resulting colliquative diarrhea is equally ex- 
hausting, and with increasing evidences of depletion, these patients die of 
exhaustion, enormously emaciated; often there are evidences of amyloid 
degeneration. 
Chronic tuberculous enteritis may follow an early stage of pulmonary BACTERIAL DISEASES 
255 
tuberculosis, when it is due to changes chargeable to toxemia, stasis, 
atrophy, atony or inflammatory swelling of the mucosa (Bandelier and 
Boepke). In this class of cases the immediate prognosis is favorable, for 
these patients may live, comparatively comfortable during many years 
unless the primary disease makes rapid progress; they may be favorably 
influenced by diet and climate. Hippocrates’ dictum may be accepted as 
true to-day. “Diarrhea added to consumption is a fatal complication.” 
By this is naturally meant tuberculous enteritis with colliquative diarrhea. 
In occasional cases, symptoms of intestinal stricture with coiling of 
intestines, follow tuberculous invasion of the ileo-cecal region, or there 
may be multiple constrictions due to ulcerations wLich have followed 
faulty healing processes. These structures are clinically often mistaken 
for carcinoma. The neighboring lymphatics are likely to be enlarged and 
adhesions are not uncommon. They may be either of primary or second- 
ary origin; about are favorably influenced by operation. In some cases 
the course is chronic. 
The Liver.—Fatty degeneration of liver tissue, either widespread or 
limited, is one of the more frequent complications of pulmonary tubercu- 
losis. Liver cells are surcharged with fat, and enlarged. In advanced 
cases the entire liver may become fatty. As the fat of the body is con- 
sumed, the deposit in the liver increases, hence prognostic conclusions are 
easily reached in the presence of subjective and objective symptoms of fatty 
liver. Lorentz proved that among the emaciated marasmic tuberculous 
subjects, 34.8 per cent were found with fatty livers, while this condition 
was absent among the acute tuberculous infections. 
Amyloid degeneration of the liver is always a late manifestation of 
chronic tuberculosis, is associated with similar change in other organs 
(spleen, kidney, adrenals, bone, etc.) and with dropsies. 
Cirrhosis of the Liver and Tuberculosis.—The examination of the 
material at the Strassburg Medical Clinic showed 21 cases of tuberculosis 
among 85 cases of cirrhosis of the liver, 25.5 per cent. Lorentz among 
4,331 post mortems found 111 cases of cirrhosis and among these 22 cases 
of tuberculosis. Among 59 cases of cirrhosis as the leading cause of 
symptoms there were 6 cases of tuberculosis, and, in 52 cases of cirrhosis 
considered incidental, tuberculosis was the primary disease among 16. 
It is positive that cirrhosis of the liver invites tuberculous diseaseJ on 
the other hand it may be concluded with certainty that primary tubercu- 
losis does not often lead to interstitial hepatitis (cirrhosis). Widespread 
or limited tuberculosis in the presence of advanced cirrhosis of the liver 
may be safely considered to have followed and not preceded the latter 
disease. 
The statistics (Bandelier and Boepke) prove the incidence of tuber- 
culosis with cirrhosis in 20 per cent of cases, while cirrhosis following 
tuberculosis is found among less than 2 per cent of the former. Bolles- 256 
SPECIFIC INFECTIOUS DISEASES 
ton states that in 706 fatal cases of cirrhosis collected from literature, 
209 (or 29.6 per cent) presented some evidence of tubercle; (the general 
incidence of tuberculosis in deaths from non-tuberculous disease is only 
about 13.5 per cent). Tuberculous lesions were found in the lungs of 22.6 
per cent of a series of 584 cases of cirrhosis. Pulmonary tuberculosis is 
the direct cause of death in from 12 (Kelynack) to 14.5 (Rolleston and 
Fenton) per cent of patients with cirrhosis. In 9 per cent of the series of 
584 cases there was peritoneal tuberculosis. As to cirrhosis following 
tuberculosis, Rolleston believes that “there is no reason to think that 
genuine cirrhosis of clinical importance is primarily produced in this 
way.” 
Cirrhosis with tuberculosis runs a rapid course with marked ascites, 
usually hemorrhagic. Pain and tenderness are slight as is jaundice also. 
Pleural effusion, usually double, adds to the suffering of the patient and 
hurries the end. 
Primary tubercle nodide in the liver is exceedingly rare; usually 
found post mortem. If palpable and large it may simulate carcinoma. F. 
Krause reports a unique case of a man, age 33, which he operated success- 
fully for primary tubercle of the liver in which the original diagnosis was 
uncertain; both cancer of the liver and transverse colon had been suspected. 
Microscopic and bacteriologic examination proved the growth to be tuber- 
culous. There was prompt and uneventful return to health. Pertik in 
1904 found but 19 similar cases in medical literature. Orth reports two 
cases in both of which he was thoroughly convinced that the growths were 
primary; in the first tuberculous peritonitis finally developed. With 
miliary tuberculous generally disseminated, the multiple deposits in the 
liver are simply a part of a general process which usually leads to death. 
With advanced chronic ulcerative pulmonary tuberculosis the liver 
may hold several large caseous nodules; often there are nodules in the 
spleen at the same time, while the intestinal glands are ulcerated and the 
intestines are involved. With such lesions death is not long postponed. 
With acute tuberculosis the enormous bacillemia naturally leads to liver 
tuberculosis, though the liver function unquestionably tends to destroy 
tubercle bacilli and other bacteria brought to it through the blood stream 
and thus prevent its own tuberculization. 
Tuberculous perihepatitis complicates tuberculous peritonitis fre- 
quently, but adds little to its seriousness. 
The prognosis of all forms of liver tuberculosis must be considered to 
be serious, for it may almost always be assumed to be a part of a wide- 
spread and progressive process. 
The Gall-Bladder.—The gall-bladder may be the seat of primary tuber- 
culosis with other ulcerative and chronic processes, or the bladder and bile 
passages may become tuberculous in association with pulmonary, peri- 
toneal, acute general miliary, or the tuberculous invasion of any of the BACTERIAL DISEASES 
257 
abdominal organs. Primary tuberculosis of the gall-bladder offers a good 
prognosis when operated early; naturally the diagnosis will as a rule be 
made by accident only. 
Ischio-rectal tuberculosis has already been mentioned and I must 
repeat that when an early complication of any form of distant tuber- 
culosis, its radical treatment can have only a salutary effect. The 
persistence of the discharge is always a weakening drain. Superficial 
treatment without the removal of the tuberculous, i. e., fistulous tract, is 
useless. I have never known in my experience of the exacerbation of lung 
symptoms after the cure by operation of tuberculosis of the ischio-rectal 
fossa. Ischio-rectal abscess is often an evidence of primary and local 
tuberculosis (Eisner), and offers an excellent prognosis when radically 
treated. Such treatment will often prove life saving, for in the predis- 
posed the ischio-rectal fossa is a favorite seat of primary tuberculous 
disease. 
References 
Albrecht. Frankf. Z. f. P., 1, 1907. 
Bandelier & Roepke. Die Klinik der Tuberculose. 1914, 414- 
Eisner (Henry L.). Gaillard’s Med. JNew York, May, 1893. 
Fischer. Munch, med. Wchschr., 1908 & 1910. 
Krause (F.). Berl. klin. Wchnschr., 1912, xlix, 677-680. 
Latham & Schlenker. Practitioner, Jan., 1913. 
Lorentz. Ztschr. f. Tuberculose, Bd. xx, H. 3. 
Orth. Uber Lokalisirte Tuberc. der Leber. Virchow Arch., 1907, Bd. Ixvi, Bd. clxxxviii. 
Piassler. Miinch. med. Wchnschr., 1906. 
Pertik. Lubarsch-Osterta, Pathol. Ergebnisse. Jahrg. 8, Bd. ii, 279. 
Rolleston. Diseases of the liver, gall-bladder and bile ducts. 1912. 
8. Tuberculous Peritonitis 
The dictum of Louis (1825) that chronic 'peritonitis is usually of 
tuberculous origin has been accepted by the profession. Tuberculous 
peritonitis may be— 
(a) Miliary peritoneal tuberculosis. 
(b) Chronic tuberculous peritonitis. 
(c) Chronic fibroid tuberculous peritonitis. 
It is difficult in the individual case to reach positive conclusions con- 
cerning the focus from which the peritoneal disease spreads. A large num- 
ber of cases w7ill always remain problematic. It is safest for our purposes 
to conclude that in the larger number of cases the disease spreads from a 
preexisting deposit; that in over 50 per cent of cases in women it is a 
part of genital tuberculosis; that the spread from the Fallopian tubes is 
most frequent; that in children the intestines may supply the infection; 
that tubercle bacilli may pass through the intestinal wall to the perito- 258 
SPECIFIC INFECTIOUS DISEASES 
neum; that there is no form of pulmonary or other tuberculous disease 
with which secondary peritonitis may not develop; that the peritoneum 
may be invaded in a process of multiple tuberculous periserositis with 
the pleura, pericardium and occasionally the meninges. 
The terminal stage of chronic cirrhosis of the liver may be compli- 
cated by an active peritoneal tuberculosis. Osier presents his statistics 
showing the disease twice as frequent in females as in males (131-60) 
and in 357 cases which he collected 27 were under 10 years: 
75 between 10 and 20 years. 
87 “ 20 “ 30 “ 
71 “ 30 “ 40 “ 
61 “ 40- “ 50 “ 
19 “ 50 “ • 60 “ 
4 “ 60 “ 70 “ 
2 above 70 years. 
He also found the disease more frequent among blacks than whites in his 
service at the Johns Hopkins Hospital. 
Borschke, in 4,250 autopsies of which 1,393 were tuberculous, found 
226, or per cent, in which the peritoneum was involved. These 
statistics vary in different sections; thus Hothnagel makes the statement 
that his experience in Vienna proved the peritoneum to be involved oftener 
than in Germany. The experiences in the United States prove the asso- 
ciation of peritoneal with other tuberculous infections in from 10 to 15 
per cent of autopsied cases. 
(a) Miliary Tuberculosis of the Peritoneum 
In these eases there is hematogenous infection, far-reaching, deposit of 
thousands of millet-seed sized tubercles on the peritoneum and on the 
liver and the spleen, with or without ascites; usually the latter is limited 
and likely to be serofibrinous, bloody or purulent. There may be circum- 
scribed areas of flatness due to sacculation. In these cases there are 
usually, as the disease advances, abundant adhesions, anatomic evidences 
of perihepatitis and perisplenitis. The disease may progress with marked 
wasting and little fever, or there may be decided febrile movement, pro- 
gressive anemia, rapid pidse: the course is acute and rapid. 
When peritoneal tuberculosis is a part of a general infection, the local 
symptoms may be marked or remain unnoticed because of the prominence 
of the changes in other organs. Diarrhea, fever and rapid pulse are occa- 
sionally prominent and an unfavorable combination. Severe pains with 
circumscribed areas of dullness and evidences of adhesions, are at times 
associated with ballooning of the intestines, evidences of partial constric- 
tion, chronic obstipation, alternation of constipation and diarrhea, with 
progressive loss of strength and flesh. This complex presents factors which BACTERIAL DISEASES 
259 
influence prognosis unfavorably. The greater the ascites with miliary de- 
posit, the better is the prognosis; this conclusion may be accepted without 
hesitation. 
Peritoneal miliary tuberculosis, a part of a general tuberculosis, with 
vomiting, pain and tympany is always serious and offers a bad prognosis. 
Miliary tuberculosis limited to the cecum,, simulating acute appendicitis, 
when promptly treated, offers a fair prognosis during the active years of 
life. Cases beginning with symptoms of enteric fever, without marked lung 
invasion, with occasional rigors, sometimes a remittent type of fever with 
slight ascites, when recognized early and radically treated, offer a fairly 
good prognosis. 
Ascites in children with acute abdominal symptoms is always suggestive 
of acute peritoneal tuberculosis; these cases are easily diagnosticated and 
their progress is usually favorable, if radically treated. 
My experience with the disseminated and mixed forms of peritoneal 
tuberculosis in children, caseous, glandular deposit and miliary disease, 
has been unusually favorable. I number among those perfectly cured and 
grown to manhood a good number, in whom, during early childhood, at 
the time of operation, the disease was so extensive as to justify only the 
gloomiest forecast. 
The prognosis of miliary tuberculous peritonitis is much better in 
children than in the adult. 
Positive evidence of active tuberculosis elsewhere than in the abdomen 
reduces the chances of recovery. The more acute the onset the more 
unfavorable the prognosis. Murphy disagrees with this conclusion. Rol- 
leston calls attention to purpura (cutaneous hemorrhages) and diarrhea 
as “very grave indications.” Mon-febrile cases in adults with negative 
tuberculin reactions have in my experience been uniformly fatal. 
(b) Chronic Tuberculous Peritonitis 
(Caseating and Ulcerative) 
I have been encouraged to believe that cases which give prompt tuber- 
culin reactions (cutaneous and subcutaneous) offer a correspondingly good 
prognosis. The fewer associated complications present, the better is the 
prognosis. The greater the ascites, the better the prognosis; bad when 
hemorrhagic or purulent. The less the diarrhea, the more favorable is the 
outlook. Associated Addisons symptom complex (suprarenal disease) 
adds decidedly to the dangers and reduces the chances of recovery. 
Mixed infection, causing fever, night sweats, an unfavorable blood pic- 
ture (Arenth “Verschiebung”) and marked leukocytosis argue against 
recovery. Favorable environment is a decided factor in preventing re- 
lapse after latency or apparent cure. The future of the patient depends 260 
SPECIFIC INFECTIOUS DISEASES 
very largely on the social conditions which prevail, for with peritoneal 
this is as important as with pulmonary tuberculosis. 
Many of these cases offer but few symptoms, run a chronic course cov- 
ering many years, during which the patient remains in statu quo, with- 
out ascites but with many adhesions and considerable thickening. The 
majority of cases run their course without ascites; the disease may be 
subacute or it may prove to be the final stage of an acute miliary tuber- 
culosis. A small proportion of cases develop intestinal symptoms; there 
may be moderate ascites, adhesions and succulation, evidences of partial 
intestinal obstruction from bands; the disease may remain afebrile dur- 
ing long periods; chronic invalidism with indefinite symptoms is not 
unusual. 
In occasional cases the retrograde process begins with acute exacerba- 
tion of symptoms, fever, increase of abdominal tension, ascites and ema- 
ciation. The number and extent of adhesions necessarily influence the 
course of the disease. It is surprising to note the extent of the disease 
at the time of operation and the favorable results which often follow. This 
agreeable experience may be found with complicating chronic tuberculous 
pericarditis and pleuritis. In the presence of nodular deposits and 
fibroid peritoneal thickening, it is not always easy to decide whether the 
process is tuberculous, a fact to which Welch, Wood and Fitz, and 
Henoch have called attention and deserves consideration in offering prog- 
noses. In these cases the peritoneum is studded with nodular growths; 
there are associated inflammatory exudates, usually serous, in which the 
prognosis is most encouraging. 
(c) Chronic Fibroid Tuberculous Peritonitis 
Surgical Treatment and Prognosis 
The influence of radical treatment (operative) on the prognosis of 
tuberculous peritonitis is of the greatest interest and importance. The 
study of a large clinical material has led me to the advocacy of early 
surgical interference in all cases of tuberculous peritonitis in which com- 
plications offer no contra-indications, with encouraging results—recovery 
in 80 per cent of such cases. The English authorities argue against 
operation in infants under 12 months. I number among my cases a lad 
now 20 years of age who was but 10 months of age at the time of opera- 
tion, with large multiple tubercle nodules in the abdomen, succulated 
serous effusion and adhesions, who has continued in perfect health and 
shows no lesions at present. 
The prognosis is unfavorable after surgical interference in the pres- 
ence of general and widespread tuberculosis. BACTERIAL DISEASES 
261 
The most favorable results follow operation for chronic tuberculosis 
of the peritoneum with ascites, and some surgeons are now limiting their 
surgical treatment of peritoneal tuberculosis to that class of cases. 
Schramm reports with children 80 per cent of cures among the operated 
and 64 per cent among non-operated cases. Pic admits recoveries among 
74 per cent of the operated against only 5 per cent of the non-operated 
cases. Sutherland makes the startling statement that he found 50 per 
cent of recoveries among the operated and 81 per cent of recoveries among 
non-operated cases. Thus Eolleston submits the result of his experience 
in cases gathered from literature and practice as follows: Of 125 cases 
treated by operation there were 88 recoveries, 70.4 per cent; of 156 
cases not operated there were 51 cures, 33 per cent. 
My experiences justify the conclusions that in carefully selected cases, 
without barring young children, basing such selection on data furnished 
in the preceding paragraphs of this chapter dealing with tuberculous peri- 
tonitis, the prognosis is enormously improved by early conservative sur- 
gical treatment. Further, while the disease may heal spontaneously, such 
incidence is not of sufficiently frequent occurrence to be depended upon in 
the majority of cases “spontaneous cures” are not always lasting; periods 
of latency are not infrequent and among spontaneous cures and latent 
peritoneal tuberculosis there are many recurrences, more by far than 
follow after operation; the dangers of dissemination are also greater 
among the apparently cured without operation than among those 
who have been helped by surgical methods. My experiences further 
agree very closely with those of Bandelier and Roepke that 96 per cent of 
untreated tuberculous peritonitides die; of these 50 per cent die in from 
1 to 6 months, 25 per cent in from to 1 year; the remaining cases may 
live with persisting symptoms during long periods, the length of time 
depending on many factors previously considered. 
My clinical material includes but two cases in which the operation 
was followed within a few days by the death of the patient. In one, 
the patient a boy age 18 seemed to present conditions that were favor- 
able, his temperature had been high, the pulse rapid and small, there was 
abundant ascites, without evidences of distant tuberculosis in physical 
signs, but the acute history justified the strong suspicion of general mil- 
iary tuberculosis. The operation was followed by continuous hyperpy- 
rexia during three days and the death of the patient. There was far- 
reaching miliary disease. The second case was practically a repetition 
of the first, with prompt lethal ending within seven days. 
References 
Bandelier & Roepke. Klinik der Tuberculose, 1914. 
Borschke. Virchow's Arch., Bd. cxxvii. 
Henoch. Berl. klin. Wchnschr., 1874, No. 20. 262 
SPECIFIC INFECTIOUS DISEASES 
Nothnagel. Spec. Pathol, u. Therapie, Bd. xvii. 
Osier. Practice of medicine. 8. ed. 
Pic. Rolleston, British Med. J., Sept. 2, 1911. 
Rolleston. British Med. J., Sept. 2,1911. 
Schramm. Idem (Rolleston). 
Sutherland. Idem (Rolleston). 
Welch. Flint’s Practice. 5. ed., 592; 6. ed., 583. J. Am. Med. Ass., 1903, xl, 701 
Wood & Fitz. Practice of medicine. 1. ed. 
9. Tuberculosis of the Pancreas 
Tuberculosis of the pancreas is so rare as to he of slight clinical or prog- 
nostic importance. If found, it is in children with generalized tubercu- 
losis, and is without marked influence on the progress of the disease. Pitt 
reports one pancreas tuberculous in 2,000 autopsies and accounting for 
per cent “of all cases in which pancreatic disease has been noted.” 
Mayo and Sendler have successfully removed tuberculous masses from 
the pancreas or from the neighboring lymphatic glands which were pal- 
pable. 
References 
Mayo & Sendler. Oser, Disease of the pancreas. Amer. translation, 1903. 
Pitt. Allbutt & Rolleston. 2. ed., iv. part I. 
10. Tuberculosis of the Spleen 
In all forms of disseminated tuberculosis, tuberculous deposits varying 
in size are found in the spleen. In some cases the capsule is more involved 
than the spleen itself and there may be consecutive perisplenitis and local 
peritonitis. Caseation of tubercle in the spleen with general tuberculosis 
is possible. 
With chronic pulmonary tuberculosis, multiple tubercles of consider- 
able size may be present in the spleen, causing enlargement, but no recog- 
nizable subjective symptoms. The tubercle grows more rapidly in the 
spleen than in the liver and is most likely to he found with tuberculosis 
of early life. 
There are cases of primary splenic tuberculosis which cause great en- 
largement of the organ, polycythemia, with positive reaction to tuberculin 
tests, in which splenectomy offers the only hope (over 80 per cent re- 
cover if operated early). Tuberculosis of the spleen should be suspected 
in all cases in which the organ is enlarged, and in which there is polycy- 
themia, without other convincing data. This combination always suggests 
tuberculin injection or other tests to establish an early diagnosis. 
The prognosis of primary tuberculosis of the spleen, if diagnosticated 
early, is favorable with rational surgical treatment. BACTERIAL DISEASES 
263 
11. Suprarenal Tuberculosis—Addison’s Disease 
(,Suprarenal Tuberculosis, Bronzed Skin Disease) 
The complex of symptoms known as Addison's disease is due to de- 
structive disease of the suprarenal glands; one or both are almost always 
tuberculous. The leading features are: increasing weakness and asthenia, 
pigmentation of the skin and mucous membrane of the mouth particu- 
larly, gastro-intestinal disturbances, increasing cachexia, small rapid pulse, 
low blood pressure, and marked emaciation. The tuberculous process in 
the suprarenals is usually bilateral and deposits in distant parts of the 
body are not unusual. 
Elsasser found in 549 cases which he studied 17 per cent with iso- 
lated suprarenal tuberculosis; in 43 per cent associated pulmonary tuber- 
culosis; in the remaining cases there were tuberculous herds in other 
organs. There are cases of hypernephroma associated with Addison’s 
complex reported by Bittorf. In 561 cases of Addison’s disease the 
suprarenals were normal in 12 per cent, tuberculous in 75 per cent (Levin). 
The description of the disease originally given by Thomas Addison in 
1S55 (“On the Effects of Disease of the Supra-renal Bodies,” London, 
1855) remains a classic in medical literature. Acute infection of the 
glands leads to a train of symptoms, without marked pigmentation, but 
with enormous asthenia, heart weakness, hypotension, depression, melan- 
cholia, at times delirium, rapid wasting of fat and muscle and death within 
from seven to fourteen days. The picture of extreme weakness is strik- 
ingly suggestive, coma or other profound nervous and toxic symptoms are 
soon followed by the end. 
In occasional cases there may be vascular changes with or without 
tuberculosis, thrombosis or hemorrhage into the gland substance, which are 
responsible for the rapidly fatal termination. Unfavorable symptoms are 
rapid wasting of tissues (faulty metabolism), subnormal temperature, per- 
sistent hypotension, diarrhea, marked blood changes, reduced hemo- 
globin and lowering of red blood count with marked large mononuclear 
lymphocytosis. Hypoglycemia, large grape sugar tolerance and adrenal- 
inemia are also unfavorable. Subnormal temperature followed by marked 
pyrexia, repeated at short intervals, are exceedingly weakening and de- 
pressing and presage an early termination. Eailure to produce glycosuria 
by the liberal injection of adrenalin with other positive symptoms must 
be interpreted as an unfavorable feature. Acute cases show but little 
or no pigmentation as a rule. 
The prognosis is better, so far as length of life is concerned, in pro- 
portion to the exent of the pigment deposit. The more chronic cases show 
the greatest pigmentation. 
Straub reports a most interesting experience with a rapidly fatal acute 
case of suprarenal disease in which the postmortem showed thrombosis 264 
SPECIFIC INFECTIOUS DISEASES 
of both suprarenal veins, and in which the symptoms of Addison’s dis- 
ease immediately developed including, after a short period of redness 
of the skin, characteristic bronzing (pigmentation), asthenia, adynamia 
and psychic disturbance. In this case the blood pressure was but little 
lowered. Syphilitic deposit in the suprarenals may simulate true Addi- 
son’s disease and may fully recover under treatment. Many reported re- 
coveries were probably of syphilitic origin. 
In chronic suprarenal tuberculosis there may be periods of latency, 
remissions, long periods of extreme weakness, during which complications, 
ordinarily insignificant, are sufficient to cause death. I number among 
my histories of chronic suprarenal tuberculosis, confirmed by autopsy, 
one of associated pernicious anemia and another case in which there were 
fully developed symptoms of exophthalmic goiter. 
Duration.—There are cases in which, including periods of latency, the 
disease may continue so long as ten years. There is no stage of the 
disease which may not be complicated by acute exacerbations, which may 
in turn lead to death within a few days or weeks. 
In chronic cases, pigmentation may be an early symptom, preceding 
during long periods the usual asthenia and the pronounced nervous mani- 
festations of the fully developed complex. In some of these cases normal 
blood pressure and hyperglycemia with adrenalinemia may continue dur- 
ing long periods, and are favorable indications. Kraus believes that all 
cases, if tuberculous, finally develop characteristic symptoms and die. 
Typical cases run their course in from two to four years. The devel- 
opment of mania or melancholia is always unfavorable. Epileptiform 
seizures may precede coma which promptly leads to death. I have never 
seen recovery from coma with suprarenal disease. Kascherininowa at the 
instigation of von Strumpell has treated a number of cases of suprarenal 
tuberculosis with tuberculin, with suprisingly good results. Munro has 
reported similar encouraging results. 
There is a class of cases in which, in the last stage of the disease, 
symptoms resembling acute peritonitis develop from which the patient 
does not recover, but dies in the course of from 3 to 7 days (Ebstein). 
I would call the attention of those interested in the literature of 
suprarenal disease to the additional references at the end of this article. 
Bertelli, Falta & Schweeger. Uber die Wechselwirkung der Driisen mil inneren Sekretion. 
Ztschr.f. klin. Med., in, No. 71. 
Biedl. Inner. Sekretion, etc. 1911-1913. 
Bittorf. Die Pathologie der Nebennieren, etc. Jena, 1908. 
Ebstein. Peritonitisartige Symptomen Complex, etc. Deutsch. med. Wchnschr., 1897, No. 
46. 
Elsasser. Arbeiten path. Anat. Inst. Tubingen, 1906, Bd. v, 45. 
Eppinger, Falta & Rudinger. Wechsclwirk., etc. Zeitschr. f. klin. Med., Bd. Ixvi-lxvii. 
References BACTERIAL DISEASES 
265 
Fait a. Mohr & Staehelin. iv. 
Erkrank der Driisen mit innere Sekretion. 1912. 
Falta & Fleming. Munch, med. Wchnschr., 1911. 
Kascherininowa. Russy Wratsch, 1911, H. 51. 
Kraus. Epstein-Schwalbe Handb. der Prak. Med., Blutdriisen. Bd. ii. 
von Mehring & Krehl Lehrbuch der inneren Medizin. 8. ed. 
Levin. Falta, Mohr & Staehelin Handbuch der Inneren Medizin. iv. 
Munro. Quoted by Bandelier & Roepke, Klinik der Tuberculose, 1914. 
Straub. Deutsch. Arch. f. klin. Med., 1909, Bd. xcvii. 
von Neusser & Weisel. Erkrankh. der Nebennieren, Wien, 1910. 
Wiesel. Virchow Archiv, Bd. clxxvi & Bd. clxxx. 
12. Tuberculosis of Lymphatic Glands 
{Scrofula, Scrofulosis, King’s Evil) 
Cervical Lymphadenitis.—All scrofula is due to the tubercle bacillus 
and in a large number of cases is purely a surgical and local affection 
leading to tuberculous adenitis. It is found, as a rule, in children, with 
the “scrofulous” or “tuberculous habit.” The disease by predilection 
selects the glands of the neck, the bronchial nodes or the mesenteries. 
There is a strong tendency toward chronicity when the neck glands are 
involved, and toward healing, while in most superficial adenitides case- 
ation and suppuration is the fate of the invaded gland. Children who 
are “scrofulous” are vulnerable. They are “below par,” as a rule, though 
intellectually active. They are prone to recurring phlyctenular conjunc- 
tivitis and keratitis, during long periods, bone tuberculosis, ulcerative 
rhinitis and otitis media; they are easily influenced by climatic changes 
and, as a rule, are not able to endure what is usually expected of the normal 
child. They are also subject to skin eruptions and ulcerations with strong 
tendency to anemia. The skin over the involved gland breaks down read- 
ily and, unless the gland when caseated or suppurating is radically removed, 
sinuses and crusting may persist during many years. Tuberculous adenitis 
provides a focus from which tuberculosis may spread at any time, and it is 
never safe to harbor such tuberculous deposits. 
Bronchial Lymphadenitis.—The invasion of the bronchial nodes has 
been frequently mentioned in connection with the study of tuberculosis 
and the importance of their prognostic significance has been accented. 
Pressure of enlarged nodes on veins may prove complicating and cause 
alarming symptoms in occasional cases. In spite of the fact that tuber- 
culous deposit in the bronchial lymph nodes may often remain latent dur- 
ing many years, there is never a time when such infection is not a menace, 
and when from it, fatal or active tuberculosis may not be spread. My ex- 
periences with these nodes as provocative of rapidly spreading tuberculous 
meningitis have been among the saddest of my professional career. 266 
SPECIFIC INFECTIOUS DISEASES 
Perforation of caseating or suppurating bronchial nodes may cause sud- 
den complications which are rapidly fatal by opening a large vein, an 
artery, one of the surrounding organs (esophagus, bronchus, lung or 
pleura), or even the heart sac. 
There are cases of widespread acute tuberculous lymphadenitis which 
resemble the acute form of Hodgkins disease. In these cases the patient 
wastes rapidly with high temperature (102°-106°F.), repeated chills and 
profuse sweating. The glandular invasion may include the lymphatics of 
the thorax, abdominal cavity, also the retroperitoneal space and often 
many superficial glands. Unless we are cautious, these cases may be 
mistaken for Ebstein s recurring fever of Hodgkins disease. The prog- 
nosis is uniformly bad, the course of the disease acute, patients die after 
a few weeks. 
With active lymphatic tuberculosis the blood changes mentioned in the 
general consideration of tuberculosis, including pronounced leukocytosis, 
are present, increased by tuberculin injection with increase of tempera- 
ture ; von Pirquet is positive in infected children with weak dilution. 
Mesenteric Tuberculosis (Tabes mesenterica).—With tabes mesen- 
terica there is tuberculosis of the mesenteric and retroperitoneal glands. 
Invasion of the glands is most frequent during early life, but there are 
cases of tuberculosis of the mesenteric glands in the adult, in which the 
infection spreads from the cecum, only occasionally from the pelvic organs 
or spine, and in which large masses, nodular and hard, are formed and are 
easily palpated. These mesenteric enlargements in the adult may remain 
latent during long periods, may present active symptoms early, with 
prompt wasting of the patient, may lead to sudden perforative peritonitis, 
or, with evidences of chronic peritonitis, alternating diarrhea and constipa- 
tion, lead to death after several weeks or months. 
Tabes mesenterica of childhood may be primary, but when thorough 
search is made it will be found that often the enlarged glands are asso- 
ciated with tuberculosis of one or more of the abdominal organs. The 
association of enlarged mesenteries with acute miliary tuberculosis, perito- 
neal tuberculosis, intestinal tuberculous ulceration, ileocecal invasion, is 
not uncommon. It may be assumed that tuberculosis of the mesenteric 
glands indicates infection by way of the intestines as a rule; that during 
early life tubercle bacilli easily wander through and beyond the intestinal 
mucosa without causing the slightest abnormality at the port of entry. 
The prognosis of all forms of mesenteric tuberculosis is bad. The pro- 
gressive cases are promptly associated with symptoms which do not keep 
the attendant in doubt; the wasting is characteristic, the increasing weak- 
ness with exhaustion, often diarrhea, rapid heart with small thready pulse, 
night sweats and fever, later added evidences of peritonitis, with or with- 
out ascites, are followed by death. Suppuration is not a frequent sequel. 
Osier calls attention as do other clinicians to the variation of the statis- BACTERIAL DISEASES 
267 
tics of abdominal tuberculosis in different countries and I quote the follow- 
ing to show these differences. “The small percentage in Hew York, less 
than one per cent of all cases (Bovaird and Mt. Sinai Hospital figures), 
contrasts with the high figure, 18 per cent for England, and the same 
has been demonstrated recently for Scotland by John Thomson, 3.57 for 
Edinburgh and 4.51 for Glasgow.” 
In considering the prognosis of lymphatic and intestinal tuberculosis 
we must once more call attention to the theory of von Behring, which is 
still sub judice, that the intestines ultimately serve as the foci from which 
pulmonary and distant infection take their origin. For the clinician who 
may or may not subscribe to this theory, the important fact must always 
remain, that in the presence of tuberculosis of the intestinal or mesenteric 
glands, the dangers of general infection with lung involvement are enor- 
mously increased. 
References 
Bovaird. Mt. Sinai Hospital figures. 
Osier. Practice of medicine. 1913. 
Pathologic and clinical data accumulated during recent years have 
entirely revolutionized our ideas concerning the prognosis and the manner 
of extension of genito-urinary tuberculosis. The profession is fast becom- 
ing convinced that most forms of genito-urinary tuberculosis are surgical 
affections. 
In no field of medicine have the newer methods made the early local- 
ization of lesions more positive than in the urinary tract. I refer more 
particularly to cystoscopy, catheterization of the ureters, with the tests 
which give information concerning the funtionating ability of the sepa- 
rate kidneys. 
There are four leading facts which influence the prognosis of genito- 
urinary tuberculosis powerfully, well established by clinical, pathological 
and surgical experiences. They are: 
(a) The kidney is primarily affected and but one kidney is at first 
involved in most cases. 
(b) If there is positive thickening of a ureter there is coexistent dis- 
ease of the kidney. 
(c) Bladder tuberculosis is not primary; “it is merely scalded and, 
as such, its irritability is the sentient expression of a suffering kidney.” 
“This, then, is the psychological moment to interfere on the chance of 
cure.” (E. Harry Fenwick.) In other words, bladder tuberculosis is 
usually secondary. 
(d) Genito-urinary tuberculosis spreads downward following along 
the course of the infected urine “with the stream” from kidney to its pel- 
vis, ureter and bladder, not in the opposite direction “against the stream.” 
13. Genito-urinary Tuberculosis 268 
SPECIFIC INFECTIOUS DISEASES 
These conclusions, accepted as they are by leading urologists and pathol- 
ogists and by those who have worked in the field of experimental medicine, 
are hard to controvert. On the other hand, we cannot deny the force of 
clinical evidence and the results of experiments, by Wildbolz, Eckehorn 
and others, which do not entirely justify the exclusion of the spread of 
genito-urinary tuberculosis from a focus below the kidney, ascending, 
therefore, not often but with sufficient frequency, to conclude that deposits 
of tubercle in the prostate, testicle, bladder or anywhere in the tract may 
spread the infection. Interference with urinary drainage is the leading 
cause of ascending infection of the genito-urinary tract. 
Tuberculosis of the Kidney 
Potent factors which influence renal and genito-urinary tuberculosis 
unfavorably, are the facts, (a) that the disease may exist, make progress, 
advancing rapidly, without causing subjective symptoms sufficient to cre- 
ate a suspicion of its presence. In one of my cases a man, age 35, died 
suddenly without evidences of preexisting disease in symptoms; at the 
autopsy there was bilateral invasion of the genito-urinary tract, no rem- 
nant of normal kidney was found. 
(b) From an early stage a large part of one kidney may he involved 
and in occasional cases the process promptly becomes bilateral (30 per 
cent). 
(c) Changed kidney function may in occasional cases lead to grave 
constitutional disturbances, toxemia, etc. 
(d) In some cases the bladder is promptly involved in an ulcerative 
process, adding to the sufferings of the patient. Mixed infection also adds 
an element of danger which is often overcome with great difficulty. 
(e) In occasional cases the functional activity of the kidney is enor- 
mously reduced, as can be established by ureteral catheterization and 
functional tests; tubercle bacilli swarm in the pus-laden urine, urea is 
reduced, and there may be grave constitutional disturbance. Gould has 
called attention to the important prognostic fact that with the presence 
of tubercle bacilli in a urine “which contains a proper proportion of urea 
and is free from pus,” surgical interference is justified and, after a thor- 
ough search of my records and a study of the literature on this subject, I 
conclude that under these conditions the prognosis may be considered 
good. 
Kidney tuberculosis associated with miliary infection is without 
marked influence on the general course of the disease which even without 
the added kidney complication leads to death within a limited time. The 
type of kidney tuberculosis which the clinician usually meets is the 
caseating and ulcerative form in which the first evidences of existing 
disease are referable to the pelvis of the kidney and are established by 
urinary examination. The symptoms are those of pyelitis. To reach safe BACTERIAL DISEASES 
269 
and early conclusions for diagnosis and prognosis every case of pyelitis 
in which no positive pathologic cause can he established at once, should 
create a strong suspicion of renal tuberculosis, and the case kept under 
observation until this conclusion is corroborated or upset by scientific 
investigation. 
Early hematuriawithout other leading symptoms, is often favorable, 
for it creates in active adults during the years of sexual activity (when 
genito-urinary tuberculosis is most frequent) the first suspicion of exist- 
ing tuberculosis, making prompt treatment possible and cure likely. It 
is a primary symptom in 6 per cent of all cases and is present in 60 per 
cent during the existence of the disease, oftener in men than in women 
(Braasch). 
The presence of bladder invasion does not argue against the possi- 
bility of complete recovery. Unexplained bladder irritation must always 
lead to the suspicion of kidney tuberculosis; it is present in 86 per cent 
of all cases (Braasch). Its significance, recognized early, will do much 
to reduce the mortality and improve the prognosis of genito-urinary 
tuberculosis. 
Spontaneous cure or surgical removal of the primary focus in the 
kidney, Avhen the disease is not widespread, as a rule results in the 
cicatrization or cure of vesical tuberculosis. When kidney tuberculosis 
is limited to one organ, the bladder and lower end of the corresponding 
ureter are uninvolved; there are but few or no constitutional disturbances; 
early recognition and treatment lead to cure in the majority of cases. 
The most important question which interests the clinician is: 
Is the disease limited to one kidney? In 30 per cent of cases the 
disease is bi-lateral early. It occasionally happens that the disease is 
active in one kidney and that a small latent deposit exists in the opposite 
kidney which escapes detection. With modern methods of diagnosis the 
chances of diagnostic failure are enormously reduced, though they will 
occur. 
I have seen cases with advanced tuberculosis in one kidney and but 
slight evidences of disease in the opposite organ, in which the removal of 
the active focus led to latency and to years of comfort, and occasionally 
to apparent cure. 
Perinephric abscess of tuberculous origin, caused probably through 
lymphatic invasion rather than perforation of the capsule of the infected 
kidney, may be an early complication of limited renal tuberculosis; its 
prognosis is not unfavorable, if the primary focus can be radically treated. 
Kidney tuberculosis of limited extent under favorable surroundings 
may occasionally undergo spontaneous cure; if this possibility suffices for 
the basis of treatment, the majority of genito-urinary tuberculoses will 
promptly follow their natural tendency toward progression and death. 
With advanced pulmonary tuberculosis and disseminated genitouri- 270 
SPECIFIC INFECTIOUS DISEASES 
nary tuberculosis the prognosis is absolutely bad. In 6 to 10 per cent of 
genito-urinary tuberculosis there is lung involvement. Limited lung 
infection does not argue against the radical treatment of renal tuber- 
culosis ; many such cases recover. The conclusions given by Braasch who 
has scientifically studied the material at the Mayo Clinic, in his “Obser- 
vations of 203 Patients Operated for Penal Tuberculosis,” may be ac- 
cepted as expressing the most advanced ideas concerning the prognosis 
and the incidence of the disease. Of the 203 patients operated, 6 died— 
2.9 per cent. Seventy per cent of the patients were followed during a 
sufficient time to allow profitable conclusions. Eighteen per cent were 
dead; of these 60 per cent died before the end of the first year, and 15 
per cent lived more than 3 years. Of the 82 per cent alive, all but 13 
per cent reported improvement or recovery from their bladder symptoms; 
their weight and strength had increased materially. Five patients had 
double infections; all of these died within one year of the operation. 
Braasch concludes that 15 per cent of renal tuberculosis is curable by 
the modern methods of treatment, while 90 per cent is fatal without it. 
Loss of weight and strength in young subjects with fever and bladder 
ulceration presents an unfavorable outlook. 
In 60 per cent of the Braasch cases of renal tuberculosis in the male, 
there was deposit either in the epididymis, the testicle, vas deferens or 
prostate, oftener in the epididymis. 
I have occasionally found that an inflammatory deposit left by gonor- 
rheal epididymitis became tuberculous; the prognosis of such cases is 
good. In one-third of all renal tuberculosis in the male the prostate is 
also invaded. General infection may be present with renal tubercu- 
losis and recovery may follow. The prognosis is less favorable when the 
kidney deposit with breakdown of tissue has advanced sufficient to make 
the organ palpable. Kidney tumor is present in from 20 to 25 per cent 
of cases. 
Persistent fever with symptoms of genito-urinary tuberculosis and 
rapid small pulse, with increasing anemia and loss of weight are all 
unfavorable. 
Besides the convincing statistics of Braasch to encourage the early 
recognition of genito-urinary, more particularly, renal tuberculosis, we 
find Bandelier and Boepke average recoveries after radical treatment at 
50 per cent, Israel 63 per cent and Caspar reports 67 cases with 50 cures. 
Pregnancy and. childbirth usually stimulate renal and genito-urinary 
tuberculosis to renewed activity. Israel has demonstrated the evil effects 
of pregnancy in a large number of cases on existing renal tuberculosis. 
In almost all of these cases rational surgical treatment has proved effi- 
cacious. 
Blood Pressure.—As in all forms of tuberculosis, so with advanced 
genito-urinary involvement and kidney degeneration, the systolic blood BACTERIAL DISEASES 
271 
pressure will be found below normal; decided hypotension is unfavorable 
and is usually found with a small and rapid pulse, disseminated disease, 
and advanced ulceration in the terminal stage of the disease. Progres- 
sive fall of blood pressure with loss of weight is always unfavorable. 
Failure to improve the circulatory condition by operation is also ominous. 
The dangers of secondary invasion of the meninges, lung, intestines, peri- 
toneum and bone, and the possibility of rapidly advancing amyloid degen- 
eration are not to he ignored in prognosis. 
References 
Baumgarten. Arch. f. klin. Chirurgie, Bd. Ixiii. 
Bandelier & Roepke. Die Klinik der Tuberculose, 1914. 
Braasch. J. Am. Med. Ass., Feb. 10, 1912. 
Caspar. Deutsche Klinik, Bd. x. 
Deutsche med. Wchnschr., 1900 & 1910. 
Eckehorn. Jores’ Anat. Grund. der Wicht. Krankh., 1913. 
Fenwick (E. Harry). Practitioner, Jan. 1913, 235. 
Gould. Practitioner, Jan., 1913, 181. 
Israel. Klinik der Nierenkrank, 1901. 
Kraemer. Zeitschr. f. Chirurgie, Bd. Ixix. 
Steinthal. Virchow’s Arch., Bd. c. 
Wildbolz. Jores’ Anat. Grund. der Wicht. Krankh., 1913. 
Genital Tuberculosis in the Female 
Menstrual Irregularities.—In the female we find with tuberculosis, 
menstrual irregularities which are usually associated with chlorotic and 
anemic conditions. 
The most frequent anomaly is amenorrhea, which is often an expres- 
sion of reduced vitality and may yield as the general condition of the 
patient is lifted and the blood picture is improved. Amenorrhea with in- 
cipient pulmonary tuberculosis without evidences of toxemia or advanced 
lung change, with chlor-anemia, almost always disappears under favorable 
surroundings unless the disease is progressive. There is in some cases, 
when advanced, atrophy of the uterus to which the amenorrhea has been 
attributed by Thorn and others. Serious .tuberculous diseases of the 
genital tract in women lead to anemia, particularly when there has been 
profuse hemorrhage or suppuration; under such conditions there may 
be amenorrhea or other menstrual irregularities. 
The Blood.—The blood condition offers valuable data for prognosis 
with genital tuberculosis or menstrual anomalies. 
The following blood picture may be considered unfavorable in the 
presence of genital tuberculosis: 
(a) Marked reduction of erythrocytes and morphologic change. 272 
SPECIFIC INFECTIOUS DISEASES 
(b) Reduced hemoglobin. 
(c) Lymphocytosis (34 per cent). Excess of small mononuclear cells. 
(d) Prominence of Arenth picture. Displacement to left. 
Can Tuberculosis Be Primary in the Female Genital Tract?—Amann 
makes the unqualified statement that there is no 'primary tuberculosis of 
the genital tract in women. Eor our purposes as prognosticians, there 
are a number of facts which contradict this dictum, though we must admit 
its truth in the majority of cases. Schlimpert is a warm advocate of 
Amann’s contention. The former claims that tuberculoses of the genitals 
are in 80 per cent of pulmonary origin, in 50 per cent they are secondary 
to intestinal tuberculosis, and that bone and lymphatic tuberculosis supply 
the foci for the remaining cases. 
The tuberculous diseases of the genitals in women are found in the 
I. Fallopian Tubes 
II. Ovaries 
III. Uterus 
IV. V agina. 
When of long duration, the disease is disseminated. 
I. Fallopian Tubes.—Kermauner claims that the Fallopian tubes 
are involved in from 70-90 per cent of all genito-urinary tuberculosis in 
women, the uterus in 40-65 per cent and the vagina in 10 per cent. The 
most patient search in many cases of tubal tuberculosis, fails at the time 
of the operation to show any other focus, and the large per cent of com- 
plete and lasting cures following, argues very strongly against the assump- 
tion that these are all of secondary origin. Naturally, the earlier tubal 
tuberculosis) is recognized the better is the prognosis, for the changes are 
prompt and may progress without subjective symptoms. Thickening of 
the tubes with caseation, the formation of creamy and cheesy tubercle 
bacilli-laden pus, and adhesions are characteristic, and from this focus 
general peritoneal tuberculosis may advance, or may be aggravated if 
already existent. 
In over 50 per cent of tuberculous peritonitides there is coexistent 
disease of the Fallopian tubes and, ovaries. 
II. Ovarian tuberculosis is as a rule secondary and is not infre- 
quent: usually the uterus and a Fallopian tube or the latter and the ovary 
are involved. Perioophoritis is a part of tuberculous peritonitis. The 
ovarian disease is usually double; one ovary may be more involved than 
the other. The disease advances in the ovary without materially inter- 
fering with the general condition of the patient in chronic cases, with 
the deposit of either multiple small foci or one or more large cheesy 
deposits. Tuberculous salpingitis may be far advanced without ovarian 
involvement. Ovarian and tubal infection often follow latent, unrecog- 
nized, or active general or localized peritoneal tuberculosis. Unrecog- BACTERIAL DISEASES 
273 
nizcd pulmonary deposit, or a tuberculous focus in some distant organ, 
may through the blood stream lead to genital infection. 
III. The Uterus.—When the uterus is tuberculous, the disease is usu- 
ally advanced in the tubes, in the ovaries, and there are likely to he 
evidences of adhesive tuberculous peritonitis, matting the pelvic organs 
together by dense adhesions. TJterine tuberculosis leads to cheesy degen- 
eration of the endometrium, which, if neglected, finally invades the mus- 
culature, limiting itself as a rule to the corpus uteri. In some cases the 
patient’s condition is reduced by the continuous discharge due to an ac- 
companying tuberculous endometritis. (Pyometra tuberculosa.) 
In considering the direction in which genital tuberculosis spreads (an 
important prognostic element), it will be found that extension is descend- 
ing under average conditions, rarely ascending. Baumgarten believes as 
the result of experimentation that in women the spread of tuberculosis is 
always in the direction of the wandering of the ovum, while in man the 
flow of the spermatic fluid marks the direction in which the disease spreads 
from, a primary focus. The unqualified acceptance of this theory is not 
justified; it unquestionably has exceptions which must be considered by 
the clinician. 
Direct infection of the genitalia in women from without is possible; 
bacilli may be introduced with the spermatic fluid or in other mechanical 
ways. 
IV. The Vagina.—Vaginal ulcers of tuberculous origin may be pri- 
mary and yield to radical treatment. In advanced genital tuberculosis 
there may be marked change in the vaginal wall, which, barring the dis- 
comfort and pain, does not materially influence the prognosis of the exist- 
ing primary disease. It is surprising to note how favorably even ad- 
vanced genital tuberculosis with vaginal invasion is often influenced by 
thorough treatment. 
In all forms of genital tuberculosis there is a strong tendency to the 
formation of protective adhesions; nature seeks to hold the disease within 
narrow limits. 
It occasionally happens that for some unknown reason general miliary 
tuberculosis promptly follows the removal by operation of tuberculous 
genitalia; this is a rare sequel. 
Generally speaking, it may be said that the prognosis of the genital 
tuberculosis of women is good; that the larger number of cases are ac- 
cidentally discovered in tubes, ovaries and uterus, though often strongly 
suspected, that in accordance with modern pathologic views “genital tuber- 
culosis in the male and in the female is not dependent for its origin upon 
urinary tuberculosis.” The safest conclusion for the practical physician 
to reach is that in the larger proportion of cases genital tuberculosis is 
secondary to a focus for which search should be made, but which may 
not be found; that the prognosis is so uniformly favorable in such a 274 
SPECIFIC INFECTIOUS DISEASES 
large number of cases that, in at least a number of these, primary infec- 
tion must be acknowledged. 
The coexistence of urinary and genital tuberculosis in both male and 
female does not of necessity lead to death; there are many cases wdiich 
are favorably influenced by surgical and medical treatment, while in 
some there may be spontaneous cure, or long periods of latency are 
established. Without an appreciation of the dangers of coexisting genital 
and urinary tuberculosis and rigorous treatment to establish resistance, 
the prognosis is grave. 
References 
Amann. Internal. Congress of Gynecologists, Rome, 1902. 
Baumgarten. Arch. f. klin. Chirurgie, Bd. Ixiii. 
Berl. klin. Wchnschr., 1904, 42. 
Kermauner. Nothnagel, Pathol, u. Therapie. Supplement, No. 6. 
Schlimpert. Arch. f. Gynaecol., 1911. 
Thorn. Kermauner-Nothnagel, Path. u. Therapie. Supplement, No. 6. 
14. Cardiovascular Tuberculosis 
Reference lias frequently been made to the heart, its small size, the 
involvement of the myocardium, and to the possibility of spreading 
miliary tuberculosis from the infected blood vessels, and the prognostic 
significance of cardio-vascular invasion. The statistics of Weigert proved 
50 per cent of all miliary tuberculosis traceable directly to vascular 
tuberculosis, while to-day statistics (Schmorl, Lubarsch, Benda) prove 
95 per cent of all miliary tuberculosis to be dependent upon this method 
of dissemination. Hence, every local tuberculous herd, closely related 
to an artery, vein, or thoracic duct, or the lymphatic stream, remains an 
element of danger. Vascular tuberculosis or infection represents there- 
fore, the link between the primary focus and miliary tuberculosis, a 
dictum of enormous prophylactic and prognostic value. 
Tuberculosis of the Aorta.—Tuberculosis of the aorta and other 
vessels may develop and lead to death. In these cases bacteria “penetrate 
the inner lining of vessels from the main channel,” in the presence of a 
forcible blood current, causing inflammatory change of the intima and 
secondary thrombosis. (Flexner, Blumer, Stroebe, Aschoff, Schmorl, 
Krumbhaar, Hekton). 
Tuberculous Pericarditis.—Tuberculous pericarditis is rarely pri- 
mary; it is usually part of a widespread process (pleural, pulmonary, 
lymphatic) which may run a chronic or an acute course. In chronic cases 
adhesive pericarditis may lead to stasis, edema, dyspnea, anginoid attacks, 
evidences of abdominal dropsy with enlarged liver and spleen, and cya- 
nosed kidney. BACTERIAL DISEASES 
275 
The acute cases often lead to hydropericardium, which may he hemor- 
rhagic with preponderance of lymphocytes (50 per cent and more) in 
the fluid. 
While the prognosis of tuberculous pericariditis is supposed to be 
unfavorable, we have found in practice that occasionally latency and cure 
may follow, and that, with disseminated tuberculosis, peritoneal and 
pleural, with but little or no lung invasion, cases have been cured by 
radical surgical interferences. We number among our medical colleagues 
one such fortunate case in which there was widespread tuberculosis of 
the pleura, peritoneum and pericardium, in which after eleven opera- 
tions, including one pericardial resection (cardiolysis of Brauer) and 
relief of adhesions thereby, there is now complete recovery, with suffi- 
cient, strength for the patient to resume practice. Romberg reports 16 
cases of tuberculous pericarditis of which only four died, while 4 of his 
10 idiopathic pericarditides died. 
Myocardium.—With miliary tuberculosis there may be deposits in 
the myocardium; these offer no symptoms which prove their pres- 
ence, and as Romberg has said, “interest the pathologist more than the 
clinician.” 
The change which is almost constant with tuberculosis is fatty degen- 
eration of the myocardium Avith marked anemia in the terminal stage of 
the disease. Tuberculous deposits in the myocardium in chronic phthisis 
are exceedingly rare. Willigk found but two hearts in which there was 
tuberculous deposit in 1,845 tuberculous subjects autopsied by him. 
Endocarditis.—Endocarditis of purely tuberculous origin is also rare. 
Occasionally there are a few vegetations on the endocardium with charac- 
teristic histologic build. But, as Marshall has demonstrated, the incident 
is not of sufficient frequency to justify the suspicion of its presence; on 
the other hand, when present, no symptoms make its recognition positive. 
Michaelis and Blum have proved the possibility of producing tuberculous 
endocarditis experimentally. 
Rot all valvular lesions found in the tuberculous subject are due to the 
tubercle bacillus. Many.of these lesions are old and of rheumatic (strepto- 
coccus rheumaticus) origin. 
In early life endocarditis tuberculosa may develop with general miliary 
tuberculosis. All of these children die. In the adult, endocarditis due to 
streptococcus infection may complicate tuberculosis or there may be 
chronic ulcerative endocarditis Avith tuberculosis, in which the Streptococ- 
cus viridans has proved to be the pathogenic factor. This complication 
may hasten the progress of the primary disease, but runs a chronic course, 
being the cause of most chronic malignant endocarditis. Klebs has also 
reported acute mycotic endocarditis Avith tuberculous phthisis. 
Thrombosis.—The formation of heart clots, thrombi in the pulmo- 
nary artery or veins of the body—ante mortem—in tuberculous sub- 276 
SPECIFIC INFECTIOUS DISEASES 
jects, is a cause of death which was recognized by Rokitansky, Klebs, 
Birch-Hirschfeld, Weichselbaum and others. In these cases, depending 
on the location and extent, there may be gradually increasing symptoms 
during several days or death may be sudden. Peripheral venous throm- 
bosis in the terminal stages of phthisis is frequent. Dodwell found the 
proportion of cases with this complication to be about 3 per cent. These 
peripheral thromboses are found in the terminal stages of the disease, when 
the circulation has become insufficient. 
Constriction of Veins.—Constriction of veins—one or more—by new 
connective tissue, causing blowing systolic murmurs in various parts of the 
lung, may appear alarming to the inexperienced; as a rule, they add but 
little to existing dangers. 
Pulse.—Changes in frequency and rhythm of the pulse often offer 
valuable prognostic data. The tachycardia of the end stage, during which 
the pulse may reach 200 per minute, is always of great prognostic impor- 
tance; with such a pulse, sudden cyanosis and death may follow. 
The Heart.—Whatever conclusions we reach concerning the size of 
the heart in the tuberculous subject, we must admit that Brehmer’s con- 
tentions (that the heart is undersized; that unless aided by proper methods 
it sends insufficient blood to the lung; that, as the direct result of its 
congenital fault, it is largely responsible for the development of pulmonary 
tuberculosis) have, with the impetus received by the approval of Dett- 
weiler, lead to the most rational and successful therapy of tuberculosis, the 
basis of which is the improvement of the tone of the insufficient heart, and 
all muscles, and the upbuilding of the patient. The theory of Rokitansky 
already mentioned in the general consideration of tuberculosis, that heart 
lesions antagonize pulmonary tuberculosis, particularly those which pro- 
duced venous stasis (initial lesions particularly) has been considerably 
shaken during the past fifty years. Fromholz found in 7870 autopsies, 
277 valvular lesions (3.5 per cent) of which 22 (8 per cent) had pul- 
monary tuberculosis. With but one exception these were associated with 
disease of the left heart. Mitral stenosis certainly antagonizes the develop- 
ment of tuberculosis of the lung as does mitral insufficiency with marked 
pulmonary engorgement and brown induration of the lungs. 
Blood Pressure.—I have already referred to the behavior of the blood 
pressure in pulmonary tuberculosis. Its progressive fall with small pulse 
is always unfavorable. Rise of blood pressure with even slight gain of 
weight is favorable, for it is suggestive of control of the process. 
Aschoff. Verhandl. d. Deutsch. path. Gesel., 1899. 
Bturner. System of medicine (Osier & M’Crae). iv, 1908, 512. 
Dodwell. Am. J. Med. Sci., 1893. 
Flexner. Johns Hopkins Hosp. Bull., 1891, in. 
References BACTERIAL DISEASES 
277 
Fromliolz. Arch. f. HeilJcunde, 1875. 
Hekton. J. Exp. Med., 1896, i, 112-193. 
Klebs. Leyden Deutsch. med. Wochenschr., Jan. 9,1896. 
Krumbhaar. Bull. Ayer Clin. Lab., Phila., 1908. 
Marshall. Johns Hopkins Hosp. Bull., 1907. 
Michaels & Blum. Deutsch. med. Wchnschr., 1898. 
Rokitansky. Handb. der Pathol. Anat. 1855. 
Romberg. Krankh. des Herzens, etc. 1906. 
Schmorl. Welch & Rolleston, Thrombosis. 
Allbutt & Rolleston. 2. ed., ix, 732. 
Schmorl, Lubarsch, Benda. Quoted by Jores. Anat. Grundlagen wichtig. Krankh., 1913. 
Stroebe. Centralb. f. allg. Pathol, u. pathol. Anat., 1897. 
Weigert. Virchow’s Archiv, No. 88; Deutsch. med. Wchnschr., 1883-1897. 
Willigk. Prager Viertel-Jahrschrift, 1856. 
15. Tuberculosis of the Nervous System 
Tuberculous Meningitis.—The prognosis of tuberculous meningitis 
is considered in connection with miliary tuberculosis. (See Miliary 
Tuberculosis.) Single tubercle nodules may exist in the brain without giv- 
ing rise to symptoms or there may be positive evidences in symptoms of 
tumor of the brain. In another class of cases there may be sufficient im- 
provement to justify the conclusion that the patient has made a fair 
recovery; periods of latency are not unusual, followed by sudden exacerba- 
tion and death; or spontaneous cure due to encapsulation or calcification, 
if the masses are small, may be followed by entire freedom from symptoms. 
Spinal meningitis, leptomeningitis, of primary origin is so rare as not 
to require consideration. When the pia is invaded, it is part of a dissemi- 
nated process, whether miliary, i. e., multiple deposit, or single large 
cheesy tubercle, with possible involvement of the cord, i. e., tuberculous 
myelitis, which offers no chance for restitution. 
Tuberculous pachymeningitis is also secondary, as a rule to bone tuber- 
culosis, the extent and its seriousness varying in accordance with the under- 
lying cause; usually the process ends in death, though life may be pro- 
longed and the disease remain stationary. There are but T4 authentic 
cases of spinal tuberculous pachymeningitis in medical literature (Bande- 
lier and Roepke). 
Myelitis.—Evidences of jnyelitis in a tuberculous subject must always 
strengthen the diagnosis of pressure due to bone disease or secondary de- 
posit in the membranes; in both the symptoms are those of compression 
and the prognosis is bad. 
The prognosis is better in those cases of tuberculous compression mye- 
litis due to caries or other bone change in which there has been ossification 
with latency. In these cases the mischief done cannot be overcome, but 278 
SPECIFIC INFECTIOUS DISEASES 
the process in the cord due to pressure does not advance and there may be 
slight improvement of the myelitic symptoms. Extra-medullary tubercle 
nodules causing compression myelitis, may, if single, be removed without 
causing destruction of cord substance and restoration of function may 
follow. Naturally the prognosis, so far as the life of the patient is con- 
cerned, must depend on the extent of the primary disease. It is surprising 
to note how superficial these nodules are often placed and how easily they 
may be removed. 
Neuritis.—There are occasionally cases of neuritis (peripheral) in 
tuberculous subjects, which, when a single nerve is involved, frequently 
yield to treatment, with full restoration of function. When there is 
limited compression neuritis, and the mass, which may be an enlarged 
gland or tuberculous bone, can be removed, the prognosis is also good. If 
in such cases there are multiple glandular enlargements at the same time, 
the advance of the process depends on many factors previously considered; 
the outlook is not encouraging, though the single neuritis may have been 
overcome. 
Multiple neuritis (polyneuritis) of tuberculous origin offers a less 
favorable prognosis than does single neuritis. It is often a terminal com- 
plication with cachexia. In alcoholics it may yield to treatment and dis- 
appears ; it is then non-tuberculous but alcoholic. 
Invasion of the cranial nerves is one of the early evidences of tubercu- 
lous meningitis as a rule, and offers a bad prognosis. (See Tuberculous 
Meningitis.) If there is early involvement of the pneumogastric or 
phrenic, death follows promptly. In children the majority of lesions 
(paralyses) referable to the cranial nerves are secondary to tuberculous 
basilar deposits; the correct diagnosis and prognosis need not be long 
postponed. 
References 
Bandelier & Roepke. Klinik der Tuberculose, 1914, 625. 
XXL Rheumatic Fever 
(Acute Polyarthritis, Inflammatory Rheumatism, Rheumatic Fever) 
Acute polyarthritis is an infectious disease in all probability due to 
the Streptococcus rheumaticus (Poynton and Paine and Rosenow) charac- 
terized by constitutional disturbances, inflammatory swelling of several 
joints in most cases, though the disease may be monarthritic. There is 
always great tendency to inflammatory changes in the serous structures of 
the joints involved and in over 50 per cent of all cases there is accompany- 
ing endocarditis. BACTERIAL DISEASES 
279 
The disease tends to relapse; following one attack during several years 
there is great tendency to recurrence. 
The disease is most frequent during the winter months (January, 
February and March) and during this season is likely to be more severe 
and its duration longer than during the warmer season, though there are 
many exceptions to this statement. 
Bacteriology 
The study of the bacteriology of acute rheumatism has not led to posi- 
tive conclusions until recently, when the observations of Poynton and 
Paine were confirmed by Rosenow. Poynton and Paine make a strong 
plea for the acceptance by the profession of their contentions, made dur- 
ing the past few years, that the Diplococcus rheumaticus is the specific 
microorganism upon which they claim the disease depends. 
The bacteriology of acute arthritis has received the attention of many 
pathologists and clinicians, including Leube, Leyden, F. Meyer, Glaser, 
Menzer, Sahli, Kraus, Schottmiiller, Jochmann, Litten and Lenhartz (See 
References), without results which to the minds of these observers justified 
the conclusion that the specific organism has been discovered. We feel 
safe in concluding, however, that the proofs offered by Poynton and Paine 
as well as Rosenow justify the conclusion that polyarthritis' is an infec- 
tious disease and is in all likelihood due to the streptococcus rheumaticus. 
Rosenow says: “The name streptococcus rheumaticus may be retained 
at present, not with the idea that organisms so-called always produce rheu- 
matism, but rather to call attention to the fact that when streptococci pro- 
duce the symptoms and lesions of rheumatism they have certain special 
features which streptococci from other sources do not usually have.” 
Mortality 
Rheumatic fever does not offer a serious prognosis. The mortality of 
all cases may be safely accepted as being between 3.Y per cent and 4.5 per 
cent. Hoffman found in his analysis of the cases at Johns Hopkins from 
1892 to 1911 that the mortality in YO males was 4.3 per cent without a 
death among the 15 females reported. 
There are many factors which influence the course of the disease and 
its severity; the study of its prognosis may be divided into the considera- 
tion of: 
Factors Influencing Prognosis 
I. The resistance of the patient. 
II. The sex and age of the patient. 
III. The character of the onset. 280 
SPECIFIC INFECTIOUS DISEASES 
IV. The nature of chronic preexisting and acute coincident disease. 
V. Complications. 
(a) Heart. 
(b) Hyperpyrexia. 
(c) Brain and Nervous System. 
(d) Blood. 
(e) Lung and Pleura. 
(f) Kidney. 
(g) Peritoneum and Appendix. 
(h) Skin. 
(i) Rheumatic nodules (Meynet). 
(j) Septic Conditions. 
(k) Purpura. 
VI. Duration. 
VII. Environment and Social Conditions. 
VIII. Relapse. 
IX. Immunity. 
I. Resistance of Patient 
As in all acute infections, those reduced in health, the weak, the obese, 
the alcoholic, and the dissipated, those who have been exposed to the 
elements without protection, those who work in damp places away from 
the sunlight and those who seem to be predisposed by heredity, present a 
lowered resistance, contract the disease after even slight exposure and 
are more likely than are those without these unfavorable factors to suffer 
from the severer forms and its complications. Poynton has called atten- 
tion to the influence of heredity in fragile children, “particularly if this 
be derived from both parents.” Such subjects are liable to destructive 
forms of carditis, to “deadly persistence of the process with increasing 
anemia, and not infrequently the development of nodules.” 
There is a greater likelihood of chorea during early life. In children 
the effect of chorea with severe carditis is always ominous and demands 
a guarded prognosis. We will again refer to the influence of age in con- 
nection with the consideration of the complications. 
II. Sex and Age 
Sex is not an important factor in prognosis; men contract the disease 
oftener than women because they are more exposed. The report of Whip- 
ham showed among 654 cases, 375 males and 279 females. In our prac- 
tice the proportion of females to males is 1 to 3; the same proportion is 
shown in our hospital service. Eemales in our service have suffered the 
same complications as men, without material differences in the prognosis. 
Between the ages of ten and twenty the proportion of female patients 
predominates. Kemp found at the Radcliffe Infirmary in Oxford that BACTERIAL DISEASES 
281 
between the tenth and nineteenth year there were among 49 cases 18 
males and 31 females, or 47.1 per cent of all of the cases reported. The 
figures of Church showed 43.5 per cent of 943 cases between the 
same ages. 
Age.—In children, the complications, particularly those involving the 
heart, are more frequent and more serious than in the adult; the disease 
is not frequent) before the sixth year. In young children, pericarditis is 
always a source of great anxiety and endocarditis is likely to leave per- 
manent valvular lesions. Langmead reports the “incidence of arthritis 
in children very high.” He examined 2,556 children, of which 133 were 
rheumatic and in all but 18 the heart was involved. “In 43 per cent of 
these cases there was some abnormality of the tonsils or pharyngeal 
mucosa.” Whipham reports that of the cases considered, 32 cases were 
under ten years of age and 80 per cent were between twenty and forty 
years of age. 
III. The Character of the Onset 
It is difficult to offer a forecast from the consideration of the method 
of onset of the disease. 
There are cases which begin without prodromata hut with sudden 
high fever and multiple arthritis in which the course is short and com- 
plications are few; while, often, cases which begin insidiously without 
fiery symptoms, with gradually increasing joint invasions, run a pro- 
tracted course, including serious complications. 
There are cases which begin with high fever, promptly develop hyper- 
pyrexia with well-pronounced cerebral manifestations, usually the ear- 
marks of meningitis; at first there is a full pulse, in which the course is 
foudroyant; death results within the first two to four days. These 
resemble the cerebral rheumatism of the older writers. 
Persistently rapid pulse during the early days of the disease with or 
without high fever must claim the close attention of the attendant, for 
it may signify myocarditis or some other early and serious complication. 
Early arhythmia, intermittence or irregularity of the heart, with evi- 
dences of myocardial weakness or dilatation, influence prognosis unfavor- 
ably, both in children and in the adult. 
Early profuse sweating, unless accompanied with heart lesions or 
other depressing complications, is not unfavorable. 
Cold extremities, small, rapid pulse with profuse sweating early, is 
an unfavorable combination. 
IV. The Nature of Chronic Preexisting or Acute Coincident Disease 
Preexisting1 Diseases.—Preexisting diseases, particularly those which 
are depressing, reduce the blood state, cause heart weakness or mental 
depression, always lower the resistance of the arthritic. 282 
SPECIFIC INFECTIOUS DISEASES 
One of the most important factors in the prognosis of rheumatism is 
the condition of the heart 'previous to the acute attack. Chronic valvular 
disease always increases the dangers of arthritis; the nature and extent 
of the preexisting lesion is important. 
Preexisting pleurisy, and myocarditis add to the dangers of acute 
polyarthritis. 
When arthritis develops in a nephritic, the prognosis must necessarily 
depend upon the stage of the nephritis, its character and the complica- 
tions. If there is chronic uremia, the added rheumatism will have an 
unfavorable influence. 
With preceding acide nephritis following acute infections and added 
arthritis, the prognosis may continue to he grave and uncertain during 
varying periods. 
Diabetes with acute arthritis superadded, is at times complicated by 
suddenly arising acetonemia and presents a serious prognosis. 
With most chronic diseases which complicate acute arthritis, the prog- 
nosis must depend upon the associated symptoms and added complica- 
tions. As a rule, the arthritis runs a favorable course and leaves the 
patient in his previous condition after a reasonable period of con- 
valescence. 
The addition of arthritis to chronic tuberculosis is considered in con- 
nection with the latter subject. (See Tuberculosis.) 
Acute Coincident Diseases.—Among the acute coincident diseases with 
which arthritis is found are tonsillitis, typhoid fever, typhus, scarlet 
fever, erysipelas, diphtheria (serum sickness), mixed infections and a 
variety of less frequently arising infections. 
Tonsillitis or tonsillar infection of some kind is present in from 70 
to 80 per cent of all acute arthritides. Tonsillitis or tonsillar infection, 
the pathogenic factor of most arthritides, does not influence prognosis 
unfavorably if the clinician appreciates its significance. 
Typhoid and typhus fever with rheumatism are, as a rule, but slightly 
influenced by the latter disease, for if is likely to be a late complication 
and in our experience has not often been severe. In children, following 
closely after typhoid or associated with it, there is greater danger of heart 
complication and the prognosis is therefore relatively worse. 
Arthritis with scarlet fever offers a good prognosis so far as life is 
concerned. In over 90 per cent of cases there is great danger of endo- 
carditis, nephritis and occasionally pericarditis, which necessarily influ- 
ence the course of the disease unfavorably and permanent damage to 
valves often results, while convalescence may be long postponed and 
relapse of the arthritis is not uncommon. 
Erysipelas with arthritis may be either suppurative or non-suppu- 
rative. When suppurative, the evidences of sepsis or pyemia are sufficient 
to warrant a guarded prognosis. These cases are always serious. Septic BACTERIAL DISEASES 
283 
thrombosis with such complications are to be feared. The nonsuppura- 
tive arthritides with erysipelas lead to recovery unless the latter disease is 
an expression of profound sepsis or both are complicated by serious heart, 
kidney or brain lesions. 
Diphtheria. Serum sickness following the use of antitoxin, with 
joint swellings and other evidences of arthritis, is of short duration and 
patients recover. 
Acute arthritis with diphtheria is less frequent than with scarlet 
fever; all of our cases have recovered. There may be sequeke including 
damaged endocardium or nephritis. The presence of arthritis does not 
in any way influence the incidence of post diphtheritic paralysis. 
Mixed Infections.—Mixed infections are always serious. Strepto- 
coccus or staphylococcus infections are often associated with malignant 
and septic endocarditis, nephritis, infarcts and justify an unfavorable 
prognosis. We will refer fully to malignant endocarditis in another 
chapter. (See Malignant Endocarditis.) The malignant rheumatic endo- 
carditis of Lenhartz and Litten is also considered with Malignant Endo- 
carditis. 
V. Complications 
(a) Heart.—Endocarditis. . In the adult there is complicating endo- 
carditis in 34.3 per cent (Pribram) ; in children the percentage is between 
60 and 80 per cent of polyarthritides, varying during different years and 
seasons. 
Arthritis is the most frequent cause of acute endocarditis and there- 
fore of chronic valvular defects. Bouillard in 1836 made the statement 
that “with severe and generalized rheumatism, endocarditis is the coinci- 
dence, pericarditis or endopericarditis the rule, absence of the lafter the 
exception. . . . With acute rheumatism which is mild, afebrile, partial, 
endocarditis is not the coincidence, and the coincidence of pericarditis 
or endopericarditis is the exception.’'1 
The prognosis of endocarditis in childhood is less favorable than in 
the adult. In the adult the majority of endocarditides complicating 
arthritis make recoveries with hut insignificant valvular damage. The 
larger number of lesions are finally found to change the mitral valve more 
than any other and the heart soon compensates for the fault. 
In both children and adults hut few who have relapses escape 
endocardial infections. Stephen MacKenzie’s statistics quoted by Osier 
show that of 116 cases, 58.1 per cent had endocarditis in their first 
attack, 63 per cent in the second attack, and 71 per cent in the third 
attack. In children the acute manifestations of the complication may, 
during many days, cause great anxiety and make the prognosis uncertain. 
When endocarditis and pericarditis are coincident in the child, or in the 
adult, the danger is greatly increased, always more in the child. 284 
SPECIFIC INFECTIOUS DISEASES 
Malignant endocarditis at all ages offers the same unfavorable prog- 
nosis (see Malignant Endocarditis) ; it is not frequent with the usual 
rheumatic infection, but when there is mixed infection, streptococcus or 
Streptococcus viridans, there is likelihood of endocardial infection. With 
Streptococcus viridans and pneumococcus endocarditis following or accom- 
panying arthritis, the course is likely to be chronic, particularly with the 
viridans infection; the outcome is always fatal. 
Severe endocarditis in children with chorea and rheumatism is among 
the most painful of all combinations, and justifies only the most guarded 
prognosis. In children as in adults many cases of acute arthritis with 
dilated hearts or slight mitral lesion make prompt recoveries and it is 
not at all unusual to find that the physical signs of endocarditis disappear 
and subjective symptoms may never recur. 
With mild grades of endocarditis in children and chorea, recovery 
is the rule. If, in these, endocarditis leads to mitral stenosis, as it some- 
times does in the more chronic cases, the outlook is more serious than 
without it. If with mitral stenosis in children and adults there are 
repeated relapses and fresh endocarditis is grafted on the old, the prog- 
nosis becomes correspondingly worse. It may be positively asserted that 
with a remnant of endocarditis shown'by positive physical signs in adults 
and in children the prognosis becomes worse with each relapse of arthritis; 
with these cases, as Povnton has said, “the prognosis, apart from this 
unknown factor (recurrence), turns mainly upon the condition of the 
heart.” Poynton’s conclusions concerning the significance of valvular 
lesions in children are applicable to the adult as well and they are here 
quoted: 
“(1) Mitral incompetence, if slight and well compensated, gives a 
favorable outlook. 
“(2) Mitral incompetence with a large feeble heart and symptoms of 
breathlessness and asystole is gloomy; such cases run a very unfavorable 
course in childhood. 
“(3) Slight mitral stenosis is compatible with a long and useful life. 
“(4) Progressive and severe mitral stenosis in childhood gives a very 
grave outlook for the future. 
“(5) Aortic and mitral disease combined are very serious when the 
aortic lesion is well marked; when this is only slight the cases fall into 
line with those of simple mitral incompetence. 
“(6) Primary aortic disease of severity is rare, but the outlook is 
grave.” 
It is often surprising to note how desperately ill patients may be 
with endocarditis complicating polyarthritis, how feeble the pulse and 
threatening the objective signs and how they may rally to make slow but 
satisfactory recoveries. BACTERIAL DISEASES 
285 
Pericarditis.—Pericarditis complicates from 5 to 6 per cent of adult 
rheumatism and from 10 to 20 per cent of the cases during childhood. 
There is, in the majority of severe cases, coincident endocarditis and 
often characteristic changes in the myocardium, to which we will refer 
in this chapter. 
During early life the prognosis of pericarditis, whether serous or 
purulent, is less favorable than in the adult. In very young children 
pericarditis is likely to prove a fatal complication. In children, peri- 
carditis with recurring attacks, in which there is a preexisting endocardial 
lesion, proves exceedingly grave. Poynton’s experience has been repeat- 
edly confirmed, i. e., that in children, “practically all the fatal first attacks 
develop pericarditis.” With asystole, adherent pericardium and hyper- 
trophy of the heart, the prognosis is unfavorable in children; in adults, 
these conditions are also exceedingly grave. 
In both children and adults the majority of serous pericarditides 
make satisfactory recoveries, though the associated endocarditis may and 
often does lead to valvular deformity. It is never to be lightly regarded. 
In the adult, and in the child, pericarditis is associated with myo- 
cardial change in many cases, which has a strong influence on prognosis. 
Suddenly arising or gradually increasing heart weakness with peri- 
carditis, from whatever cause, clouds the forecast; in most cases it leads 
to death unless promptly overcome. 
It will always be wise to give a guarded prognosis in cases which 
recover as to the future of the heart, for slowly forming adhesions may 
interfere with the functioning ability of the heart and lead to irre- 
parable cardiac asthenia. 
Myocarditis.—Thrombo-myo-endocarditis.—The myocardium is the 
most important organ for prognosis in arthritis, as in all acute infections. 
Myocarditis is present in 15 per cent of all cases. 
It may be assumed that with an unchanged myocardium and the 
absence of vasomotor paralysis, the prognosis of polyarthritis is favorable; 
icith a changed myocardium the prognosis remains uncertain. Severe 
rheumatism with endocarditis is usually associated with changes in the 
myocardium which are characteristic, differing from those found with 
other infections. Aschoff and Tawara described this peculiar myocar- 
ditis of polyarthritis. It consists in a leukocytic infiltration of the myo- 
cardium ; there are foci of large round cells, mononuclear with basophilic 
colored protoplasm; there is a unique wreath-form arrangement of the 
cells. These foci are found in the perivascular connective tissue, they 
are subendocardial, there is thrombus formation near the surface, pro- 
ducing the thrombo-endocarditis of Aschoff. Poynton and Paine pro- 
duced this type of thrombo-myo-endocarditis experimentally with the germ 
which they claim to be the specific organism of polyarthritis (Diplococcus 
rheumaticus). 286 
SPECIFIC INFECTIOUS DISEASES 
In cases of, moderate severity without marked symptoms referable to 
the myocardium, it is often difficult to tell the depth of the change in the 
muscle. Subsequent histories prove that unrecognized myocarditis leads 
to dilatation and faulty function during many months and with added 
interstitial change may cause permanent damage or death. Most cases 
of myocardial weakness without valvular lesions in children and in adults 
eventually lead to recovery. Many systolic murmurs heard during acute 
polyarthritis are due to myocardial change and are not of endocardial 
origin. Ventricular dilatation due to myocardial weakness may cause 
these and they usually disappear as the relative insufficiency is relieved. 
The strength of the myocardium or the “heart’s working capacity” is best 
tested by learning, as Kemp has claimed, the “amount of physical 'work 
which each individual can do in earning his or her living.” This natu- 
rally requires a full consideration of the individual case after the period 
of convalescence. 
Sudden Death.—Sudden death is not frequent. As a rule it is due 
to myocarditis, thrombosis or embolism. With hyperpyrexia death may 
be sudden. We have seen such patients die within a few minutes after 
convulsions. 
Blood Pressure.—At the height of the attack blood pressure is usually 
low; in the average adult and moderately severe polyarthritis it averages 
100 mm. Ilg. Hypotensive conditions which increase or persist influence 
prognosis unfavorably. 
With marked myocarditis rheumatica (Aschoff type) the prognostic 
conclusions will be materially strengthened by the intensive study of 
blood pressure. High blood pressure early, with tense pulse and previous 
nephritis, is unfavorable. In patients whose previous history is vague, 
with persisting high blood pressure during the height of the disease, the 
preexistence of chronic nephritis may be strongly suspected and the 
prognosis may be accordingly framed. 
Bradycardia.—Bradycardia during convalescence is not serious. It 
often follows cases of long duration in which digitalis has been given. 
It may follow under other conditions. In old patients with arteriosclerosis 
it may indicate heart-block (Adams-Stokes phenomenon) and it is 
serious. With meningitis bradycardia may be present early, but does 
not continue long and is soon followed by a small rapid and compressible 
pulse. 
Tachycardia.—Persistent tachycardia during the acute period is a 
grave symptom, particularly if there is progressive lowering of blood 
pressure with other evidences of myocardial weakness. 
(b) Hyperpyrexia.—Rheumatism is one of the three conditions which 
may be associated with the highest temperature found in the practice of 
clinical medicine. (The other two are sunstroke and meningitis.) The 
modern treatment of arthritis has unquestionably reduced the incidence BACTERIAL DISEASES 
287 
of hyperpyrexia. Hyperpyrexia with rheumatism is more frequent in 
hospital than in private practice. 
Hyperpyrexia, is always life threatening; there are usually symptoms 
referable to the meninges, kidney, and to the heart. Wild and active 
delirium is followed by coma; these symptoms may follow each other in 
rapid succession. The patient is cyanosed, conjunctiva is congested, 
Kernig symptom is present, there may be convulsions (particularly in 
children), there is albuminuria, concentrated and acid urine, materially 
reduced in quantity and evidences of rapidly failing heart strength. In 
some cases there are paralyses with spasticity. 
The duration of cases with marked hyperpyrexia is short. Death may 
follow in from twelve to forty-eight hours. Many of these cases are the 
prototypes of Trousseau’s “cerebral rheumatism.’’ 
With hyperpyrexia, the prognosis is almost always fatal. We have 
never seen recoveries, when, with the symptoms mentioned, the tempera- 
ture has mounted above 106°F. In rare cases the temperature may reach 
as high as 108°-110c before death. 
(c) Brain and Nervous System.—Meningitis (see Hyperpyrexia, 
preceding paragraphs) is usually a fatal complication of rheumatism. 
There are cases of transitory meningismus in children and in adults which 
recover without the development of active or progressive meningitis. 
Delirium and other mental symptoms are not uncommon during the 
acute period; these are not of serious import in most cases. But few' 
severe or widespread arthritides are exempt from psychic disturbances. 
They are often marked in young subjects, in alcoholics and in the plethoric; 
but are by no means limited to these. Acute psychoses are occasionally 
present with hallucinations; at times active mania and manic-depressive 
states, also stupor. These conditions are rarely lasting, they are of toxic 
origin and yield in the course of a few weeks to several months. 
Neuritis may be either an early or a late complication. There may 
be multiple neuritis or a single nerve trunk may be involved. Most 
peripheral neuritides are.associated with more or less muscular atrophy. 
The single neuritides may include either the sciatic, the motor oculi, the 
trifacial or other nerves. 
The prognosis of all forms of neuritis with arthritis is good. 
(d) The Blood.—Uncomplicated cases of polyarthritis wdth fever and 
joint swelling show an average leukocytosis of 15,000; higher counts are 
rare. Serious infections with complications such as pleurisy, pericarditis, 
pneumonia, etc., present much higher leukocytic counts. 
Improvement, fall of temperature and reducing swelling of the joints, 
is followed by a lowered leukocytic count. Fresh infection may be sus- 
pected when there is a sudden leukocytic increase. Naegeli showed that 
there is a decided neutrophilic increase, occasionally mononuclear also. 
At the height of the acute symptoms there is a decided decrease of 288 
SPECIFIC INFECTIOUS DISEASES 
lymphocytes and eosinophils; an increase of these is found with improve- 
ment of constitutional and local symptoms and argues in favor of an early 
convalescence. 
Anemia is characteristic of acute arthritis, there is a prompt destruc- 
tion of erythrocytes in severe cases, and the blood elements including the 
red corpuscles and hemoglobin reform very slowly during convalescence. 
Persistent anemia is always a serious indication. Fibrin and blood plates 
are always increased. 
Cases beginning with typhoid symptoms, in which there is slight en- 
largement of the spleen (Naegeli), may prove puzzling for diagnosis and 
prognosis. In these, the leukocytosis and increase of fibrin preclude the 
possibility of typhoid. Joint symptoms develop after from thirty-six to 
sixty hours in most cases. 
(e) Lung and Pleura.—Pneumonia.—Croupous or bronchopneumonia 
may complicate rheumatism. Pneumonia is an occasional terminal infec- 
tion in alcoholics, in the aged or in children. Croupous pneumonia is not 
often the cause of death. When pneumococcemia or other types of pneu- 
monia are complications, they are secondary. (See Pneumonia). Hypo- 
static bronchopneumonia may complicate the more serious and persistent 
cases. (See Bronchopneumonia). 
Pleurisy.—Pleurisy may be due to extension from the pericardium; 
when associated with endocarditis and pericarditis, in the presence of large 
serous effusion it adds to the discomforts of the patient and to the dangers. 
Recovery is possible, and follows in a large proportion of cases. It has 
been our experience that the exudate is promptly absorbed, also that the 
symptoms yield to one or two aspirations. 
The association of pleuritis and pericarditis (polyserositis) was found 
by Mosler in 15 of 142 cases of arthritis; in these the prognosis cannot be 
given early. The cases demand long periods of observation that the re- 
sulting adhesions and heart damage may be considered. 
Empyema.—Empyema does not often complicate rheumatism; when 
it does it is secondary. It yields to radical treatment unless the underly- 
ing sepsis or pyemia is overpowering. 
Bronchitis.—Bronchitis associated with rheumatism, unless second- 
ary to serious heart lesions, is usually insignificant. 
(f) Kidney .—Albuminuria with rheumatism does not necessarily in- 
dicate the presence of nephritis and though frequent, particularly during 
the febrile period, it is not per se of serious import. 
Concentrated acid urine is the rule and does not materially in- 
fluence the course of the disease. It offers indications for treatment, which 
when recognized, can in most cases be controlled. 
Nephritis is a rare complication. With mixed infection, cases that 
prove to be septic, or with infarct due to malignant endocarditis, renal 
changes are ominous. BACTERIAL DISEASES 
289 
(g) Peritonitis and Appendicitis.—In a large experience we have met 
but one case of rheumatic peritonitis; it ended fatally. Jochmann has 
never seen a case. 
Appendicitis is in some cases held to be of rheumatic origin. There 
are cases which remain unexplained; some are associated with or follow 
tonsillitis; it may be that these are dependent upon the same infection. 
However, the question is still sub judice; Poynton and Paine have caused 
it experimentally with an organism which they isolated from cases of 
rheumatism. 
(h) The Skin .—Sudaminous eruptions are the rule and are unim- 
portant prognostically. 
Erythematous eruptions, intertrigo and occasional herpes, are with- 
out prognostic significance. 
Erythema nodosum.—Erythema nodosum is unquestionably of in- 
fectious origin and presents many of the earmarks of rheumatism and 
should in the present state of our knowledge be classified with it. Children 
suffer oftener than adults. Only rarely are there serious complications 
referable to vital organs (heart, etc.). The prognosis is uniformly good. 
The duration varies, the disease may run an acute course in seven to ten 
days, may show tendency to relapse, may become subacute and in rare 
cases, usually in the adult, becomes chronic. 
(i) Rheumatic Nodules (Meynet).—These nodules first described by 
Meynet are about the size of a pea, rarely larger; they are located on the 
fingers, hands, wrists and in the neighborhood of the elbows. They rarely 
form during the height of the disease, usually follow the febrile period. 
Osier says they are common in children with mitral lesions. All authors 
have found the nodules oftener in children than in adults. 
Kemp holds that “the presence of rheumatic subcutaneous nodules has 
a definite bearing on prognosis, and when present, especially in children, 
are always accompanied by gross damage to the heart.” They are more 
frequent in children than in adults. They probably hold infecting agents 
and are responsible for fresh attacks. Rheumatic nodules do not in- 
fluence prognosis in adults materially. 
(j) Septic Conditions.—The septic condition is due to mixed infec- 
tion, is always serious when complicating rheumatism. It may be either 
early or late and is likely to be associated with septic endocarditis, septic 
thrombo-myocarditis and offers an unfavorable prognosis (See Sepsis and 
Malignant Endocarditis). 
In occasional cases symptoms of septic fever precede polyarthritis 
(non-suppurative) during several days before there are positive evidences 
of joint disease. Many of these recover. 
Sepsis is in rare cases associated with multiple suppurative arthritis. 
In some of these, the septic condition precedes the joint symptoms during 
several days. Thorough search usually reveals the primary focus. Our 290 
SPECIFIC INFECTIOUS DISEASES 
experience with these cases has been unfavorable; they often present the 
clinical picture of malignant septicemia. 
(k) Purpura.—Whether purpura rheumatica should be included in 
the consideration of polyarthritis remains undecided. In this work it will 
be separately considered (See Purpura). 
Purpuric and hemorrhagic conditions complicating arthritis are al- 
ways suggestive of malignant infection and demand a guarded prognosis. 
When purpuric conditions are due to hemophilia or are attributable to the 
usual causes of non-malignant purpura (purpura simplex, rheumatica, and 
hemorrhagica) the prognosis of arthritis is not unfavorably influenced by 
the complication; on the other hand, septic conditions, with limited or ex- 
tensive petechise, with or without endocarditis, are always serious. These 
conditions are embolic. 
Blebs or vesicles which contain blood often show a tendency to necro- 
biosis of the underlying cutis, are also of embolic origin, and are evidence 
of malignant infection. 
VI. Duration 
It is never safe to make a prophecy which will commit the clinician to 
a time limit of polyarthritis. It is absolutely impossible in any case to 
give any reliable information on the subject, for apparently mild cases at 
the beginning finally prove to be rebellious to treatment and those in which 
the initial symptoms argue in favor of a long period of arthritis often run 
a short course. 
Number of Joints Inflamed.—The early and persistent inflammation 
of a single joint (monarthritis) in the majority of cases argues in favor 
of a slow process and occasionally leads to subacute disease or chronicity. 
In rheumatism the prognosis as to length of time the disease lasts seems, 
as the result of the observation of many clinicians, in many series of cases, 
to be less favorable when the disease is monarticular and stationary, than 
with the invasion of several joints or the leaping of the disease from joint 
to joint. If with polyarthritis the features of the disease change, and one 
joint is selected with tendency to thickening and swelling, a long period 
may be expected during which the local and some constitutional symptoms 
will continue troublesome. Migratory lesions of the joints often yield 
within a reasonable period. 
Recurring rheumatism is usually either subacute or may approach 
chronicity. It is not at all unusual to find the second or the third attack 
associated with endocarditis and multiple joint invasion continuing dur- 
ing four to eight months. The average duration of the benign case is 
from three to six weeks. BACTERIAL DISEASES 
291 
VII. Environment and Social Conditions 
In considering the factors which influence the course of the disease 
we referred to sunlight, dampness and other baneful conditions which 
lower the resistance of the patient; these are also included in the study 
of the environmental and social factors which influence prognosis. Un- 
healthy homes, faulty ventilation, insufficient and faulty food, humidity, 
exposure, dissipation, excesses of all kinds prepare the culture media 
within the body which are needed for the proliferation of the micro- 
organism which is the cause of the disease. 
It is not at all unusual to find patients who have suffered repeated 
attacks of arthritis relieved permanently by a change of residence or 
climate; in other cases, change of occupation and methods of living prove 
to have a wholesome influence. 
VIII. Relapse 
Relapses are frequent, and exert an enormous influence on the subse- 
quent history of these patients because endocardial complications are 
aggravated and valvular deformities are thereby increased. Relapse often 
leads to chronic changes in the joints with deformities and muscular 
atrophies. Muscular atrophies increase with each attack of rheumatism, 
particularly with those forms in which the symptoms continue subacute 
during long periods and remain limited to the same joints. 
IX. Immunity 
Arthritic infection is not followed by immunity. In many a predis- 
position is developed which invites repeated attacks. It not infrequently 
happens that the predisposition continues during four to six years follow- 
ing the initial attack, after which there may never he a return of the 
disease. These facts thoroughly appreciated by life insurance companies 
have led to the postponement or rejection of applicants during a number 
of years after acute attacks of arthritis. 
References 
Aschoff & Tawara. Grundlagen der Herzschwache, 1906. 
Aschoff Pathol. Anat. 1913. 
Church. Allbutt & Rolleston System of Medicine. London, 1906, ii. i. 603. 
Hoffman. The statistical experience. Data of Johns Hopkins Hosp., etc., Baltimore. 
Johns Hopkins Hospital Reports, New Series, No. 4, 72. 
Kemp. Quarterly J. of Med., Oxford, April, 1914, vii, No. 27. 
Langmead. Osier's Practice of medicine. 8. ed., 1913, 372. 
Mosler. Rudolph Virchow, Krankenhaus Reports. 
Naegeli. Bluterk. u. Blutdiagnose. 1912. 292 
SPECIFIC INFECTIOUS DISEASES 
Poynton. Practitioner, London, xc, No. 2. 
Quarterly J. of Med., Oxford, 1909-10. 
Poynton & Paine. Researches on Rheumatism. London, 1913. 
Rosenow (E. C.). J. Infect. Dis., Jan., 1914, xiv, No. 1, 61-80. 
Whipham. Report Collective Investigation Committee of the British Med. Ass. 
XXII. Tonsillitis 
The Influence of the Tonsil on Prophylaxis and Prognosis 
The tonsil serves as the port of entry of pathogenic organisms and has 
an enormous influence in spreading infection to distant organs through 
the chain of lymphatics with which it is intimately connected and through 
the hlood-stream. The normal tonsil harbors disease-producing micro- 
organisms at all times; the diseased tonsil is a greater menace, for in its 
crypts conditions are offered which invite local proliferation and con- 
secutive constitutional infection. 
All changed, enlarged and adherent tonsils powerfully influence the 
prognosis of many pathologic conditions. I considered the influence 
of the tonsils in connection with the study of tuberculosis. (See Tuber- 
culosis.) Recent investigations by Mitchell dealing with the infection 
of children with bovine tuberculosis accent their importance and prove 
the enormous influence of the faucial tonsils in tuberculosis of the upper 
cervical glands; they also prove that in a large proportion of cases a well- 
marked tuberculosis of the deep glands “is secondary to a small tuber- 
culous focus in the tonsil.” In children, Mitchell reportsi the “high per- 
centage of faucial tonsils in which the bovine virus was present,” and 
claims it “is further striking proof of the frequency of tuberculous cows’ 
milk as a source of infection.” Wood in 1,671 cases showed, that in 88 
(or 5.2 per cent) the tonsils were tuberculous. Lartigan contends that 
Wood’s figures are less reliable than his own in which he did not rely 
upon histologic studies alone, but added the results of inoculation tests 
and found that 12 of his 75 cases gave positive results to animal inocu- 
lation and therefore placed the percentage of tubercular involvement of 
the pharyngeal tonsil at 16. 
Tonsils in which there are no apparent changes have been proved 
experimentally and clinically to hold the organisms of cerebrospinal 
meningitis, pneumonia, rheumatism, streptococcus endocarditis, poliomye- 
litis and many other grave diseases, and have served as the port of entry 
of these disease-producing agents. 
Further it may be contended with considerable certainty that many 
chronic disases, the causes of vjhich have not been understood in the past, 
are being favorably influenced by the enucleation of both large and small BACTERIAL DISEASES 
293 
tonsils. Among these diseases are the various forms of so-called chronic 
rheumatism and rheumatoid arthritis. 
There are acute infections of the tonsils in which these organs are 
involved. Among these are diphtheria and suppurative peritonsillitis. 
To such tonsils, after convalescence has commenced, serious constitutional 
disturbances which threaten life may be traced; they continue to hold in 
their crypts and tissues colonies of the original pathogenic microorganism 
which they throw into the blood-stream from time to time. Pyemia, 
sepsis, nephritis and other infections have followed from such source. 
Diphtheritic paralyses, in which there are acute exacerbations with 
evidences of sensory neuritis, have been favorably influenced by the 
enucleation of tonsils, in which, weeks after the acute process had run its 
course, diphtheria bacilli were found. 
In a number of cases of Hodgkin's disease there has been a clear his- 
tory of persistent enlargement of cervical glands following tonsillar infec- 
tions. In some of these, the glands remained stationary during a number 
of months before showing the progressive enlargement and extension of 
the fatal disease. 
The prophylaxis and prognosis of many constitutional diseases as well 
as many conditions, the cause of which we have been unable to under- 
stand, will be favorably influenced by the thorough appreciation of the 
importance of the faucial tonsil as a reservoir from which many and 
serious infections may proceed, and the further fact that the defensive 
function of the organ is readily overcome. 
Acute Follicular Tonsillitis 
Angina, Amygdalitis, Streptococcus Tonsillitis 
Tonsillitis is an acute infection of the tonsil leading to inflammation, 
membranous deposit, constitutional disturbances, occurring usually dur- 
ing early life, with complications either early or late which may lead to 
grave organic changes in one or more organs. It may he sporadic or 
epidemic. Most acute tonsillitides are of streptococcus origin. The 
majority of these run a favorable course and lead to convalescence with 
considerable weakness, and at times long periods of ill-defined symptoms 
with a general condition below par. 
Sporadic Cases.—There are acute sporadic cases in which, for sev- 
eral days, there are free and outspoken constitutional manifestations, 
including, with the tonsillar lesions, high temperature, rapid pulse, mitral 
systolic murmur due to muscular insufficiency and albuminuria; often 
there are evidences of nephritis. These cases under treatment and rest 
offer a good prognosis; rarely does death follow except in those reduced 
by previous disease, burdened by depressing and undermining diatheses 
or some one of the early complications to be mentioned later. 294 
SPECIFIC INFECTIOUS DISEASES 
The subsequent history proves the importance of the infection as a 
cause of chronic and permanent disease in neglected and malignant strep- 
tococcus infections. In all cases the extent of the glandular invasion 
(enlarged cervical glands) is an index of the depth of the infection. 
There are all grades of severity in the sporadic cases. 
Streptococcus tonsillitis may accompany and materially influence 
the course of other infections; among these are influenza, measles, scarlet 
fever, infantile paralysis, cerebrospinal meningitis, and in young children 
bronchopneumonia occasionally. In rare cases it may precede these 
infections. 
Sporadic cases may infect entire households or wards of hospitals 
and it sometimes happens that an outbreak of streptococcus tonsillitis in 
a surgical ward leads to erysipelas among the operated cases. 
Mild sporadic cases run their course in from three to six days. 
Those with marked constitutional disturbances average between six and 
nine days. 
Convalescence is usually slow, sequelae are numerous and often serious. 
These will be considered with the epidemic type of the disease. 
Endemic and Epidemic Streptococcus Tonsillitis.—The most frequent 
source of endemic or epidemic tonsillitis is infected milk. The infection 
is almost always due to organisms belonging to the streptococcus group. 
Miller, who investigated the Chicago epidemic, found that “an epidemic 
of mastitis existed in cows and sore throat in farmers” in the territory 
which supplied the contaminated milk, and emphasizes the fact that 
“streptococci which cause mastitis in cows may be pathogenic for animals 
and virulent to man.” 
Epidemic streptococcus tonsillitis which prevailed in Cortland and 
the adjacent counties of Central Yew York during .1912 was virulent 
and was the cause of many deaths. The old and feeble, also very young 
children offered lowered resistance. The complications of the Cortland 
epidemic were numerous and included nephritis, endocarditis, pneumonia, 
metastatic parotitis (see Metastatic Parotitis) and a variety of conditions 
which lead to tardy convalescence. 
Capps and Miller made an exhaustive report of the Chicago epidemic 
due to the contaminated milk supply above mentioned; 10,000 cases were 
included. 
Epidemic cases are always much prostrated by the infection and show 
marked leukocytosis. 
Second attacks within a few days are frequent and lead to slow 
convalescence. 
Capps and Miller report peritonsillar abscesses in occasional cases 
which, when promptly opened, lead to prompt recovery. 
Complications.—The unfavorable cases are those in which there is bac- 
teremia, which leads to numerous complications. Otitis media compli- BACTERIAL DISEASES 
295 
cated 6 of 173 typical cases observed by Capps and Miller. Arthritis 
is a frequent complication of epidemic tonsillitis; it is present in 10 per 
cent of the cases and occasionally leads to suppuration of the joints. 
Erysipelas complicated two cases seen by us during the epidemic in 
Cortland and adjoining counties. In one, the complication was migra- 
tory, covered the entire body in its acute exacerbations; the patient, a 
man aged about thirty, finally developed streptococcus meningitis and 
died. The other case was a woman who recovered. She was over seventy, 
developed secondary pneumonia, suppurative metastatic parotitis and 
erysipelas, after initial streptococcus tonsillitis. 
Nineteen of the 173 cases reported by Capps and Miller died. Nine 
of these died of peritonitis, four of pneumonia and three of septicemia. 
An investigation made at the time of the Cortland epidemic by Dr. Charles 
E. North of New York City, who, with two assistants, cooperated with 
the Public Health Committee of the Cortland County Medical Society, 
resulted in, the finding of two cows in one dairy that were affected with 
garget. This dairy furnished about 7 per cent of the total milk supply 
and tabulation showed that this dairy furnished milk to families in which 
about 72 per cent of the whole number of cases occurred. Eleven throat 
cultures were examined and all of them revealed the presence of a certain 
species of streptococcus of the same type found in the discharge from the 
udders of the two affected cows. Of 669 cases 13 died, cause of death 
as follows: 
Age. Cause of Death. 
50 Edema of Larynx. 
51 Heart Failure. 
69 Lobar Pneumonia. 
39 Peritonitis. 
66 Peritonitis. 
60 Peritonitis. 
62 Peritonitis. 
70 Erysipelas. 
80 Erysipelas. 
82 Pneumonia. 
72 Heart Disease. 
78 Erysipelas. 
Unknown Peritonitis. 
In addition, there were reported seven other cases of erysipelas; nearly 
all cases had enlarged cervical glands, many of them forming abscesses; 
and a very large number of protracted cases of rheumatism. Also cases 
of pleurisy and pericarditis. 
Epidemic cases occasionally run a prolonged course—three to seven 
weeks, after which the convalescence is slow and the patient continues 
weak during a long time. Mild cases recover in from two to three days. 
Heart Complications.—The cardiac complications which follow all 296 
SPECIFIC INFECTIOUS DISEASES 
forms of tonsillitis may be either due to streptococcus endocarditis and 
myocarditis, to relative insufficiency of the myocardium, to functional 
disturbances depending on the reduced state of the patient or to distant 
complications, such as nephritis, arthritis, et cetera. All of these offer a 
favorable prognosis except those forms of malignant endocarditis of 
streptococcus origin. Permanent damage often follows in the non-malig- 
nant cases and the patient recovers with an irritable heart and valvular 
lesions. In these cases, either with subsequent tonsillitis or without, there 
are acute endocardial exacerbations in which there may be complications 
which are serious, including nephritis and possible cardiac insufficiency 
and increasing anemia. Many of these patients fall into extremely dan- 
gerous conditions including general dropsy, from which they may with 
proper care and treatment recover, i. e., return to their former state with 
an added endocardial scar. 
Pericarditis if purulent complicating or following tonsillar infection 
is always serious. 
Hot all murmurs following streptococcus tonsillitis are due to endo- 
carditis. The majority of mitral systolic murmurs are due to relative 
muscular insufficiency and disappear as the patient regains strength. 
Chorea is frequently associated with an initial tonsillar infection; 
there is with these cases often acute endocarditis. The prognosis is good; 
in obese children endocarditis may be severe and occasionally, without 
relief of the choreic symptoms, the child dies. Malignant endocarditis 
may prove to be a sequel. 
Functional disturbances causing arhythmia and annoying intermis- 
sions and irregularities also yield after long periods of rest. 
Bradycardia is an occasional sequel or an accompaniment of the 
acute stage, without unfavorably influencing the prognosis. 
Kidney.—Nephritis, which follows within seven to twenty-one days 
after acute tonsillitis, is often rebellious and occasionally leads to dropsies 
and to fatal uremia. 
Early nephritis and albuminuria usually yields during the slow con- 
valescence. 
Arthritis (Rheumatism).—Arthritis is a frequent complication of 
tonsillitis and shows the characteristics of polyarthritis in most cases, is 
often complicated with endocarditis, is subject to relapse and usually 
leads to full recovery without permanent damage to the joints invaded. 
(See Polyarthritis.) 
Paralysis.—We have never chanced to find a single case of paralysis 
in which the bacteriologic diagnosis of streptococcus tonsillitis was posi- 
tive. Such cases are recorded, but must be exceedingly rare. 
Septicemia without, evidences of local disturbance or with endocarditis 
is the most serious sequel of tonsillitis. It offers only the most unfavorable 
forecast. BACTERIAL DISEASES 
297 
Among the other complications of streptococcus tonsillitis are 
osteomyelitis, appendicitis, empyema, liver abscess, perinephric abscess, 
meningitis, and empyema. (See separate chapters for further prognostic 
data.) 
Pneumonia.—The prognosis of streptococcus pneumonia following 
tonsillitis depends on the factors fully considered in connection with the 
pneumonias. (See Pneumococcemia.) 
Generally speaking it may be concluded that the migratory types of 
the disease offer a grave prognosis, the acute cases justify the figures and 
conclusions to which reference has been made elsewhere. (See Migratory 
Pneumonia.) 
Mortality.—Our average mortality of all forms of streptococcus 
tonsillitis in private practice does not reach 2 per cent. Hospital statistics 
include neglected cases and show a higher mortality. 
Phlegmonous Tonsillitis. (Septic) 
In occasional infections there are marked constitutional symptoms, 
nephritis, large albumin loss and destructive gangrenous changes in the 
tonsils, foul smelling with symptoms of deep sepsis at once, including 
delirium and final coma which lead to death in from three to seven days. 
These cases are rare, they occur in adults as a rule, and before death 
show decided purpuric tendencies; they are not to he confounded with 
suppurative tonsillitis. 
Acute Suppurative Peritonsillitis 
Quinsy, Peritonsillitis 
Most forms of quinsy invade, besides the tonsil, the 'peritonsillar tissue; 
they may be either primary or secondary. 
When secondary the suppuration may he a complication of general 
infection (pyemia, septicemia, scarlet fever, typhoid, erysipelas, et 
cetera) or it may he associated with nephritis, diabetess or other constitur 
tional diseases. Syphilitic and carcinomatous ulcers at times lead to 
tonsillar suppuration. 
Most primary suppurative peritonsillitides offer a good prognosis if 
rationally treated. 
Edema of the glottis and larynx is at times a sudden complication 
with both primary and secondary tonsillar suppuration and unless 
promptly relieved by surgical means ends fatally. Edema of the uvula 
complicates all cases of suppurative peritonsillitis. 
The prognosis of the acute secondary suppuration of the tonsil per se 
is not bad; occasionally it suddenly leads to edema particularly in cases 
of chronic and acute nephritis and threatens life. The nature of the 298 
SPECIFIC INFECTIOUS DISEASES 
disease naturally influences the prognosis of the associated sup- 
puration, but as a rule the patient recovers from it. 
Some subjects develop primary suppuration of the tonsil and peri- 
tonsillar tissue repeatedly at short intervals; in almost all, the prognosis 
is good and recurrence is prevented by the excision of the tonsils. 
Ulceration of large arteries with consecutive bleeding (internal caro- 
tid artery) is exceedingly rare. 
Convalescence is often very slow and patients are subject to many of 
the complications of acute non-suppurative tonsillitis. (See Acute Ton- 
sillitis.) 
(e) Vincent’s Angina 
Vincent’s angina is due to a fusiform bacillus which may also cause 
noma (see Cancrum Oris), laryngitis, pneumonia, mastoid inflammation 
and bronchopneumonia. The bacillus was found by Tunnicliffe to be the 
pathogenic germ in a case of pyemia. The germ is usually found in 
connection with other disease-producing organisms (aerobic). Halsted 
says that “like the other organisms with which it is associated, it occurs 
in healthy mouths, but more particularly in mouths and throats in which 
there is some unhealthy condition, such as diseased tonsils, decayed teeth 
and inflamed gums” . . . “it rarely produces disease when the tonsils, 
teeth and mucous membranes are in a normal condition.” 
Vincent’s angina may accompany any of the tonsillar infections of 
diphtheria, scarlet fever, syphilis, streptococcus or other inflammations 
associated with the formation of false membranes. 
Rolleston in 18,187 cases in which diphtheria was suspected admitted 
to the London Metropolitan Hospital Board that he found during 1905- 
1907, 3,047 non-diphtheritic cases; of this number 95 were due to the 
fusiform bacillus, or Vincent’s angina. 
The disease presents in an ulcerative or destructive form, or remains 
membranous. Two cases reported by Halsted proved to be fatal. Pearce 
in his cases found great prostration with feeble and rapid pulse, marked 
involvement of the nervous system, the hippocratic facies and death from 
toxemia. 
Purpuric symptoms argue in favor of malignancy of infection, as 
does also necrosis of included tissue. The clinical picture of the malig- 
nant cases is much like the fatal cases of cancrum oris. 
The prognosis is worse in patients who are reduced and previously 
infected. The limitation of the disease to the tonsils without marked 
constitutional symptoms offers a good prognosis. Invasion of the larynx 
adds an enormous element of danger, particularly during early life. 
Non-diphtheritic membranous croup and tonsillitis should always 
create a suspicion of Vincent’s angina. The diagnosis can be cleared 
only by bacteriologic tests. BACTERIAL DISEASES 
299 
Ulcerative stomatitis may be caused by the fusiform bacillus without 
involvement of the tonsils. (See Ulcerative Tonsillitis) (Aschoff.) 
References 
Halsted (T. H.). Vincent's Angina, etc. The Laryngoscope, St. Louis, 1912. 
Rolleston. British J. Dis. of Children, 1910, vii. 
Tunniclitfe. J. Infect. Dis., Jan., 1912. 
Pearce. Boston Med. & Surg. J., Nov. 9,1911. 
Aschoff. Path. Anatomie, 3. Aufl., Jena, 1913. 
Chronic Tonsillitis 
(Chronic Naso-pharyngeal Obstruction, Mouth Breathing, Aprosexia, 
Adenoids of the Pharynx) 
Chronic tonsillitis may result from preceding acute tonsillar infection 
and may include persistent enlargement of the neighboring lymphatic 
glands or it may be a part of a chronic hypertrophy of all the adenoid 
tissues of the pharynx in which the vault of the pharynx is occupied by 
succulent adenoid structures which cause mouth breathing and many 
secondary changes. 
The influence of adenoids and chronic enlargement of the tonsils on 
the growing child is paramount. Development, both mental and physical, 
is impeded by the handicap which results. Insufficient oxygenation is 
one of the results of the obstructed breathing. The advance of rhinology 
has been of great value in calling the attention of the profession to the far- 
reaching effects of chronic tonsillitis, adenoids and associated lymphatism. 
The facies of the children suffering from adenoids are characteristic. 
The direct results of faulty breathing due to the disease are, besides those 
mentioned, developmental anomalies of the thorax, chicken breast, barrel 
chest, and funnel breast. Deafness or faulty hearing is frequent. Con- 
vulsive tics are occasional. These children are hypersensitive, contract 
the acute infections which spread from the tonsils oftener than do normal 
children, their breaths are offensive, the crypts of the tonsils hold foul- 
smelling cheesy masses and when they develop scarlatina the throat symp- 
toms are always severe. The removal of the tonsils and the adenoids 
promptly changes the picture and from a stupid, mouth-breathing, sickly 
and apathetic youngster, there is a complete metamorphosis to a normal 
child in almost all cases. Captain Catlin in his pamphlet published in 
1861 probably overestimated the importance of adenoids and enlarged 
tonsils, when he contended that to these anomalies all of the ills of man- 
kind are attributable, but there is much of value and truth in his aphorism. 
“Shut your mouth and save your life.” 300 
SPECIFIC INFECTIOUS DISEASES 
Iloffinan shows the mortality from all diseases of the tonsils to be 
1.8 per cent in males and 1.1 per cent in females including 225 cases. 
References 
Capps & Miller. J. Am. Med. Ass., June 15, 1912. 
Hoffman. Statistical Experiences, etc., Johns Hopkins Hospital, 1892-1912. 
Lartigan. King. J. Am. Med. Ass., Iviii, 2026. 
Miller. J. Am. Med. Ass., June 15, 1912. 
Mitchell. Science Committee Report of the British Med. Ass., 1914. 
Wood. J. Am. Med. Ass., May 6, 1905. 
XXIII. Metastatic Parotitis 
(Secondary Parotitis, Infectious Parotitis, Parotitis metastatica) 
Inflammation of the parotid not due to epidemic mumps may be con- 
sidered to be secondary to existing infection, is usually one-sided and an 
expression of grave constitutional invasion and malignancy of the pri- 
mary disease. 
The infections to which parotitis has been added include all forms of 
pyemia, typhoid fever, scarlet fever, pneumonia, dysentery, cholera 
asiatica, malignant endocarditis, streptococcus infections, sinus thrombosis, 
cerebrospinal meningitis, small pox, angiocliolitis, yellow fever, all naso- 
pharyngeal infections, syphilitic ulcerations of the mouth, peptic ulcers, 
measles, tuberculosis and in rare cases mild infections and mumps lead 
to chronic enlargement of the gland. 
Many of these melastases are due to direct infection through the 
mouth and some of these might be prevented by more thorough cleansing 
of the upper air passages and the nasopharynx, more particularly, than 
is usually practiced. 
The glandular ducts and gland substances themselves may serve to 
infect and finally a large number of secondary parotitides may be traced 
to infection through the blood stream. 
During a recent large epidemic at Cortland, Mew York, which was 
traced to milk infection, of streptococcus origin, I saw a case with Dr. 
Higgins of streptococcus tonsillitis in a woman over 70 years of age who 
developed streptococcus pneumonia, then streptococcus parotitis, with 
small pockets of degeneration and suppuration, who finally made a full 
recovery. This history with its fortunate outcome is rarely repeated. 
With most serious infections the development of secondary parotitis may 
be viewed with concern. It is an evidence of the gravity of the original 
infection and adds an element of danger at the same time. In some cases 
suppuration advances to the cellular tissue of the neck (Angina of Lud- NON-BACTERIAL EUNGUS INFECTION 
301 
wig) and to the ear and skull, when sub-acute and chronic infection may 
follow with facial paralysis, caries or meningitis. Tuberculosis invading 
the parotid may cause caseation. 
Metastases to the parotid occur with equal frequency in children and 
adults. Early metastases to the parotid are more serious than the late 
infection of the gland. The invasion of the parotid during acute gouty 
arthritis is a painfnl and weakening complication which, as a rule, yields 
to treatment in from two to three weeks without suppuration. 
C. Diseases due to Non-Bacterial Fungus 
Infection 
1. Actinomycosis 
(StrahlenpilzkranJcheit) 
Actinomycosis is caused by the Actinomyces bovis (Ballinger, 1877), 
also known as the uray fungus,” which is a Gram-positive streptothrix. 
The disease is found in animals—horses, pigs and other cattle—most 
frequently involving the jaw, mouth and tongue, and is in all probability 
caused by the eating of ordinary grain or barley holding the actinomyces. 
Man is more frequently infected than woman (3-1). 
The disease leads to a condition of subacute or chronic pyemia .due 
to the infiltration and suppuration of the infected tissues, around which 
there is promptly connective tissue proliferation. In man as in cattle 
the jaw and tongue are the usual foci of the disease, though other parts 
of the body may be infected. The ac omycetes as they enter the tissues 
cause hyperemia, infiltration, chronic suppuration and consecutive con- 
stitutional disturbances. The diagnosis can be made positive by the pres- 
ence of the ray-fungus in the pus. 
The characteristic swellings of the disease may follow in any part of 
the body to which the streptothrix is carried and the fungus may migrate 
to surrounding tissues and organs or in severe cases blood vessels may be 
invaded, more particularly veins, which opens the avenues for the entrance 
of actinomycetes into the blood stream and their dissemination to distant 
organs (lung, liver, brain, etc.). 
The disease may invade: 
1. The alimentary tract 
2. The respiratory tract 
3. The skin 
4. The brain or other internal organs. 
Forms of Actinomycosis 302 
SPECIFIC INFECTIOUS DISEASES 
1. Alimentary Actinomycosis.—The course of alimentary actinomy- 
cosis, the most frequent form of the disease, is characteristic. The fungus 
finds a point of entrance in the mucosa surrounding carious teeth, through 
the mucosa of the floor of the mouth or through the tonsils. The changes 
already mentioned promptly follow; the local swelling depends upon the 
direction of growth and the extension of the fungus and the amount of 
infiltration and suppuration. As a rule there is more or less 'periostitis of 
the jaw and there are fistulous tracts which discharge a thin yellow pus, 
in which the yellow ray-fungi are promptly detected. 
The tongue is less likely to show suppuration than the surrounding 
tissues, hut the separate nodules are readily palpated. 
The posterior pharyngeal wall may be invaded when the disease may 
extend downward attacking the esophagus which it may perforate. As the 
process progresses the stomach and intestinal mucosa may be infiltrated. 
Perforative peritonitis due to intestinal perforation may follow. 
Appendicitis develops in occasional cases. Intestinal actinomycosis 
may lead to fistulous openings through the abdominal wall, to abdominal 
swellings and adhesions of intestines or to intestinal stenosis. The pos- 
terior mediastinum may be attacked through migration of the actinomyces 
and the pleura and the lungs invaded through this avenue. 
2. Actinomycosis of the Respiratory Tract.—Actinomycosis of the 
respiratory tract is rare, save as it is secondary to alimentary invasion or 
follows the aspiration of infected foreign bodies. The fungus causes an 
obstinate fetid bronchitis or as a rule the dependent part of one lung is 
slowly infiltrated (chronic pneumonia) causing constitutional symptoms, 
including fever, rapid heart action, increasing emaciation, and the expec- 
toration of purulent sputum, with fungi and acid crystals. 
In chronic cases there is adva to the pleura and to the chest wall, 
with chronicity and consecutive deformity. 
In pulmonary actinomycosis the pericardium may also be the seat of 
deposit. 
3. The Skin.—The skin, through an abrasion or wound may be in- 
vaded by the fungus and multiple lesions result vfith the symptoms of 
chronic pyemia accompanying the suppuration. 
4. The Brain and Other Internal Organs.—The brain and liver inva- 
sions are found in those cases in which the actinomycetes have invaded 
the walls of a blood vessel and have been carried to these organs through 
the blood stream. 
In the brain the symptoms of tumor are prominent and death is the 
result, the duration varying in accordance with the location of the deposit. 
The liver, when involved, presents the symptoms of abscess of that 
organ and offers an unfavorable prognosis unless the abscess is superficial 
and operable. DISEASES DUE TO METAZOAN PARASITES 
303 
Prognosis of Actinomycosis 
The prognosis of all forms of actinomycosis must depend on the loca- 
tion of the disease, the ability to remove the focus early by radical surgical 
treatment. When the disease is disseminated the chances of recovery by 
medical treatment are small. 
Spontaneous recoveries have been reported, but are rare and can only 
be imagined to have followed limited swelling. The chronic pyemia of 
unrelieved cases wdth its long periods of remittent fever leads to exhaus- 
tion, emaciation, and after months of suppuration, with increasing anemia 
and edema, albuminuria with other positive evidences of far-reaching amy- 
loid degeneration of the internal organs develop and death results. 
It may be positively concluded that the skin infections offer the most 
favorable prognosis. When the neck and face are the seat of the disease, 
Poncet and Thevenot found that death followed in one case in 16; with 
lung and abdominal (visceral) actinomycosis 25 per cent died. 
Reference 
Poncet & Thevenot. Lommel, Handbuch der Inneren Medizin (Mohr and Staehelin). 
1911. 
D. Diseases due to Metazoan Parasites 
(.Internal Parasites) 
Of the animal parasites which infect the body (non-microscopic), (1) 
the tapeworms or cestodes, and the (2) round worms, or nematodes, are 
the most important. 
1. The principal varieties of the Cestodes are: 
(a) Tenia solium. 
(b) Tenia saginata or mediocanellata. 
(c) Bothriocephalus latus. 
(d) Tenia echinococcus (or hydatids). 
2. The Nematodes are: 
(a) Ascaris lumbricoides. 
(b) Oxyuris vermicularis. 
(c) Ankylostomum duodenale or hookworm. 
(d) Tricocephalus dispar. 
(e) Trichina spiralis. 
(f) Filaria sanguinis hominis. 
3. The Bilharzia hematobia belongs to the Trematodes and also de- 
mands consideration. 304 
SPECIFIC INFECTIOUS DISEASES 
1. Cestodes 
(a) Tenia solium 
(Armed Tapeworm) 
This worm is not as common in English speaking countries as is the 
Tenia saginata. It is due to the eating of improperly cooked or raw pork. 
When fully grown it is from eight to twelve feet long and inhabits the 
small intestines, where as a rule it is solitary, though multiple tenke are 
not uncommon. Its life history and other characteristics are best studied 
in works on pathology and diagnosis. It must be remembered, however, 
in connection with the cysticercus of the worm, that it may in occasional 
cases lodge in one or more vital organs of man and give rise to local changes 
and symptoms. To this I will again refer. The armed worm as a rule 
causes no serious symptoms and does not threaten life; the passage of the 
head is assurance that the host has been freed. If the head in its passage 
escapes discovery or if the proglottides are passed without the head, the 
host continues uncertain of the fate of the worm during several, usually 
three months; the time required for the development of the worm and the 
passage of its proglottides. 
While the symptoms caused by the Tenia solium are not of serious 
import, the worm may by its presence interfere with stomach and intestinal 
functions, causing nausea, diarrhea, other symptoms of indigestion, in- 
cluding abnormal appetite, loss of flesh and mental torpor; with some 
anemia, all of which symptoms disappear with the passage of the worm. 
The worm eliminates a 'poison which enters the blood stream and is 
directly responsible for the eosinophilia and anemia which are constant 
accompaniments of the tapeworm and of many other intestinal parasites. 
The prognosis of the fully formed tapeworm as it inhabits the intes- 
tinal tract from the study of its life history and the preceding paragraphs 
may be said to be uniformly good and is readily influenced by suitable 
anthelmintics. 
The deposit of the cysticercus in the brain may cause but few or no 
symptoms, in occasional cases the brain may tolerate the growth during 
long periods, depending upon the seat of the tumor caused by it; on the 
other hand it may threaten life by its presence and may cause the usual 
symptoms of a neoplasm. It may infest the base and cause pressure 
symptoms including paralysis of one or more of the cranial nerves. It 
may grow to considerable size, causing destructive changes as it enlarges. 
The cysticercus racemosus may lie loose in brain tissue, usually in the 
ventricles of the brain. In occasional cases chronic basilar leptomeningitis 
may be provoked. Jacksonian and other forms of epilepsy, ependymitis 
and hydrocephalus internus, cerebral anemia and obliterating cerebral 
endarteritis are mentioned by Askanazy as complications due to the pres- 
ence of the cysticercus in the brain. DISEASES DUE TO METAZOAN PARASITES 
305 
The cysticercus with its dense membrane may continue to live in the 
tissues of man for years, may die, when calcification usually follows. The 
skin may harbor cysticerci, also the muscular tissue, the liver, spleen, the 
intestinal wall, the heart, the lung, the pleura, the lymphatics and bone, 
The favorite seat of the cysticercus is the brain and the eye. 
Cysticerci are not usually the cause of local inflammatory changes or 
congestion, neither do they give rise to marked sensory symptoms when in 
the skin. 
In the eye, atrophic changes may follow (phthisis bulbi) (Askanazy). 
(6) Tenia saginata or mediocanellata 
Tenia saginata is the most common form of tapeworm in man; it is 
transmitted by the eating of infected beef, and grows to an average length 
of twenty (20) feet. This variety of tapeworm causes fewer complica- 
tions than does the Tenia solium, may be carried without inconvenience 
in many cases, save the loss of the proglottides from time to time. In 
some cases there are colicky pains, indigestion, abnormal appetite and per- 
sistent malaise. Reckzeh reports the occurrence of pernicious anemia 
caused by the worm. The cysticercus of the saginata is rarely imbedded 
in the tissues of man. From 60 to 65 days lapse between the swallowing 
of the cysticercus and the appearance of proglottides in the stools. 
The prognosis of Tenia solium is uniformly good. It occasionally hap- 
pens that several trials must be made before the head passes, but full 
restoration of gastro-intestinal function to normal invariably follows the 
passage of the worm. 
(c) Bothriocephalus latus 
The bothriocephalus is the largest of all tapeworms, its immediate host 
is the fish almost always of the pike family and it is distributed over Cen- 
tral Europe (Switzerland) and in Japan. Tn America we occasionally 
find the worm in subjects who were infected abroad. 
The bothriocephalus usually causes greater gastro-intestinal disturb- 
ances than do the other varieties of tenia; these include diarrhea, persist- 
ent nausea, mental lethargy, depression and at times great irritability. 
In rare cases convulsions and other explosive nervous manifestations 
have been charged to the worm. 
The greatest danger to the host is the development of grave anemia 
which has all of the characteristics of pernicious anemia and is now con- 
sidered by hemotologists to be identical with that disease. (For the bene- 
fit of the student of the literature of bothriocephalus anemia I have 
appended the leading references on this subject from which in turn the 
full bibliography may be obtained). 
It may be assumed in the light of our present Icnowledge that the dis- 306 
SPECIFIC INFECTIOUS DISEASES 
eased or dead bothriocephalus adds a poison to the blood stream which is 
hemolytic in its effect and causes the blood picture and constitutional dis- 
turbances of progressive pernicious anemia. Ehrlich, Biermer, Laashe 
and Schauman, the leading authorities on this subject have all reached 
this conclusion. 
The prognosis of even advanced cases of bothriocephalus anemia is 
good, if the worm, dead or alive, is promptly expelled by treatment. Full 
recovery is slowly reached. Schauman proved that the daily regeneration 
of the erythrocytes after the expulsion of the worm varied between 60,000 
and 214,000. In the beginning of the improvement he found the aver- 
age midway between the extreme figures given; the microcytes disappeared 
early; macrocytes may at first be increased; later these disappear entirely 
and the normal blood picture is reestablished. This subject will be fur- 
ther considered in connection with progressive pernicious anemia. 
(d) Tenia echinococcus 
(Ilydatid Disease) 
The adult worm is not found in man. The worm itself is one-quarter 
inch long, occupies the intestine of the dog and wolf. The sheep is often 
the intermediate host. In man, the cysticercus stage makes him an inter- 
mediate host. 
The six booklets of the embryo set free by the digestion of the shell of 
the ovum, migrate through the intestinal wall and enter the blood stream 
or in some other way gain entrance to the brain, the liver, the spleen or 
other organs of the body. When the booklets are deposited they disap- 
pear, and the embryo is slowly converted into a cyst of small size with 
two layers, one external or the capsule; the other internal or the endo- 
cyst. The cyst ivall encloses a light clear fluid. The fluid of the cyst has 
an average specific gravity of 1010, neutral reaction as a rule; contains 
98.5 per cent of water. Of the solid constituents sodium chlorid is in 
the ascendency. The albumin content is infinitesimal. The fluid con- 
tains a toxin which when injected into animals causes paralysis of the 
heart in diastole, lowered blood pressure and temperature. Soon there is 
a connective tissue enclosure which strengthens the cyst. Daughter cysts 
develop within the parent cyst and from these daughter cysts, other or 
grand-daughter cysts develop. 
The echinococcus may live many years, or may die, when remnants of 
the original cyst are found within the fibrous wall in the invaded organs„ 
calcified or otherwise changed. 
Cysts may rupture and according to their location give rise to symp- 
toms. Hydatid cysts are not frequent in America. In our practice we 
have seen but three. One we saw in 1878 at the Billroth clinic in Vienna 
(involving the neck, successfully removed) one in the clinic of Detmoldt DISEASES DUE TO METAZOAH PAEASITES 
307 
in Hew York (liver echinococcus), and one of liver echinococcus which 
died, in our own practice. Lyon recorded 241 cases of hydatid disease 
in the United States and Canada “and several of these occurred amongst 
the Icelanders settled in Manitoba.” Of the 241 cases 177 were in the 
liver; 26 in the omentum, the peritoneal cavity and mesentery. Eleven 
cysts were passed per rectum; in 7, the cysts or hooklets were expecto- 
rated and two escaped through the urethra. 
The following statistical records taken from Allbutt and Rolleston 
show the incidence of echinococcus cysts in the various organs of the body: 
In 1,000 autopsies at the Adelaide Hospital, South Australia, 49 bod- 
ies were found to contain hydatid cysts, i. e., 5 per cent. In 11 the cysts 
were multiple; in 5 two organs were infested; in 6 three or more viscera. 
In 36 the liver contained a cyst. 
In 9 the lung contained a cyst. 
In 6 the spleen contained a cyst. 
In 5 the peritoneum contained a cyst. 
In 4 the brain contained a cyst. 
In 1 the heart contained a cyst. 
Thomas in 1,900 cases of hydatid disease found the liver infested in 
5 per cent; the lung in 11.6 per cent; the kidneys in 4.7 per cent; the 
brain in 4.4 per cent; the spleen in 2.1 per cent; the heart in 1.8 per 
cent; the-peritoneum, omentum and mesentery in 1.4 per cent. 
The average of all statistics shows the liver to he the seat of the echino- 
coccus disease in one-half of those infected. 
Hydatid of the Liver.—There may he one or more cysts in the liver; 
the right lohe is the favorite location of these. The prognosis for life 
depends on the fate of the cyst, its location, size and the mischief which 
its presence causes. 
Suppuration of Liver.—Echinococcus cysts may lead to grave constitu- 
tional and local disturbances, which unrelieved by surgical interference 
usually leads to death. 
Perforation of hydatids of the liver may take place into one or more 
of several surrounding organs; into the stomach; the intestines; the peri- 
toneal cavity; the lung; the bronchus; the kidney or into the portal vein. 
Rupture into the lung or pleura may lead to fatal pneumonia, to gan- 
grene, to empyema, sudden asphyxia, pyo-pneumothorax and threatening 
hemoptysis. 
With all perforations there is besides the local lesions great danger 
of poisoning by the entrance of toxins from the fluid of the cyst. 
After aspiration of the cyst in many cases, distressing urticaria, also 
an evidence of toxinemia is frequent. Hence aspiration adds to the dan- 
gers unless operation follows immediately. 
A large number of liver cysts remain latent during many years and 
the carriers die of intercurrent disease. 308 
SPECIFIC INFECTIOUS DISEASES 
Death may be caused by compression of 'the portal vein or toxinemia 
associated with obstruction of the bile passages. 
Fistulous openings may result from the suppurating of liver cysts, 
and their burrowing to the surface; such patients unless relieved by surgi- 
cal interference die from sepsis, emaciated and with the cerebral symptoms 
of toxineniia. 
Spontaneous cure may follow perforation; not of sufficient frequency, 
however, to justify expectant treatment. 
All operable cases of single liver echinococcus cyst offer a good prog- 
nosis. Multiple liver cysts are almost uniformly fatal. 
Hydatid Cysts of the Lung.—Hydatids of the lung, as already stated, 
represent 11.6 per cent of those who suffer from echinococcus disease. 
Pleural invasion may lead to the symptoms and include the dangers of 
effusion, compression and its results. In many cases encysted hydatids 
in the lung do not threaten life; they may cause few or no symptoms. In 
other cases compression with inflammatory changes, cavity formation, per- 
foration, occasionally into the pericardium, septic fever and repeated hem- 
orrhages follow, with occasional perforation into the pleura; empyema and 
pyo-thorax. Death follows lung hydatids in one-third of all cases. 
Hydatid of the Kidney.—Echinococcus of the kidney may he present 
without interfering with the health of the host during many years. They 
may be passed per urethram and without consecutive damage to the genito- 
urinary tract. In some cases the entire kidney is converted into a sac 
giving the physical signs and subjective symptoms of hydronephrosis. 
The prognosis is good, when, as a rule, the condition proves to be operable. 
Rupture into the pelvis of the kidney is the usual fate of the cyst; this 
is followed by pyuria, fever and offers a good prognosis when radically 
treated. Spontaneous recoveries are recorded after rupture. 
Kidney cysts may rupture into the peritoneal cavity, causing perito- 
nitis; into the lung or bronchus, when the prognosis is unfavorable. The 
external rupture of kidney hydatids offers a good prognosis, the removal of 
the kidney with included cyst usually leads to cure. 
Hydatid of the Spleen.—This condition is rarely recognized without 
exploration, aspiration or post mortem. Its surgical treatment is prompted 
and justified by the physical signs of enlarged spleen and persistent pain; 
when the prognosis is favorable. Unrelieved by surgical treatment the 
cyst itself, during long periods may not threaten life; it may, however, per- 
forate into some one of the surrounding viscera and thus lead to serious 
complications and death. In rare cases sloughing and hemorrhage have 
followed and have caused death. 
Omental, mesenteric and peritoneal hydatids present palpable tumors 
which are all operable and offer a good prognosis, better when the cyst is 
not broken during its manipulation thus preventing poisoning. 
Hydatid Disease of the Brain.—Intra-cranial hydatids often grow to DISEASES DUE TO METAZOAN PARASITES 
309 
enormous size without causing symptoms. The cyst may be found either 
large or small in any part of the brain. Naturally its symptoms and prog- 
nosis in most cases are those of brain tumor and depend upon its size and 
location. Occasionally there are multiple hydatids in the brain. The 
cerebral hydatid is fourteen times as frequent as is the cerebellar (Sterling 
and Verco) growth. 
Epileptic convulsions are a frequent accompaniment of hydatids of the 
brain; most patients die during an epileptic fit; they may fall into coma 
after a period of meningeal symptoms; they may live during a long period 
of paralysis, or, as often happens, they die of intercurrent disease. 
Superficial hydatid cysts of the brain when localized by the diagnos- 
tician and attacked surgically, offer a fair chance of recovery. 
Hydatids in the remaining organs of the body are so rare as to* re- 
quire no further consideration. 
References 
Allbutt & Rolleston. 2. ed., ii, 1,014- 
Askanazy. Aschoff, Pathologische Anatomie. 2. ed., Bd. i., 245. 
Biermer. Progressive Anemie. 1872. 
Botkin. Cited by Schauman (See below). 
Ehrlich & Lazarus. Die Anaemie. 
Die Klinik der Anaemie, 1913. 
Grawitz. Klinische Pathologie des Blutes. 4• ed. 1911. 
Hoffman (F. A.). Die Lehre der Konstitut. Krankheiten. Stuttgart, 1893. 
Laache & Ehrlich. Die Anaemie. Christiania, 1883. 
Deutsch. med. Wchnschr., 1891, No. 5. 
Lyon. Am. J. Med. Sci., cxxii. 
Osier. Practice of medicine. 8. ed., 1913, 88. 
Reckzeh. Quoted by Ehrlich u. Lazarus. Die Anaemie. 1913,122. 
Reyher. Deutsch. Arch. f. klin. Med., 1886, Bd. xxxix. 
Schauman. Gives the best resume of the literature. 
Bothriocephalus Anaemia. Berlin, 1894. 
Berl. klin. Wchnschr., 1889, No. 1. 
Deutsch. klin. Wchnschr., 1912, No. 26. 
Volkman’s Sammlung klin. Vortrage, 1900, No. 287. 
Deutsch. med. Wchnschr., 1910, No. 26. 
Schauman & Talquist. Deutsch. med. Wchnschr., 1898, No. 20. 
Sterling & Verco. Allbutt & Rolleston [l. c.], 1025. ii. 
Thomas (Adalaide). Hydatid Disease. 1884. 
2. Nematodes 
(a) Ascaris lumbricoides. (b) Oxyuris vermicularis 
The (a) Ascaris lumbricoides, and (b) the Oxyuris vermicularis, the 
most frequent of all worms, the former inhabiting the small intestines of 310 
SPECIFIC INFECTIOUS DISEASES 
children, the latter the colon, are without serious significance and promptly 
yield to the well known anthelmintics. Barring occasional febrile move- 
ment, irritability, petulance, rectal uneasiness, rarely reflex disturbances, 
such as convulsions, we have never found either of these round worms 
the cause of disease in our practice. Only rarely are distressing condi- 
tions caused by the wandering of the ascaris. Worms are vomited; at 
times they enter the postnasal space from the esophagus, the eustachian 
tube or the larynx. Asphyxia and gangrene of the lung are recorded 
among the accidents due to the wanderings of the worm (Osier);. They 
may find their way to the liver, causing abscess, or to the bile ducts. 
(c) Ankylostomiasis 
( Uncinariasis, Hookworm Disease, Miner’s Anemia, Egyptian Chlorosis, 
Dochmiose, Ankilostomoanemia, Tunnel Disease) 
Ankylostomiasis is a form of progressive and grave anemia with symp- 
toms referable to the gastro-intestinal tract and nervous system due to the 
Ankylostoma duodenale, originally described and recognized by Dubini 
in 1843. 
The Papyrus Ebers, according to Scheuthauer and Joachim, about 3,550 
years B. C. mentions a disease due to a worm Heltu ‘which caused all of 
the symptoms of ankylostomiasis and has been known by the Egyptians 
from times immemorial. It is questionable whether the disease mentioned 
in the papyrus Ebers was identical with the present day hook-worm dis- 
ease ; Oefele denies it. 
Occurrence.—The disease caused by the worm prevails in tropical 
and subtropical countries. On the Continent of Europe it is found among 
the miners of Erance, Austria, Hungary, Germany, Switzerland and Bel- 
gium. In England, the disease prevails among the Cornish miners (Boy- 
cott and Haldane) (Montgomery). In Egypt the disease is found among 
the natives and the Indian coolies. The credit for our exact knowledge 
of the hook-worm and its resulting disease as found in the United States 
belongs entirely to C. W. Stiles, whose conclusions are now fully accepted 
by the profession. (Full references to the contributions made by Stiles 
are given in the bibliography at the end of this chapter.) 
The Infection.—The worm which causes the disease in the United 
States, it is now believed, does not belong to the Uncinaria but is given the 
name of the “Hew World Hook-worm or Necator americanus of Stiles, in 
contra-distinction to the “old world worm” or Ankylostoma duodenale. In- 
fection is due to the development of the eggs, millions of which are passed 
with each stool of the infected patient. These develop in feces mixed with 
the earth or sand at a temperature of from 70° to 90° F. The human 
being is infected as a rule through the skin; from the fingers through the DISEASES DUE TO METAZOAK PARASITES 
311 
mouth, which latter method is unusual. Loos has demonstrated the course 
followed by the larvse after entering the skin. They pass from the veins 
to the heart, into the lungs, through the pulmonary vessels, into the bronchi, 
and from there into the post-pharyngeal space to the esophagus and out 
through the stomach and intestinal tract. The lack of caution in caring 
for the infected stools is the paramount factor in the spreading of the 
disease. 
The “ground itch” is prevalent among 90 per cent of those infected 
according to Ashford and King (H. W.). 
Clinical Manifestations.—The leading clinical manifestations of hook- 
worm disease include a period of malaise with increasing languor, after 
which gastro-intestinal symptoms predominate with circulatory and respira- 
tory disturbances. The anemia is characteristic and is probably due more 
to the hemolytic action of the poison elaborated by the worm than by the 
direct loss of blood. The red blood corpuscles are reduced in proportion 
to the severity of the anemia from 1/4 to 1/10, the hemoglobin falls to 
15 and 20 per cent in grave cases. It will be noticed that the color index 
continues high. Eosinopliilia is a constant attendant, reaching as high 
as 40 per cent of all leukocytes in the more pronounced cases. Leukocy- 
tosis is rarely marked. 
The complication of ankylostomiasis by pneumonia at once reduces the 
existing eosinopliilia. Leichtenstern found a drop of eosinophils to 6-7 
per cent from 72 per cent. Warburg from 65 per cent to 0 and a return 
of the eosinopliilia with the recovery of the patient. Acute sepsis has 
the same effect. 
Sufferers from the disease are lethargic; children continue dull and 
apathetic, they remain undersized, drag themselves about shiftlessly, and 
fail to attain their growth until years after puberty. The graver cases 
which continue unrelieved by treatment show the marked anemia, the 
faulty development, asthenia, dilated heart, respiratory embarrassment, the 
mental sluggishness, the skin changes of itch and the infected stools. 
Incidence and Prognosis.—The incidence and prognosis of the disease 
have been enormously influenced by the education of the people which has 
resulted in concerted action to destroy the worm by removing the baneful 
conditions which make its multiplication possible and inducing the 
infected to care for themselves and to take advantage of specific treat- 
ment. The wearing of shoes to protect against infection through the skin 
has also been a powerful prophylactic factor. 
Barring cases which have advanced to threatening asthenia with heart 
insufficiency and a blood condition which is extreme, the prognosis of 
treated cases is surprisingly good. In some cases there are relapses. The 
return to full health is often slow but certain. The blood is regenerated 
after varying periods. 312 
SPECIFIC INFECTIOUS DISEASES 
References 
Ashford & King (H. W.). Study of Uncinariasis in Porto Rico. American Medicine, 
Philadelphia. 
New York Med. J., April 14, Ixxi, 552-556. 
Boycott & Haldane. J. of Hygiene, Cambridge, Hi, 95-136. 
Loos. Mense Tropen Krankheiten. i. 
Montgomery. Quoted by Loos. In: Mense Tropen Krankheiten. 1. 119. 
Oefele. Studien fiber AUagypt. Parasitologie I. Arch. Paras., iv, 481-530 (bes. 512). 
Scheuthauer & Joachim. Virchow's Archiv. Ixxxv, 343-354- 
Stiles (C. W.). Uncinariasis in man and animals in the United States. Texas Med. 
News, July, 1901. 
Recent American cases, etc. The Annual Report, Bureau of Animal 
Industry, Washington, 1902. 
Am. Med., Philadelphia, May 10,1902. 
Hookworm disease in the South. Public Health Report, Washington, 
D. C., Oct. 24, 1902. 
Report, Prevalence and geographical distribution of hookworm disease 
in the United States. Bulletin (X) Hygienic Laboratory, U. S. 
Public Health and Marine Hospital Service, Washington, 1903. 
Newly recognized factor in American anemias. Brooklyn Med. J., xvii, 
1903. 
See also articles by Stiles in Osier’s Modern medicine, Philadelphia. 1 & 
2 ed., 1913, 1914. 
(d) Trichocephalus dispar 
The whip worm or Trichocephalus dispar infects the large intestine of 
man. It is a small worm of peculiar build, with marked differences in 
the anterior and posterior parts of the body, being thin anteriorly and 
broad posteriorly; its length is from 4 to 5 cm.; the female is longer than 
the male. 
The worm is not common in the United States but is frequent on the 
Continent of Europe. 
Hundreds of worms may be present without causing symptoms or 
materially interfering with the health of the host. The prognosis is 
always good. 
(e) Trichinosis 
Trichinosis is an infection of man due to the eating of imperfectly 
cooked or raw pork or ham which holds in its muscle the larval or encysted 
form of the Trichina spiralis. The worm is a nematode, unusually 
resistant and infests the muscular tissue of man, giving rise to charac- 
teristic subjective and constitutional symptoms with a blood picture in- 
cluding eosinophilia. (Thayer and Brown.) 
The Infection.—In the process of digestion the ingested larvae are freed 
in the stomach; in 3 days the period of sexual activity begins in the intes- 
tinal tract. The sexes unite in the intestines and innumerable embryos 
are produced within from 1 to 9 days. The embryonic worm does not 
penetrate the intestinal wall as was formerly supposed, but the female DISEASES DUE TO METAZOAN PARASITES 
313 
worm finds her way from the muscular and mucous coat of the intestine 
by way of the lymphatics, the veins and the blood stream secondarily, to 
the striped muscles (mainly) of the host, in which they are easily recog- 
nized when bits of the muscle tissue are harpooned and examined micro- 
scopically. In occasional instances the worm is encapsulated within 
about 6 weeks. Nature finally provides the encapsulated worm with a 
dense fibrous membrane which, within from 4 to 6 months, becomes cal- 
carious. In occasional cases, coincident with trichinosis, there are sec- 
ondary infections which materially modify the course and the prognosis 
of the disease (cocci, etc.). The encysted worm may live undisturbed 
during many years. 
Symptoms.—In most cases the infection is promptly followed by a stage 
of intestinal symptoms. These symptoms vary in accordance with the 
severity of the infection. In the severer cases, diarrhea, colic and vomit- 
ing are in the ascendency; all severe and exhausting. The mild cases 
may present none of these intestinal manifestations; on the other hand, 
there are severe cases in which the early symptoms of intestinal invasion 
are not outspoken at once, but these symptoms gradually develop or may 
he entirely absent. 
In all cases the prognosis is largely influenced by the number of the 
invading worms. Grave symptoms often follow before the embryonic 
worm has had time to settle in the muscular tissues of the patient. These 
symptoms, including great exhaustion and muscular weakness, are due 
to the poisoning influence of the worm (metabolic products of the trichinse 
themselves), for it has been proved experimentally that the blood serum 
of the trichinous animal is poisonous early, i. e., before muscle invasion. 
The prognosis, after muscular invasion, depends, besides, upon the 
resistance of the patient, the degree of constitutional disturbance, the ex- 
tent and location of the muscular invasion, the severity of the nervous 
manifestations and the gravity of the complications. 
Marked muscular rigidity and severe and widely spread muscular 
pains, with high fever, rapid pulse, albuminuria, diarrhea, delirium, the 
Kernig symptom following the period of intestinal symptoms, and evi- 
dences of edema of the glottis are among the more serious manifestations 
of trichinosis and demand a guarded prognosis. 
Involvement of the respiratory muscles, including invasion of the 
muscles of the larynx and diaphragm, associated with hoarseness and 
dyspnea, at times marked air hunger and cyanosis, is always alarming and 
is present in the graver forms of the disease and demands great caution 
in offering a forecast. 
When the constitutional symptoms include a long-continued typhoid 
condition with increasing weakness and emaciation, and an unfavorable 
blood picture, the prognosis remains doubtful and grave during several 
days. 314 
SPECIFIC INFECTIOUS DISEASES 
The presence of albuminuria with other favorable symptoms is not 
of serious import. 
The presence and persistence of the Diazo-reaction does not influence 
prognosis. 
Bronchitis is a frequent and not a serious complication when limited; 
when the smaller tubes are invaded and there is also respiratory embar- 
rassment due to muscle disturbance (diaphragm, etc.), the bronchial 
catarrh may add an element of danger and cloud the prognosis. 
When myocardial weakness is present sufficient to cause edema of the 
extremities and other evidences of heart insufficiency, unless the disease 
has run its course or the heart responds to treatment, the outlook is 
exceedingly grave. 
Pneumonia, whether lobar or lobular, is always a grave complication; 
this is the rule in those cases in which respiratory symptoms due to 
trichinosis already exist and the dyspnea is associated with a feeble and 
non-dependable circulation. 
Limited peripheral thrombosis, when without other serious complica- 
tion, adds but slight danger to the disease. Cerebral thrombosis or throm- 
bosis of other vital organs is almost always unfavorable. 
In the chronic cases, those dragging along during several months, the 
development of bed-sores retards recovery and may lead to secondary 
infection. 
Enlargement of the spleen is in all probability due to secondary infec- 
tion, its disappearance is always to he interpreted favorably. During the 
first two w7eeks of the disease the spleen offers no prognostic data. 
Blood.—The blood shows characteristic changes which demand its 
close inspection for diagnostic and prognostic purposes. The red blood 
corpuscles show no marked change. Leukocytosis in mild cases is not 
excessive. The more severe cases show a decided tendency toward poly- 
morphonuclear leukocytosis. There is an enormous increase of eosino- 
phils with displacement of neutrophils. This may mount to from 30 to 
60 per cent. (Thayer and Brown.) Staubli and Hegar claim that in 
spite of the relative reduction of the neutrophilic leukocytes there is an 
absolute and marked, increase of these, sometimes reaching as high as 
three times the normal count and therefore the high eosinophilia is not 
present at the expense of the neutrophils. It has been shown that as a 
rule the graver forms of the disease are associated with the highest eosin- 
ophilic counts. Schleip found percentages varying in accordance with 
the gravity of the disease, between 20 and 62 per cent. Kerr found 86 
per cent in one of his cases. Thayer and Brown found 16,000 eosinophils 
(in 1 c. mm.) as against the normal count of 150-250. 
Moderate eosinophilia may persist long after convalescence, and in 
occasional severe forms of the disease may be limited and insignificant. 
Improvement usually follows the appearance of moderate lymphocytosis DISEASES DUE TO METAZOAN* PARASITES 
315 
and a striking increase in the number of blood-platelets. Eosinophilia is 
not likely to be marked during the stage of intestinal invasion, but depend- 
ing upon the metabolic products of the Trichina spiralis, is coincident 
with the deposit of the worm in the muscles of the body. 
The duration of mild cases is from 16 to 35 days. The severe infec- 
tions may continue during several months; these cases are followed by a 
slow convalescence, long periods of muscular weakness, asthenia, myalgic 
pains and occasional intestinal anomalies. 
Most deaths occur between the third and fifth week of the disease; in 
over 60 per cent of these, there is invasion of the respiratory muscles and 
often secondary bronchopneumonia. 
Owing to a guarded quarantine and the thorough examination of 
pork and its products, trichinosis is at present comparatively infrequent. 
Mortality.—The mortality varies in different epidemics and is influ- 
enced by the factors already considered. I have in my experience found 
the mortality of our hospital cases low. The average mortality may be 
placed between 4 and 30 per cent. Children bear trichinosis much better 
than do adults. 
It must be remembered that rheumatic pains and vague symptoms 
may continue during many years. 
Kerr. Lommel, Mohr & Staehelin, 1911, i, 1022. 
Schleip. Deutsch. Arch. f. klin. Med., 1904, Bd. Ixxx. 
Staubli & Hegar. Trichinosis. Wiesbaden, 1909. Deutsch. Arch. f. klin. Med., 1905, 
Bd. Ixxxv. 
Munch, med. Wchnschr., 1909, No. 7, 825. 
Thayer & Brown. Lancet, London, Sept. 25, 1897, 777. 
References 
(f) Filariasis 
There are a number of round worms belonging to the family Filaridce, 
which infect the blood of man or other portions of the body, discovered 
by Wucherer, 1866, in Bahia and by Lewis in 1872 (Filaria sanguinis 
Jiominis), which give rise to symptoms. Most of these worms pass during 
the night from the lymphatics into the blood stream. The leading symp- 
toms caused by these nematodes are hematuria, chyluria, elephantiasis, 
lymph-scrotum, chylous ascites and elephantoid fever. 
The blood filarhe which interest us are: 
a. Filaria Bancrofti (Cobold, 1877). 
b. Filaria diurna (Manson, 1891). 
c. Filaria perstans (Manson, J891). 
The filaria of Bancroft causes hematocyturia and the lymph-scrotum. 
The blood shows the presence of the worms during the sleeping hours, 316 
SPECIFIC INFECTIOUS DISEASES 
whether the patient sleeps during the day or night. The blocking of the 
lymph-channels causes most of the conditions already mentioned and 
elephantiasis. 
All of these conditions may persist during many years without causing 
marked inconvenience or affecting health. 
The lymph-scrotum may lead to great inconvenience because of its 
size, the thickening of the skin and the change in the lymphatics, but it is 
not directly dangerous to life. 
There are cases of fiiariasis in which there are a number of weeks or 
months, occasionally years, of lymphangitis with erysipelatous inflamma- 
tion and fever. (Elephantoid fever.) Abscesses may develop in these 
cases; surgical treatment has relieved some of them. 
The prognosis of scrotal elephantiasis after amputation is good; occa- 
sionally recurrences have followed cases in which the incision was made 
in diseased tissue. 
In women, the infection may produce elephantiasis of the external 
genitals, and the mammary glands of both sexes may show enormous 
enlargements. With persistence of chyluria and hematochyluria patients 
may live undisturbed during many years. 
Occasionally anemia causes weakness and threatens life. Only rarely 
does the patient die without intercurrent disease. 
Spontaneous cure can only occur in the most favorable surroundings 
where fresh infection can be prevented. 
3. Trematodes 
{Bilharzia hematobia—Bilharz) 
The blood fluke (Schistosomum hematobium) or Bilharzia hema- 
tobia was first recognized by Bilharz in 1851. The male worm is one- 
half inch long, the female three-quarter inch. The adult worm carries 
the female in a curved canal (gynecophoric canal). The worm is found 
mainly in Northern and Southern Africa, in Persia, Arabia and along 
the west coast of India. Griesinger in 1851 called attention to the fre- 
quency of the worm in Egypt, where in 363 autopsies bilharzise were 
found in 117. 
The leading inconveniences caused by these blood flukes are hemdr 
turia, bladder and kidney irritability, consecutive cystitis and secondary 
anemia. There are in some cases rectal and vaginal disturbances leading 
to tenesmus and dysenteric symptoms and chronic vaginitis, due to direct 
local infection. 
Among the complications which materially influence prognosis are 
profuse hematuria with secondary anemia, pyelitis, nephritis, renal and 
bladder calculosis, dysentery, asthenia and marasmus. In some cases the INFECTIONS OF UNKNOWN ORIGIN 
317 
low hemoglobin content of the blood is characteristic with a relatively high 
red blood corpuscle count (oligochromemia). There is some leukocytosis 
(40 per cent) (Grawitz). Lymphocytes and eosinophils reach as high as 
53 per cent. 
The gravest forms are found in men oftener than in women. 
Multiple urinary fistulas often complicate bilharziasis very materially 
and unless relieved may lead to septic conditions or tend to drain and 
exhaust the patient. Even the grave forms of bilharziasis do not run an 
acute course but in the overwhelming number of cases are chronic, cover- 
ing years, and patients may die of intercurrent disease besides the com- 
plications already mentioned. 
Liver flukes are rare in America or on the Continent of Europe. In 
Japan, China and India, they are found infecting the bile passages, 
causing enlargement of the liver, icterus, pain, gastro-intestinal symptoms 
and in the terminal stages dropsies and ascites with marked anemia. The 
disease is chronic and usually causes death. 
References 
Grawitz. Klin. Path, des Blutes. 1911. 
Gresinger. Arch. f. phys. Heilk., 1854, 554. 
E. Infections of Unknown and Doubtful 
Origin 
I. Poliomyelitis 
(Infantile Paralysis, Heine-Medin Disease: 1840-1887) 
1. Acute Anterior Poliomyelitis 
The revelations of the past fifty years have led the pathologist and 
clinician to positive views concerning the various forms of poliomyelitis, 
and justify a definition which proves the infection to be far-reaching in 
its effects, by no means limited to the anterior multipolar cells in the 
cord, in which by predilection, it is true, the greater changes are pro- 
duced and are promptly recognized. To the reader who is eager to 
study the history of the disease, we would commend the references ap- 
pended to this chapter. 
Our present conception of infantile paralysis justifies the conclusion 
that it is an infectious disease of early life, as a rule communicable. In 
all probability it is due to a filterable organism which is ultramicroscopic, 
causing a short period of indefinite symptoms followed by the prompt 
development of paralysis in most cases, and other features of invasion 318 
SPECIFIC INFECTIOUS DISEASES 
of the nervous system; these depend entirely upon the location and extent 
of the lesions. The clinical types are numerous and well defined, making 
localization and accurate pathologic conclusions possible. 
It is not at all unlikely that the minute organisms found by Flexner 
and Noguchi, consisting of globoid bodies 0.15 micron to 0.3 micron in 
diameter, and arranged in pairs, chains or masses, are the true cause of 
the disease. This question is still sub judice. Flexner and Noguchi 
have grown the cocci in human ascitic fluid. They pass through the 
Berkefeld filter, are capable of reproducing the disease in the monkey, 
and from these they can be again recovered in pure culture. The organ- 
ism is anaerobic. 
When the clinician for either diagnostic or prognostic purposes con- 
siders the underlying pathologic changes of anterior poliomyelitis, he must 
remember that he is dealing with an infection in which all structures of 
the nervous system may be involved, with a strong preference for the 
motor neuron. Hence to focus our attention upon the structures most 
prominently included in the pathologic picture, we consider the various 
manifestations of the disease as expressions of either neuritis, acute ante- 
rior poliomyelitis, meningitis, meningomyelitis or poliomveloencephalitis. 
Occasionally the paralysis is of the Landry type, to which we will again 
refer. The above conclusions are corroborated by a study of the epoch- 
producing contributions to the literature of this subject by Heine, Medin, 
Wickman, Strumpell, P>ergenholtz, Flexner and Homer. Clinical and 
pathological material thoroughly studied, is convincing. The fact which 
we wish to impress is that so-called anterior poliomyelitis can no longer 
be considered to be a disease of the anterior horns alone, but that its 
pathology and symptomatology may include changes in the central and 
peripheral nervous system as well as in the membranes of the cord and 
brain, in a large number of cases. 
The disease is now more frequent than ever before, and is also spread 
over a larger territory. Rosenau in the followung table shows the num- 
ber of outbreaks and the number of cases from 1880-1910: 
Cases. 
Outbreaks. 
Average Number 
of Cases per 
Outbreak. 
1880-1884 
23 
2 
11.5 
1885-1889 
93 
7 
13 
1890-1894 
151 
4 
38 
1895-1899 
345 
23 
15 
1900-1904.. . 
349 
9 
39 
1905-1909 
8,054 
25 
322 
Of the 8,054 cases reported between 1905 and 1909, 5,514 or about five- 
sevenths were found in the United States, INFECTIONS OF UNKNOWN ORIGIN 
319 
The cases have been more severe during the past few years than ever 
before, and in certain sections the number of ascending paralyses in 
adults, of the Landry type, have been correspondingly frequent and fatal, 
A further interesting feature is the greater fatality and relative frequency 
in the country districts and small villages than in the crowded cities. It 
has been my experience that outlying districts of cities, and sparsely 
settled sections, offer more cases than do central and thickly populated 
centers of cities. The majority of cases occur during the warmer months 
of the year; while sporadic cases are found regardless of season. 
It is not within the province of this work to consider the port of entry 
of the infecting agent: the consensus of opinion favors the nasopharyngeal 
route. We might add, however, that in our last case, which was severe 
and of the bulbar type, the disease followed within six days after the bite 
of a large horsefly, in a child four years of age. (See Rosenau.) 
It is further to he remembered that the disease may he conveyed by 
uhealthy carriers” who harbor infecting material in their nasal secretions 
—a fact which Flexner, Clark and Fraser have proved experimentally. 
There are no positive proofs that the disease is not directly contagious 
and in the present state of our knowledge, including the larger experi- 
ences of the Swedish observers, it is safe to so consider it. The period 
of incubation may be placed at from eight to ten days, with an average 
of seven days. 
The Prodromal Period.—The prodromal period offers practically no 
positive prognostic data. There are cases in which the pulse is rapid 
and feeble from the beginning and in which the disease proves grave, 
often of the bulbar type. 
The temperature and pulse taken together during the prodromal 
period are not to be relied upon for prognosis. Early involvement of the 
respiration, rapid and superficial breathing during this period is always 
significant and is found with the bulbar type of paralysis, or may be due 
to bronchopneumonia, which is a frequent cause of death. 
Gastrointestinal symptoms are among the most frequent accompani- 
ments of the first stage of the disease; they are controlled or yield spon- 
taneously in most cases. 
The blood examination in this stage may be of great diagnostic and 
prognostic value, for it shows marked leukopenia. 
The nervous manifestations of the prodromal stage include more or 
less somnolence without psychic disturbances. Drowsiness and stupor 
during the early stage of the disease are not of unfavorable significance, 
and are more favorable than alertness. This experience was confirmed 
by the results of the investigations made by Draper of the Rockefeller 
Institute. 
In very young children convulsions need not be interpreted as serious; 
often they are followed by the stage of paralysis and other symptoms, 320 
SPECIFIC INFECTIOUS DISEASES 
which at once clear the horizon, making the diagnosis of the disease and 
its type possible, and often permitting of a tentative but not a positive 
prognosis. 
The pains and rigidity during the prodromal period are in proportion 
to the extent of the meningeal infiltration {leptomeningitis). 
Profuse perspiration is usually present in both severe and mild cases. 
It is impossible to gain accurate diagnostic or prognostic data during 
the early stage, for as Romer has well said, “the initial symptoms are not 
characteristic of any one type of disease, but they are conglomerate, with 
the possible prominene of one symptom referable either to the meninges, 
the gastro-intestinal tract, the respiratory organs; or the features of infill- 
enzal fever may predominate.” This period is usually short, from twelve 
hours to three to seven days, and is followed by the second stage, the 
stage of paralysis. 
Stage of Paralysis.—It is in the stage of paralysis that we recognize 
the nature and the type of the disease. The diagnosis cannot he positively 
made before the appearance of paralysis; during endemics it can only he 
suspected. 
We recognize the following types (Romer) : 
(a) Abortive 
(b) Spinal 
(c) Landry 
(d) Bulbar and pontine 
(e) Cerebral 
(f) Ataxic 
(g) Polyneuritic 
(h) Meningeal 
(a) Abortive Type.—Wickman’s statistics showed that of 1,028 
cases thoroughly investigated by him, 157 were of this type (15.3 per 
cent). In these the prognosis is uniformly good. The toxins in this type 
do not attach the motor neuron nor the other central organs, and there is 
therefore no paralysis. 
The features which are prominent and yield after a few days are 
fever, pains in the head and back, tonsillar invasion, bronchitis and all 
of the other manifestations of the prodromal stage of the more severe cases. 
Edward Midler has described cases which offer a good prognosis, in 
which there are transitory paralyses of a single group of muscles, or there 
may be evanescent loss of the tendon reflexes. These he has characterized 
as “rudimentary poliomyelitis.” Midler places the incidence of the 
abortive types much higher than does Wickman. The former claims that 
during epidemics fifty per cent of all cases are of this type. My experi- 
ence proves that not all epidemics are alike in their virulence, and we 
have often found the coincidence of other acute infections with infan- INFECTIONS OF UNKNOWN ORIGIN 
321 
tile paralysis, which may have been considered abortive forms of the 
disease, and which may account for these varying conclusions. The 
larger number of abortive cases were found between the ninth and eleventh 
year, and during this period it will be noted from the study of Wickman’s 
tabulation, there are the fewest paralyses. 
(b) Spinal Type.—The spinal type is the most frequent of all forms. 
The paralyses are promptly evident “paralysis of the morning.” It is a 
complete motor paralysis. It soon proves to be flaccid; it may in some 
cases be extensive, involving all four extremities; it may be irregularly 
distributed, or it may from the beginning limit itself to one group of mus- 
cles. When two or more extremities are paralyzed, one extremity usually 
suffers more than do the others. The peroneal and quadriceps muscles are 
oftenest involved and permanently damaged. The cranial nerves includ- 
ing the ocular apparatus are only rarely involved; neither are there sphinc- 
ter paralyses. Sensory symptoms are due to associated cellular infiltra- 
tion of the meninges or the sensory tract, and are of short duration as a 
rule. Muscular atrophy is the fate of the muscles which remain paralyzed; 
with the flaccid paralysis the reaction of degeneration is present. 
The reaction of degeneration does not argue against the possibility of 
final restoration of function. Its persistence without motor improvement 
from six to twelve months after the onset, leaves but little hope for cure 
of the remnant of paralysis. 
With the atrophy of the paralyzed muscles there are trophic changes. 
The more developed the latter, including shortening of the affected ex- 
tremity, interference with the bone growth, marked and persisting lower- 
ing of the local temperature, the less favorable are the chances of restora- 
tion of function. 
Persistence of changed deep and superficial reflexes is unfavorable; in 
these cases the paralysis is likely to persist though the education of acces- 
sory muscles may prove of great assistance. 
Urinary retention during the prodromal period or following, is not, 
in the spinal form, an unfavorable symptom. We have found it both in 
the adult and in early life. In young boys (2-6 years) the urethra is 
not infrequently plugged with a dense phosphatic deposit, which is likely 
to recur, but is not unfavorable. 
Consecutive contractures remain and can only be overcome by ortho- 
pedic treatment. Equinovarus is the characteristic contracture which re- 
mains when the lower extremity is paralyzed. 
Resulting deformities such as kyphosis and scoliosis may often be 
prevented by proper treatment. When developed, they are likely to re- 
main, though in rare cases modern methods of mechanical treatment may 
result in marked improvement. In rare cases there may be exacerbations 
with fresh paralyses which are not usually extensive and are likely to dis- 
appear. 322 
SPECIFIC INFECTIOUS DISEASES 
(c) Landry Type.—Our experience justifies the conclusion that Lan- 
dry’s ascending paralysis is identical with poliomyelitis, there being two 
forms of the disease. 
In the first form there is the characteristic and prompt development 
of ascending paralysis, usually beginning in the lower extremities, ascend- 
ing, and in the course of three to five days involving the diaphragm and 
respiratory muscles; finally there is the pneumogastric and glossopharyn- 
geal ; with spasm of the glottis, air hunger and death, usually before the 
end of the seventh day. The majority of patients die between the third 
and fifth day of the disease. Schluckpneumonia (aspiration) is not un- 
common. 
In the second form we have during the first twenty-four hours rec- 
ognized the ascending paralysis. The respiratory muscles are less in- 
volved; the upper extremities are paralyzed before the end of the fourth 
day; but the pneumogastric and glossopharyngeal are not involved in 
the process. The patient may live and continue paralyzed. Such cases 
are rare but they do occasionally present. We saw a student with this 
complex of symptoms ten years ago, who has since entered the practice 
of law in which he is making a brilliant success in spite of the motor 
paralysis of his four extremities, which has remained unchanged. 
(d) Bulbar and Pontine Type.—The bulbar and pontine form of 
poliomyelitis was described by Medin and includes the involvement of 
the cranial nerves in the motor paralysis. As a rule the bulbar and 
pontine invasion is coincident with the spinal form of the disease, as 
in a case (age four) at present under observation, in which there is paral- 
ysis of both lower extremities and both arms—the left greater than the 
right—and in which during the first four weeks the left facial nerve was 
also included. In this case the facial paralysis has disappeared (six 
months) with marked improvement of all other paralyses. The facial is 
oftener paralyzed than any of the other cranial nerves. The ahducens and 
motor oculi are rarely included. Our material includes one case in which 
the optic nerve was involved. 
(e) Cerebral Type (Polioencephalitis).—These forms of the disease 
are a mixture of poliomyelitis and encephalitis and were originally de- 
scribed in a brilliant article of Striimpell, whose observations have since 
been verified by Medin. The characteristic cerebral paralysis includes 
hemiplegia in children with marked trophic changes, developmental anom- 
alies, contractures, accompanied by the usual adduction of the arm, with 
flexed elbow and well marked clubfoot (pes equinovarus). The reflexes 
in children with these symptoms are likely to continue abolished; in the 
adult they may be present or exaggerated; Bahinski persists or may be 
absent. In children athetosis may finally develop. 
Cerebral polioencephalitis may involve the cerebellum and its paths. 
The paralyses due to this form of poliomyelitis may improve, but com- INFECTIONS OF UNKNOWN ORIGIN 
323 
plete return of function cannot be expected. The majority of these chil- 
dren remain bright, but go through life hemiplegics. 
(f) Ataxic Type.—Medin, Wickman, and Zappert observed symp- 
toms in some of their cases which after the prodromal period resembled 
Friedreich’s hereditary ataxia. In these cases the prognosis for full 
restoration of function is unfavorable. 
(g) Polyneuritic Type.—These cases present all of the features 
of multiple neuritis. They arise during epidemics of the more common 
forms of poliomyelitis, and are held by Medin to be due to the same virus 
which causes all other types. They are associated with sensory symp- 
toms and tender nerve trunks; there are often evidences of meningeal in- 
flammation, including the Kernig symptom. The prognosis of the poly- 
neuritic type of the disease is favorable, though recovery may be slow. 
(h) Meningitic Type.—In this form of the disease there are, during 
the early days, many of the symptoms of acute leptomeningitis arising in 
the midst of an epidemic of poliomyelitis, including the Kernig symp- 
tom. This is followed in most cases by well developed paralyses with the 
usual characteristics of infantile paralysis. ISTetter reports that twenty- 
nine per cent of his cases are of the meningitic type of the disease. 
General Considerations 
Lumbar Puncture.—In the fatal cases of Landry’s ascending 'polio- 
myelitis the fluid escapes under high pressure and contains albumin in 
appreciable quantity. There are no polymorphonuclear cells but the 
French have confirmed the observations made by some American observ- 
ers that there are a good number of lymphocytes present. 
In the usual forms of the disease the fluid escapes under moderate in- 
crease of pressure, the quantity of the fluid being increased; it is usu- 
ally clear, contains no microorganisms, and gives a negative Wassermann 
reaction. For both prognostic and diagnostic purposes it is of interest 
to note that while the withdrawn spinal fluid continues negative, the 
blood (as reported by Plaut and Schottmuller) is likely to give a posi- 
tive Wassermann reaction during the acute period, and becomes nega- 
tive at the end of four weeks—with the improvement of all symptoms. 
The globulin reaction is positive, according to the experience of most 
clinicians, though in the recently published work of Plaut it is claimed 
to be absent. Lmphocytes are present in the fully developed cases in the 
fluid. 
Electrical Reactions.—Oppenheim believes that the electrical response 
of the paralyzed muscles gives important prognostic information. Those 
muscles, he claims, in which the reaction to the faradic current is not 
entirely lost after the third week will be likely to recover full power 
ultimately. 324 
SPECIFIC INFECTIOUS DISEASES 
Groups of muscles in which at the end of the first week of paralyses 
there is complete reaction of degeneration are not likely to recover in 
the majority of cases, though the prognosis is not had in all of these, as 
has already been indicated. We have seen full return of power with 
both complete and partial reaction of degeneration. Eckert believes that 
inability to move the toes is unfavorable for the full restitution of motor 
power in the paralyzed leg. 
Conclusions.—A study of the preceding pages must lead to the con- 
clusion that poliomyelitis is not an innoce?it disease; that deaths are not 
infrequent as the direct result of the infection—a fact which is not sur- 
prising in the light of our present conception of its pathology. The most 
convincing conclusions must rest on the study of a large number of cases 
cautiously investigated. This has been conscientiously done by Wick- 
man (Governmental investigation, 1905) in 1,028 cases. Of these 868 
were paralyzed, 157 were abortive cases (15.3 per cent) and showed nr 
paralysis, or only transitory motor symptoms. Of the entire number 
159 died (12.2 per cent). The average number of days these lived was 
fifteen. Following the cases paralyzed which finally died, we find that 
by adding these to the early deaths, the mortality of poliomyelitis was 16.7 
per cent. The mortality varies in different epidemics from ten to forty- 
two per cent. The mortality as given by nine collective investigations 
(Romer, page 27) was between 10.8 per cent and 22.5 per cent. In the 
monkeys infected experimentally the mortality is very high, 75 to 76.4 
per cent (Homer, Flexner and Lewis). 
Of Wickman’s 157 deaths, 14 died after the fifteenth day and 143 
between the first and the fifteenth day. The following table (Wickman) 
proves that the fourth day claims the larger number of children (25.5 
per cent). 
Table showing number of deaths between the first and fifteenth days 
of the disease inclusive: 
Died on 1st day of disease 1 
“ “ 2d “ “ “ 6 
“ “ 3d “ “ “ 22 
“ “ 4th “ " “ 36 
“ “ 5th “ “ “ 25 
“ “ 6th “ “ “ 15 
“ “ 7th “ “ “ . 16 
“ “ 8th “ “ “ 3 
“ “ 9th “ “ “ 5 
“ “ 10th “ “ “ 7 
“ “ 11th “ “ " 2 
“ “ 12th “ “ “ 1 
“ “ 13th “ “ “ 2 
“ “ 14th “ " « 1 
« " 15th “ “ “ 1 INFECTIONS OF UNKNOWN ORIGIN 
325 
The following table taken from Wickman’s report of his collective in- 
vestigation proves that adults are not exempt from the disease and that 
the death rate is higher in adults than in children: 
Table showing ages, number paralyzed, number of abortive cases, 
number of deaths during first fifteen days, and mortality in per cent 
of paralyzed cases. 
Age, 
Year. 
Cases with 
Paralysis. 
Abortive 
Cases. 
Died During 
First 15 Days. 
Mortality in 
Per Cent, of the 
Number of 
Paralyzed Cases. 
0- 2 
169 
14 
17 
10. 
3- 5 
181 
33 
21 
11.6 
6- 8 
154 
25 
23 
14.9 
9-11 
88 
35 
10 
11.4 
12-14 
77 
29 
22 
28.6 
15-17 
59 
8 
14 
23.7 
18-20 
53 
5 
15 
28.3 
21-23 
24 
3 
8 
33.3 
24-26 
14 
1 
3 
21.4 
27-29 
11 
1 
3 
27.3 
30-32 
12 
2 
4 
33.3 
33-35 
3 
0 
0 
0. 
36-38 
10 
0 
1 
10. 
39-41 
6 
0 
2 
33.3 
41-44 
0 
1 
0 
0. 
45-47 
2 
0 
0 
0. 
48-50 
1 
0 
1 
100. 
51-53 
1 
0 
0 
0. 
54-56 
2 
0 
1 
50. 
65 
1 
*0 
0 
0. 
868 
157 
145 
There were 592 cases with 71 deaths in children between 0-11 years 
of age (mortality of 12. + per cent), whereas between the 12th and 32d 
year there were 250 cases with 69 deaths (mortality of 27.-j-per cent). 
In one case the father of nine children (all in the same house) contracted 
the disease without a single infection among the children. 
If children live beyond the 15th day the chances are that life will 
not be longer threatened. Children living beyond the 7th day are not 
likely to die. 
Twenty per cent of all paralyses recover fully, according to ISTeuroth. 
Wickman claims in children from 9-11 years, 48.4 per cent; after 11th 
year 32.2 per cent. Leegard’s figures show children to the 14th year, 
30.4 per cent, and after the fourteenth year 22.2 per cent of recoveries 
from paralyses. 
We are justified in concluding that poliomyelitis leads to death in 
a larger number of cases than has been heretofore supposed; that the 
prognosis for life therefore must be guardedly given until beyond the 326 
SPECIFIC INFECTIOUS DISEASES 
first week; that paralyses which are well developed may yield; that in 
the larger number of paralyses remnants will remain; that paralyses 
which persist beyond six to twelve months will prove to he permanent, 
with hut slight modification; that trophic changes persisting beyond twelve 
months remain uninfluenced; and that the most fatal form is the ascend- 
ing type with symptoms of Landry’s disease. 
So-called sporadic cases offer an excellent prognosis so far as the life 
of the patient is concerned, though the paralyses are more likely to be 
permanent than are those of the epidemic types. 
Cases of human and experimentally produced poliomyelitis prove that 
the length of the period of incubation offers no positive data for prognosis. 
2. Chronic Poliomyelitis 
There are a number of cases of unknown origin occasionally following 
trauma, in which there is a subacute or chronic course with paralysis, 
closely resembling the spinal type of the acute disease. These cases are 
found in adults without the acute period of the epidemic forms and re- 
semble, when fully developed, the spinal type of muscular atrophy. They 
ditfer from progressive muscular atrophy because of the early paralysis 
and the atrophy which follows it. There may he exacerbations during 
which further paralysis develops, involving separate groups of muscles in 
which atrophy follows, with the flaccid paralysis. There is loss of reflexes 
and the reaction of degeneration. 
In occasional cases there may he marked improvement of all symp- 
toms. In a number of cases the exacerbations lead to progression of the 
atrophy, and with ascending symptoms and increasing weakness the pa- 
tient dies. These cases represent degenerative processes in the anterior 
horns, are often difficult to differentiate from progressive muscular atrophy, 
though as already mentioned, the early flaccid paralysis offers a differ- 
ential feafure. The atrophic changes are secondary, never primary. The 
lower extremities are usually involved first, though there may he mono- 
plegia, and later extension to other parts. 
The prognosis so far as life is concerned is less favorable than pro- 
gressive muscular atrophy, for the disease when progressive, ends fatally 
in from one to four years. 
References and Literature 
Bergenholtz. Romer. epidemische Kinderlahmung. Berlin, 1911. 
Berliner. Wien. med. Wchnschr., 1909, No. 21. 
Flexner (S.). Contributions of exper. medicine, etc., to human poliomyelitis. J. Am. Med. 
.dss., 2Ih 9, 1910. J. of Exper. Med., xii, 1910. J. Am. Med. ylss., 
1909, 58; 4, 1909; No. 29, No. 18. Munch, med. Wchnschr., 
1910, 2. J. Am. Med. Ass., 50, 1910; idem, 1910, No. 14, No. 22, 
No. 55; idem, lx, 362. INFECTIONS OF UNKNOWN ORIGIN 
327 
Flexner & Lewis. J. Am. Med. .Ass., liii, 1909; 20, IS, 11, 1909. 
Flexner, Clark & Fraser. Idem, lx, 201. 
Gibney & Wallace. J. Am. Med. Ass., xlix, 1907, No. 25. 
Heine. Beobacht, etc., Stuttgart, 1840. 
Spinal Kinderldh. 2. ed., Stuttgart, 1860. 
Koplik. Arch, of Pediatrics, May, 1909. 
Landsteiner & Popper. 
Deulsch. med. Wchnschr., 1909, 1995. 
Handbuch, etc. Jena, 1911, Fischer. 
Medin. X Med. Intern. Congress, Berlin, 1890. 
Nord med. Arkiv., Bd. xxviii, 1896, i. 
Arch, de med. des enfants, 1898. 
Mueller (Edward). Munch, med. Wchnschr., 1909, 48. 
Spinal Kinderlahm. Berlin, 1910. 
Arch. f. Kinderheilk., Bd., liii. 
Netter. Bullet, de VAdcad. de Med., 31, 5, 10. 
Bullet, et Mem. de laSoc. Med. des Hop. de Paris, 21, 10,1910. 
Neuroth. Jahrb.f. Kinderheilk. 1905, Bd. Ixi, Hft. 5,742. 
Oppenlxeim. Lehrbuch der Nervenkrank. 1913. 
Arch. f. Psych., 1888. 
Arch. f. Psych., 1892. 
Berlin klin. Wchnschr., 1889. 
Peabody, Draper and Dochez. Monograph Rockefeller Institute, etc. New York, 1912. 
Plaut, Rehm & Schottmuller. Leitfaden, etc. Zerebrospinalfliissigkeit. Jena, 1913. 
Romer. Die Epid. Kinderlahm. Berlin, 1911 (includes full bibliography). 
Rosenau. Preventive medicine. 1913. Appleton. 
Schottmuller. Der Liquor Cerebrospinal bei Infectionskrankh., etc., Munch, med. 
Wchnschr., 1912. 
Strumpell. Deutsch. Arch. f. klin. Med.,Bd., xxxv. 
Jahrb. f. Kinderheilk., 1885, Bd. xxxii. 
Beitrage, etc., Leipzig, 1887. 
Wickman. Ztschr. f. klin. Med., Bd. Ixiii, 362. 
Beitrage, etc. Helsingfors, 1905. 
Beitrage, etc. Berlin, 1907. 
Ztschr., f. die gesammte Neurol, u. Psych., 1910. 
Acute poliomyelitis. Berlin, 1911. 
Zappart. See Article in Pfaundler and Schlossman 1910; also bibliography in Romer. 
II. Scarlet Fever 
{Scarlatina, Ger. Scharlach) 
Scarlet fever is an acute infectious contagious disease, of unknown ori- 
gin, and of early life, characterized by fever, a far-reaching (scarlatinal) 
erythematous eruption, usually followed by desquamation and associated 
with throat complications of varying intensity, lymphatic enlargements 
and a strong tendency to sequelae in which the kidney, heart and joints may 
suffer serious damage. Children between 3 and 8 years of age are most 
disposed to scarlet fever; resistance seems to increase with increasing years. 328 
SPECIFIC INFECTIOUS DISEASES 
In considering prophylaxis and prognosis, let it be remembered that the 
disease is contagious until the end of desquamation and one or two days 
before the outspoken symptoms of the disease. The corpse also holds and 
spreads the infection. The so-called “mild scarlet fever” may spread the 
infection and cause malignant disease in others. There are cases of scar- 
let fever without rash and with slight tonsillitis. It is exceedingly diffi- 
cult, in fact impossible, to offer any forecast of value during the early days 
of the disease, save in those cases which may be recognized at once as 
malignant, in which the duration is short and death prompt, often before 
the rash has appeared. There are so many and such serious complications 
which may influence the course of scarlet fever, whether the initial symp- 
toms are mild or severe, that it is never wise or safe to offer a forecast 
which commits the physician. Cases beginning with mild symptoms may 
be finally complicated with serious organic diseases of vital organs, while 
it is not at all uncommon to find those with alarming symptoms during 
the first five or six days of the disease march to complete recovery without 
an untoward incident. It is safe to consider those cases gravest, in which, 
during the period of invasion, there are marked cerebral symptoms, much 
vomiting, rapid pulse, high temperature and suppressed urine with albu- 
min in the little that is voided. 
Occasionally a case presents with symptoms so grave during the period 
of invasion, including those of profound and sudden sepsis, with immediate 
heart weakness, that death results before the appearance of the rash. 
These cases are not so frequent as formerly; it is a question whether the 
nature of the infection has not been influenced favorably by some un- 
known factor, for those who practised during the dark days of “malignant 
scarlet” and “masked scarlet fever” have lived to repeat these experiences 
only at rare and long intervals. Those were the days when entire families 
of children were stricken and died within twenty-four hours. In Central 
Yew York thirty years ago these experiences were frequent; I know of 
no repetition within the last twenty years in my own or in the practices of 
my colleagues, though now as before it is clear that the mortality varies 
in different epidemics and in different countries from 3 to 50 per cent. 
The highest mortality has been found during October and the winter 
months. The depth of color of the eruption varies, hut experience teaches 
that early mottling of the skin, cyanosis, purple-tinted, purpuric, or hem- 
orrhagic eruptions are strongly suggestive of severe infection, offering 
unfavorable prognosis in direct proportion to the degree of myocardial 
weakness. Widespread deposit on tonsils, pharyngeal wall and uvula, 
membranous in character, diphtheritic or streptococcic, is proof of mixed 
infection, and should lead to a guarded prognosis. 
Considerable involvement of the cervical lymphatics, with widespread 
angina, is found with the more severe infections, and should be given 
considerable weight in offering a forecast. INFECTIOUS OF UNKNOWN ORIGIN 
329 
If with pharyngeal and cervical invasion the nasal mucosa is also in- 
volved, and the symptoms of general infection manifest, more particularly, 
if the heart is showing evidences of added burden, the prognosis becomes 
grave. These cases are usually diphtheritic and reference to them will he 
repeated. Termination of the febrile period by crisis is in the majority of 
cases favorable. 
What complications may follow in any of these cases no diagnostician 
can foresee. Increase of symptoms, including great unrest, somnolence, 
delirium, persistent vomiting, between the second and fourth days of the 
disease, with deepening color of the eruption, cyanosis, with or without 
tonsillar change, but with increasing rapidity of the heart action and dila- 
tation of ventricles is of grave import (Toxic scarlatina) (Schick). 
Diphtheritic Infection.—Necrosis, sloughing of tonsillar tissue with 
symptoms of grave diphtheritic infection (positive bacteriologic diagno- 
sis), between the 3-5 days of the disease, often with middle ear and nasal 
invasion, is found in the graver forms of the disease. If the sloughing is 
deep, and, as individual sloughs are cast off, there is no tendency to heal, 
the prognosis is more serious than in those cases in which, as often hap- 
pens, the slough (i. e., process of necrobiosis) is superficial with prompt 
healing, decrease in size of lymphatics and constitutional disturbances. 
Persistent high temperature without decided fall during the morning 
hours with sloughing, is indicative of deep infection and is serious. 
The depth and extent of destruction of pharyngeal tissue are impor- 
tant factors in prognosis. Extension to the larynx with widespread phar- 
yngeal destruction is serious, as is also laryngeal croup. The lower the 
temperature on the second day of the disease (eruptive period) in cases 
remaining uncomplicated, the more favorable is the prognosis. 
The Ear.—The ear offers important data for prognosis; its early 
infection in cases with symptoms of spreading infection (particularly diph- 
theria) and associated deep necrosis of tissues, is always serious. Acute 
otitis causes increase of temperature, interferes materially with nutrition 
and may lead to acute meningitis from mastoid invasion or may he the 
cause of sinus thrombosis, with its serious accompaniments. 
Chronic changes may follow early or late otitis media suppurativa, 
causing deafness, spreading infection, pyogenic disease of the brain, 
months and years after the initial disease. 
Chronic mastoiditis with latent abscess continues to he a menace and 
may remain unrecognized, to he suddenly lighted into activity, and may 
cause meningitis and death. 
Otitis suppurativa may spread infection to distant organs; the peri- 
cardium, endocardium and joints have been infected by pus producing 
organisms from this source. 
The Respiratory Organs.—Pneumonia (staphylococcus or streptococ- 
cus) secondary to otitis has followed with serious results in many cases. 330 
SPECIFIC INFECTIOUS DISEASES 
Purulent 'pleurisy (empyema) dependent on otitis is always a grave 
complication. 
A very large number of middle ear suppurations are late complica- 
tions, often during convalescence, which, when recognized early and rad- 
ically treated, offer a very favorable prognosis. 
The Blood.—There is a moderate leukocytosis and eosinophilia with 
scarlet fever; a decided drop or absence of the latter is unfavorable. 
Keckzeh reports that leukocytosis and eosinophilia are at their height as 
the eruption begins to fade. 
The Cardiovascular System.—Children bear a rapid pulse well during 
the early stages of scarlet fever, hence rapid heart action without evidences 
of dilatation or myocardial weakness, secondary cyanosis or mottling of 
the skin, is not of itself serious. Persistently rapid heart action (140 and 
above) is usually evidence of profound infection and grave. 
Small, thready, rapid pulse, above 150 on the first day, in children, 
with other grave symptoms is always ominous. 
Acute myocardial degeneration with dilatation is promptly shown in 
symptoms of circulatory insufficiency, congested skin, cyanosis, dyspnea, 
and is among the serious complications whenever present. Endocarditis 
(acute) and pericarditis are frequently associated with myocardial degen- 
eration. 
Scarlatinal endocarditis is, next to rheumatism, the most frequent 
cause of chronic valvular disease. When acute endocarditis and nephritis 
are co-existent, as often happens, the prognosis is less favorable than if but 
one of these complications exists. Many cases, however, recover and it is 
surprising to find among these but scant remnant of disease in either heart 
or kidney if patients are cautiously watched and scientifically treated. 
To improve the chances of scarlet fever patients, the endocardium demands 
the same watchful care in this disease as in rheumatism. Often an endo- 
carditis may run its course ending in serious damage without subjective 
symptoms; physical signs, however, prove its presence in most cases early, 
hence the prognosis is improved in proportion to the early diagnosis and 
subsequent care given these patients. It must be remembered that, in rare 
cases, post-scarlatinal endocarditis may develop without subjective symp- 
toms and may lead to permanently damaged valves. Septic or malignant 
endocarditis may complicate otitis, diphtheria or other mixed infections 
with scarletina and always ends fatally. 
Irregularities of the heart, erratic behavior, at times surprisingly slow 
hearts alternating with sudden acceleration, are complications present dur- 
ing convalescence which are relieved by continued rest and abundant time. 
Increasing systolic blood pressure with or without albuminuria during 
the first 2 or 3 weeks of scarlet fever, indicates obstruction in the renal 
circuit—hence nephritis. It is compensatory, and should be accepted as 
an evidence of Nature’s effort to assist in the cure. When dilatation fol- INFECTIOUS OF UNKNOWN ORIGIN 
331 
lows this condition, slight and insufficient hypertrophy, diffuse area of car- 
diac impulse, the prognosis is less favorable. 
Increased systolic blood pressure may be present during the early days 
of albuminuria, before there are other evidences of nephritis, and is likely 
to be the first suggestion of that complication. 
The Kidneys.—Acute nephritis complicates one-seventh (1/7) of all 
cases of scarlet fever, and is a frequent cause of chronic kidney disease 
(interstitial and parenchymatous). Recovery is the rule in the majority 
of cases of scarlatinal nephritis, though it often leads to death. True 
scarlatinal nephritis is not likely to develop before the third week, and 
should not be confounded with the febrile albuminuria of the disease. It 
may begin to show itself as late as the 6th or 8th week. The greatest 
source of danger is uremia. + 
Uremic poisoning, usually arising suddenly, may be found with the 
mildest as well as the more severe nephritides. As a rule the complica- 
tion may be expected if there have been the usual premonitory symptoms 
of uremic poisoning, including vomiting, headache, markedly reduced uri- 
nary secretions, slow pulse, with increased blood pressure. While uremia 
is a serious complication, the prognosis is not entirely bad and cases which 
appear serious, in which the coma and other evidences of surcharged blood 
are threatening, may fully recover. It is surprising to note how long chil- 
dren bear uremic poisoning in individual cases, and how completely they 
lift themselves out of it. No case of uremia in a child is so severe that it 
may not recover. I have seen children profoundly uremic with complete 
suppression of urine during 2, 3 and even 4 days, recover with return 
to normal kidney function and final restoration of normal kidney tissue, 
so far as I could tell from the subsequent histories of these cases. Patholo- 
gists and clinicians have repeatedly proved that two-thirds (2/3) or even 
more of our total kidney substance can be spared without serious incon- 
venience (Bradford). I have already referred to the association of heart 
and kidney lesions. Nephritis is a frequent cause of cardiac asthenia, 
leading to severe dyspnea, cyanosis and edema of the lungs. Endo- and 
pericarditis with nephritis are always serious. Dropsies, particularly 
hydropericardium and single or double hydrothorax, are complications due 
to nephritis, of grave significance. The prognosis in these cases should 
not be given as positively bad, for recovery does take place occasionally 
in spite of multiple complications. . The height of the fever in scarlatinal 
nephritis when the symptoms are acute does not offer much of prognostic 
value. I have seen many cases in which the temperature for several days 
has continued high, which finally proved tractable and ran a short course. 
In my practice I have found the quantity of urine secreted and the 
heart condition to offer most reliable prognostic data. Until the quantity 
of urine has increased and its color cleared, with reduction of casts and 
blood and a fair urea output, no positive prognosis can be given. Even 332 
SPECIFIC INFECTIOUS DISEASES 
in these cases we must leave a loop-hole in our prognosis for occasionally, 
for some reason, there is sudden suppression and. a return of uremic 
symptoms. If with uremia or nephrkis the heart fails to respond to 
treatment, if the pulse grows more tense and has periods of flabbiness 
and continues rapid, a guarded prognosis must be given, v 
Increasing anemia with eye symptoms, and persistence of edema, are 
evidences of extensive and obstinate kidney lesions, and influence prognosis 
accordingly, worse with cardiac instability. 
Cases of nephritis which may he characterized as almost completely 
unon-albuminuric>'> in which a trace of albumin and fe\y casts are found 
at long intervals, usually on arising in the morning (orthostatic albumin- 
uria), yield to rest and treatment. When these remain unrecognized or 
untreated they are likely to be followed by chronic nephritis. 
The duration of average nephritis with scarlet fever is from 2 to 4 
weeks. 
Arthritis.—Non-suppurative polyarthritis complicates scarlet fever in 
6 per cent of cases. Developing during the second week usually or later as 
a rule it leads to recovery without damaged joints or endocardium. Occa- 
sionally endocarditis with positive physical signs develops, and almost all 
of these recover with but slight damage. In cases of scarlatinal arthritis 
rapid pulse and high temperature are not necessarily serious. In most 
cases both are high and yet recovery is the rule. 
Adenitis.—Most cases of suppurative adenitis lead to full recovery. 
The types of diphtheritic and gangrenous adenitis complicating mixed in- 
fection (diphtheria, etc.), at the height of the disease, have been mentioned 
above and are always part of a serious process. 
Adenitis with nephritis is a combination of serious moment though the 
larger number of these finally recover. 
Resume.—Pneumonia (post-scarlatinal) is often associated with em- 
pyema and offers a grave prognosis. 
It may be accepted as a rule for the prognosis of scarlet fever that, 
I. Added infection of any kind adds to the danger of the original 
disease. 
II. ZTSTo disease requires such a long period of observation of the kid- 
ney and the cardio-vascular system. 
Finally, to classify systematically cases for prognosis, we accept 
Moser's division. 
I. and II.—Favorable cases. 
III. Doubtful cases. 
IV. Hopeless cases. 
Division I.—Includes cases without serious symptoms, reasonable tem- 
perature. Few or no pharyngeal symptoms, good general condition. 
Division II.—Includes moderate intensity of symptoms. But one or INFECTIONS OF UNKNOWN ORIGIN 
333 
two symptoms in the ascendancy. Moderate pharyngeal invasion. No 
suppurative otitis media. Moderate erythematous eruption. No heart 
weakness, no cyanosis. Fairly high temperature and pulse of good quality. 
Divisions III. and IV.—Include the severe cases, grave, toxic and in- 
fectious forms (diphtheritic) above described, usually in children between 
the 1st and 4th year of life. 
Mosers. Behandlung des Scharlachs. 1903. 
Reckzeh. Deutsch. Arch. f. klin. Med., 1903, Bd. Ixxvii. 
Schick. Pfaundler & Schlossmann, Handbuch der Kinderheilkunde. 2. ed., ii. 
References 
III. Smallpox 
{Variola, Ger. Blattern, Fr. Petite verole, It. Vaiuolo) 
Smallpox is an eruptive disease of unknown origin, epidemic or en- 
demic, probably due to ultramicroscopic life, possibly of protozoic origin 
(Cytoryctes variolse), and associated with skin lesions, invasion of mucous 
membranes, and constitutional disturbances. 
Historical Data.—The disease was known long before the birth of 
Christ; it raged in China and India, and was brought to Egypt and the 
continent of Europe during the sixth century. Until the sixteenth century 
the disease remained in Southern Europe, when Germany was invaded. It 
is strange that during the thirteenth century serious epidemics decimated 
England without reaching Northern Europe. During the sixteenth 
century it was brought to America by the Spaniards. In 1718, Lady 
Mary Wortley Montague introduced inoculation into Europe, but it was 
associated with such painful results that it failed to gain a foothold. In 
1798 the illustrious Jenner gave to the world the epoch-producing discovery 
of vaccination which robbed smallpox of its terror, and will with proper 
supervision, strict quarantine, and concerted action of the lay world and 
the medical profession as represented in the modern Science and Art of 
Preventive Medicine, ultimately efface it. 
General Considerations.—The character of the vaccination, it is now 
universally conceded, affects prognosis. The non- and insufficiently vac- 
cinated are likely to suffer from the severer types of smallpox, either dis- 
crete or confluent. 
There seems in some families to be complete immunity to the disease, 
in some, repeated vaccinations remain negative. One colleague I have vac- 
cinated seventeen times without reaction. He has been in the midst of 
malignant smallpox, treated many cases, but has never contracted the 
disease. 334 
SPECIFIC INFECTIOUS DISEASES 
One attach as a rule gives immunity, but there are so many exceptions, 
that the rule must be ignored if the public and the individual are to be 
protected. I have met several examples of mild first attacks of smallpox, 
in which second infections were severe and hemorrhagic. Reverse expe- 
riences I have also had. 
Epidemics vary in virulence and are likely to present many features in 
which they differ. Some may be characterized as malignant, others be- 
nign. It is a rule that the milder cases are'found at the close of the epi- 
demic. 
Ro age is exempt from the ravages of smallpox. It may attack the 
fetus in utero—usually with fatal result. Between the ages of one to 
forty the disease claims most of its victims. It is found in old age less 
frequently than during the active years of life. Prognosis of the disease 
in old age is bad. “The prognosis improves up to the age of ten, is more 
favorable until fifteen, and then gradually becomes less so, although the 
case mortality in discrete cases remains very small, at least until advanced 
old age” (White and Biernaski). The sexes are equally attacked and prog- 
nosis does not differ though pregnancy and miscarriage, resulting from 
smallpox of the fetus and the mother, add to the number of serious cases 
in women. It has been proved in all epidemics that smallpox in pregnant 
women is likely to be malignant and strikingly fatal. Pregnancy invites 
the disease. 
The disease is prone to attack negroes and the mortality among these, 
in the unvaccinated, is larger than among the whites. 
Stage of Incubation 
The stage of incubation (10 to 13 days) offers no symptoms nor note- 
worthy data of use for prognostic purposes. 
The stage of invasion may be either mild or severe. The rule that an 
invasion with mild symptoms argues in favor of a benign smallpox, has so 
many exceptions that these must he kept in mind and should protect the 
clinician against a positive prognosis too early. There have been within 
my experience a number of cases in which the symptoms of this stage were 
unusually mild and reassuring, in which during the period of eruption I 
faced malignant disease of the pustulo-hemorrhagic and hemorrhagic types. 
The severe backache (rachialgia) may be out of all proportion to the 
ultimate severity or benign nature of the disease. 
Profound cerebral invasion is occasionally met in non-malignant cases. 
As a rule it is safe to consider somnolence, coma, delirium and marked 
subsultus indicative of the more severe form of the disease. If these symp- 
toms are present early in the period of invasion, and are associated with 
Stage of Invasion INFECTIONS OF UNKNOWN ORIGIN 
335 
high temperature in the adult or child, if the pulse is correspondingly dis- 
turbed, irregular and erratic, rapid and small, we may expect a severe 
course of the disease. Hurried respiration during the period of invasion, 
with rapid pulse, high temperature and delirium, argue against mild small- 
pox. Marked enlargement of the spleen early is evidence of deep infection, 
and is of serious import though with “black smallpox” there is no enlarge- 
ment as a rule. Albuminuria, during invasion with nephritis, is always 
suggestive of great danger. 
Bashes or prodromal exanthemata (invasion) may differ. In some 
cases these are scarlatinal, in others they resemble the measle eruption and 
are likely to be macular. They are evanescent in almost all cases (12 to 
24 hours) and do not lead to desquamation. The deep scarlatinal eruptions 
are more significant prognostically than the moderate erythematous rash 
or the measle-like eruption. Macular eruptions as a rule are favorable; 
the hemorrhagic prodromal eruption is likely to remain, and is always of 
serious significance. When both hemorrhagic and non-hemorrhagic 
macules are present during this period, the prognosis must be guardedly 
given, for while, this adds an element which may be interpreted as serious, 
a fair number of these cases recover. 
Convincing symptoms of use for prognosis are found toward the end 
of the period of invasion and the established stage of eruption. 
Stage of Eruption 
In connection with the study of the prognosis of smallpox it will he 
wise at this juncture to present the accepted classification of its varieties 
made clear as a rule, only during the stage of eruption. 
I. Variola vera. 
(a) Discrete smallpox. 
(b) Confluent smallpox. 
II. Variola hemorrhagica (hemorrhagic smallpox). 
(a) Purpura variolosa (black smallpox). 
(b) Variola hemorrhagica pustulosa (pustular hemorrhagic small- 
pox). 
III. Varioloid. 
IV. Variola without eruption. 
Pustulation.—Pustulation in the average case must be expected after 
vesiculation on the ninth day of the disease. A marked tendency early 
during pustulation to-confluence is found in the more severe forms of the 
disease. Pustulation, with limited eruption, few lesions of the mucous 
membranes and but few constitutional symptoms, is always favorable. Few 
pustules filled with blood—this probably due to self-inflicted trauma—are 
not significant. With the pustulo-hemorrhagic type of the disease, a few SPECIFIC INFECTIOUS DISEASES 
336 
bloody pustules do not influence the outcome. Many pustules—hemor- 
rhagic—with symptoms of pyemia, are usually indications of severe in- 
fection and make the prognosis grave. The earlier the hemorrhagic nature 
of the eruption in any form of the disease, the ivorse is the prognosis. 
Those cases justify a serious forecast in which there are hemorrhages 
into the shin early, and before pustulation or the pustulohemorrhagic con- 
dition is manifest. These cases are unusually virulent. The prognosis is 
grave if separate pustules, without hnown trauma fill with blood. 
The invasion of the mucous membranes (usually the mouth and throat, 
sometimes also the larynx, stomach, intestines, vulva, and rectum) is not 
as a rule of significance unless there are many pustules. If the invasion 
is far-reaching, the result is weakening and adds materially to the danger 
of the disease. Large hemorrhages from mucous membranes are serious 
and are usually associated with variola hemorrhagica. 
Temperature.—A decided fall of temperature shortly after the ap- 
pearance of the eruption, is always welcome and favorable. This is not at 
all unusual in cases which during the period of invasion, because of nerv- 
ous symptoms, were considered serious. In severe cases there is but little 
fall of temperature with the appearance of the eruption. The temperature 
promptly rises to the height of the period of invasion and even higher; 
cerebral and other grave symptoms persist. It is safe to interpret a de- 
cided drop of temperature as vesiculation begins, favorably, if it does not 
again mount to its former height. In severe cases the drop of tempera- 
ture even though appreciable, is of short duration; it is not likely however 
to be decided. 
Persisting high temperature during pustulation is pyemic or strepto- 
coccic in its nature, and when associated with far-reaching confluence, is 
serious. 
Blood.—During the stage of eruption the blood shows marhed leuko- 
cytosis (12,000 to 24,000) with lymphocytic increase. This begins on 
the fourth to the sixth day of the disease and may continue during several 
Aveeks or months after full recovery. Neutrophilic leukocytes are only 
relatively diminished. Macgrath, Brinkerhoff and Bancroft found in 
fatal cases and in those in which the skin lesions were severe and wide- 
spread, a decided lowering of the leukocytic count. These obseiwers also 
found increase of mononuclear lymphocytes. 
General Statement.—The general statement is justified that small-pox 
(I. Variola Vera) may be either benign or malignant, that the average 
mortality of all cases—and most of these are unvaccinated—varies in dif- 
ferent epidemics from 15 to 35 per cent. 
I. Variola vera 
(a) Discrete Smallpox.—Discrete smallpox has a mortality of 5 to 
10 per cent. INFECTIONS OF UNKNOWN ORIGIN 
337 
(b) Confluent Smallpox.—The mortality of confluent smallpox is 
high: the greater the confluence, the worse the prognosis. If confluence is 
not spread over the back, the prognosis is correspondingly better. If con- 
fluence is limited to the face and extremities the prognosis is worse than 
in the discrete form, but better than if over the trunk at the same time. 
Infants below two years of age all die when the eruption is confluent. Be- 
tween two and five years of age one-fourth recover; after five years of age 
the mortality is lower; from ten to fourteen “the patient is more likely 
to recover than at any other age.” “After fifteen years of age the per- 
centage of deaths to recoveries increases steadily with advancing years” 
(MacCombie). 
Laryngeal and pulmonary complications with confluent smallpox, cellu- 
litis, and those unfavorable conditions mentioned under General Consid- 
erations add to the danger of confluence. 
(a) Purpura variolosa (Black Smallpox).—Purpura variolosa is al- 
most invariably fatal: recovery is so rare as to justify the gloomy forecast 
given. These patients die early in the disease, and as has already been 
mentioned, without demonstrable enlargement of the spleen—a fact of 
some prognostic value. 
(b) Variola hemorrhagica pustulosa (Pustular Hemorrhagic Small- 
pox).—In the preceding pages mention has been made of a number of 
conditions which materially modify the prognosis of these cases. It is 
not as fatal as black smallpox (Purpura variolosa) but is more frequent. 
The disease if fully developed is grave; the majority of patients die, usu- 
ally in collapse between the seventh and twelfth day of the disease. 
II. Variola hemorrhagica (Hemorrhagic Smallpox) 
III. Varioloid 
This is a modified form of smallpox. The overwhelming proportion 
of patients if inoculated, were probably not properly vaccinated—hence not 
entirely protected—or have gone beyond the period of immunity. The 
duration of all the periods of the disease is materially reduced; many 
features of variola vera are absent; fever disappears with the modified 
eruption and rarely returns: when it does, it is of short duration and due 
to absorption of pus during pustulation. 
Vesiculation and pustulation may not follow the formation of the 
papule; mucous membranes are usually untouched by the disease; recovery 
is prompt, and as a rule without complication or sequel. 
IV. Variola without Eruption 
This is always mild; it is usually found in well-protected subjects, or 
as the epidemic is fading. The symptoms of the stage of invasion sug- 338 
SPECIFIC INFECTIOUS DISEASES 
gest as a rule a mild form of the disease; occasionally there may be consid- 
erable constitutional disturbance, fever, rachalgia and anorexia. The 
appearance of the patient continues good, there may be a prodromal rash 
—usually macular, non-scarlatinal—the disease ends favorably at the end 
of the period of invasion. 
Complications 
These modify the prognosis as a rule during pustulation. Complica- 
tions after the beginning of convalescence are infrequent. 
Among the debilitating incidents are added multiple phlegmons, deep 
abscesses of the muscles and suppurative adenitis. 
Erysipelas is always a serious complication, worse with the severer 
types of the disease: when facial and widespread with meningeal symp- 
toms it usually leads to death. 
Gangrene, local or widespread is serious. 
Deep sepsis and pyemia with confluence are among the serious com- 
plications. 
Bronchitis limited in extent is not unfavorable. 
Invasion of the smaller tubes by bronchial catarrh (bronchiolitis) adds 
a large element of danger in the possible development of bronchopneu- 
monia, which is not unusual. 
Croupous pneumonia is not frequent, occasionally when present, it is 
followed by lung abscess. 
Purulent thrombosis is always a serious complication. 
Pleurisy and empyema occasionally follow; as a rule the latter is 
the more serious, but if a late manifestation and relieved by drainage, 
most patients recover. Occasionally pulmonary tuberculosis has been a 
sequal of smallpox. Roily makes the statement that all lung and pleural 
complications give a bad prognosis. 
Invasion of the mucous membranes has been mentioned in the preced- 
ing pages, also edema of the glottis—a threatening complication. 
The complications due to eye, ear and nose invasion demand the con- 
sideration of workers in special fields. They are often destructive and 
permanent. Eye complications are present in from six to ten per cent 
of all cases. .Blindness due to suppurative disease of the eye, opacities 
of the cornea, and other deforming and damaging conditions depend on 
eruptive lesions, sepsis or pyemia. 
Brain complications have been mentioned as occurring during the 
acute stages of the disease and their prognostic significance discussed. 
There are cases in which acute encephalitis, aphasia consecutive to soften- 
ing of brain substance, have proved fatal. Leyden has reported cases 
complicated with diffuse myelitis, insular sclerosis and acute ascending 
paralysis (Quoted by Roily). In the epidemics of Central Rew York, INFECTIONS OF UNKNOWN OKIGIN 
339 
peripheral neuritis was exceedingly rare and psychic disturbances men- 
tioned by many observers have been absent. 
Suppurative arthritis is a serious and damaging complication: when 
these patients recover, anchyloses are the rule. 
The degenerative changes lead in serious cases to myocardial weakness, 
kidney invasion, while septic endocarditis is associated with a limited 
number of cases and invariably leads to death. Pericarditis, occasionally 
purulent, has proved fatal. 
Vaccination—Vaccinia 
But little space need be given to the prognosis of vaccination itself; 
when done'under strict antiseptic precautions, and these are continued, 
or if after a septic vaccination such strict cleanliness of the wound and 
person as the intelligent physician directs is practiced, there is practically 
no danger of infection if a pure animal lymph is used. The following 
conclusions are justified by large clinical experience and will prevent com- 
plications and annoyance if heeded, and the prognosis of vaccination will 
be uniformly good. 
Conclusions:—1. Arm to arm inoculation is justified. 
2. Human scabs or crusts are never to be used. 
3. Vaccination with animal lymph from reliable sources, preferably 
under State control, offers the best prognosis. 
4. Attention to detail and strict asepsis are demanded; the subject and 
the operator need to be equally clean. 
5. A sick child should not be vaccinated unless in the midst of an 
epidemic, or immediately after exposure to the disease. 
6. Children or adults showing acute syphilitic lesions will react unfa- 
vorably and should first be subjected to_ antispecific treatment and later 
vaccinated, unless there is danger of immediate smallpox infection. 
7. The same advice should be accepted in connection with congenital 
syphilitics. 
8. Children or adults, reduced in health, with active tuberculosis, 
strikingly anemic, cachectic, with suppurating glands or those suffering 
from acute disease of the nervous system, including chorea, should first be 
prepared and later vaccinated. 
9. Tetanus will not follow vaccination unless there has been contami- 
nation either through the lymph, from the body of the vaccinated subject 
or through dressings, or as the result of faulty technic (instruments, 
skin, etc.). 
10. Auto-infection is avoidable, and is evidence of carelessness on the 
part of the vaccinated or those responsible for his care. 
11. Disease, i. e., syphilis, acute infection, tuberculosis, “scrophula,” 
and smallpox itself, is never spread by clean vaccination. 340 
SPECIFIC INFECTIOUS DISEASES 
12. The vaccination of children lias no influence in preparing ready 
culture media in the body for the development of the other acute ex- 
anthemata (measles, scarlet fever, etc.). 
Considerations and Statistics.—How the prognosis of smallpox has 
been influenced by vaccination requires no detailed consideration: even 
the intelligent layman has this knowledge at his tongue’s end. A few 
telling statistics may be added to round this chapter. There was a time 
when smallpox was the direct cause of 1/7 of all deaths, and this, in 
the civilized countries of the earth—as fatal as was tuberculosis during 
the last quarter of the 19th century. During the 18th century 30,000 
victims were annually claimed in France; in 1796, 25,646 died in Prussia 
when its population was 7,000,000. In Berlin 1/12 of all deaths were 
due to smallpox during the last decade of the 18th century. 
In countries today where vaccination is obligatory, note the change. 
Smallpox has been reduced, among the properly vaccinated to 0.25 to 
0.35 per 100,000 population. The detailed statistics of Prussia show 
the disease to be present among 0.25 per 100,000 of population. In Eng- 
land and Wales during 1910 there were but 19 deaths due to smallpox. 
In the United States during 1909 and 1910 there were 54,451 cases of 
smallpox with 565 deaths—about 1 per cent mortality among the infected. 
Proper regulation of vaccination, making it obligatory in all countries, 
in all of our own states, well guarded quarantine after the early recogni- 
tion of the disease, revaccination at regular intervals (six to ten years) 
will surely lead to the disappearance of the disease. 
Finally we would call attention to the fact that protection conferred 
by vaccination is in direct proportion to the thoroughness of the operation 
and the number of cicatrices. Marson (London Smallpox Hospital) 
brought the results of his observations to the notice of the Royal Commis- 
sion of England through Sir Richard Thorne, from which I take the fol- 
lowing data: 
Cases of Smallpox Classified According 
to the Vaccination Marks Borne by 
Each Patient Respectively. 
Percentage of Deaths 
in Each Class 
Respectively 
Uncorrected.* 
Percentage of Deaths 
in Each Class 
Respectively 
Corrected.* 
1836-51 
1852-67 
1836-51 
1852-67 
1. Stated to have been vaccinated, but 
having no cicatrix 
25.5 
40.3 
21.7 
39.4 
2. Having one vaccine cicatrix 
9.2 
14.8 
7.6 
13.8 
3. Having two vaccine cicatrices 
6.0 
8.7 
4.3 
7.7 
4. Having three vaccine cicatrices 
3.6 
3.7 
1.8 
3.0 
5. Having four or more vaccine cicatrices. 
1.1 
1.9 
0.7 
0.9 
Unvaccinated 
37.5 
35.7 
35.5 
34.9 INFECTIONS OF UNKNOWN ORIGIN 
341 
Vaccination 
Scars. 
Total 
Cases. 
Confluent and 
Hemorrhagic. 
Deaths. 
One 
886 
177 or 20. per cent. 
101 or 11.4 per cent. 
Two 
589 
83 or 14.1 per cent. 
44 or 7.3 per cent. 
Three 
94 
13 or 13.8 per cent. 
4 or 4.2 per cent. 
Four 
74 
9 or 12.2 per cent. 
2 or 2.8 per cent. 
* The terms uncorrected and corrected are used to signify the inclusion or exclusion 
of those fatal cases of smallpox in which the patient suffered from some other disease 
superadded to the smallpox. 
References 
Macgrath, Brinkerhoff & Bancroft. J. of Med. Research, 1904. 
MacCombie. Allbutt & Rolleston, System of Medicine. 2. ed., 529. 
Roily. Mohr & Staehelin, Handbuch der Inneren Medizin. 1911, i, 169. 
Thorne (Sir Richard). M’Vail, Allbutt & Rolleston, System of Medicine, ii, part 
i, 2. ed., 785. 
White & Biernaski. Bain, Text Book of Medicine. 
IV. Varicella 
(Windpocken, Gr. Spitzpocken, Chicken pox, Varicelle, Fr. Petit verole 
volante) 
Chicken pox is a highly contagious disease of childhood (adults are 
rarely attacked) of unknown origin; it is characterized by a vesicular 
skin eruption, which finally becomes pustular; is associated with mild con- 
stitutional symptoms, promptly yields and ends in full recovery, with 
developed immunity (99 per cent of cases) to the disease. 
The prognosis of varicella is almost uniformly good. In an experi- 
ence of thirty-five years I number hut one death due to the disease, that 
of a feeble child, four months of age, who died in convulsions with the 
characteristic rash fully developed. Deaths attributed to varicella, have, 
in all probability in the majority of cases been unrecognized smallpox, 
unless in correctly diagnosticated cases there have been serious complica- 
tions—which are exceedingly rare. 
Roily reports the autopsy of a child who died on the thirty-sixth day 
of the disease after a long period of dysentery following chicken pox, 
in which one of the pustules became gangrenous. There was also albu- 
minuria with hyaline casts. The autopsy showed dysenteric lesions in 
the large intestines, enlarged mesenteric glands, and cloudy degeneration 
of the cortical substance of the kidney. In this case dysentery was prob- 
ably an accidental accompaniment of varicella. 
Occasionally a death has been reported during chicken pox epidemics 342 
SPECIFIC INFECTIOUS DISEASES 
due to hemorrhagic accompaniments. In most of these cases the children 
were either sick or reduced by previous illness. 
Complications 
Nephritis is a rare complication, usually ending in recovery. This is 
likely to he of hemorrhagic nature. 
Chorea has followed close upon convalescence, in children predisposed. 
Hemiplegia, encephalitis, pericarditis, pleurisy, suppurating adenitis, 
mediastinal abscess are also among the rare sequelae. 
Poly- or monarthritis, usually mild, have been present in a very small 
per cent of cases. Recovery without endocardial disturbance is the rule. 
Roily makes the following statement: “Chicken pox influences tuber- 
culous disease, as does measles, unfavorably. Tuberculosis is positively 
lighted into activity to such a degree that the patients usually die within 
a short time.” The combination of chicken pox with other acute exan- 
themata, scarlatina and measles, is an occasional coincidence. The prog- 
nosis depends entirely in these cases upon the severity of the infection 
other than varicella, which is not materially influenced by the presence of 
the latter disease. 
Roily. Mohr & Staehelin, Handbuch der Inneren Medizin, i., 142. 
Reference 
V. Measles 
(Morbilli, Rougeole, Rosolia) 
Measles is an acute exanthematous, directly contagious disease of 
early childhood (1st to 5th year) ; it is epidemic, characterized by fever, 
catarrhal inflammation of the air passages and photophobia, a disease in 
which positive immunity is not produced by one or more attacks, though 
as a rule the disease is not repeated. The bacterial cause of the disease 
is unknown. Its period of incubation is from seven to fourteen days. 
Patients continue to carry the contagion during at least sixteen days, 
the length of the period of safe quarantine. The blood and secretions, the 
desquamated skin, the clothing and bedding, hold the contagious element 
and transfer the disease to the healthy, in all probability, by direct contact. 
The disease is contagious during the period of invasion (3 to 4 days 
before the eruption) and after, during from ten to sixteen days. The 
severity of subsequent attacks is not influenced by previous infection. 
The prognosis of uncomplicated measles is almost uniformly good. 
The disease is either mild or malignant. Malignant measles is rare 
and is of hemorrhagic character, associated with deep discoloration of the 
eruption, marked invasion of the nervous system, degenerative changes in INFECTIONS OF UNKNOWN ORIGIN 
343 
the heart and kidneys, and causes death in most cases between the second 
and fifth day of the eruption. In some malignant cases the period of 
invasion is characterized by severe symptoms. There may be hemorrhages 
from mucous surfaces (epistaxis, etc.), a purpuric eruption, and children 
may die before the true measle rash appears. Fortunately, as already 
stated, these cases are exceedingly rare. 
The number of Koplih spots bears no relation to the severity of the 
disease. 
Temperature.—In the majority of favorable cases the temperature aver- 
ages between 102°-104° F., with corresponding acceleration of the heart 
action. The more severe cases are characterized by the deeper, “darker,” 
papular eruptions. The papules of mild measles disappear as a rule on 
deep pressure, the hemorrhagic papules do not disappear. 
Conjunctivitis.—The severity of the conjunctivitis in the majority of 
cases bears no relation to the severity of the disease. It not infrequently 
happens that measles with mild constitutional symptoms may have severe 
catarrhal conjunctivitis, as well as harassing bronchitis. 
Blood.—Leukopenia is the rule in measles; there is in favorable cases 
disappearance of lymphocytes (usually in the ascendency during early 
childhood) and relative increase of neutrophilic leukocytes. The white 
count in the average case is between 2,800 and 3,400. Leukocytosis dur- 
ing the period of eruption indicates the presence of a complication. Lym- 
phatic (cervical, mainly) enlargements are the rule are not of serious 
moment, and recede during the period of convalescence. 
Urine.—Febrile albuminuria is frequent and is found with marked con- 
stitutional involvement; it is not of serious importance save in the hemor- 
rhagic types of the disease. 
The mildest cases are those without catarrhal symptoms or few only, 
a modified rash, and but slight febrile movement. 
The severe types (non-malignant) of the disease in which the prog- 
nosis may be doubtful are those in which with a deep colored eruption there 
is hyperpyrexia, brain symptoms including the typhoid conditions, de- 
lirium, involuntary discharge of urine and frequent diarrheal stools, with 
rapid small dicrotic pulse. The periods of incubation and invasion may 
be associated with the symptoms of severe infection, which in occasional 
cases cease with the appearance of the eruption—the entire picture of the 
disease changing for the better suddenly, with fall of temperature and 
improved pulse. The reverse may also happen, i. e., mild periods of incu- 
bation and invasion with increase in the severity of the symptoms during 
the period of eruption. 
The Skin.—Cyanosis of the skin, a blue appearance of the papules, is 
found in the graver forms of the disease. The heart in these cases offers 
the best indications for prognosis; with evidences of cyanosis its muscu- 
lature is usually weakened by toxins, previous or associated disease. 344 
SPECIFIC INFECTIOUS DISEASES 
Mortality.—The rule may be accepted that measles without complicar 
tions offers an exceptionally favorable prognosis. The average mortality 
of all cases of measles, with and without complications, is between four 
and 6 per cent, varying with different epidemics. The mortality is high- 
est during the first three years of life and lowest between the fourth and 
twentieth year. Measles after the forty-fifth to fiftieth year is less favor- 
able than during the more active years of life. 
Complications 
Bronchopneumonia is the gravest of all of the complications of measles; 
one-half to three-quarters of all deaths following measle infection are due 
to it. 
Bronchitis invading the smaller tubes is always a menace and when 
in these cases there is sudden increase of respiration with rising tem- 
perature and active playing of the accessory muscles of respiration, the 
development of secondary bronchopneumonia may be expected, and the 
prognosis is correspondingly serious. In some of these cases atelectasis 
may follow bronchiolitis—always a serious complication—or it may accom- 
pany or follow bronchopneumonia. 
Bronchopneumonia is a complication of measles in epidemics of average 
severity and duration in from five to eight per cent of all cases. The 
mortality of bronchopneumonia varies in different epidemics and ranges 
between 40 to 70 per cent. 
Measle infection invites the development of pulmonary tuberculosis 
and lights latent tuberculous diseases into activity. Besides this, the 
glandular system is so changed by the infection that it offers a suitable 
habitat for the tubercle bacillus from which long periods after infection, 
tuberculosis may spread. This is particularly true of the bronchial nodes 
in measles as well as whooping cough and other non-tuberculous infections 
of the upper respiratory organs. In some cases the tuberculosis resulting 
runs an acute and rapid course. 
Laryngitis may at times he severe, considerable edema may be present, 
and at times, ulceration; recovery is the rule. Croup with modern treat- 
ment offers a favorable prognosis. 
Whooping cough accompanying measles always increases the dangers 
of complications; bronchopneumonia is always to be feared and likely to 
be fatal with this combination. 
Ulcerative stomatitis or the usual less severe forms add painful symp- 
toms, but without further complication recovery follows slowly. 
Cancrum oris (Noma) is always serious, it may lead to large loss of 
tissue and has in my experience proved fatal in three-fourths of all cases. 
Otitis media suppurativa is present in about 7 per cent of all cases 
of measles, usually during convalescence. But few cases receiving prompt INFECTIONS OF UNKNOWN ORIGIN 
345 
attention lead to serious complications, such as mastoiditis, sinus throm- 
bosis or consecutive meningitis. 
Non-tuberculous adenitis, enlarged lymphatic glands following measles 
—usually in the cervical region—are likely to be associated with adenoids, 
and under surgical treatment and improved hygienic surroundings yield 
promptly. 
Persistent enlargement of cervical glands after measles even without 
fever or evidences of cheesy degeneration should be considered to be of 
tuberculous origin. Prognosis and treatment should he accordingly 
framed. 
Diarrhea and other symptoms of gastroenteritis early or late, may 
weaken the child but offer a favorable prognosis in the absence of other 
complications. 
Jaundice has never complicated my cases. It has been reported by 
others (Friedjung), with favorable outcome. 
Heart complications are rare. The malignant cases promptly show 
vasomotor paralysis, the governing spinal centers are soon fatigued by the 
toxins, and there are also degenerative changes in the myocardium itself. 
Nephritis is rare; it is not as serious as with scarlet fever and only 
rarely does it lead to death. If present it runs a benign course and leads 
to recovery and full restoration of kidney tissue in from three weeks to 
two months. 
Permanent damage to the eye resulting from catarrhal conjunctivitis 
is unusual. Occasionally with Tceratitis slight opacities have remained. 
Brain complications are usually secondary when late. Early convul- 
sions in young children are not always of serious import. Early delirium 
and the typhoid condition are present in the severer infections and with 
complicating meningitis and bronchopneumonia. They may also follow 
or accompany otitis, mastoid invasion and nephritis. 
Tuberculous meningitis may promptly follow measles; in the majority 
of these cases latent deposits were stimulated to activity by the added 
infection. Rarely is measles followed by polyarthritis with or without 
mild endocarditis; the same is true of pleurisy. The prognosis of these 
complications is good. 
Roily contends that when scarlet fever complicates measles, the prog- 
nosis is usually good; when however measles is added to existing scarlet 
fever, the course of the measle infection is severe and long and the mortal- 
ity is higher. 
The association of measles and ivhooping cough has already been men- 
tioned in connection with bronchopneumonia as a serious complication. 
Diphtheria (positive presence of the diphtheria bacillus in the dis- 
eased tonsils, etc.) when coincident with measles, is likely to prove serious 
and justifies a guarded forecast; when measles follows after diphtheria has 
run its course, the prognosis is decidedly better—usually full recovery 
results. 346 
SPECIFIC INFECTIOUS DISEASES 
References 
Friedjung. Allgem. Wien. med. Ztschr., 1910. 
Roily. Mohr & Staehelin, Handbuch der Inneren Medizin. 1911, i. 
VI. German Measles 
{Rotheln, Epidemic Roseola, Rubeola, Roseole epidemiqu 
German measles is an acute contagious disease of uncertain origin, 
epidemic or endemic; in its typical development it includes a rash, 
inflammation of the cervical lymphatics, and moderate elevation of tem- 
perature. It is less contagious than measles, and is probably transmitted 
by fomites. 
Second attacks are frequent. 
Children between the ages of two and ten are usually attacked. 
The period of incubation is unusually long—fourteen to twenty days. 
The disease is so mild in its manifestations that the physician’s usual 
function is to satisfy the parent by his differential diagnosis and the 
assurance of prompt recovery of the patient in from four to eight days. 
Cases with severe symptoms are exceedingly rare. 
Occasionally an epidemic includes cases in which separate symptoms 
are severe, as general lymphatic enlargement and slight nervous mani- 
festations, with possible convulsions in the younger children, hut these 
too make satisfactory recoveries. 
Recrudescence and relapses are occasional experiences. 
Complications 
Complications are infrequent. In our experience we have rarely been 
called to attend a child for any sequel of German measles. 
Among the complications mentioned by others are, bronchitis, wdiich 
always yields to treatment promptly; bronchopneumonia, which, rarely 
present, is less dangerous than with other exanthemata, as measles; acute 
gastroenteritis of transitory duration; and mild, slight enlargement of 
the thyroid gland with tenderness; and in some cases persistence during 
several months of enlarged lymphatics. 
Koplik has reported abortive cases without marked enlargement of 
lymphatics, no eruption, slight febrile movement leading to prompt 
recovery. 
Reference 
Koplik. Arch. f. Kinder krankh... 1900. INFECTIONS OF UNKNOWN ORIGIN 
347 
VII. Yellow Fever 
{Black Vomit, Fr. Fievre jaune, Span. Fiehre amarilla, Span. Vomito 
negro or prieto, I tat, Febbre gialla, Ger. Gelbes Fieber, Lat. Typhus 
icteroides) 
Yellow fever is an acute pestilential infectious disease, epidemic, of 
uncertain origin, conveyed by the mosquito, Stegomyia fasciata (calopus), 
which in the past has raged in tropical and insular America between 
the 45° north and 35° south latitude. The disease is characterized by a 
fever continuing for two or three days, followed by a marked remission 
which may end either in convalescence or the patient may pass into a 
critical stage in which there is “black vomit,” jaundice, hemorrhages, 
albuminuria, possible suppression of urine, and a typhoid condition with 
mental and nervous symptoms. 
The disease is always dependent on a temperature not lower than 
70° T., hence the epidemic ends with the first frost. 
The disease was brought to San Domingo and Porto Pico by Colum- 
bus in 1493 in all probability. It rages along river and ocean fronts and 
is not likely to make much headway in country districts. Crowded cities, 
especially the neglected parts near the water, suffer most during epi- 
demics. Filth, marsh, faidty sanitary conditions invite the mosquito and 
spread the disease. 
Any American writing on the prophylaxis and prognosis of yellow 
fever must be stimulated by the achievements of American medicine. 
What the unselfish and practically unrewarded sacrifices of Walter Peed, 
Carroll, Lazear, Agramonte in the Western Hemisphere, and Myers of 
the Liverpool Commission, which resulted in the control of the disease 
in tropical and insular America, with the practical application by Colonel 
Gorgas of the facts thus furnished have accomplished for mankind, can- 
not be fully estimated today. The “Augean stables”1 have been cleansed, 
cities have been made safe, commerce, formerly stagnant during epidemics 
and long after, has been extended without obstacle, and the Panama Canal, 
the greatest achievement of modern times, has been completed, connect- 
ing the Atlantic and Pacific oceans, at the same time transforming a zone 
formerly pestridden into an inviting and healthy country. 
There has been no serious epidemic in the United States since 1897 
when the disease last raged in Hew Orleans with a much lower death 
rate than during former epidemics. In all probability the disease will 
be completely effaced and the writing of the chapter on its prognosis will 
consequently prove to be a work of supererogation. 
Special Considerations.—There are a few points bearing on the progno- 
sis which should be considered. The degree of the fever of the period 
of invasion is usually in direct proportion to the severity of the disease. 348 
SPECIFIC INFECTIOUS DISEASES 
The more rapid the pulse the more serious is the infection. 
Early black vomitus or hemorrhage is always serious. 
The collapse following the fall of temperature may promptly end life, 
for in no other disease does the heart muscle degenerate so rapidly as in 
yellow fever. Fatty granules displace the normal muscle; the heart cavi- 
ties are filled with dark brownish black blood. 
With the end of the remission in the serious cases symptoms referable 
to various internal organs present. Deep jaundice with hemorrhagic 
tendencies, profuse black vomit and albuminuria with casts, or complete 
suppression of urine make the prognosis bad, and with these symptoms 
from 50 to 60 per cent of patients have died. 
Disappearance of albumin and casts, and return of urinary function 
are favorable indications. 
Cases without deep jaundice, hemorrhages and with hut slight albu- 
minuria, few casts, moderate vomiting after remission offer a favorable 
prognosis. 
Large bloody stools are often found with profuse black vomit and are 
an expression of hemorrhage, and are serious. 
Free perspiration during the first stage is always favorable. 
An algid state of the patient at any time, with collapse, with or with- 
out hemorrhages, is among the most dangerous conditions presented by the 
yellow fever patient. 
Hemorrhage is a cause of death in a proportion of cases. 
Ecchymotic spots with multiple symptoms are unfavorable. 
Hemoglobin is reduced. White blood corpuscles vary between 5,000 
and 20,000. Polynuclears are increased; eosinophilia is rare. Ilemo- 
globinemia and hypoleukocytosis are to be expected in the average cases. 
Marked degenerative changes in the liver are present and accompany 
the serious cases, with deep jaundice, great collapse and associated neph- 
ritis. In spite of great weakness following the first stage of the disease, 
those patients are likely to recover who do not have a return of fever, 
whose skin does not become dusky, and who are without typhoid symptoms. 
Rapid pulse in the second stage of the disease with typhoid or brain 
symptoms, including stupor, sordes accumulating on the teeth, dark and 
dry foul tongue, increasing jaundice, occasional convulsions, and suppres- 
sion of urine are unfavorable. 
If the patient enters the third stage, and the temperature shows a 
decided rise and many of the untoward symptoms mentioned in the pre- 
ceding paragraph are present, death is likely to follow. 
The period from the fifth to the seventh days is most ominous. 
No case of yellow fever is safe until convalescence has been fully 
established. 
The negro is less susceptible to yellow fever than is the white man, 
and when infected bears the disease better. There is a difference of 30 INFECTIONS OF UNKNOWN ORIGIN 
349 
per cent in the mortality in some epidemics between the death rate of 
whites and blacks. 
The Chinese are more resistant than whites. 
The American Indian is but little less liable to the disease than is 
the European (Davidson). 
The larger number of victims are claimed between the twentieth and 
fortieth years of life. Yellow fever is more fatal to men than to women; 
children bear the disease better than do adults. 
Immunity follows a single attack of the disease: exceptions to this 
are rare. The mortality varies in different epidemics from 15 to 85 per 
cent and is highest among alcoholics; lower in precincts where hygienic 
conditions are good. 
Reference 
Davidson. Allbutt & Rolleston, System of Medicine, ii., part ii. 
VIII. Foot and Mouth Disease 
The disease rarely occurs in man. It is characterized by the forma- 
tion of vesicles, blebs and bullce in the mouth, nose, lips, on the tongue 
(often with salivation), and on the fingers and toes. The bacteriologic 
cause of the disease is unknown. The disease is contracted from cattle— 
goats, sheep and pigs. The udder and mammary glands of cattle are often 
diseased and from these sources the disease may be spread. 
The contagion may be conveyed through milk, butter, cheese, sputum, 
nasal secretions; particularly by the rich cream of the infected animals. 
Boiling the milk destroys the disease-producing power, simple heating 
does not. Direct contact with the infected does not cause the disease 
save in the rarest instances: the skin of workers in dairies is seldom 
infected. The most frequent cause is the drinking of raw milk, rich 
cream and milk products (cheese, etc.). 
The formation of vesicles is associated with more or less febrile move- 
ment in man. The buccal mucosa is the most frequent seat of the vesicular 
eruption after a period of incubation varying from two to ten days. 
Fever with malaise, and often other evidences of constitutional disturb- 
ances, are present from the beginning. Dryness and burning sensation 
in the mouth are among the disagreeable symptoms. The vesicles appear 
on the third to sixth days of the disease with a fall of temperature and 
salivation. The symptoms in the adult need cause no alarm in spite of 
an added diarrhea in some cases. In very young children, nurslings par- 
ticularly, who are infected, depleting diarrhea may occasionally cause 
death and the prognosis is less favorable than in the adult. Symptoms 
are likely to persist during two weeks in mild cases, as long as four to 
eight weeks in the severer infections, with considerable loss of flesh and 
strength. The healing process is complete, the ulcers left by the vesicles 350 
SPECIFIC INFECTIOUS DISEASES 
are promptly covered with epithelium and the neighboring inflammation 
subsides. 
The lesions about the fingers and toes are characteristic. Vesicles or 
bullse form, leading to limited superficial losses of tissue, often pus de- 
posits about the nails (paronychia)—all of which heal in from two to 
eight weeks. 
The average duration of the disease is fourteen days. In occasional 
large epidemics the mortality has reached eight per cent. 
When there are doubts concerning the diagnosis, consequently prog- 
nosis as well, these may be overcome by the inoculation of sheep or goat 
with the serum or pus of the vesicle. 
Prophylactic measures will ultimately lead to the extermination of 
the disease, for it is easy to recognize the presence of the epizootic in a 
dairy and to institute prompt quarantine against the infected cattle and 
the milk. 
IX. Ephemeral Fever 
(Febricula, Symptomatic Fever) 
Ephemeral fever is a febril condition of short duration and of un- 
known origin, which in all probability is symptomatic and hardly deserves 
to he dignified as a disease per se. 
It has always seemed to me that whenever the clinician has been 
forced to diagnosticate “Ephemeral fever” he admits ignorance of the 
cause of the febrile disturbance. Symptomatic fever would in all proba- 
bility better characterize the complex; than “ephemeral fever.” 
Ephemeral fever may be an expression of one of several infections, 
and is in some cases an abortive form of typhoid, paratyphoid, scarlet 
fever, measles, rheumatism (arthritis) or even pneumonia. This con- 
clusion is justified because the disease is found at times of epidemics of 
the above mentioned diseases. Sporadic cases are frequent. 
In children the complex is often coincident with digestive disturb- 
ances due to dietetic errors. It has, in children susceptible to febrile 
movement on slight cause, repeated itself at short intervals during a 
number of years, usually ending, never to return after the seventh to 
tenth year of life. The duration is rarely longer than three days: usually 
from twenty-four to thirty-six hours. I know of no fatal cases of the 
disease. 
X. Infectious Jaundice—Weil’s Disease (1886) 
(Epidemic Catarrhal Jaundice, Morbus Weilii) 
Weil’s Disease is an epidemic acute infection, characterized by gastric 
symptoms, fever, jaundice, constitutional symptoms, albuminuria, and INFECTIONS OF UNKNOWN ORIGIN 
351 
severe muscular pains. There is in severe cases delirium, nephritis, 
hematemesis, melena and epistaxis.- The pulse is rapid in proportion to 
the severity of the infection. 
In the average cases the temperature may be continuously high dur- 
ing from six to seven days. In some of these there may be delirium 
which is not of serious import. 
As a rule, the evidences of constitutional infection begin to improve 
with the end of the first or the beginning of the second week. 
Prostration may appear alarming during several days but if the pulse 
remains of fair character, the disease being self limited, patients bear 
the symptoms through the critical period and recover. The disease 
appears among consumers of meat mainly, and has been found in butchers 
very largely. 
As patients recover, the spleen and liver recede and with the disap- 
pearance of jaundice and albuminuria, normal functions are restored. 
The disease shows a low mortality, though in some endemics it has reached 
10 per cent. 
Relapse after the end of seven to ten days complicates one-half of all 
cases; in some, the fever then continues during three to four weeks; most 
of these recover. Convalescence is slow. In fatal cases there is an in- 
crease of kidney symptoms, and deep invasion of the nervous system; 
purpuric spots cover the body and there are hemorrhages from the mucous 
membranes. Marked heart weakness with myocarditis may end the scene. 
In some cases pneumonic infection may prove a serious complication. 
XI. Sweating Sickness 
(Febris miliaris) 
Sweating sickness is characterized by fever, excessive sweating, and 
an eruption of miliary vesicles. It has never been epidemic in the United 
States so far as I can determine by a search of medical literature. The 
disease proved fatal at the end of the fifteenth century in a large number 
of cases during the first epidemic of which there is a record in England, 
and has been known since in Germany and on the continent as the “Eng- 
lish sweat.” Hirsch in his monumental work reports 194 epidemics 
between 1718-1879. Epidemics begin and end suddenly, and never con- 
tinue long. Large numbers are stricken during epidemics; the active 
and healthy adult and women are most subject to the disease. 
The duration of the disease averages seven days. 
The disease during the initial English epidemic had a high mortality, 
80 to 90 per cent; in recent epidemics, on the Continent, the death rate 
has been 20 per cent. Death took place on the third or fourth day usually. SPECIFIC INFECTIOUS DISEASES 
352 
The prognosis is worse early in the epidemic than after it has spent 
its force and is ending. 
In some cases death has been sudden during the first or second day 
of infection. 
Hirsch. Handbuch der Histor.-Geograph. Pathologie. 2. ed., 1881. 
Reference 
XII. Herpetic Fever 
(Febris herpetica) 
Herpetic fever is a symptom complex of unknown origin, character- 
ized by fever—usually mild—with some constitutional disturbances, in 
rare cases severe, slight enlargement of the spleen. All of these symptoms 
continue during two to five days when the herpetiform vesicular eruption 
appears, usually covering a considerable portion of the body, though at 
times only a cheek and adjacent skin or an ear or the neck; occasionally 
the eruption may become hemorrhagic. In rare cases in which there is 
an hemorrhagic tendency, nephritis hemorrhagica develops. The prognosis 
is good; recovery is the rule; the duration is short. Relapse often occurs 
and is of short duration, lasting about one day. 
XIII. The Fourth Disease 
{Dukes’ Disease, Filaton-Dukes’ Disease, Rubeola scarlatinosa, 
Scarlatinoid) 
This is an acute symptom complex which the Americans and Germans 
have not yet entirely accepted as a disease per se, fully described by 
Dukes, bearing close resemblance to abortive scarlet fever and also rotheln, 
with less desquamation than follows the former but greater than in the 
latter. 
The constitutional disturbances are of short duration; the period of 
transmission of infection is also short, while the period of incubation is 
unusually long (9 to 20, or even 30 days). 
The prognosis is uniformly good and there are no complications or 
sequelae. 
XIV. Epidemic Parotitis 
{Mumps) 
Mumps is an acute epidemic disease, characterized by swelling and 
non-snppurative inflammation of both parotid glands, contagions, of un- 
certain origin, associated with moderate constitutional disturbance, a long 
period of incubation (eighteen days) leading to full recovery in from 
seven to ten days. Immunity follows a single attack with rare exceptions. INFECTIONS OF UNKNOWN ORIGIN 
353 
Complications.—In about 25 to 30 per cent of male adults, rarely in 
young boys, the infection is associated with orchitis, usually single, and 
attacks the right testicle oftener than the left. The complication runs 
its course in from seven to fourteen days causing some atrophy of the 
testicle in from 30 to 40 per cent of cases. In rare cases the changed 
testicle in after years has been found tuberculous. There is but insig- 
nificant enlargement of the spleen. In exceptional cases, a chronic swell- 
ing of the parotid gland follows which persists during many years. 
Among the serious complications reported in medical literature which 
have resulted in death, are meningitis, encephalitis, gangrene of the paro- 
tid, nephritis and laryngitis {croup). Less serious complications have 
included otitis media and externa, Meniere's disease, and insignificant 
ocular disturbances, such as conjunctivitis, keratitis and iritis—rarely 
paralysis of the ocular nerves. Nephritis is rare; slight albuminuria 
with few hyaline casts is present in occasional cases. 
Symptoms referable to the nervous system if serious are an expression 
usually of added infection. There may, in rare cases, be a transitory 
typhoid condition from which the patients promptly lift themselves: this 
is an early complex. 
Serious heart lesions, endo- and pericarditis I have not met in my 
epidemics though others have reported these at long intervals. Poly- 
arthritis when present is of short duration, benign and without endo- 
carditis. 
Severe joint and muscle pains (myalgia) are frequent. I have never 
met a case of oophoritis due to epidemic parotitis. Many hold that there 
is a reciprocal relation which invites change in the ovaries when the paro- 
tid is diseased, and vice versa. 
Mortality.—The low mortality of epidemic mumps is shown by the 
statistics of Ringberg who found seven deaths in 58,331 cases of the 
disease. 
Reference 
Ringberg. Quoted by Krause. Mohr & Staehelin, Handbuch der inneren Medizin. 1911. 
i, 239. 
XV. Glandular Fever—Pfeiffer’s Disease 
(Driisenfieber) 
Pfeiffer’s disease or glandular fever is an acute febrile disease of 
childhood—it also occasionally attacks adults—of uncertain origin, char- 
acterized by headache, dysphagia, congested tonsils and pharynx, by 
enlargement of the cervical lymphatics (usually bilateral) with tender- 
ness ; in some cases many distant glands are involved (axillary, inguinal, 
mesenteric, et cetera). The febrile period ends in from three to seven 
days; the glandular enlargement and pharyngeal redness may appear any 
time between the second and fifth day. 354 
SPECIFIC IHFECTIOUS DISEASES 
In a recent epidemic in Dry den, Hew York, there were as a rule, 
bilateral enlargements of the cervical lymphatics which appeared with- 
out redness of the skin. The children were without marked consti- 
tutional disturbances after the fourth day; the glandular enlargements 
gradually melted away in from seven to twenty-one days. 
In the counties between Central and Eastern Hew York sporadic cases 
have occasionally followed very limited endemics. As a rule in these 
districts the disease has not attacked many children. 
The duration of the disease is short. The fever ends before the 
seventh or eighth day. Recovery has been complete in all cases seen, and 
without complication. Ho case of which I have knowledge has ended in 
suppuration, though such cases have been reported by others; neither has 
nephritis, otitis nor retropharyngeal abscess followed. 
Suppuration has seemed to be more frequent in the adult than in 
children. 
The associated edema of the soft palate and palatine folds may prove 
exceedingly painful and extension to the glottis serious. 
In the anemic, and children otherwise reduced in health, convalescence 
has been somewhat protracted. 
XVI. Hydrophobia 
{Rabies, Lyssa, Wuthrankheit) 
Hydrophobia is a disease the bacterial origin of which is unknown, 
transmitted to man by the bite of rabid animals through the infected 
saliva, especially that of the dog. The deeper the bite the greater the 
laceration and the more saliva introduced, the more likely is hydrophobia 
to follow. 
The majority bitten by rabid dogs never develop rabies. The figures 
given by Romberg, showing 15 to 20 per cent of those bitten to he infected, 
correspond very closely with those of American and other continental 
observers. 
Hydrophobia follows bites of the exposed parts of the body—hands 
and face oftener than bites where clothing has served to protect and hold 
the saliva of the rabid animal. The development of the disease depends 
in all probability upon the injury and infection of the peripheral nerves 
which serve to transmit the infection to the central nervous system, i. e., 
the cord and the medulla. 
An important prognostic fact is the possibility of the transmission 
of the disease from the infected animal to man several days before the 
onset of symptoms in the former. 
The period of incubation is unusually long, varying from one to nine 
weeks—occasionally several months. INFECTIONS OF UNKNOWN ORIGIN 
355 
Those bitten by rabid dogs who have not received the Pasteur treat- 
ment, in spite of a negative condition are not to be considered immune 
until the end of at least three months. 
The healing of the wound inflicted by a rabid animal, in one unpro- 
tected by inoculation (Pasteur), does not in, any way argue against or in 
favor of ultimate infection. 
Burning, itching, throbbing and pain, when not due to autosuggestion, 
are soon followed by swelling, depression, melancholia, malaise, great 
uneasiness and restlessness, anorexia—all positive evidences of the pro- 
dromal stage of the disease. These symptoms may continue from three to 
eight days. The typical uneasiness referred to the throat and mouth 
begins before the end of the first stage. 
The second stage, or period of excitation, is associated with spasms, 
pain in the throat—the latter promptly provoked by the attempt to swal- 
low liquids—alarming dyspnea, cyanosis and irregular breathing, due to 
spasm of the respiratory muscles. 
The frequency of the spasms increases as the disease advances and 
the true “phobia” is fully established; the sight of fluid, the noise of 
running water, the touching or moving of the patient, any jar, noise or 
the passing of a light are each sufficient to provoke spasms. The intervals 
between the spasms grow shorter, and the patient cannot be nourished; 
there may be slight febrile movement, 100-103° F., occasionally higher 
(104-105° F.), the pulse grows small and rapid and after from one to 
three days of spasms varying in different cases and during which death 
may occur, the majority of patients fall into the third stage or stage of 
paralysis, in which the weakness is overpowering. 
There may be paralyses (usually of the extremity bitten) at times 
hemiplegia, or in occasional "cases ascending paralysis. Coma 
and death results from respiratory paralysis in most cases; in some syn- 
cope suddenly ends life. 
The duration of the third stage is from three to twenty-four hours. 
Death may occasionally follow the prodromal period without the symp- 
toms of the second stage of the disease. The third stage (paralysis) 
promptly follows and is of short duration. 
Conclusions.—From the foregoing abstract of symptoms and the course 
of the disease as presented in its three stages, it is clear that the prognosis 
is absolutely bad in all cases of fully developed hydrophobia. Occasional5 
cases have been reported cured, in which it may be assumed that the diag- 
nosis rested on a doubtful foundation. I feel justified in repeating that 
the hope of the subject actually infected lies in the prompt cleansing of 
the wound and the early prophylactic treatment mentioned (the latter is 
now readily obtainable} ; that the greater the laceration of tissues and the 
deeper the bite, the greater is the danger of rabies developing. 
The Pasteur treatment requires three weeks, during which, at inter- 356 
SPECIFIC INFECTIOUS DISEASES 
vals, the patient is inoculated with the virus of rabies (dogs) which has 
been modified by the repeated inoculation of rabbits. The antirabic 
material is an emulsion of the spinal cord of the inoculated rabbits and 
to be effective the prophylactic treatment must have been completed at 
least two weeks before the end of the period of incubation. 
Statistics.—Statistics prove further that of those bitten by rabid ani- 
mals only 0.5 to 1 per cent who have been treated prophylactically, develop 
rabies, against 15 to 20 per cent among the untreated. 
Reference 
Romberg. Die Acuten Infedionskrankheiten von Mehring u. Krehl. 8. ed. 
XVII. Dengue 
(Breakbone, Dandy Fever) 
Dengue is a rare disease except in tropical and subtropical climates. 
It is acute and of unknown origin, characterized by sudden onset, severe 
pains in joints and muscles, fever with cutaneous erythema, and charac- 
teristic stiffness of gait (“dandy gait”). It is usually panepidemic or 
epidemic, attacking a large proportion of the population suddenly. It is 
rarely found above the 41° north latitude, and Manson has expressed the 
opinion that the disease follows slowly along the lines of sea travel. The 
disease is likely to attack entire families, all under a single roof, and 
spreads from house to house along the same street. 
While the specific germ is unknown, Ashburn and Craig proved that 
the disease is conveyed by the mosquito (Culex fatigans). (Investiga- 
tions regarding the Etiology of Dengue Fever, 1907.) 
There have been no epidemics in the Northern United States. The 
last large epidemic in America was in 1897 when 20,000 of Galveston’s 
inhabitants were stricken, with practically no deaths. In a limited epi- 
demic in Charleston in 1828, three deaths were reported. 
From the above data it is clear that the prognosis is good and that 
complications are exceedingly rare. Convalescence may be slow, asso- 
ciated with prostration and weakness, with a persistence of erythema, 
and at times marked inertia and mental torpor. These symptoms yield 
fully, though considerable time is often required for full restoration to 
health. 
The average length of the attack is from seven to eight days. 
Immunity is of short duration, averaging about twelve to fourteen 
months. 
Reinfection during the same epidemic has been noted by several 
clinicians. Section II 
Diseases of the Respiratory 
Apparatus 
A. Diseases of the Nose 
1. Acute Catarrhal Rhinitis 
(Coryza) 
Acute catarrhal inflammation of the nasal passages is either a primary 
infection characterized bv all of the usual changes in the mucosa of catar- 
rhal disease, in which the secretion is materially increased, and finally 
purulent, or secondary to other infections, oftener in children with 
measles, whooping cough, bronchitis, laryngitis, syphilis, scarlet fever, 
diphtheria, or it may follow the use of the iodin compounds in both chil- 
dren and adults (often with idiosyncrasies). 
Children suffering from hereditary syphilis are particularly subject 
to continuous snuffles, as are also those of lymphatic temperament, who 
on the slightest exposure are liable to contract “cold.” 
Both adults and children are subject to “colds” which are transitory 
as a rule, and without complications lead to recovery in a few days. 
Most secondary (infectious) rhinitides are associated with more or 
less pharyngitis; the constitutional symptoms and gravity depend entirely 
on the nature of the primary disease. In all uncomplicated rhinitis the 
disease is self-limited, and does not materially interfere with the patient’s 
activities. With grippal infection, scarlet fever, diphtheria and nasal 
involvement, extension to the surrounding sinuses is possible. With in- 
vasion of the middle ear, there may be mastoid suppuration or final 
pyogenic disease of the brain (meningitis, encephalitis, invasion of the 
veins, etc.). In children, neglect, particularly during periods of influ- 
enza, may lead to extension into the air passages, and final broncho- 
pneumonia. 
Much depends upon the resistance which the subject offers to the 
357 358 
DISEASES OF THE RESPIRATORY APPARATUS 
infection as well as its malignancy. With diphtheria, nasal and glandular 
involvement is always serious (See Diphtheria). 
Syphilitic coryza in children—non-malignant—usually yields to treat- 
ment. If the deep structures are involved, recovery is naturally slow 
(See Syphilis). 
Polypoid growths in adults often continue catarrhal discharges which 
are relieved by radical treatment. There are adults who develop nasal 
catarrh on slight cause, in whom there is also asthmatic breathing. Unless 
there are local disturbances, these symptoms are dependent upon neural 
or constitutional causes—and the prognosis should be given accordingly. 
Catarrhal conditions of the nasal mucosa are often continued by 
pharyngeal adenoids. In these cases, usually children, the removal of the 
succulent growths brings relief. These patients are always worse during 
wet seasons. Children with lymphatic enlargements (cervical) and nasal 
catarrh dependent upon local lesions demand prompt attention, and are 
cured by modern radical treatment. The recurrence of coryza in the 
hypersensitive adult and child is favorably influenced by treatment which 
increases resistance. 
2. Hay Fever 
(Bose Cold, Autumnal Catarrh) 
Most cases of hay fever are found in subjects who are predisposed to 
catarrhal disturbances, when have an abnormal and sensitive naso-respira- 
tory mucosa. The leading clinical features of hay fever which follow 
the action of the pollen of certain plants, grasses, or the inhalation of 
irritating dust, are catarrhal and spasmodic. The catarrhal symptoms 
include coryza, free discharge, conjunctivitis; the spasmodic, repeated 
sneezing and asthmatic attacks. 
Naturally the pollen of a certain plant being the cause of the symp- 
toms in the individual case, the onset of the symptoms corresponds with 
its appearance in the air, and the release must be materially influenced 
by its disappearance and the immunity which it produces. The latter is 
short lived and questionable. 
The prognosis of hay fever for life is good—it is self-limited and 
subject to recurrence. Complications are exceedingly rare. Occasionally, 
for some reason, without change of climate during subsequent seasons of 
pollen irritation, the complex does not return. There are probably no 
cases of rose cold which are not favorably influenced by climatic change. 
I have never met a death directly traceable to autumnal catarrh, nor 
a single extension to the air cells to cause bronchopneumonia. The asth- 
matic breathing and paroxysms disappear with the nasal symptoms. 
Emrys-Roberts has demonstrated an interesting blood picture in con- DISEASES OF THE NOSE 
359 
nection with hay fever and asthma, which includes increased eosinophilia 
coincident with the asthma. He believes that there is an alteration in 
the blood picture, which besides the eosinophilia includes a decrease of 
hemoglobin, marked polycythemia, and increase in large mononuclear 
lymphocytes, the presence of vacuolated and degenerated leukocytes and 
a degree of leukopenia. “An altered, but modified blood picture persists 
during the intervals between the seasonal attacks.’’ 
Occasional cases have been benefited by the surgical treatment of 
local anomalies; considering the number treated, the results so far as 
the relief of nasal and respiratory symptoms during the periods of exacer- 
bation, have not been encouraging. 
The influence of vaccination against hay fever is at present sub judice; 
its influence on the control of the disease cannot be decided without fur- 
ther investigation. Lowdermilk claims good results from the use of toxin 
extracted from pollen with the addition of an autogenous vaccine, in all 
cases complicated by the presence of a bacterial infection (Freeman, I.). 
Dunbar’s investigations justify the use of his pollantin; if his con- 
clusions are correct, relief and a moderate added immunity ought to 
follow. In the majority of cases it will be found that at present we have 
no remedy which positively aborts the symptoms. Cocaine, used by 
physicians or patient,’ can only lead to temporary relief and encourages 
the formation of an enslaving drug habit. 
3. Epistaxis 
{Nosebleed) 
Nosebleed which is not due to mechanical insult (traumatism) is 
dependent upon lesions of the nasal mucosa (ulceration, catarrhal inflam- 
mation, dilated or diseased veins) or it is secondary to constitutional 
defects, including the hemorrhagic diathesis, purpura, scorbutus, hemo- 
philia, the grave anemias, leukemias, carcinomatosis, malignant and non- 
malignant infections, sepsis, malignant endocarditis, typhoid fever, yellow 
fever, measles, smallpox, scarlet fever, pertussis, icterus and various 
poisonings. 
Nosebleed is often an early evidence of arteriosclerosis, it may 
recur repeatedly with this condition; particularly does this happen with 
associated interstitial nephritis and hypertension. It may prove a salu- 
tary warning; slight bleeding with uncomplicated arteriosclerosis is 
insignificant. 
Nosebleed is a frequent symptom of heart lesions and cirrhosis, or 
other liver lesions. 
Epistaxis is not to be considered pathologic if moderate, when sudden 
changes to a high altitude cause it. Occasionally nosebleed may be an 360 
DISEASES OF THE RESPIRATORY APPARATUS 
expression of vicarious menstruation and is of no importance. The sig- 
nificance of nosebleed which is secondary to the conditions above men- 
tioned has been fully considered in connection with the separate infec- 
tions; with malignancy it is always grave, also with the constitutional 
diseases and grave anemias. 
ISTosebleed per se does not often threaten life. In the exceedingly 
weak, with hemophilia, grave anemias, severe and uncontrolled bleeding 
does occasionally hasten death. Children during the period of growth, 
very often have recurring nosebleed which ceases at puberty; it is with- 
out significance. With the diseases of the ductless glands I have occa- 
sionally found insignificant nosebleed; one of my cases of acromegaly 
had frequent recurrences without ulcerative changes in the mucosa. 
B. Diseases of the Larynx 
1. Acute Laryngitis 
Acute catarrhal laryngitis may be either primary or secondary. 
Primary laryngitis is rarely associated with significant constitutional 
symptoms; occasionally there may be slight elevation of temperature, but 
this is evanescent, and barring the discomfort due to the changed larynx, 
hoarseness and cough, there are no evidences of illness. Such laryngitis 
runs its course in a few days to a favorable termination. Most cases show 
some associated inflammation of the trachea. When the larynx is 
inflamed from strain, the symptoms disappear after a short period of 
laryngeal rest. 
The severity of laryngitis which is secondary depends entirely on the 
primary cause. With corrosive poisoning, edema may promptly follow 
or the swelling may be sufficient to cause asphyxia. Life is threatened; 
prompt surgical or local relief is demanded in such cases. 
The acute laryngitis of croupous diphtheritic origin is separately con- 
sidered (See Diphtheria). 
With measles, in occasional cases, laryngo-tracheitis causes alarming 
symptoms which may be complicated by bronchopneumonia. Without the 
latter complication most of these children recover (See Measles and 
Bronchopneumonia). 
Acute laryngitis with edema following fracture of the larynx or other 
wounds may prove dangerous. Foreign todies caught in the larynx may 
cause laryngitis and swelling. These conditions are within 
the domain of the surgeon, who with modern devices succeeds in relieving 
most of them. 
Primary or secondary catarrhal laryngitis in children often causes DISEASES OF THE LARYNX 
361 
symptoms of croup and is known as “catarrhal croup” or “Pseudocroup.” 
It is as a rule found in children who are subject to catarrhal laryngitis, 
and who whenever they “catch cold” are “croupy.” In some there is 
slight elevation of temperature. This condition, when uncomplicated, is 
relieved in a few days after a period of cough, hoarseness and nocturnal 
increase of symptoms. Sudden increase in the frequency of the respira- 
tions with rising temperature and pulse, create the suspicion of compli- 
cating bronchopneumonia. 
The laryngeal picture of laryngitis, when uncomplicated, will prove 
reassuring and is an aid in foretelling the course of the disease—also in 
diagnosticating the subglottic form, which mjay prove serious. The im- 
provement of tbe general condition of the patient, the relief of associated 
lesions of the nasopharynx or other inflammatory conditions in the upper 
air passages, the relief of a rheumatic diathesis when present, favorable 
housing, climatic conditions (environment)—all prove powerful factors 
in not only relieving these patients in the acute attacks, but in preventing 
their return and final chronic laryngeal change. 
2. Chronic Laryngitis 
Chronic laryngitis is either primary or secondary. 
The cases which follow repeated acute attacks (primary) can only be 
cured by long periods of rest, often climatic changes. 
Chronic primary laryngitis due to the continuous inhalation of dust, 
tobacco or other irritating substances, if unrelieved leads to organic changes 
in the vocal cords, which continue annoying. ISTone of these cases are 
relieved if repeatedly subjected to the factor which causes them. Laryng- 
ologists are agreed that but few laryngitides of the chronic type are pri- 
mary, “except from the improper use of the voice” (Ballinger). 
Secondary laryngitis may he due to nasal, nasopharyngeal or tonsillar 
disease. Removal of the primary lesion acts favorably on the laryngeal 
changes. 
Chronic gastritis due to alcohol is frequently associated with chronic 
laryngitis, as are also cirrhosis of the liver, chronic gastro duodenitis, 
heart lesions causing venous enlargement, mediastinal growths of Hodg- 
kins and leukemic origin and long residence in an unfavorable climate. 
The prognosis in all of these cases necessarily depends upon the depth 
of the change (hypertrophy, atrophy, polypoid or other productive lesions) 
and the ability to remove the underlying cause in the individual case. 
The voice in chronic alcoholics who have had long-continued symptoms 
often remains hoarse in spite of the discontinuance of stimulants. 
Pulmonary tuberculosis and chronic bronchitis, chronic interstitial 
pneumonia (the pneumoniokonioses) may be complicated by non-tuber- 
culous chronic laryngitis—persistent and often unyielding to treatment. 362 
DISEASES OF THE RESPIRATORY APPARATUS 
3. Edema of the Larynx 
{Edematous Laryngitis, Edema of the Glottis) 
Primary laryngitis may cause marked edema of the larynx. As a 
rule edema of the larynx is secondary to vascular obstruction, dependent 
upon the pressure of growths—malignant or non-malignant (cervical- 
mediastinal, etc.); heart, kidney, lung lesions, constitutional diseases—- 
diabetes, syphilis, the grave anemias (pernicious and leukemic), also 
purpura. 
Syphilitic tuberculous ulcerations may cause edema of the larynx. 
The general dropsies of nephritis at times include sudden edema of the 
glottis. 
Peritonsillar suppuration (quinsy) may suddenly cause edema of the 
glottis, as may other infections which cause cellulitis or perichondritis, 
including erysipelas, Ludwig’s angina, and malignant growths of the neck. 
With measles, typhoid fever, scarlet fever, diphtheria or other infec- 
tions, the glottis may become edematous; life is always threatened when 
such edema exists—it causes acute and alarming symptoms, whether de- 
pendent upon grave underlying causes or conditions which uncomplicated 
do not threaten life. This is particularly true of angioneurotic edema 
(Quincke’s disease) separately considered. We have seen one case of 
diabetes in which there was one-sided swelling of the larynx, demanding 
immediate operation. 
Edema due to injury, foreign bodies and surgical affections is men- 
tioned in connection with the laryngitides. 
The laryngoscope leads to the recognition of the extent of the danger 
and often suggests treatment which prevents fatal asphyxia. The imme- 
diate prognosis for life must always depend upon the ability to overcome 
the obstruction and prevent recurrence. Our art (laryngology) is so far 
advanced that whatever the primary cause, but few will lose their lives 
from the edema itself who are treated early and rationally. 
The organic diseases of the vital organs which serve as the most fre- 
quent cause of edema of the glottis usually terminate fatally. 
4, Laryngismus stridulus 
{Spasmodic Laryngitis) 
The “holding of the breath” by the child is the characteristic feature 
of laryngismus stridulus. Spasm of the glottis may be caused by a 
variety of laryngeal and nervous disturbances. It is an affection of the 
nervous system of infant life (6 months to 3 or 4 years) and is often 
provoked by emotional causes. Children often while crying “hold their 
breath” without any serious result. I consider spasm in connection DISEASES OF THE BRONCHI 
363 
with tetany and infantile convulsions, to which section the reader is 
referred. 
The majority of my cases have been found in children with neurotic 
tendencies, rachitic, underfed, and emotional. Some of these show the 
characteristic reactions of tetany. The spasm involves the diaphragm as 
well as the adductors of the larynx and for the fraction of a minute the 
appearance (cyanosis) alarms the parent. The inspiratory stridor which 
follows is always welcome to the over-anxious observer. Probably the 
deaths which have been attributed to laryngismus stridulus are charge- 
able to the status thymolymphaticus. I have never in our practice seen 
a death from laryngismus stridulus. 
Adult stridulus is occasionally met in practice; it may be hysterical or 
evidence of another neurosis. It is not serious. 
The laryngeal crisis of tabes dorsalis includes characteristic stridor 
and may recur at short intervals without serious result. 
Mueller (Fr.) claims that in rare cases laryngeal crises may cause 
sudden death by asphyxia. 
3. Tuberculous Laryngitis 
See Tuberculosis, Section I, B. 
6. Syphilitic Laryngitis 
See Syphilis, Section I, A. 
References 
Ballinger. Disease of the nose, throat and ear. Philadelphia, 1914. 
Dunbar. Deutsch. med. Wchnschr., 1911, xxxvii, 578—583. 
Emrys-Roberts. Blood in hay fever. British Med. J., 1914, 1176—1178. 
Freeman (J.). Vaccination against hay fever. Lancet, London, 1914, i, 1178-1180. 
Lowdermilk (R. C.). Hay fever. J. Am. Med. Ass., 1914, Ixiii, 11+1- 
Mueller (Fr.). von Mehring u. Krehl. 8. Aufl., Jena, 1913, Bd. i. 
C. Diseases of the Bronchi 
1. Acute Bronchitis 
Acute bronchitis is one of the most frequent of all diseases, at the 
same time one of the most benign. It is easily the most frequent of all 
diseases of the respiratory tract. The majority of acute cases are pri- 
mary, more frequent during the fall and winter months always mate- 364 
DISEASES OF THE RESPIRATORY APPARATUS 
rially influenced by sudden climatic changes and exposure. In otherwise 
healthy subjects, without added complications, it offers an absolutely 
favorable prognosis. 
Many acute bronchitides begin as laryngeal or pharyngeal catarrh 
and descend after a day or two of local symptoms. 
Bronchial Catarrh.—Bronchial catarrh is associated with more or less 
tracheitis. The bronchi are symmetrically inflamed (both sides) and the 
medium-sized bronchi are mainly involved. The bronchitis of early life 
and old age when neglected or extensive is likely to extend to the smaller 
bronchi; hence it is always serious and there is great danger of secondary 
bronchopneumonia. The bronchiolitis of early and late life is often sec- 
ondary and is a complication of influenza, measles, whooping-cough, diph- 
theria and other infections. 
When in the young or old, bronchopneumonia develops with bron- 
chiolitis, or disseminated bronchitis extends to the capillaries and air cells, 
an enormous element of danger is added. (See Bronchopneumonia.) 
The prognosis of bronchopneumonia following the bronchitis of measles 
and whooping-cough is always grave (see Measles and Whooping-cough), 
particularly in very young and feeble children. 
Atelectasis—collapse of air cells—is one of the serious complications 
of bronchiolitis and bronchopneumonia. With bronchiolitis or fully de- 
veloped islands of bronchopneumonia, and extensive collapse of air cells 
(atelectasis) the condition of the patient is always serious—marked 
cyanosis and cardiac insufficiency may end the scene. 
Whenever with acute bronchitis there is persistent high temperature 
and respiration is correspondingly accelerated, the possibility of compli- 
cating pneumonia should be considered. 
In uncomplicated bronchitis the acute symptoms begin to yield on the 
third or fourth day; the expectoration becomes more profuse and purulent; 
the acute symptoms (malaise, slight fever, anorexia and cough) show 
marked improvement, and uninterrupted return to health is the rule. 
Dyspnea and rapid respiration in all cases when present demand im- 
mediate interpretation; they are not symptoms of uncomplicated bronchitis. 
Cough may not cease entirely before the end of the second week. If 
it persists beyond that time and there is some evening temperature, with 
or without acceleration of the pulse, the suspicion of a tuberculous infec- 
tion in the absence of other infection or cause should be strongly enter- 
tained, and the case treated (watched) accordingly. 
Heart weakness in the aged and infants with disseminated bronchitis 
is always of serious import. 
Primary uncomplicated bronchitis in otherwise healthy individuals 
always leads to recovery. The virulence of primary infections with which 
bronchitis may be associated must always be considered to be of para- 
mount importance. DISEASES OF THE BRONCHI 
365 
Acute bronchitis, complicating chronic heart lesions, nephritis or 
other visceral diseases may seriously influence the prognosis. The prog- 
nosis in these cases depends largely on the general condition of the patient, 
the resistance and the extent of the bronchial infection. The same is 
true of bronchitis as it arises suddenly with cerebrospinal meningitis, 
polyarthritis, cqronary disease, pulmonary emphysema, mitral lesions, 
rachitis, sepsis, typhus and smallpox. 
2. Chronic Bronchitis 
Chronic bronchitis may follow acute catarrhal bronchitis. As a rule, 
chronic bronchitis depends upon long-continued hyperemia of the bron- 
chial mucosa which is secondary to pulmonary obstructions and dependent 
upon valvular lesions, weakness or disease of the right ventricle, pulmonary 
emphysema, the pneumonokonioses; particularly the inhalation of dust 
laden air. With chronic bronchitis there is but little tendency toward 
return of the membrane to a normal state. While the atrophic or hyper- 
trophic changes are not overcome, life may not be threatened, for some 
of the patients live to reach old age and many die of intercurrent disease. 
Bronchiectasia and bronchial stenosis may result from long continued 
bronchitis. Chronic bronchitis is a frequent cause and accompaniment of 
pulmonary emphysema. With this complication the right heart is over- 
taxed, and finally dilates and hypertrophies. 
There are forms of chronic bronchitis which are materially affected 
by seasonal and climatic influences. Thus with “winter cough” the 
patient may cough or have symptoms only during cold weather, and is 
promptly relieved by climatic treatment. Most chronic bronchitis is favor- 
ably influenced by warm weather or by a dry equable climate. 
There are cases in which chronic change in the mucosa causes an exces- 
sive mucopurulent secretion with cough and final secondary heart and 
trophic changes—clubbed fingers (See Chronic Pulmonary Arthropathy). 
These cases are exceedingly chronic; they are types of bronchorrhea. In 
these as in most chronic types of bronchitis there is more or less peribron- 
chial proliferative change. The dry bronchial catarrh of Laennec is at 
once exceedingly troublesome and chronic, because of the persistent dry 
cough, with only the occasional expectoration of a small pearl-shaped plug 
and the secondary heart changes, emphysema with dyspnea, which are 
practically uncontrollable. 
Chronic bronchitis dependent upon chronic heart lesions is often mate- 
rially relieved during long periods by the improved condition of the myo- 
cardium. But few of these cases cease coughing entirely during the peri- 
ods of improvement, but they remain comparatively comfortable. In a 
large number, the cough with excessive expectoration (bronchorrhea) con- 366 
DISEASES OF THE RESPIRATORY APPARATUS 
tinues without materially interfering with the general condition of the 
patient. The primary disease always determines the outcome. 
Any form of bronchitis may be associated with asthma, and in most, 
emphysema is more or less developed. 
While as above stated chronic changes in the bronchi do not tend to 
mend, the outcome so far as life is concerned is not discouraging, save 
as it is influenced by the primary circulatory or other faults which cause 
the disease, or by the secondary lung or heart changes which the bronchitis 
itself produces. 
Chronic bronchitis with “fixed thorax” may he materially improved in 
well selected cases by plastic operations on the thorax (See References). 
Chronic purulent bronchitis with asthma (purulent bronchorrhea,) and 
emphysema may be associated with polypi, adenoids, or nasal perfora- 
tions; while the majority are not cured by radical surgical treatment of 
the nasopharyngeal anomalies, many are materially relieved. Climatic 
and seasonal changes influence these cases favorably. 
Chronic putrid or fetid bronchitis is secondary to gangrene of the lung, 
empyema, tuberculosis, syphilitic or malignant disease. These cases are 
not curable; the length of life is measured by the primary cause and its 
extent. Distant secondary changes (metastases) may promptly end life 
(brain abscess, infarct, amyloid disease, etc.). 
3. Bronchiectasis 
Dilatation of the bronchi may he either (1) congenital or (2) ac- 
quired. 
(1) The congenital type (Grawitz) (bronchiectasis universalis) is ex- 
ceedingly rare. Most congenital cases have been found to he unilateral. 
There is no treatment which influences these defects; the amount of dis- 
turbance and influence on the life of the child depends upon the extent 
of the bronchiectasis. In those who live, secondary pulmonary and heart 
changes must he expected. 
(2) The acquired brochiectasis is always secondary. Reference is 
made to bronchial dilatations in connection with infectious pulmonary dis- 
eases and chronic bronchitis (See separate sections). 
Classification.—Barty King classifies the acquired bronchiectasis as 
follows: 
1. Chronic bronchitis. 
2. Bronchopneumonia. 
3. Chronic pneumonia. 
4. Pneumonic. 
5. Pleuritic. 
A. Pure 
B. Tuberculous. 
C. Traumatic 
Bronchiectasis 
1. Aneurism. 
2. Tumor. 
3. Foreign body. 
4. Syphilis. DISEASES OF THE BRONCHI 
367 
All bronchiectases are either (a) diffuse or cylindrical, or (b) circum- 
script or saccular. 
(a) The diffuse or cylindrical forms are not as a rule extensive. 
(b) The circumscript or saccular forms are either single or multiple. 
In severe cases a section of the lung shows the appearance of innumer- 
able saccular dilatations resembling multiple cavities. 
Symptoms and Course of Complication.—The symptoms and course of 
the complications depend on the size and number of the bronchiectatic 
cavities, the character of their contents and the amount of constitutional 
disturbance caused by absorption and the nature and extent of the primary 
lesion. 
Causes and Development of Bronchiectasis.—The most frequent cause 
of bronchiectasis is chronic inflammation of the bronchial wall which is 
associated with or is a sequel of measles, whooping-cough and influenza— 
usually during early life. A large number of bronchiectatic cavities which 
develop during early life increase in size with advancing years. In these 
cases the walls are thickened by growth of connective tissue. With chronic 
bronchitis there may be no advance in the size of the cavities or there may 
be diffuse dilatation of many bronchi which increases (Aschoff). With 
pressure from tumors or stenosis due to the presence of a foreign body, 
syphilitic cicatricial tissue following ulceration, tuberculous ulcerations or 
aneurismal growths, the cavity, one or many, may increase and the symp- 
toms are correspondingly aggravated. 
Associated Symptoms.—Atelectasis and bronchiectasis may be associ- 
ated conditions. If the former is extensive and arises suddenly, the dan- 
gers are at once apparent because of cyanosis, respiratory and circulatory 
embarrassment. In children and in the aged with bronchopneumonia, 
acute bronchiectasis with or without atelectasis is always serious and usu- 
ally leads to death. The symptoms which are associated with good sized 
dilatations are characteristic. Cough may be absent during the larger 
part of the day, troublesome early in the morning when it is accompanied 
by the emptying of the pocket which brings relief. The size of the cavity 
may be approximately decided by the quantity of secretion (expectoration) 
which it holds. 
The complications depend, as already hinted, upon the primary causes 
and the changes consecutive to the dilatations—local and constitutional. 
The average chronic case without excessive and multiple dilatations 
lives on, never without some symptoms, but in fair health; not a good 
subject for added infection—pneumonia particularly. With extensive and 
multiple dilatations and excessive purulent secretion, with fetid expectora- 
tion the prognosis is always grave. Patients, with febrile movement after 
many years of invalidism become septic, develop anemia (secondary), are 
exhausted and emaciated, and often die with advanced amyloid degen- 
eration in many organs. We have seen cases, particularly syphilitic, re- 368 
DISEASES OF THE RESPIRATORY APPARATUS 
main stationary and in good general health after intensive treatment dur- 
ing many years. 
4. Bronchial Asthma 
Bronchial asthma is a neurosis, usually of reflex origin; characterized 
hy paroxysmal dsypnea, narrowing of the bronchi by spasm, hyperemia or 
exudation; commencing suddenly, as a rule; soon accompanied with loud 
wheezing breathing, spasmodic cough, prolonged and defective expiration, 
in which the respiratory muscles are all overtaxed, the lung is distended, 
expectoration is usually profuse, there is associated bronchitis and emphy- 
sema, and in chronic cases changes in the heart, thorax and blood—all of 
these symptoms are without attending fever. 
Charcot-Leyden crystals (small colorless octahedra) are found in the 
sputum in most cases and are not of prognostic significance, neither are 
the Curschmann spirals. Curschmann considered the presence of the 
spirals as positive proof of inflammation of the finer bronchi (bronchio- 
litis exfoliativa). The presence of blood in the sputum is not necessarily 
or usually ominous; in the severer attacks the sputum is at times bloody. 
Large hemoptysis is not a symptom of primary asthma. Eosinophilic cells, 
usually present in the sputum, are of no prognostic significance. The 
individual attack may end in less than one hour; as a rule it continues 
several hours (2 to 4). Severe attacks may continue during several days 
with only slight and not complete remission. 
Meltzer in 1910 called attention to the resemblances of asthma to 
anaphylactic shock and offered the suggestion that “it is an anaphylactic 
phenomenon.” Certainly there are a number of facts which strengthen 
the theory of Meltzer, particularly those which prove the frequency of 
recurrence under similar conditions and exposure to the same causes which 
prove hypersensitivness, abnormal reaction, or as Meltzer says “asthmatics 
are individuals who are sensitized to a specific substance.” 
The disease is not fatal per se. There are facts which prove the enor- 
mous influence of a psychic element in inviting and continuing symptoms, 
particularly in neurotic individuals in whom no organic lesion can be 
found. In some cases suggestion has been powerful in determining the 
onset of attacks. West mentions the presence of premonitory symptoms 
which if heeded may abort or prevent the paroxysm—“like the aura in 
epilepsy.” 
Trousseau a sufferer from bronchial asthma had his attacks with 
great regularity “as the clock struck three in the morning.” . 
One attack usually leads to more; it is unusual to find one attack the 
only paroxysm during the entire life of the patient. The more frequent 
the attacks, the lighter they are, as a rule, though there are exceptions to 
this. Postponing of attacks or increasing the length of the intervals is DISEASES OF THE BRONCHI 
369 
favorable and in some cases such behavior is followed by almost complete 
immunity. 
Heredity.—Heredity is a factor of some importance in connection with 
prognosis. It is noted in about 2 of 5 cases. Salter’s statistics in 217 cases 
showed 84 with a strong heredity, and often direct from parent to child 
and through several generations. Salter and West report the occurrence 
of asthma among several children of a family without the disease in the 
parent. The prognosis for complete relief is better in the cases without 
inherited taint. 
Sex.—Salter’s statistics show 153 cases of which 102 were males, and 
51 females. 
Age.—Asthma in young children often disappears after one or more 
attacks. Salter offers the following table to show the age at the time of 
the first attack in 225 asthmatics: 
During 1st year 
1-10 years 
11 cases 1 
\ 81 • 
per 
cent. 
10-20 years 
30 cases 
12.8 
per 
cent. 
20-30 years 
39 cases 
17. 
per 
cent. 
30-40 years 
44 cases 
19. 
per 
cent. 
40-50 years 
24 cases 
9. 
per 
cent. 
50—60 years. 
5 
per 
per 
cent. 
60-70 years 
1.4 
cent. 
70-80 years 
1 case 
0.4 
per 
cent. 
Salter says that the chances of cure are good when asthma develops 
before the age of 10 years; if before 20 it may be cured; if between 20 
and 40, it will probably not be cured; if after 60 it will certainly not be 
cured. 
Occupation.—Occupation is not of as much importance in etiology or 
prognosis as is generally supposed. Those most exposed are not likely to 
develop asthma unless they are predisposed and work in an atmosphere 
of dust. It has seemed that those who use their voices most are subject 
to asthma (preachers, lawyers, school teachers, etc.) hut this remains with- 
out confirmation. Once present, occupations which continue irritating, pro- 
voke seizures and prevent long periods of immunity. 
Additional Influences and Symptoms.—Gouty and diabetic families 
show a surprisingly large number of asthmatics, and in these the prognosis 
for complete freedom is not encouraging. In young children the associa- 
tion of intractable eczema and asthma is striking and frequent. A num- 
ber of our cases with this combination proved subject to pneumococcus in- 
fection. In one child we had, as a complication, four threatening broncho- 
pneumonias during four consecutive winters. This boy has grown to man- 
hood cured of both asthma and eczema. Another active chap with the 
same clinical picture, was less fortunate; he died in his third broncho- 
pneumonia. 
Asthma is comparatively frequent with urticaria. Bulkley’s figures 370 
DISEASES OF THE RESPIRATORY APPARATUS 
are high (7 per cent). Asthmatics both young and old, are as a rule, unusu- 
ally active and alert and when at work are strenuous. 
Location and climatic conditions are of great importance in most cases 
but there are absolutely no indications which the individual case offers 
which can lead the clinician to determine the location or climate which will 
most favorably influence the majority of “idiopathic asthmas.” Most 
asthmatics, it may he safely concluded, are favorably influenced by change 
to a higher altitude, particularly if they are living in the lowlands. Pa- 
tients are able to get some relief from 'postural change, particularly by 
raising the shoulders and the scapulae. Clavicles and spine are fixed, the 
patient leans forward, the hack is curved, the head rests on the hands, 
the anteroposterior diameter of the chest is increased while the diaphragm 
is depressed and the respiratory effort is extreme as it raises the ribs. 
The respirations are long, noisy, wheezing, though not abnormally rapid. 
Profuse expectoration gives considerable relief, while in the more trou- 
blesome attacks the sputum is scanty and the asthma “dry.” 
Blood Pictuke.—The leading characteristic of asthmatic blood is 
eosinopliilia. The eosinophils are often increased to from 10 to 40 per 
cent of the leukocytes. Higher counts are recorded. Early in the attack 
the eosinophils are usually reduced hut soon there is a decided increase; 
with the decrease of eosinophils early, there is a lowering of the lympho- 
cytes and the polymorphonuclear cells increase. Later in the attack 
there is evident eosinophilia, as suggested above with marked lympho- 
cytosis, all of which fall as the attack is relieved. Asthmatics often 
show persistent lymphocytosis. But little of value for prognosis is gained 
from blood examination though in the terminal stages of some secondary 
asthmas (heart and pulmonary lesions) polycythemia may he present. 
General Considerations.—I have elsewhere mentioned the paroxysmal 
breathing, cyanosis, and asphyxia which lead to sudden death (thymic 
death) now known as the status thymo-lymphaticus. This is not to be 
confounded with bronchial asthma. 
Cardiac asthma is usually a terminal symptom of heart or cardiovas- 
cular disease in which myocardial degeneration is the prominent feature 
and in which pulmonary edema is likely to lead to death. 
Renal asthma is not unusual with nephritis in which the heart muscle 
is advanced in degeneration and uremia may he chronic or acute. The 
heart is erratic, feeble and arhythmic, and with increasing evidences of 
cardiac and respiratory insufficiency—pulmonary edema—death follows. 
There are cases dependent upon gastric or gastro-intestinal or hepatic 
disease, either organic or functional. Many asthmatic paroxysms may he 
traced to faulty digestion or organic disease of the digestive apparatus in 
which diet and radical treatment exert a marked and favorable influence on 
the asthmatic attacks. When asthma is symptomatic of grave organic dis- 
ease (cardiac, renal, pulmonary or gastric) the prognosis is had; this, DISEASES OF TIIE BRONCHI 
371 
however, is not veritable asthma. Spasmodic or bronchial asthma which 
is a neurosis as originally defined in this chapter, is the only variety which 
should be included in the consideration of true asthma. 
With vagotonia of Eppinger and Hess (see Diseases of the Sympa- 
thetic System) the subjects develop asthma with the other symptoms in- 
cluded in the complex (increased susceptibility to pilocarpine, nervous 
dyspepsia, hyperacidity and erratic heart) and are materially relieved 
by adrenalin. As in hay fever, so in vagotonic asthma the eosinophilia 
is characteristic. 
There are occasional asthmas which seem reflex from some genito- 
urinary disturbance. Menstrual anomalies, pregnancy and uterine dis- 
placements in the female, and sexual disturbances and neurasthenia in 
the male have occasionally been considered among the causes. Most of 
these patients are neurotics and are influenced by suggestion rather than 
by radical treatment in most cases. 
There is practically no danger to life during the attack. There are 
so few cases recorded in which death occurred during an attack that it 
may be safely assumed that in these there was some complication. Fagge, 
Franzee and Bamberger each report one case of death during the asthmatic 
attack. Asthma does not per se shorten life. It has been noted that 
asthmatics often live to old age. I saw the case of a salt boiler who 
had asthma over 60 years and died at about 90 years of age. In chronic 
asthmatics with marked secondary changes including emphysema and 
heart lesions (dilated right ventricle) life may be shortened by such com- 
plications. In young subjects and in the aged there is danger from bron- 
chopneumonic infection. 
The association of asthma and tuberculosis is strikingly rare, though 
in some cases the x-ray shows calcified and tuberculous glands in asthmatic 
subjects (Fr. Mueller). When attacks increase in frequency and severity 
at the same time and their length increases, the chances of cure are re- 
mote. The chances of relief are increased by decreasing severity of the 
attacks and lengthened intervals. The positive discovery of the cause 
of the reflex materially improves the chance of amelioration or cure. I 
have often been disappointed by radical nasal treatment in cases which 
seemed to depend upon nasal growths or other anomalies, though occa- 
sionally success either complete or partial has followed. 
West says: “Although it is clear from what has been stated that there 
is more in the relation of nasal irritation to asthma than has been until 
recent years believed, and although most marked relief is given in some 
cases, still so far as we know at present it is impossible to recognize be- 
forehand with certainty the cases in which relief will be given and those 
in which it will fail.” The conclusions of West are sound and safe to 
follow in offering a forecast in those cases in which some nasal abnormal- 
ity seems to be the irritant. 372 
DISEASES OF TILE RESPIRATORY APPARATUS 
Asthma sometimes disappears after intercurrent disease or it may 
alternate with other and graver diseases of the nervous system. Salter, 
Lloyd, and Taylor report cases in which asthma alternated with epilepsy; 
Trousseau reports the cure of asthma after gout but persistent hemicrania 
followed. Eulenberg records a parallel case in which asthma alternated 
with hemicrania and angina pectoris. Savage and Conolly Xorman prove 
the relation between asthma and insanity; the two affections alternate at 
times. There was freedom from asthma so long as the insanity contin- 
ued; on cure asthma returned. 
Long-continued asthma, while it does not, as already suggested, shorten 
life without some added complication, in the advanced stage may lead to 
the “fixed thorax” with emphysema and all the associated physical signs. 
In these cases dyspnea may finally he continuous and with heart changes, 
dilatation of the right heart, edema of the lung may develop and threaten 
life. I have seen two cases, in extreme condition, relieved hv plastic 
operation on the thorax. The improvement of both was prompt and 
seems to continue. But few chronic asthmatics are without evidences of 
incurable chronic bronchitis between their paroxysms. 
Secondary asthma depending on pressure of growths upon the pneumo- 
gastric offer no hope of relief. Among the most distressing cases of 
asthma are those due to metastases or primary growths (mediastinal). 
In many of these the dyspnea and cough are paroxysmal, the breathing 
noisy and characteristic of true asthma. In the terminal stages with 
these conditions the breathing is continuously bad with marked cyanosis. 
To prevent serious accident or death ‘the anaphylactic action of diph- 
theria and other antitoxins administered to asthmatics demands serious 
attention in the presence of the diseases for which these are used. 
References 
Bamberger. Quoted by Staehelin [l. c.], 372. 
Bulkley (L. Duncan). British Med. J., 1885, ii. 
Eppinger & Hess. Die Vagotonie; Samml. klin. Abhandl., etc., von Noorden. Hft. 9-10. 
Berlin, 1910. 
Eulenberg. Nervenkrank., Berlin, 1871. 
Fagge. S. West. [Z. c.], 589. 
Franzee. Quoted by Staehelin [l. c.], 372. 
Lloyd & Taylor. Lancet, London, June 10, 1893. 
Meltzer (S. J.) Transactions, Assoc. Am. Physicians, 1910. 
Mueller (Fr.). Ztschr. f. arztl. Fortbild. 1912, No. 14- 
Salt er {Hyde). On asthma, its pathology and treatment. 2. ed., London, 1868. 
Savage & Norman. J. Mental Sci., April, 1885. 
Insanity. 1889. 
Staehelin. Mohr & Staehelin; Ilandbuch der inneren Med. Bd. 2., Berlin, 1914. 
Sokolowski. Brustkrankheiten. Berlin, 1906. DISEASES OE THE LUNGS 
373 
Trousseau. Clinical Medicine, Paris; also quoted by S. West [Z. c.]. 
Unger. Arch. f. klin. Med., xxi, 455. 
West (S.). Diseases of the organs of respiration. London, 1902. 
5. Fibrinous Bronchitis 
(Croupous Bronchitis) 
Eibrinous bronchitis may be either acute or chronic. When acute 
it is usually secondary and molds—fibrinous casts of the bronchi—are 
formed because of descending croupous inflammation with diphtheria, 
occasionally with croupous pneumonia or any pseudomembranous disease 
of the upper respiratory organs. With all of these conditions extension 
into the finer bronchi and air cells with the formation of casts adds enor- 
mously to the danger of the primary disease. Caustic poisons may in 
rare cases cause fibrinous bronchitis. In occasional malignant neoplasms 
of the lung casts of the bronchi have been formed. 
Primary fibrinous bronchitis is exceedingly rare. In an active prac- 
tice of over thirty ears I have seen but one case. This was chronic; 
it commenced in a girl at the age of eight years. Casts of the bronchi 
formed without materially affecting her growth or general condition, vary- 
ing at intervals during six years, after which she made a full recovery and 
has never, after thirty odd years, had recurrence. Ho treatment influ- 
enced this case; it ran its course and the habit of making casts was lost. 
This patient never had asthma during the active years of the disease. 
6. Whoopinjj-Coujjh 
See Infectious Diseases (Section I). 
D. Diseases of the Lungs 
(The Pneumonias and Pulmonary Tuberculosis are considered in Sec- 
tion I—Infectious Diseases.) 
1. Circulatory Disturbances of the Lunjjs 
Congestion 
(a) Active 
(b) Passive 
(c) Edema of the lungs. 
(a) Active Congestion of the Lungs (Woillez disease).—It is 
questionable whether active congestion of the lung ever exists as an inde- 374 
DISEASES OF THE KESPIRATORY APPARATUS 
pendent disease. Most of these cases have been strongly suggestive of 
abortive pneumonia. Woillez in 1854 called attention to congestion pul- 
monair e idiopathique, which develops after chilling of the surface (usu- 
ally from a fall into cold water or injury of the thorax) and in which there 
is sudden chill, some fever, pleuritic pain, cough, dyspnea and expectora- 
tion which settles in two layers one frothy and yellowish, the other muci- 
laginous ; usually there are pneumococci present. In occasional cases the 
expectoration is absent. The symptoms run a favorable course in four 
or five days. There is leukocytosis. The disease in rare instances runs 
a more protracted course but ends in recovery. 
Active hyperemia not depending on pneumonia, with sunstroke, inha- 
lation of poisonous gases or acute miliary tuberculosis is of no clinical 
importance (Staehelin), and of such rare occurrence that its occurrence 
is questioned. 
(b) Passive Congestion.—Passive congestion of the lung may fol- 
low mechanical obstruction secondary to tumor, insufficient heart force or 
decompensation. The condition is always secondary and serious because 
of the gravity of the initial disease. In the terminal stages of malig- 
nancy, constitutional diseases, the wasting and acute diseases of the aged, 
with valvular lesions, most frequently initial disease, chronic and acute 
nephritis, and purpura, passive congestion may develop, and in some con- 
tinue long enough to produce brown induration (Aschoff). 
I have, with all primary disease to which passive pulmonary hyper- 
emia may be secondary, dilated on its prognostic significance. Unless 
the circulation can be sufficiently stimulated or the pressure removed when 
present, the prognosis is absolutely bad. 
The suddenly arising engorgement of the pulmonary vessels witli 
heart disease is usually associated with edema (See heart lesions, also 
pulmonary edema). Hypostatic congestion of the lung is always secon- 
dary; it is a frequent attendant of all long continued infections and in 
these cases causes engorgement of the dependent portions of both lungs, 
as a rule. It is almost constantly present with pneumonia, severe typhoid 
infection, the infections of old age and early life; when in the latter they 
are serious when the patient has been kept on the back during long periods. 
Hypostatic congestion may prove a serious complication with fractures of 
the hip and other bones, particularly in delicate old and non-resistant 
patients. With marked dyspnea, cyanosis and weak heart, also with 
edema, the prognosis is grave. 
Hypostatic congestion with the majority of infections does not lead 
to death or materially influence the chances of recovery unless it is exten- 
sive, and the heart is enfeebled by overpowering toxemia. Postural change 
and other prophylactic treatment do much to prevent the development and 
advance, when present, of the complication. 
With cerebral apoplexy, opium poisoning, brain tumor and other brain DISEASES OF THE LUNGS 
375 
lesions, uremia and a variety of other unfavorable 'primary diseases hypo- 
static congestion may prove to be the leading cause of death. 
(c) Pulmonary Edema.—Edema of the lung is never to be lightly 
regarded whatever the primary condition which causes it. References 
to the clinical and prognostic significance of pulmonary edema are fre- 
quently made in all separate sections dealing with conditions which may 
cause it. There is no more alarming condition, none which demands 
prompter relief that life may he prolonged than that which presents when 
the patient is literally drowning in his own serum. I say “life pro- 
longed” for in the larger number of cases pulmonary edema is secondary 
to grave conditions. On the other hand, there are occasional edemas from 
which patients make full recoveries; these are with such underlying con- 
ditions as can be relieved, or they do not recur. I have found among 
my favorable cases the edema secondary to acute nephritis, to sudden 
cardiac insufficiency with acute infections, pneumonia, typhoid, measles, 
myocardial weakness with endocarditis and polyarthritis, specific aortitis, 
coronary sclerosis and myocardial degeneration; in all of these active 
treatment proved sufficient to bridge the patient over the critical period. 
The unfavorable hypostatic congestions are those in which the heart 
is so far degenerated or the toxemia so malignant that response to general 
and local stimulation is impossible. I have called attention (see Pneu- 
mococcemia) to those rapidly fatal cases of pneumonia in which the air 
cells are promptly filled with blood serum which in a few hours drowns 
the patient. With nephritis, heart insufficiency, arteriosclerosis, the prog- 
nosis in the presence of an acute pulmonary edema is bad. With angina 
pectoris and acute edema the chances of recovery are small. In many 
of these cases overeating is an important exciting factor of the attack. 
With any heart lesion which leads to insufficiency—decomposition— 
the addition of edema is life threatening. 
With emphysema and heart {right) dilatation, suddenly arising edema 
leads to cyanosis and often to death. These patients are usually among 
the more chronic and debilitated. 
Sudden edema with obesity and fatty heart, is, as a rule, fatal. Angio- 
neurotic edema may cause edema of the lung; it is rarely fatal—in 
fact it is not frequent. I have seen epilepsy with edema recover. Any 
cause which weakens the left heart sufficiently to interfere with the pul- 
monary circuit and cause edema, as already strongly hinted, unless promptly 
relieved will lead to death. 
The duration of the single edema of the lung in severe cases cannot be 
long, for when severe, it is associated with such reduced myocardial strength 
that death is likely to follow soon. Pulmonary edema by rigorous treat- 
ment with fatal primary conditions may be overcome. It is likely to 
recur, and may finally claim its victim. 376 
DISEASES OF THE RESPIRATORY APPARATUS 
Aschoff. Path, anatomie. Jena, 1913. 
Davis. British Med. J., 1910, i, 257. 
Frankel. Specielle Pathol, u. Therap. der Lungenkrank. Berlin, 1904. 
Jores. Deutsch. Arch. f. klin. Med., Bd. Ixxxvii, 389. 
Woillez. Arch. General de Med., Paris, 1854, i, 385. 
References 
2. Pulmonary Hemorrhage 
(a) Hemoptysis 
(b) Pulmonary Infarct 
(a) Hemoptysis 
Coughing or raising of blood from the air passages is symptomatic 
of many primary conditions; the most frequent cause of blood spitting is 
tuberculous disease of the lung (See Tuberculosis). 
Hemorrhage from the pulmonary vessels may be due to traumatism 
when the nature of the injury and extent will make prognosis easy. Ac- 
tive hyperemia causing hemoptysis is inflammatory in most cases. The 
causes are acute pneumonia, tuberculosis, and Staehelin mentions ma- 
laria. With pneumonia we have never seen hemoptysis sufficiently pro- 
fuse to deplete the patient or cause weakness. The pure bloody sputum of 
pneumonia is not encouraging—such complication is found in the graver 
cases. (There are occasional exceptions.) 
The hemorrhages—hemoptysis of malignant growths, rarely cause 
serious weakness. In the terminal stage occasionally large vessels may be 
eroded, and weakness already extreme becomes threatening. 
Vicarious menstruation may include hemoptysis which, aside from the 
psychic effect of the bleeding, is without depressing or weakening effect. 
Ulcerative disease of the upper air passages, pharynx, larynx and tra- 
chea may cause slight hemoptysis. Hemoptysis due to mitral stenosis 
often relieves the patient’s breathing; it rarely causes more than transitory 
weakness. In all such cases the possibility of tuberculosis should be con- 
sidered. 
Wilson has grouped his cases of hemoptysis in heart disease in three 
principal groups: 
“(1)Those in which with an antecedent or concomitant lesion of the 
heart, the hemoptysis is essentially of pulmonary origin, as in tuberculosis, 
croupous and sometimes bronchopneumonia, infarct, acute and chronic 
bronchitis, emphysema, bronchiectasis and malignant growths.” 
“(2) Those in which vascular structures are the seat of hemorrhage, 
as aneurism, erosion caused by foreign bodies or malignant growths, and 
primary and secondary diseases of the blood.” 
“(3) Those which are primarily and essentially of cardiac origin.” DISEASES OE THE LUNGS 
377 
In the first two groups the prognosis is grave as the primary disease 
undermines resistance and the hemoptysis is profuse. In this chapter we 
consider the hemoptysis from many of the sources mentioned without asso- 
ciated heart disease, the latter naturally under certain conditions adds to 
the danger. With a good myocardium, and in the majority of cases be- 
cause of the limited loss of blood, the prognosis is good so far as the 
hemoptysis is concerned, except in aneurism. All clinicians have noted 
that moderate hemoptysis in mitral stenosis is usually followed by material 
relief of dyspnea and other cardiac symptoms. Mackenzie says that with 
mitral stenosis “at various stages the patients may be seized with great 
bleeding from the lungs. There doubtless the cause is the back pressure 
in the pulmonary circulation and rupture of the blood vessels. As a rule, 
this is a grave sign, the patient dying sometimes shortly after the attack.” 
We have not often met these large hemorrhages with mitral stenosis. 
In most hemoptyses due to heart lesions the immediate prognosis is good; 
naturally the course of the disease is molded by the nature of the primary 
heart defect. 
The bleeding of pulmonary gangrene is not as a rule profuse; in one 
case we saw a fatal hemorrhage—this is exceptional. 
The slow bleeding of the aortic aneurism is ominous, while the rupture 
of the sac into the air passages is always promptly fatal. Aneurismal bleed- 
ing from whatever vessel into the bronchi, whether slow, sudden or profuse, 
leads to death. 
With chronic bronchitis blood streaked sputum is frequent. Hemop- 
tysis is rarely profuse. The admixture of blood is usually due to violent 
coughing. Ho significance need be given to this bleeding. 
With whooping-cough and measles in children and adults during vio- 
lent paroxysms, hemoptysis often occurs without influencing the general 
condition. 
With syphilitic ulceration of the upper air passages, hemorrhage is not 
often severe. There is usually only a slight addition of blood (See 
Syphilis). 
With malignant purpura, hemoptysis may be either slight or it may be 
profuse. When it is present it is only one of several complicating condi- 
tions with profound constitutional changes and should be accordingly in- 
terpreted (See Purpura; also Scurvy). Some cases which often look 
serious finally recover. 
Hemophiliacs occasionally bleed freely from the bronchial mucosa, 
particularly when there are catarrhal or other inflammatory changes. The 
general and circulatory condition of the patient, the blood state, the 
nature of the primary disease, and the quantity of blood lost make progno- 
sis possible and usually correct. 
Hemoptysis with arteriosclerosis and chronic interstitial nephritis in 
gouty subjects particularly, will usually prove more alarming than serious; 378 
DISEASES OF THE RESPIRATORY APPARATUS 
the underlying primary disturbances make prognosis possible. The loss 
of blood is not usually great. 
Abscess of the lung rarely causes large hemorrhage; with a persisting 
cavity there may he repeated small hemorrhages. In these cases the 
blood and pus are mixed. These slight bleedings do not influence the 
course of the primary disease materially. 
Profuse hemorrhage from any cause into the air cells may, particu- 
larly in patients weakened and reduced by chronic disease, lead to suffo- 
cation or heart weakness. 
The presence of blood in the lung may by aspiration to distant parts 
of either lung—if it holds pathogenic germs (the pneumococcus particu- 
larly)—lead to acute inflammatory processes, just as, after pulmonary 
hemorrhage in tuberculosis, the bacillus and other microorganisms may 
he aspirated to dependent parts of the lung, and acute pneumonic tuber- 
culosis may result. 
(b) Pulmonary Infarct 
(Pulmonary apoplexy) 
Wedge-shaped (usually) or other infarcts into the lung tissue are 
dependent upon chronic heart lesions, malignant or septic infections with 
embolism or thrombosis of the pulmonary artery, mechanical obstruction 
from pulmonary or circulatory anomalies which produce the characteris- 
tic 'heart lung.” If the blood effused is not great, there may he hut slight 
hemoptysis and few subjective or objective symptoms. In such cases the 
clot is finally expectorated as a black or dark purple airless lump (West, 
S.). If there is extensive infarct (malignant endocarditis and other 
septic conditions, chronic nephritis) an entire lobe of a lung is suddenly 
filled. It is impossible always to tell from the hemoptysis how extensive 
the infarct may be. I have seen large infarcts with but little blood 
spitting. In these cases the physical signs, dyspnea, and heart condi- 
tions decide the immediate prognosis. 
Infarct of a large branch of the pulmonary artery or sudden obstruc- 
tion with myocardial insufficiency (left ventricle) in which with hemop- 
tysis the subjective symptoms are severe, promptly leads to death. 
Pulmonary infarct may, after varying periods of hemoptysis, lead to 
pulmonary gangrene with change in the expectoration; these patients die 
with symptoms of sepsis. The conditions which lead to the majority of 
pulmonary infarcts are serious and are separately considered with the 
infections, heart and other lesions. There are many chronic heart and 
other lesions in which pulmonary infarcts do not lead to death; they may 
recur. We have, with chronic cases of malignant endocarditis had re- 
peated hemoptysis due to infarcts from which the patients have rallied, 
to die of brain infarcts or other complications. Multiple infarcts are not 
infrequently found in many organs of the body, post mortem. DISEASES OF THE LUNGS 
379 
Mackenzie {James). Diseases of the heart. Oxford, 1910; also 1808, 226. 
Samson (4. E.). Allbutt & Rolleston, System of Medicine. 1909, vi, 866. 
Staehelin. Mohr & Staehelin, Handbuch der Inneren Med. Bd. ii, Berlin, 1914. 
West (S.). Diseases of the organs of respiration. ii., London, 1902. 
Wilson {J. C.). Bloodspitting in heart disease. Transact, of the Amer. Climatological 
Ass. 1913, xxix, 40. 
References 
3. Chronic Non-tuberculous Pneumonia 
Included in this consideration of Chronic Non-tuberculous Pneumonia 
are: 
(a) Chronic pneumonia. 
(b) Chronic interstitial pneumonia. 
(c) The pneumonokonioses. 
(a) Chronic Pneumonia 
There are occasional cases in which the exudate present in the air cells 
in the third stage of pneumonia remains unchanged and continues an 
irritant, producing changes which lead to chronic pneumonia. These are 
the so-called cases of delayed resolution or unresolved pneumonias. As 
already suggested (croupous pneumonia) the majority of “unresolved 
pneumonias” prove ultimately to be tuberculous; they are cases of em- 
pyema, or the persisting symptoms are due to some other added complica- 
tion. It is however possible for delayed resolution or “unresolved 
pneumonia,” either fibrinous or catarrhal, to lead to chronic, non-tubercu- 
lous changes in the lung. The tendency is toward the proliferation of 
connective tissue and carnification. There is, with both types of pneu- 
monia which become chronic, more or less peribronchitis with the changes 
mentioned. It is impossible to differentiate these cases from chronic inter- 
stitial pneumonia; indeed, the pathology of both is identical when the 
disease is fully developed. Further references to the prognosis of chronic 
pneumonia are therefore included in this chapter. 
Chronic pneumonia is usually the outcome of the atypical types of the 
acute disease; it often follows measles and whooping-cough in children 
who are burdened by diatheses (tuberculous or rachitis), and in all cases 
there is great danger of the ultimate tuberculization of the lung. 
(6) Chronic Interstitial Pneumonia 
(1ST on-Tuberculous ) 
{Chronic Pneumonia, Cirrhosis of the Lung, Fibroid Phthisis) 
Chronic interstitial pneumonia is a productive inflammation of the 
lung, characterized by the formation of fibrous tissue ivhich is the product 380 
DISEASES OF THE RESPIRATORY APPARATUS 
of granulation tissue, causing induration and contraction of the organ. 
The process may be peribronchial or interalveolar. 
A large number of these cases follow chronic pleurisy and empyema 
(pleurogenous pneumonia). The disease is therefore associated with 
dense adhesions which lead to retracted and misshapen thoraces with re- 
sulting respiratory embarrassment and further secondary changes, to 
which I will again refer. 
Mediastinal growth, aneurism, abscess of the lung, peribronchitis, 
syphilis of the lung, hydatid disease and traumatism are among the causes 
of pulmonary fibrosis to be considered in making the prognosis. 
(c) The Pneumonokonioses 
( Zenker) 
Pneumonokoniosis is an occupation disease in which there is fibrosis 
of the lung. The disease may be caused by the inhalation of dust, flour, or 
other noxious substances. 
The inhalation of coal dust (antliracosis), steel dust (Zenker’s sidero- 
sis), stone particles (silicosis)-, mineral dust (chalicosis) and cotton 
(byssinosis) are among the leading causes of fibroid proliferation in the 
lung. 
In most of these cases the greater changes are in the apices of the lung 
where macroscopically there are abundant evidences of fibroid growth, 
misshaped and contracted lung, and collapse of large portions of the lung, 
while other changes are included which must be appreciated to justify safe 
prognosis. 
General Conclusions 
The prognosis of (a) chronic pneumonia following the acute lobar in- 
fection is often good. This is true of those cases in which the process is 
limited—the fibrosis does not extend—where there are no secondary heart 
changes, and after a reasonable time the lung learns to adapt itself to the 
slight abnormality which remains unchanged. This forecast is applic- 
able to chronic lobular pneumonia of limited extent. 
When the process is extensive, patients are made uncomfortable be- 
cause of cough, respiratory insufficiency, consecutive heart changes, and 
resulting deformities. They may live during many years and die of in- 
tercurrent disease, but they are never well and their activities are limited 
unless perchance they are favorably influenced by climatic conditions. 
Bronchiectasia, atelectasis, tuberculization, right heart insufficiency and 
stasis within the pulmonary, portal, and renal systems (ultimate dropsies) 
are among the complications which influence prognosis. 
The further consideration of the prognosis of (b) chronic (non-tuber- DISEx\SUS OF THE LUAGS 
381 
culous) interstitial pneumonia, and (c) the pneumonokonioses, justifies 
the following conclusions: 
Unless the process is due to specific deposit (rare) there are no means 
at our command which influence existing fibroid changes. 
Cases of pleurogenous origin may live during many years in compara- 
tive comfort without advance of the process; if the heart has accommo- 
dated itself to the changed conditions there are no threatening symptoms. 
These patients are easily fatigued and are often short of breath. 
In all chronic cases the heart offers valuable prognostic data. The 
right heart is naturally overtaxed by the obstruction in the pulmonary 
circuit and with extensive fibrosis, dilates; this leads to hypertrophy with 
accentuation of the second pulmonic sound. With advancing disease the 
dangers of myocardial insufficiency and degeneration are added. 
In the terminal stage, the patient’s life is threatened by the resulting 
obstruction in the venous system, causing in turn cyanosis, liver and kid- 
ney changes, splenic hyperemia, ascites and edema. 
The extent of the bronchiectasis and atelectasis in these cases is a 
powerful and unfavorable factor with failing heart strength. 
The involvement of the bronchial glands (lymph nodes) is of great sig- 
nificance and often lays the foundation for extension of tuberculosis. 
A surprisingly large number of chronic interstitial pneumonias includ- 
ing the pneumonokonioses develop tuberculosis. 
We found in the knife grinders who worked over emery wheels, before 
the modern protective appliances were installed, that all developed chronic 
interstitial pneumonia; that over 90 per cent of these who lived over ten 
years, showed positive evidences of pulmonary tuberculosis. We have 
found the workers in an American knife factory who came from Sollingen, 
Germany, where they had previously worked and who had continued at 
their work more than five years, that, in spite of modern appliances, all 
of them showed evidences of siderosis; many of these have died of tubercu- 
losis. 
The chronic interstitial changes of the workers in coal mines and in an 
atmosphere of coal dust, as has been proved by experiences in America 
and oil the continent, rarely become tuberculous. “All forms of chronic 
interstitial pneumonia may develop and die of tuberculosis” (Jiiergem 
sen). Juergensen makes the following statement: “I hesitate to diagnose 
interstitial pneumonia and to exclude tuberculosis so long as there is 
normal physical strength and great mental activity, a quiet and strong 
heart.” 
The chronic pneumonia offers reduced resistance to acute infection, 
and many die of acute pneumonia. 
Restitution to full health is impossible. The process due to the pneu- 
moniokonioses is often stayed when not too far advanced. When the pa- 
tient changes climate and his work, he may live many years. 382 
DISEASES OF THE RESPIRATORY APPARATUS 
The prognosis is often influenced unfavorably by an intolerant stom- 
ach due to consecutive hyperemia. 
Persistent evening rise of temperature, with accelerated pulse and loss 
of weight are'unfavorable, and suggests tuberculosis or some other added 
infection. 
Emphysema, when limited, is physiologic, when extensive it adds to 
the respiratory embarrassment and is unfavorable, increasing the work of 
the right heart. 
With bronchiectatic cavities there may be absorption of septic and 
pyemic organisms, which reduce vitality and lead to serious constitutional 
disturbances. 
Uncomplicated non-tuberculous cases have only rarely caused alarm- 
ing hemoptysis in our experience. Heredity materially influences the in- 
cidences of the tuberculization of chronic pneumonics. 
Children of tuberculous parents are handicapped. 
The prognosis is more favorable in the adult than in children, so far as 
length of life is concerned. 
Apex fibrosis is less favorable than is change at the base of the lungs. 
Persisently rapid pulse, regardless of other symptoms is always 
ominous, and demands the most cautious search for its cause; usually the 
complication of which it is an expression is serious. 
Reference 
Juergensen. Ziemssen, Handbuch der spec. Path. Therapie. 1877. 
4. Emphysema 
{Pulmonary Emphysema) 
Emphysema is a condition in which the air cells are abnormally 
dilated and the lung enlarged. Surgical emphysema, the escape of air 
into the pulmonary walls, following injury or surgical operation is not 
included in my consideration of this subject. 
Vesicular or pulmonary emphysema may be either 
(a) Compensatory 
(b) Hypertrophic 
(c) Atrophic. 
(a) Compensatory emphysema 
Compensatory emphysema develops when after collapse of lung tissue 
or extensive consolidation, unaffected portions of the lung assume increased 
function and till the void. With atalectasis associated with bronchopneu- 
monia, chronic pleurisy, adhesions, and with fibroid overgrowth—chronic 
interstitial pneumonia—large and chronic pleural effusion, pyopneumo- DISEASES OF TI1E LUNGS 
383 
thorax and pneumothorax, compensatory lung changes including em- 
physema follow. The prognosis depends entirely upon the ability to 
influence the primary condition; once this is removed the lung accomodates 
itself, and function is practically normal. The discouraging feature is 
the inability to influence the underlying process. Each case naturally 
demands separate consideration (See separate sections). 
Most forms of emphysema are of the mixed type; there is enlargement 
of the lung, the alveolar walls are dilated and the interstitial tissue is more 
or less atrophied. Emphysema is relatively frequent. Frankel found 
positive evidences of emphysema in 5 per cent of 911 post mortems. We 
found 4 per cent of 6,300 cases of internal disease. Emphysema is not a 
disease of early life, though children with chronic bronchitis or stenoses 
of the respiratory tract develop it. It is more frequent after the fortieth 
year and most frequent in those of advanced age. 
Men develop emphysema oftener than women. 
Heredity bears the same relation to emphysema as it does to asthma. 
James Jackson, Jr., found in Louis’ wards 18 of 28 cases with positive 
heredity. 
Emphysema, asthma and chronic bronchitis are usually associated 
conditions. Bronchitis is the primary lesion in the majority of emphyse- 
mas. Bronchiectasia and emphysema are frequently present together; in 
these cases there is preceding and persistent bronchitis also. 
Fixed thorax is being more and more considered as a cause of emphyse- 
ma and asthma (favorable for operation). Emphysema is probably 
dependent upon inspiratory or expiratory stenosis or enfeebled respiratory 
strength. Emphysema is often found in cases in which there is both in- 
spiratory and expiratory obstruction. 
Emphysema is aggravated by occuptions which require heavy work, 
lifting heavy loads, the playing of wind instruments or the inordinate use 
of the vocal organs (glass blowing, etc.). When emphysema develops with 
chronic bronchitis (winter cough) or any bronchial catarrh which con- 
tinues unrelieved, it is progressive and is likely to lead to secondary circu- 
latory changes. 
Chronic bronchitis, “fixed thorax,” and emphysema lead to aggrava- 
tion of all subjective symptoms during cold and damp weather, also on 
exertion. Cyanosis and marked dyspnea are evidences of associated heart 
insufficiency, as a rule. Asthma recurring at short intervals or unrelieved 
during long periods increases existing emphysema and invites secondary 
changes. The greater the respiratory weakness (muscular insufficiency of 
the respiratory muscles) and the more advanced the dilatation of the right 
ventricle, the less likely are the symptoms of emphysema to improve. 
(6) Hypertrophic Emphysema 384 
DISEASES OF THE RESPIRATORY APPARATUS 
Persistent cough aggravates existing conditions, showing unrelieved 
bronchitis or secondary change. Abnormally prolonged expiratory move- 
ment is evidence of advanced emphysema in the presence of subjective 
symptoms. Marked change in the shape of the thorax (barrel-shaped 
thorax) is evidence of chronicity, and with the emphysema remains un- 
changed. Marked change in the size of the heart, particularly to the right, 
is present in advanced emphysema, and when associated with myocardial 
insufficiency is serious. In chronic and extensive cases the area of heart 
dullness is masked by the overlying dilated and enlarged lung. 
Chronic nephritis, dilated heart, bronchitis and emphysema is a quartet 
of conditions at once serious, and while life may be prolonged, is fatal in 
the end. 
Hypertrophy of the heart may prove sufficient during many years to 
carry some emphysematous patients along. In all of these suitable climatic 
and cautious treatment are important factors in prognosis. Rapid pulse 
with increasing dyspnea with or without increasing cough is always 
ominous. Arhythmia after long or short periods of emphysema is unfavor- 
able and indicates degenerative change. Dropsies either limited or general 
are always unfavorable. Dropsy is a terminal complication. 
Relative mitral and tricuspid insufficiency may develop after overtax- 
ing the heart, or during acute exacerbation of existing bronchitis and 
asthma. With stimulation and rational treatment these threatening condi- 
tions often yield; they return on slight cause. Myocardial degeneration 
is the usual cause of death. Stasis unrelieved leads to liver changes, con- 
gested kidney with albuminuria, gastrointestinal disturbances and cerebral 
congestion. 
Naturally the extent of the existing bronchitis is paramount in most 
cases, as is also asthma to which we have repeatedly referred. 
Emphysematous patients who develop pneumonia (bronchopneumonia 
usually) offer an unfavorable prognosis. 
I saw one case of fatal pneumothorax follow the rupture of the apex 
of an emphysematous lung in a post mortem made by Fischer (Frankfurt). 
In this case other dilatations were seen on the surface with thin walls like 
tissue paper. The apex was converted into cavities, several of which had 
ruptured. 
Emphysema, without serious complication, even with asthma and 
bronchitis, may not shorten life; such patients may live many years and 
die of intercurrent disease. Many cases do not advance to involve larger 
parts of the lung or cause marked secondary heart changes. Inherent 
weakness of the alveolar walls (Virchow) invites progression. The two 
factors of greatest importance in the prognosis of emphysema are the be- 
havior of the bronchial element and the ability to prevent disturbance of 
heart function with consecutive changes (stasis). Cardiac insufficiency 
once present, though it may yield to treatment, is certain to recur. Dyce DISEASES OF THE LUNGS 
385 
Duckworth has reported fatal hemoptysis with emphysema, and Osier 
mentions “an old emphysematous patient death followed the 
erosion of a main branch of the pulmonary artery by an ulcer near the 
bifurcation of the trachea.” 
(c) Atrophic Emphysema 
I have considered cases in which there are atrophic changes in con- 
nection with the hypertrophic form of the disease, and there mentioned 
that most emphysemata were of the mixed type. 
The characteristic atrophic form is found in old subjects in whom there 
is persistent respiratory embarrassment because of great dilatation of the 
air cells, the disappearance and atrophy of the alveolar walls and consecu- 
tive cavities. bTo treatment influences these cases. 
References 
Fraenkel. Quoted by Staehelin, (See below). 
Jackson (J. Jr.). Quoted by Osier, (See below). 
Mueller (Fr.). von Mehring & Krehl, Lehrb. d. Inneren Med. 8 Aufl., Bd. i., Jena, 1913. 
Osier. Practice of medicine, New York, 1914. 
Staehelin. Mohr & Staehelin, Handbuch der Inneren Med., Bd. ii., Berlin, 1914 (with 
bibliography). 
Tendeloo. Studien iiber Ursachen der Lungenkrank. Wiesbaden, 1902. 
Virchow (R.). Emphysema pulmonum. Berl. klin. Wchnschr., 1888, xxvi, i. See also 
iv, 2. Series. Index Catal. Library Surgeon General’s Office, 897-8. 
5. Gangrene of the Lung 
Gangrene of the lung is always a secondary infectious process in which 
the death of either a circumscribed portion of the lung or diffuse areas 
takes place. Pulmonary gangrene is either embolic (metastatic) or 
bronchogenic. In my experience I never met but one case in which re- 
covery followed the positive diagnosis of pulmonary gangrene—it was a 
sequel of an apex pneumonia in an adult aged 30 years. Lehert claims 
6 recoveries in 36 cases; no other clinician has ever approached such en- 
couraging results. 
Pneumonia is the most frequent primary infection. Infections in 
which there are infectious emboli may cause the death of lung tissue. The 
clinical history of gangrene with the characteristic sputum and odor make 
its recognition relatively easy. 
Pneumonia in diabetics invites pulmonary gangrene, which is promptly 
fatal (See Diabetes Mellitus). 
Pneumonia with erysipelas or other streptococcus infections has sup- 
plied several cases in our series, all fatal. Hemorrhagic infarct with sep- 
tic conditions in nephritis occasionally leads to pulmonary gangrene. The 386 
DISEASES OF THE RESPIRATORY APPARATUS 
gangrene of pulmonary malignancy is one of the factors which increases 
the septic and typhoid condition and causes death. 
Thrombosis or embolism of a branch of the pulmonary artery with 
septic conditions—typhoid, smallpox, pneumonia, or any other malignant 
infection—may cause gangrene. With all the prognosis is the same. Re- 
covery is so rare as not to be expected. 
Wilson Fox found one lung involved in 90 per cent of the cases investi- 
gated; the right in 54; the left in 36; the lesions were multiple and scat- 
tered in 22.5 per cent; limited to one lung in 77.5 per cent. 
Laennec saw 2 cases in his entire practice. We have had 5 cases in 
6,300 internal diseases. In over 37 years of active practice we do not 
recall 10 cases in private and hospital practice. 1.6 per cent is the propor- 
tion to other causes of death given by several observers (See West, S.). 
Multiple lesions are not uncommon with gangrene. Rarther reports 8 
cerebral abscesses in 49 autopsied cases of pulmonary gangrene—16 per' 
cent. 
Gangrene is exceedingly rare with pulmonary tuberculosis. Lung ab- 
scess and gangrene are occasionally coincident. Infection following pul- 
monary injury may lead to fatal gangrene. Our patients have usually 
died after from 5 to 14 days with symptoms of general sepsis and asthenia. 
In all cases the prognosis should be guardedly given; small abscesses with 
moderate necrobiosis may lead to recovery. In these cases, as in all who 
recover, a cavity remains from which there is more or less expectoration, 
often fetid, and in subacute or chronic cases there may be intermittent 
septic fever with final multiple foci and death after many weeks or months. 
Hemoptysis—profuse bronchial hemorrhage—occasionally causes 
death. 
Wherever possible, x-ray examination is indicated. With increased 
surgical technic the future may prove the prognosis of pulmonary gangrene 
to be more encouraging than it is at present. 
Aschoff. Pathol. Anatomie, Band ii, Jena, 1913. 
Fox (Wilson). Quoted by S. West (See below). 
Laennec. Treatise on diseases of the chest. Translated by Forbes, Philadelphia, 1823. 
Lebert. Klinilc der Brustkrank, Tubingen, 1873-4. 
Narther. Deutsch. Arch. f. klin. Med., xxxiv., 169. 
West (S.). Diseases of the organs of respiration. London, 1902. 
References 
6. Abscess of the Lung 
Lung abscess is a surgical affection; unless cured by nature’s proc- 
esses or surgery, it is always fatal. It offers only reasonable hope of DISEASES OF THE LUNGS 
387 
recovery when superficial and surgically treated. To accomplish its 
relief by surgical means it must he favorably located, single and circum- 
scribed. Multiple lung abscesses are almost always fatal. The outcome 
must depend upon the primary location and extent of the infection as 
well as the resistance of the patient, his age, and nature’s ability in the 
absence of surgical intervention to wall off the disease. It may be sec- 
ondary to pneumonia, pyemia, septicemia, injuries to the lung and chest 
wall, malignant growths, subphrenic abscess, liver abscess, and hydatid 
disease of the liver and lung. With pulmonary tuberculosis abscess of 
the lung often develops, also with pyopneumothorax which condition it 
may also cause. 
There are a number of cases recorded which followed the aspiration 
of foreign bodies, also neck and thorax operations. With malignant 
growths of the lung or surrounding organs (esophagus) abscess may 
develop. The pyemic abscesses are of embolic origin and are usually 
multiple. Perforation of lung abscess may suddenly fill the air cells 
causing threatening or fatal asphyxia; pyopneumothorax follows pleural 
perforation and is always a serious complication. 
In those cases which nature or the surgeon cures, there is gradual 
improvement of the general and local conditions; the sputum diminishes, 
the physical signs disappear very largely, and finally x-ray shows cica- 
tricial contraction or a cavity walled off, or in other cases, a contracted 
cavity communicating with the bronchial tree. 
The extent of lung abscess may be studied by means of the Rontgen 
ray, and valuable diagnostic and prognostic data are thus obtained. 
7. Neoplasm of the Lung 
New growths in the lung are either (a) primary or (b) secondary, 
(a) Primary Neoplasms.—The primary neoplasms are exceedingly 
rare and these are usually carcinomatous, taking their origin in a bronchus, 
usually of considerable size (Aschoff). The occlusion of a large bronchus 
by the new growth leads to bronchiectasis. Primary cancer soon invades 
large portions of the lung, offers characteristic physical signs and x-ray 
picture. In some there is pleural infiltration and bloody effusion. En- 
largement of supraclavicular, at times axillary, glands may be among 
the early secondary pathologic changes. The upper lobe is most likely 
to be the seat of primary carcinoma. Pulmonary gangrene may compli- 
cate primary carcinoma. Primary pulmonary cancer may originate in 
the epithelium of the air cells (rarely) or in the metaplastic bronchial 
epithelium (See Isaac Adler’s splendid monograph for full data concein 
ing the origin and growth of primary neoplasm of the lung). Aschoff 
claims that primary neoplasms of bronchial origin often originate in 
tuberculous cavities. In some of these cases the primary growth is small 388 
DISEASES OF THE RESPIRATORY APPARATUS 
and gives rise to but few symptoms, while distant metastases offer the lead- 
ing clinical data and cause death; thus, metastatic brain tumor may offer 
the only prominent symptoms. When the growth is infiltrating (a variety 
of primary lung cancer), large areas of lung tissue are involved. 
I base my conclusions upon pathologic data which seem justified, 
and to these I add my unfortunate clinical experience with primary 
malignant growths of the lung. Adler, who has given this subject great 
thought and investigation, concluded one of his chapters as follows: 
Neglecting in this place all further detail, it may be briefly stated 
that it is at present the common consensus of opinion, and probably justly 
so, that the great majority of primary carcinomata of the lungs develop 
from the bronchi and that a cancer of the lung is, taken strictly, a bron- 
chial carcinoma; that, on the other hand, a carcinoma starting from the 
lung tissue itself occurs, but is extremely rare, and is built up, not of 
flat, but of cylindrical epithelium.” 
The course of 'primary lung cancer may be either rapidly fatal, acute 
and galloping, or with symptoms of increasing pressure and bronchopneu- 
monic symptoms the typical picture of lung cancer is presented; in some 
cases the features of mediastinal compression are in the ascendency, or 
the invasion of the pleura may materially influence symptoms and the 
course of the disease. In none of these clinical types is there hope of 
recovery. The x-ray examination offers hope of early diagnosis aided 
by the direct inspection of the bronchi, but unfortunately symptoms are 
not sufficiently pronounced early to lead either the physician or the patient 
to take advantage of these refinements of diagnosis. 
(b) Secondary Lung Growths.—Secondary lung growths may fol- 
low primary cancer of distant or near organs. The breast and thyroid 
offer the primary seat of most metastases; they also follow stomach, pan- 
creatic or genito-urinary growths. Secondary lung growths are usually 
multiple and infiltrate both lungs. With secondary lung growths, cancer 
or sarcoma, lymphatic involvement, bronchial, axillary, cervical or in- 
guinal may develop. The pleural invasion or pressure leads to hydro- 
thorax, usually bloody. 
With cachexia, enormously emaciated, and with respiratory embar- 
rassment, these patients die of exhaustion. Besides cancer and sarcoma, 
fibroma, lipoma, myoma, teratoma, and osteoma have been found in the 
lung (Aschoff). 
References 
Aschoff. Pathol. Anat. 8. Aufl.,Bd. ii., Jena, 1913. 
Adler (Isaac). Primary malignant growths of the lungs and bronchi. London & New 
York, 1912. 
Bain. Textbook of the medical 'practice. London & New York, 1904. DISEASES OF THE PLEUBA 
389 
E. Diseases of the Pleura 
1. Pleurisy 
(a) Fibrinous Pleurisy 
{Dry Pleurisy, Pleuritis sicca) 
When dry pleurisy is of primary origin it usually follows in a pre- 
viously healthy subject after cold or traumatism. Probably but few 
reach middle life without having at some time had limited pleurisy; in 
many the process of repair, after the plastic deposit on the pleural surface 
leads to agglutination of the visceral and parietal pleura, or adhesions, 
which may or may not give rise to symptoms. Primary dry pleurisy 
runs its course with but slight constitutional disturbance in from 2 to 7 
days. In all of these cases the clinician must bear in mind the possibility 
of an underlying primary lesion (tuberculosis, pneumonia, etc.). 
Associated Symptoms.—When pleurisy is secondary to carcinoma, gam 
grene, traumatism in which there is fracture, or abscess, the prognosis of 
the plastic pleurisy is of no importance; the primary disease offers the 
leading data. 
Pleurisy with croupous pneumonia often adds to the discomfort and 
may, when severe, influence prognosis unfavorably though the toxemia 
and extent of the primary disease with the resistance of the patient remain 
the paramount factors. 
(6) Serofibrinous Pleurisy 
{Pleurisy with Effusion) 
We consider tlie tuberculous pleurisies separately (see Tuberculous 
Pleurisy—Section on Tuberculosis). Many cases considered non-tuber- 
culous during long periods finally prove to be tuberculous. Besides 
tuberculous infection serofibrinous pleurisy may depend upon the 'pneumo- 
coccus, streptococcus, influenza bacillus, typhoid, diphtheria, and a variety 
of other infections. The majority of pneumococcus pleurisies are pleuro- 
pneumonic and their prognosis depends upon the virulence of the lung 
inflammation and all other conditions which we have considered in con- 
nection with the prognosis of pneumococcemia (See Pneumococcemia). 
Pneumococcus pleurisy often becomes purulent when it offers a good 
prognosis, early detected and radically treated (See Empyema). The 
septic or streptococcic or staphylococcic pleurisies must naturally depend 
upon the nature and malignancy of the infection as well as the extent of 
the pleural change, the amount of the fluid, the early recognition of its 
presence, and a variety of other data which we consider in connection 390 
DISEASES OF THE RESPIRATORY APPARATUS 
with the symptoms and rational treatment. Most influenzal infections 
in which there is serous effusion are pleuro- or bronchopneumonic. The 
prognosis depends upon the same factors as are considered with the pre- 
ceding clinical types. 
Associated Symptoms.—With typhoid fever, diphtheria, scarlet fever, 
polyarthritis and nephritis the addition of pleural effusion is always a 
serious complication, more, because it is evidence of malignancy or severity 
of the primary disease. 
Serofibrinous pleurisy associated with abscess, bronchiectasis, gan- 
grene, pericarditis, peritonitis, purpura and polyarthritis is considered 
with these conditions in separate chapters. 
Most pleurisies of childhood are of pneumococcus origin and offer a 
fair prognosis. The prognosis of serofibrinous pleurisy depends on the 
nature of the primary infection, the associated lesions in other organs, 
the height of the fever and tissue degeneration, the mechanical effect of 
the effusion, the effect of all upon the circulation, the early diagnosis and 
rational treatment. 
High temperature persisting with effusion particularly after early 
aspiration, with or without repeated chill, leads to the suspicion of puru- 
lent change. The height of the temperature offers no clue to the nature 
of the infection. Fall of temperature or decided remissions before aspira- 
tion may in most cases be interpreted as indicating a mild course. Slight 
temperature persisting after aspiration is not unusual, neither is it unfa- 
vorable. In uncomplicated cases we have expected the temperature to 
fall to or near normal in seven days after aspiration. Persisting tem- 
perature after the seventh day with increase of fluid and good pulse is 
not unfavorable in the non-tuberculous cases. In cases which have been 
considered non-tuberculous, continued temperature, physical signs of fluid, 
rapid pulse, with or without night sweats, the chances favor an unrecog- 
nized tuberculosis. Gastro-intestinal symptoms are usually present and 
yield with the relief of the pleural pressure. Cough persisting is sug- 
gestive of unrelieved pressure, associated bronchitis, or lung involvement. 
The severity of pain during the early hours does in some cases indi- 
cate the depth and extent of the pleurisy. This is not to be accepted with- 
out considering the possibility of exceptions. Increase of urinary secre- 
tions, at times polyuria, is favorable and denotes absorption of fluid unless 
there is proof to the contrary of its dependence on other factors. 
Blood pressure in favorable cases is not materially changed from the 
normal. Decided fall is unfavorable. Emaciation is to be expected, but 
loss of flesh after radical treatment, failure to enter upon a satisfactory 
convalescence is indicative of associated complication, should lead to thor- 
ough investigation and suggests the possibility of tuberculous complication. 
The amount of effusion is not an expression of the malignancy of the 
infection. There are cases of malignant infection in which the effusion DISEASES OE THE PLEURA 
391 
is not large; on the other hand, the less malignant infection may be asso- 
ciated with large exudate. There is no rule. 
Associated collapse of lung (atelectasis) with weak heart is unfavor- 
able. Grocco’s triangle is usually present with most fair sized effusions; 
it is of diagnostic, not of prognostic value. Encapsuled effusion may 
remain unrecognized longer than free fluid in the pleural cavity, and 
convalescence is therefore correspondingly retarded. The average favor- 
able serofibrinous pleurisy runs its course to a favorable termination in 
from 3 to 4 weeks. The fever gradually falls, the heart strength increases, 
the physical signs improve, the dullness or flatness does not disappear 
entirely either after aspiration or absorption, but in the course of several 
months return of normal percussion note is to be expected. 
The return of the friction sound after its original disappearance is fa- 
vorable, for it indicates absorption or removal of fluid. In favorable cases 
the deformity of the thorax which follows from adhesions and neglect of 
proper treatment can be favorably influenced by pulmonary gymnastics 
and climatic change. The former alone, in primary non-tuberculous 
cases is sufficient. 
Persistent dyspnea with or without weak myocardium in rationally 
treated cases is unfavorable and demands thorough search for its cause. 
In cases which promptly lead to adhesions and in which the lung is com- 
pressed and bound, unable to expand, there will be a long period before 
there is compensation. In these cases mechanical treatment (pulmonary 
gymnastics) often leads to brilliant results, but patience and perseverance 
are necessary. 
The unfavorable pleurisies are those which have been neglected, in 
which the lung and other organs are misplaced, in which the heart is weak, 
the fever uncontrolled, the absorption slow, the improvement unsatisfac- 
tory after aspiration, and in which there is the picture of sepsis. In 
spite of these unfavorable features a number of these cases in which 
tuberculization does not follow, recover fully with more or less misshapen 
chests. 
Delirium and other evidences of involvement of the sensorium, with 
rapid pulse and typhoid condition, are characteristic of the graver pleu- 
risies. But few cases run an absolutely acute course. 
General Considerations.—The sudden deaths reported by some are ex- 
ceedingly rare. In our practice we never met but one sudden death from 
serofibrinous pleurisy. In that case the effusion had not been detected 
during many weeks; preparation was being made for aspiration during 
which the patient suddenly expired without preceding alarming heart 
weakness. 
Double serofibrinous pleurisy is exceedingly rare: most of these cases 
are in reality hydrothorax dependent upon circulatory or other obstruction. 
Interlobular pleurisy is more frequent than has been heretofore sup- 392 
DISEASES OF THE RESPIRATORY APPARATUS 
posed. The diagnosis is easily made, as is that of all serofibrinous 
pleurisies by x-ray examination. Interlobular pleurisy (involving the 
surfaces between two lobes) may cause considerable malformation and 
troublesome adhesions, and unless the possibility of such encapsuled 
serofibrinous effusion is considered in the absence of the Rontgen rays 
the diagnosis will not be made. We refer to interlobular purulent pleurisy 
in the consideration of empyema. Fraenkel and Dietlen have done yeo- 
man’s service in this field by giving convincing clinical and pathologic 
data. The prognosis of interlobular pleurisy is favorable. The prognosis 
of serofibrinous pleurisy of early life (children) is not unfavorable. 
Pleurisies limiting themselves to the diaphragm, the mediastinum and 
the pleuritic thickening and effusion of pleuropericarditis (polyserositis) 
are not primary, and their significance must be separately considered 
with the associated conditions (See Polyserositis). The differential diag- 
nosis of the tuberculous and non-tuberculous pleuritides is enormously 
assisted by the leukocytic blood count. We have invariably found low 
white counts in our tuberculous cases and have prognosticated accord- 
ingly. The lymphocytes are relatively increased with tuberculous pleurisy 
as in other forms of tuberculosis. The average white count in non- 
tuberculous pleurisies is between 10,000 and 15,000. 
Staelielin reports 13 deaths in 400 of serofibrinous pleurisy. In those 
previously depleted by disease (infection) with resistance lowered, the 
prognosis is correspondingly influenced. The influence of early recogni- 
tion and timely aspiration on prognosis is paramouunt. Complicating 
pulmonary embolism and thrombosis are among the rare but fatal accidents. 
Chronic interstitial pneumonia follows only those cases which lead to 
chronic pleurisy. 
References 
Bain. Textbook of medical 'practice. London, 1904. 
Dietlen. Ergebnisse der inneren Med. Bd. xii, 196. 
Fraenkel {A.) Therap. d. Gegenwart. 1910, 337. 
Frick. J. Am, Med. vlss., vol. 55, Dec., 1910, 2042. 
von Mehring & Krehl. Lehrbuch der inneren Med., 8. Aufl., Jena, 1913. 
Osier. Practice of medicine, New York, 1914. 
Staehelin. Mohr & Staehelin, Handbuch der inneren Krank. Bd. ii, Berlin, 1914. 
(c) Purulent Pleurisy 
{Empyema—Pyothorax) 
The larger number of purulent pleural effusions are secondary, and 
most of these are found with the various types of pneumonia, either 
during the period of active inflammation of the lung or as a sequel fol- 
lowing in the course of a fewT days or weeks. DISEASES OF THE PLEURA 
393 
The more virulent types of empyema are those in which the bacterial 
invasion is greatest, in which the accumulation has remained unrecog- 
nized or neglected and time has been given for burrowing and distant 
infection, secondary pus accumulation in kidney, spleen, or other organs— 
occasionally purulent meningitis. The prognosis is also materially influ- 
enced by the previous condition of the patient, the character of the pri- 
mary pneumonia, its extent and the behavior of the cardiovascular and 
renal organs, and the ability of the patient to resist disease. 
Associated Symptoms.—Either typical or atypical pneumonias may 
have pus accumulation added. The more frequent are pneumococcus 
infections, but influenzal or streptococcus pneumonias are likely to suffer 
from this complication. In all, the prognosis is materially influenced by 
the added lesion hut it may be positively concluded that in all, the early 
recognition of the pus, and its prompt removal, in the absence of asso- 
ciated depressing conditions, particularly if the primary disease has run 
its course, allows a reasonably good prognosis to be given. 
Pneumococcus empyema offers a more favorable prognosis than do 
any of the other infections above mentioned. 
Abscess of the lung associated with empyema offers a less favorable 
prognosis than does the latter alone. Yet in these cases in children and 
in adults during the active years of life, while the condition must be con- 
sidered to be serious, the prognosis is not absolutely bad. I have the 
records of a number of cases of this kind in which, after a slow conva- 
lescence and long drainage, the patients have made a complete recovery, 
though with misshapen and sunken thoraces which finally improved under 
well regulated and long continued pulmonary gymnastics, in favorable 
surroundings. 
Empyema with metastases, occasionally found with puerperal fever, 
erysipelas, diphtheria, traumatism, tonsillitis, endocarditis, either benign 
or malignant infections of the ivalls of the thorax, or tuberculosis with or 
without pneumothorax, offers a very grave prognosis. The prognosis is 
unfavorably influenced by a rapid pulse if this does not yield within a 
reasonable time to the radical treatment of the empyema. 
Constitutional symptoms, such as fever and delirium, the former high 
and persistent, with or without chills, are found in the more malignant 
types of the disease; if they do not yield after rational treatment in a. 
reasonable time argue against recovery. 
Active delirium with rapid pulse and high fever in the acute period 
of pneumonia with pyothorax is suggestive of malignant infection and 
justifies an exceedingly grave prognosis. 
General Statements.—Spontaneous resorption of pus from the pleural 
cavity is not likely to occur. It certainly does not deserve to be considered 
in the prognosis or treatment of the typical disease, and he who depends 
upon it to the exclusion of radical methods of treatment is adding to the 394 
DISEASES OF THE RESPIRATORY APPARATUS 
dangers of his patient, reducing the chances of restoration to health, and 
is inviting rupture into lung or bronchus, deformity—usually irreparable 
—or death from exhaustion with general infection and possible amyloid 
changes. 
Empyema necessitatis offers a poor prognosis for final complete func- 
tionating ability of the lung. Its ravages are often difficult of treatment, 
and may continue to prove a drag upon the patient during his entire 
life; they leave an avenue for future infection and almost continuous 
discomfort, besides the possibility of amyloid and other degenerations. 
In these as in all cases of empyema the great danger of pyemia and sepsis 
must be considered. 
In double empyema of pneumococcus origin the prognosis is less 
favorable than with invasion of but one pleural cavity, but it is still good 
and the majority of these cases, promptly recognized and treated, recover. 
With the more malignant and far-reaching double empyemata of strepto- 
coccus origin the condition is graver; death usually follows, the dura- 
tion depending upon associated conditions. 
It is often surprising to note how promptly patients with empyema, 
with all appearances of serious illness, recover after the free evacuation 
of the pus. 
The prognosis during early life is good in the large majority of cases. 
It is safe to place the recoveries above 90 per cent. Even during the first 
two or three years of life these figures are justified. In the adult during 
the active years of life, uncomplicated empyema offers an exceptionally 
good prognosis. Complications above mentioned must be considered. In 
old age, beginning with the fifty-fifth year of life, the prognosis is less 
favorable; fortunately the number of cases of empyema at this time of 
life is strikingly small. 
The time of the complication is of great importance in prognosis. At 
the height of pneumonia of whatever bacterial type, the prognosis is less 
favorable than after the crisis. If in these cases there is cerebral inva- 
sion, if alcoholism, nephritis or arterial degeneration, or chronic metabolic 
fault (diabetes mellitus, gout, etc.), the prognosis is grave, and death 
follows promptly as a rule. 
Recently Gerhardt, D., has described a type of empyema to which he 
refers as parapneumonic empyema. This condition is as a rule (I) asso- 
ciated with pneumonia at its height, (II) is of limited extent, (III) offers 
a favorable prognosis and (IV) the pus is remarkably free from micro- 
organisms. The larger number of these cases will remain unrecognized, 
for the pus accumulation has been found so small and the added symptoms 
so few that it appears to the writer that its diagnosis is uncertain. Ger- 
hardt claims however that in the Basel Clinic in 4-J years he recognized 
20 cases of parapneumonic empyema in 300 cases of pneumonia, while 
in Wurzburg in 95 cases he found but 3 cases. DISEASES OF THE PLEURA 
395 
If we accept the contentions of Gerhardt that such limited pus accu- 
mulations are frequently present with pneumonia, and adopt his charac- 
terization of the complication as parapneumonic empyema, we are justified 
in concluding that the condition does not materially influence the prog- 
nosis of the primary disease and that its own prognosis is good. 
Gerhardt (/).). Mittheil. aus denGrenzgeb. der Med. u. Chir. Band xxvi, Hft. 5, 46. 
Reference 
(d) Tuberculous Pleurisy 
See Tuberculosis (Section I). 
(e) Chronic Pleurisy 
There are cases of pleural effusion which persist during many months, 
which after the chest is emptied by aspiration return; they remain non- 
purulent. Most of these in the end prove to be symptomatic and not 
true primary pleurisies. Some are tuberculous from the beginning and 
some of these may finally yield to time or radical surgical treatment; in 
others the fluid is finally absorbed; a number of cases are finally compli- 
cated by lung involvement and die of general tuberculosis. There are 
cases of a chronic character in which subjective symptoms and pleural 
thickening persist after pleuritis sicca. Such patients continue more or 
less out of health; they have some respiratory embarrassment, chronic 
cough, at times no cough at all—while pleuritic pains recur with the 
change of weather. All of these symptoms may follow any form of 
pleurisy including empyema, and are of no grave significance. Another 
class of cases is that in which pleurisy causes gradually increasing 'pro- 
liferative changes, resulting in thickening of the surfaces and extension 
to the interstitial tissue of the lung with resulting fibroid pneumonia, 
always chronic (See Chronic Interstitial Pneumonia). These cases pri- 
mary pleural, may extend so slowly as to cause but few symptoms or little 
inconvenience during many years; the patients recognize their limitations 
and are worse during the winter and damp weather. Tuberculization is 
not uncommon. 
Chronic pleurisy ivith multiple adhesions is frequently found post 
mortem without having caused symptoms during life. There are chronic 
pleuritides in which adhesions and proliferative lung changes lead to 
emphysema, bronchiectasis, and dilated heart. With increasing heait 
weakness dropsies may develop; also albuminuria and death results from 
exhaustion. 
It not infrequently happens that pleural effusions are encysted, form- 
ing small or large serofibrinous cysts. The prognosis of these, when 396 
DISEASES OF THE RESPIRATORY APPARATUS 
primary, is good. X-ray examination when possible should be used to 
determine the location and extent of these. 
Hemorrhagic pleurisies are usually symptomatic of either carcinoma 
or sarcoma of the pleura or lung, malignant infection, hemorrhagic in- 
farcts, terminal nephritis, tuberculosis or other grave primary lesions. 
These are therefore not true pleurisies. In all the prognosis is bad. 
2. Hydrothorax 
The transudation of non-inflammatory fluid in the pleural cavities is 
secondary, and purely symptomatic. It is usually an expression of circula- 
tory insufficiency or compression and a part of general dropsy with myo- 
cardial insufficiency. Circulatory obstruction or insufficiency leading to 
hydrothorax may fill one or both pleural cavities. With heart lesions the 
hydrothorax is often unilateral; renal hydrothorax is almost always double. 
Causes.—Carcinoma, grave constitutional anomalies, the graver ane- 
mias, Hodgkin’s disease, pericardial adhesions and growths of the lung 
and pleura may by pressure cause hydrothorax. The prognosis of all these 
conditions is bad. 
Associated Symptoms.—With heart lesions there may be material tem- 
porary improvement but hydrothorax is usually a terminal complication 
and when persistent during several weeks, without relief of the myocardial 
weakness, death is not long postponed. Ascites and hydrothorax are 
usually present at the same time. 
3. Pneumothorax 
(a) Hydropneumothorax 
(b) Pyopneumothorax 
Air in the pleural cavity is symptomatic. Pneumothorax is rarely 
present without either serum (a) hydropneumothorax, or pus (b) pyo- 
pneumothorax. Pneumothorax results when the pleural cavity is in com- 
munication with the external air; hence in the larger number of cases there 
is, either because of disease or trauma, perforation of the lung. In consid- 
ering emphysema we call attention to the rupture of superficial emphyse- 
matous cavities; in our consideration of tuberculosis we also mention this 
accident. With whooping-cough, in rare cases, rupture of the lung may 
occur during a violent fit of coughing. Abscess and gangrene of the lung 
superficially located or burrowing, empyema rupturing into the lung, the 
breakdown of malignant nodule (carcinoma or actinomycosis or sarcoma) 
or perforation from the stomach through the diaphragm, perforation of 
the esophagus, aneurismal rupture, abscess of the liver, injuries to the DISEASES OF THE PLEURA 
397 
chest wall, following the use of the aspirator needle, and in occasional cases 
rupture of the healthy lung during sleep or on only slight exertion, may 
all cause pneumothorax. We have recently received the history of a pneu- 
mothorax in an apparently healthy young man while playing billiards. 
These accidents do not always cause inflammatory changes (pleuritis) but, 
as a rule, they do. S. West believes that 90 per cent of all pneumothorax 
is secondary to the rupture of a tuberculous cavity or the breakdown of 
superficially located tubercle. 
Statistics.—Osier mentions the “spontaneous development” in pleural 
exudates of the gas bacillus (B. aerogenes capsulatus, Welch). Emerson 
reports 48 cases of which 22 were tuberculous, 6 due to trauma, 10 of aspi- 
ration, 2 spontaneous, 2 with bronchiectasis, 2 abscess of the lung, 2 due to 
empyema, 1 gangrene of the lung, and 1 abscess of the liver. 
Saussier’s statistics show 62 per cent due to tuberculosis. Of 131 cases 
he found 29 due to empyema. 
General Considerations.—The statistics of Walshe correspond with 
those of S. West. West, considering the possibility of rupturing a healthy 
lung “by any force which respiration can bring to bear upon it” concludes 
that it is possible, and cites pneumothorax resulting from whooping-congh 
and straining during labor. The direct results of pneumothorax are the 
collapse of the lung, and the displacement of organs. The danger from 
collapse of lung tissue which makes it useless is great, particularly when 
the breathing surface of the opposite lung is lowered by infiltrating disease. 
Besides the collapse of the lung on the side of the pneumothorax, the op- 
posite lung suffers more or less from collapse, contains a reduced quantity 
of air, and “a smaller aerating surface on which the blood vessels are ex- 
posed to the air.” With these conditions there is “embarrassment of the 
circulation which pneumothorax causes” (West). Because of these facts 
the greatest danger of pneumothorax immediately follows the perforation, 
within the first hour, and West contends that “the immediate prognosis 
improves with every hour that life is prolonged.” 
The ability to accommodate the lung function to the suddenly changed 
respiratory conditions, and the condition of the heart and the opposite 
lung, are important factors in framing the early prognosis. Naturally the 
prognosis is best when the lung has been previously normal. In cases of 
advanced tuberculosis the early symptoms may be largely cardiac and less 
pulmonary. Perforation leading to pneumothorax without advanced infil- 
tration, or in the apparently healthy because of sudden change of respira- 
tory conditions leads to greater respiratory embarrassment. In both, the 
ability of the heart to come to the rescue largely influences the prognosis. 
In some cases of tuberculosis where the process is not far advanced, pneu- 
mothorax without causing hydro- or pyothorax, may have a salutary effect, 
just as artificially produced pneumothorax in properly selected cases 
proves beneficial in a proportion of cases. 398 
DISEASES OF THE RESPIRATORY APPARATUS 
Sudden cardiac insufficiency with collapse is the leading danger of 
pneumothorax. Pneumothorax is not of necessity a complication of the 
more advanced cases of tuberculosis; the rapidly advancing cases are most 
liable to perforation. Much depends upon the local change at the point 
of rupture; it may be extensive there, but limited elsewhere. 
Persisting dyspnea is always significant of danger; with its relief and 
a fairly strong heart the immediate danger is decreased. It is possible for 
the perforation to seal itself and the air to absorb, if effusion is absent. 
Naturally the primary tuberculosis may be so far advanced as to prove 
the immediate cause of death. 
Additional Statistics.—West in a series of 101 cases was positive of 
the duration in 39 and knew approximately in 37. Of the 39 cases, 10 
patients died within the first 24 hours; “2 within 20 minutes and 30 min- 
utes respectively of the attack; the other 8 within a few hours.” “18 had 
died by the end of the first week, and 21 by the end of the fortnight ; to 
which may be added 8 more cases, in which the duration cannot be quite 
determined, though it was certainly less than 14 days, making thus 29 out 
of 39 cases which were fatal within the fortnight, i. e., nearly 75 per cent. 
In other words, 3 out of every 4 cases.” Six more died within the second 
fortnight. “Of the 35 cases in which the duration was uncertain, 9 were 
admitted with pneumothorax and died in the hospital; 10 developed 
pneumothorax in the hospital, and left at varying dates after the attack, 
some of whom were known to have died subsequently at their own homes; 
while 18 patients were admitted with pneumothorax and left with it. Of 
this second group, taking all the cases together, 10 died within the first 
month, 8 more within the second, and 2 more within the third—making 19 
in all.” 
“Taking the two series together of 74 cases, 45 died within the month, 
i. e., 60 per cent; 9 more died within the second month, making 71 
per cent.” Seven were alive at the end of the third month, one at the 
end of the fifth, one at the end of the ninth. West reports 20 cases 
under his immediate care of which 12 died and 8 recovered—60 per cent 
mortality. The records of St. Bartholomew’s Hospital for 14 years give 
the same mortality. 
Special Considerations.—Pneumothorax due to empyema—rupture 
through the chest wall or into the lung with empyema necessitatis—offers 
a more favorable prognosis than does tuberculosis or other pneumothorax. 
The clinician in offering prognosis must consider as suggested by West: 
(1) “The immediate risk to life.” 
(2) “The possible duration of life.” 
(3) “The chances of ultimate recovery.” 
(1) The Immediate Risk to Life.—We have called attention to the 
greater danger immediately following the perforation. In deciding on DISEASES OF THE PLEURA 
399 
the outcome, the dyspnea and circulatory obstruction, as shown by dyspnea, 
the condition of the opposite lung, the resistance of the patient and the 
underlying (primary) cause are the leading factors to be considered. 
(2) The Possible Duration of Life.—The length of the patient’s life 
depends largely on the extent and nature of the primary lesion, the heart 
condition, the resistance, the character of the effusion and the complica- 
tions. 
(3) The Chances of Ultimate Recovery.—We have seen recoveries in 
our series. We are watching a physician who almost two years ago after a 
number of years of latent tuberculosis (supposed cured) without warning, 
developed threatening pneumothorax. He is living, engaged in literary 
work, walks well and seems to be making a slow convalescence under favor- 
able climatic conditions. 
West places the average of recoveries at 10 per cent. The St. Barthol- 
omew’s statistics yield over 25 per cent. West’s own statistics in “20 
cases show 5 complete recoveries, in 3 the recoveries from pneumothorax 
were complete, but the patients died subsequently of phthisis; and in 3 
others recovery was incomplete. Besides these, I have seen one other case 
in consultation in which recovery was complete and the patient remained 
well for many years.” 
Without effusion the prognosis is always more favorable. Purulent 
effusion (pyopneumothorax) offers the most unfavorable prognosis. X-ray 
examination will prove of great assistance in showing the extent of the 
primary deposits and the amount of effusion and displacement. 
References 
Emerson. Johns Hopkins Hospital Reports, xi. 
Osier. Practice of medicine, 8. ed., New York, 1914. 
Saussier. Theses de Paris. 1841. 
Walshe. Diseases of the lungs. London, 1871. 
West (S.). Diseases of the organs of respiration, ii, London, 1902, 798. 
Lancet, London, May 3, 1884. 
4. Mediastinal Diseases 
Because of the relative importance of the organs within and in close 
relation to the mediastinum, the fact that most mediastinal lesions lead to 
pressure, the prognosis of all mediastinal lesions is grave. 
The leading mediastinal tumors are: sarcoma—these may arise from 
lymphatic glands, the thymus or cellular tissue (Woodwark, Aschoff and 
Mueller), secondary cancer, lymphadenoma (glandular), dermoid and 
hydatid cysts. 400 
DISEASES OF THE RESPIRATORY APPARATUS 
Associated Symptoms.—The pressure symptoms and physical signs 
with all of these conditions are positive, as they are also with aneurism, 
specific lymphadenitis, abscess and emphysema following injury or per- 
foration of surrounding organs. Tuberculous glands may lead to suppura- 
tion and pressure. Hare made an exhaustive study of the diseases of 
the mediastinum, including 520 cases. He found 134 cancers, 98 of sar- 
coma, 21 lymphoma, 7 fibroma, 11 dermoid cysts, 8 hydatid cysts; lipoma, 
gumma and enchondroma. Sarcoma is oftener primary than cancer. 
The prognosis of mediastinal growths is absolutely bad. With increas- 
ing dyspnea, cyanosis, edema and heart insufficiency these patients often 
die after weeks of wretchedness. 
The x-ray pictures make it possible to watch the growth, locate it and 
recognize the changed relations of the included and surrounding organs 
(Rieder, Ilolzknecht). Mediastinal abscess may perforate; it has been the 
cause of death with erysipelas or it may develop without known cause. 
Mediastinitis which is suppurative is always a serious disease. Recovery 
from abscess may be expected in about one-half the cases. Hare says 40 
per cent. Acute thymus death has been separately considered. Pressure 
from an enlarged thymus gland, if great, impinges on the mediastinum 
with fatal result, if not relieved at once. We have seen several cases in 
which death followed a few days of suddenly increasing mediastinal pres- 
sure with Hodgkins’ disease and lymphatic leukemia. 
The heart changes materially influence prognosis with all mediastinal 
displacement; usually the displacement is to the left. Venous stasis is 
common and in cases which are terminal, the engorgement of the face and 
arms, one or both, w-ith dyspnea and deep cyanosis tell of the approaching 
end. Tumors which press on the trachea and esophagus show their pro- 
gression by increasing stridor and dysphagia. Hydrothorax and palpable 
nodules, enlarged supraclavicular glands all aid diagnosis and prognosis. 
Cachexia is often extreme with mediastinal malignancy. According to 
Mueller, Fr., death follows in about one year in the average case. The 
course of the disease depends upon the nature and rapidity of the growth. 
Blood counts particularly leukocytic counts will often prove of value 
in differentiating thyroid, thymus enlargement and malignant growths. 
With thyroid or thymus pressure there are the blood changes mentioned in 
our separate consideration of disease of the ductless glands. The increased 
lymphocytosis (30 to 50 per cent) with these is of great diagnostic and 
prognostic value (See Thyroid and Thymus Disease). 
Displacement of the mediastinum due to pleural or pericardial effusion 
may prove fatal unless promptly relieved. Hare includes 6 cases of 
hematoma in his series of 520 cases of mediastinal disease. Most hema- 
toma of the mediastinum are of traumatic origin and are exceedingly grave. 
The extent can be decided by x-ray examination, but the subjective symp- 
toms will offer the best guide for the forecast. If dyspnea and cyanosis DISEASES OF THE PLEURA 
401 
are relieved or improving, if the pulse is correspondingly better there is 
hope of ultimate relief unless there are associated unfavorable conditions. 
References 
Aschoff. Pathol. Anatomie. Band ii, Jena, 1913. 
von Bergman. Mohr & Staehelin, Handbuch, etc. Bd. ii, Berlin, 1913. 
Charcot & Bouchard. Traite de Medicine, Tom. iv. 
Hare. The pathol. clin. history and diagnosis of affections of the mediastinum, etc., Phila- 
delphia, 1889. 
Hoffmann. Nothnagel, Spec. Path. u. Therapie. Bd. xiii. 
Holzknecht. Die Rontgendiagnostic der Brust Organe. 
Mueller (Fr.). von Mehring & Krehl, Lehrbuch, etc. Bd. i, Jena, 1913. 
Rieder. Roentgenunters. des. Mediast. Bd. i., Leipzig, 1913 (Rieder-Rosenthal). 
Woodwork. Manual of medicine. London, 1912. Section III 
Diseases of the Circulatory 
Apparatus 
A. Arteriosclerosis 
(Arteriocapillary Fibrosis, Atherosclerosis, Atheromatous Degeneration, 
Endarteritis chronica deformans, Endarteritis chronica nodosa, 
Arterial Degeneration) 
Arteriosclerosis is a progressive nutritional disturbance of the arterial 
wall, with swelling, thickening and sclerosis of the intima primarily, in- 
crease and degeneration of cellular elements, partial necrosis and calcifica- 
tion, either diffuse or nodular, in which all coats are finally involved; 
the media more particularly when the arteries of the extremities are 
affected. There is in advanced cases, change of a productive character in 
the adventitia (peri-arteritis). This definition of Marchand is almost 
universally adopted by clinicians and pathologists and at once demon- 
strates the possibility of either limited degeneration, or what is more fre- 
quently found—almost universal invasion of the arterial tree with con- 
secutive changes in many organs. The correct conception of the causes 
and nature of the pathologic processes included in arterial degeneration 
proves the complex character of the lesions in the individual case, that 
the prognostic and clinical problems are among the most complicated and 
obscure in the whole field of internal medicine, and that the dictum of 
Bimce finds profitable application in connection with our study of this dis- 
organizing process, in which he holds: “The best prognostic use to make 
of symptoms and signs is indirect; not to value them individually, but to 
diagnose by them the cause and nature of the pathologic process, and then 
to frame our forecast by these.” 
Arteriosclerosis furnishes the fundamental morbid processes in the 
larger number of deaths after the fortieth year. Arteriosclerosis of the 
heart, kidney and brain is the cause of 22 per cent of all deaths after the 
fortieth year of life. 
Advanced arteriosclerosis is synonymous with old age. Whenever 
402 ARTERIOSCLEROSIS 
403 
present, the changes are suggestive, for we find the skin altered and 
wrinkled, the parenchymatous organs and muscles atrophied, the hones 
show trophic changes and fracture easily and the mental status is below 
par. 
The pressure in the aorta and peripheral vessels in the aged is not 
necessarily the same, it is higher in the ascending aorta and in conse- 
quence is lower in the periphery. 
The increase of cardiovascular disease during the past two decades has 
been recognized by all clinicians. This increase is greater the farther we 
are separated from hospital practice. 
Of 5,708 cases of internal disease seen in our private practice during 
the past seven years of which we have full records, there were 623 cases of 
marked and advanced arteriosclerosis 10.8 per cent, 101 cases of angina 
pectoris, 1.77 per cent, and 110 cases of chronic interstitial nephritis, 1.9 
per cent. 
The change is appreciated when we quote from a long-hand written 
report of the lectures of Benjamin Rush delivered over 125 years ago, in 
which that experienced and busy clinician makes the statement that he 
had seen but “one case of angina pectoris” and mentions the name of 
another Philadelphia physician who had also seen but one case. 
The gravity of arterial degeneration is shown further by the increase 
of other heart lesions directly dependent upon the same process. Thus in 
an analysis of our cases, we find 4.2 per cent showing evidences of degen- 
erative endocarditis; (in contradistinction to inflammatory) 4.7 per cent 
of aortic obstructive and degenerative lesions of the aorta, and 8.6 per cent 
of myocardial degenerations. 
The study of our material justifies the conclusion that hurry, worry 
and excesses are at the bottom of the majority of our cases; the stress of 
modern life, syphilis, and the enormous influence of heredity are among 
the leading factors with which we must reckon. 
In all cases there is a period of hypertension, either recognized or un- 
recognized which precedes the fully developed symptoms which are directly 
due to arteriosclerosis—to this we will again refer. 
There is a physiological hyperplasia of the intima during early life. 
For purposes of diagnosis and prognosis we consider the separate 
artery as an organ, a part of the body which has positive functions to per- 
form; its task is not single but multiple; the performance of its daily 
undisturbed work is attended even during the earliest years of life with a 
compensatory deposit for the preservation of these organs and the con- 
tinuity of the circulation. As soon as this physiological hyperplastic change 
of the intima because of age, overwork, strain, toxemia, or from any other 
cause is forced into a stage of hypertrophy, we have the beginning of 
arteriosclerosis. 
The leading factors which influence prognosis are the following: 404 
DISEASES OF THE CIRCULATORY APPARATUS 
1. Age 
Arteriosclerosis is present more or less advanced in most subjects who 
have lived beyond the fiftieth year. If the arterial tree is subjected to 
critical microscopic examination this fact is fully established. 
Arteriosclerosis may persist for years without giving rise to a single 
symptom, without in any way interfering with the comfort of the indi- 
vidual ; it is well borne when it is associated with the tolerance and com- 
pensation that are expected in the subject advanced in life. These favor- 
able conditions do not prevail during early life. 
Young subjects do not bear arteriosclerosis well; in these, evident and 
palpable lesions are not long present without marked evidences of progres- 
sion and the development of organic lesions in vital organs, unless the 
process is promptly controlled by proper treatment. If of syphilitic origin 
and not far advanced the artery may and often does yield to intensive 
treatment. 
No person is too young or too old to be thoroughly searched for arte- 
rial change; the prognosis so far as tolerance and length of life are con- 
cerned is unfavorable in the younger subjects. 
Romberg in 174 male patients, excluding all juvenile arteriosclerosis at 
the Marburg Klinik found arteriosclerosis: 
Between the 20th and 29th year in 4.89 per cent. 
Between the 30th and 39th year in 14.28 per cent. 
Between the 40th and 49th year in 29.67 per cent. 
Between the 50th and 60th year in 41.55 per cent. 
Between the 60th and 69th year in 57.77 per cent. 
Among 703 females: 
Between the 30th and 39th year in 0.78 per cent. 
Between the 40th and 49th year in 6.1 per cent. 
Between the 50tli and 59th year in 34.25 per cent. 
Between the 60th and 69th year in 52.00 per cent. 
Severe arteriosclerosis in young subjects involving the aorta and other 
vessels are not uncommon. Andral, Pischl and Chiari, found in all sub- 
jects examined in Prague between 2 and 25 years of age 48.7 per 
cent with beginning evidences of arteriosclerosis in the intima of the 
aorta. 
When arteriosclerosis is the prime cause of death, it is likely to claim 
its victims during the productive years when they ought still to be able 
to continue their occupations; as Bruce has said “when work ought to be 
still carried on in the interest of the family and country, at an age when 
a man’s reasonable ambitions, as a rule, have not been attained.” Grass- 
man offers the following data which corroborate our conclusions: Of 151,- 
083 who died in Germany 13,247 had cardiovascular lesiohs, including 
cases of cerebral apoplexy. Prom 15 to 30 years he found diseases of the ARTERIOSCLEROSIS 
405 
circulatory organs the cause of death in 7 per cent; between 30 and 60 
years 14.5 per cent of all deaths were due to the same causes. In Bavaria 
in 1907, 17,000 died of diseases of the cardiovascular system and 7,000 of 
cancer, thus two groups were responsible for 25 per cent of all deaths. 
2. Heredity 
The influence of family history on the prognosis of arteriosclerosis 
is paramount. In subjects burdened with the family history of arterio- 
sclerosis there is progression of the degeneration on slight cause. 
Histories in which one or both parents and several of their children 
have died of coronary disease are not uncommon; neither are the instances 
of cerebral hemorrhage in many members of a family at almost the same 
age unusual. 
The appreciation of the influence of heredity on prognosis, interpreted 
by the physician and the patient, may if heeded, lead to rational cautious 
living and appropriate occupation, which will often postpone unfortunate 
tendencies and thus prolong life. 
3. Syphilis 
We have elsewhere considered the influence of specific infection on the 
arterial tree (See Syphilis of Arteries) and will also consider aneurismal 
dilatations which are often of specific origin, separately. 
It is a fact that arteriosclerosis (arteritis specif ca), of syphilitic origin 
when early recognized is amenable to treatment and may yield after severe 
and threatening subjective symptoms. 
4. Worry and Stress 
The arteriosclerosis which follows long continued worry and stress, par- 
ticularly with unfavorable family history, is likely to advance insidiously, 
to involve vital organs (heart and kidney), before subjective symptoms 
are sufficient to bring the patient to the physician. The obstruction in the 
arterial tree is shown by persistent hypertension and hypertrophy of the 
left ventricle, all of which make the prognosis grave. It is surprising, 
however, to note how in individual cases, if the patient is removed to a 
favorable environment, where rest, relaxation with freedom from care and 
rational living obtain, he improves, and how his life may be prolonged. 
With the baneful factors continuing, such lives are promptly ended, usu- 
ally with evidences of added myocarditis and chronic interstitial nephritis. 
(See Occupation in this chapter.) 
5. Alcohol 
Alcohol is directly and indirectly a factor of the greatest importance 
in the causation and prognosis of arteriosclerosis. Alcoholics are as a rule 406 
DISEASES OF THE CIRCULATORY APPARATUS 
careless of their health, some are inordinate eaters, some have perverted 
appetites, others to tempt their appetites use deleterious condiments (pep- 
per, etc.) ; they eat at irregular hours; while alcohol itself may not pro- 
duce hypertension and arterial change, the productive changes wrought in 
liver, heart, brain and kidney, with the factors above mentioned lead indi- 
rectly to arteriosclerosis and the inclusion of the changes in the vital or- 
gans which lower the resistance of these subjects and lead to death. The 
contention of Richard Cabot that alcohol does not cause arteriosclerosis 
based on the examination of the arteries of alcoholic inebriates has not 
been generally accepted by the profession; as we have intimated we know 
that a large number of alcoholics die of cardiovascular disease, particu- 
larly arteriosclerotic processes and must accept that fact as proved in 
framing a forecast. Ilarlow Brooks’ report of 400 autopsies and the clin- 
ical evidences obtainable are sufficient to establish the influence of alcohol 
on arterial disease. 
The following is the table compiled from Brooks’ statistics: 
Artery. 
Cases. 
Etiological Factors. 
400 
Alcohol, 149; among laborers, 115; nephritis, 51; 
syphilis, 38; old age, 38. Males, 275; females, 
125. 
Aorta 
301 
Visceral trunks 
368 
Coronary arteries 
270 
Alcohol, 107; nephritis, 35; syphilis, 27; excessive 
tobacco, 9. 
Alcohol, 48; nephritis, 21; syphilis, 19. 
Alcohol, 43; nephritis, 10; syphilis, 10. 
Alcohol, 19; syphilis, 9; senility, 9. 
Alcohol, 12; nephritis, 8; syphilis, 6; senility, 3. 
Alcohol, 9; syphilis, 7; nephritis, 4; endocarditis, 
2; senility, 2; tuberculosis, 2. 
Alcohol, 4; syphilis, 5; senility, 5; tuberculosis, 4; 
nephritis, 2. 
Most of them with alcoholism. Sclerosis of 
mesenteric, all cases with adiposis. 
Alcohol, 4; syphilis, 4; most of the rest in primary 
spinal diseases. 
Brain 
132 
Renal 
81 
Pancreas 
74 
Hepatic 
43 
Splenic 
35 
Lungs 
Celiac axis 
19 
Spinal vessels 
20 
Alcoholic parents beget children who are likely to develop arterio- 
sclerosis early in life. 
6. Lead 
Lead poisoning leads to hypertension, arterial thickening, chronic ne- 
phritis and when advanced offers an unfavorable prognosis for Restitutio 
ad integrum. When detected early, and the patient is removed from the 
atmosphere of lead, the prognosis is not unfavorable, though the arteries 
remain permanently altered. ARTERIOSCLEROS1S 
407 
7. Tobacco 
Lauder Brunton says of the influence of nicotin, “The rise of blood 
pressure is so great that I have never seen it equaled after the injection 
of any drug, with the exception of suprarenal extract. The rise is due to 
contraction of the arteries. The ultimate effect is to increase the rapidity 
of the heart.” I am fully satisfied that in many cases tobacco is among 
the cause of arteriosclerosis, that it aggravates existing hypertension and 
arterial degeneration, that unless used in moderation it is injurious to 
adults and that for growing boys it is “distinctly harmful.” 
The use of tobacco in the presence of hypertension and arteriosclerosis 
acts unfavorably on the organic process. 
8. Infection 
The influence of infection in causing hypertension and arterial change 
has been noticed and studied by most clinicians. Thayer and Brush ex- 
amined 4,000 consecutive cases admitted to the Johns Hopkins Hospital 
and found changed arteries in the percentages noted of the patients under 
fifty years of age who had been the subjects of the following factors: 
After scarlet fever, radials palpable in 16.4 per cent. 
No causal factors with palpable radials in 16.5 “ “ 
Pneumonia, radials palpable 17.0 “ “ 
Diphtheria, radials palpable 17.0 “ “ 
Malaria, radials palpable 20.0 “ “ 
Typhoid fever, radials palpable 26.0 “ “ 
Rheumatism, radials palpable 34.0 “ “ 
Alcoholics, radials palpable 46.8 “ “ 
Hard work, radials palpable 57.5 “ “ 
Added infection of any kind in subjects with pronounced arteriosclero- 
sis is always serious and adds enormously to the danger. Pneumonia is 
almost uniformly fatal in the presence of advanced arteriosclerosis, while 
typhoid fever, sepsis, rheumatism, and erysipelas also offer unfavorable 
prognoses. 
With some acute infections in the presence of arteriosclerosis the pulse 
may continue slow, full and reasurring during the first forty-eight hours 
(particularly with pneumonia), but soon there is a break, the blood pres- 
sure falls and the heart becomes insufficient. 
9. Occupation 
Occupation is of paramount importance in the etiology and prognosis 
of arteriosclerosis. 
Arteriosclerosis is the result of long continued wear and tear, more 408 
DISEASES OF THE CIRCULATORY APPARATUS 
tear, “which is the result of abuse,” than wear which as Weir Mitchell 
said is “the result of use.” 
The busy brain worker, the man of enormous responsibilities, the 
worker who with his worries is obliged to hurry, whose rest is insuffi- 
cient, who is wearing his bearings and holding the string taut, is grad- 
ually but certainly encouraging arterial degeneration, he may work dur- 
ing months or even years with hypertension, no warning has led him to 
relax until he has run to a fall and is beyond the stage of hypertension and 
has fully developed arteriosclerosis. This is the history of hypertension 
and arterial degeneration as it is found among professional men, includ- 
ing physicians, lawyers, bankers, brokers, engineers, all occupations which 
tax the brain and are sedentary. In physicians, the tendency is toward 
coronary disease. With but one notable exception all members of the 
Vienna faculty who have died within the past two decades have yielded 
to coronary sclerosis and myocardial degeneration. In our own country 
the number of physicians who are claimed by coronary disease or general 
arteriosclerosis is surprisingly large. 
Romberg says “Everyone acquires his arteriosclerosis within the circuit 
which he has taxed most.” 
There is no more interesting question in connection with the etiology 
and prognosis of arteriosclerosis than nervous stress. It “winds up the 
best brains in the community” (Bruce). The combination of “intellectual 
stress and emotional stress” which characterizes the “strenuous life” is at 
the bottom of physiological collapse. 
The early appreciation of the effect of occupation with appropriate 
treatment during the period of hypertension often does much to relieve 
the tension and prevent progression to organic change. In these cases 
the timely detection of a trace of albumin and an occasional hyalin cast is 
a warning which if recognized may prove life saving. 
The truth of Romberg’s dictum is proved by the location of the greater 
changes in the arteries in the different occupations. 
The brain, heart and kidney vessels show greatest changes in those of 
sedentary habits—i. e., in brain workers. In workingmen, the arteries of 
the extremities are most involved. In the wives of farmers the arteries 
of the legs are the seat of degeneration; among wealthy females we often 
find the mesenteries involved, often the coronaries, sometimes both. 
In all, when arteriosclerosis develops rapidly after an unrecognized 
period of hypertension there is likely to be kidney invasion; this is true 
of those cases in which there is enormous accentuation of the second pul- 
monic sound, in which the pulse continues tense, and there are evidences 
of hypertrophy of the left ventricle. Some of these apparently subacute 
cases may lead to death within a few months. 
In the majority, an early appreciation of the effect of occupation on 
prognosis by the individual, with prudent and cautious self-control, the ARTERIOSCLEROSIS 
409 
ability to bring appetite to reason, the practice of sobriety, temperance 
and abstinence, much can be accomplished to prevent the onward march of 
the degeneration. Benjamin Franklin’s aphorism is applicable, “Against 
diseases known, the strongest fence is the defensive virtue, abstinence.” 
10. Overeating 
The arteriosclerotic who cannot control his appetite, is unable to con- 
trol the process which threatens his life. Overeating invites and produces 
degeneration; it increases it because it throws an extra burden on the 
heart, vessels and digestive organs. It interferes with metabolism and 
chokes the furnace to the disadvantage of the cardiovascular system as well 
as most organs within the domain of the splanchnic and renal vessels. 
A single error of diet has often ended life which might have contin- 
ued in comfort during many years. This is particularly true of coronary 
sclerosis and myocardial degeneration. These are the deaths which are 
incorrectly attributed to “Acute indigestion” which are increasing with 
noticeable frequency. 
11. Mechanical Factors 
Mechanical factors have a decided influence on prognosis, the sclerosed 
artery has been robbed of its elasticity, it is lengthened and abnormally 
tortuous, it demands auxiliary force (vis a ter go) which in the end may 
prove insufficient. The ability of the heart muscle to continue to compen- 
sate for the lack of assistance normally offered by artery and muscle, to 
which it has been accustomed, naturally influences the prognosis enor- 
mously. 
Mechanical strain aggravates existing sclerosis and may lead to rup- 
ture and sudden death or to aneurism. 
12. Chemical and Toxic Factors 
Chemical and toxic factors unquestionably exert a baneful influence. 
These may be provocative of hypertension, or when present the continuous 
poisoning increases the ravages of the process in all directions. The re- 
tention of wornout material, the results of faulty metabolism, persistent 
hyperglycemia (Diabetes mellitus), the blood surcharged with uric acid 
and its products, with gout, the other toxic states which are associated 
with faulty secretion and excretion, the influence of the ductless glands, 
particularly the adrenals in throwing their secretions into the blood-stream, 
are all factors which need to be considered in framing the prognosis of 
the individual case. 
The “Metabolic group” is important, for in these cases there is mal- 
nutrition, the tissues are poisoned by the products of malassimilation and 
as Bruce has well said are starved at the same time.” 410 
DISEASES OF THE CIRCULATORY APPARATUS 
Diabetics usually show evidences of marked arteriosclerosis, the dis- 
ease is rarely hypotensive, usually there is a normal or elevated blood 
pressure and often the pancreatic arteries are markedly changed. (See 
Diabetes mellitus.) Gout shows cardiovascular changes in almost 50 per 
cent of cases. 
13. Hypertension 
There is a considerable period of hypertension which precedes pro- 
found changes of an organic nature in the arterial tree, which however, 
in the majority of cases is not recognized, because of a natural tolerance; 
and the almost immediate compensation. 
If hypertension persists unrelieved, and the factors which continue it 
remain uncontrolled, organic changes in vital organs are usually present, 
particularly in the heart, kidneys and within the splanchnic area, before 
the patient presents subjective manifestations. 
Hypertension long continued is the leading cause of arterial degen- 
eration. 
Prognosis of hypertension depends entirely upon the time of its rec- 
ognition, in no other way than by early recognition can its influence on 
heart, peripheral vessels, kidney and brain be controlled. 
‘ When arteriosclerosis is established, hypertension is not a necessary 
feature; our statistics elsewhere given in this chapter prove that arterio- 
sclerosis may show normal, subnormal or high blood pressure. (See Blood 
Pressure Study.) “As a raised blood pressure is itself productive of 
degenerative changes in the vessels, we have good grounds for believing 
that if the rise be detected early, and counteracted by proper regimen and 
treatment, the vascular changes which it would otherwise produce might 
be prevented, and life very considerably prolonged. The earlier this is 
done the better, and I think it is only likely to be done by the sphygmo- 
manometer being used as frequently by the physician as the stethoscope or 
thermometer are at present.” (Lauder Brunton.) 
The prognosis is good when with hypertension there are no evidences 
of associated lesions. 
Hypertension in young subjects with uniformly thickened arteries, 
smooth and tense, who appear prematurely old, demands a guarded 
prognosis; it is usually progressive. 
Hypertension with marked renal symptoms, often without albumin, 
“non-albuminuric nephritis” is no longer uncomplicated, but in such sub- 
jects the degeneration of the arteries has commenced and the prognosis 
must be made accordingly; these are amenable to treatment. While the 
organic changes cannot be overcome or influenced unless specific, the prog- 
nosis so far as life is concerned is not necessarily bad. 
It may be safely concluded that uninfluenced hypertension in most 
cases is associated with changes in the renal vessels, the process is partly 
glomerular and partly includes the lesions of the granular kidney. ARTERIOSCLEROSIS 
411 
14. Kidney Invasion 
With advanced arteriosclerosis there are, as a rule, marked changes 
in the kidney substance; the evidences of nephritis are positive. Patholo- 
gists and clinicians in the study of arteriosclerosis have during the past 
sixty years made repeated attempts to satisfactorily explain the sequence 
of invasion of the heart, arteries and kidney and their reciprocal relations 
without reaching conclusions which may he accepted as final. The clini- 
cian knows that there are cases in which the process in the kidney seems 
to he primary and the arterial and heart changes secondary, on the other 
hand, there are cases in which the clinical history proves the presence 
of arteriosclerosis and heart compensation before there are positive evi- 
dences of interstitial, or mixed nephritis. Post mortem investigation 
shows the invasion of the kidney in the overwhelming number of cases 
of advanced arterial degeneration. 
The recent investigations of Fischer, J., who'examined 550 cases of 
marked hypertension in which the clinical and pathological evidences of 
nephritis were carefully noted are interesting: 62 per cent of these 
showed positive evidences of nephritis; 15 per cent were suspicious; 23 
per cent gave normal urines. Excluding cases with blood pressure below 
160 mm. Hg. in only 3.6 per cent was the urine normal. Autopsies of 42 
cases showed positive nephritis; in 14 of these the urine during life 
showed no evidences of kidney disease. Krehl from his material reports 
in patients with a blood pressure of 200 mm. Hg. or higher 87.4 per cent 
with nephritis—of these he autopsied 43 cases, of which 42 gave positive 
evidences of nephritis. 
Adami says “arteriorenal problems are among the most complicated and 
obscure in the whole of pathology.” 
In presenting this subject we feel the safest conclusion to reach is 
that arteriosclerosis and hypertension may occur without the symptoms 
of renal invasion, that with high blood pressure, tense thick arteries, 
hypertrophy of the left ventricle, there is nephritis in almost all cases. 
The absence of albumin and casts from the urine during long periods 
with such positive objective features does not argue against the presence of 
nephritis and the prognosis should be accordingly made. 
With arteriosclerosis in any of its stages the prognosis is unfavorable in 
proportion to the extent of kidney involvement. 
15. Coronary, Myocardial, Endocardial and other 
Heart Lesions 
In all cases of arteriosclerosis in which there have been evidences of 
coronary disease the prognosis for Restitutio ad integrum is had, though 
life may he prolonged, and the patient may die of intercurrent disease 
years after the initial symptom of angina pectoris or anginoid disease. 
The coronary trunks may he atheromatous, tracing them into their 412 
DISEASES OF THE CIRCULATORY APPARATUS 
intramuscular network, the finer branches may be free from any trace of 
disease and thus sufficient blood is sent to the myocardium to maintain 
the left ventricle. Such cases, unless overtaxed, may live many years 
with but few symptoms. Patients may have a single severe attack of 
angina pectoris or suffer repeated “small attacks,” symptoms may he 
present which prove deep involvement of the coronaries and yet the heart 
pang and other reminders of coronorary sclerosis may he absent for 
months or years at a time; and it is not at all unusual, particularly in 
thoroughly treated specific cases, or in cases which have developed mur- 
murs and slight dilatation to find the symptom complex permanently re- 
lieved. We refer the reader for the full consideration of the prognosis 
of coronary disease to the chapter on Angina Pectoris. 
Myocardial degeneration associated with arteriosclerosis is always 
ominous; this is especially true of the senile heart, when overtaxed. The 
prevention of mechanical strain often makes it possible for these patients 
to live comfortably during many years; life may be sacrificed by a sin- 
gle indiscretion. 
Arteriosclerosis of specific origin leading to myocarditis may yield to 
treatment. 
With long continued hypertension and an overworked heart, there is 
great danger of sudden revolt of the heart muscle with disastrous results. 
With necrotic processes in the myocardium resulting from coronary occlu- 
sion, the prognosis is bad. Coronary disease is the most frequent cause 
of disorganizing changes in the myocardium. The closure of one branch 
of the coronary does not always lead to death. Such advanced disease is 
always serious. 
The condition of the heart muscle is the most important factor in the 
prognosis of arteriosclerosis, in the myocardium rests the key of the heart 
and upon it we must depend. 
In our experience myocardium degeneration accompanied one-sixth of 
all cases of arteriosclerosis at the time of its detection. The prognosis 
of myocardial degeneration is fully considered in another chapter {Myo- 
carditis) . 
Advanced arteriosclerosis is associated with compensatory hypertrophy 
of the left ventricle. So long as these changes'are sufficient, m the ab- 
sence of added complications, the prognosis for life is good. Such subjects 
may live for years without inconvenience unless they overtax their cardio- 
vascular system. We cannot subscribe to the dictum which holds that such 
hearts prove as resistant as normal hearts. They are not, they do not brook 
insult, they revolt on slight cause. 
With advanced coronary sclerosis there is reduced heart strength and 
dilatation may lead to sudden death. 
Long continued hypertension with hypertrophy of the heart is asso- 
ciated with nephritis in most instances and offers a bad prognosis. ARTERIOSCLEROSIS 
413 
The condition of the peripheral arteries and the kidney are important 
factors to be considered in connection with the heart anomalies of arterio- 
sclerosis. 
Marked accentuation of the aortic second sound is proof of increased 
peripheral resistance and with aortic obstruction (vascular), showing itself 
in a well marked basic systolic murmur, we may be sure of advanced 
sclerosis, usually including the ascending aorta; conditions which are 
permanent but with favorable environment and right living the patient 
may live during many years. 
Naturally aneurismal dilatation of the aorta alters the prognosis. 
With marked widening of the ascending aorta and a corroborative 
x-ray picture, we have often found an area of tympany and exaggerated 
breathing to the right of the sternal edge in the aortic space and around 
it and the aortic impulse increased; this is of serious moment. Usually 
these cases are associated with coronary disease. (See Aneurism of the 
larger arteries.) 
The frequency of the pulse with persistent high blood pressure is of 
prognostic significance. Rapid pulse, whether intermittent or arhythmic, 
with myocardial or other heart lesions, with or without high blood pres- 
sure tires the heart and reduces the chances of prolonging life. Inter- 
mission, arhythmia and irregularity, may persist during years without 
shortening the life of the patient. Such anomalies are well borne in older 
subjects; in the young in whom they arise suddenly, life is at once threat- 
ened. The prognosis is always better in those cases in which the heart 
has gradually fallen into the habit of being erratic and the muscle has 
learned to accommodate itself. None of the hearts with the above men- 
tioned anomalies are dependable, though they may serve when undisturbed 
by added complications during surprisingly long periods. 
Cardiac asthenia and pulmonary edema due to cardiovascular degen- 
eration are usually terminal conditions and of grave import. Even these 
threatening complications may with proper care be followed by long 
periods of comparative comfort. 
The endocardial changes of arteriosclerosis are degenerative and not 
inflammatory. The greater the invasion of the aortic cusps and the adja- 
cent endocardium the worse is the prognosis. Simple aortic obstruction 
without incompetence due to roughness of the valves and the ascending 
aorta may persist during years without causing damage or symptoms 
when uncomplicated. 
When the aortic cusps are so malformed as to become insufficient, a 
different picture is presented; the heart has an added burden, its further 
hypertrophy follows, the pulse amplitude shows the enormous load which 
such hearts are carrying and degenerative myocarditis, apoplexy, uremia 
or other complications must be expected. Such hearts are ready to sur- 
render on slight cause. 414 
DISEASES OF THE CIRCULATORY APPARATUS 
Increase of 'physical signs particularly in arteriosclerotics with dia- 
betes and gout, fresh murmurs (aortic) with evidence of insufficiency 
is always ominous and shortens life. With aortitis and diabetes the prog- 
nosis is bad; there is always danger of corna. 
Gangrene when an evidence of endarteritis obliterans is not a limited 
process, there are often associated metabolic faults (diabetes, gout), the 
arterial tree is extensively involved and prognosis as a rule is bad. Life 
has been prolonged in some cases by surgical interference but the exten- 
sion is not usually long. 
16. Vascular Crisis 
(Spasm) 
et Vascular crisis” is a term which was introduced very largely as the 
result of the investigations of Pel to characterize recurring, suddenly 
arising symptoms of a painful character in the domain of changed 
arteries. 
Vascular crises are associated with diseased arteries in which the 
definite symptom-complex is due to vascular contraction, temporary nar- 
rowing of the artery; occasionally extreme dilatation or vasodilator 
paralysis may predominate. 
Vascular spasm or crisis explain the sensory symptoms included in 
anginous attacks, intermittent claudication, some cases of Adams-Stokes 
phenomenon, evanescent muscular pains and cramps in the subjects of 
arteriosclerosis, abdominal angina, or the Dyspragia intestinalis inter- 
mittens of Ortner; the crisis of tabes in cases associated with arterial 
degeneration, a condition which is often present early in young tabetics 
and many cerebral and spinal symptoms of short duration. 
Vascular crises are provoked by factors which throw an extra tax 
upon the heart and the organ invaded. This is a fact of enormous impor- 
tance to be considered in prognosis and treatment. 
Vascular spasm is evidence of developed arteriosclerosis, and is not 
present, in our experience during the early stage of hypertension; it 
always adds to existing dangers; more when vital organs (heart and 
brain) are involved. 
The anginous attacks we have considered elsewhere; most of these 
are due to coronary spasm. 
Intermittent Claudication 
(Dysbasia intermittens angiosclerotica) 
Vascular spasm of the lower extremities usually provoked by walk- 
ing or movement of the limbs to which Erb called attention, and which ARTERIOSCLEROSIS 
415 
is increasing with the increase of arterial degeneration may recur during 
long periods, may be associated with erythromelalgia, Raynaud’s Disease, 
or may in cases of advanced obliterating endarteritis precede gangrene 
during long or short periods. Erythromelalgia as we have demonstrated 
(Eisner) is usually due to arteriosclerosis. Its symptomatology includes 
the ured neuralgia” of Weir Mitchell, but contrary to his original con- 
tention it may ultimately lead to sufficient obstruction of the circulation 
to cause gangrene or limited necrobiosis. (See Erythromelalgia.) 
Acroparesthesia and many of the other sensory disturbances of the 
extremities are due to arteriosclerosis and associated vascular spasm. (See 
Acroparesthesia.) 
Threatening brain symptoms—vertigo, transitory paralyses, aphasia, 
also paraplegia and temporary abeyance of function in other organs are 
often warnings of approaching danger due to vascular spasm. 
Transitory blindness in one eye in the subject of arteriosclerosis may 
be dependent upon vascular spasm. In this connection the experience 
of Wegenmann is corroborative. Wegenmann’s patient was a man aged 
sixty-three years who had arteriosclerosis and who had transitory periods 
of blindness in his right eye. On one occasion Wegenmann was present 
when the patient became suddenly blind. An ophthalmoscopic examina- 
tion was made; the arteries during the period of blindness were found 
empty. They were converted into threadlike shining strands, yellow in 
color. ISTormal pulsation had ceased. The veins resembled threadlike 
but red strings. Pressure on the eye did not cause pulsation. This con- 
dition continued during ten minutes, the observer found as the spasm 
was relieved, the arteries filled and the veins dilated, with a return of 
pulsation and of sight. 
It is a question whether the pains of lead colic, in which we know 
there is arterial change (hypertension) are not due to vascular spasm. 
The prognosis of arterial spasm is not encouraging—an expression of 
fully developed arteriosclerosis—it is a symptom of a far-reaching 
process. 
When vascular spasm causes the Adams-StoJces phenomenon because 
of arterial change in the vascular supply of the intraventricular septum, 
a condition which is not unusual, the prognosis of non-specific cases is 
absolutely bad. With specif c arteritis it may cause sudden death. 
Vascular spasm of the cerebral and spinal vessels has in some of our 
cases persisted during a number of years; finally these patients invariably 
succumbed to the underlying conditions. 
Unless vascular spasm is dependent upon a removable cause such as 
syphilitic end-arteritis there may be improvement and temporary relief 
but never cure. 416 
DISEASES OF THE CIRCULATORY APPARATUS 
The influence of cerebral, spinal and peripheral changes of the ner- 
vous system and psychoses are separately considered. Neurasthenic 
conditions are common and rebellious. (See Neurasthenia.) 
17. Cerebral, Spinal and Peripheral Changes 
18. The Blood Pressure Study of Arteriosclerosis 
{after the stage of hypertension) 
The revelations of the sphygmomanometer (blood-pressure study) are 
too often misinterpreted to the disadvantage of the patient; this is par- 
ticularly true of blood pressure in connection with arteriosclerosis. The 
suggestion to the patient that he “has blood pressure” is often depressing 
and starts an autosuggestion which may prove injurious. 
With increased blood pressure sufficient to “meet physiological de- 
mands” the various tissues of the body are given a sufficient blood supply. 
Occasionally a high blood pressure causes weakness of the diseased walls 
of the vessel and rupture results, “a high blood pressure with this excep- 
tion is not to be regarded as something evil, but as an attempt on the 
part of the body to keep our various organs working at their physiological 
optimum” (Fisher). Elevated or changed blood pressure is therefore 
often a conservative and compensatory process to be left undisturbed; at 
times encouraged; it is a balancing and protective measure. 
Blood pressure study alone offers much less information of value in 
framing prognosis than is generally supposed. 
Arteriosclerosis may be far advanced without marked change in the 
systolic pressure, it may remain normal; in some cases there is, after 
the initial period of hypertension persistence of the same pressure, while 
in another class of cases there may even be hypotension. 
In the cases of advanced arteriosclerosis mentioned in the beginning 
of this chapter in connection with the study of 5,708 cases of internal 
disease I found persisting hypertension (above 180 mm. Hg.) in 181 
cases or 3.17 per cent and striking hypotension in 21 cases. In 623 
arteriosclerotics the per cent of hypertension cases was 29. Sawada 
found of 206 cases of arteriosclerosis, 122 not complicated with marked 
lesions, 12.3 per cent with high blood pressure. In 75 with heart com- 
plication and albuminuria 30.6 per cent showed hypertension. Janeway 
found 11.9 per cent of all of his cases of internal disease (7,872 patients) 
with systolic blood pressure above 165 mm. Hg. and 458 of these had 
permanent hypertension. Of 870 patients with hypertension at some 
time 62.4 per cent were men and 37.6 per cent were women. Of the 
458 cases of persisting hypertension 67 per cent were men and 33 per 
cent women. Janeway found at the end of the nine year period the 
number of men dead were 6.2 per cent more than living; women living ARTERIOSCLEROSIS 
417 
were 35 per cent more than dead. Thus 20.6 per cent more men died 
than women. This experience is confirmed by all observers—women 
bear arteriosclerosis better than men, unquestionably the prognosis would 
be the same if both sexes were exposed to the same conditions. 
Arteriosclerotics bear operations badly, this is particularly true of 
men with high blood pressure who subject themselves to prostatectomy. 
A number of these develop uremic symptoms with suppression of urine 
within 24 to 48 hours of the operation fall into coma and die. 
It will be seen from the statistics of Janeway and those which I offer, 
that arteriosclerosis is not necessarily a hypertensive disease. My figures 
differ because Janeway included all cases above 165 and I only those above 
180 mm. Ilg. 
Blood pressure study calls attention to possibilities and should be so 
interpreted. 
Young subjects who appear prematurely old with persistingly high 
blood pressure offer unfavorable prognoses. 
High pressure with renal changes, also cases of “non-albuminuric 
nephritis” and dilated heart or associated coronary disease offer unfavor- 
able prognoses. 
Pulse Pressure 
The study of the minimum or diastolic pressure which gives also the 
pulse pressure (difference between the systolic and diastolic pressure) is 
more important for prognostic purposes than the systolic pressure alone. 
It makes clear “the burden” which the heart is bearing. “Pulse pressure 
measures the energy of the heart in systole in excess of the diastolic 
pressure” (Stone). 
A sustained diastolic pressure of from 100-110 signifies hyperten- 
sion; it measures peripheral resistance and is therefore a “better index 
of hypertension than the systolic pressure” and “is less influenced by 
physiologic factors than the systolic pressure” (Stone). 
In cases in which the blood pressure is high, but the normal ratio 
between the maximum and minimum (systolic and diastolic) pressure is 
not markedly altered, we are justified in offering a favorable prognosis 
for the chances are against grave organic change in favor of a stage of 
hypercontractility of the walls of the vessels, which rational treatment 
may relieve. 
Sudden reduction of high pressure may lead to serious conditions, 
including anuria, coma, myocardial ■weakness and death. 
Low systolic blood pressure after a period of hypertension with neph- 
ritis usually leads to sudden death because of “cardiac defect” (Allbutt). 
The greatest differences in systolic and diastolic pressure, hence the 
highest pulse amplitude or pulse pressure, are found with advanced 
aortic disease (insufficiency), chronic interstitial nephritis with double 418 
DISEASES OF THE CIRCULATORY APPARATUS 
aortic murmurs and marked cardiac hypertrophy. All offer grave 
prognoses. 
Invasion of the splanchnics (the mesenteric arteries) is associated 
with high pressure during long periods and with persisting toxemia 
usually due to intestinal disturbance throws added work on the cardio- 
vascular system, influencing prognosis unfavorably unless promptly 
relieved. 
The great difficulty which we face in the problem of arteriosclerosis 
and blood pressure study is that we do not know the strength of the 
arterial wall; with normal or increased pressure miliary aneurisms of 
the cerebral arteries or ulcerating defects of the larger vessels may lead 
to hemorrhage {rupture) ; dilatations and various other irreparable 
complications. 
With changed blood pressure, cerebral warnings, including vertigo, 
spasm or convulsions, lapses of memory, active or passive cerebral hyper- 
emia, associated edema, sudden dyspnea, increase of kidney symptoms 
including uremic poisoning or indiscretions may be followed by a decided 
break leading to death. 
19. Thrombosis 
Arteriosclerosis is a frequent cause of thrombosis; the complication 
is always serious. With coronary disease suddenly developing thrombosis 
is a frequent cause of death. 
With sclerosis of the pulmonary artery, multiple organized and firmly 
attached thrombi are not infrequently found post mortem which must 
have antedated death during comparatively long periods; the patients 
dying of other causes. Arteriosclerosis of the pulmonary artery may 
exist without change in the arteries of the body; it is often found with 
mitral lesions and emphysema; in such cases there is increased blood 
pressure in the pulmonary circuit and hypertrophy of the right ventricle. 
Thrombi are more frequent in the smaller arteries and consecutive 
changes due to occlusion must be expected. 
Thrombi in the aorta are frequent and may start emboli to the brain 
or other vital organs. Hemorrhagic infarct secondary to aortitis with 
thrombosis in the brain, spleen, kidney or liver may lead to death. The 
thrombus of aortic aneurism is not so firmly attached as is the organized 
plug in the pulmonary artery. 
20. Ocular Changes 
Advanced arteriosclerosis particularly when associated with inter- 
stitial nephritis shows evidences of change in the retinal vessels. The 
presence of retinitis albuminuria with arteriosclerosis never justifies anv 
other than an unfavorable prognosis. Such patients stand on the edge ARTERIOSCLEROSIS 
419 
of a precipice and may fall at any moment. They rarely live two years 
after the onset of the retinitis. Cerebral apoplexy, uremia, pneumonia 
and sudden myocardial failure are the causes of death. 
Large and suddenly arising retinal hemorrhages are evidences of the 
terminal stage or far advanced disease. 
Advanced arteriosclerosis shows involvement of the retinal vessels in 
the majority of cases. The ophthalmoscope therefore is a valuable prog- 
nostic aid. 
21. X-ray 
The revelations of the Rontgen picture in individual cases will prove 
of value in prognosis. This is particularly true of changes in the aorta 
(aneurism, etc.), and in the differentiation of specific and non-specific 
arteritis. 
Our views concerning the prognosis of arteriosclerosis have been ma- 
terially changed during the past fifty years. This fact is proved by the 
following quotations from Bamberger, who represented the climax of 
medicine in Germany sixty years ago, and from Romberg, who stands 
today as the exponent of all that is advanced in cardiovascular pathology 
and diagnosis. Bamberger said, “Atheromatous processes cannot be 
cured, hence they cannot be treated.” Romberg holds: “While we are 
not able to alter the anatomic changes in the blood vessels, the seat of 
arteriosclerosis, we can nevertheless improve the functions of the organs 
invaded and exert material influence on the advance of the process.” 
The prognosis in every case of arteriosclerosis must be based not only 
on the subjective and objective manifestations which are evident, but a 
thorough inquiry into the patient’s entire history, the influence of his 
occupation and his habits, the diseases which he has had, his “constitu- 
tional strength and physical training and disposition in earlier years, and 
more remote than these, his inheritance.” (Bruce.) 
In no other process does inheritance, the character of the individual, 
his disposition, temperament and circumstances play such an important 
role. 
In arteriosclerosis there is often a single and .preventable cause, not 
an extension of the degeneration which produces the death of the patient. 
Much naturally depends on the location of lesions; limited arterio- 
sclerosis—a small plaque at the mouth of a coronary vessel—a small 
miliary aneurism of a cerebral vessel, circumscribed sclerosis with local- 
ized myocardial degeneration and rupture, may cause sudden death, while 
with disseminated change in the arterial tree, the patient may live for 
years in comfort, oblivious of his lesions. 
“The first requisite for longevity must clearly be the inherent or 
inborn quality of endurance; of steady, persistent nutritive force, which 420 
DISEASES OF THE CIRCULATORY APPARATUS 
includes reparatory force and resistance of disturbing effects; and a good 
proportion or balance between the several organs. The second requisite 
is freedom from exposure to the various casualties, indiscretions, and 
other causes of disease to which illness and early death are so much 
due.” (Humphry.) 
References 
Adami. Principles of pathology, etc. 
Allbutt. Brit. Med. J., April 22, 1911, 937. 
Andral, Fischl, Chiari. Quoted by Marchand. Eulenberg RealEncycl. etc. 2.ed.,i. 
Bamberger. Lehrbuch d. Krankh. d. Herzens, etc. Wien, 1857. 
Brooks (Harlow). Am. J. Med. Sci., 1906, cxxxi. 
Bruce. Lumeleian Lecture. Lancet, London, July 8, 1911. 
Cabot (Richard). Relations of alcohol to arteriosclerosis. J. Am. Med. 1904, xliii, 
774. 
Eisner. New York Med. News, 1897; idem, 1901. 
Erb. Deutsch. Ztschr. f. Nervenkrankh., Bd. xiii. 
Fischer (J.). Deutsch. Arch. f. klin. Med., 1913, cix, 469. 
Fisher. Nephritis, etc. 1912. 
Grassman. Munch, med. Wchnschr., Nov. 11, 1913. 
Humphry. Old Age. 11 & 12. 
Janeway. Arch. Int. med., Dec., 1913. 
Krehl. Lehrbuch der inner. Med. 8. ed. (von Mehring). 
Lauder (Brunton). Longevity and the means of attaining it. 
Ortner. Volkmann’s sam. klin. Vortrage N. F. No. 347. 
Pel. DieGefass Krisen. Leipzig, 1905. 
Romberg. Deutsch. Arch. f. klin. Med., Bd. xlviii; Kongress f. Innere Med., 1904. 
Krankheilen des Herzens u. Blutgef. 1906. 
Sawada. Deutsch. med. Wchnschr., 1904, xix, 435. 
Stone. J. Am. Med. Ass., Oct. 4, 1913. 
Thayer. Am. J. Med. Sci., 1904, cxxvii, 391. 
Thayer & Brush. J. Am,. Med. Ass., 1904, xliii, 726. 
Wegenmann. Quoted by Ortner [£. c.]. 
B. Aneurism 
Aneurism may be defined as a chronic dilatation of a blood vessel 
with productive (connective tissue) change of its wall, the cavity always 
communicating with the lumen of the artery. For our purpose we con- 
sider only the circumscribed and diffuse dilatations. The most common 
form of the former is the saccular aneurism, of the diffuse—the spindle 
shaped. 
Miliary aneurisms will be considered in connection with cerebral 
apoplexy. ANEURISM 
421 
Dissecting aneurisms are due to incomplete rents in the walls of a 
blood vessel; the layers of the vessel are undermined by the blood and 
consecutive deposit. This variety is of interest pathologically only. 
The leading pathogenic factors to be considered in the formation of 
aneurismal dilatations are diseased blood vessels, arteritis—usually spe- 
cific arteriosclerosis; besides syphilis, typhoid fever, diphtheria, endo- 
carditis (malignant) and other infections, traumatism and increased 
blood pressure. 
In our hospital and consultation practice we have found at least 90 
per cent of all cases due to syphilis. Malmsten found 80 per cent 
syphilitic. Recent experiences give positive Wassermann reactions with 
almost all aneurisms, particularly the aortic dilatations. 
Unquestionably syphilis leads to arteritis and arteriosclerosis in 
young subjects and thus lays the foundation for dilatation on slight cause. 
The prognosis of all aneurismal dilatation so far as life is concerned 
depends upon its location, its size, the condition of the arterial wall, the 
blood pressure, the strength and condition of the myocardium and valves, 
the extent of degeneration of the arterial tree, the relation of the growth 
to the surrounding organs, the amount of pressure it exerts, the extent of 
paralysis (particularly of the vagus'), the amount of pressure upon nerve 
trunks and bone tissue, the protecting influence of coagulation and throm- 
bosis within the sac, the results and amount of obstruction to the blood 
stream which folloivs, as well as many other factors, including lesions in 
vital organs, brain, liver and kidney, which are likely to be associated 
with cardiovascular disease. More than two-thirds of all aneurisms are 
found in men between the 38th and 60th year. Cominotti found aneu- 
rism five times as often in men than in women. He found 24 between the 
ages of 24 and 40 years, 29 between 40 and 50, 18 between 50 and 60. 
Marchand in 28 autopsies of aneurisms found 20 men and 8 women, 
2 were between 30 and 39 years of age, 6 between 40 and 49 years, 10 
between 50 and 59 years, 4 between 60 and 69 years and 6 between 10 
and 90 years. 
The greater frequency of aneurism in England and in the United 
States than on the Continent of Europe is established by statistical study. 
The negro is more disposed to aneurism than is the white man. Myers 
found in 320 deaths of soldiers in the English Army resulting from 
cardiovascular lesions 138 aneurisms; of 1,346 invalided soldiers 35 had 
aneurisms. Crisp reports 551 aneurisms, spindel and saculated, located 
as follows: 
Aorta (thoracic) 175 
Popliteal artery 137 
Femoral artery 66 
Abdominal aorta 59 
Carotid artery 25 422 
DISEASES OF THE CIRCULATORY APPARATUS 
Subclavian artery 23 
Innominate artery 20 
Axillary artery 18 
Iliac artery 11 
Arteries of the internal organs 8 
Cerebral arteries 7 
Pulmonary artery 2 
Cominotti found in 181 aneurisms, 37 of the ascending aorta, 49 of 
the arch of the aorta, 29 of the descending aorta and 16 of the abdom- 
inal aorta. 
Nature may either protect the arterial wall or occasionally, by its 
reparative process, cause obliteration of the sac and relative cure. Thus 
dense and organized coagula in moderate sized dilatations, without 
marked interference with heart or distant organs, may exist during years,, 
and death may be due to other causes. By the reinforcing of the aneurism 
with fibrous tissue the growth may become stationary. The tendency of 
all aneurismal dilatations is towards progression, with compression and 
adhesion to the surrounding organs. Rupture of the wall is the most 
frequent cause of sudden death. 
Thrombosis may prove sufficiently extensive to close the aneurismal 
sac and present a smooth surface to the blood stream. 
Moderate dilatations may be smoothed aud protected during long 
periods by dense and firmly organized thrombi. 
A small artery with aneurismal dilatation may be side-tracked by 
Nature’s processes without interfering with the heart or the general 
health. (Collateral Circulation.) (Jores.) 
Infectious processes, tuberculosis particularly, may cause ulcerative 
changes in the arterial wall leading to aneurismal dilatation. This 
method of producing aneurisms holds only for the smaller arteries. 
The mycotic-embolic aneurisms which arise during the course of 
malignant or infectious endocarditis are usually multiple and follow 
ulcerative changes in the walls of arteries. This is a part of a process 
which is always fatal. 
Embolic detachments from aneurismal walls are not frequent; occa- 
sionally they may lead to sudden death, hemorrhagic infarcts in the 
lung, spleen, kidney, brain or other organs; rarely to gangrene. 
X-ray examination of all aneurisms gives positive data which make 
clear the location, the size, the relations to surrounding organs, as well as 
other important facts ivhich bear upon the diagnosis and prognosis in 
individual cases. 
The further complications which influence prognosis are considered 
in connection with the separate aneurisms. ANEURISM 
423 
1. Aneurism of the Ascending Portion of the Arch 
of the Aorta 
Aneurism of the ascending portion of the arch of the aorta is a sequel 
of syphilitic aortitis, and is always fatal. 
When the x-ray shows the presence of the dilatation, the radial pulses 
are unequal, there are other evidences of pressure with secondary heart 
changes, death may be expected at any time. 
With aneurism of the aorta in any of its parts and associated coronary 
disease the patient’s life is in constant jeopardy; such a patient is “always 
dying.” 
The thickness of the aneurismal wall and the size of the aperture 
communicating with the aorta influence the force of the pulsation (“ex- 
pansile thrill”). The growth increases by expansion. 
Thin aneurismal dilatations just above the aortic valve or of one of 
the cusps of the valve may rupture into the pericardium without having 
caused previous symptoms (Aneurism of a Sinus of Valsalva). With 
these cases coronary invasion and aortic insufficiency is not uncommon, 
the latter at times leads to hypertrophy of the left ventricle. 
Dyspnea and cyanosis are not long endured, they indicate a tired 
heart and pressure with pulmonary obstruction. 
Edema of the upper extremities—one or both—when once established 
is likely to persist until death. 
Pulmonary ede?na on slight cause, particularly during and after 
coitus, is often a terminal symptom. 
All pressure symptoms, once established are likely to continue. 
The extent of compression showing itself in symptoms, is a valuable 
guide for prognosis and justifies conclusions which the experienced can 
usually reach concerning the average time which the patient may live—- 
barring sudden rupture which is always to he expected with all aortic 
aneurisms. 
2. Aneurism of the Transverse Portion of the Arch 
of the Aorta 
The anatomic location of the arch leads to symptoms of compression 
often before dilatation is far advanced. Aneurism of the arch of the 
aorta is likely to be associated with some change of the ascending por- 
tion also, as the process advances. 
The displacement of the heart, usually to the left, may exist without 
marked hypertrophy of the ventricle. When the aortic valve is insuffi- 
cient, as often happens, the hypertrophy is enormous. 424 
DISEASES OF THE CIRCULATORY APPARATUS 
Marked systolic bruit and tracheal tugging are evidences of advanced 
aneurism. 
Paralysis of the left recurrent laryngeal nerve is proof of advanced 
aneurismal dilatation in the presence of other physical signs and persists 
unrelieved to the end. If the innominate is involved, or if there is suffi- 
cient pressure, the right recurrent may also suffer; under these condi- 
tions the end will not be long postponed in the average case. 
The papillary changes are due to involvement of the sympathetic 
system and are proof of advanced disease. 
3. Aneurism of the Descending Portion of the Arch 
of the Aorta 
Aneurism of the descending ‘portion of the aortic arch may exist 
during a considerable period without causing symptoms. The recogni- 
tion is often postponed because of the failure to interpret the significance 
of the multiple symptoms of many intrathoracic lesions which are included 
when subjective complaints are made, and the further failure to take 
advantage of Rontgen examination. 
The aneurism may cause intercostal pain during a long period when 
finally positive evidences of compression in erosion of the dorsal vertebrae 
(usually third to the sixth) is added; there may be evidences of bronchial 
and lung pressure, or the mass may present externally in the scapular 
region. Rupture into the pleura, bronchus or lung is the fate of a large 
number of aneurisms of the descending portion of the arch. 
Early recognition of aortic aneurism wherever located which is pos- 
sible by x-ray examination with immediate rational treatment, including 
the indicated rest, offers the o?ily encouragement for the prolongation 
of life. 
4. Aneurism of the Descending Thoracic and 
Abdominal Aorta 
Aneurism of the descending aorta below the arch, may cause but few 
symptoms until advanced, when pains—intercostal and lumbar—with 
epigastric or thoracic pulsation persist. The stomach and liver may be 
displaced. With abdominal aneurism the systolic bruit can be distinctly 
beard posteriorly, a symptom of great diagnostic and prognostic value in 
doubtful cases. 
Erosion of bone (vertebrae) and other symptoms of compression, 
edema of the extremities are present in advanced cases. ANEURISM 
425 
3. Aneurisms of the Celiac Axis 
Aneurisms of the celiac axis or its branches may prove of anatomic 
interest, they may not be diagnosticated intra vitanu as there may be no 
symptoms. In one case I found the symptoms of hemorrhagic pancreatitis 
arise suddenly in a man age 65. The autopsy showed rupture of the 
disorganized axis into the pancreas. 
The prognosis of splenic, hepatic and renal aneurism is equally bad. 
There may be aneurismal dilatation of one of the mesenteric arteries, 
usually the superior, which causes vague symptoms, may lead to death 
from rupture or it may be accidentally discovered at autopsy. 
6. Aneurism of the Coronary Artery 
Aneurism of the coronary arteries is exceedingly rare, leads to death 
by rupture into the pericardium or heart muscle. (Wardrop.) Griffith 
has collected these cases in a splendid article. 
7. Aneurism of the Pulmonary Artery 
Aneurism of the pulmonary artery or its branches is also rare. Our 
experience includes one case in which we failed to make the correct diag- 
nosis (though aneurism was strongly suspected) because the aneurismal 
dilatation rested on the heart wall anteriorly and consequently did not 
show in the skiagram. Death resulted from rupture into the pericardium. 
8. Aneurism of the Subclavian Artery 
With subclavian aneurism we have seen long periods during which 
there was no advance of growth or symptoms. 
The growth of an aneurism is rarely continuous; there seem to be 
sudden exacerbation in many. The hope of prolonging life rests in the 
strengthening of the arterial wall and the organization of coagula 
(thrombosis) by Nature’s processes. 
Landraf reports a case of aortic aneurism in which paralysis of the 
recurrent laryngeal disappeared. This is exceedingly rare. 
The dissecting aneurism usually leads to early perforation; other 
aneurismal dilatations perforate in the later stages, after long periods 
of compression and expansion. Fifteen to twenty per cent of all aneu- 
risms perforate. The perforation usually leads to prompt death; in ex- 
ceptional cases a rent may be closed by a thrombus or perforation may 426 
DISEASES OF THE CIRCULATORY APPARATUS 
take place into organized tissue, into a vein or into the substance of a 
solid organ when death may be postponed for a short time. Location of 
an aneurism does not change the prognosis so far as its influence on life 
is concerned; with all, the outlook is equally grave, all stand on the edge 
of a precipice; when the fall is to follow no clinician can prophesy. 
We may safely conclude that aneurism is rarely cured by any method 
of treatment. Nature's methods of spontaneous relief we have already 
considered. 
Death is the fate of most patients with aneurism within from six to 
eighteen months after the diagnosis has been fully established. There 
are exceptions to this rule; cases are recorded by all experienced clini- 
cians which lived during years, but these are notable exceptions. 
References 
Cominotti. Wien. med. Wchnschr., 1901, No. 86. 
Crisp. Cited by Birch- Hirschfeld, Path. Anatomie. 
Griffith. Brit. Med. J., Feb. 2, 1901, 266. 
Landraf. Berl. klin. Wchnschr., 1901, No. 27. 
Malmsten. Aortic aneurism. Stockholm, 1888. 
Marchand. Romberg, Krankh. d. Herzens. 1906. 
Meyers. The frequency and causes of heart diseases, etc., 1875. 
Jores. Anat. Grundlage wichtige Krankheiten. 1913. 
C. Diseases of the Pericardium 
1. Acute Pericarditis" 
Acute pericarditis is a secondary inflammation of the pericardial sac, 
rarely primary, associated in the order of frequency with rheumatism, 
tuberculosis, pneumonia, pleurisy, scarlet fever and typhoid fever. It 
may also occur with other exanthemata as measles, smallpox, etc., and is 
not an infrequent accompaniment of septic and pyemic infection. It is in 
many cases coincident with valvular lesions—endocarditis and myocarditis. 
Echinococcus disease and actinomycosis may provoke it; it is occa- 
sionally found with gonorrhea, may follow extension of cancer and sar- 
coma from the surrounding organs, may be secondary to perforation of 
the esophagus or of the pleura with empyema; abscess of the liver and 
subphrenic abscess may perforate into the pericardium as may pyopneumo- 
* The reader is also referred to chapters on the separate infections where the 
prognostic significance of pericarditis is considered among the complications. DISEASES OF THE PERICARDIUM 
427 
thorax; gastric and intestinal ulcers with adhesions and inflammation may 
lead to pericarditis. 
Chronic interstitial nephritis is often associated with pericarditis. 
Romberg quotes Frerichs and Rosenstein as having found the sac in- 
flamed in 13 of 292 and 8 of 114 cases respectively—5.1 per cent. 
Pericarditis may also complicate scorbutus, other purpuric conditions, 
leukemia and pernicious anemia. 
Penetrating wounds of the thorax, gunshot wounds, erysipelatous in- 
flammation of the thoracic walls or phlegmonous infiltration with suppura- 
tion when they involve the heart sac usually cause purulent pericarditis as 
do also the malignant perforating diseases already mentioned; all offer 
unfavorable prognoses. 
The so-called idiopathic pericarditis of children is almost always of 
tuberculous origin in the absence of positive proof of other causes. (Rheu- 
matism, scarlet fever, etc.). 
When pericarditis accompanies puerperal sepsis it is likely to be 
purulent and fatal. 
Naturally pericarditis is found in those of all ages since it is an accom- 
paniment of so many infections, as well as other constitutional anomalies 
and accidents. 
The pericarditis of rheumatism is present in from 5 to 6 per cent of 
fully developed cases in adults and from 10 to 20 per cent in children. In 
the majority of these endocarditis with some change in the myocardium is 
present. There are occasional severe cases in which the heart sac is in- 
volved before there are evidences of arthritis. A large number of fatal 
cases of chorea with and without joint symptoms and tonsillitides are at 
times complicated by pericarditis and are of rheumatic origin. 
The prognostic significance of pericarditis depends almost entirely on 
the nature and gravity of the primary disorder. The reader will find the 
subject separately and fully treated in connection with the consideration 
of the complications of rheumatism, tuberculosis, pneumonia, scarlet fever, 
pleurisy, typhoid fever, erysipelas, chorea, tonsillitis and all other infec- 
tions, beside septic and pyemic conditions, to which he is referred. 
When pericarditis does not advance beyond the first or dry stage (peri- 
carditis sicca) it has, per se, very little influence on the course of primary 
disease. 
Romberg, however, reports 85 cases of pericarditis with 24 deaths, a 
high mortality. At Johns Hopkins Hospital Hoffman’s statistics show 
among 1,770 medical cases admitted (1902-1911) 1,317 (1,044 males, 
273 females) cases of circulatory diseases, among these were 22 diseases of 
the pericardium (14 males with 5 deaths—35.7 per cent) (8 females—2 
deaths—25 per cent), of these 11 males had pericarditis with 3 deaths, 
27.3 per cent, and 6 females with 1 death, 16.7 per cent. 
The effusion may be fibrinous, serofibrinous, purulent or blood stained. 428 
DISEASES OF THE CIRCULATORY APPARATUS 
The less severe types are fibrinous and serofibrinous with rheumatism; 
purulent effusion is associated with septic and pyemic infections and is 
always serious, usually fatal. 
Those purulent effusions are most serious which are associated with 
puerperal sepsis, pyemia, malignant endocarditis and in cases in which 
there are bands of adhesion which bind the heart anteriorly when the pus 
is held in the dependent portion of the pericardium beyond the easy reach 
of the operator. 
The blood stained eff usion is usually found with tuberculosis, cancer, 
sarcoma, purpura or scorbutus. It is always an indication of serious con- 
stitutional disturbance and is likely to end in death. 
The serofibrinous effusions with the infections (rheumatism, scarlet 
fever, tonsillitis) are, unless the primary disease leads to death, absorbed 
in the course of a limited period with resulting temporary or permanent 
adhesions. 
The extent of the adhesions and their permanency are important fac- 
tors in limiting the action of the heart and are considered in connection 
with adherent pericardium. 
Moderate adhesions with partial obliteration of the heart sac do not 
often lead to permanent subjective symptoms after recovery. 
Calcareous Pericarditis.—In a few cases there may be calcareous 
deposits in the pericardium, the prognostic significance of these depends 
entirely upon the extent of the degeneration, the condition of the heart 
muscle and the nature of the accompanying chronic changes in other 
organs. Purulent pericarditis may be followed by calcareous deposit; this 
is exceedingly rare as most purulent cases die. 
Acute Myocarditis.—Acute myocarditis may be complicated by peri- 
carditis. In these cases the spread is from the myocardium and invades 
the pericardium in the neighborhood of the primary muscle change. 
But few cases of pericarditis are without more or less myocarditis. 
The extent of the latter is of paramount importance. 
Myocardial inflammation associated with pericarditis when far reach- 
ing or in a previously weakened or diseased heart may lead to cardiac 
insufficiency. Dilatation of the heart is not infrequent; usually the right 
heart is involved, with relative muscular weakness. If in such cases the 
patient lives and there are adhesions or lowered vitality, myocardial de- 
generation may follow and there may be cellular infiltration, fibroid 
change or atrophy. 
The heart and surrounding organs are tolerant of pericardial effusion 
during long periods. The sac may contain a large quantity of fluid with- 
out threatening life. 
Rapidly increasing exudate is more threatening to life than is the 
gradual accumulation. 
X-Ray Examination.—The assistance received from the Rontgen DISEASES OF THE PERICARDIUM 
429 
picture is not always to be relied upon in the presence of moderate effu- 
sion ; it will nevertheless prove a valuable aid in prognosis in many cases. 
Pericardial adhesions are often beautifully clear in the picture, more par- 
ticularly the extrapericardial hands. 
Displacement of the lung with tracheal pressure and involvement of 
the mediastinum, often with paralysis of the recurrent laryngeal nerve, 
may prove serious and unless relieved becomes life-threatening. 
Pulmonary edema with insufficiency of the right heart and dilatation 
of the ventricle may lead to sudden death. 
When pressure leads to dropsy and there is associated myocarditis the 
prognosis is grave. 
Thrombosis, either pulmonary or in the left innominate, increases ob- 
struction and is usually fatal. 
Pericarditis with chronic Bright’s disease is a terminal complication 
(See Nephritis). 
Sy?nptoms referable to the nervous system as delirium, coma, convul- 
sions, marked apathy and prolonged insomnia are evidences of the graver 
infections. With osteomyelitis, pericarditis adds a large element of 
danger to an infection already malignant. 
The behavior of the temperature offers but little to guide in offering a 
forecast. Pericarditis may develop insidiously without marked rise of 
temperature or other symptoms; the temperature may on the other hand 
remain unchanged by pericardial involvement in the presence of the 
primary disease. 
With pyemic and septic pericarditis the advent may be heralded by 
a distinct chill and rise of temperature above the previous level. These 
chills as in all similar infections are likely to recur, to be followed by 
fever and excessive sweating, with or without added pericarditis. 
Physical signs, i. e., friction sounds, are more dependable than any one 
other symptom to mark the beginning of the pericardial complication. 
If large effusion continues unrelieved during long periods and in cases 
where after its removal it promptly reforms, the prognosis is bad. These 
patients fall into a chronic state of invalidism which ends in asthenia with 
symptoms of compression. 
Among the unfavorable symptoms are unusually large effusions, 
marked dyspnea, advanced myocardial weakness, small, feeble, erratic and 
rapid pulse, the pulsus parodoxus in cases with thickened pericardium, 
cyanosis, delirium, coma, albuminuria with scanty urine and evidences 
of septic nephritis, marked tremor, and in children persistent vomiting, 
hiccough and increasing anemia. 
The prognosis during early life is under all conditions less favorable 
than in the adult. In children under ten years of age most pericardial 
effusions are purulent. Mediastinal lesions with pericardial inflammation 
or extension of mediastinitis to the pericardium often lead to dense and 430 
DISEASES OF THE CIRCULATORY APPARATUS 
troublesome adhesions and heart weakness. These cases are likely to be 
subacute or chronic; reference is again made to them under “adherent 
;pericardium,.” 
The duration of the disease depends upon the nature of the primary 
infection. The average case runs its course in from 14 to 21 days, but 
there are so many factors to influence the complication that it is never 
safe to commit oneself to a time limit. 
In but few cases does pericarditis per se lead to death. 
Evidences of heart weakness, including dyspnea on exertion, fatigue, 
syncope, and erratic heart action may continue long after the beginning of 
convalescence. 
Valvular Lesions and Pericarditis.—Gerhardt, C., calls attention to 
the frequency of pericarditis with valvular disease of rheumatic origin. 
The evidences of endocarditis may remain unrecognized until the peri- 
cardial effusion has been absorbed. He further accents the fact already 
mentioned that in the presence of chronic valvular lesions pericarditis may 
arise without known cause insidiously, and may lead to permanent myo- 
cardial damage. The frequent association of pericarditis and aortic val- 
vular disease was shown in an analysis of 197 rheumatic cases with 
pericarditis in 17, and in 13 of these, the aortic valve was involved, once 
alone, in nine cases the aortic lesion was not prominent, in only four cases 
was the disease limited to the mitral valve alone. The relatively infre- 
quent involvement of the aortic valve with rheumatism would, from Ger- 
hardt’s anatomic experiences prove the greater tendency to complicating 
pericarditis with lesions of the aortic valve, the nearness of the overlying 
pericardium may be an important factor. 
Pericarditis complicating old heart lesions, chronic valvular defects or 
myocarditis is always serious. In these cases it matters- little what the 
primary cause of the pericarditis may be, the heart revolts, becomes rapid, 
dilates, there is pulmonary engorgement, general venous stasis, cyanosed 
kidney and unless treatment proves promptly efficacious, death results. 
In many cases the sequelae of pericarditis interfere with comfort and 
the prolongation of life. There may be adhesions, distortion and consecu- 
tive interference with the functional power of the heart which may finally 
lead to irreparable myocardial weakness. 
2. Adherent Pericardium 
(Chronic Pericarditis, Mediastinopericarditis) 
Adherent pericardium results from either acute or subacute inflam- 
mation. Stokes, Gardner and Walshe understood the results of pericardial 
adhesions. 
Their consideration of the results of adherent pericardium is unequaled DISEASES OF THE PERICARDIUM 
431 
by anything which has appeared since, with the exception of Broadbent’s 
treatise on the subject. 
Barlow and Chevers were agreed that hypertrophy and dilatation of 
the heart were not necessary sequences of obliteration of the heart sac or 
uncomplicated adherent pericardium. 
Walshe proved that after adhesions an atrophic condition of the muscle 
was more likely to result. In the light of more recent clinical data as 
reported by Krehl and Romberg, with pathologic observation, the fact is 
fully corroborated that hypertrophy or dilatation never follow complete 
obliteration of the pericardial spaces and that the heart itself may not be 
unfavorably influenced. 
With mediastinopericardial and pleural adhesions, fixation of the 
heart to the thorax, and the systolic retraction which is associated with 
adherent pericardium, immobile thorax often follows. The heart is forced 
to overexert, it dilates, it hypertrophies and may finally break; marked 
fibroid and atrophic changes follow. This is most likely to occur with asso- 
ciated valvular defects. 
In some cases, particularly where there are mediastinal pleuroperi- 
cardial adhesions, the x-ray examination will offer valuable assistance. 
With mediastinal, pericardial and pleural adhesions the veins at the 
base of the heart may be compressed leading to marked secondary changes 
in the heart and in distant organs. 
Probably the dilatation which exists in a large number of adherent 
hearts is due more to the diseased condition of the heart muscle than to 
pericardial interference. 
When hypertrophy follows in these cases the idght heart is usually most 
enlarged, the hypertrophy becomes a necessity because it must overcome 
the effect of preceding dilatation. In many cases in which the heart itself 
is tied down to the chest wall at some point or to the surrounding tissues, 
the prognosis will depend very largely upon the ability of the heart to help 
itself by increasing its muscular fibre, hence its systolic strength. 
Adhesions early in life interfere materially with the development of 
the heart. 
Adherent pericardium with arteriosclerosis, especially coronary disease, 
is threatening. The combination may end life without warning. 
The heart muscle always remains the paramount issue in the prognosis 
of adherent pericardium, for in many cases there is either consecutive or 
preceding myocarditis, as often happens for example with tuberculous 
pericarditis. Moderate superficial fatty degeneration of the myocardium, 
originally described by Virchow, is not often of serious significance. 
Adherent pericardium, mediastinal and pleural agglutination with 
added work thrown upon the heart muscle because of increasing valvular 
disease, asthma and emphysema, recurring bronchiolitis, kyphosis or pneu- 
monia (usually bronchopneumonia), advancing arteriosclerosis, chronic 432 
DISEASES OF THE CIRCULATORY APPARATUS 
interstitial pneumonia (which often follows chronic mediastino-pleuro- 
pericarditis) becomes a serious condition which continues during long pe- 
riods to threaten life, usually with evidences of extreme dilatation and 
dropsies, and causes death. 
In connection with tuberculous pericarditis with adhesions I mention 
the influence of the operation of Cardiolysis of Brauer on these cases (See 
Cardiovascular Tuberculosis). The literature of this subject is sufficient 
with our present experience to prove the enormous influence of the opera- 
tion of Brauer on adherent pericardium and the “fixed thorax”—“Starrer 
Thorax”—of the Germans. 
Adherent pericardium with general tuberculosis, valvular disease, 
nephritis or other grave constitutional defect offers an unfavorable outlook. 
Adherent pericardium may persist during many years with but few 
symptoms and without shortening life. 
3. Chronic Pericardioperitonitis 
('Chronic Polyserositis, Pick’s Disease, Zuckerguss Krankheit) 
Curschmann and Pick both called attention to productive changes in 
the serous coverings of the peritoneum, the liver, the spleen, the pleura 
and the pericardium in which there is enormous fibrous thickening of the 
various serous coverings with the characteristic appearance which follows 
the deposit and the drying of a saturated solution of white sugar on a 
smooth dry surface, to which Curschmann therefore gave the name of 
“Zuckerguss Krankheit.” 
The various serous membranes seem to be simultaneously affected or 
the inflammation of one covering may follow close upon the other. 
The pericardium may become adherent, the sac obliterated, always 
with enormous thickening. 
Pari passu, with the changes in the pericardium and peritoneum, 
ascites develops. The ascites persists during many years without causing 
death; to prolong life repeated tapping is necessary. In two cases seen 
during the past ten years we were obliged to tap on an average of once 
every four to six weeks. In several of our cases there was hydrothorax 
and hydropericardium with ascites. 
The spleen is often much enlarged, its serous covering so thickened as 
to be unrecognizable. 
The liver shows organic changes which suggested to Pick the name of 
"pericardial pseudocirrhosis of the liver.” 
In all of these cases the obstruction of the portal circuit is the leading 
symptom, the evidences of chronic peritonitis persist, the pericardium may 
be deeply involved without causing serious subjective manifestations, but 
at some stage of the disease the myocardial weakness is sure to develop DISEASES OF THE PERICARDIUM 
433 
and leads to increasing circulatory embarrassment, extensive dropsies, 
cyanosed kidney and death, unless intercurrent disease interferes earlier. 
The evidences of pericardial thickening and obliteratiort may be so few 
as to make the positive anatomic diagnosis impossible. It may be assumed 
that with Pick’s Disease which has persisted during a long period, the 
pericardium and multiple serous surfaces are thickened, particularly if the 
patient is an alcoholic and with recurring ascites shows evidences of myo- 
cardial weakness with pleural changes. 
One of our cases lived over twenty years and died as the immediate 
result of an ill advised laparotomy, the surgeon having diagnosed tubercu- 
lous -peritonitis. 
One boy who came to the hospital when about 12 or 13 years of age 
was observed during eight years and disappeared. 
The average length of life is between ten and fifteen years, during 
which paracentesis abdominalis and in some cases repeated aspiration of 
the thorax are necessary to prolong life. 
Patients who do not die of myocardial degeneration usually yield to 
intercurrent disease, pneumonia frequently. The process being multiple, 
radical surgical interference offers no encouragement. I have found death 
hastened by it. 
4. Hydropericardium 
The accumulation of fluid in the pericardial sac when non-inflamma- 
tory in its origin is usually the result of stasis, interference with the nor- 
mal emptying of the veins and lymphatics of the heart, an accompaniment 
of all possible heart lesions, changes in the walls of the blood vessels due 
to constitutional diseases, including the anemias and leukemias, hydremic 
conditions and chronic nephritis. 
The fluid is usually of low specific gravity, often contains sugar and 
chyle. 
With heart lesions and hydropericardium there is usually dilatation of 
the ventricles. 
The prognosis of hydropericardium is grave because it depends entirely 
upon an underlying cause which is usually serious; the accumulation is 
likely to be a terminal complication. 
5. Hemopericardium 
The presence of pure blood in the pericardial sac may be due to trauma- 
tism, to the rupture of small or large pericardial vessels, to the rupture of 
an aneurism, either of the heart, aorta or coronary artery or other large 
vessel, including the pulmonary artery, also malignant growths. 434 
DISEASES OF THE CIRCULATORY APPARATUS 
With hemorrhages of considerable size, collapse is prompt, anemia 
characteristic, the pulse small and death not long postponed. Compression 
of the heart by the surrounding blood is an important factor in causing 
death. 
6. Pneumopericardium 
This condition is exceedingly rare. I have no record of a case in my 
own practice. Walter James collected 38 cases of which 26 died. 
Traumatism, rupture of esophageal or gastric cancer, surrounding ab- 
scess or ulceration, instrumentation followed by accidental perforation of 
the esophagus, trachea or lung, empyema, pyopneumothorax with tubercu- 
losis and adhesions, have been known to cause pneumopericardium. 
The effect on the heart depends upon the cause of the pneumopericar- 
dium. External causes leading to prompt surgical interference, improve 
the patient’s chances of living. 
Internal perforations promptly lead to suppurative (purulent) peri- 
carditis and usually to death. 
When for some reason a small amount of air enters the pericardium 
without causing purulent or other pericarditis, it may be absorbed without 
interfering with the functions of the heart and unless the underlying cause 
is serious the patient is likely to recover. 
7. Neoplasms of the Pericardium 
The leading new growths of the pericardium are tubercle, carcinoma, 
sarcoma and gumma. 
Tuberculous pericarditis is separately considered; it is always second- 
ary to disease in other organs (See Cardiovascular Tuberculosis). 
When cancer invades the pericardium the disease is likely to extend 
from the immediate neighborhood. 
The larger number of sarcomata of the pericardium are spindle or 
round celled and never primary. 
Gummata of the pericardium are always associated with myocardial 
syphilis, either single or multiple, with muscle degeneration. 
All new growths of the pericardium cause some symptoms of pericar- 
ditis, usually with effusion which is blood stained or purulent. 
The prognosis of pericardial new growths is absolutely had. 
Barlow. Gulstonian Lecture, 1843. 
Brauer. Arch. f. klin. Chirurg., Bd. Ixxi. 
Ztschr. f. Chirurgie, 1903, No. 86. 
Broadbent. Adherent Pericardium, etc. 
References CONGENITAL DEFECTS OF THE HEART 
435 
Chevers. Guy’s Hospital Reports, ix. 
Curschmann. Deutsch. med. Wchnschr., 1884, No. 85, 564• 
Frerichs & Rosenstein. Quoted by Romberg. 
Gardner (W. T.) The favorable termination of pericarditis, Adhesions of the pericardium. 
Edinburgh Monthly J. Med. Sci., 1851. 
Gerhardt (C.). Herzklappenfehler. Wien, 1913. 
Hoffman. Johns Hopkins Hosp. Reports, 1913. 
James (Walter). Tr. .Ass. Am. Phys., Philadelphia, 1904, viii, p. 28-27. 
Krehl. von Mehring Lehrbuch der inneren Medizin. 8. ed., i. 
Pick (F.). Ztschr. f. klin. Med., Bd. xxix, 885. 
Romberg. Krankheiten des Herzens. 1906. 
Stokes (Wm.) The diseases of the heart and aorta. 1851. 
Virchow. Cellular pathologie. Berlin, 1871; also Virchow's Archiv. (repeated references) 
Walshe. Diseases of the lungs and heart. 1851, 280. 
D. Congenital Defects of the Heart 
The leading congenital defects which interest the clinician are: 
1. Stenosis of the Pulmonary orifice. 
2. Defective Ventricular Septum. 
3. Perforate Foramen Ovale. 
4. Dextrocardia. 
5. Stenosis of the aortic orifice. 
6. Insufficiency and stenosis of the mitral and bicuspid valves. 
7. Transposition of the aorta and pulmonary artery; perforate and 
premature closure of the ductus arteriosus. 
It is by no means easy to diagnosticate with anatomic precision the 
location of congenital defects in all cases where one or more exist, for the 
subjective and objective manifestations of all are much the same and 
several are likely to be present in many cases. 
1. Stenosis of the Pulmonary Orifice 
Stenosis of the Pulmonary Orifice causing obstruction of the pul- 
monary valve with narrowing of the conus arteriosus of the right ventricle 
is the most frequent of all congenital heart defects (GO per cent). Of 
those who live with congenitally defective hearts after the twelfth or thir- 
teenth year, over 80 per cent show pulmonary stenosis. When only mod- 
erate, and stenosis of the pulmonary orifice or the vessel exists, without 
other defect, compensatory hypertrophy of the right ventricle makes it 
possible in the absence of added complication for the subject to live many 
years in good health. These patients are often conscious of the murmur, 
hut disregard it and are not materially inconvenienced. 436 
DISEASES OF THE CIRCULATORY APPARATUS 
If with pulmonary stenosis there is perforate foramen ovale—a fre- 
quent combination—the patient’s chances of living are materially reduced. 
It is unusual for such patients to live beyond the fifteenth year; to live 
longer is exceptional. 
With stenosis and a defect in the intraventricular septum, life is rarely 
prolonged beyond puberty. Most of these die during the first years of life. 
The right ventricle hypertrophies enormously to send the blood into the 
aorta. 
With pulmonary stenosis, patent interventricular septum and open for- 
amen ovale the forecast is graver than with stenosis alone. Peacock says 
“the open state of the foramen ovale and the imperfection in the ventricu- 
lar septum, so far from adding to the danger, really afford the means of 
relief to the overcharged right auricle and ventricle without which life 
could not be prolonged for any considerable period.” This “relief,” how- 
ever, is comparative and under the slightest stress or with complications 
proves insufficient. 
Congenital pulmonary stenosis is usually coexistent with auriculoven- 
tricular lesions or other evidences of fetal endocarditis. 
Fetal endocarditis is not infrequent and is a cause of congenital steno- 
sis and other defects (B. Fischer). 
Pulmonary stenosis with patent ductus arteriosus (Botalli) leads to 
early death. Colbeck says “life is rarely prolonged beyond the thirteenth 
year.” 
Complete occlusion of the pulmonary artery leads to early death. 
With a high degree of stenosis the blood which reaches the lungs must 
pass from the aorta through the ductus arteriosus which latter remains 
open. 
When stenosis of the pulmonary orifice is the only congenital defect, 
there is a fall of pressure in the pulmonary artery, the pressure in the pul- 
monary veins is elevated, also in the right ventricle with consecutive 
hypertrophy of both right auricle and ventricle. In many of these cases 
there is marked cyanosis. In some cases tricuspid insufficiency is super- 
added. 
Pulmonary stenosis and perforate foramen ovale with closed inter- 
ventricular septum was found by Abbott in 12 per cent of her cases of 
congenital heart lesions. This makes it possible for much of the blood to 
find its way along the channel of least resistance through the opening 
from the right to the left auricle without going through the lung. Natu- 
rally the amount of cyanosis will then depend upon the quantity of Mood 
which finds its way through the lungs via, the pulmonary artery. When 
these conditions prevail, it takes but the slightest added effort, such as 
exercise, overeating and emotion, leads to prompt increase of cyanosis and 
dyspnea. 
Peacock found that 74 of 101 of his cases were “blue babies” morbus CONGENITAL DEFECTS OF THE HEART 
437 
coeruleus) at birth, or they showed characteristic cyanosis before the end 
of the second year. 
Cyayiosis, dyspnea, convulsions, headaches, clubbed fingers and poly- 
cythemia are the leading features of this and most congenital anomalies 
with associated physical signs. 
Nosebleed and purpuric conditions are also frequent. 
(For a detailed account of the physical signs of congenital heart de- 
fects and further pathologic data, the reader is referred to Hirschfelder’s 
classic work on “Diseases of the Heart and Aorta” (Lippincott, Philadel- 
phia and London) and Maude Abbott’s article (Vol. IV. Osier’s Modern 
Medicine). 
Almost all who live long enough with congenital stenosis of the pul- 
monary orifice develop pulmonary tuberculosis. 
Abbott reports 80 per cent. B. Fischer (personal communication) 
says that all who live beyond the fifteenth year show tuberculous changes 
in the lungs. 
Increasing enlargement of the liver, spleen, with cyanosis, albumin- 
uria and ascites in the average case do not continue long before death 
follows. 
Blood counts during all stages of all congenital defects are interesting. 
The polycythemia of pulmonary stenosis with septum defects may reach 
as high as 9,000,000, even higher. 
Hirschfelder gives Stoelker’s statistics showing “53 cases with 32 
deaths at birth, 12 during the first year and 11 during the first decade. 
Only 4 reached the fourth decade.” 
Abbott’s statistics are also quoted by Hirschfelder. 
Age at Death. 
Pulmonary Stenosis. 
Pulmonary Atresia. 
Ventricular 
Septum 
Closed. 
Foramen 
Ovale 
Closed. 
Defective 
V. S. 
F. 0. 
Patent 
Defect 
V. S. 
Ventricular 
Septum 
Closed. 
Foramen 
Ovale 
Closed 
Defect 
V. S. 
F. 0. 
Patent 
Defect 
V. S. 
Before 1 year 
0 
4 
3* 
6 
2 
10* 
1- 7 
2 
16 
8 
0 
3 
0 
7-14 
4 
5 
4 
0 
0 
0 
3 
8 
5 
0 
0 
0 
20-28 
6 
3 
0 
0 
0 
0 
28-45 
1 
0 
0 
0 
0 
0 
16 
36 
20 
6 
5 
10 
*9.7 per 
*78 per 
cent. 
cent. 438 
DISEASES OF THE CIRCULATORY APPARATUS 
2. Defective Interventricular Septum 
We have referred to the defects of the interventricular septum in the 
preceding paragraphs. The defect was an accompaniment of other 
anomalies in 78 per cent of Abbott’s cases (149). In 58 per cent of these 
there was stenosis or atresia of the pulmonary orifice or artery. In 24 
cases, i. e., 16.1 per cent the ventricular septum defect was uncomplicated. 
We are rarely called to offer a prognosis in cases of defective ventricular 
septum for the condition per.se is not usually diagnosticated. The defects 
which are coincident, justify the prognosis given in considering stenosis 
of the pulmonary orifice with this complication. Uncomplicated defects 
of the septum have been found post mortem in subjects as old as fifty years. 
3. Perforate Foramen Ovale 
Uncomplicated perforate foramen ovale is the least serious of all con- 
genital defects; it may not cause symptoms. There are many cases in 
medical literature showing life to have remained uninfluenced; death being 
due to other causes. The influence which the open foramen exerts on the 
more frequent pulmonary stenosis is considered in the preceding para- 
graphs. 
Associated mitral lesion may lead to recoil of blood from the left to the 
right auricle, to venous stasis and cyanosis—a serious and life-threatening 
complication. Emboli may form and reach the pulmonary artery from the 
left ventricle and pass to remote parts of the body causing fatal infarcts. 
4. Dextrocardia 
Dextrocardia, without other serious lesions, is usually associated with 
the transposition of other viscerae and exerts little influence on life. It 
has been thought by some to predispose to acute infections but there are no 
positive data which bear on the subject. 
5. Stenosis of the Aortic Orifice 
Stenosis of the aortic orifice may be due to fetal endocarditis or to the 
congenital displacement of the aortic septum and the unequal division of 
the aorta and pulmonary artery. 
The result of stenosis of the aortic orifice is invariably hypertrophy of 
the left ventricle. If the aorta is completely closed, the left ventricle re- 
mains undeveloped and the circulation is carried forward through the 
right ventricle assisted by the perforate ductus arteriosus. The prognosis 
is grave, but few survive birth. Abbott found this defect in 2 per cent of 
her cases. CONGENITAL DEFECTS OF THE HEART 
439 
The length of life of subjects with stenosis of the aortic orifice depends 
largely on the narrowness of the opening and the associated lesions. If 
the interventricular septum is patent but few live after the ninth or tenth 
year. 
Stenosis of the first portion of the aorta and stenosis of the arch of the 
aorta at the ductus arteriosus may develop congenitally. Abbott reports 
this lesion in 198 of her 412 cases—a common anomaly therefore. With a 
well compensated collateral circulation life may not be shortened, though 
the heart may suddenly revolt, the peripheral vessels dilate and tire, offer 
no assistance, cerebral hyperemia may prove serious and fatal. 
6. Insufficiency and Stenosis of the Mitral and 
Tricuspid Valves 
Insufficiency and Stenosis of the mitral and tricuspid valves of con- 
genital origin depend upon fetal endocarditis. Romberg calls attention to 
the fact that complete closure of the tricuspid may exist when the blood is 
conveyed through the perforate foramen ovale and a slit or leak in the 
ventricle. 
7. Transposition of the Aorta and Pulmonary Artery 
Perforate Ductus Arteriosus and Premature Closure 
(Botalli) 
Occasionally transposition of the aorta and pulmonary artery with or 
without transposition of the auriculoventricular valves is found. In some 
cases there is either absence or partial deficiency of the septum between 
the aorta and pulmonary artery allowing the two vessels to communicate. 
The ductus arteriosus normally closes within the first week after birth; 
failure to close leaves the opening between the aorta and left branch of the 
pulmonary artery. 
Patent ductus arteriosus as already mentioned is, as a rule, combined 
with pulmonary stenosis or aortic narrowing. 
Uncomplicated patent ductus arteriosus may give rise to no symptoms, 
and may not interfere with life; its presence remains unsuspected and is 
discovered post mortem. When uncomplicated, the symptoms are not con- 
tinuous but recurring cyanosis and dyspnea may at times prove trouble- 
some. 
Transposition of the aorta and pulmonary artery promptly leads to 
death; it is incompatible with continuance of extra-uterine existence. 
It is often surprising to find the subjects of congenital heart defects 440 
DISEASES OF THE CIRCULATORY APPARATUS 
looking robust; the lesions are irreparable and as Adelman has recently 
said, they remain “infaust,” “the sword of Damocles hangs over these 
children.” 
While the lesions do not heal, the physical signs may often change, 
murmurs disappear or their character is modified. 
Most congenital heart defects show insufficiency at birth and therefore 
many die during the first month of life or shortly after. 
If life is prolonged beyond the first year they may live for several 
years without severe symptoms because of a degree of compensation. The 
heart muscle becomes an important factor. 
With increase of weight, extra work is thrown upon the crippled organ 
to meet the demands of development, and a break is likely to follow. 
Tuberculosis and other pulmonary complications are the most frequent 
causes of death in those who live beyond the eighth or tenth year. Tuber- 
culosis, the most frequent complication of pulmonary stenosis, does not 
develop during the first years of life. 
Death may take place while children are crying or exercising, during 
excitement, emotion, from acute, often insignificant infection, during con- 
vulsions or with other cerebral complications. 
In many cases, repeated x-ray examinations will prove of inestimable 
value for both diagnostic and prognostic purposes; by this method com- 
pensatory efforts can be watched. 
Each case demands separate consideration; there are no rules which 
are of value; extreme pictures may improve temporarily, cyanosis and 
dyspnea threatening at one time may disappear to recur later. 
Severe dyspnea and persistent cyanosis with edema are always un- 
favorable. 
Cyanosed kidney, scanty and albuminous urine or nephritis are un- 
favorable complications. 
The character and frequency of the pulse, i. e., the condition of the 
heart muscle remains the most prominent prognostic guide with congenital 
as with all other heart anomalies. 
References 
Abbott. Osier's modem medicine. Philadelphia, 1908, iv. 
Adelman. Diagnose u. Prognose der angeborene Herzfehler. Ergeb. d. inner. Med. u. 
Kinderheilk., 1913, Bd. xii. 
Colbeck. Diseases of the heart. London, 1901. 
Fischer (B.). Fetale Endocarditis. Frankfurter Zlschr. f. Pathol., 1911, No. 7. 
Peacock. Malformations of the heart. London, 1966. 
Romberg. Krankheilen des Herzens, etc. 1906. DISEASES OF THE MYOCARDIUM 
441 
E. Diseases of the Myocardium 
The myocardium influences prognosis oftener than does any other 
organ of the body. 
In this chapter I consider those conditions which are associated with 
change of myocardial function usually due to degenerative and toxic, 
rather than to inflammatory lesions. 
It is repeatedly demonstrated in this work that with many constitu- 
tional conditions the myocardial degeneration or cardiac toxemia is the 
direct cause of death. 
It is unnecessary to repeat in this chapter what is thoroughly consid- 
ered in connection with the myocardial changes as they complicate the 
separate infections diseases; to these the reader is referred for details. 
The same may be said of the results of myocarditis or, more properly 
speaking myocardial degeneration as found in the majority of lesions of 
the heart, including the endocardium, and the valves. These are also 
separately considered. 
I have aimed to impress upon the clinician the overpowering influence 
of the myocardium in the prognosis of all internal diseases whenever 
involved. 
The hypertrophy and dilatation of the heart resulting from, or associ- 
ated with valvular defects, arteriosclerosis, kidney lesions, syphilis and 
many other individual diseases have also received separate consideration. 
Idiopathic Hypertrophy of the Heart.—There are cases of idiopathic 
hypertrophy of the heart in which the most careful search fails to show 
valvular lesions, arterial or kidney disease. Ho cause can be given for 
many of these hypertrophies. Some of these die with dilatation after a 
period of cardiac asthenia, including the usual features of broken compen- 
sation. In occasional cases there may be few pericardial adhesions. In 
some of these cases death is caused by bullet shaped thrombi which, as 
Jores showed, form by predilection between the trabeculae of the right 
ventricle. These cases of idiopathic hypertrophy of the heart ultimately 
prove to be due to degenerative and myocarditic lesions. 
There is another type of idiopathic hypertrophy in which both halves 
of the heart are enlarged, dilatation is not marked, it is usually absent, 
the heart muscle is of a reddish brown color without characteristic micro- 
scopic appearances. There may be stasis in vital organs, there is usually 
slight arteriosclerosis of the abdominal aorta and of the renal arteries. 
Neither the arteriosclerosis nor the renal lesions are sufficient to be con- 
sidered causative of the hypertrophy. These cases strengthen the theory 
of Bollinger that cardiac hypertrophy and arteriosclerosis are “coordinate 
processes of the same cause.” 
Idiopathic hypertrophy is often associated with polycythemia, very 442 
DISEASES OF THE CIRCULATORY APPARATUS 
often in alcoholics and without arterial and kidney changes. This condi- 
tion is frequent in beer drinkers, the heart may ultimately become fatty. 
Idiopathic hypertrophy is also found in growing children without 
known cause. Most of these subjects finally develop dilatation which con- 
tinues during a varying period and leads to death. 
The following lesions of the myocardium will be considered: 
1. Acute Purulent Myocarditis. 
2. Acute Interstitial Myocarditis (Parenchymatous Myocarditis). 
3. Chronic Myocardial Insufficiency. 
(a) Fibroid degeneration (including the arhythmias). 
(b) Fatty heart. 
(c) Fragmentation and Segmentation. 
(d) Brown Atrophy. 
(e) Coronary sclerosis with associated myocardial degenera- 
tion. (Angina Pectoris.) 
(f) Senile Heart. 
4. Hypertrophy and Dilatation due to, 
(a) Overstrain. 
(b) Hypertension. 
(c) Secondary to lung diseases, asthma, kyphosis, fixed thorax, 
and non-valvular heart lesions. 
(d) With masturbation, uterine fibroids and Hyperthyroidea. 
5. Stokes-Adams Disease. 
6. Syphilis of the Heart. 
I. Heart Weakness due to insufficient exercise. 
8. Inherent muscular weakness. 
9. Insufficiency with the anemias, metabolic faults and toxic states. 
10. Neoplasms. 
II. Parasites. 
12. Rupture of the Heart. 
13. Aneurism of the Heart. 
1. Acute Purulent Myocarditis 
Acute purulent myocarditis is of septic embolic origin; it is usually 
an accompaniment of malignant endocarditis, localizes itself as a rule in 
the right conus arteriosus and in the papillary muscles of the left ventricle, 
may lead to embolic abscesses, necrosis and even to heart rupture by ulcer- 
ation. The prognosis is always unfavorable, death follows a period of 
positive symptoms including petechise and the other usual manifestations 
of septic endocarditis. DISEASES OF THE MYOCARDIUM 
443 
2. Acute Interstitial Myocarditis 
(Parenchymatous myocarditis) 
Acute interstitial myocarditis and parenchymatous myocarditis may 
he: 
(a) Simple acute interstitial myocarditis, 
(b) Acute septic interstitial myocarditis. 
(a) Simple Acute Interstitial Myocarditis 
(Romberg) 
These conditions have been fully considered in connection with diph- 
theria, typhoid fever, scarlet fever, smallpox, gonorrhea, rheumatism, 
measles and other infectious diseases. In some cases the parenchymatous 
changes are in the ascendency. Some are of the mixed type showing both 
interstitial and parenchymatous changes. The prognosis depends largely 
on the virulence of the primary infection. 
(b) Acute Septic Interstitial Myocarditis 
Acute septic interstitial myocarditis is almost always fatal. 
It is a serious question whether the differentiation made by Aschoff 
of (1) Acute purulent myocarditis and the (2) Acute interstitial septic 
myocarditis requires consideration for clinical purposes. Anatomic diag- 
nosis during life is impossible. The prognosis of both of these septic proc- 
esses is unfavorable. 
3. Chronic Myocardial Insufficiency 
(a) Fibroid Degeneration 
(“Weak Heart” Debilitas cordis, Myodegeneration of the Heart, 
Myocardial degeneration) 
Myocardial degeneration is the most frequent of all lesions of the heart 
causing death. It is a disease of advanced life; when found early in life 
it usually leads to prompt death if not due to syphilis. Women are not 
as often affected as men, and when they are the disease shows itself later 
than in men. The heart lesions which are increasing with surprising 
rapidity are of a degenerative fibroid character, they progress insidiously 
without marked physical or subjective symptoms during a long period; 
the patients present for treatment as a rule, after the initial stage, when 
complex conditions exist. 
It may be assumed that the degenerative 'process is brought about by 
interference with the proper nourishment of the heart muscle through 
the coronary arteries. The result is sclerotic or fibroid, change in the mus- 444 
DISEASES OF THE CIRCULATORY APPARATUS 
culature of the heart. The heart in these cases passes through a period 
during which it is overtaxed because of faulty pabulum to its muscle ele- 
ments and there is usually a long existing and unrecognized hypertension 
with added toxic conditions. 
The influence of faulty metabolism, long continued worry and strain, 
syphilitic infection and obstructive changes in the peripheral capillaries as 
found with arteriosclerosis of the kidney and mesenteric vessels is of 
paramount importance for prognosis and etiology. 
An overworked heart with peripheral obstruction and associated high 
blood pressure is likely to yield when extra demand is made upon it. This 
is particularly true when there is advanced coronary disease. Cases de- 
tected in the initial stage without marked distant (arteriosclerotic) changes 
and not progressive, which are tractable and able to follow the directions 
of the physician, are often favorably influenced by treatment. The prog- 
nosis will depend entirely upon the associated conditions, the capacity of 
the myocardium, which can he tested by safe methods, the age of the 
patient, and the underlying cause. 
Conditions are often complex even in the early stage of myocardial 
weakness and in many cases make prognosis exceedingly difficult, often 
impossible. 
If during the initial stage there are attacks of stenocardia (angina 
pectoris) and these are severe, the chances of materially prolonging such 
a life are small (See Angina Pectoris). 
Early evidences of stasis, particularly enlarged liver and spleen with 
cardiac asthma are among the unfavorable features, as are also dyspnea 
and symptoms referable to the peripheral vessels. 
It is unfortunate for many of these cases that the patient is often 
unconscious of myocardial disease until the heart reserve has been ex- 
hausted. The symptomatology associated with similar lesions is so vari- 
able in different cases, as to mislead the clinician and the patient. Mac- 
kenzie says that “at first sight the ‘symptoms’ are hopelessly confused.” 
“I have submitted to Professor Keith a large number of hearts affected 
by the changes associated with arteriosclerosis from patients ranging 
from forty-two to seventy-seven years of age, and in all the post mortem 
appearances had such a close resemblance that it might have been assumed, 
that during life the symptoms would have been identical.” This how- 
ever is not the case. Some patients suffer from serious anginous attacks 
and in the intervals present no evidences of myocardial disease, while 
others with exactly similar lesions present the continuous symptoms of 
muscular weakness; still others present no evidences of any lesion in 
either subjective or objective symptoms, but suddenly, there is either an 
acute dilatation, a pulmonary edema, the development of arhythmia, 
extra systoles, suddenly arising evidences of extreme muscular insuffi- 
ciency, the pulsus alternans and prompt death. Others develop dropsies, DISEASES OF THE MYOCARDIUM 
445 
while with exactly the same lesions there are often no dropsies. The 
functional disturbances therefore are differently influenced in different 
cases by the same lesions. It is impossible for the physician as Allbutt 
has said to draw a parallel “in the living patient between the formidable 
works of decay described by the pathologists; how and when these degen- 
erations are manifested; how, in the long course of cardiac decay the 
imminence of death is to be foreseen and provided against; or how, in- 
deed, we are to know that any such process is at work at all; or lastly, 
how in a case of known heart disease the degrees of its advancement and 
of the cardiac reserves are to be noted and tested.” “Thus we have the 
physician and the pathologist trotting each on his own side of the hedge, 
each intent upon his own scouting and his own bearings, and neither able 
as yet to reconcile his own observations with those of his comrade.” 
The blood pressure study of fibroid degeneration offers varying results. 
Early high blood pressure (hypertension) with symptoms of myocardial 
degeneration sufficient to make the diagnosis possible is as unfavorable as 
hypotension with the same subjective complaints. 
Sudden decided fall of blood pressure with small and rapid pulse and 
distant heart sounds is always evidence of insufficient heart power. High 
blood pressure, without evidences of coronary involvement in subjective 
symptoms, without aortic insufficiency, without arhythmia, with or with- 
out an aortic systolic murmur, but with the pulse pressure approaching the 
normal (40 to 60 mm. Hg.) may be considered favorable for the continues 
tion of life, and the patient is often able to continue his occupation if it is 
not too taxing, mentally or physically. These patients are materially 
influenced by autosuggestion; the personal element plays an important 
role, and the prognosis is often improved by the tactful consideration of 
existing conditions with abundant and justified reassurance and the judi- 
cious planning for the future. 
Too much importance has been given to systolic blood pressure by the 
lay world, often by the physician, without a just estimate of the many col- 
lateral conditions to be considered in all cases of myocardial degeneration. 
High systolic blood pressure with myocardial fbrosis in patients be- 
yond 55 years is often without unfavorable effect. There is a class of 
cases in which the myocardial degeneration progresses rapidly; it in- 
cludes men who work under unusual strain who often develop hyperten- 
sion which is promptly followed by hypertrophy of the left ventricle, and 
for some reason the associated kidney cirrhosis progresses with equal 
rapidity. The prognosis of these rapidly developing cases is bad. The 
duration of some, from the beginning of the subjective symptoms which 
brought the patient to the physician to the end, has been less than four 
months. These are exceptional conditions. The revolt of the myocardium 
in the terminal stage is associated with dyspnea, erratic heart action and 
nocturnal pulmonary edema in some, cardiac asthma in others. 446 
DISEASES OF THE CIRCULATORY APPARATUS 
Early evidences of edema are nob encouraging neither are the symp- 
toms of stasis within the portal circuit (Liver engorgement and gastritis). 
Pallor with vertigo arising suddenly, with or without arhythmia, 
particularly on slight exertion, are warnings of weakness, which when un- 
heeded lead to serious results, at times sudden death. 
Physical signs which show marked dilatation and embryonic heart 
sounds in any stage of fibroid or any other form of myocarditis are always 
suggestive, worse with dilatation of the left than the right ventricle. 
With angina pectoris and myocarditis the ventricles are not dilated as a 
rule, though the outlook may he exceedingly grave. 
With emphysema, chronic bronchitis and marked kyphosis the evi- 
dences of right ventricular dilatation are often borne during long periods 
and with improved conditions (often possible) the dilatation disappears. 
Accented second pulmonic sound is always evidence of insufficiency of 
the mitral valve and with fibroid degeneration the insufficiency is likely 
to he relative. 
The advanced and unfavorable symptoms often follow an acute exac- 
erbation ; an angincus seizure or a suddenly arising cardiac asthma, or 
nocturnal pulmonary edema may be followed by continuous symptoms of 
decompensation. Severe dyspnea may persist after such acute attacks 
and may never disappear. In a number of cases evidences of stasis in the 
liver and dropsies of the serous cavities (hydrothorax, hydropericardium, 
occasionally ascites and edema of the extremities) develop; marked 
arhythmia becomes continuous, there is albuminuria with reduced urine, 
excessive nervousness, finally orthopnea and death ends the scene. 
Physical examination of the heart in the terminal stages shows 
marked dilatation of the left ventricle; systolic murmurs over the mitral 
and aortic areas are frequent, the second pulmonic sound is accented and 
with hypertension and interstitial nephritis the second aortic sound is 
also snappy and loud. 
In another class of cases the heart is so exhausted that the sounds are 
indistinct, distant and embryonic in character. With increasing weak- 
ness, the heart becomes rapid and as already suggested arhythmia is a 
further evidence of myocardial insufficiency. 
There are cases of serious fibrosis of the myocardium in which the 
pulse gives absolutely no indications of the existing condition—this is of 
great importance. Even with normal frequency, rhythm and blood pres- 
sure, advanced degeneration may be present and increase rapidly. 
A normal pulse which is markedly influenced, i. e., accelerated by 
slight exertion, is always suggestive of myocardial degeneration. Persist- 
ent rapidity, as well as marked bradycardia and instability as shown by 
decided variation in the frequency and character of the pulse are serious. 
Experience teaches that a heart which has been overtaxed or in which a 
lesion has been recognized which, suddenly becomes erratic or shows that DISEASES OF THE MYOCARDIUM 
447 
its reserve is being reduced by the development of any form of arhythmia, 
is an organ which demands a guarded prognosis. Many such hearts may 
again “find themselves,” but they are not dependable, such organs are eas- 
ily fatigued, they revolt on slight cause, are likely to desert when but little 
overtaxed, they dilate unexpectedly. On the other hand favorable cases 
are met which after serious evidences of weakness regain sufficient force to 
live in comfort with proper care during long periods. “In no organ is this 
lack of concord between the signals of life and death so disconcerting as 
in the heart.” (Allbutt.) 
The Arhythmias 
The irregularities of the heart which interest the clinician in connec- 
tion with myocardial degeneration are: 
(i) Sinus irregularities. 
(ii) Irregularities due to depressed conductivity. 
(iii) Irregularities due to extrasystoles (premature contractions). 
(iv) Pulsus alternans. 
(v) Auricular fibrillation. 
By the use of graphic methods we are now able to gain information 
for diagnosis and prognosis which have metamorphosed cardiac pathology. 
By the simultaneous study of the jugular and the arterial pulses we now 
obtain a clear conception of the clinical significance of, and the factors 
which cause the arhythmias. 
In this work we concern ourselves with the prognostic significance of. 
the separate arhythmias, basing our conclusions on the work of Mackenzie, 
Lewis, and Price. 
i. The 'prognostic significance of Sinus irregularities 
The usual form of sinus irregularity is of little prognostic signifi- 
cance. Lewis excludes “the prolonged and sudden cessation of the heart 
beat and the true phasic variation of pulse rate.” Sinus irregularity is 
not frequent with myocarditis but is usually found in young subjects and 
in those who have been taking digitalis. 
ii. Irregularities Due to Depressed Conductivity 
We do not include all of the fully developed Stokes-Adams phenomena 
in this consideration. (See Adams-Stokes Complex.) 
The prompt impulse along the auriculoventricular bundle is disturbed 
or delayed with depressed conductivity. Price suggests three grades of 
impairment: (1) The stimulus from auricle to ventricle is merely de- 
layed—that is, there is merely a prolongation of the interval which sepa- 448 
DISEASES OF THE CIRCULA TORY APPARATUS 
rates the commencements of contraction of the auricle and contraction of 
the ventricle. (2) The stimulus does not at times cross over; in other 
words, the ventricle does not at times respond to the stimulus from the 
auricle (this is called “partial heart block”) and (3) no impulses at all 
reach the ventricle from the auricle, so that the auricles and ventricles beat 
quite independently of each other, the ventricles at an approximate rate 
of 30 per minute (“complete heart block”). 
Our clinical experience teaches that heart block of any form with myo- 
carditis is a serious condition, it certainly indicates a diseased and weak- 
ened myocardium. 
In all forms of irregularity due to depressed conductivity there is great 
danger from sudden cerebral anemia and revolt of the heart muscle which 
may lead to sudden death. We are not considering the temporary disso- 
ciation of febrile disease in which the prognosis is fairly good, but the 
graver condition which is due to an organic and permanent change in the 
myocardium. 
iii. Irregularities Due to Extrasystoles 
(Premature Contractions) 
Extrasystoles represent the commonest of all intermissions—an extra- 
systole is a premature contraction either of the auricle or ventricle or of 
both together, while the sinus rhythm is maintained. 
The normal rhythm of the heart is interrupted by either frequent, or 
occasionally by a premature beat; the following pause is abnormally long 
which is termed the “compensatory pause.” The beat which follows is 
more powerful because of the long period of rest after the extrasystole. 
The pulsus bigeminus is due to a regularly recurring extrasystole after 
each normal heart beat. 
Feeble extrasystoles may not be felt at the wrist, the pause simply is 
recognized as “dropped beat” or intermittent pulse. 
Extrasystoles are most frequent during middle life and directly after, 
in men oftener than in women, and oftener with fibroid myocarditis 
(cardiosclerosis) than with valvular disease. The Mackenzie school does 
not consider extrasystoles as bearing seriously upon prognosis. The con- 
sensus of the modern school is summed up in the following quotation, 
“Unfortunately the public has come to attach a serious significance to 
them, (extrasystoles). This is absolutely without foundation. When 
extrasystoles are considered by themselves, that is, without reference to 
the condition with which they may be associated—there is no evidence for 
supposing that extrasystoles can be taken as an indication of an impaired 
heart or add to the gravity of an already diseased heart.” (Price.) To 
this Mackenzie and Lewis subscribe. We are, however, dealing with myo- 
cardial fibrosis, and while many cases live for years with extrasystoles DISEASES OF THE MYOCARDIUM 
449 
the arhythmia must be considered indicative of a diseased myocardium 
and should never be disregarded though its importance is less than are 
most other arhythmias. I know that extrasystoles accompany grave 
heart lesions and safe reasoning leads the clinician to the conclusion 
that the associated lesions must give their own prognostic indications. 
Wr, do not deny the possibility of a healthy heart falling into the bad 
habit of producing premature contractions. The work of the degenerated 
heart muscle will certainly be increased finally by the presence and per- 
sistence of extrasystoles, and in direct proportion to their frequency— 
Lewis, it seems to us offers the safest conclusion. “Premature contrac- 
tions constitute and bear witness to defects” . . . “while premature con- 
tractions have unquestionably a relatively insignificant import, as com- 
pared to many forms of cardiac irregularity, entire neglect of their pres- 
ence is not advisable.” 
iv. Pulsus alternans 
With the alternating pulse, the heart beats regularly, blit each alter- 
nate beat is larger than the beat immediately preceding, hence with the 
contraction of the left ventricle the quantity of blood thrown into the 
aorta is larger and smaller at alternate contractions. The size of the 
pulse is necessarily influenced and the tracings are correspondingly clear. 
Alternate pulse is sometimes found when the heart contracts with un- 
usual frequency as with paroxysmal tachycardia, under such conditions 
it is less serious than in those cases with which it is most frequently asso- 
ciated, i. e., when the heart rate is not accelerated; the pulse may be 
of normal frequency or even reduced in frequency with fibroid myocarditis, 
angina pectoris, hypertension with chronic interstitial nephritis and in 
all forms of decomposition associated with dilatation of the heart and 
fatigue. 
The pulsus alternans is evidence of an overtaxed heart; it means that 
the heart is struggling to carry its burden, that its reserve is exhausted, 
and it always adds to the gravity of the case and is always serious. Lewis 
says “It ranks with subsultus tendinum, with optic neuritis, with the 
risus sardonicus and other ill-omened messengers. It is the faint cry of 
an anguished and fast failing muscle, which, when it comes, all should 
strain to hear, for it is not long repeated. A few months, a few years 
at most and the end comes.” The alternating pulse, being a symptom 
of advanced myocardial degeneration, is associated with other grave symp- 
toms in most cases, these include angina pectoris, hypertension, nocturnal 
dyspnea, often with pulmonary edema or cardiac asthma, Cheyne-Stohes 
breathing, or it may be the only evidence of a crippled myocardium which 
suddenly balks when death is entirely unexpected. 
“These results support the teaching of Dr. Mackenzie. In his expe- 450 
DISEASES OF THE CIRCULATORY APPARATUS 
rience, the inception of the pulsus alternans in aged people has invariably 
been followed by fatal heart failure within two or three years.” (Windle.) 
Windle in his article on “The Incidence and Prognostic Value of the 
Pulsus Alternans in Myocardial and Arterial Disease” offers the follow- 
ing in 
Table 1 
Pulse irregularities observed in 202 cases of arteriosclerosis: 
Nature of Irregularity. 
Number 
of Cases 
Observed. 
Percentagf 
109 
54.5 
Complete irregularity 
61 
30.5 
23 
11.5 
3 
1.5 
1 
0.5 
Complete heart-block 
4 
2.0 
Sinus irregularity 
1 
0.5 
y. Auricular Fibrillation 
(Auricular Flutter) 
The “flick” or “flutter” of the auricle with fibrillation is rapid, erratic 
and is produced by “stimulus production at multiple auricular foci.” A 
large number of irregularities are due to auricular fibrillation. The in- 
fluence of auricular fibrillation on the ventricle according to Lewis is 
twofold. “The normal regular and coordinate contractions in the auricle 
are in abeyance and consequently the ventricle is robbed of the regular 
impulses which form its accustomed supply. These are replaced by numer- 
ous and haphazard impulses, escape to the ventricle from the turmoil 
which prevails in the upper chamber; the change is consequently pro- 
found.” 
The condition is most frequent during advanced life when degenera- 
tive processes are numerous. 
It is not present during the first decade of life. 
It is more frequent in men than in women. 
It is a frequent accompaniment of mitral stenosis. Lewis says 
“Mitral stenosis and auricular fibrillation are bosom companions.” 
Ventricular fibrillation is promptly fatal, and is the cause of sudden 
death in a number of cases. 
Auricular fibrillation is synonymous ivith muscular degeneration of 
the auricle and characteristic of advanced changes. 
It is the precursor of cardiac surrender in many cases—in other DISEASES OF THE MYOCARDIUM 
451 
cases tlie heart learns to accommodate itself to the flutter and cases are 
recorded which lived ten years and longer after the initial seizure. 
In some favorable cases the fibrillation is paroxysmal. 
The frequency of the beat influences prognosis; the more frequent 
the flutter the greater the danger of exhaustion. 
The results of digitalis treatment on auricular fibrillation influences 
the forecast. The drug in favorable cases acts as a specific and promptly 
controls the symptom, if it fails■, the prognosis is absolutely bad. 
The conclusions of Gossage and Braxton Hichs are appended: 
“1. That the exact cause of auricular fibrillation is unknown. 
“2. That it usually comes on in a heart where there has been for a 
considerable period disease of the valves or myocardial change from 
inflammation or degeneration. 
“3. That it sometimes arises suddenly where there has been no pre- 
vious sign or symptom of heart disease. 
“4. That possibly in some of these cases it occurs in hearts which 
were previously perfectly healthy. 
“5. That if this is true its essential cause must lie outside the heart 
and not in any anatomical or pathological change in the heart itself. 
“6. That sudden death in auricular fibrillation is probably due to 
the onset of fibrillation of the ventricles, and that some cases of sudden 
death both in diseased and healthy persons may be due to the simulta- 
neous onset of fibrillation of both auricles and ventricles.” 
The prognostic significance of the Atropin reaction in diseases of 
the heart has received considerable attention from various sources. The 
hypodermic injection of 1/50 to 1/25 grain of atropin produces a de- 
cided increase in the heart rate by paralyzing the pneumogastric. It acts 
directly on the vagus and not on the myocardium. Cushny first sug- 
gested “releasing of the vagus by means of hypodermic doses of atropin, 
so-called atropin reaction in the study of digitalis action” (Talley). 
The polygraph or sphygmograph is used to register the pulse rate 
and to show the contrast. The rate is to be averaged by ten minutes’ 
observation before taking the hypodermic, the reaction is again averaged 
by ten minutes’ observation, when after .the injection, the pulse is at its 
maximum. The normal reaction is from 30 to 40. Talley should be 
consulted for a full understanding of the method, his conclusions follow: 
“1. The atropin reaction in the normal heart is probably from 
30 to 40. 
“2. A reaction of 20 or less, in a heart not recently subjected to 
exhausting disease, points to a degenerative process in the cardiac tissue 
which makes the outlook for improvement under treatment unpromising. 
“3. Cases of auricular fibrillation with normal response or above, 
are promising subjects for treatment. 452 
DISEASES OF THE CIRCULATORY APPARATUS 
“4. Two atropin reactions in case of auricular fibrillation, one before 
and one on full digitalis, enable us to determine whether the vagal or 
the cardiac tissue factor is the greater. The patients with a large cardiac 
tissue factor are the ones who usually are sufficiently improved by treat- 
ment to return to their occupations.’’ 
Fibroid myocarditis once established is never cured. It can be con- 
trolled m many cases by rational living. Its extent naturally influences 
the prognosis as well as the course of many associated conditions. 
Sudden death occasionally occurs without previous warning of the 
existence of any lesion. This is not frequent. But few die in whom a 
thorough consideration of symptoms and physical examination would 
have failed to lead to a correct diagnosis. 
Diabetes, gout, and other diseases, as well as a faulty diet for metab- 
olic faults, the use of thyroid extract for obesity, continued mental strain, 
acute disease, particularly influenza, often prove depressing factors which 
promptly invite progression of existing degeneration. 
The fate of the myocarditic patient often depends on his own acts. 
It is surprising to note how many of these patients with weak hearts 
(degenerated) continue to live in favorable surroundings and conditions 
with a minimum of symptoms during many years, when they give the 
heart the rest which it needs. 
Errors of diet, excesses of any kind, may promptly shorten life, which 
with rational treatment, temperance and sobriety might have continued 
during a considerable period. 
The effect of tobacco, tea, coffee, alcohol and sexual indulgence de- 
mands the closest scrutiny in the individual case, and if the patient wishes 
to prolong his life, he must be willing to make sacrifices and forego 
many pleasures. 
In favorable cases the effect of rest and treatment is comparatively 
prompt and is followed by the disappearance of threatening symptoms. 
(6) Fatty Heart 
Fatty disease of the heart may be due either to the accumulation of 
fat in the sub pericardial tissue, which may also deposit between the mus- 
cular fibers of the heart, a condition found with obesity, at times with 
carcinoma and tuberculosis, or to the “fatty degeneration of the heart” 
in which the muscular tissue has undergone a fatty degeneration, which 
may be diffuse or more or less localized. The heart cavities are dilated, 
hypertrophy is impossible in advanced cases because there is insufficient 
muscle element left; the heart is therefore usually flabby and dilated. 
With obese patients the small and feeble organ is insufficient to meet 
the demands made upon it by the enormous body when the changes are 
advanced. The association of obesity with coronary sclerosis, and a DISEASES OF THE MYOCARDIUM 
453 
high diaphragm to which Romberg calls attention is an unfavorable 
combination. 
In many obese subjects the two forms of fatty disease are combined. 
When with fatty accumulation in obese subjects there is also fibroid 
myocarditis the prognosis is bad. 
In obese subjects with diabetes and gout, a combination which is not 
infrequent, or with diabetes alone, the evidences of heart fatigue and 
insufficiency may arise suddenly, and promptly end fatally. 
Whenever an obese patient develops arhythmia suddenly9 it is proof 
of cardiac insufficiency and is serious. 
Fatty degeneration of the heart is also found with all wasting dis- 
eases, pernicious anemia, with phosphorous poisoning, pericarditis, endo- 
carditis and with the myocarditis of many acute infections. 
The myocardial degenerations are not infrequently of the mixed type, 
i. e., fibroid and fatty degeneration or parenchymatous may be present 
together. 
So long as the heart muscle itself in the obese subject is intact and 
the deposit of fat in the surrounding tissues is not serious, the danger 
lies in the invasion of the myocardium—the extent of fatty and fibroid 
degeneration. 
Leyden holds that in such cases dropsies have been overcome. This 
in our experience is exceedingly rare. 
The influence of diet and carefully supervised exercise and the Ber- 
gonie treatment is favorable in occasional cases. 
With dilated hearts in obese subjects and evidences of stasis, the 
prognosis is grave. 
Arteriosclerosis and obesity with heart symptoms develop conditions 
which advance insidiously and lead to death. 
The increase of dullness to the right of the sternum is less serious 
than similar increase to the left of the nipple line which is proof of dila- 
tation of the left ventricle. The former is often due to fatty deposit 
rather than degeneration. 
The prognosis of fatty degeneration of the heart is primarily influ- 
enced by its cause. With the acute infections under proper 
it may disappear or cause no further symptoms after fully established 
convalescence; the sarqe is true of anemic conditions which are amenable 
to treatment. 
Feeble and distant heart sounds with dilatation, relative mitral insuf- 
ficiency, dyspnea, arhythmia, faintness, syncope, cyanosis, and stasis in 
the abdominal viscera, are among the unfavorable features of fatty heart. 
Fatty degeneration due to coronary disease is usually of the mixed 
fatty, fibroid type and is fatal. Rupture of fatty heart is a frequent 
cause of death./ One such case we met during a gall-stone colic. Sudden 
death during gall-stone or other colics {renal) is at times due to fatty 454 
DISEASES OF THE CIRCULATORY APPARATUS 
and insufficient heart. In Y7 per cent of fatty hearts Hamilton reported 
spontaneous rupture. 
(c) Fragmentation and Segmentation 
Fragmentation and segmentation cannot be diagnosticated ante mor- 
tem, they interest the pathologist. The true significance and cause of 
fragmentation is undecided. Post mortem, the heart muscle with frag- 
mentation shows transverse breaks or fractures across its fibers; with 
segmentation, the muscle fibers themselves are separated along the line 
of contact. 
Fragmentation has been found in hearts without degenerative changes 
and may be due to ante mortem or post mortem changes. 
id) Brown Atrophy 
Brown atrophy is frequently found with chronic valvular disease in 
the senile heart and with cachectic states. 
The heart is small and usually insufficient. When brown atrophy 
exists during a comparatively long period fibroid changes are also found 
in the myocardium. 
With the small heart of brown atrophy there is feeble systolic force 
and hyotension. 
The prognosis depends on the cause; brown atrophy can only he sus- 
pected during life, never positively diagnosticated. 
Starvation Atrophy.—The enormous tolerance of the heart makes full 
recovery possible after atrophy due to starvation and long continued wast- 
ing disease. 
(e) Coronary Sclerosis 
(Angina pectoris) 
Seneca wrote of angina pectoris, “To have any other malady is to 
be sick; to have this is to he dying.” 
John Hunter, himself a victim of Heberden’s disease and his con- 
temporary, said “my life is in the hands of any rascal who chooses to 
annoy or tease me.” 
We have no clearer or more classic picture to offer of angina pectoris 
than is included in the original description of the disease by Heberden 
in his Commentaries on the History and Cures of Disease. In the pres- 
ent state of our knowledge reasoning from the prompt appearance of the 
symptoms of angina when the heart muscle is taxed in those suffering 
from the disease, whatever the lesion found on post mortem, we are 
justified in including the complex with the diseases of the myocardium DISEASES OF THE MYOCARDIUM 
455 
and subscribe to the dictum of Mackenzie “that angina pectoris is an 
evidence of exhaustion of the function of contractility” and that the 
pain “is a viscerosensory reflex.” 
Coronary disease is unquestionably the leading lesion of angina pec- 
toris. It is associated in a proportion of cases with aortic disease— 
aortic aneurism, simple dilatation of the aorta, aortic valvular disease 
and in but few cases do ive fail to find myocardial degeneration, a result 
of faulty nourishment through the coronary vessels. 
Hypertension is often associated with some o?ie of the above men- 
tioned lesions, but is by no means a constant attendant of the disease 
either during the paroxysm or in the interval. 
Fiessinger contends that the danger to life of angina pectoris has 
been somewhat exaggerated and divides cases of the disease into six 
groups, according to the cause, viz.: 
coronary involvement, 
aortitis, 
myocarditis, 
interstitial nephritis, 
obesity and 
aerophagia—this order of enumeration is that of decreasing gravity. 
The exhausted left ventricle is an important attendant of angina 
pectoris in all cases. In most cases the ventricle is struggling against an 
increased pressure, this relieved, the sensory symptoms are long post- 
poned or may never recur. It has been the experience of all clinicians 
to find the fading of anginous attacks with the appearance of ventricular 
dilatation and mitral insufficiency. Musser, Broadbent, Mackenzie, 
Abrams, and Eisner report similar experiences. The heart during the 
attacks is perceptibly reduced in size; with broken compensation and 
dilatation the prognosis so far as angina pectoris is concerned is better 
in direct proportion to the amount of dilatation. 
After severe illness, the symptoms of angina pectoris often disappear. 
Ortner mentions such cases. We include in our series the case of a 
woman who almost twenty years ago had typical angina wdth chronic 
nephritis and advanced aortic lesion. She developed uremia, passive 
cerebral hyperemia, was unconscious during a long period with a threat- 
ening pulse, she finally rallied from the acute symptoms and never again 
had the slightest suggestion of coronary spasm. 
I count among my cases a number of men and women in whom 
there was complete recovery from anginous symptoms during many years 
after the development of added heart and kidney lesions. One of these 
was a clergyman who had severe angina during several months when he 
was stricken with vague febrile symptoms associated with marked cerebral 
manifestations; he made a full recovery from these and for nineteen 456 
DISEASES OF THE CIRCULATORY APPARATUS 
years continued at the head of a large congregation when he developed 
anew the symptoms of angina with nephritis. 
I do not consider “pseudo angina3 a disease per se. 
There are occasional cases of pain and other associated symptoms in 
which it may be assumed that there are no lesions in the coronaries or 
heart muscle but which are due to vaso-constriction or spasm of the 
arteries, in which the symptoms of stenocardia are of secondary origin. 
Nothnagel’s article on “Angina pectoris vasomotoria” describes these 
fully. These patients are easily influenced by cold, after and during 
exposure they have the characteristic pang, and this is likely to persist 
until they are thoroughly warmed. My experience is in accord with 
that of Mackenzie that the blood pressure is not high in these cases either 
during the attack or in the interval. The prognosis of vasomotor angina 
is more favorable than is that of other forms of the disease. 
The enormous increase of stenocardia, or coronary disease is striking. 
This is especially true among professional men. In 6,155 cases of in- 
ternal disease I found 110 fully developed (1.78 per cent) coronary 
scleroses. This is in striking contrast to the rarity of the disease during 
the days of Benjamin Bush; out of his enormous experience he reported 
in a lecture to his students that he had seen but one case of angina pec- 
toris, and he mentioned the name of a colleague practicing in Philadelphia 
who had also seen but one case. 
Coronary sclerosis may truly be considered “the doctor’s disease” for 
it is more prevalent among physicians than among any other class of men. 
Over 80 per cent of deaths among the teaching medical faculties of the 
large universities of the world during the past ten years have been due to 
this disease. Bomberg has said that arteriosclerosis is most advanced 
in the vessels which are most taxed; physicians tax their hearts and brains 
most, hence their coronaries and cerebral vessels must bear the burden. 
There is no disease of the arterial tree in which family history is a 
more striking pathogenic and prognostic factor than in angina pectoris. 
It is not at all uncommon to find several members of a family in which 
the father or mother had fully developed angina pectoris. With a strong 
family tendency to the disease, the symptoms, are likely to develop in 
the fourth decade, occasionally in the third, and the course of the disease 
is more rapid than when developed later in life. 
My experience justifies the statement that almost all cases of angina 
pectoris developed before the fortieth year are either associated with a 
direct hereditary tendency or are of syphilitic origin. In the subjects 
burdened with heredity there is usually an unrecognized period of hyper- 
tension and the development of the complex is hastened sooner than 
it is in other subjects who are exposed to the same hurry, worry and 
overwork. 
When we consider the prognosis of angina pectoris from the purely DISEASES OF THE MYOCARDIUM 
457 
clinical manifestations which are produced, two pictures stand out in 
bold relief. 
First. The large attack, suddenly arising, usually after excitement, 
worry or a hearty and full meal, in which the anguish is great, the pain 
severe, breathing uninfluenced as a rule, a sense of impending death, the 
sensation of a heavy load resting on the thorax, at times the “heart is 
pressed in a vise,” blood pressure presents no distinctive features, it may 
be high, is usually however nearly normal or may be slightly depressed; 
the pulse is equally non-committal, it may be slow or normal, if the attack 
is long there may be extrasystoles; with advanced myocardial degenera- 
tion, there may be great rapidity, the pulse small and sometimes alter- 
nating. The pulse in many cases seems entirely unchanged from the 
normal, to the moment of death. The heart may suddenly stop during 
diastole often at a time when its systolic force seems reassuring. 
Second. The small attack. The majority of cases which now present, 
suffer from the “small attacks”; these are suggestive of the larger attack 
but are less severe and in many cases, after the disease has continued 
during a varying period, are likely to recur on slight cause; they are eva- 
nescent and the varying sensations described by different patients promptly 
cease with rest. In the advanced cases the small attacks are promptly 
provoked by the slightest extra tax on the heart, but they are rarely 
associated with the severe pain of the larger attacks, neither does the 
pain often radiate from the sternal regions into the neck or beyond the 
left shoulder; the patient is not materially weakened by recurrence. 
Each one of the large attacks has been said to “add a peg to the coffin”; 
the smaller attacks are often borne during many years without serious 
results in patients who profit by rational living. The first larger attack 
may kill the patient; as a rule there are several larger attacks before the 
fatal termination. The large attack may never recur, the patient may 
fall into a condition of chronicity covering many years during which he 
has many small attacks, or several months or years may intervene after 
which severe attacks follow. It is impossible, in the absence of physical 
signs, to give a prognosis of value. 
No disease presents more prognostic problems than does angina pec- 
toris. uThe cardinal fact in real angina is its (Walshe). 
The small attacks rarely kill, they make the lives of the victims 
wretched and uncertain; they do not often interfere (nor should they) 
with light occupation, and with care the patients may continue to live 
during many years. 
I have found that the effect of vasodilators offer valuable prognostic 
data. Angina pectoris (either large or small) which is promptly relieved 
by small doses of glonoin, given dry on the tongue, offers a favorable fore- 
cast so far as the prolongation of life is concerned. Thus many men who 
have angina pectoris, by the aid of infinitesimal doses of glonoin are 458 
DISEASES OF THE CIRCULATORY APPARATUS 
able to take exercise and prevent serious symptoms during long periods. 
This effect is by no means the result of suggestion. The author has given 
the method too many trials to be mistaken. 
Cessation of activity during the first moments of a large or small 
attack has a favorable effect in most cases. 
Large or small attacks recurring during rest or during the night, 
arousing the patient from sleep are always serious, they indicate advanced 
disease. 
Women hear angina longer and better than do men. They are better 
able to rest and their worries are fewer and their activities more limited. 
Large or small attacks in young subjects unless specific, are more 
likely to end life sooner than are similar seizures in older subjects. 
Arhythmias persisting or arising during attacks are an expression of myo- 
cardial weakness. 
Extrasystoles are easily borne during years by many who suffer from 
the milder form of the disease. 
Persistent and intensive antisyphilitic treatment in the presence of 
a positive Wassermann reaction offers a good chance of complete cure. 
The number of cases associated with aortitis prove the frequency of 
syphilis as a cause. 
Closure of both coronaries leads to prompt death. 
One coronary may be sclerosed during a long time without causing 
death. The trunks may be atheromatous tracing them into their intra- 
muscular network to find the finer branches free from disease and thus 
there is sufficient blood to maintain the heart wall and prevent serious 
revolt. 
With aneurism and aortic disease and angina, the prognosis is abso- 
lutely bad. 
With aortic insufficiency and coronary disease (a frequent combina- 
tion), there is constant danger and death is not long postponed. 
Evidences of aortic (valvular) degenerative change (arteriosclerotic) 
with coronary disease and small attacks with slight hypertrophy of the 
left ventricle and a reasonably dependable blood pressure are found in 
many cases which live for years, are always in danger; they hold their 
lives in their own hands. Indiscretion is not long tolerated in these cases. 
An aortic systolic murmur should not always be seriously interpreted, for 
it is present in many cases which live many years. 
A single debauch, a single error of diet, with the overloading of the 
stomach, may lead to prompt death. These are the cases which are 
reported by laymen and often by physicians as uacute indigestion.” 
uAcute indigestion” does not kill a man with a normal heart. 
Thrombosis or embolism of the coronaries is a frequent cause of death. 
It cannot be influenced by any known treatment. Acute dilatation added 
to coronary sclerosis either during an attack or in the interval, if extreme, DISEASES OF THE MYOCARDIUM 
459 
is serious; moderate dilatation which may he provoked by forcibly strik- 
ing the cervical vertebrae with a percussion hammer often relieves the 
attack and saves the patient. Osier has called attention to angina pectoris 
as an early symptom of aortic aneurism. 
Anginoid attacks occur in children with valvular disease and with 
adherent pericardium. I have seen a number recover, particularly 
with valvular defects, our experience with adherent pericardium in chil- 
dren has been limited. 
In the adult, I saw one case in which cardiolysis cured the patient, 
a physician who is now engaged in active practice. 
Angina pectoris of toxic origin offers a favorable prognosis if the 
coronary sclerosis and myocardial degeneration are not too far advanced. 
Tobacco angina is amenable to rational treatment, as are also those 
indefinite cases attributed to tea, coffee, etc. When symptoms persist 
in spite of discontinuance of the supposed cause, it may be concluded 
that grave organic disease exists. 
Abdominal angina (dyspragia intermittens intestinalis et abdominalis 
of Ortner) is due to sclerosis of the superior mesenteric artery, as a rule; 
it may alternate with angina pectoris, or the coronaries may not be in- 
volved. The prognosis depends on the extent of the general process. 
With abdominal angina life may be materially prolonged in most cases. 
Interstitial nephritis with angina, is usually associated with marked 
hypertension and advanced arteriosclerosis. In these cases death is not 
often due to the coronary disease directly; most of our patients have died 
of uremia or other complications. Sometimes there has been a period of 
decompensation without recurring angina, but with dropsies. 
In all cases of angina pectoris excessive coitus, at times even moderate 
indulgence, influences the case unfavorably. 
Pulmonary edema has complicated a number of our cases immediately 
following coitus. 
Agreeable occupation is necessary in those cases which are about; 
idleness and a self-centered state increase all symptoms. 
In no other disease of the cardiovascular system is the patient so 
promptly influenced by his psychic condition. The exalted and over- 
wrought brain is associated with the tear which often kills these patients. 
The painful seizures accompanying Graves’ disease yield to treat- 
ment. It is questionable whether they belong among the true anginas. 
There are occasional neuroses which justify the term “anginoid”; 
these are all symptomatic and offer a good prognosis. In all cases the 
condition which caused the symptoms must give the data upon which the 
forecast should rest. This requires of the physician the most painstak- 
ing investigation of all details, a task which is not without its reward. 
The severest “large attack” in which the life of the patient seems lost 
may yield and the patient may live to enjoy life, while the “smaller 460 
DISEASES OF THE CIRCULATORY APPARATUS 
attack,” almost unnoticed, if neglected may lead to death. This is not 
the rule. I repeat—the prognosis is unfavorable in proportion to the 
ease with which the attack is produced by seemingly insignificant causes, 
in cases with marked arterial degeneration, with hereditary tendencies, 
with carelessness of the patient, under unfavorable surroundings and 
social conditions, failure, to rest, with associated progressive metabolic 
faults, gout, diabetes, lead-poisoning, added acute infections and with 
pneumonia. 
Self cure of angina pectoris is possible. 
The revelations of the Rontgen rays are needed in all cases to assist 
in clearing the horizon and often lead to valuable data for prognosis. 
The task of the physician in conveying to the patient the necessary infor- 
mation to lead him safely over a path which is never without danger is 
by no means easy. Enormous tact is required to prevent the autosugges- 
tion which is harmful and which aggravates existing conditions. To 
absolutely ignore the dangers invites prompt death; to pilot with intelli- 
gence, with concert of action of the attendant and the patient often adds 
many years of life. What this means to mankind is apparent, when we 
consider the intelligence and the usefulness of those whom the disease 
attacks by predilection. 
(/) Senile Heart 
Balfour is probably responsible for the final acceptance of the “senile 
heart” as presenting a complex of symptoms which may justify the diag- 
nosis. Senile heart is not a clinical entity. The symptoms depend 
upon degenerative changes in the cardiovascular system of the aged or 
prematurely old and include all of the usual clinical manifestations 
of such complex lesions with myocardial weakness in the- ascendency. 
The prognosis depends upon the extent of the myocardial and arterial 
disorganization; it is always unfavorable, though the subjects of “senile 
heart” cautiously guarded, may live quietly during many months. 
4. Hypertrophy and Dilatation 
Hypertrophy and dilatation due to: 
(a) Overstrain 
Permanent or transitory dilatation and hypertrophy of the heart mav 
follow severe strain, undue muscular exertion and prolonged worry. The 
possibility of preexisting disease of the heart, or its muscle must always 
be considered. In the majority of these cases the history will prove that 
the heart was not normal before the strain. DISEASES OF THE MYOCARDIUM 
461 
Undue strain long continued may certainly lead to hypertrophy. 
In Erance the country letter carriers, who walk all day, suffer no ill 
effects from their long continued, and at times laborious marches, prob- 
ably because the normal heart, more than any other muscle, accommodates 
itself to its work. 
Rieder, Spillman, Bernheim, Thurn, assert that with a healthy condi- 
tion of the heart it is exceptional to find cardiac insufficiency and dilatation 
with consecutive hypertrophy following severe bodily exercise, and most of 
these observers believe that the normal heart never tires, that in those who 
are perfectly healthy in spite of exhausting effort there is no typical 
cardiac insufficiency. 
A full consideration of this subject leads us (Eisner) to the conclusion 
previously expressed. “It is safe and conservative to conclude, that the 
heart muscle, like all muscles, demands the natural stimulation which fol- 
lows moderate functional activity and mechanical movements, but ex- 
cessive functional activity, mechanical strain or prolonged mental pang and 
worry, cause malnutrition and irritation, giving rise to chronic degenera- 
tive changes” and may lead to hypertrophy and dilatation. This hyper- 
trophy may take place in the perfectly healthy heart and is not to be 
considered pathologic. 
In making life insurance examinations it should be remembered that 
the hearts of young men and growing boys often show marked increase 
of systolic force and slight hypertrophy of the left ventricle. This is par- 
ticularly true of the college student who is at all athletic, and should not 
argue against the acceptance of the risk. These hypertrophied hearts due 
to overwork which are to be included in the class of “work hypertrophies" 
never show degenerative changes if they were previously absolutely normal. 
The “overtrained” heart which was previously normal, which during 
periods of stress shows the effects on the cardiovascular system, after a 
time, varying in different cases, as a rule, returns to its normal condition 
and remains so. These experiences have been confirmed by many ob- 
servers (Inndell). 
(b) Hypertension 
The influence of hypertension is considered with the separate condi- 
tions with which it is associated, and requires no repetition in this chapter. 
I once more warn against misinterpretation of the prognostic value of 
blood pressure study, agree that long continued hypertension is a frequent 
cause of hypertrophy, that most of these cases are associated with estab- 
lished arteriosclerosis and renal involvement ivhen detected, that its early 
detection and rational treatment often leads to satisfactory results, that in 
itself “raised blood pressure . ... is productive of degenerative changes 
in the vessels" .... Lauder Brunton further says “we have good 462 
DISEASES OF THE CIRCULATORY APPARATUS 
grounds for believing that if the rise be detected early, and counterbalanced 
bv proper regimen and treatment, the vascular changes which it would 
otherwise produce might be prevented and life very considerably pro- 
longed.” 
(c) Hypertrophy 
(Secondary to lung diseases, asthma, kyphosis, fixed thorax and non- 
valvular heart lesions) 
The prognosis of the hypertrophy secondary to the diseases above men- 
tioned requires no separate consideration, it must necessarily depend upon 
the seriousness of the underlying pathologic lesions. It is surprising to 
note the salutary influence of hypertrophy on the general condition of these 
patients; in most cases it may safely be considered compensatory and 
therefore favorable. Extreme sudden dilatation occasionally causes sud- 
den death or serious decompensation. 
Fixed thorax and some non-valvular diseases of the heart including 
hyperthyroidea with marked hypertrophy are often favorably influenced 
by surgical interference. This is true of the former (Starrer-Thorax), a 
fact not generally understood by the profession. 
(With masturbation, uterine-fibroids and hyperthyroidea) 
(d) Hypertrophy 
With masturbation the heart is often irritable and overactive, the sys- 
tolic force abnormally strong. These symptoms are associated with mod- 
erate hypertrophy, which yield with the dropping of the habit, and leaves 
no remnants. 
Uterine growths are often associated with enlargement of the thyroid 
Sind, other symptoms of hyperthyroidea and heart hypertrophy. I have 
called attention to this frequent association of uterine, thyroid and heart 
lesions in an article (Eisner) which proves this possibility and its unusual 
frequency. 
All abdominal growths by pressure and added circulatory obstruction 
add to the work of the heart muscle. With uterine myofibromata of con- 
siderable size it is not surprising to find the myocardium insufficient with- 
out the loss of blood from flooding. The prognosis of the heart condition 
has been studied in the French hospitals, particularly by Pozzi, it is favor- 
ably influenced by surgical interference. 
A small uterine polyp may cause heart symptoms, often continuous, and 
when persistent, hypertrophy may result; removal brings relief. DISEASES OF THE MYOCARDIUM 
463 
5. Stokes-Adams Disease 
{Heart Block) 
The Stokes-Adams complex when fully established (See also reference 
in this chapter to Irregularities due to depressed conductivity) is an ex- 
pression of advanced disease of the bundle of His making it impossible for 
impulses to reach the ventricle from the auricle; the ventricles and auricles 
heat independently of each other. The phenomena of heart block include, 
bradycardia, epileptiform seizures, often syncope, visible auricular im- 
pulse in the neck, the rhythm usually 3 to 1, in all cases myocardial disease, 
often, positive evidences of arteriosclerosis. The myocardial lesion always 
includes change of some kind in the auriculoventricular bundle (His 
fibers). 
Lewis grouped his cases as follows showing the age distribution of 
Stokes-Adams disease: 
Age 
10-20 
20-30 
30-40 
40-50 
50-60 
60-70 
70-80 
90-90 
Cases 
7 
6 
3 
5 
2 
3 
4 
1 
The symptom complex may occur at any age; the age distribution de- 
pends on the diseases which produce it. 
The rheumatic and choreic cases include most cases between 10 and 35 
years. The specific and arteriosclerotic group includes the cases between 
35 and 70. The senile group includes a large number of cases with asso- 
ciated heart lesions. 
Our series of cases shows the disease to he twice as frequent in men 
than in women. 
Lewis calls attention to the presence of heart block with the acute in- 
fections in young subjects, particularly with rheumatism, diphtheria, in- 
fluenza, typhoid, and pneumonia. 
Our chronic cases have been either in the subjects of previous rheuma- 
tism, syphilis or with marked arteriosclerosis. 
Heart block is often found during and after acute infections, or with 
valvular lesions in which large doses of digitalis have been responsible for 
the dissociation. 
Heart block is always serious, it is in almost all cases the evidence of 
local disturbance which is a part of a widely disseminated process, just as 
a small placque over a coronary artery is a limited hut fatal lesion of far- 
reaching arteriosclerosis. 
Heart-block may be borne during long periods by some, but when the 
pulse falls to a very low level (15-25) the epileptiform, at times apoplecti- 
form state clouds the sensorium and death after convulsive movements 464 
DISEASES OF THE CIRCULATORY APPARATUS 
follows. The larger number of deaths are due to the associated fibroid 
degeneration, uremia at times, cerebral apoplexy and sudden acute dilata- 
tion of the left ventricle. 
The mild rheumatic type and those cases of partial block associated 
with the acute infections entirely disappear during convalescence. 
The specific cases offer a better prognosis when intensive treatment is 
instituted, than do the arteriosclerotic or fibroid types. I have in pri- 
vate and hospital practice seen encouraging results from the combined 
modern treatment (mercury and neosalvarsan) (Weintraud, Huchard, 
Barries). 
Heart block, properly speaking, should include only those cases in 
which complete block does not exist; Stokes-Adams disease represents 
cases of complete block. 
The occurrence of convulsions always increases the danger, though it 
must be conceded that they are more frequent with partial, than with com- 
plete block. 
In my experience no patient has recovered in whom the underlying 
cause was of degenerative origin; the only recoveries included in the series 
were the syphilitic and those acute cases in young subjects, dependent on 
infection, rheumatism usually, pneumonia and influenza. Most acute in- 
fections which are sufficiently severe to include the complex, lead to death 
during the active days of the toxemia. 
The longest duration of Stokes-Adams disease in my experience was 
in a man who for fifteen years had persistent bradycardia, his pulse beat 
v/as below the average of the respiratory frequency at all times, he had 
epileptiform seizures at varying intervals during three years before his 
death in coma. Ilis age at death was 79. 
I have had no experience with the so-called "neurotic cases” described 
by Edes and Councilman, which fail to show pathologic lesions on post 
mortem examination. 
Death is usually sudden. Sapegno found lesions of the auriculoven- 
tricular fibers in 50 per cent of all sudden deaths. 
Sternberg found some lesion of the bundle in 70 per cent of cases of 
all heart affections. 
6. Syphilis of the Heart 
See Cardiovascular Syphilis 
7. Heart Weakness due to Insufficient Exercise 
The myocardial weakness which results from insufficient exercise is 
often an accompaniment of long continued invalidism, or is due to other DISEASES OF THE MYOCARDIUM 
465 
causes; at times the inertia of the patient and paralytic conditions make 
exercise impossible. The heart muscle may weaken in aged patients with 
fractures, usually of the hip joint. There may be alarming syncope when 
the patient first tries to change his position or stands, but the heart soon 
gathers strength and' in the absence of organic change become normal. 
8. Inherent Muscular Weakness 
There are occasional cases of inherent muscular weakness with an 
asthenic state, in which the myocardium promptly shows evidence of 
fatigue on slight cause. Such hearts bear any added tax badly; the patient 
is without resistance and when overtaken by infection is unable to make 
the average fight against its advance. Children who are constitutionally 
weak, in whom there is a distinct diathesis, may be influenced by many 
factors to overcome the inherent weakness, which, when it persists, leads to 
an unhappy existence. I have found a number of these cases of inherent 
weakness among the intractable cases of Akinesia algera originally de- 
scribed by Moebius, which may lead to years of invalidism and which 
offer a doubtful prognosis (See Akinesia algera). 
9. Insufficiencies with the Anemias, Metabolic Faults 
and Toxic States 
Myocardial insufficiency is likely to develop with the advance of all of 
the graver anemias, with faulty metabolism and with many toxic condi- 
tions. The prognosis must depend entirely upon the character of the 
primary disease and cannot be separately considered. 
10. Neoplasms 
IsTew groivths of the heart are either primary or secondary. The 
gumma of specific origin is of greatest interest to the clinician; all other 
growths are interesting pathologically, but remain as a rule undiagnosti- 
cated during life. 
The primary growths are: 
Fibromata 
Myxofibromata 
Lipomata 
Lymphangiomata 
Cavernous myomata 
Rhabdomyomata. 
Myxomatous growths may form on the separate valves. 466 
DISEASES OF THE CIRCULATORY APPARATUS 
The secondary or metastatic growths are: 
Carcinomata (often from the esophagus) 
Tubercle 
Syphilitic gummata 
Lymphadenomata 
Extension of Hypernephromata 
Sarcomata 
Melanosarcomata 
X anthosarcomata 
Osteosarcomata. 
Direct invasion of the heart from the pericardium may follow sarcoma 
of the thymus, cancer of the lung and pleura. 
Leukemic growths may also invade the myocardium. 
The Stokes-Adams complex follows invasion of the intraventricular 
septum occasionally with neoplasms; with syphilitic gummata, this is 
comparatively frequent. 
Some of the innocent growths, when small, may give rise to no symp- 
toms during life, the malignant and semimalignant naturally hasten the 
death of the victim. 
Tuberculosis and actinomycosis are separately considered. 
11. Parasites of the Heart 
The Echinococcus may find a resting place in the heart muscle (See 
Hydatid disease) usually in the right ventricle and unless of considerable 
size, causes no symptoms. When the cyst ruptures, embolic infarcts lead 
to death. These are found in the lung and distant organs. 
The Cysticercus of the Tenia solium may settle in the myocardium. 
When symptoms are produced by the growing cyst, they never lead to a 
diagnosis. Marked hypertrophy, dropsy and severe pectoral pains pre- 
ceded death in the few recorded cases. I have had no personal experi- 
ence with either Echinococcus nor Cysticercus of the heart. We have 
found the heart infected with Trichinae spiralis, hut their presence in the 
heart muscle as a rule does not materially influence the prognosis of trichi- 
nosis, so far as we know (See Trichinosis). 
For a full consideration of the parasites of the heart the reader is re- 
ferred to Hosier’s articles. (See reference.) 
12. Rupture of the Heart 
I referred to rupture of the heart in connection with fatty heart and 
mentioned the fact that in 77 per cent of spontaneous ruptures Hamilton 
found fatty degeneration of the myocardium. DISEASES OF THE MYOCARDIUM 
467 
13. Aneurism of the Heart 
Aneurism, of the heart is exceedingly rare; it is an occasional cause of 
rupture. It may accompany ulcerative malignant endocarditis and fibroid 
myocarditis. 
Fibroid degeneration and the mixed forms of degeneration may also 
lead to aneurism and rupture. 
Partial rupture may not prove immediately fatal. We found one case 
in which a partial rupture preceded death by a number of days, which was 
sudden and due to a second complete rupture. A thrombus may plug a 
small rent and prolong life during only a limited time. 
Abscess of the heart wall may cause rupture—the majority of heart 
abscesses are micotic—are found with malignant endocarditis, pyemic and 
septic conditions—they may be multiple or single. 
References 
Allbutt. Brit. Med. Jour., March 23, 1913. 
Brit. Med. Jour., 1912. 
Aschoff. Path. Anatomie, 1913, xi. 
Balfour. The Senile Heart. 
Ballinger. Quoted by Jores [l. c.]. 
Barries. Cceur et de V aorte, 3. ed., Paris, 1912. 
Brunton (L.). Longevity and the means of attaining it. 
Eisner. Am. Jour, of the Med. Sd. 1, 1914. 
Fiessinger. Bullet, de VAcad. d’Med., Oct. 1, 1912. 
Gossage and Hicks (Braxton). The Quart. J. of Med., Oxford, July 1913, vi, 440. 
Hamilton. Cited by Hirschfelder. 
Heberden. Commentaries on the History and Cures of Disease. Philadelphia, 1845. 
Hirschfelder. Diseases of the Heart and Aorta, Lippincott. 
Huchard. Traite Clinique des Malad. du Coeur et de Vaorte, Paris, 1899-1905. 
Inndell. Nord. Med. Ark., 1913, H. 3—9. 
Jores. Anat. Grundlagen der Wichtigen Krankh., Berlin, 1913. 
Lewis. Med. Disorders of Heart Beat, 1912 & 1914. 
Leyden. Deutsch. Med. Wochenschr., 1899. 
Mackenzie. Diseases of the Heart, London. 
Moebius. Zeitschr. f. Neurolog., 1-11. 
Mosler. Zeitschr. f. klin. Med., Bd. v, vi, 215. 
Musser, 
Broadbent, 
Mackenzie, 
Abrams, 
Eisner. 
Quoted by Eisner. Arch, of Diag. New York, Jan., 1909. 
Nicolai & Kraus. Berlin, 1910. 468 
DISEASES OF THE CIRCULATORY APPARATUS 
Nothnagel. Deutsch. Arch. f. klin. Med., 1867, 309. 
Ortner. Ueber klin. Prognose. Wien, 1908. 
Volkman’s Klin. Sammlungen. No. 347, Innere Med., 854 
Osier. Angina pectoris. Med. Chron., Manchester, 1906; also Monograph-Angina pectoris 
and allied states. New York, 1897. 
Practice of medicine. New York, 1915. 
Price. Brit. Med. J., March 8, 1913. 
Rieder, 
Spillman, 
Bernheim, 
Thurn. 
Quoted by Eisner, Arch. f. Diagnosis, Jan., 1909. 
Romberg. Krankheiten d. Herzens. 1906. 
Sapegno. Path. riv. quindicio. Geneva, 1909-1910, 175. 
Sternberg. Verhandlung der Deutsch. Path. Gesellschaft, 1910, xiv. 
Talley. Prognostic significance of atropine reactions, etc. Am. J. of the Med. Sci., Oct., 
1912, 514- 
Walshe. Diseases of the heart and great vessels, London, 1873. 
Weintraud. Therapie der Gegenwart, Oct., 1911. 
Windle. Quart. J. of Med. Oxford, July, 1913, vi, 462. 
F. Endocarditis 
Endocarditis is either (1) acute or (2) chronic. 
1. The varieties of Acute Endocarditis are: 
(a) Simple Acute Endocarditis (Thrombo-endocarditis simplex 
of Ziegler). 
(b) Septic Endocarditis. 
(Malignant or ulcerative endocarditis, Thrombo-endocarditis sep- 
tica ulcerosa) (Aschoff) 
2. The varieties of Chronic Endocarditis (Chronic Cardiopathy) are: 
(a) Valvular Deformities (resulting from previous Acute Endo- 
carditis) 
(b) Degenerative Endocarditis (Arteriosclerosis—Syphilis) 
Endocarditis is always of infectious origin, is secondary and not a 
disease per se. 
To recognize its prognostic significance its pathology demands consid- 
eration. The extent of the endocardium, the unevenness of its surface, as 
well as its irregularity, the mechanical factors continually present, invite 
the deposit and proliferation of bacteria. 
The endocardium offers a suitable and inviting culture medium, more 
particularly with changed conditions of the blood, and possible slight ab- 
normality of the endocardial surface. This is especially true of the malig- 
nant, septic or ulcerative type of endocarditis. ENDOCARDITIS 
469 
1. Acute Endocarditis 
(a) Simple Acute Endocarditis 
(Thrombo-endocarditis simplex of Ziegler, also known as Endocarditis 
verrucosa) 
The prominent lesion of this form of endocarditis is the deposit of 
warty or papillary masses or bodies along the edges of the valves. The 
amount of deposit varies; it may be so insignificant as to escape the eye, or 
it may be prominent, forming masses of considerable size—uneven, irreg- 
ular and of warty appearance. These masses on section show the character 
of thrombi, and hold within the included fibrin, platelets, lymphocytes with 
colonies of the infecting bacteria. There may be evidences of necrosis of 
the tissue of the endocardium or valve upon which the warty or papillary 
masses rest. The extent of the necrosis is in direct proportion to the 
severity of the infection. The danger of embolic infarct increases with the 
extension of the necrosis and the loose attachment of the thrombi. The 
replacing of the thrombi and of the underlying endocardium by connective 
tissue in the process of cure, including the valve structure, result in thick- 
ening, contraction, adhesions, leading to stenosis (narrowing) or insuffi- 
ciencies in accordance with the extent of the original lesions. Endocar- 
ditis may limit its ravages to the free surface of the endocardium without 
involving the valves. This fact must be considered in the diagnosis and 
prognosis of infections in which unexplained symptoms of constitutional 
disturbance persist. The following figures show the relative frequency 
of the invasion of the valves: 
The mitral valve is involved in 60 per cent; the aortic in about 9 per 
cent. The tricuspid and pulmonary rarely; the inflammation of both 
mitral and aortic valves is found in about 30 per cent of all cases. With 
simple endocarditis it is exceedingly rare to find the tricuspid inflamed 
with the mitral alone, or with the mitral and aortic valves combined. It is 
unusual to find all four valves attacked (Aschoff). 
In simple endocarditis the bacterial invasion is not usually overpower- 
ing, there is limited loss of endocardial tissue, there may be none at all, 
the formation of emboli is infrequent—all these conditions prevail in the 
septic or malignant type of the disease—hence the prognosis so far as life 
is concerned, is good. Romberg denies the possibility of complete anatomic 
restitution after even simple acute endocarditis. 
The extent of the damage done by an acute endocarditis cannot be 
foretold—this fact calls for a guarded prognosis concerning the future of 
the functional powers of the heart and at the same time suggests such 
prophylactic measures as should lead to the conservation of the organ. All 
forms of acute endocarditis are associated with more or less myocarditis, 470 
DISEASES OF THE CIRCULATORY APPARATUS 
a further fact, which must he considered in connection, with the primary 
disease during the period of endocardial involvement and the months fol- 
lowing convalescence. Pericarditis (See Chapter Pericarditis) is also a 
frequent accompaniment of endocarditis; the significance of the former 
must be considered in connection with the degree of virulence of the 
primary infection and the extent of the endocarditis, as well as the charac- 
ter of the effusion. (See Pericarditis.) The mortality of the combined 
lesions reaches between 25 and 35 per cent. 
All factors which overtax the heart during or after acute endocarditis 
invite permanent damage. 
Endocarditis is subject to relapses; this is due to the tendency of poly- 
arthritis to recur (the most frequent cause of the complication) ; and the 
further fact that the endocardium harbors bacteria in its folds and on its 
surface during long periods. 
In the acute types, non-malignant, the left ventricle is usually the seat 
of the infection; with severer and ulcerative septic endocarditis, the right 
heart is frequently the seat of profound changes as well as the left ventricle. 
I have considered the significance of endocarditis in connection with 
the many infections which it complicates and refer the reader to the sep- 
arate chapters; they include Polyarthritis, Scarlet fever, Tonsillitis, 
Typhoid fever, Pneumonia, Erysipelas, Diphtheria, Chorea, Syphilis, 
Tuberculosis, Gonorrhea, Pyemia, Sepsis, Nephritis, etc. 
With some forms of grave anemia and cachexia, endocarditis may de- 
velop and seriously complicate the prognosis. Probably some of these cases 
are of toxic rather than of infectious origin. 
Endocarditis complicating gout, diabetes and other constitutional dis- 
eases, may, in the light of our present knowledge be included in the 
“toxic type.” The prognosis with acute symptoms and material change in 
the heart muscle is to be guardedly given; all features of the case demand 
the closest consideration. These cases are not to be confounded with the 
endocarditis of degenerative (arteriosclerotic) origin which is frequent 
with faulty metabolism. 
The Physical Signs.—In offering a prognosis, the clinician is not 
to interpret the loudness of the systolic murmur which is present and 
widely disseminated over the precordium in almost all cases, as indica- 
tive of a serious condition. 
Let the greater reliance for prognosis be placed upon the virulence 
of the infection, the extent of the primary lesions, the general condition 
of the patient, the amount of dilatation of the heart, the character of the 
pulse, the functional ability of the kidney, the blood pressure, the size of 
the liver (enlarged in serious cases), the size of the spleen, the presence of 
infarcts, the blood picture and a variety of symptoms which are unearthed 
by close observation, 
In children, while the prognosis is less favorable than in adults, iu ENDOCARDITIS 
471 
the absence of edema and in the presence of apparently serious endo- 
carditis, recovery may follow with but limited damage to valvular 
structures. 
Even with edema and multiple systolic murmurs in children and 
adults, recovery may folloiu ivith surprisingly insignificant damage in 
cautiously treated cases. 
Loud, and multiple murmurs with chorea, may disappear entirely, 
never to return, within a number of years. Return of chorea may in 
some cases remain uncomplicated, in others there are acute exacerbations 
of endocarditis. The prognosis of chorea with complicating endocarditis 
is not bad. In a large experience I have seen but two deaths; both chil- 
dren were enormously obese—in one the endocarditis was malignant. 
With recurrences and extension, the damage resulting with increas- 
ing physical signs of myocardial insufficiency arid dilatation, may lead 
to long periods of uncertainty, but in most cases life is saved; occasion- 
ally underlying conditions are serious, resistance is reduced and death 
cannot he averted. 
Pulmonary edema, pneumonia, purulent pericarditis, thrombosis, 
embolism with hemorrhagic infarct and a mitral obstructive lesion are 
unfavorable complications, and include the most frequent causes of death. 
Duration.—It is never possible to foretell the length of time during 
which the acute symptoms will continue; cases which often drag along dur- 
ing weeks and months without change in physical signs or subjective symp- 
toms, gradually regain health with ultimate limited damage to the heart. 
The previous condition of the heart is an important factor in prog- 
nosis. There is always danger of malignant endocarditis in cases of 
acute exacerbation of chronic heart lesions. 
With early aortic insufficiency, the danger is greater than with the 
more frequent mitral insufficiency; the danger is greater with early mitral 
than with aortic obstruction. 
The influence of age, sex, occupation and habits is considered with 
the resulting permanent valvular lesions. In all cases of simple acute 
endocarditis treatment, especially rest and right living enormously influ- 
ences prognosis. Many lives have been doomed to wretchedness and 
chronic invalidism by failure on the part of the physician, oftener the 
patient, to realize the great curative and prophylactic value of rest after 
acute endocarditis. 
(6) Septic Endocarditis 
(Malignant, Infectious, Ulcerative Endocarditis; Thrombo-endocarditis 
septica s. ulcerosa—Aschoff) 
In contradistinction to the superficial character of the lesions with 
simple acute thrombo-endocarditis, septic endocarditis shows deep inva- 
sion of valvular structures and of the free endocardium in a destructive, 472 
DISEASES OF THE CIRCULATORY APPARATUS 
necrobiotic process; the formation of vegetations, abundant thrombotic 
deposit, and the presence of the virulent microorganism in great num- 
bers. Bacteremia is present and can be demonstrated by blood-cultural 
methods in most cases. 
Septic endocarditis should he considered to he of secondary origin in 
all cases; the exceptions are so rare as to require no consideration. There 
is no one pathogenic organism which causes the disease, it may follow 
in order of frequency streptococcus, pneumococcus, staphylococcus, influ- 
enza bacillus, gonococcus infection and in the chronic forms of the disease 
the streptococcus viridans (Schottmtiller, Rosenow, Libman) is now 
established as the leading factor, though there are many cases of chronic 
pneumococcus endocarditis and in all forms mixed infection may ulti- 
mately exist. Aschoff suspects that the viridans is a modified pneumo- 
coccus. 
The avenues of entrance of the infecting agent are numerous and 
often furnish surprises. 
The hlood is furnished with the specific organism from diseased ton- 
sils, the lung, the genitalia (women oftener than men), the puerperal 
uterus and adnexae, the hone marrow, the skin and from any source to 
which infection may he carried and from which the hlood current is 
infected. Insignificant (apparently) traumatism has in several of our 
cases led to malignant endocarditis. In two cases we found the passing 
of a urethral sound with slight bleeding followed by fatal endocarditis. 
In the cases following the unnoticed and insignificant primary infec- 
tion, the malignant nature of the endocarditis comes as a surprise. Often 
the primary disease is unheralded and overlooked—“In the endocarditis 
following the graver infections, one is dazed by the gravity of the pri- 
mary malady and fails to look for secondary and malignant disturb- 
ances” (Eisner). 
For prognostic purposes the frequency of septic endocarditis grafted 
or preceding valvular disease must be considered, the chronic lesion 
becomes an important and inviting factor. Goodhart showed that 61 of 
69 cases presented old thickening of the valves, and mentions the occur- 
rence of malignant endocarditis with aneurismal disease. He further 
says: “Patients with chronic sclerotic valves are walking mushroom beds, 
in common times without spawn, but in periods of epidemics germs enter 
by various channels, which fertilize in these cases into ulcerative endo- 
carditis ; in others to suppurative processes.” Osier also mentions the 
frequency with which sclerotic disease of the aorta and valves is asso- 
ciated with malignant endocarditis. This is an exceedingly important 
fact for prognosis and with all primary infections, in the presence of 
chronic heart lesions it should not be ignored. Sir James Paget offered 
the data which proved the frequency with which changed valves suffer 
from acute disease. Of 84 cases of infectious endocarditis seen in St. ENDOCARDITIS 
473 
Bartholomew’s Hospital from January, 1890, to March, 1897, 51 were 
found in males, or 60.71 per cent, and 33 in females, or 39.29 per cent. 
The greatest number was found from the thirtieth to the fortieth years; 
most of the cases between twenty and forty. In these cases all but 10 
were found either in patients suffering from old cardiac disease, or there 
was positive evidence of an infecting lesion. The tendency of old dis- 
eased valves in pneumonics to take on chronic malignant inflammation 
is surprising. 
It has been established experimentally by Wyssokovititch, Oliver and 
Rosenow that infectious material introduced in the blood stream attacks 
by preference the valves and endocardium which have been traumatically 
robbed of their protecting endothelium. To Heiberg belongs the credit 
of establishing the fact that in these cases, the vegetations on the valves 
were bacterially contaminated. The complication of malignant endo- 
carditis with septic conditions is fortunately comparatively rare, but 
with increased diagnostic skill it is more frequently found than formerly. 
Lenhartz found in the Hamburg Hospital 21 per cent of all general sepsis 
with endocarditis. 
Romberg reports in 33,539 of internal diseases during 8 years, 243 
cases of sepsis with 42 malignant endocarditides. In 6,670 cases of inter- 
nal disease I found in my private and consultation practice 20 cases 
of malignant endocarditis including gonococcus and pneumococcus infec- 
tion. Of 7,770 cases of internal disease among whites admitted to Johns 
Hopkins Hospital (1902-1911) there were 1,317 diseases of the circulatory 
organs, among these endocarditis was diagnosticated in 38 males with 21 
deaths, 55.3 per cent, and in 12 females, 33.3 per cent. How many of 
these were malignant is not stated. 
Endocarditis which is at first benign or appears to be so, may in the 
course of a few days end fatally with symptoms of malignant infection, 
while other cases which commenced with symptoms of malignancy may 
prove to be benign or non-septic. 
It is exceedingly difficult in practice to draw a line which shall sepa- 
rate the severer benign, from the malignant types, either by clinical study 
or blood cultural methods during long periods in individual cases. Re- 
peated negative cultures in cases of malignant endocarditis not infre- 
quently leave the clinician uncertain as to diagnosis and prognosis 
during long periods. In some of these cases the involvement of the right 
heart argues in favor of malignant infection. Bitten called attention to 
a variety of simple acute endocarditis associated with rheumatism which 
he styled “Non-septic Malignant Rheumatic Endocarditis,” in which 
many cases prove unusually severe and often fatal. This type of endo- 
carditis presents distinct features which must be considered separately 
and are not identical with those of malignant or septic endocarditis. In 
the favorable cases there is the same tendency to contraction and changes 474 
DISEASES OF THE CIRCULATORY APPARATUS 
in the valves found in the less virulent forms. The right heart escapes 
involvement. There may be infarcts and metastases but these are never 
malignant, there is greater tendency to pericardial involvement, and 
recurrences of acute exacerbations in those who recover are frequent. 
There are no paralyses nor symptoms of embolism or purulent throm- 
boses. Death usually results with cerebral symptoms; albuminuria is 
transitory, the spleen is less enlarged than in malignant endocarditis. 
Tn 209 cases of septic endocarditis, Osier reports the tricuspid valve 
involved in 19 cases; the pulmonary in 15; the aortic and mitral together 
in 41; the aortic alone in 53, the mitral alone in 77, the heart wall in 
33, and in 9 cases he found the right heart involved alone. These figures 
prove the involvement of the right heart out of all proportion to the left 
sided disease in the less malignant or other forms of secondary endo- 
carditis. The grave prognosis which is justified in all cases of malignant 
or septic endocarditis depends on the virulence of the primary infection, 
often mixed infection, the far-reaching local and general disturbances, 
the tendency of the diseased tissue to break down into minute particles 
which act as carriers of the infectious material to distant parts causing 
deep changes, hemorrhagic infarcts, mycotic aneurisms, and the further 
tendency to miliary abscesses, and purulent infarct in the various organs 
of the body, including the kidneys, spleen and heart. Ilarbitz and Lib- 
man claim that with the virulence of the infecting agent reduced, the 
local endocardial lesions may heal and cicatrice though the resulting 
damage to the valves and endocardium is greater than with single endo- 
carditis. We have no case to report, in which if such healing process 
did occur the life of the patient was saved in our practice; in no case 
in which the diagnosis of septic endocarditis was positively established 
clinically and bacteriologically has recovery followed—this is the expe- 
rience of nearly all clinicians. The following classification of Septic 
Endocarditis is most serviceable: 
I. Intermittent of pyemic form. 
II. Fulminating intermittent form. 
III. Typhoid form. 
IY. Cerebral form. 
V. Chronic Cardiac form. 
I. Intermittent or Pyemic Form.—Kirke and Traube dilated fully 
on the possibility of chills and fever and all of the symptoms of inter- 
mittent fever, with endocarditis. In these cases there is as a rule the 
history of preceding septic or purulent infection. Most cases are of 
streptococcus origin, show marked leukocytosis, the spleen is enlarged; 
with delirium, rapid pulse, moderate albuminuria, occasional hematuria, 
positive physical signs, early changes in the quality of the heart sounds 
and equally early embolic infarcts, cutaneous and deep, they die. ENDOCARDITIS 
475 
In some of these cases where there are preexisting heart lesions and 
consecutive murmurs, the character of these is often changed, and with 
this change there are transitory paralyses; sometimes evidences of em- 
bolic infarct in the skin, lung, brain, kidney or intestine, obstructive 
murmurs are often changed in character and occasionally become in- 
audible—for a time at least. 
Intermittent types with puerperal phlebitis run a short course to a 
fatal termination. Petechiae are often abundant. 
In these cases, as with all forms of septic endocarditis, the endocardium 
may be plastered ivith granulations and deeply ulcerated without causing 
murmurs or other physical signs until within a few hours or days of death, 
or these may never appear. The chronicity of some of these cases is strik- 
ing. Some persist with final irregular intermittent fever during from four 
to six months. Most die within four to six weeks. The diagnosis of inter- 
mittent malarial fever has often been made in cases seen before the days of 
blood cultural tests; at present these errors are rare. Quinin is entirely 
without influence on the course of the disease. Most patients die with 
symptoms of cerebral infarct. 
Among these intermittent cases, we recognize (a) pyemic or septic 
form, (b) erratic intermittent form, (c) late cardiac, intermittent form 
and (d) intermittent form with preexisting heart lesions. To the first 
of these, 
(a) Pyemic or septic form belong the cases of pyemia following 
puerperal fever. These patients carry pus foci (one or more), may be 
about for a time, but the course of the disease is usually short, always 
fatal. 
(b) The erratic intermittent form may have erratic chills, more or 
less continuous fever, the chills are very severe, the patient finally falls 
into a .typhoid condition with a zigzag temperature curve during which 
the chills observe no periodicity, there is delirium, coma and death. 
(c) The late cardiac intermittent form is characterized by absence 
of positive physical signs during considerable periods, unexplained chills, 
fever and pyemic symptoms persist during several weeks when the ob- 
jective features become clear and death follows. 
(d) Intermittent form with preexisting heart lesions includes those 
cases upon which a malignant infection is grafted. This group of cases 
bears the strongest resemblance to malaria. 
II. Fulminating Intermittent Type.—This type includes a number of 
cases which run a rapid course, terminating fatally in from ten to seven- 
teen days, occasionally sooner. 
Our series includes one case in which there was an infarct into the 
right eye causing complete blindness with characteristic quotidian fever 
and marked mitral systolic murmur. There were no petechiae. The 
source of infection remained undiscovered. The patient died before the 476 
DISEASES OF THE CIRCULATORY APPARATUS 
end of the second week. Another death with fulminating intermittent 
symptoms was a child (obese) aged 12 years with violent chorea. There 
was, with the chills, hyperpyrexia, hematuria, cutaneous hemorrhages, 
delirium cordis, death in coma on the 13th day of the disease. Many 
of these cases show chronic endocardial lesions and they are likely to be 
of staphylococcus origin. 
III. Typhoid Form.—The typhoid forms may persist as such from 
the beginning, or the typhoid state may precede or follow any of the 
other types. Most cases belong to this form. Pure intermittent cases 
often merge into a typhoid state and die in that condition. 
Without chills, with more or less looseness of the bowels, enlargement 
of the spleen, leukocytosis (12,000-20,000), increasing anemia, albu- 
minuria, mental torpor with final cerebral infarct, in many, and with 
positive blood cultural finds, in almost all cases, these patients die in the 
course of from 6 to 12 weeks. 
IV. Cerebral Form.—Bramwell suggested the consideration of this 
type in his work on “Diseases of the Heart.” In all of these forms there 
is a strong tendency to coma and other cerebral symptoms as the disease 
advances. There is a strong resemblance to cerebrospinal meningitis or 
meningitis. In occasional cases there has been pneumococcus infection 
with pneumonia. In two cases, convulsions preceded death. One of 
our cases was associated with purulent pericarditis. In some cases the 
vegetations were so placed as not to give rise to murmurs. 
V. Chronic Cardiac Type.—This group includes all cases of chronic 
endocardial disease in which infection has led to mycotic endocarditis. 
The chronicity of these infections is characteristic with persisting bac- 
teremia, usually either pneumococcus or streptococcus viridans, erratic 
fever, anemia, leukocytosis, enlarged spleen, often joint pains, late in the 
course of the disease hematuria due to infarct, finally in most cases 
death from cerebral infarct or exhaustion. Septic Nephritis develops in 
most cases. In some there are mycotic aneurisms. Petechiae are found 
in almost all cases at some time during the long duration of the disease. 
Some of our patients have lived from seven to thirteen months. Death 
is usually caused by one or more good sized infarcts. I have found 
the association of infarcts into the brain, lung, spleen and kidney. Occa- 
sionally one or more of the multiple infarcts are found sterile. It may 
be assumed with considerable certainty, that the streptococcus viridans 
is the cause of most forms of chronic malignant endocarditis and that 
the prognosis is uniformly fatal. 
Gonococcus Endocarditis which should he included among the malig- 
nant types of endocarditis, offers only the most discouraging prognosis. 
It is fully considered in the chapter on gonococcemia. 
The unfavorable prognosis which I offer in all cases of septic and 
gonococcus endocarditis is justified by my experience in spite of those ENDOCARDITIS 
477 
cases in which from “time to time” greatly deformed cicatricial valves 
and remnants of infarct are found in patients who have died from other 
causes. Broadbent after mentioning these possibilities, concludes: “The 
number of authenticated cases recorded, however, in which recovery is 
reported to have taken place, is extremely limited, and it has not been 
my good fortune to see an undoubted case recover. 
Aschoff. Pathol. Anatomie. 8. Aufl., Bd. ii, 21. 
Bramwell. Diseases of the heart and aorta. Edinburgh, 1884. 
Broadbent. The Practitioner, London, July, 1910. 
Eisner. Malignant endocarditis. Jacobi's Fetschrifft. 
Goodhart. Transact. London Path. Soc., xxxiii. 
Heiberg. Virchow's Arch. etc. Bd. vi, 1896. 
Kirke. Eisner’s Malignant endocarditis [l. c.]. 
Lenhartz. Nothnagel Spez. Pathol, u. Therap. Bd. iii„ iv. Theil, Wien, 19th. 
Munch, med. Wchnschr., 1901, Nos. 28 & 29. 
Libman. Am. J. Med. Sci., 1912, No. 144- 
Litten. Ztschr. f. klin. Med., 1881, Bd. ii. 
Oliver. Int. Clinics., Philadelphia, 1895, series 5, i. 
Osier. Gulstonian Lectures, Lancet, London, March, 1888. 
Paget (Sir Jas.). Transact. London Med. Chirurg. Soc., xvii. 
Romberg. Krankh. des Herzens, 1906. 
Rosenow. Transact. Med. Soc., State of New York, State J., 1912. 
Report Med. Section, Med. Soc. of the State of New York, 1912. 
J. Am. Med. Ass., 1912-1913. 
Schottmuller. Munch, med. Wchnschr., 1910, No. 12. 
Traube. Gesammelte Abhandlung II. Therap., 270. 
Wyssokovititch. Quoted by Leube. Specielle Diagnose der inner. Krankh. Leipziq, 
1895. 15. 
References 
2. Chronic Endocarditis 
( Cardiopathia chronica—Aschoff) 
General Considerations Included in the Prognosis of the Valvular 
Lesions of the Heart 
Acute or recurring endocarditis leads to cicatricial changes in the 
valves of the heart making one or more of these insufficient or stenosed, 
causing consecutive changes in the heart and distant organs, in accord- 
ance with the character of the lesion. 
There is, in truth, no true chronic endocarditis; the lesions 'produced 
are the results of gradual reparative changes which finally influence cardiac 
function and lead to the chronic endocardial and valvular defects above 
mentioned. 478 
DISEASES OF THE CIRCULATORY APPARATUS 
The general acceptance of the term “Cardiopathia chronica ” offered 
by Aschoff is suggestive, and at the same time explanatory, and would 
do much to clear the horizon of the indefinite notions which are asso- 
ciated in the minds of many clinicians and students in connection with 
the misnomer “Chronic Endocarditis.” 
It is important to associate the chronic cardiopathies with two distinct 
primary processes, one inflammatory; the other degenerative. The first, 
or inflammatory process—is likely to attack the mitral valve by predilec- 
tion and the neighboring endocardium; the second, or degenerative proc- 
ess—(arteriosclerotic) selects the aortic valve and the surrounding tissue, 
and often the aorta itself, is part of an existing general arteriosclerosis 
and is often associated with coronary disease and myocardial fibrosis. 
With mitral lesions the degenerative or retrograde processes of the 
myocardium start in the coronary veins; with aortic disease, the lesions 
in the coronary arteries are likely to start the muscular insufficiency 
which is the threatening complication of all heart lesions. We are justi- 
fied in considering the faulty compensation of mitral disease as a “venous 
cirrhosis,” that of aortic disease as “purely arterial.” 
It is impossible to consider the diagnosis or prognosis of the car- 
diopathies (vascular lesions) without at once accenting the most impor- 
tant fact in cardiac pathology that in the majority of cases murmurs give 
hut little clue to existing dangers, that we find in the heart muscle “the 
hey to the pathology of the heart” (Stokes). Whatever the valvular 
lesion, “the symptoms depend mainly upon the strength or weakness, the 
irritability or paralysis, the normal or abnormal condition of the heart 
muscle.” 
It cannot be too often repeated that for safe prognosis we must 
assume that valvular lesions per se, have hut little influence on the gen- 
eral condition of the patient so long as the heart muscle remains healthy 
and sufficient. 
Gee’s aphorism teaches a valuable lesson. “A beginner can hear mur- 
murs and detect valvular disease, it requires long experience to appreciate 
nervous and muscular affections of the heart.” 
The seat and severity of the valvular defects naturally determine 
the secondary changes in the heart and other organs. 
(a) Hypertrophy.—The heart learns to accommodate itself to changed 
conditions, it is built to bear insult, it is the most tolerant of all the 
necessary organs of the body. 
With stenosis or insufficiency the heart undergoes such changes as 
are demanded by the increased tax made upon it. These must always 
be considered in connection with the separate valvular lesions. The gen- 
eral rule may be accepted without reservation, that whenever extra force 
and added energy are required, Nature makes a prompt attempt to de- 
velop the heart muscle to meet the demands; in other words the prognosis ENDOCARDITIS 
479 
is influenced by the growth of the muscle, its increased strength, indeed 
the separate fibers show characteristic change (Tangl). 
Only cases in which valvular lesions have existed a short time, fail 
to show some compensatory increase of strength. (Hypertrophy.) 
For prognosis, the important factors to be considered are, 
A. The reserve force of the heart. 
B. Compensatory hypertrophy. 
With the average defect, there is “a stasis behind the diseased valve 
and an anemia in front; the arteries consequently receive too little blood.” 
A. When called upon, the normal heart is competent to increase its 
force and strength of action thirteen fold (Zuntz). 
The reserve power of the heart makes it possible for the organ when 
disturbed by a valvular lesion to prevent circulatory disturbances and 
embarrassment so long as the body is kept at rest, or the organ is not 
overtaxed, and the distant organs receive their quantum of blood and 
the arteriovenous balance remains undisturbed. 
When extra work is thrown on the heart, the seat of any valvular 
lesion, the reserve is lowered. 
B. Compensatory hypertrophy becomes an immediate necessity to 
equalize the circulation and to prolong life. 
The demand which is made upon the heart to overcome an existing 
fault must determine the amount of necessary compensatory hypertrophy; 
under such conditions the prognosis is favorable in direct proportion to 
the ability of the heart muscle by increasing its volume, if conditions are 
continuous, to meet the added requirements. Under these conditions the 
prognosis is necessarily influenced by the ability of the patient to reduce 
the heart’s labor, in other words, the subject of valvular disease if he 
fails to give the heart muscle the sleep or rest to which it is entitled adds 
an element which reacts unfavorably, for the overtaxed and overtired 
muscle hypertrophies or compensates slower than does the muscle which 
has been subjected only to physiological strain. The prognosis is fur- 
ther influenced by the spontaneity of the response of the muscle to react 
to the added task; the nature of the valvular lesion, the method of its 
onset and the other factors which influence the outcome of all heart 
lesions. 
With aortic obstruction, the pressure within the left ventricle is 
increased during systole, the resistance offered by the narrowed or uneven 
ostium (valve) must be overcome and with a favorably reacting left 
ventricle, hypertrophy.leads to sufficient strength to overcome the obstruc- 
tion and the quantity of blood enters the aorta with sufficient force to 
meet all demands. These favorable conditions continue during many 
years in a large number of cases, are promptly influenced by conditions 
which increase obstruction in the periphery, by advancing degenerative 480 
DISEASES OF THE CIRCULATORY APPARATUS 
changes in the arteries and increased blood pressure, by degeneration of 
the myocardium and other factors considered in connection with aortic 
obstruction and stenosis. 
The prompt hypertrophy of the left ventricle which follows aortic 
stenosis is not characteristic of the behavior of the left auricle when the 
mitral valve is stenosed. Here the auricle because of its anatomic struc- 
ture—poor muscular development—is less likely to hypertrophy, besides 
there are conditions in the pulmonary circuit which increase the amount 
of blood in the left auricle early during diastole, it is overtaxed during 
its systole, dilatation is invited and the extra work then thrown upon 
the right ventricle leads to its hypertrophy. 
With moderate, almost insignificant mitral stenosis, a limited hyper- 
trophy of the left auricle may prove sufficient to overcome the obstruc- 
tion and the circulation may continue undisturbed. 
With a high grade of mitral stenosis the pressure within the pul- 
monary circuit and in the left auricle is increased, and unless the hyper- 
trophy of the right ventricle continues sufficient, a break follows which 
influences prognosis unfavorably. This condition is separately consid- 
ered but it cannot be too often repeated that it is the leading danger of 
mitral stenosis. 
With valvular insufficiencies, physical and mechanical conditions are 
different than with the stenoses. In the former we are dealing with the 
regurgitation of blood into a cavity of the heart (with aortic disease into 
the left ventricle, with mitral insufficiency into the left auricle) and with 
both of these conditions the heart must of necessity contract with added 
strength to empty the respective cavity, but the cavity itself must accom- 
modate itself to hold the surplus or extra blood which it receives. More 
blood must be forced onward than the cavity normally receives during 
the period of rest. The result is change in the musculature to hold the 
extra blood and to force it onward. 
In favorable cases compensation is synonymous with the increase of 
strength of the muscle and a sufficient degree of physiologic dilatation. 
If dilatation is extreme, compensatory hypertrophy is less likely to 
prove prompt or satisfactory. 
Extreme pathologic dilatation always retards or lowers the chances 
of the growth of the muscle fibers to meet the demands. 
Regurgitant lesions (insufficiencies) tend to enlarge the openings 
situated behind the seat of the lesion. In most favorable cases in which 
the left side of the heart is enlarged, the right ventricle hypertrophies, 
thus maintaining the blood pressure in the pulmonary circuit. 
(b) Dilatation.—The physiologic widening of a cavity of the heart 
to accommodate itself to a surplus of blood is compensatory as already 
suggested and with increase of systolic force conditions continue favorable. 
If the heart muscle is weakened, the cavity is not entirely emptied/ ENDOCARDITIS 
481 
there is with increasing accumulation increase of dilatation and added 
demands are made upon the musculature of the organ. Unless this is 
successfully met, the stretching or dilatation of the heart may become 
extreme and evidences of such cardiac insufficiency are shown by added 
dyspnea and physical signs. 
With aortic insufficiency there are two sources from which blood 
enters the left ventricle during diastole: the regurgitation from the aorta 
because the cusps are not completely closed, and the normal supply from 
the left auricle. The heart muscle is called upon to exert itself to empty 
the ventricle during systole of the added quantity of blood, besides the 
content which is normally present ; sufficient force is demanded to send 
into the arterial tree all of the contained blood, besides contracting the 
ventricle to as nearly as possible its normal size. So long as this com- 
pensation continues undisturbed there is no fear of troublesome dilata- 
tion; when disturbed, the muscle lags behind, the blood accumulates in 
the ventricle, and pathologic dilatation without sufficient hypertrophy 
results. 
The dilatation of the left ventricle which results from mitral insuffi- 
ciency when associated with compensatory hypertrophy allows of suffi- 
cient discharge of blood into the aorta to compensate, without disturbing 
the circulatory balance. 
Conditions.—The conditions which bring about the compensation 
necessary to insure a favorable prognosis with valvular insufficiencies 
are therefore a sufficient or physiologic dilatation to allow of the regurgi- 
tated blood and muscular strength to empty the chamber completely of 
its contents. 
Blood Pressure.—When there is heightened blood pressure with in- 
sufficiency, dilatation becomes a serious condition and with the added 
systolic force needed to overcome the resistance in the periphery, there 
is, under failing conditions, an increase of residual blood in the ventricle, 
dilatation without hypertrophy and decompensation is the result. 
With increasing dilatation of the left ventricle, relative mitral insuf- 
ficiency may result; this in turn leads to dilatation of the left auricle and 
rise of pressure in the pulmonary circuit. The right ventricle is soon 
overtaxed in its attempt to overcome the resistance in the pulmonary 
artery, it dilates in unfavorable cases, tricuspid incompetence results with 
all of the secondary disturbances including dilatation of the right auricle 
and the evidences of stasis in the systemic veins and in the portal circuit. 
Under these conditions, the prognosis is exceedingly grave, the picture of 
circulatory embarrassment or break is complete. 
Simple uncomplicated hypertrophy of the left ventricle is exceedingly 
rare. When present, without other physical signs it is due to arterial- 
aortic disease and often to some one of the nephropathies. With persist- 
ently high blood pressure the latter may be strongly suspected. Under 482 
DISEASES OF THE CIRCULATORY APPARATUS 
these conditions with proper care, life may be prolonged during many 
years. (See Myocarditis, also Nephritis.) 
(c) Decompensation.—The full compensation of a valvular defect 
may persist during many years and patients may die of intercurrent dis- 
ease. In most cases of (valvular) defects, added work thrown upon the 
heart is promptly followed, even in the average unfavorable case, by some 
subjective or objective symptom of revolt. 
In the majority of organic valvular lesions the heart tires ultimately 
and decompensation is more or less in evidence, in direct proportion to 
the weakness or lack of resistance of the myocardium. 
In many cases the patient is responsible for the unfavorable condi- 
tion because of overwork, excitement, excesses in diet, tobacco, coffee or 
alcohol, faulty living, exposure and a variety of depressing factors. Other 
agencies which invite decompensation are beyond the patient’s control; 
they include acute infections and many other diseases (metabolic) recur- 
ring endocarditis, worry, pregnancy, traumatism, etc. 
The myocardium always remains the prime factor in decompensation. 
With aortic disease and increase of degenerative changes in the arterial 
tree (arteriosclerosis), the myocardium suffers and symptoms are in- 
creased ; the forecast is made less favorable. 
Increase of valvular changes (contraction, insufficiency) necessarily 
adds to the work of the muscle and calls for further compensation. 
With valvular lesions the reserve force of the heart is reduced, the 
work which the organ accomplishes is often maximum or near the limit of 
its power, when this is exceeded, decompensation is likely to follow if the 
baneful factors persist. 
In practice, it is never safe to assume, in spite of statements by ex- 
cellent authorities to the contrary, that the hypertrophied heart is equal 
to the normal heart in its functional ability, that it is able to endure 
equal strain, that the reserve power of both is the same. The safest rule 
to accept for prognosis is that the heart which is changed to compensate 
for an existing fault is never as dependable as is the normal heart, that to 
overtax such an organ adds an element of danger which may lead to 
irreparable damage and when the insult is persistent decompensation must 
be expected. For the further study of hypertrophy, dilatation and de- 
compensation and degenerative changes in the myocardium, associated 
with valvular lesions, the reader is referred to the chapter on Myocarditis 
and to the following works: Krehl and Romberg, Dehio, Stokes, Aschoff 
and Tawara and Gerhardt (See References at end of chapter). It is 
impossible to separate the study of the myocardium from the valvular 
lesion in prognosis, the latter is of secondary importance, a fact to which 
the clinician must cling at all times. 
I have referred to increased blood pressure with arteriosclerosis as 
a cause of myocardial weakness and ultimate decompensation; in these ENDOCARDITIS 
483 
cases the prognosis, even with included aortic valvular lesions is best in 
syphilitic arteritis. 
Arteriosclerosis of the pulmonary artery or its branches with valvular 
lesions, aortic and mitral, in which the left ventricle is weakening, adds an 
element of danger and throws an added burden upon the right ventricle 
which may prove insufficient and lead to changes in the lung—bronchitis, 
pulmonary congestion or edema. Under these conditions the right ven- 
tricle is hypertrophied and insufficient. 
The prognosis of dilatation of the right ventricle under all conditions 
is more favorable than is that of the left ventricle. The former may de- 
velop suddenly and promptly disappear, the latter is usually threatening 
and serious. 
Hypertrophy of the right ventricle which continues during a consid- 
erable period is likely to prove permanent. On the other hand dilatation of 
the left ventricle may yield to treatment, there are many associated fac- 
tors to be considered in making the forecast. Acute, suddenly arising 
dilatation of the left ventricle is always of the gravest import. 
(d) Frequency of Valvular Lesions.—From three to five per cent 
of all internal diseases are due to chronic valvular lesions. Gerhardt 
gathered the following statistics showing the frequency of valvular dis- 
ease. He found that in hospital practice from two to five per cent of all 
internal diseases were due to valvular anomalies. Leuch claimed 2.1 per 
cent, Schmidt 3.3 per cent, Guttman 5 per cent, Duchek 2.3 per cent, 
my own statistics 5 per cent (private practice). In private practice the 
number of heart lesions are greater than in most general hospitals. Ger- 
hardt found that of 1,200 patients seen in private and consultation prac- 
tice, 289 complained of heart symptoms with 65 valvular lesions, 115 
myocardial disturbances, 109 neuroses. Of those complaining of heart 
symptoms 25 per cent have valvular lesions. 
(e) Sex.—Sexes run nearly evenly with a small per cent in favor 
of the female. 
The prognosis of heart lesions, i. e., valvular defects is more favor- 
able in women than in men. This is true of all organic diseases of the 
heart, including its arterial supply. 
Hoffman’s statistics gathered at Johns Hopkins Hospital (1902-1911) 
show that of all forms of endocarditis 55.3 per cent of white males and 
only 33.3 per cent of white women died. 
(f) Heredity and Family History.—Heredity has a powerful influ- 
ence on the prognosis of the chronic cardiopathies; this is particularly 
true of lesions of the aortic valve. Schott found 26 per cent of all valvu- 
lar lesions with a family tendency. The prognosis is always less favor- 
able with a clear family history of heart disease. To this fact I refer in 
connection with angina pectoris. 
With an aortic valvular lesion, the history of anginous attacks and an 484 
DISEASES OF THE CIRCULATORY APPARATUS 
unfavorable family history the prognosis is correspondingly grave. Eich- 
horst and Mohr offer data which show positive hereditary tendency to 
valvular lesions in some families. 
(g) Age.-—Age is an important factor in the prognosis of chronic 
valvular lesions. 
Young children with permanent valvular defects offer an unfavor- 
able prognosis. 
During the active years of life the prognosis of the lesions which 
result from inflammatory disease (mitral usually) is relatively favorable. 
The degenerative (aortic lesions) valvular lesions, however, offer an un- 
certain and usually an unfavorable forecast. 
Valvular lesions during old age are likely to be associated with such 
other senile defects as justify only clouded prognoses. With such patients 
arteriosclerosis is the most frequent accompaniment; the prognosis natu- 
rally depends upon the rate of its progression. In a large percentage of 
these cases the advance of the sclerosis is slow and not infrequently the 
process remains stationary during a number of years. Compensation for 
valvular faults in advanced life is often surprisingly prompt. The heart 
instead of undergoing atrophy is stimulated and enlarges. Leyden says, 
“the heart is the only organ the size of which increases during old age.” 
He claims that the heart of the youth is “more likely to exhaust itself 
than is that of the older individual.” 
(h) Occupation and Social Conditions.—The influence of occupa- 
tion and social status on the course of valvular lesions is of paramount 
importance. From the data given in the preceding paragraphs it is at 
once evident that occupations which require considerable physical effort, 
if continued, are less favorable than are those in which the patient is kept 
comparatively quiet. 
Valvular diseases {usually aortic), in those who are subjected to men- 
tal strain, worry, hurry and excitement are not likely to hold their com- 
pensation. Myocardial degeneration with aortic and coronary lesions 
and interstitial nephritis (sclerotic) are the complications which lead to 
death, 
The factors included in the stress of modern life lead many active busi- 
ness and professional men to an early fall in the presence of a chronic 
cardiopathy. 
With mitral stenosis and aortic insufficiency the prognosis is often 
favorably influenced by occupation which conserves the patient’s energies 
and strength and does not add a burden to the overworked heart. 
The ability of the patient to control his movements, to take advan- 
tage of favorable climatic influences guided by intelligence and sobriety 
become enormous factors in his favor. 
Though valvular lesions are usually incurable, patients are often re- 
sponsive to intelligent supervision, and if their social status permits of ENDOCARDITIS 
485 
the control indicated in the individual case with a healthy suggestion and 
sufficient optimism life is often made comfortable during many years. 
(i) The Influence of Intercurrent Diseases.—Infections.—In spite 
of serious valvular lesions, the heart, under extra strain, in the presence 
of added disease, which in the perfectly healthy subject requires the assist- 
ance of a resistant organ, does its work satisfactorily and in the end the 
disease terminates favorably. The heart under such conditions bears the 
burden during the acute period of the complication, hut there may be and 
often is a revolt during convalescence in some cases; with the disappear- 
ance of the acute symptoms the myocardium may be found weakened or 
degeneration may follow and insidiously undermine its strength. On the 
other hand, the heart may not be unfavorably affected, and after the added 
tax, the previous lesion is found unchanged. 
Hearts, the seat of organic lesions with kidney complication, do not hear 
added infection well; this is especially true during the active years of life. 
Old subjects with organic lesions of the valves, even aortic, bear acute 
non-malignant exacerbations fairly well provided the myocardium func- 
tionates normally; this is not true of aortic insufficiency or marked mitral 
stenosis. 
The heart, the seat of a valvular defect with chronic infection super- 
added, bears the strain surprisingly well during weeks and months in the 
presence of high fever, rapid pulse and wasting disease. This is demon- 
strated by the chronicity of many infections of which tuberculosis, pyemia 
and viridans streptococcemia are examples. Some infections promptly 
establish cardiac tolerance, which for prognosis is of great importance, 
while with other toxic conditions the heart muscle seems without resist- 
ance and promptly wilts. 
In the consideration of the infectious diseases we considered the 
chronic lesions which they complicate. A few general conclusions are 
here added to make reference easy and prompt. (The reader is also re- 
ferred to the separate infections and their complications). 
Pneumonia.—With aortic lesions and general arteriosclerosis in old 
individuals the prognosis in the presence of pneumococcemia is unfavor- 
able. 
All cases of pneumonia in subjects with valvular disease are grave, 
recovery is not impossible and takes place in a good number of cases. 
Polly and Blumstein report 1,048 pneumonics of which 17 had valvu- 
lar lesions; of these 5 died—29.4 per cent against the average mortality 
of 21.6 per cent. A number of our cases made uninterrupted recoveries 
from pneumonia -with chronic valvular defects of all kinds. The recovery 
is slow, the course of the disease is likely to be atypical, and the disease 
usually terminates by lysis. 
Influenza does not influence valvular lesions favorably. If pneumonia 
develops, the prognosis becomes grave. The period of convalescence from 486 
DISEASES OF THE CIRCULATORY APPARATUS 
uncomplicated influenza in the subjects of valvular disease is slow, and 
the heart continues irritable during long periods, the myocardium is often 
weakened and existing compensation is unfavorably influenced. 
In influenza and pneumonia the prognosis depends largely on the de- 
gree of existing compensation and the general condition. 
Erysipelas.—My experience with erysipelatous infection and 
chronic cardiopathies has been limited. Gerhardt reports that two of 
his patients made prompt recoveries. In both the lesions were old and 
well compensated with mitral stenosis and moderate aortic insufficiency. 
With decompensation and erysipelas the prognosis is unfavorable. In such 
patients, as Gerhardt says, the erysipelatous inflammation is likely to 
attack the edematous extremities. 
Bronchitis involving the smaller tubes with advanced valvular disease 
may lead to sudden death or to serious symptoms which often continue 
threatening during many days. 
Bronchiolitis and bronchopneumonia in young subjects and in the aged 
are always serious and are among the most frequent causes of death of 
old subjects in hospitals. 
Recurring tonsillitis in young subjects is a frequent cause of acute ex- 
acerbations of chronic cardiopathies and increases all factors which lead 
to greater permanent damage than previously existed. 
Malignant Endocarditis.—The dangers of malignant endocarditis 
as a complication of chronic valvular disease has been separately consid- 
ered in this chapter. (See Septic or Malignant Endocarditis.) 
(j) The Influence of Marriage and Pregnancy on Valvular Disease. 
—My personal experience with the results of pregnancy on the subjects 
of valvular disease has been surprisingly favorable. In an active prac- 
tice of over thirty-seven years I recall but three deaths of patients with 
valvular disease during pregnancy, or as the result of childbirth. There is, 
however, a great difference of opinion in the profession as to the influence 
of marriage and pregnancy in women with chronic valvular lesions and as 
to the advisability of recommending marriage to them. 
The variation in the statistics of observers in the mortality of heart 
lesions during labor is shown by the following percentages of death: 
Mueller 3.0 per cent. 
Gusserow 6.0 “ “ 
Wiesenschal 12.5 “ u 
Lewoff 12.0 “ 11 
Jess 31.5 “ “ 
Guerard 34.0 u a 
Schalyer 48.0 “ “ 
Wessner 49.3 “ “ 
Von Leyden 55.0 “ u 
Lublinsky 60.0 “ “ 
MacDonald 61.0 “ “ ENDOCARDITIS 
487 
Fellner’s statistics prove two important prognostic facts. One, that 
the percentage of reported cases was much too low and did not include 
many with organic diseases of the heart, which were discovered on careful 
routine examination; (it was found that six of seven cases of compen- 
sated heart diseases were escaping the attention of the examiners at the 
clinics) and the other was the cautious treatment and watching of these 
cases which lead to the advice at the Schauta Clinic to “terminate preg- 
nancy in cases of mitral stenosis as soon as the slightest signs of broken 
compensation appear” or whenever evidences of danger were present in 
previous pregnancies. (Hirschfelder.) There was but one death in 
twenty-one pregnancies complicated with valvular lesions at the Schauta 
Clinic. In ten years Fellner found 81 cases, in which three mothers 
were lost and 26 children. The highest mortality was found in mitral 
uncompensated stenosis among the newborn. Seventeen mothers with 
one death, ten children died. Among 900 pregnant women there were 
twenty with valvular lesions, one death and five children lost. The one 
death was in a case of mitral stenosis uncomplicated. Ilirschfelder says: 
“These statistics from unselected cases are much more favorable than 
the previous reports would indicate, and are in accordance with the con- 
clusions of Hicks and French that few women with heart disease are 
sterile, that they are not particularly liable to abort and that most of 
them bear children well.” 
Occasionally sudden death takes place before labor during advanced 
pregnancy, of chronic mitral insufficiency, broken compensation and renal 
invasion. I have seen cases in which, without the approach of labor, 
and evidently no factor added save the changes which accompany preg- 
nancy, after a few days of increased dyspnea, death followed suddenly 
from acute dilatation. 
Relative tricuspid insufficiency persisting during pregnancy or organic 
insufficiency with increasing dyspnea and cyanosis, enlargement of the 
liver, with or without edema of the extremities is a serious condition, and 
may in the pregnant woman lead to death at the time of labor or before. 
Much will depend on the care of these cases. I have recently seen such 
a case which we referred to a young and conscientious obstetrician, in 
which all symptoms seemed unfavorable, but which with persistent atten- 
tion to detail, in a appointed hospital was carried safely through 
labor and is still living. 
The persistence during pregnancy or labor of the usual severe symp- 
toms of broken compensation with any chronic valvular lesion is of 
serious import. 
With dyspnea, orthopnea, cyanosis and albuminuria and an uncompen- 
sated valvular lesion, ivomen rarely live long beyond labor. Hirschfelder 
says, “in from 25 to 40 per cent of patients with severe heart lesions the 
pregnancy does not reach term, but premature labor occurs spontaneously 488 
DISEASES OF THE CIRCULATORY APPARATUS 
owing to partial asphyxia of the fetus.” These statistics, so far as the 
premature expulsion of the fetus are concerned, are much higher than 
any which we have been able to gather in our own practice or from our 
colleagues. The statistics of mitral stenosis give a higher mortality for 
mother and child and approach those of Ilirschfelder. Abortion is also 
more frequent in these. Fellner found 2G per cent of stillbirths among 
women with valvular lesions. Occasionally aortic lesions which are very 
rare during the child bearing period cause sudden death. 
Mackenzie holds that dilatation during pregnancy affects the right 
heart, and that a woman otherwise normal may develop a definite tricuspid 
insufficiency as shown by the presence of a systolic murmur in the tricus- 
pid area and venous pulse. This murmur may come and go, returning 
under varying conditions of the patient, it is therefore a relative insuffi- 
ciency. These hearts may break compensation and pulmonary edema 
develops. This is most likely to happen with added mitral stenosis and 
pulmonary engorgement preceding. 
Slemon and Goldsborough and Williams and Slemon have studied the 
influence of labor on the heart and they report that the act of labor itself 
does not add to the strain of the heart unfavorably. This is certainly true 
of a heart with a good myocardium. 
With marked or limited myocardial degeneration of whatever nature, 
with or without valvular lesions the added strain of pregnancy and labor 
is likely to lead to a very serious condition in which the life of both the 
mother and the fetus are jeopardized. 
If there is any one condition which justifies the interdiction of mar- 
riage it is valvular disease with persistent myocardial insufficiency. 
Marriage is not without its dangers to the woman who has a valvular 
defect. The question which presents to the physician—whether marriage 
is to he sanctioned—can only he answered by a painstaking survey of the 
individual case. 
In the presence of a well compensated heart, with mitral insufficiency 
or moderate aortic obstruction or a combination of valvular lesions which 
are ivell borne, in the absence of other defects, with a normal urine and 
favorable surroundings, marriage may be sanctioned. 
With aortic insufficiency and with mitral stenosis both marked, with 
consecutive changes, there is just reason for hesitation. Marked hyper- 
trophy and moderate dilatation with the former, in our opinion is suffi- 
cient to interdict marriage. Moderate mitral stenosis with compensation 
may under favorable conditions justify marriage, but an advanced degree 
of stenosis with secondary changes in the right heart does not justify the 
clinician, who must assume the enormous responsibility of deciding the 
question to recommend marriage. The same holds true of the advisa- 
bility of the marriage of a man who has similar valvular defects and sec- 
ondary changes. ENDOCARDITIS 
489 
The social status with all that is included in environment becomes an 
important factor in deciding upon the future life of the woman as well 
as of the man in the presence of valvular and myocardial disease. 
(k) Influence of the Usual Complicating Diseases on the Course of 
the Chronic Cardiopathies.—Pericarditis is separately considered (See 
Pericarditis) as a frequent complication of all forms of endocarditis. 
There are occasionally acute forms of pericarditis which complicate 
chronic valvular lesions and arise suddenly; many of these are of the 
dry type (pericarditis sicca), others accompany acute exacerbations of 
rheumatic origin. Unless there is considerable effusion or purulent peri- 
carditis, the addition of dry pericarditis does not affect the chronic cardi- 
opathy unfavorably. With added septic infection and pericardial invasion 
the prognosis is always had. 
Diseases of the Respiratory Organs.—Persistent disturbances— 
bronchitis and pulmonary stasis are found in the more serious cases and 
terminal stages of valvular disease, they influence prognosis unfavorably. 
Degenerative changes in the endocardium (arteriosclerosis) myocar- 
dial fibrosis and chronic bronchitis proves a complex which is rebellious to 
treatment, is occasionally favorably influenced by climatic change, but 
allows of only the gravest forecast. 
Cardiac Asthma and Dyspnea.—Por prognosis, in the presence of 
a valvular lesion, a prompt test of the resistance of the heart can be made 
by cautiously leading the patient to exercise and noting the result on res- 
piration and pulse. Dyspnea on slight exertion is evidence of insuffi- 
ciency and gives the safest indications for treatment and prognosis which 
we possess. Relative muscular insufficiencies are thereby developed which 
are also significant. 
Severe dyspnea and cardiac asthma appear threatening at times, but 
under treatment in many instances disappear even in the presence of drop- 
sies and other symptoms of insufficiency. The prognosis should in the 
average case be made only after the trial of rational treatment and rest. 
In these cases, particularly with mitral insufficiency, results are surpris- 
ing and improvement is held during long periods. 
With hydrothorax, hydropericardium, dilated left ventricle and an 
insufficient right heart and general anasarca the prognosis is grave. 
With aortic lesions and cardiac asthma and dsypnea, the prognosis is 
less favorable than with mitral insufficiency. With aortic lesions and 
coronary sclerosis, cardiac asthma, with or without stenocardia, the chances 
for the patient to lift himself out of the attack are much reduced, though 
the heart may mend during considerable periods under such unfavorable 
conditions. 
Dyspnea and cardiac asthma depending on auricular insufficiency are 
more favorable than are similar symptoms with ventricular disease (dila- 
tation, etc.). 490 
DISEASES OF TIIE CIRCULATORY APPARATUS 
Cardiac asthma with pulmonary edema when a sudden complication 
makes the presage unfavorable in almost all cases. 
Bkown Induration of the Lung.—Brown induration of the lung is 
always proof of long continued insufficiency. The weakness and dilata- 
tion of the left ventricle with bronchiolitis and the characteristic “cells 
of heart failure” in the sputum must lead to a guarded, usually unfavor- 
able prognosis. In these cases of bronchitis due to brown induration, and 
congestion or edema, the sputum is rich in albumin in contradistinction to 
the sputum of uncomplicated bronchitis. (The Fr. v. Mueller test aids 
in diagnosis and prognosis. Add to the sputum three times its volume of 
a three per cent acetic acid solution, shake thoroughly and filter; then 
add a few drops of ferrocyanid of potassium solution when the albumin 
content will be precipitated). 
Pulmonary edema due to dilatation of the left ventricle is more serious 
than stasis caused by right heart change. The latter is often of short dura- 
tion, the former in the presence of marked valvular insufficiencies and 
organic muscle change frequently leads to prompt death. 
The significance of hemoptysis depends entirely upon its cause. There 
are cases of moderate stenosis of the mitral valve in which hemoptysis 
continues during long periods without seeming to have any unfavorable 
influence. The bronchial or pulmonary hemorrhages are not as a rule 
threatening or profuse. Aortic lesions rarely lead to hemoptysis. 
In occasional cases of mitral stenosis, tuberculosis may prove to be 
the cause of hemoptysis. 
With congenital or acquired pulmonary stenosis, tuberculosis is fre- 
quent and the bleeding is a symptom of ulcerative or disorganizing change. 
Embolic infarct may be a cause of hemoptysis; when present with the 
exacerbation of a chronic endocarditis it is of malignant or septic origin 
and offers an unfavorable prognosis. Infarcts also accompany non-malig- 
nant valvular lesions and are always to be interpreted as being of serious 
moment. They are found in the lungs of patients who during considerable 
periods had broken compensation. Pulmonary infarcts usually lead to 
death within a limited period because they are in the majority of cases 
coincident with fully developed cardiac asthenia; an occasional infarct 
may not be followed by death, recovery may slowly follow and compensa- 
tion restored. Ginsburg presents interesting data. Of 250 autopsies 
in subjects who died of heart diseases there were 197 with valvular lesions; 
of these 85, 34 per cent showed emboli, 35.4 per cent had endocarditis 
of the left ventricle, 47.1 per cent of both ventricles, 29.4 per cent myo- 
carditis, 20 per cent dilatation and hypertrophy. Infarcts were found in 
the kidney in 62 cases, spleen 23, brain 15, lungs 14, intestinal mucosa 3, 
tibial, bronchial, brachial, coronary arteries each once and once each in 
the pia mater and uterus. 
Tuberculosis.—The association of tuberculosis and chronic valvular ENDOCARDITIS 
491 
lesions is considered in the chapter on tuberculosis (Cardiovascular 
culosis). Congenital pulmonary stenosis, mitral and aortic stenosis are 
often found with lung tuberculosis. 
Pleurisy.—Pleurisy may complicate valvular lesions, is often present 
with pulmonary infarct; if the effusion is small it does not influence the 
case unfavorably, if large it adds to the danger. 
Most pleural accumulations are non-inflammatory and are the direct 
result of cardiac insufficiency. (See Hydrothorax and the separate Valvu- 
lar Lesions.) 
(l) Blood.—When with advanced valvular lesions there is polycy- 
themia, it is an indication of insufficient heart strength and imperfect 
oxygenation. The loss of the watery element of the blood with extreme 
concentration in the terminal stages with dropsies is unfavorable and 
death under these conditions is not long postponed. With insufficiency of 
the right heart, cyanosis and polycythemia are often long tolerated and 
may yield to treatment. 
Increased viscosity of the blood is found in cyanosed patients and with 
extreme insufficiency—evidence of extreme danger. 
Various grades of anemia are found during the course of most valvu- 
lar lesions at different times, their prognostic significance depends upon 
the underlying condition rather than on the blood state. 
(m) Skin.—The skin shows changes which the experienced clinician 
interprets at a glance in many cases. The mottling and cyanosis, the 
cold extremities, the clubbed fingers and the evidences of chronic stasis 
with dermatitis or eczema are among these. 
(n) Nephritis.—True nephritis is only rarely an accompaniment of 
valvular disease. Chronic congested or cyanosed kidney including the 
accompanying albuminuria is a frequent expression of stasis and muscu- 
lar insufficiency. Infarcts into the Icidney are frequent with malignant 
and benign endocarditis. These give rise to so-called hemorrhagic 
nephritis. 
Chronic Interstitial Nephritis or the arteriosclerotic Icidney (See 
Chronic Interstitial Nephritis) with aortic lesions and general arterioscle- 
rosis deserve separate consideration and is part of a general process. When 
present with any form of valvular disease it adds to the dangers and influ- 
ences the course of the disease. 
(o) Liver.—Enlargement of the liver, acute or chronic, with valvular 
disease is a frequent complication, and is often an expression of insuffi- 
ciency of the right ventricle, is present in mitral disease with decompen- 
sation. Advanced stasis, the cause of liver enlargement in these cases 
leads to ascites, gastritis, enlarged spleen and many depleting intestinal 
symptoms. Organic change may lead to cirrhosis. (See Pericardial 
Pseudocirrhosis). 
Tricuspid insufficiency is a frequent cause of liver enlargement. Jaun- 492 
DISEASES OF THE CIRCULATORY APPARATUS 
dice, when persistent or with cyanosis and other symptoms of stasis has in 
our experience proved to be of serious significance. It is not infrequent in 
cases of malignant endocarditis, grafted on chronic valvular lesions. 
Gall-stone colic may lead to sudden death in the presence of a thin 
heart muscle and valvular disease. We include one such case in which 
an obese woman with chronic mitral obstruction and fatty heart died dur- 
ing a gall-stone colic of rupture of the left ventricle. 
Frequent exacerbations of cholangitis and cholecystitis with gall- 
stone disease and valvular defects may lead to acute infection of the dis- 
eased endocardium, malignant endocarditis and death. Naunyn, Lenhartz 
and Eisner call attention to these cases. 
(p) Nervous System.—Psychic Disturbances.—Psychoses are 
relatively frequent with valvular lesions. Kraepelin believes that venous 
stasis accounts for most of these. Romberg found thirteen psychoses 
among 1,200 heart diseases, mainly of the depressive forms. 
Complications.—Epilepsy, hysteria, neurasthenia, persistent insomnia, 
somnolence, involvement of the respiratory center, Cheyne-Stokes breath- 
ing, persistent headaches, vertigo, chorea, and anomalous sweating are 
among the many complications referable to the nervous system. All of 
these conditions, particularly the psychoses, epilepsy, hysteria and neu- 
rasthenia, may develop without in any way influencing the valvular 
lesions; the psychoses themselves offer a less favorable prognosis with 
chronic valvular lesions than do those which complicate rheumatic acute 
endocarditis. 
(q) Dropsies.—To these the author has referred in considering the 
prognostic value of other symptoms and in connection with the dangers 
of the separate valvular lesions. 
(r) Pulse.—In considering the pulse we are again reminded of the 
fact that whatever prognostic data we obtain from its study must he 
furnished by the myocardium, upon its efficiency, its ability to overcome 
and accommodate itself to existing faults, clearly demonstrated by mod- 
ern methods of examination depends the future of the patient. The pulse 
is fully considered in connection with the lesions of the individual valves 
and with myocarditis. 
(s) Blood Pressure.—(See Consideration of the Lesions of the Indi- 
vidual Valves.) 
(t) Rontgen Examination.—The use of the x-ray for purposes of 
diagnosis and prognosis has become invaluable in practice. By the aid of 
the fluoroscope and the Rontgen photogram we are at once, in most cases, 
given a view of the size of the heart, more particularly the left ventricle 
and the right auricle and the relation of the organ to its surroundings. 
These results can he corroborated by the orthodiagram. Repeated x-ray 
examinations permit of the close observation of the effect of treatment 
and its influence on the organ. The changes which follow in the blood ENDOCARDITIS 
493 
vessels closely related to the heart and in distant organs which influence 
the course of valvular lesions are easily followed. For a full study of 
this subject the reader is referred to the splendid works of Groedel and 
Schwarz. To gain valuable data for prognosis, the examinations should 
always be made by those who devote themselves to this special work. In- 
terpretation demands experience. 
(u) Sudden Death and Valvular Anomalies.—Sudden death is an 
exceedingly rare occurrence with chronic valvular disease of the heart. 
There are warnings in almost all cases given by the failing muscle and 
the increase of secondary manifestations. The heart may occasionally, as 
in aortic insufficiency with dilatation and faulty compensation, stop with- 
out warning, but such sudden end is exceptional. 
With an unchanged or compensated muscle the heart will continue 
the struggle; under such conditions there is sufficient reserve force to 
prevent stasis and sudden acute dilatation. When there is increasing 
secondary engorgement and the reserve is insufficient, the abundant symp- 
toms and physical signs give timely warnings. 
Aortic lesions associated with coronary disease (angina pectoris) may 
lead to sudden death. Such patients stand on the edge of a precipice, they 
may fall at any time. Under control, women particularly, may live dur- 
ing long periods. Less than two per cent of mitral lesions lead to sudden 
death. (Leyden.) 
Obese patients—large portly men—with small fatty hearts, weak and 
rapid pulse, with arteriosclerosis and aortic stenosis (degenerative) are 
always threatened and often die suddenly. 
(v) Anatomic Cure of Valvular Lesions.—Unquestionably there are 
cases of acute endocarditis which are followed by well marked physical 
signs of valvular deformity, murmurs, and muscular changes, in which 
all physical and subjective symptoms disappear and the patients continue 
well. 
Post mortem examinations prove the possibility of the complete ana- 
tomic cure of valvular lesions. 
Mitral insufficiencies of organic origin have disappeared, never to 
recur. (Amsler, Leyden.) The clinician should assure himself that he 
is not dealing with relative insufficiencies in these cases. 
(w) The Influence of Treatment on Prognosis.—With full compen- 
sation, well regulated life, quiet temperament and a healthy suggestion 
which allows the heart to remain light while the brain is agreeably occu- 
pied; many patients with valvular lesions live in comfort during many 
years. 
The psychic element in all forms of heart lesions is overpowering, it 
influences longevity materially for good or ill. The physician is largely 
responsible through his personality and included tact for the creation of 
a healthy optimism which means so much to the patient. 494 
DISEASES OF THE CIRCULATORY APPARATUS 
The influence of rest, well chosen and properly directed hatlis and 
exercises is often paramount in the presence of the waning heart muscle. 
The reaction of 'properly selected cases to digitalis is of enormous value 
in piercing the future of the cardiopath. Prompt reaction to digitalis in 
the presence of mitral disease is always encouraging. The prognosis is 
best in those cases in which the favorable effect of the remedy continues 
during a comparatively long period. When the effect is evanescent or of 
short duration, and the remedy is necessarily required at correspondingly 
short intervals there is danger that it may soon fail to produce the satis- 
factory strengthening of systole. Naturally the prognosis depends upon 
the ability of the therapeutist to administer the remedy secundum artem 
and upon the continuous supervision of the life of his patient. 
There are cases in which dropsies with incomplete compensation and 
threatening symptoms due to distant stasis yield and under rational treat- 
ment such patients may live during many years. 
The specific (syphilitic) lesions of the valves, usually the aortic, offer 
favorable prognosis in direct proportion to the improvement which follows 
modern treatment. (See Cardiac Syphilis.) The prognosis of heart le- 
sions has been enormously influenced by the indications for treatment sug- 
gested by the Wassermann reaction of the blood in the larger number of 
aortic lesions. 
(x) The Influence of Physical Signs.—The prognostic significance of 
physical signs is readily shown by the relative dangers of the different 
valvular lesions to which reference is made in considering these. 
The fact which should he forcibly impressed upon the beginner is that 
loudness of the murmur as a rule, hears no relation to the gravity of the 
lesion. It is often more favorable than soft or low murmurs. 
Systolic murmurs are more favorable than are the diastolic; in many 
cases they finally prove to be of functional origin (hemic, etc.). Naturally 
in offering the forecast, attention must be given to all of the many details 
considered in this chapter. 
Diastolic and presystolic murmurs are almost always of organic origin 
and demand serious thought and attention for prognosis. 
The abnormalities of rhythm—intermission and arliythmia—are con- 
sidered with the separate lesions and in the chapter on myocarditis. 
Delirious hearts (delirium cordis) are often well borne. They always 
add to the danger. When due to auricular fibrillation the prognosis is 
much better than with the ventricular disturbance; alternating pulse with 
any form of arliythmia or myocardial disturbance is unfavorable. 
(y) The Fate of the Chronic Cardiopathies.—Romberg found that 
the duration of the period of compensation averaged seven years. One- 
third of his cases went beyond that time without a break, and the maxi- 
mum period was found to be thirty-eight years; one-third of his cases re- 
mained without compensation from the beginning. ENDOCARDITIS 
495 
Gerhardt reports 300 cases of which 123 allowed positive conclusions: 
No. OF 
Duration of Compensation. Cases. 
0- 5 years 37 
6-10 years 33 
11-20 years 30 
21-30 years 9 
31-40 years 12 
41-44 years 2 
The average was twelve years. 
The average duration of primary compensation in man is nine years, 
in woman ten years (Gerhardt). 
Localization of Valvular Lesions and their Forms 
The prognosis of chronic valvular disease largely depends upon the 
valve affected and the degree of resulting deformity. There is an enor- 
mous difference as has already been hinted in the dangers of mitral and 
aortic disease. Most authorities claim that aortic insufficiency is the most 
serious of all valvular lesions, including Osier, while a large number in- 
cluding Colbeck and Gerliardt claim that mitral stenosis is the most 
serious. Osier calls attention to the fact that, in women particularly, 
mitral stenosis is almost on a level with mitral insufficiency. Uncompli- 
cated aortic stenosis is the most favorable of all lesions, mitral insufficiency 
when well compensated offers a good prognosis. 
Aortic stenosis and mitral insufficiency are the most frequent valvular 
lesions after the thirtieth year. 
Mitral Insufficiency.—Over 50 per cent of all valvular lesions are 
due to mitral insufficiency. Mitral insufficiencies both alone and asso- 
ciated with other valvular lesions were present in 64 per cent of the Johns 
Hopkins Hospital cases, occurring alone in 29 per cent. 
Mitral insufficiency offers greater encouragement for complete anatomic 
cure and insures longer periods of compensation than does any other 
valvular lesion. With mitral insufficiency the following facts require 
consideration in offering a forecast besides those included in “General 
Considerations of the Valvular Lesions.” 
The cause of the lesion hears directly on prognosis. Rheumatism, 
chorea and scarlet fever justify the most hopeful outlook, because in the 
large proportion of cases there is no danger of exacerbation after reason- 
able immunity. 
Full compensation may never be disturbed, the future is often in the 
hands of the patient. Reasonable care insures safety in most cases. 
Mitral regurgitant murmurs due to chorea disappear after a few years. 
Sir Andrew Clark taught that they never were found after ten years. 
Mitral insufficiency is more amenable to treatment than any of the 
other valvular lesions. 496 
DISEASES OF THE CIRCULATORY APPARATUS 
Dropsies which have existed only a short time with mitral insufficiency 
and without extreme loss of compensation often yield, and life may con- 
tinue many years. Extensive dropsies always add to cardiac embarrass- 
ment. Mitral insufficiency with long continued dropsy and evidences of 
broken compensation justify a guarded prognosis, the result of treatment 
must clear the horizon. Associated conditions bear directly on the out- 
look. 
With mitral insufficiency, “arteriosclerosis-insuffisance mitral-arte- 
rielle” of Iluchard—which is usually caused by gout, lead poisoning, or 
dietetic excesses, is frequently associated with renal disease,” and dyspnea 
is often severe and prognosis grave (Moon). 
With arteriosclerotic changes in the endocardium, there is tendency to 
progression and a less favorable outlook than with the “endocarditic form 
of valvular disease” 
Blood Pkessure.—Much depends on the resistance in the peripheral 
vessels. With abnormally heightened blood pressure the force of the 
regurgitation is increased, the backward pressure in the left auricle is 
augmented and an added demand is made on the right ventricle. 
Pulse Pressure (amplitude) is far more reliable than simple systolic 
blood pressure, for it gives an index of the burden which the heart is carry- 
ing. Undue frequency of the pulse with arhythmia perpetua due to auric- 
ular fibrillation need not always to be seriously interpreted. Digitalis will 
usually control the symptom. The perpetual arhythmia is less significant 
with mitral disease than with aortic. 
When in mitral insufficiency the heart which has been regular and 
its frequency within reasonable limits suddenly develops perpetual 
arhythmia it signifies increased weakness or dilatation of the left auricle 
and nothing more, but this fact must be added to the many details 
of the individual case if safe conclusions for prognosis are to be 
reached. 
Decided fall of blood pressure (hypotension) is unfavorable; it usu- 
ally signifies myocardial insufficiency. 
In all cases of mitral insufficiency physical signs should be watched 
for evidences of dilatation (increase in the transverse diameter) and 
evidences of stasis. 
The pulse is increased in size so long as compensation is sufficient, 
therefore a favorable sign. 
A small, thin, rapid pulse (umitralized pulse”) is proof of insufficient 
muscle strength. 
Pulmonary stasis and dyspnea go hand in hand; they indicate broken 
compensation. The strength of the left ventricle is of greater prognostic 
value in considering pulmonary stasis than is that of the right ventricle, 
for the former when acting well empties its own cavity of more blood 
than the right ventricle pumps into the pulmonary artery. There is ENDOCARDITIS 
497 
therefore a surplus of blood leaving the lungs under these conditions 
until the congestion is relieved. 
Hirschfelder says, “The whole condition may be summed up by the 
statement that a weakly acting left ventricle overfills the lungs with 
blood, while a strongly acting left ventricle bails them out. The whole 
of pulmonary engorgement is, as rightly claimed by V. Basch, a problem 
not of the right ventricle, but of the left.” 
Accentuation of the second pulmonic sound indicates involvement of 
the pulmonary circuit, this is not always significant. Mitral insufficiency 
may continue during years with an accented second pulmonic sound with 
good compensation without the addition of serious complications, The 
following summary may be safely followed: 
The favorable cases of mitral insufficiency are those in which com- 
pensation is sufficient; there is no dyspnea, no dropsies, the pulse is full, 
not excessively rapid, pulse pressure within normal limits, general con- 
dition satisfactory, urine free and non-albuminous, no enlargement of 
liver or spleen, and physical signs correspondingly encouraging, includ- 
ing moderate enlargement of the left and right sides of the heart; the 
second pulmonic moderately accented. 
The unfavorable cases are those in which the leakage is large, pulse 
is “mitralized”—weak, rapid, irregular, pulse pressure and blood pres- 
sure are reduced, heart cavities dilated, the right ventricle particularly, 
and the left insufficiently hypertrophied; the murmur obliterates the 
first sound of the heart entirely, the second pulmonic is greatly accented, 
the radial artery cannot be felt between the beats, there is continuous 
dyspnea and evidences of pulmonic and systemic engorgement.” 
Lung complications—pulmonary edema, pleurisy with effusion add 
to the work of the heart, overtax the rigid ventricle and cloud the prog- 
nosis. For the significance of embolic infarct, thrombosis, pericarditis 
and other complications, the reader is referred to the General Considera- 
tions, etc., of Valvular Lesions. 
Mitral Stenosis.—The outlook is influenced by the degree of mitral 
obstruction. 
Moderate stenosis is tolerated during many years, in fact during a 
long and comfortable life without causing subjective symptoms and is 
often accidentally discovered post mortem. 
Extreme stenosis leads to secondary changes because insufficient blood 
is forced into the left ventricle, the arterial tree is correspondingly empty, 
there is stasis in the left auricle, the pulmonary circuit, and the right 
ventricle is called upon to overcome the obstruction by added muscular 
force, hypertrophy and dilatation result. When the right ventricle is 
overtired and overtaxed, dilatation increases, the reserve muscular force 
is exhausted and decompensation with all of its complications is in 
evidence. 498 
DISEASES OF THE CIRCULATORY APPARATUS 
Mitral stenosis almost always includes a degree of insufficiency, it 
is not infrequently associated with aortic insufficiency also. The ma- 
jority of mitral stenoses are moderately developed or mild. 
With proper rest and cautious living and without added burden 
thrown upon the heart such cases live in comfort during many years, 
barring complications. 
Unfavorable Features.—Unfavorable features are increase of dilata- 
tion of the left ventricle, thrombosis and embolism, increasing arterial 
anemia, added pulmonary complications including cardiac asthma and 
dyspnea, edema, hydrothorax; albuminuria, added tricuspid insufficiency 
with decided hypotension and lowered pulse pressure and the engorge- 
ment of the abdominal viscera. 
Marked dropsy with mitral stenosis is due to the associated insuffi- 
ciency of the valve; with stenosis alone, it is not likely to be extensive. 
The pulse, with good compensation is small, regular, of good force 
and of nearly normal frequency. The pulse is easily obliterated by 
pressure, but under favorable conditions it is palpable between the beats. 
Blood pressure may not be changed. The greater difference is in the 
reduced pulse pressure because the arterial tree compensates in a large 
degree; the minimal pressure rises because of the vasoconstriction. The 
difference between systolic and diastolic pressure is not so marked as in 
well compensated mitral insufficiency. 
The process of cicatrization may continue in the muscle, change the 
chordae tendinae, “impairing at other places the functional activity of 
the heart muscle, and affecting the a.-v. bundle, depressing conductivity 
or producing nodal rhythm, thereby profoundly modifying the nature of 
the rhythm of the heart” (Mackenzie). 
With marked incompetence of the valve and stenosis, the character of 
the pulse is changed, it becomes rapid, small, partaking of the character 
of the “mitralized pulse.” 
Mitral stenosis which develops early in life is more serious than when 
developed in adult life, because of the tendency toward increase of ob- 
struction and the further fact, that the stenosed opening does not increase 
in size while the growth of the heart is progressive. Moon says that 
“such cases seldom reach the age of forty.” Broadbent gives the average 
age at death of these cases at thirty-three years for men, and thirty-seven 
years for women. Hirschfelder thirty-three and thirty-eight respectively. 
The significance of mitral stenosis in women is considered in con- 
nection with marriage and valvular disease. 
When the second sound is inaudible at the apex, there is great danger 
of decompensation, any added effort proves the presence of muscular 
insufficiency. 
The progressive character of the lesion in many cases accounts for 
the change of physical signs and other symptoms. ENDOCARDITIS 
499 
Fading or weakening of the presystolic murmur, with diminishing 
second pulmonary sound is evidence of failure of the right ventricle. 
The presystolic murmur is likely to disappear with the appearance 
of continuous irregularity of the heart and rapid pulse. 
Mitral stenosis associated with arteriosclerotic endocardial change 
offers a less favorable prognosis than do other forms of the disease. 
With the arteriosclerotic form of the disease, arhythmias are more fre- 
quent and often denote myocardial degeneration. 
Aortic Stenosis (obstruction).—Probably the majority of murmurs 
heard over the aortic valve are not due to true organic stenoses. Pure 
aortic obstruction is exceedingly grave. The murmurs are either func- 
tional (hemic), of arteriosclerotic or inflammatory origin. 
Eomberg analyzed 670 cases of valvular disease and found 17 un- 
complicated aortic stenoses—2.53 per cent. At Johns Hopkins Hospital 
aortic stenosis was found in 5 per cent of the valvular diseases. 
In practice it is found that most aortic stenoses after middle life 
are of arteriosclerotic origin, and that an aortic systolic murmur is often 
the first sign of the presence of the process; under such conditions there 
is increase of the second aortic sound with or without raised blood 
pressure. 
Hypertrophy of the left ventricle is a necessity to overcome the effects 
of aortic obstruction when it is decided. 
Marked dilatation is evidence of added insufficiency of the valve, a 
frequent combination; in these cases the pulse gives additional evidence 
for prognosis. 
The loud systolic murmur is often out of proportion to the amount 
of obstruction offered by the uneven or contracted cusps. 
Dilatation in varying degree is produced by aortic stenosis; hyper- 
trophy of the left ventricle is more dependable and lasting with aortic 
stenosis than with any other valvular lesion. 
Unfavorable Cases.—The unfavorable cases are those in which the 
obstruction is progressive, in which there may also be invasion of the 
coronary arteries and with final aortic insufficiency, dilatation, sec- 
ondary distant changes and arteriosclerotic changes in the kidney, with 
obstruction in the peripheral vessels. The terminal stage includes aortic 
insufficiency with myocardial degeneration and the usual picture of 
decompensation. 
The graphic study of the pulse offers valuable prognostic data. 
As a rule, in favorable cases the pulse is slow, regular, of good force, 
and the artery is easily palpable between beats. The pulse wave is small, 
is well sustained, its rise and fall are slow. The pulsus tardus is not 
unfavorable. The pulse tracing is more characteristic than with most 
other valvular lesions. 
Arhythmia shows itself in irregularity, in serious cases—the pulsus 500 
DISEASES OF THE CIRCULATORY APPARATUS 
alternans and in occasional periods of extrasystoles, these depend upon 
the condition of the myocardium. True alternating pulse is always of 
serious significance. 
Blood pressure depends largely on the amount of sclerotic change in 
the peripheral vessels and in the aorta, as well as on the condition of 
the myocardium, the kidney vessels and many other factors. In the 
average case without serious complications the pressure is normal. 
Sudden death is less frequent than with aortic insufficiency; in most 
cases, long periods of symptoms of myocardial insufficiency precede 
death. This is not true of cases complicated with coronary disease and 
advanced myocardial weakness. 
Mitral stenosis is favorable to the development of pulmonary tuber- 
culosis. (See Tuberculosis.) Babcock found seven of his twenty cases 
of aortic stenosis with pulmonary tuberculosis. 
The prognosis of aortic stenosis will often be favorably influenced 
by the revelation of the Wassermann reaction of the blood and its prompt 
acceptance for therapeutic indications. 
Aortic Insufficiency.—Since the original classification of the disease 
by Corrigan, two forms of insufficiency have been considered: 
(a) The Functional Form, 
(b) The Organic Form. 
(a) Functional Form.—The functional form is due to the dilatation 
of the mouth of the aorta and is associated as a rule with aneurismal 
dilatations of the aorta or it is an accompaniment of pulmonary insuffi- 
ciency. It is exceedingly difficult to diagnosticate functional aortic 
insufficiency; I do not remember to have met with a case in which the 
diagnosis seemed to have been justified save as I found the aortic mouth 
wide open post mortem in connection with disease of the aorta. 
(b) Organic Form.—At this point we must once more impress upon 
the clinician the great value for prognosis of recognizing the character 
of the lesion, whether inflammatory (endocarditic) or arterial and degen- 
erative (arteriosclerotic). 
When rupture of the valves occurs from mechanical strain or trau- 
matism, it is associated with either ulcerative or sclerotic change, there- 
fore requires no separate consideration. This question has an important 
medicolegal hearing. I do not believe that rupture of the normal valve 
follows strain or accident. Experimentally it cannot be ruptured by the 
highest pressure to 'which it is ever subjected by man. 
The larger number of aortic insufficiencies are found in men, are of 
the arteriosclerotic form, are most frequent after middle life and depend 
upon the same factors for their production as general arteriofihrosis. 
A large number are of syphilitic origin; this is especially true of the 
many cases which have no history of acute endocarditis preceding and ENDOCAKDITIS 
501 
develop between the third and fourth decade of life. The positive Wasser- 
mann reaction proves the truth of these conclusions. 
The heart changes depend entirely upon the fact that the left ven- 
tricle is forced to supply the arterial tree with sufficient blood; this it 
can only do by compensating for the return of blood to its cavity during 
diastole through the insufficient valve which during systole was forced 
into the aorta. 
Naturally the amount of extra work thrown upon the left ventricle 
and the seriousness of the lesion depend upon the size of the leak, the 
length of time of the regurgitation, the pressure which must be overcome 
in .the arterial system (aorta particularly) and the extent of associated 
lesions in distant organs. 
Aortic insufficiency offers an unfavorable prognosis because the larger 
number of cases are advanced before treatment is instituted and being 
dependent upon arteriosclerosis are likely to be progressive. 
In the moderately advanced cases or where the processes are stationary 
patients may live during many years with compensation which makes 
light occupation possible and life comfortable. 
The endocarditic type offers a much better prognosis than does the 
arteriosclerotic. 
Arteriosclerotic insufficiency in young subjects with evidences of 
progression, uninfluenced by specific treatment advances rapidly to a fatal 
termination with a number of complications in distant organs. 
The Flint murmur, presystolic, heard over the mitral area accom- 
panies many cases of aortic insufficiency. Austin Flint first described 
this murmur and claimed that it was due to the functional narrowing of 
the orifice between the mitral cusps which was closed at the beginning 
of auricular systole. There has been much discussion and controversy 
over the true cause and significance of the Flint murmur. (Thayer, 
Guiteras, Gibson and others.) The consensus of opinion is in favor of 
Flint’s original contention, but for prognosis it must not be forgotten 
that true mitral stenosis may complicate the organic lesion. I have not 
found that the presence of the Flint murmur influenced the course of aortic 
insufficiency unfavorably. 
So long as the left ventricle is sufficiently compensated pulmonary 
stasis is prevented, but with its failure and its persistent dilatation, it 
develops and is not easily overcome. 
Blood pressure in the inflammatory form of aortic insufficiency is 
not so high as in the arteriosclerotic cases. A normal pulse rate with a 
nearly normal systolic and diastolic pressure is found only in cases with- 
out marked sclerosis and with very limited insufficiency. 
Fall of blood pressure is often unfavorable, whether produced by a 
weakened myocardium or by drugs. 
Hypertension and high pulse pressure are characteristic of aortic 502 
DISEASES OF TIIE CIRCULATORY APPARATUS 
insufficiency and offer valuable data for prognosis as well as diagnosis. 
In no other cardiovascular disease is there such enormous difference in 
the maximum and minimum pressure. Once established, the general 
features of the Corrigan or trip-hammer pulse persist until changed by 
myocardial fatigue. 
The wave is large, the upstroke sudden, the pulse is collapsed during 
diastole. The sphygmographic tracing may be safely relied upon for it 
is characteristic and promptly shows the break when it occurs, which is 
due to extreme dilatation and myocardial revolt. 
In favorable cases the pulse rate is slow and regular. With a rapid 
pulse, ventricular extrasystoles, evidence of dilatation and myocardial 
weakness, and the bigeminal and irregular pulse the outlook is serious. 
The laboring heart, thickened and visible throbbing arteries are evi- 
dences which must be studied with the associated features for the correct 
interpretation of their prognostic significance, also the capillary pulse. 
The snappy second sound is found in cases in which the peripheral 
resistance demands the “slamming of the door” as Lauder Brunton has 
so forcibly expressed the phenomenon. 
Suddenly arising mitral insufficiency (muscular relative insuffi- 
ciency) is due to extreme dilatation of the left ventricle and is un- 
favorable. 
The association of coronary disease with aortic insufficiency offers 
only the most dismal forecast and yet life may be prolonged by rational 
living in many of these cases. (See Angina Pectoris.) It is in these 
cases that family history is of great prognostic value. 
The recurring strain to which the arteries are subjected by the enor- 
mous hypertrophy of the left ventricle in many cases is a factor in pro- 
ducing or increasing arteriosclerotic change. 
The influence of arteriosclerotic changes in the brain, kidney, and 
within the splanchnic area is paramount. (See Cerebral Apoplexy, 
Arteriosclerotic Nephritis and Arteriosclerosis.) 
Sudden death is more frequent with aortic insufficiency than with any 
other valvular lesion, (See same chapter, General Considerations.) 
Subjective symptoms which are unfavorable include faintness, pre- 
cordial pains, dyspnea, somnolence and mental torpor. 
In the prognosis of aortic insufficiency no single symptom can serve 
to give a reliable forecast. The multitude of lesions which may be pro- 
duced by the sclerosis, of which the valvular defect is only a part, takes 
the clinician into an enormous field. In the final analysis there are 
naturally many factors to be considered, but the paramount issue must 
always include the accommodation of the ventricle to withstand the strain 
by sufficient dilatation and hypertrophy, i. e., to hold compensation. 
“The field of cardiac response is the only true and safe guide” (Mac- 
kenzie). ENDOCARDITIS 
503 
Tricuspid Insufficiency.—Lesions of the tricuspid valve are rare. In 
the preceding pages we have considered the association of tricuspid in- 
sufficiency with other heart and lung lesions. It is not likely to exist 
independently. It is frequently present as an expression of muscular 
and relative insufficiency, and with diseases of the lung or the left heart, 
it is always a serious complication. 
The recognition of insufficiency is made possible by the accompany- 
ing venous pulse and pulsating liver. 
True tricuspid insufficiency leads to death. We have no exception 
to report. Colbeck says “the precise estimate of the leakage is of less 
importance than the determination of the exact causes which have led 
to the occurrence of the lesion.” The chief points to be considered are: 
1. “The degree of enlargement of the right ventricle and auricle. 
2. “The presence or absence of venous pulsation in the neck. 
3. “The presence or absence of pulsation of the liver and the degree 
of enlargement of the organ. 
4. “The degree of arterial anemia.” 
Tricuspid Stenosis.—Tricuspid stenosis is not found without insuffi- 
ciency, compensation is out of the question (Romberg). Sphygmographic 
tracings may lead to the suspicion of the existence of the lesion. 
Congenital defects are sometimes associated with fetal endocarditis 
causing tricuspid stenosis. (See Congenital Defects of the Heart.) 
The acquired form is more frequent in women than in men and is 
secondary to mitral stenosis. The two lesions are almost always asso- 
ciated, and both are more common in women. The rise in pressure in 
the right ventricle following mitral stenosis “causes strain and irrita- 
tion,” and invites tricuspid change. 
The right side of the heart is more frequently the seat of valvular 
murmurs with the malignant than with the usual forms of endocarditis. 
The blood stream through the tricuspid orifice is obstructed and in- 
creased, demand is made on the right auricle, hypertrophy results with 
more or less dilatation. The amount of dilatation also depends on the 
associated insufficiency of the valve. 
Unfavorable conditions with all tricuspid disease are congestion of 
the portal and general venous system. The amount of hypertrophy and 
dilatation of the right ventricle depends largely on the degree of mitral 
stenosis, as does the pulmonary engorgement also. 
Defects of the Pulmonary Valve.—Most murmurs heard in the pul- 
monary area are of functional hemic origin, they are systolic and, con- 
sidered alone, are of but little significance. Cardiorespiratory murmurs 
and mitral murmurs are often heard in the pulmonary area. 
Stenosis is usually of congenital origin and predisposes to tubercu-  DISEASES OF THE CIRCULATORY APPARATUS 
504 
losis. For a full consideration of its prognosis see Congenital Stenosis 
of the Pulmonary Valve. 
Pulmonary Insufficiency.—Pulmonary insufficiency is rarely acquired, 
it may occasionally be of syphilitic origin. It occurs with kyphosis, 
mitral stenosis and narrowing of the pulmonary artery or its branches, 
when it is a relative insufficiency. Aneurism of the aorta may also be 
associated with relative pulmonary insufficiency (Romberg). 
Barie reports 58 cases and claims that it may be an acquired lesion 
most frequent between the ages of eighteen and thirty-four. The right 
ventricle enlarges, there is great venous congestion, jugular and hepatic 
pulsation, cyanosis and clubbed fingers. The prognosis is only favorable 
so long as the right ventricle proves sufficient. The regurgitation is 
probably slight if the murmur does not efface the second sound. 
The complete effacement of the second sound is evidence of serious 
insufficiency of the valve. 
3. Arteriosclerotic and Syphilitic Endocarditis 
The influence of the degenerative types of valvular disease depending 
on arteriosclerosis and syphilis is fully considered in this chapter and in 
connection with the study of cardiovascular syphilis and need not he 
repeated. The progressive and unfavorable cases of valvular disease are 
those of the degenerative or arteriosclerotic type, particularly between the 
twentieth and fiftieth year. In older individuals the process is better 
borne and may remain stationary during many years. 
The beginner may be led by the presence of a systolic aortic murmur 
with moderate arteriosclerosis to offer a grave prognosis, this is not justi- 
fied in the average case which remains under reasonable control. 
The blood pressure study of these cases gives valuable information 
in connection with a thorough appreciation of the coronary circulation 
and the kidney function. 
In the degenerative types of disease particularly, the frequent Ront- 
gen examination and the use of graphic methods are a necessity for the 
valuable information which they add. 
4. Combined Valvular Lesions 
From the foregoing consideration of the acute and chronic cardiop- 
athies it is clearly evident that combined lesions are more frequent than 
are the single defects. 
We have seen mitral and aortic lesions together with full compensar 
tion during many years and death resulting from intercurrent disease. 
The mitral lesions combined, as has been shown, may also continue ENDOCARDITIS 
505 
without causing serious inconvenience in many cases; there are always 
the dangers of decompensation to which we have repeatedly alluded. 
There are combinations of lesions which act favorably; thus aortic 
stenosis may reduce the amount of regurgitation in aortic insufficiency, 
and the same occasionally happens when stenosis and insufficiency are 
combined at the mitral opening. The prognosis of the lesions included in 
the combination can only be given after the consideration of the facts men- 
tioned in connection with the individual valvular defects. 
Romberg’s statistics show mitral insufficiency and mitral stenosis 
combined in 19.7 per cent alone, and in 7.97 per cent with valvular 
lesions. Aortic and mitral insufficiencies were combined in 12.69 per 
cent. In 4.93 per cent aortic and mitral insufficiencies with mitral 
stenosis were combined. The gravest combination is aortic insufficiency 
and stenosis 5.2 per cent. In 4.05 per cent there were besides aortic 
insufficiency and stenosis other valvular lesions. Tricuspid and mitral 
lesions were combined in 1.97 per cent of Romberg’s cases. 
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der Leipziger Klinik, 1893, 83). 
Lenhartz. Die Septische Erkrank., Nothnagel Handbuch. 
Leyden. Uber die Prognose der Herzlcrankheiten. Munch, med. Wchnschr., 1889. 
Leuch. Statist, klin. Mittheil. ueber HerzklappenFehler. Zurich, 1899. 
Mackenzie. Diseases of the heart, 1908, 2 ed. 
Mohr. Ueber Familien Klappenfehler. Med. Klinik, 1905, No. 28. 
Moon. The prognosis and treatment of diseases of the heart. London, 1912. 
Naunyn. Die Klinik der Cholelithiasis. 
Oppenheim. Lehrbuch der Nervenkrankheiten. Bd. i, 1913. 
Osier. Practice of medicine. 1913. 
Roily & Blumstein. Klinische Beobacht. bei Krup. Pneumonie. Fortschrit. der Med., 
1911. 
Romberg. Krankh. des Herzens u. Blutgef. 1906; also Arch. f. klin. Med., 1906, Bd. liii. 
Schmidt. Statistik, etc. Jena, 1893. 
Schott. Verhand. d. Kongress. f. inner. Med., 1892. 
Schwarz. Rontgen Untersuch. des Herzens. Leipzig u. Wien, 1911. 
Slemon & Goldsborough,—Johns Hopkins Bull., 1908, 194- 
Williams & Slemon.—Idem, 1908. 
Starr. Diseases of the nervous system. 1 & 2 ed. 
Stokes. Diseases of the heart. 1851-1855. 
Tangl. Hypertrophie u. physiologisches Wachstum des Herzens, Virchow's Archiv, etc. 
Bd. cxvi. 
Thayer. Am. J. Med. Sci., cxxii, 538. 
Zuntz. Landwirthschaft Jahrbuch 27. Supplement. 
G. Functional Disorders of the Heart 
In most cases the functional disorders of the heart are not diseases 
\per se, hut include the symptoms which are produced hy the derangement 
of the nervous or muscular mechanism of the heart, or both; associated 
with true organic lesions. There are exceptions to this definition but as 
Colbeck has truly said, after committing himself to practically the same 
definition, “In other words, ‘functional disorders’ of the heart form part 
of many different groups of symptoms, which severally constitute ‘a dis- 
ease’ properly so called. A clear grasp of this conception will go far to 
dissipate much of the difficulty and confusion that has grown up around 
the subject of functional affections of the heart.” 
Functional affections of the heart which include among their leading 
symptoms, palpitation, arrhythmia pain and a train of neurasthenic symp- 
toms, may arise from changes in many organs. We find functional dis- 
turbances with all cardiovascular diseases, affections of the nerves and 
ganglia of the heart, the pericardium, the myocardium, the aorta and FUNCTIONAL DISORDERS OF THE HEART 
507 
coronaries, with arteriosclerosis and with vasomotor disturbances which 
influence arterial pressure. 
Diseases of the nervous system are often associated with functional 
disturbances of the heart. Neurasthenia and hysteria are prominent 
among these. 
Grave organic diseases of the brain and cord—tabes dorsalis, menin- 
gitis, brain tumor, apoplexy, epilepsy, injury to the brain, lesions of the 
medulla, mania, manic depressive states and general progressive paral- 
ysis, all, at some time during their progress develop characteristic evi- 
dences of functional derangement of the heart. 
The thyroid heart (hyperthyroidea) is separately considered. (Dis- 
eases of the Ductless Glands.) 
The influence of the diseases of the lung, tuberculosis particularly, 
is paramount in causing disturbed heart function and is separately con- 
sidered. (Tuberculosis.) 
The large number of neurasthenics with derangements of the gastro- 
intestinal tract adds an enormous material in which nervous manifesta- 
tions are in the foreground. These cases include neuropathies ivith ptoses 
(Glenard’s Disease) who are rarely without phobias of some hind, due 
to deranged function of the heart of reflex character. 
The influence of constitutional diseases including all forms of anemia, 
gout, diabetes, so-called rheumatism, the leukemias, the acute and chronic 
infections, each is a factor in producing perverted heart function. 
In considering myocardial disease and hypertrophy we mentioned the 
influence of masturbation, ovarian and uterine disease. 
Toxic states, including uremia, acidosis, the excessive use of alcohol, 
tea, coffee, tobacco, each modifies the action of the heart. The effect of 
lead and other drugs including digitalis, strophanthus, aconite, bella- 
donna, the bromids, and iodids, is largely influenced by existing resistance 
and idiosyncrasy when used in small doses, when in larger dosage, the 
physiologic effect on the separate functions of the heart are promptly 
manifested. We consider among the functional derangements: 
1. Palpitation. 
2. (a) Paroxysmal Tachycardia and (b) Simple Tachycardia. 
3. Bradycardia. 
4. Arhythmia. 
5. The Neurasthenic State. 
1. Palpitation 
The sensation which is distinctly perceptible to the individual, caused 
by the undue frequency of the regular or irregular heart, is known as 
palpitation. It is probably the most frequent of all sensations referred 508 
DISEASES OF THE CIRCULATORY APPARATUS 
to the heart, causes in the overwrought and neurasthenic or nervous 
patient the fear of death and in the majority of cases is not associated 
with organic disease of the heart. Palpitation in most cases is due to 
influences which act through the nervous system and is caused by hurry, 
worry, excitement, fatigue and kindred factors which are evanescent in 
their effect. The subjects whose hearts are promptly ungeared belong to 
the neurasthenic class—true neuropaths. 
Palpitation may he an expression of a weak heart muscle, when, as a 
rule, there are extrasystoles. Hirschfelder has demonstrated that palpi- 
tation may persist “without any motor disturbance in the heart’s action 
and without any change in the reflex response of the heart to various 
stimuli.” 
The majority of palpitations are without serious significance and 
exist without organic disease of the heart. 
In the majority of cases in which the symptom is not of organic 
origin it either disappears suddenly to return when depressing or toxic 
factors are added, or it yields after a painstaking investigation of the 
patient’s history leads to the relief of its cause. In all cases which remain 
unexplained by physical examination the possibility of tea, coffee, tobacco, 
alcohol, coal tar preparations, thyroid extract and other drugs as the 
possible exciting cause should be considered. Distant and unexpected 
lesions are often recognized as provocative of palpitation, their relief is 
followed hy the disappearance of the rapid hearty 
The disagreeable and depressing mental pang which neurotics suffer 
with palpitation makes them wrretched during the continuance of the 
symptom. 
The palpitations due to the infections, usually during the period of 
convalescence (pneumonia and diphtheria particularly), offer a good 
prognosis with rest and reassurance. 
Palpitation with menstrual anomalies at the menopause, puberty and 
during menstruation may appear serious at times, but always yield when 
without organic fundament. 
There are some women, men occasionally, who from the slightest 
imaginable cause between the fifteenth and about the thirty-fifth year of 
life promptly “blush and palpitate,” in whom the attacks are evanescent, 
exceedingly annoying, hut without effect on their general condition. 
2. (a) Paroxysmal Tachycardia 
For over half a century paroxysmal tachycardia has been recognized 
by the profession as a symptom complex without a clear conception of its 
nature or the method of its production. In all cases the striking features 
are those which were included in Bouveret’s article and the works of 
A. Hotfman. FUNCTIONAL DISORDERS OF THE HEART 
509 
Clinical experiences prove that in most cases the tachycardia begins 
without warning and ends with equal suddenness. Hoffman’s tracings 
show the characteristic change of the heart rate within a single cycle. 
The heart rate during the 'paroxysm is either double, treble, or quadruple 
that of the patient’s heart rate just before the attack commenced. These 
characteristics differentiate paroxysmal and simple tachycardia or exces- 
sive palpitation. 
For our purposes of prognosis the differential diagnosis of the vari- 
eties of tachycardia is important. 
My experience with paroxysmal tachycardia does not agree with those 
who claim that it is as frequent in men as in women. I have rarely 
found paroxysmal tachycardia in men without positive evidences of 
hyperthyroidea, this is not true of women who have presented the uncom- 
plicated idiopathic variety of the disease, which justified the diagnosis 
of paroxysmal tachycardia. 
The author does not consider those of auricular fibrillation with mitral 
stenosis (not infrequent) as essential tachycardia. 
With serious attacks, pulmonary congestion may become alarming, 
the pressure in the pulmonary circuit is then high, while the systolic 
blood pressure and pulse pressure is usually low. The alarming symp- 
toms include the enormous tachycardia, pulmonary stasis, cerebral 
anemia, low blood pressure and pulse pressure, occasionally dyspnea and 
albuminuria. 
There are cases in which no remedy influences the paroxysm which 
yields without known cause and often leaves the patient without marked 
weakness. 
In occasional cases sudden acute dilatation causes death after the 
tachycardia ceases. A case which we watched over twenty years, with 
attacks recurring at intervals of from three or four months to as many 
years, recovered from a slight attack, seemed uninfluenced; the following 
day while shopping she fell forward on the counter and immediately 
expired. This is not a frequent occurrence. 
The fluoroscope has demonstrated to the satisfaction of those who 
have had opportunity to examine the heart during the attack, that the 
heart is not dilated but is decreased in size and that in severe cases it 
dilates toivard the end of the paroxysm. 
The embryonic sounds (originally so characterized by Hothnagel) are 
heard during the attack. 
In the more severe cases the liver remains permanently enlarged. 
The duration of paroxysmal tachycardia is variable. I have had two 
cases under observation (both women) during the past twenty years. 
Occasionally the seizures cease after a few years of recurrence. The 
only death in our series is above mentioned after insufficient rest follow- 
ing an apparently insignificant paroxysm. 510 
DISEASES OF THE CIRCULATORY APPARATUS 
Osier reports a case of H. C. Wood in a physician “who in his eighty- 
seventh year had had attacks at intervals from his thirty-seventh year.” 
In this case “the taking of ice-water or strong coffee would arrest the 
attacks.” When the attacks cease all patients promptly recognize the 
“Hop” for which they have learned to wait. 
2. (b) Simple Tachycardia 
An abnormally rapid heart in which the individual is as a rule uncon- 
scious of the heat, which is without the features of paroxysmal tachy- 
cardia, may be considered simple tachycardia. In many cases tachycardia 
is physiological, as during pregnancy, during lactation; there are per- 
fectly normal hearts which continue abnormally rapid throughout life 
without causing inconvenience. 
The abnormally rapid hearts and their baneful influence on prognosis 
of the acute infections are considered with the separate diseases. 
In all acute infections prolonged tachycardia is evidence of serious 
cardiac toxemia. 
It must be accented that tachycardia during the incipient stage of 
most acute infections is evidence of virulent infection and vasomotor 
paralysis. 
Tachycardia with cerebral lesions is evidence of a lesion of the 
pneumogastric nerve, which is due to an anatomical lesion of the nerve 
or to pressure which after a period of irritation led to paralysis. 
Causes.—Thrombosis and embolism, brain tumor, bulbar paralysis, 
myasthenia gravis, Landry’s paralysis, acute myelitis, acute poliencepha- 
litis, lateral sclerosis (amyotrophic), disseminated sclerosis and hemor- 
rhage of the fourth ventricle are mentioned by von ISTeusser among the 
causes of simple tachycardia. Charcot and Oppenheim also mention the 
crises of tabes and syringomyelia with bulbar manifestations. 
There is no disease of the- brain or cerebral injury (fracture in- 
cluded), which may not cause tachycardia. In all cases tachycardia 
influences prognosis unfavorably but the prognosis depends entirely on 
the nature and extent of its cause. 
Irritable hearts and delirious hearts (Delirium Cordis) are asso- 
ciated with enormous rapidity of action, usually there is some precordial 
pain, the subjects are nervous individuals, easily ungeared. J. M. 
Da Costa reported the cases of 200 soldiers with fever and overstrain in 
17 per cent, diarrhea with mild typhoid fever in 30.5 per cent; hard 
field service; excessive marching 38.5 per cent; doubtful causes in 18 
per cent; in which there were irritable hearts. 
Many cases of irritable hearts are associated with myocardial degen- 
eration and demand a guarded prognosis. In some cases the irritable 
heart is found in young recruits unaccustomed to “the strain, mental FUNCTIONAL DISORDERS OF THE HEART 
511 
excitement and insufficient training.” Hypertrophy is occasionally 
followed by dilatation in grave cases. 
3. Bradycardia 
An abnormally slow heart is synonymous with bradycardia. 
True bradycardia includes only those cases in which all of the heart 
chambers beat equally slow. The other forms of bradycardia according 
to Mackenzie are “false”—they are due (a) to a missed beat, in which 
the ventricle contracts, but the pulse wave because of the feeble contrac- 
tion fails to reach the wrist, (&) “certain cases of nodal rhythm where 
the auricle has ceased to beat, or does so synchronously with the ven- 
tricle,” and (c) “where the stimulus is blocked between auricle and 
ventricle so that the auricle beats at its normal rhythm and the ventricle 
does not respond to the auricular systole, but pursues an independent 
and slow rhythm” (heart block). 
Bradycardia is not necessarily pathologic. There are individuals who 
always have a slow pulse and are never influenced unfavorably thereby. 
During labor, the pulse may be normally slow. 
The leading causes of bradycardia summarized by von Neusser are: 
Toxic substances: 
Tobacco—Nicotine 
Lead 
Physostigmin—Muscarin 
Potash salts—Picric Acid. 
Autotoxic substances: 
Ptomain poisoning 
Bile 
Urea 
Acetone—Acetic Acid. 
Convalescence from Acute Infectious Diseases—Rheumatism and 
Pneumonia particularly. 
StoTces-Adams Disease. 
Coronary and Myocardial Disease. 
Diseases of the brain: 
Gummatat Tuberculous and other tumors 
Lesions of the medulla oblongata 
Hyperemia of the vagus center 
Meningitis 
Concussion of the brain 
Cerebral apoplexy 
Thrombosis and Embolism 
Acute hydrocephalus 512 
DISEASES OF THE CIRCULATORY APPARATUS 
Hemorrhage of the fourth ventricle 
Facial Paralysis 
Cysticerci of the fourth ventricle. 
Hysteria. 
Melancholia. 
Basedow’s Disease (during transition from Basedow to myxedema). 
Pressure on the vagus: 
Carcinomatous glands and tuberculous growth of the neck. 
Cancer of the Stomach, gastric ulcer and gall-stone colic. 
Injuries to the spinal cord. 
Diseases of the Ear: 
Foreign bodies in the external ear; reflex irritation from the 
auricular branch of the vagus. 
Each of these many possible causes of bradycardia suggests its own 
prognosis. 
When bradycardia arises suddenly during the active period of pneu- 
monia or any grave infection, it usually indicates incipient meningeal 
invasion. During the period of convalescence it is not usually of signifi- 
cance with proper care and is not infrequent. 
With cerebral hemorrhage moderate bradycardia is more favorable 
than tachycardia, which with high temperature is almost always fatal. 
With cancer of the stomach bradycardia during the early stage may 
assist in diagnosis, for it is not infrequent and may, by leading to prompt 
recognition influence prognosis favorably. 
Bradycardia due to syphilitic lesions offers a favorable prognosis— 
when attacked early and vigorously. 
Heart block has been separately considered. The influence of digi- 
talis and kindred remedies in slowing the heart must be considered in 
connection with the study of individual cases. 
4. Arhythmia 
The Arhythmias have been considered in connection with the dis- 
eases of the myocardium. 
S. The Neurasthenic State 
There are but few neurasthenics without complaints referable to the 
heart. These complaints are numerous, vary from day to day and are 
always interpreted as serious by the patient who soon becomes self- 
centered with the heart symptoms in the ascendency. 
There are often acute exacerbations of symptoms resembling organic FUNCTIONAL DISORDERS OF THE HEART 
513 
crises which are aggravated hy the autosuggestion and associated fear of 
the patient. 
In some cases symptoms continue during long periods; in other cases 
nocturnal attacks and periodicity are characteristic. 
Anginoid attacks with marked development of an emotional element 
accent the fears of the neurasthenic. 
Some patients are fairly well between the acute attacks hut live in 
fear of this recurrence. 
The mental pang suffered hy the cardiac neurasthenic is often pitiful. 
The pulse shows great variations in frequency and in character at 
different times, and under varying conditions. It may be surprisingly 
slow at one time, exceedingly rapid at another. Intermission and ar- 
hythmia with marked excitement and great fear of impending danger 
and associated hysteria are noted in some cases. 
Sensory symptoms referable to the extremities, with hyperesthetic 
areas, at times to the precordium are frequent, and add to the discom- 
forts and fears. 
The prognosis of the neurasthenic state is favorable. The most potent 
factor in its prognosis is the personal equation of the attendant whose 
tact and resources will often be taxed during long periods, but by so 
regulating the lives of these individuals as to remove them from them- 
selves and substituting a healthy suggestion for the ever recurring and 
depressing autosuggestion and other appropriate mental pabulum, these 
patients make satisfactory recoveries. 
Relapse is frequent when depressing factors are usually responsible. 
References 
Bouveret. De la tachycardie paroxstique essentielle. Rev. de Med., Paris, 1889, ix, 
753-836.' 
Charcot & Oppenheim. Quoted by von Neusser [Z. e.]. 
Colbeck. Diseases of the heart. London, 1901. 
DaCosta (J. MS). Am. J. Med. Sci., Philadelphia, 1871, Ixi. 
Hirschfelder. Johns Hopkins Hosp. Bull., Baltimore, 1906, xvii, 299. 
Hoffman. Die Paroxysm. Tachycardie. Wiesbaden, 1900. 
Pathol. u. Therapie der Herzneurosen. 1901. 
Mackenzie. Diseases of the heart. 1912. 
Osier. Practice of Medicine. New York, 1913. 
Von Neusser. Bradycardie u. Tachycardie. 1908 (Translated by MacFarland). Section IV 
Diseases of the Blood and 
Hemopoietic Organs 
A. Anemia 
1. Symptomatic Secondary Anemia 
Formerly the term “Anemia” included only a reduction in the num- 
ber of red blood corpuscles. Anemia is now defined as a condition in 
which the blood as a whole, the red blood corpuscles or the hemoglobin, 
or both, are diminished. 
Oligemia includes a condition of the blood in which all of its con- 
stituents are diminished. 
Oligocythemia is a condition in which the red blood corpuscles are 
reduced. 
Chlorosis or oligochromemia denotes a marked reduction in the amount 
of hemoglobin in the individual cell. 
Local anemia or ischemia is usually either transitory or permanent. 
I consider both these conditions in connection with vascular spasm and 
arterial changes, such as endarteritis, which may choke the parts beyond 
the point of obliteration and lead to deep tissue changes—gangrene, 
necrobiosis and cyanosis (See separate diseases). 
General Anemia 
The larger number of aneviias are of secondary origin and symp- 
tomatic. 
Anemia due to loss of blood may be (a) acute or (b) chronic. 
(a) Acute Anemia (Hemorrhagic).—Hemorrhage may cause sudden 
acute anemia reducing at once every element which normally floats 
through the vessels and naturally the amount of blood. 
514 ANEMIA 
515 
Suddenly arising pallor, anemia, should always lead to the suspicion 
of hemorrhage. When external, the recognition of the cause is easy; 
when hemorrhage is internal, it is more difficult. With typhoid fever, 
sudden pallor and collapse without symptoms of peritonitis or intestinal 
perforation should always lead to the suspicion of intestinal hemorrhage, 
the blood may be held in the intestine for several hours before it appears 
in the stool. (See Typhoid Fever.) Sudden anemia in women whose 
menstrual flow has been irregular or absent, should always lead to the 
strong suspicion of ectopic pregnancy with tubal rupture. The prog- 
nosis of this condition is brilliant in cases recognized early and promptly 
treated radically. The clinician wall make no more satisfactory con- 
quests in the practice of his profession than in the prompt diagnosis of 
ruptured tubal pregnancy. These patients may be thoroughly exsan- 
guinated and still recover. Accidents during delivery, placenta previa, 
uterine inertia, and laceration may cause serious and threatening- 
depletion. 
Malignant growths ulcerating or rupturing, may cause sudden and 
fatal anemia. One of our cases died suddenly from internal hemorrhage 
due to the rupture of a rapidly growing encephaloid cancer of the liver. 
The ability of the individual to immediately furnish much of the water 
content of the separate organs to the blood vessels as these are depleted 
by sudden hemorrhage, is one of the important factors in saving life in 
acute anemia resulting from hemorrhage, by tiding him over the critical 
period. 
Patients who are depleted or below par, do not bear sudden loss of 
blood well, for the response to the added demand on the bone marrow is 
slow and unsatisfactory. The young and healthy bear the loss of blood 
better and react quicker than do older subjects. It has been found experi- 
mentally, that with the loss of from £ to of the total blood volume 
(1/13 of the body weight) regeneration usually follows in from 2 to 6 
weeks (Turk). Bierfreund found that with the loss of 25 per cent of 
the entire blood in children, complete regeneration followed in 22| days, 
in healthy adults in 17-| days, and in the aged in 28 days. 
It may be assumed that oligocythemia and oligochromemia are con- 
ditions which, with the reduction of the blood plasma are promptly com- 
pensated by nature’s processes. The danger point in all acute hemor- 
rhage is reached if one-half or more of the entire volume of blood is lost. 
Morawitz says that “the loss of more than two liters must be viewed 
writh great concern and offers an unfavorable prognosis.” A low blood 
count and cellular changes which show lack of regenerative power and 
marked enfeeblement is an unfavorable combination. If the underlying 
factor is removable, even under these threatening conditions, recovery 
often follows. Tiirk makes the unqualified statement that the exhaus- 
tion of the patient offers the indications for the immediate attempt to 516 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
overcome the prime factor because extreme conditions may ultimately 
yield to radical treatment. 
The plasma of the blood increases first after depleting hemorrhage, 
the regeneration of the red blood corpuscles is slower, while the hemo- 
globin is last to return to the normal level. Sudden hemorrhage stimu- 
lates both the erythroblastic and myelogenic tissues to activity, which 
accounts for the prompt leukocytosis (posthemorrhagic leukocytosis) 
which follows the loss of blood. The return of normoblasts and young 
red cells in abnormally large numbers is always favorable. The leuko- 
cytosis and excess of normoblasts, if present, are promptly changed to 
approximately average conditions. 
The pulse may be small and rapid, the heart sounds distant and 
feeble, the associated symptoms extreme; all these conditions usually 
yield with the control of the hemorrhage. The prognosis must depend 
finally upon the cause of the hemorrhage, the extent of damage done to 
the tissues, the resistance of the patient and a variety of other conditions 
which present in the individual case. 
(b) Chronic Anemia (Hemorrhagic).—The anemia which is chronic 
and associated with hookworm disease, has been separately considered 
(See Ankylostomiasis). Long continued drain leads to chronic blood 
changes. The gravity of the anemia depends upon the amount and dura- 
tion of the hemorrhages, its localization and the cause. The leading 
causes of chronic hemorrhagic anemia are excessive menorrhagia, metror- 
rhagia, bleeding piles, intestinal and gastric hemorrhage due to ulcers of 
the duodenum, intestine or neoplasms (cancer), varices, epistaxis, pur- 
pura, hemophilia, hematuria due to organic disease or parasites. 
The grave anemia of bothriocephalus latus is separately considered 
(See Pernicious Anemia and Bothriocephalus Anemia). 
The blood changes of chronic (hemorrhagic) anemia include a char- 
acteristic picture. In extreme cases hemoglobin may sink below 20 per 
cent, and if the cause can be overcome, complete return to health usually 
follows. In the grave types normoblasts, polychromatic erythrocytes, 
megaloblasts and megalocytes are found. In the more favorable cases 
normoblasts, polychromatic erythrocytes, poikilocytes and microcytes are 
present. The red count falling below 1,000,000 in the acute and chronic 
cases is always ominous with the correspondingly low color index. Turk 
says 20 per cent of such cases offer a doubtful prognosis. 
The secondary chronic anemias due to malignancy, cachexia and 
infection influence the forecast of these conditions. 
Tuberculosis, cancer, sarcoma, nephritis, typhoid fever, malaria, the 
intoxicants, including lead, mercury, arsenic, antimony and other poisons 
are all associated with more or less anemia as these diseases advance. 
There is slow “latent bleeding” due to malignant growths of the intestine 
which during long periods offers no subjective or objective symptoms ANEMIA 
517 
save gradually increasing anemia, the cause of which may be detected by 
the presence of occult blood in the stools. The prognosis of all depends 
upon the ability to remove the cause. The slow bleeding of cancer (gas- 
tric and intestinal) is likely to show greater cachexia than anemia and 
this is of value in differentiating pernicious anemia, in which the anemia 
is out of proportion to the cachexia. Faulty living, ventilation, diet and 
social conditions influence the blood state besides leading to primary 
conditions upon which anemia is usually dependent. With chronic 
bleeding and associated anemia or any form of secondary chronic anemia 
the unfavorable features include besides heart weakness and the unfa- 
vorable blood picture, edema, vertigo, tinnitus aurium, headache and 
dyspnea. 
In cases which are operable the prognosis is best in which the hemo- 
globin per cent does not fall below 40. Von Voorden believes that any 
form of anemia may ultimately lead to complete exhaustion of the bone 
marrow which may present the clinical features and the blood picture 
of pernicious anemia. If this is true the occurrence is exceedingly rare. 
The author has never in practice seen a case of secondary anemia develop 
the pernicious or essential disease. 
Bierfreund. Arch. f. klin. Chirurg., 1890, Bd. xli. 
Bramwell. Anemia and some of the diseases of the blood-forming organs and internal 
glands. Philadelphia, 1899. 
von Limbeck. Klin. Path. desBlutes. 1896, 2. Aufl. 
Morawitz. Mohr & Staehelin, Handb. d. Inner. Krankh. Bd. iv. 
von Noorden. von Mehring & Krehl, Lehrb. der inneren Medizin. Jena, 1913, Bd. ii, 
736. 
Turk. Vorlesungen iiber klin. Hematol. Wien, 1912, 2. Theil, Bd. ii, 2. 
References 
2. Primary or Essential Anemia 
(a) Chlorosis 
(Green sickness, Oligochromemia) 
Chlorosis is a condition of the blood in which there is a decided 
lowering of blood coloring matter—hemoglobin—which is limited to the 
female, is likely to develop during the period of sexual development, is 
relieved by iron, is never per se a serious disease, though it recurs easily, 
is materially and promptly influenced by the general condition of the 
patient. The blood picture of chlorosis is characteristic. Chlorosis may 
be diagnosticated in the absence of the picture of true anemia when there 
is a decided reduction in the percentage of hemoglobin. Most chlorotics 518 
DISEASES OF BLOOD AND HEMOPOIETIC OKGANS 
are also oligocythemic (red corpuscles reduced). In the severe cases 
the red corpuscles number from 2,5u0,000 to 3,500,000 per c. mm. 
Hayem reports extreme counts as low as 1,300,000 per c. mm. Cabot 
averaged 77 cases at 4,050,000 per c. mm. Bramwell averaged 80 cases 
at 3,437,000 per c. mm. Mild cases show but slight reduction in the 
red count. Besides the reduced hemoglobin, there is an excess of blood 
serum (polyplasma), the regenerative power of the blood is reduced, the 
leukocytic count is not materially disturbed, the blood platelets are in- 
creased. The pathologic, cause of chlorosis is unknown. Virchow be- 
lieved that there was, in most cases, a congenital narrowing of the larger 
blood vessels (aorta). 
Extreme chlorosis is associated with marked subjective symptoms; 
prominent among these are dyspnea, palpitation, exhaustion, menstrual 
anomalies, gastro-intestinal disturbance, obstipation and excessively devel- 
oped emotional element, perverted appetite, vertigo, tinnitus aurium and 
the characteristic pallor of the mucous membranes and green colored 
skin. The extremities are cold much of the time. Chlorotics lack normal 
resistance. In these cases hemic murmurs (systolic) are usually present. 
The foregoing features are present and persist until relieved by some 
form of treatment. The majority of chlorotic girls yield to proper diet, 
ventilation and prolonged rest. Uncomplicated chlorosis always yields 
to iron and other rational treatment. ISTo patient dies of chlorosis unless 
there has been some complication. Pulmonary embolism and thrombosis 
are rare but fatal complications; many men of large experience have 
never met such cases. The tibial or femoral vessels are occasionally the 
seat of thrombosis. With improvement of the general condition the color 
index is raised, the blood picture changes and all attending symptoms 
gradually yield. The return to a normal condition is often exceedingly 
slow and an irritable heart may persist during varying periods. The 
perverted appetite is also a source of annoyance in some cases during 
long periods. Chlorotics are liable to relapse on slight, sometimes with- 
out hnown cause; seasonal and climatic influences are powerful. Change 
of scene with rest often effects lasting cure. 
Progressive loss of weight with chlorosis or any form of anemia argues 
against uncomplicated blood changes and demands search for the underly- 
ing cause before a forecast is justified. 
The influence of intestinal toxemia in continuing or causing chlorosis 
should be considered in the individual case. Sir Andrew Clark strongly 
advocated the intestinal origin of chlorosis and believed that constipation 
was the leading factor. 
In America, foreign girls between the ages of 12 and 16, shortly after 
their arrival, often become chlorotic and amenorrheic. This condition 
usually yields after a few months of treatment. Girls coming to cities 
from the country also develop chlorosis very frequently and menstrual ANEMIA 
519 
anomalies. It has been noted that recurrence is finally prevented by 
pregnancy. Occasional cases remain but slightly changed during long 
periods; they are veritable chronic chlorotics without many annoying 
symptoms, but the blood picture does not return to normal. Some of 
these continue chloranemic throughout their lives. Among the frequent 
complications of chlorosis is gastric ulcer. The prognosis of this condi- 
tion is separately considered. (See Gastric Ulcer.) Chlorosis with 
exophthalmic goiter is repeatedly met in practice and usually yields with 
the other symptoms of hyperthyroidea. Acute nephritis and endocarditis 
mentioned by Bramwell as sequelae of chlorosis we have never experi- 
enced. There is a strong tendency to self cure after the twenty-fifth or 
thirtieth year. 
Bramwell. Anemia, etc. Philadelphia, 1899. 
Cabot. Clinical examination of the blood. New York, 1904. 
Ehrlich-Lazarus. Die Anaemie. 2. Aufl., Berlin, 1909. 
Grawitz. Klin. Path, des Blutes. 4- Aufl. 
Hayem. Du sang et de ses alterations anatomiques. Paris,"1889. 
Morawitz. Mohr & Staehelin, Handb. der Inneren Krankh., Bd. iv, Berlin, 1912. 
Naegeli. Blutkrankh. u. Blutdiagnos. Leipzig, 1908. 
von Noorden. von Mehring & Krehl, Lehrbuch der Inneren Krankh. Jena, 1913. 
References 
(6) Pernicious Anemia 
(Addisons Anemia (1855), Progressive Pernicious Anemia, Malignant 
Anemia, Infectious Anemia, Biermers Essential Anemia, Megalo- 
blastic Anemia) 
Pernicious anemia is a chronic progessive, possibily infectious disease 
characterized by (hemolysis) destruction of large numbers of red blood 
corpuscles in which the remnant of corpuscles contains a high hemoglobin 
per cent; the disease presents a blood picture which is classic, though not 
absolutely pathognomonic; it often shows long periods of latency, has 
periods of exacerbation which are followed by remission in some cases, 
may either early or late present striking features showing involvement of 
the nervous system and in almost all cases leads to death with symptoms 
of toxemia. In rare cases the course is acute. There are besides the 
destruction of the blood elements, marked changes in the bone marrow, 
surprising retention of the body fat in spite of advancing disease, hemor- 
rhages into the skin and serous cavities, dilatation of the heart, also 
myocardial degeneration, usually atrophy of the gastric and intestinal fol- 
licles; in the terminal stages, enlargement and fatty degeneration of the 
liver, which organ contains an excess of iron, with or without slight en- 
largement of the spleen. As a rule, the spleen remains negative so far 
as its size and contour are concerned. The changes in the bone marrow 520 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
are easily recognized. The color is abnormally red, lymphoid cells and 
a large number of normoblasts (Ehrlich’s gigantoblasts) are seen. Licht- 
heim first called attention to the symptoms and changes in the nervous 
system. These are important in the diagnosis and prognosis of individual 
cases and include sclerosis of the cord in patches, mainly affecting the 
posterior columns and the ganglionic cells of the sympathetic. I char- 
acterize the nervous symptoms as “ Lichtheim symptoms” and will again 
refer to the complex. There is no treatise which details the clinical his- 
tory of the disease more accurately than that given by Addison in 1855 
under the caption of idiopathic anemia. 
History.—Grawitz in considering the history of pernicious anemia 
mentions Combe as having reported a case in 1822, another by Marshall 
Hall in 1843 and Lebert in 1853 and 1868 call attention to parallel cases 
developed during pregnancy. Cazenave, in 1860 with Lebert, called at- 
tention to essential anemia without pregnancy. Combe in reporting the 
original case wrote “A marked instance of a very peculiar disease—If any 
train of symptoms may be allowed to constitute anemia a generic disease, 
the following may be considered a sample of it. in its most idiopathic 
form.” 
The disease is known on the continent of Europe as Btermer’s Pro- 
gressive Anemia or Essential Anemia; the original classic description 
of the disease by Addison which antedated Biermer’s redescription by at 
least 17 years had been practically ignored even in England; in spite of 
the fact that the colleagues of Addison at Guy’s Hospital were acquainted 
with his description but little attention was given to its diagnosis until 
their minds were refreshed by Biermer’s treatise. The failure to recog- 
nize this form of anemia during those days is accented by the fact that 
Pye Smith in 1882 presented a complete bibliography and was unable to 
gather more than 102 cases from various sources. 
Heredity.—Any grave anemia, pernicious particularly, in which there 
is a strong hereditary element is likely to be rapidly progressive and long 
periods of latency are not frequent. We have in our cases noted the fre- 
quency with which several members of the same family are afflicted. It 
is not unusual to find one or more brothers and sisters, or one parent and 
one or several children with essential anemia; all running the typical 
course to death. We have never met a case of pernicious anemia in a 
child below the age of 15 years. Osier reports one case in a boy ten years 
of age. The large majority of our cases were between 33 and 40 years 
of age. We do not include a single case in our old or new series in which 
pregnancy or prolonged lactation caused the disease. Pepper, Channing 
and Gusserow called attention to the influence of pregnancy on the pro- 
duction of essential anemia. Probably with modern hematologic methods 
of differentiation most of these cases would now prove to be secondary and 
dependent upon long continued drain. ANEMIA 
521 
Blood Picture.—The blood picture of pernicious anemia is sufficiently 
characteristic to lead to its diagnosis in the majority of cases. There are 
occasional exceptions for thorough hematologists have been forced to 
concede that rare grave anemias, non-pernicious, do present pictures which 
so closely resemble the pernicious type that error is possible. 
Ehrlich contends that the blood picture alone is so characteristic as to 
make diagnosis possible. The dictum to which the Ehrlich school adheres 
is that “Megaloblasts and Megalocytes show megaloblastic degeneration 
and this is the main cause of pernicious anemia.” 
Bothriocephalus anemia which in cases not too far advanced offers a 
fair prognosis, presents blood features which are so closely allied to the 
essential pernicious type of the disease as to make differentiation impos- 
sible and most authorities agree that the blood pictures are parallel (See 
Bothriocephalus Latus). Unquestionably advanced bothriocephalus latus 
anemia cannot from the blood picture be differentiated from true perni- 
cious anemia and such patients die with all of the clinical manifestations 
of essential anemia. I have seen recovery from grave bothriocephalus 
anemia follow the expulsion of the worm which is usually dead or sick 
and by its presence caused toxemia. 
The erythrocyte count is lowered in the advanced or most serious cases 
to 1,000,000 per c. mm. or below. The average in our cases early has 
been between 2,500,000 and 3,500,000. The blood is pale yellow, abnor- 
mally fluid, and clotting is slow and unsatisfactory. In some cases the 
prick is followed by oozing and the surrounding skin becomes ecchymotic 
(spurious hemophilia). 
Blood counts in which the erythrocytes fall below 1,000,000 are rapidly 
fatal. Prognosticating from the blood picture we quote Cabot: 
“1. Severe (rapidly fatal) 
(a) Extreme progressive anemia. 
(b) High color index. 
(c) Increase in size of red cells. 
(d) Denegerative changes. 
(e) Numerous megaloblasts. 
(f) Few or no normoblasts. 
(g) Lymphocytosis.” 
“2. Less severe (slower course) 
(a) Remissions. 
(b) Normal or low color index. 
(c) Normal sized cells. 
(d) No degenerative changes. 
(e) Few megaloblasts. 
(f) Numerous normoblasts. 
(g) Normal percentage of adult 
cells.” 
The size of the red cells is increased—megaloblasts and megalocytes 
are abundant. There is marked macrocytosis—the number of small sized 
red corpuscles is striking and these vary in size and shape (anisocytosis). 
Misshapen red corpuscles (poikilocytosis) are abundant. The high color 
index (high hemoglobin value of the individual cell) is one of the con- 
stant features and serves in doubtful cases to make diagnosis and prog- 
nosis positive. Polychromasia is the rule. Normoblasts or nucleated 522 
DISEASES OF BLOOD AFD HEMOPOIETIC ORGANS 
red blood corpuscles are usually, but not always present. During the 
early history of individual cases (not acute or rapidly fatal) normoblasts 
are present. Their presence indicates response of the bone marrow to 
the stimulation necessary to make new blood elements. The complete ab- 
sence of nucleated red corpuscles may be interpreted as indicating failure 
to respond and is always of bad prognostic significance. The myelogenic 
reaction which brands an anemia as pernicious and consequently fatal is 
of great importance. Xeusser says “We find the expression of reaction 
of the bone marrow, which is regenerative, in the appearance of nucle- 
ated red blood corpuscles (normoblasts) while the production of megalo- 
blasts with degenerated small and badly tinged nuclei are the expression 
of degeneration.” The leukocytic count in the average case may not be 
materially changed but as the disease advances there is a reversion of 
the entire blood to the embryonic state. The presence of myeloblasts in 
increased numbers (5 to 10 per cent) is not unusual and blood platelets 
may drop to 75,000-100,000. 
In our consideration of the subject we assume that pernicious anemia 
because of its uncertain pathogenesis should include “any profound and 
(apparently) causeless anemia which is characterized by peculiar altera- 
tions in the blood—which tend to pursue a progressive and pernicious 
course.” (Bramwell.) 
Bramwell believes that the question whether the clinical condition 
termed pernicious anemia “may result from a variety of causes or whether 
it is a singular clinical entity, the causation of which is always one and the 
same, should be left an open one.” We are safe in concluding that in the 
typical cases there is excessive and rapid blood destruction (hemolysis) 
and defective blood formation. 
For our purposes of prognosis the consideration of the unsettled the- 
ories relating to the etiology of the disease is unnecessary. Indeed the 
profession is by no means agreed. There are data both clinical and ex- 
perimental which strengthen the infectious and toxic origin of the dis- 
ease, that increased destruction of blood in the portal system is due to the 
absorption of toxins from the gastro-intestinal tract, and that oral sepsis 
(Hunter, Wm.) is an important factor in causation. 
In considering various pathologic data wdiich influence prognosis the 
frequency of achylia gastrica (Einhorn 1892—Martins 1897) associated 
as it is with atrophy of the gastric follicles, a frequent, almost constant 
attendant deserves consideration (Grawitz, Fenwick, Quincke, Nothnagel, 
Jurgens, Friedenwald). While Friedenwald does not subscribe to Gra- 
witz’s contentions that with achylia gastrica resulting toxemia, the hemo- 
lytic action of toxins elaborated in the stomach and intestines cause perni- 
cious anemia; he found in 70 per cent of his pernicious anemias the pres- 
ence of atrophy of the gastric follicles (achylia gastrica) and in 20 per 
cent of the remnant marked reduction of hydrochloric acid. Friedenwald ANEMIA 
523 
believes that the same toxic agent is at once the cause of the achylia gas- 
trica and the pernicious anemia. 
Lazarus expresses the same view, believing that both conditions are the 
result of an unknown poison. 
Faber and Bloch believe that the changes in the gastro-intestinal tract 
are post mortem and that there is no direct proof of the existence of such 
lesion intra vitam. This contention has not received support. We know 
that during life in most cases there is absence of free hydrochloric acid 
and we have often in our cases found long periods of improvement or 
latency follow the administration of free HC1. in large doses after the 
method of Croftan. 
Whatever we conclude concerning the relation of achylia gastrica and 
essential anemia the fact remains that life is shortened by the complete 
anorexia and gastro-intestinal disturbances associated with atrophy of the 
gastric and intestinal glands. We have seen the more rapidly fatal course 
in those cases in which after a period of intestinal symptoms, diarrhea) 
usually, hemolysis has been rapid, the general condition has promptly 
failed, complete anorexia and stomach intolerence has been marked and 
without remission, but with increasing involvement of the sensorium death 
has followed. There are a number of cases in which during years pre- 
ceding the development of essential anemia, chronic diarrhea has been a 
prominent feature. This remains uncontrolled in most cases and finally, 
there are added the complete blood picture and other clinical features of 
pernicious anemia. These patients are not likely to have periods of remis- 
sion or latency, but the onward march to death is prompt, with symptoms of 
sepsis. 
Pernicious anemics without prominent and persistent gastro-intestinal 
symptoms live longer and are more likely to have periods of remission and 
latency than do those with such complications. 
Grawitz who bases his pathogenesis on the absence of free hydrochloric 
acid in the stomach contents reports repeated cures. Critics are agreed 
that none of the cured cases have been proved to be true pernicious anemia. 
Grawitz does not consider the blood picture of pernicious anemia diagnos- 
tic and has, according to Tiirk, included all forms in his list of the essen- 
tial anemias. Lazarus, Cabot, Tiirk and FTaegeli disagree with Grawitz 
and believe that cases of primary hemolytic anemia in which there is a 
characteristic blood picture and in which there are positive evidences of 
the failure of the bone marrow to react to normal stimuli, are fatal. 
Pernicious Anemia and the Spleen as a Hemolytic Organ.—The suc- 
cessful issue in Banti’s Disease in which there are evidences of anemia 
and hemolysis which have followed splenectomy with the results of experi- 
mental research, have led a number of clinicians to consider the influence 
of splenectomy on the prognosis of pernicious anemia. The literature of 
this subject is growing and while in a few individual eases thus treated 524 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
patients have withstood the operation, no positive conclusions are justified 
at the present time. Eppinger reports two cases of pernicious anemia with- 
out death following the operation. He believes that the extirpated spleens 
of pernicious anemia, hemolytic jaundice, and experimental toluylendia- 
min are identical, all filled with erythrocytes. The urobilin in the stools 
of all splenectomized patients showed marked reduction and convalescence 
was without incident. 
Eppinger’s material besides the two cases of pernicious anemia included 
2 of hemolytic jaundice, 3 of Banti’s disease, 2 of hypertrophic cirrhosis 
and one of grave catarrhal icterus. There are isolated cases in medical 
literature in which there seemed to he improvement but we are not justified 
in reporting any cured. We would further refer the reader to the reports 
of George Klemperer and Hirschfeld, Banti and the experimental work 
done by both American and German pathologists in this field. 
Acute Pernicious Anemia.—There are cases in which pernicious ane- 
mia runs a rapid course to a fatal termination; such behavior is excep- 
tional. I have recently seen a case in which, after a short period 
of indefinite “Lichtheim symptoms” within two weeks there was such 
prompt hemolysis and utter loss of marrow reaction that the blood picture 
of the gravest megaloblastic anemia was complete. There are cases of 
syphilitic anemia which we have met in families with positive hereditary 
tendency to pernicious anemia, in which the blood picture of the disease is 
completed within a few weeks. Such a case I now have under observation 
in which one parent and one brother died of pernicious anemia; a sister 
suddenly developed the cord symptoms which are often present early in 
the grave types of the disease, the hemolysis was most destructive, the 
count fell to almost 1,000,000 within two weeks, the cell elements and 
high color index were characteristic of true essential and pernicious ane- 
mia. The intravenous injections of neosalvarsan promptly brought relief 
of both objective and subjective symptoms. Such cases, before a positive 
prognosis can be given, demand long periods of observation for it is not 
at all safe to conclude even in the acute cases with positive Wassermann 
reaction and the blood picture of genuine pernicious anemia that the treat- 
ment has not proved sufficient to awaken the bone marrow to renewed 
activity and that later there will not be a return of classic symptoms and 
the onward march of the disease. Certainly the syphilitic history and 
the satisfactory reaction following salvarsan in acute cases argue in favor 
of a good prognosis in cases of grave anemia which in the end, if the 
patient remains permanently cured, proved that they were not true megalo- 
blastic anemia. 
With acute pernicious anemia marked glossitis, gastro-intestinal symp- 
toms, rapid loss of strength, dyspnea and symptoms referable to the cenr 
tral nervous system, (brain particularly) the chances of remission are 
small and death may be expected before the end of the eighth week. ANEMIA 
525 
While the sudden, severe and 'persistent character of blood destruction 
—hemolysis—is the feature which is in the ascendency even in acute cases, 
the striking power of regeneration is a factor which is paramount and it 
does in a proportion of cases, which begin with acute symptoms and rapid 
blood destruction (in the more favorable cases), lead to marked improve- 
ment, long periods of remission and the restoration of sufficient strength 
to return the patient to his work. Such patients may remain immune 
from symptoms during varying periods in spite of the acute onset and 
enormous hemolysis, but in the end the symptoms return; there may be 
several remissions but the end follows a period of continuous symptoms 
just as in those cases which were chronic and progressive from the begin- 
ning. 
Remissions and Periods of Latency.—Nature’s attempt to stimulate 
the blood producing organs to renewed activity after hemolysis is strik- 
ingly successful in over 50 per cent of all cases. Indeed it is the excep- 
tion to find an idiopathic anemia which leads to a fatal termination with- 
out one or more remissions of varying length. 
Cabot reports 524 cases of which 
296 had one remission 
118 “ two remissions 
65 “ three remissions 
21 “ four remissions 
24 “ five remissions 
In 6,300 cases of internal disease tabulated, I have seen 46 cases of 
pernicious anemia, in over 15 per cent of these, remissions led to such 
marked improvement as to materially change the blood picture and not 
infrequently the original diagnosis has been doubted. I number among 
my older cases one of a young girl in whom I made the diagnosis from 
the positive blood picture 10 years ago, who improved and married, 
indeed the blood apparently became normal until within the past 
six months, when she returned after a short period of severe Lichtheim 
symptoms with a blood count of 1,510,000 erythrocytes; 7,800 white 
corpuscles, color index 1 + and the disease is now rapidly progressive. 
This case had the longest period of remission of any case in my experi- 
ence. It proves that it is not safe to offer rose colored prognosis in these 
cases. I have never met true pernicious anemia, it matters not how 
long the period of improvement or remission, which did not finally lapse. 
The length of life depends upon the natural powers of recovery of the 
blood producing organs which as Hunter has said, “are very striking and 
constant,” as well as upon the complications. 
I would warn against the assumption that any particular form of 
medical treatment is the paramount factor in stimulating the inherent 
power of the bone marrow to regenerative function after even long periods 526 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
of inactivity. It would seem that when hemolysis has produced the char- 
acteristic degenerative changes the bone marrow attempts to come to the 
rescue and as already suggested succeeds during varying periods. 
Bramwell reports that one of his patients remained well for 12 years 
and then relapsed and died almost fourteen years after the first attack. 
Nervous Symptoms.—I have repeatedly referred to “Lichtheim 
symptoms” in considering prognosis. These include a variety of subjective 
complaints, the leading early symptoms are a “numbness and awkward- 
ness of the hands” often the legs are paresthetic at the same time. These 
paresthesias and accompanying reactions are often “tabetic” in charac- 
ter and include unsteadiness of gait and loss of patella tendon reflex. In 
rare cases pupillary changes are present as well as sphincter disturbances. 
It is interesting to note that paresthesias and disturbances of locomotion 
at times antedate anemia. In another group of Lichtheim cases there 
may be hut slight paresthesia of the hands early, no tabetic symptoms, in 
which the nervous complex increased with progression of the anemia. 
There are, in the most severe cases, in which remission is scarcely to he 
expected, early evidences of cerebral toxemia, from which the patient may 
only partially rally to finally fall into profound coma. Such behavior is 
unusual, characterizes the terminal stage, hut whenever there are profound 
mental disturbances the prognosis for life is had and death promptly fol- 
lows. While the gravity of the anemia is not in direct proportion to the 
nervous symptoms in all cases, our experiences justify the conclusion that 
once established, Lichtheim symptoms are likely to persist and that marked 
tabetic and cerebral symptoms when present are found in the most advanced 
stages or in those cases least likely to have long periods of remission. When 
remission is decided in cases with few Lichtheim symptoms the slight 
numbness and other abnormal sensations are usually borne without com- 
plaint. In my 46 cases of pernicious anemia among 6,300 patients over 
80 per cent developed Lichtheim symptoms either early or late—usually 
during the first 12 months of the disease. 
Heart and Blood Vessels.—With the initial hemolysis the pulse is 
small, thready and rapid with a low blood pressure and a strong tendency 
to edema of the ankles. When the edema becomes general the myocardium 
is enfeebled and there is hydremia in most cases. Small, feeble, rapid 
pulse, low blood count, dyspnea, edema and evidences of toxemia showing 
themselves in increasing mental and nervous disturbances, form a complex 
which with the blood picture is characteristic of the terminal stage of the 
disease. Small feeble pulse with tinnitus aurium, vertigo and palpitation 
with some Lichtheim symptoms and low red count may still be followed by 
remissions, one or more. Edema of the lung with feeble heart and other 
complications, marked enlargement of the liver and albuminuria are unfa- 
vorable, and soon lead to death. 
Persistent tricuspid regurgitation, epistaxis and purpura are unfavor- ANEMIA 
527 
able. Usually there is marked edema, at times hydrothorax and retinal 
hemorrhage. Venous hum over the neck veins (external jugular) may be 
present early and persists during the periods of exacerbation until the end; 
the same is true also of hemic murmurs heard best at the base of the hearu 
With an improved blood these murmurs may disappear. 
Retinal hemorrhages may be an early or late complication. Probably 
50 per cent of essential anemias have retinal hemorrhage at some time. 
The hemorrhages are not, as a rule, large. I have never seen a case in 
which the hemorrhage led to blindness. Retinal hemorrhage and pallor 
of the fundus are of diagnostic and prognostic value. Deep purpuric con- 
ditions once present, there is small hope of remission or improvement of 
the blood state. 
Temperature.—Slight elevation of temperature is frequent. Some 
cases have a continuous slight elevation of temperature which does not seem 
to interfere materially with the disease. In most cases the higher con- 
tinuous fever which is associated with other toxic symptoms—central nerv- 
ous manifestations—is present late in the disease and is not influenced by 
treatment. The fever is almost always irregular and atypical. It is an 
expression of toxemia. 
In chronic cases death is often hastened by acute exacerbations during 
which elevation of temperature is the earliest symptom. Such cases may 
be following a typical course, with periods of remissions, when without 
known cause, there may or may not be a chill; continued fever, not always 
high, but with a slight morning fall persists. With increasing malaise 
and extreme exhaustion and increasingly rapid and small pulse, symptoms 
of toxemia including delirium and coma follow. The temperature curve 
is between 100|° F. and 103° F. (may be higher). Death may be ex- 
pected before the end of the fourth week. The mental (toxic) symptoms 
are always prominent from the beginning of such exacerbations. 
The urine offers no marked features to influence prognosis. Cases 
which show no tendency to improve may often die without showing a trace 
of albumin. In other cases as already suggested, with general dropsy in 
the terminal stage, albuminuria is present. High colored urine with uro- 
bilinuria is often an expression of blood destruction (blood crisis) and 
unfavorable. 
Indicanuria is of no prognostic value in pernicious anemia; it is not 
unusual. 
Tongue.—“Oral sepsis'” has been strongly advocated by Hunter as be- 
ing of great importance and provocative of pernicious anemia; the same 
author believes that with relief of the septic element, the blood picture 
and the general condition of the patient improves. There are in some cases 
from the beginning marked changes in the tongue which are best consid- 
ered to be inflammatory, atrophic, at times ulcerative. 
Glossitis is by no means a constant attendant of pernicious anemia. In 528 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
the late stages the shining, wrinkled, dry, often cracked and bleeding tongue 
is present. In all cases the tongue is pale. Marked evidences of dry 
tongue—the glazed, shining denuded tongue with ulcerative gingivitis and 
bleeding gums are evidences of malignancy of the anemia and indicate 
advanced disease. 
Atrophy of the gastro-intestinal glands with glossitis and correspond- 
ingly low blood state are not often followed by long or satisfactory remis- 
sions. 
Retention of the body weight, fat particularly, does not in any way 
influence prognosis. Cachexia is not frequent or striking. The marked 
anemia is out of all proportion to the cachexia or loss of weight, while as 
already suggested with malignant disease, the cachexia is out of proportion 
to the anemia (Henry). 
Intravenous and intramuscular injections of salvarsan, intensively used 
have been advocated by many during the past 3 or 4 years. Personally, 
after a reasonably large experience with the remedy we are unable to 
positively say that a single case has been saved. In the graver specific 
anemia it does yeoman service. In those cases of pernicious anemia in 
which it has seemed to have a wholesome effect in stimulating the blood 
producing organs and improvement has resulted, there is no assurance 
that relapse may not follow. Indeed the improvement when it does fol- 
low is usually short-lived. 
Bramwell in a recent article in which he reports his results of 21 
cases treated by salvarsan and neosalvarsan had “6 without improvement 
(28.5 per cent) ; in 3 (14.2 per cent) there was slight improvement; in 5 
(23.8 per cent) there was marked improvement and in 7 (33.3 per cent) 
there was complete ( ? temporary) recovery. 
Ultimate results of BramwelPs series show “of 21 cases treated by 
salvarsan or neosalvarsan and recorded in this paper, in 1 case (4.7 per 
cent) the patient remains fairly well; in 5 cases (23.8 per cent) quite 
well; in 15 cases (71.4 per cent) the patients have died.” 
Such statistics are of no practical value. They are too recent and in- 
definite. 
Bramwell correctly states the case as follows: “In order to judge fairly 
and accurately of its value, a series of consecutive and unselected cases, 
slight as well as severe, in which no other treatment has been employed, 
should be taken and the results compared with a series of similar cases 
treated by other methods.” 
The great majority die in coma, after a period of brain symptoms vary- 
ing from two to four or more weeks. Complications are exceedingly rare. 
Occasionally bronchopneumonia or added infection causes death, not often. 
Pernicious anemia with atrophy of the gastric follicles and tuberculosis of 
the suprarenals (including bronzed skin) were found in one of our cases ANEMIA 
529 
References 
Addison. London Med. Gazette, March, 1849. On the Constitutional and Local Effects 
of Diseases of the Suprarenal Capsule, 1855. 
Banti (G.). Semaine Medicale Annee, xxxiii, 313. 
Biermer. 42. Versam. deutsch. Naturf. u Aerzte, Dresden, 1868. Korrespond. Schweizer 
Aerzte, Bd. ii, 1872, No. 1. 
Billings (Frank). Boston Med. & Surg. Jour., cxlvii, Nos. 9 & 10. 
Bramwell. Med. Times & Gaz., 167. 
Edinburgh Med. Jour., 1877. 
Anemia, etc. Philadelphia, 1899. 
Brit. Med. Jour., i, 1915. 
Cabot. Boston Med. & Surg. Jour., 1896. Clinical Exam, of the Blood, New York, 1894. 
Cazanave. Jour, de Med. de Bordeaux, 1860, 53. 
Combe, 
Hall, Marshall. 
Transact. Med. Clin. Soc. Edinburgh, May, 1822. Quoted by Turk, 
[Z. c.]., 374- 
Croftan (A. C.). Deutsch. med. Wochenschr., xxxviii, 1912, 84-2-844- 
Ehrlich. Die Anemie, Nothnagel Handbuch, Wien, 1898. 
Einhorn (Max). New York Med. Rec., 1892, 650. 
Eppinger. Berl. klin. Wochenschr., Jg. 50, No. 83, S. 1509, also No. 84, 1572, 1913. 
Eppinger u. Rauzi. Ueber Splenektomie bei Bluterkrankungen. Mitth. a. d. Grenz. der 
Med. u. Chir., Bd. 27, 1914, 796. 
Faber & Bloch. Zeitschr. f. klin. Med., xl, 1900. Arch. f. Verdauungs-Kr., Bd. x, 1904. 
Fenwick. London, Lancet, 1877, also cited by Turk [L c.]. 
Friedenwald. Boston Med. and Surg. Jour. ii. 1912, 160-162. 
Grawitz. Lehrb., etc., 4■ Aufl., 1913. 
Henry & Osier. Am. J. Med. Sci., 1886. 
Hunter (Wm.). Lancet, London, 1888. 
Practitioner, 1889. 
Severest Anemia, i, London, 1909. 
Jurgens. Quoted by Turk [l. c.], ii, 386. 
Klemperer (G.) & Hirschfeld (II.). Therapie der Gegenwart, Jahrgang liv, 885. 
Lebert. Essential Anemie. Wien. med. Wchnschr., 1858. 
Lichtheim. 6. Kongress f. inner. Med., Wiesbaden, 1887. 
Martius. Achylia Gastrica. Leipzig & Wien, 1897. 
Neusser. Wien. klin. Wchnschr., 1899, No. 15. 
Nothnagel. Ztsch.f. klin. Med.,Bd. vi, 1882. 
Osier. Practice of medicine. 8. ed., New York, 1914. 
Osier & Gardner. Centralb. f. d. Med. TFiss., April, 1877. 
Pepper (Wm.). Am. J. Med. Sci., Oct., 1875. 
Pye-Smith. Guy’s Hosp. Rep., xxvi, 1882. 
Virchow’s Arch., 1875, Ixiv, 507. 
Quincke. Deutsch. Arch. f. klin. Med., Bd. xx, 25, 27. 
Turk. Vorles. ii. Hematologie. Bd. ii, Wien, 1912. 530 
• DISEASES OE BLOOD AND HEMOPOIETIC ORGANS 
B. Leukemia 
1. Leukocytic Leukemia. 
Synonyms: Myelocytic Leukemia. 
Splenomyelogenous Leukemia. 
Myeloid Leukemia. 
Myelemia. 
Lienal Leukemia. 
2. Lymphatic Leukemia. 
Synonyms,: Lymphemia. 
Leukocythemia. 
Chloroleukemia. 
Pseudoleukemia. 
3. Acute Leukemia. 
4. Leukanemia (Leube). 
5. Mixed Leukemia. 
1. Leukocytic or Splenomyelogenous Leukemia 
The original description of leukemia with the clinical and blood pic- 
tures given by Virchow was so exact that but little which has been offered 
since has materially altered his original conception of the disease. Eb- 
stein, who has made a careful investigation unhesitatingly concludes that 
Virchow recognized the disease before Bennett to whom the credit is usu- 
ally given. The references appended make it possible for the student of 
medical history to study that question for himself if he desires from the 
literature within easy reach. Virchow did not appreciate the part played 
by the bone marrow until Neumann, in 1870, called attention to it. Leu- 
kemia may he defined as a condition of the blood in which the white blood 
corpuscles are enormously increased so as to be in the proportion of 1 to 
20 of the red cells or there may be greater disproportion (1-10 or 1-5), 
in which there are changed relations of the normal varieties and numbers 
of white blood corpuscles depending on a specific cause (unknown) and 
irritative growth in the blood producing tissues (hyperplasia of the leuko- 
blastic tissues) which result in the flooding of the blood with either myelo- 
cytes or lymphocytes, in accordance with the variety of leukemia present. 
The true nature of the disease is unknown. Some believe it resembles or is 
closely related to sarcoma and myeloma. 
Leukocytic or Splenomyelogenous Leukemia 
Blood.—The myelocytes, large mononuclear cells of Ehrlich, are in 
the ascendency and are supposed to differ from the large mononuclear LEUKEMIA 
531 
lymphocyte. All blood, therefore, which contains myelocytes is abnor- 
mal. The myelocyte is normally present in the bone marrow. In leuko- 
cytic leukemia there is an overdevelopment of the myelocytes and their 
casting off into the blood stream. 
Relatively the proportion of the polymorphonuclear cells is decreased. 
They are actually increased. There are many polymorphonuclear leuko- 
cytes, a preponderance of myelocytes, eosinophils and eosinophilic myelo- 
cytes; increased mast cells; an occasional normoblast; poikilocytes, inegalo- 
cytes, microcytes, pale red blood corpuscles, and in advanced cases Char- 
cot-Leyden crystals. The alkalinity of the blood is decreased; the specific 
gravity reduced (1,025-1,040); there is finally a positive reduction of 
hemoglobin (average early 60 per cent lower as the disease advances). 
Bennett characterized the disease as “suppuration of the blood.” 
A high myelocytic count, irrespective of the number of leukocytes is 
essential for the diagnosis of splenomyelogenous leukemia, just as megalo- 
blasts are necessary for the diagnosis of pernicious anemia. The average 
white count in our series at the height of the disease was between 275,000 
and 300,000. We have, in rapidly fatal cases made counts much higher. 
In one case seen many years ago with marked hemorrhagic tendencies in 
the terminal stage, the red and white counts during the last few weeks of 
life ran practically parallel—500,000 to 800,000 per c. mm. The poly- 
morphonuclear cells average between 25 and 50 to 55 per cent; the myelo- 
cytes from 30 to 50 per cent. Almost all of our cases were without hered- 
itary taint—with the male decidedly in the ascendency. 
In some cases the red count may remain normal or nearly so for a 
considerable period, rapid or progressive drop of erythrocytes is unfavor- 
able, particularly if at the same time, there are evidences of increasing ex- 
haustion, hemorrhages, purpura or increasing mental symptoms. Marked 
morphologic change in red corpuscles with increasing hemolysis is unfa- 
vorable for the prolongation of life. 
High fever, or even continuous elevation of temperature, slightly above 
100° F. with evening rise, is evidence of advancing change and unfavorable 
for prolongation of life. Symptoms referable to the nervous system often 
resemble the Lichtheim complex of pernicious anemia. The greater the 
involvement of the nervous system the shorter is the course of the disease, 
as a rule. Invasion of the sensorium is indicative of deep toxemia or in- 
filtrating changes in the brain and is promptly followed by death. There 
is greater paresthesia than tabetic symptoms though the latter may be 
present, also neuritis. Tinnitus aurium and vertigo are evidences of pro- 
found anemia in most cases. Hemorrhages into the auditory system lead- 
ing to deafness and uncontrollable vertigo are unfavorable symptoms. 
The spleen is enormously increased in size. In some cases in which, 
as the result of treatment or nature’s processes, the white count improves, 
the splenomegaly shows some retraction, but this is not to be relied upon 532 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
as occurring uniformly. In my cases treated with Rontgen Rays and 
Benzol, the spleen did not change in size with the improved blood .picture. 
Perisplenitis has not been a frequent source of pain in my cases. It 
has no great bearing on the progress of the disease. I have never met a 
death due to rupture of the spleen in my material, occasional cases have 
been reported in which rupture was the cause of death. Marked dyspnea, 
cough, expectoration and physical signs of infiltration are indications of 
advancing disease. Dyspnea and cough may be due either to leukemic in- 
filtration of the lung or myocardium or to extreme weakness and myocar- 
dial weakness. The physical signs of infiltration of the lung may also be 
due to complicating tuberculosis. These cases all progress rapidly to a 
fatal issue. We consider elsewhere the influence of added tuberculous in- 
fection on the white blood count. Dyspnea and respiratory embarrass- 
ment may also be due to pressure from hydrothorax, hydropericardium, en- 
larged spleen and liver. The prognosis is unfavorably influenced by gas- 
tro-intestinal complications or symptoms. In severe cases, often in the 
last stage, anorexia, vomiting and diarrhea, with hemorrhage, rapidly 
weaken the patient. 
In the terminal stages ascites and general edema are in evidence. It 
may happen that after the removal of the abdominal fluid toxic symptoms 
increase. At times life may be prolonged during a short time by such 
procedure. With fbrotic and nodular changes in the liver and fatty de- 
generation, or the latter alone, there may be slight jaundice. The liver 
as suggested elsewhere in this section may show leukemic infiltration. 
All of these conditions are unfavorable for the prolongation of life. Peri- 
tonitis is the terminal complication in rare cases. 
The urine shows an increase of uric acid (characteristic condition) ; 
there may be moderate albuminuria, hyalin casts and evidences of acute 
or chronic nephritis. In some cases barring the excess of uric acid, even 
in severe cases, there are no changes in the urine. Occasionally the urine 
is of a greenish hue and Bence-Jones albumose has been present as in 
multiple myeloma (Kahler’s Disease). Such complications are most fre- 
quent with lymphatic leukemia. 
I have seen several examples of priapism which has persisted unre- 
lieved by any treatment. In one woman, the clitoris was in a state of 
chronic erection and with vaginal irritation caused great discomfort. 
The behavior of the heart is much like pernicious anemia as the end 
approaches. From the beginning of symptoms there is rapid action, small 
and thready pulse, systolic blood pressure is low. As the disease advances 
the systolic force grows more and more feeble, the heart sounds embryonic 
and dilatation with hemic murmurs, jugular pulsation, tricuspid insuffi- 
ciency and frequent syncope may precede death. 
Pulmonary edema due to heart insufficiency is a cause of death. Early 
or late, usually late, evidences of hemorrhagic retinitis are in evidence with LEUKEMIA 
533 
associated ocular subjective symptoms. Sight is not lost; optic neuritis is 
not frequent. 
2, Lymphatic Leukemia 
{Lymphemia, Leukocythemia, Chloroleukemia, Pseudoleukemia) 
The essential features of lymphatic leukemia are changes in the lym- 
phatic glands of the body causing multiple enlargements (increase of lym- 
phocytic forming tissue) and the resulting lymphocytosis. The blood 
changes are characteristic. 
Blood.—The color index is low, the hemoglobin reduced, the coagula- 
bility, alkalinity and specific gravity are much like the splenomyelogenous 
form. There is true lymphemia, The small lymphocytes are in the as- 
cendency. There is increase in the number of polymorphonuclear leuko- 
cytes, though less than in leukocytic leukemia. The red blood corpuscles 
usually number 3,000,000 or below, as the disease advances. Few nucle- 
ated red cells are seen, less than in the other variety of the disease; a few 
myelocytes and a small fraction of eosinophils. In both varieties of leu- 
kemia the blood platelets are increased. 
The lymphatic type shows a predilection for children and young adults, 
though older subjects may develop the disease. Males are more frequently 
afflicted than females. 
The lymphatic enlargements may at first be limited, beginning in the 
neck, and extending to the axilla with, in advanced cases, multiple enlarge- 
ment in the glands of the body—mediastinal, postperitoneal, mesenteric 
and inguinal. There are also changes in the internal organs due to infil- 
tration. 
The spleen may not be materially enlarged. The anemia is slower to 
develop in this form than with myelogenous leukemia. In some cases the 
color may remain good in spite of mulitple lymphatic enlargements. The 
fever is not likely to be an early symptom. It is often long postponed. 
Skin pigmentation and nodules are relatively frequent. The involve- 
ment of the oral mucosa, teeth, tonsils and postnasal glandular tissue, in- 
creases septic symptoms and hastens the end. 
Chloroma is a condition of lymphemia with nodules in the skull, green 
color of the lesions as the glandular structure proliferates, the presence of 
exophthalmos and facial paralysis in most cases. Chloroma may be asso- 
ciated with or is a part of either myelogenous or lymphatic leukemia, usu- 
ally as above stated the latter. It may be associated with the acute or 
chronic leukemias, usually the former, but cases have been reported which 
lived from two to four years (Ward). The average duration of life 
is below seven months. 534 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
3. Acute Leukemia (Ebstein) 
Acute leukemia may be either leukocytic or lymphatic. The large 
majority of cases are typically lymphatic, though the spleuomyelogenous 
form is occasionally met (Naunyn). In the latter form we have seen two 
cases which commenced suddenly without prodromata, with high fever fol- 
lowing repeated chills. The spleen and liver were enlarged at once, the 
former was somewhat tender. One of these was a girl about 15 years of 
age who during several months was favorably influenced by Rontgen ther- 
apy, indeed the high leukocytic count was at once reduced and after a few 
weeks her physician reported counts approaching leukopenia, when her 
fever and chills were under control. So striking was the improvement that 
the case was reported at the meeting of the Medical Society of the State 
of New York by her attendant, who wTas much encouraged by the result. 
(Schuyler.) The improvement was short-lived. She died as did all other 
cases. 
The typical cases of acute leukemia begin suddenly with marked febrile 
disturbances, the lymphatics are involved, there is lymphemia and increas- 
ing anemia. Fraenkel has reported the constant presence of abnormally 
large mononuclear cells, wasting and toxic symptoms, enormous prostra- 
tion, hemorrhages from the mucous surfaces and purpura, (skin) and the 
enlarged spleen are among the symptoms. 
The blood changes are exceedingly rapid. Death results in coma after 
a period of typhoid condition in from four weelcs to three or four months. 
Russell and Taylor have reported 55 cases of acute leukemia. We have 
never known of recovery. Cases in which there is depleting diarrhea die 
early. Ulcerative colitis and enteritis have accompanied some acute leu- 
kemias. Thymus and tonsillar infiltration, gingivitis (ulcerative) and 
ulceration of the buccal mucosa lead to inanition and early death. Rapid 
leukemic infiltration of vital organs, lung, liver, and kidney with skin 
nodules—pigmentation and leukoderma are found in both forms of acute 
leukemia. The more extensive the leukemic nodules, the sooner will death 
follow. The brain may be the seat of infiltration causing hemorrhage with 
resulting paralysis and other focal symptoms. Hemiplegia has been re- 
ported as well as ocular and aural lesions with consecutive symptoms. 
There are occasional cases reported in which decided increase of lympho- 
cytes has failed to appear until within one or two weaks of death. (Litten, 
Waldstein, Villinger.) 
The majority of acute leukemias are found in children and before the 
age of 20 years. 
4. Leukanemia (Leube) 
Leube called attention to blood changes and a clinical history in which 
there are evidences of myelogenous or lymphatic leukemia with grave LEUKEMIA 
535 
anemia. The lesions present depend upon the variety of leukemia with 
which the grave anemia is associated. The prognosis is bad. 
5. Mixed Leukemia 
There are also mixed forms of leukemia in which the blood picture 
shows cellular elements characteristic of both forms of the disease. 
The influence of treatment on the prognosis of all forms of leukemia 
has not been encouraging. Beginning with x-ray therapy and ending with 
benzol and mesothorium, enthusiasts have been deluded by the surpris- 
ing influence of the Rontgen Ray over the long bones and spleen, and the 
benzol internally administered in reducing the leukocytic count. Periods 
of improvement of subjective symptoms have followed but we have no 
record at hand after wading through a large literature hearing on the sub- 
ject which justifies the conclusion that a single case has been permanently 
benefited. All relapse and all leave died. There is great danger from the 
sudden and overpowering poisoning due to the destruction of large num- 
hers of leukocytes following the Rontgen Ray and the use of benzol. 
The influence of splenectomy on leukemia is being considered, hut in 
spite of a few reported cures (?) there are no data at hand which warrant 
the conclusion that the “cured” were veritable cases of the disease. Until 
we are better informed by experimental study on the influence of the spleen 
in these cases, no hope is justified by the removal of that organ. The aver- 
age duration of life in uncomplicated cases is between six to eight months 
and between three and five years. My lymphatic cases have lived longer 
than the myelogenous. 
Remissions with considerable periods of improvement are character- 
istic, but not so strikingly frequent as in pernicious anemia. Many spleno- 
myelogenous leukemias are progressive from the beginning without a stay 
of symptoms, either subjective or objective. 
Lymphatic leukemia frequently shows tendency to remain latent dur- 
ing long periods. Once symptoms of deep toxemia show themselves or with 
purpuric or hemorrhagic complications, with acute exacerbations and high 
temperature, edema, ascites or other evidences of dropsy, heart degenera- 
tion, remission cannot be expected. The subjective symptoms of all forms 
of leukemia have practically the same influence on the forecast. 
Complications.—The influence of acute or chronic added infection 
upon the blood count is striking. I called attention to the influence of 
added tuberculosis in connection with Groat in a case of splenomyelogenous 
leukemia. With tuberculous infiltration of the lung and its advance, the 
myelocytic count was promptly reduced (Eisner and Groat, also George 
Dock). These observations have been confirmed by other observers in con- 
nection with a variety of complicating infections. There are but few com- 
plications. Death results from asthenia in coma, in most cases. Pulmo- 536 
DISEASES OF BLOOD AND HEMOPOIETIC OKGANS 
nary edema, bronchopneumonia, exhaustion following hemorrhages and 
sudden syncope are among the causes of death. In all forms of leukemia 
the greater the number of leukemic nodules in the internal organs and skin, 
the more rapid is the course of the disease. 
Bennett {I. H.). Two cases, etc., etc., in which death took place from the presence of purulent 
matter in the blood. Edinburgh, Med. & Surg. J., 1845, Ixiv. 
Leukocythemia, etc. London, 1852. 
Dock {George). University Med. Magazine, Philadelphia, 1898. 
Am. J. Med. Sci., 1904. 
Dock & Warthin. Chloroma. New York Med. News, 1904. 
Transact. Ass. Am. Phys., 1904, xix, 64-115. 
Ebstein (Wm.). Die Pathol., etc., der Leukaemie. Stuttgart, 1909. 
Ehrlich. Anemia, Nothnagel, Spec. Path. u. Therapie. 1901. 
Eisner & Groat. Am. J. Med. Sci., March, 1901, {contains full references to influence of 
infection on blood count in leukemia). 
Fraenkel (A.)* Verhandlungen, 15. Kongress f. Inner. Med., 1897, 359. 
Fussell & Taylor. Philadelphia Med. J., 1899. 
Transact. Ass. Am. Phys., 1898, xiii, 124-146. 
Leube. Deutsch. Klinik, Bd. Hi, 1903. 
Deutsch. Klinik, 1891, ii, 177-202. 
Litten. Ebstein [Z. c.], 29. 
Naegeli. Blutkranlc., etc. Leipzig, 1908. 
Naumann. Arch. d. Heilkunde, Bd. Ixxvii, 1870, 1. 
Naunyn. Deutsch. med. Wchnsch., 1898, Vereinsbeilage, No. 8, 47• 
Villinger. Acute Leukemie. Tubingen, 1900. 
Virchow. Weisses Blut, etc., In Frorieps. Neue Notizen a. d. Geb. d. Natur. u. Heilk. 
Nov., 1845. Abhand. z. Wissensch. Med., 1856, 14- Med. Zeit. d. 
Vereinsf. Heilk. in Preussen, 1846, Nos. 34-36. 
Virchow’s Arch., Bd. v., 1853, 80. 
Krankhafte Geschwiilste, Bd. ii, Berlin, 1864-5. 
Virchow's Arch. {Prof. Bennett u. Leukemie) 1854, Bd. vii, 564• 
Waldstein. Ebstein [l. c.], 29. 
Ward. Clinical Hematology. Philadelphia, 1914. 
References 
C. Hodgkin’s Disease Lymphoblastoma 
{Pseudoleukemia, Lymphadenoma, Malignant Granuloma, Adenie, 
Lymphogranuloma) 
Hodgkin’s Disease is characterized by marked enlargement of the 
lymphatic glands of the body, beginning, as a rule, in the cervical region 
and extending to distant parts (axillary, mediastinal, bronchial, mesen- 
teric and inguinal) with more or less enlargement of the spleen and liver 
.as the disease advances and finally the blood picture of grave secondary 
anemia. To sum up and contract the definition, Hodgkin’s Disease may HODGKIN’S DISEASE; LYMPHOBLASTOMA 
537 
be considered a far-reaching disease of the organs which elaborate blood 
cells, including the lymphnodes, the spleen and bone marrow, which bears 
external resemblances to leukemia but is without the typical leukemic 
blood picture (Naegeli). 
The disease bears close resemblance to tuberculosis without the pa- 
thologic changes which prove it to be of bacillary origin, while there are 
some features which resemble the leukemias, which led pathologists to 
name it “pseudoleukemia.” The entire history of the disease, its symp- 
tomatology and pathology create a strong suspicion of the presence of an 
infectious agent. Within the last few years this suspicion has been 
strengthened by the experimental and pathologic researches of various 
men, foremost among these are Bunting and Yates who, as the result of 
their studies are strongly of the opinion that the diphtheroid organism 
which they have cultivated from cases of the disease in man and with 
which they have successfully inoculated monkeys, reproducing lesions 
similar to those of the disease in man, will ultimately prove its infectious 
nature. They say “we feel fully assured of the etiologic relationship of 
the diphtheroid organism (Bacterium Hodgkini) to Hodgkin’s Disease.” 
The early and tonsillar and alveolar symptoms in many cases create the 
further suspicion of infection and point strongly to the tonsils (teeth 
and mouth) as the port of entry. 
Hodgkin’s Disease may be accepted as a clinical entity in which the 
pathologic changes in the lymph glands are characteristic and include 
marked increase of the gland tissue, multiplication of the endothelial 
and reticular cells and as has been shown (Andrewes and Dorothy Reed) 
lymphoid cells are enormously increased and are of uniform size and 
shape; giant cells, the lymphadenoma cells, hold multiple nuclei; while 
eosinophils are constantly present. The hardness of the gland is due to 
the fibroid change—reticular increase. Suppuration is rare, and when 
this happens, there is in all probability added pyogenic infection. In 
some of the monkeys inoculated by Bunting and Yates, the “softening” 
was found, but without the presence of any added microorganism. The 
Bacterium Hodgkini alone grew in the cultures of these cases. 
[The study of the life of Hodgkin who in 1832 described the disease 
which bears his name, proves him to have been one of the three clinical 
and pathological giants of the early half of the nineteenth century who 
added fame to Guy’s Hospital. The other two were Addison and Bright. 
(Stroud, Wm.) Hodgkin deserves to be remembered not only as having 
made clear the clinical and pathologic characters of the disease bearing 
his name but as an unselfish and humane physician.] 
Haegeli considers Hodgkin’s Disease or pseudoleukemia a symptom 
complex of these diseases: 
A. Lymphocytoma.—Lymphocytoma, or those in which there is pro- 
liferation which he characterizes as lymphocytic and aleukemic, in which 538 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
the lymphatic system is largely involved, in which the spleen, bone mar- 
row, liver or periosteum may, in individual cases present the greater 
changes during varying periods. Included in the lymphocytoma are: 
(a) The Aleukemic Lymphadenomata (Hodgkin’s Disease of most 
clinicians). 
(b) Lymphosarcomatosis (Kundrat’s Disease). 
These are localized sarcomata originating in lymphatic tissue (lymph 
nodes usually), never disseminated beyond the lymphatic system. Liver 
and spleen are not enlarged. 
B. Granuloma.—The granulomata are inflammatory growths and not 
true Hodgkin’s Disease, they may be: 
(a) Malignant. 
(b) Tuberculous. 
(c) Syphilitic. 
When, therefore, we consider “Hodgkin s Disease” we include the 
lymphocytomata or the aleukemic lymphadenoma. 
The course of Hodgkin’s Disease may be either (a) acute or (b) 
chronic: 
(a) Acute Hodgkin’s Disease.—The acute form of the disease usually 
begins with tonsillar symptoms which resemble very closely the sub- 
jective features of acute leukemia. The advance of lymphatic inva- 
sion with associated constitutional disturbances, changes in the spleen, 
thymus and blood are often surprisingly rapid and ultimately fatal. In 
most of these cases there is fever, often marked hyperpyrexia with 
prompt emaciation, cachexia, and toxic symptoms (cerebral). In several 
of our cases, with slight enlargement of the spleen and liver, there has 
been edema of the extremities, purpuric spots over the body and deplet-> 
ing epistaxis. These cases are to be differentiated from the typical acute 
or subacute relapsing cases described by Pel and Ebstein. The non- 
relapsing acute Hodgkin’s Disease is always fatal and runs its course in 
from three weeks to as many months. The Hodgkin’s process of Pel and 
Ebstein may continue during many months. In this form of the disease 
the symptoms often resemble the more acute type but there are varying 
periods of relapse (7 to 14 days) after high and weakening fever, with 
excessive sweats, wasting and increasing secondary anemia. There may 
be enlargements alone of the internal glands, or as we have seen in sev- 
eral hospital cases, the lymphatic invasion is general and one of our cases 
died with mediastinal pressure of asphyxia which increased suddenly. 
In the Ebstein pseudoleukemia the temperature during the afebrile 
period may be subnormal from which there is a gradual rise to the climax. 
In one of our cases there was, at the beginning of each relapse, a well 
defined chill during which the temperature reached 104-5° E.. where it HODGKIN’S DISEASE; LYMPHOBLASTOMA 
539 
remained much of the time for three or four days, when it fell gradually 
to below normal. These patients may develop purpuric symptoms, have 
hemorrhages, fall into a typhoid condition; usually have evidences of 
nephritis with the blood picture of secondary anemia. 
Ziegler called attention to cases in which there are constitutional 
symptoms, elevation of temperature and increasing evidences of anemia 
without palpable external glandular enlargement, but involvement of the 
internal glands. The spleen is usually enlarged in these cases, and it 
has been suspected that occasionally the disease originates in the lym- 
phatic structure of the spleen. In some cases the retroperitoneal glands 
alone may be involved, in others the bronchial or both thoracic and 
abdominal glands may be enlarged at the same time. These are con- 
sidered under the head of the “Latent type.” We know of no recovery 
from a single well authenticated case of these types of the acute disease. 
Heffron’s case presented a typical history in which mediastinal pressure 
promptly caused death. Such cases are not infrequent. For the full 
study of the symptomatology of the relapsing type of Pel-Ebstein the 
reader is referred to McNally’s paper (See References). 
(b) Chronic Hodgkin’s Disease.—The onward march of the disease 
is slow, the first evidences are the enlargement of the cervical glands, 
usually one sided, at the angle of the jaw. The extension to the opposite 
side may be long postponed but careful examination in most cases will 
detect an abnormal hardness and some enlargement of one or more deep 
cervical glands long before the growth extends to the other side of the 
neck. The enlargement of the lymphatics may be surprisingly extensive 
as the disease advances and multiple skin nodules are not uncommon. A 
recent case showed extensive bronzing of the skin—probable involvement 
of the suprarenals. This man in spite of the existence of the disease 
during several years (3) and glandular enlargements in all possible direc- 
tions, palpable spleen and liver, with a blood count with all the charac- 
teristics of moderate secondary anemia and albuminuria, was able to 
work his farm and walked without discomfort. 
When the mediastinal glands are involved the pressure symptoms are 
persistent and increase; the suffering is acute and with edema of the 
face and arms, or at times with only symptoms of compression death 
promptly follows. 
The blood picture is not pathognomonic. As already intimated 
Hodgkin’s Disease in the chronic type leads to blood changes which cor- 
respond with those of secondary anemia (anemia gravis). There are 
eases in which the glandular enlargements are prominent without dis- 
coverable changes in the blood. These are among the most chronic cases; 
life is not threatened during long periods unless death is caused by 
pressure or other complications. In the average case the leukocytic count 
is not markedly increased. Even in the acute cases this rule holds and 540 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
makes differential diagnosis easy. In some, particularly during febrile 
exacerbations, there is moderate leukocytosis (10,000-30,000). Lympho- 
cytes may be increased with the fall of polymorphonuclear cells. In 
these cases they may represent 75 per cent of all white cells. Pinkus 
holds that the relative lymphocytosis is typical of the disease. Bunting 
believes that tbe diagnosis can “be made with a considerable degree of 
accuracy” from the blood picture, and does not agree with Pinkus that 
lymphocytosi': is typical. It may be safely concluded that the more 
chronic and serious cases show the greater changes in the blood, anemia 
and some leukocytosis. The “two constant features” which Bunting 
holds for diagnosis and therefore for prognostic data, “an increase in 
blood platelets and an absolute increase in the transitional leukocytes,” 
cannot be accepted in all cases. We are agreed that the majority of late 
cases show marked neutrophilic leukocytosis “and a diminution in per- 
centage of all other elements except the transitional leukocyte.” 
There are cases (ISTaegeli and Baumler) in which the lymphocytes 
are markedly reduced with marked neutrophilic leukocytosis, eosin- 
ophilia and increase of mast cells. With the cases which have been 
characterized as “infectious granuloma” the neutrophils continue normal 
and the lymphocytes are much decreased. 
Yates who has collaborated with Bunting makes the following state- 
ment, “In spite of Dr. Bunting’s work, on the blood picture of Hodgkin’s 
Disease, it is almost universally accepted that there is manifested herein, 
nothing essentially or constantly characteristic.” In the chronic cases 
without marked change in the size of the enlarged glands there may be 
decided remissions. In rare cases the glands appear somewhat reduced, 
that may have been imaginary. The remission may be due to an im- 
provement of the periadenitis which is present in some cases. 
The remissions are not as oft repeated or as long as in pernicious 
anemia. During periods of remission the appetite improves, the general 
condition is better and patients are often able to continue at their work. 
Relapse is the fate of all and progression to a fatal termination. 
The duration of the chronic cases varies. The average of our cases 
was in the neighborhood of three years. We have seen cases which lived 
much longer, one, the longest of our series lived over seven years. Mora- 
witz reports the possibility of the extension of life beyond ten years in 
some cases. 
There is in almost all chronic cases a period which Trousseau char- 
acterized as the “periode latente,” this with glandular enlargement and 
no constitutional symptoms may continue during surprisingly long peri- 
ods; one to three years are the extremes. The “period progressive” is 
variable; once the symptoms and lesions are prominent and are progres- 
sive there is not much hope of long periods of remission. The final 
uperiode cachectique,, of Trousseau is coincident with the terminal stage HODGKIN’S DISEASE; LYMPHOBLASTOMA 
541 
and from this there is no release. The symptoms of the cachexia are 
the pallor, weakness, low red blood count, dyspnea, albuminuria, hemor- 
rhages and purpuric skin changes, bronzing and nodes in the skin, increase 
of persistent fever, marked enlargements of the spleen and liver, ascites, 
edema of the extremities, and a period of toxic nervous (brain) symp- 
toms, with small, thready pulse, hemic murmurs, jugular pulsation and 
tricuspid insufficiency (relative) at times. 
Hemorrhagic symptoms are rarely present early; petechiae with or 
without large hemorrhages from mucous surfaces are ominous. The 
transition of an original pseudoleukemia to leukemia is possible and 
occasionally happens. In rare chronic, as in the acute cases, limited 
lesions—localized forms of the disease may offer but few or indefinite 
symptoms during long periods; thus the disease may begin in the mesen- 
teric or postperitoneal glands, be followed by latent periods; extension is 
sure to follow. 
The leading causes of death are toxemia, exhaustion, pressure and 
added infection. 
Tuberculosis is rarely a complication. 
The surgical treatment of Hodgkin’s Disease has in my experience 
been absolutely unsuccessful. On the other hand, it has often seemed to 
stimulate the growth with extension of lymphatic enlargement. Able 
clinicians believe that in some cases the progress is halted by early 
removal. Ho form of treatment—x-ray, surgery, vaccine, serum, drugs, 
climatic or hygienic, has so far as we have been able to discover, saved 
a single life. In making the foregoing statement, we are not unmindful 
of the reported experiences of Yates, who in concluding his article says 
“. . . even these few cases indicate that primarily Hodgkin’s Disease 
is a localized process, susceptible of cure wffien properly treated as a 
malign, though chronic infection. It may persist for years without mani- 
festing itself save in the blood picture so that cures may not be assumed 
until after an uninterrupted duration of years of persistently normal 
conditions.” 
Syphilitic granuloma offers a favorable prognosis. This is not a true 
Hodgkin’s process nor are any of the granulomata to be so considered. 
(See Haegeli’s Classification in this article.) The inflammatory and 
tuberculous granulomata offer an unfavorable forecast. 
References 
Andrews. Transact. Pathol. Soc. of London, 1902, liii, SOB. 
Baumler. Munch. Med. Wchnschr., 1904, Ifi. 
Bunting. Johns Hopkins Hosp. Bull., 1911, xxii, 114; also June, 1914. 
Bunting & Yates. J. Am. Med. Ass., Nov. 15,1913; also Feb. 14,1914. 
Ebstein. Berl. klin. Wchnschr., 1885, No. 1; also 1887, No. 35. 542 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
Heffron (John L.). Acute lymphatic pseudoleukemia, Am. Med., April 12, 1902. 
Hodgkin (Thomas). Med. Chirurg. Transact. 1832, xvii, 68-114. 
McNally. Lymphadenoma with relapsing pyrexia, Quart. J. Med., Oxford, 1911-12, 12, 
v, 58-108. 
Morawitz (P.). Mohr & Staehelin, Handb. d. Inner. Med.,Bd. iv, Berlin, 1912. 
Naegeli. Bluterk. u. Blutdiagnos. 1912. 
Pinkus. Die Pseudoleuk., Nothnagel’s Handbuch, Bd. viii. 
Reed (Dorothy M.). Johns Hopkins Hosp. Report, 1902, x., 133. 
Stroud (Wm.). Bibliographic Sketch. London, 1858, Dudd & Glass. 
Trousseau. Gaz. hebd. d. Med. Paris, 1864, 2. 8.1. 837; idem 1865, 2-3-11. 5. 
Med. Klin., Hotel Dieu in Paris, 1868, Bd. Hi. 
Yates. Johns Hopkins Hosp. Bull., June, 1914. (Clinical Consideration of Hodgkin's 
Disease). 
Ziegler. Monograph, Die Hodgkinsche Krankheit. Jena, 1911. 
D. Purpura 
Hemorrhagic Diathesis 
In considering the prognosis of the symptom complex of purpura we 
adhere to the following classification which is based upon the hypothesis 
that the hemorrhagic diathesis includes a variety of symptoms of a large 
number of heterogeneous diseases (Naegeli) and further that all so-called 
“primary purpuras” including simple purpura and purpura hemorrhagica, 
acute or chronic, are all identical, they simply differ from each other in 
degree and intensity of constitutional symptoms. 
Classification 
Purpura -I 
1. Secondary. 
(a) Simplex. 
(b) Rheumatica (Schoenlein’s disease). 
(c) Hemorrhagica (Werlhof’s disease) 
(Morbus maculosus Werlhofi). 
(d) Chronic purpura. 
(e) Henoch’s purpura. 
(f) Hemophilia. 
2. Primary 
1. Secondary Purpura 
Secondary purpura as we have demonstrated repeatedly in this work is 
an expression of a septic or toxic process; symptomatic always of one of 
many constitutional disturbances and may include scorbutus, hemophilia 
or the hemorrhagic diathesis. Among the leading conditions with which 
purpura may he associated are the leukemias, pernicious anemia, Hodgkin’s 
lymphadenoma, malignant endocarditis, carcinoma, sarcoma, the infec- 
tions (usually the more severe), vasomotor disturbances associated with 
nervous disorders, tabes dorsalis, myelitis and hysteria, all cachexias from PURPURA 
543 
whatever cause and the various intoxications from drugs or other sources 
(Ergot, belladonna, mercury, iodin and snake bites). Purpura in those 
with a strong diathesis may follow mechanical insult. 
Classifying the above causes of secondary purpura into separate groups 
we find them to be infectious, toxic, cachectic, neurotic and mechanical. 
(Osier.) The forecast of secondary purpura always depends upon the 
malignancy or nature of the underlying cause. In all of these conditions 
the addition of purpura may, if it is extensive, unfavorably influence the 
progress of the disease, but it should rather be interpreted as an expression 
of a grave infection or disturbance. 
(The reader is referred to the separate diseases of which purpura is 
a symptom for fuller data.) 
Hemorrhagic scarlet fever and smallpox are examples of malignant 
infection associated with secondary purpura. Erysipelas offers another 
example. 
It may be safely concluded that the grave infections which are “hemor- 
rhagic(purpuric) at their height, always offer a grave prognosis. This 
is not always true of purpura which follows the infections, either shortly 
after the acute symptoms have subsided or later. 
Severe bleeding from many surfaces may follow typhoid fever and 
the patient may show marked depletion, secondary anemia. Nevertheless, 
recovery is the rule under favorable surroundings and rational treatment. 
The larger hemorrhages with the anemias and leukemias weaken the pa- 
tient and hasten the course of the disease. 
With cancer and sarcoma, purpura is almost always included among 
the terminal symptoms. With myelitis, tabes dorsalis, cerebrospinal menin- 
gitis and the depleted neglected alcoholic, the downward course is promptly 
evident after the advent of purpura. Extensive ecchymosis of the genitals 
in tabetics is a late symptom in the more reduced subjects. In children 
the administration of iodin in any form (we have found it after even 
small and continuous doses of syrup of the hydroiodic acid) may cause 
purpura, hematuria usually, and threatening anemia. With the discontinu- 
ance of the drug and proper care, the child in the absence of serious pri- 
mary disease recovers. In the adult with decided hemorrhagic diathesis 
iodin in small or large doses may cause hemorrhagic purpura. 
2. Primary Purpura 
(a) Purpura Simplex 
Simple hemorrhage into the skin, without known cause, may he lim- 
ited or universal and may develop at any age. It is usually found in early 
life. It is often an expression of reduced vitality and resistance. The 
malaise anorexia, and (occasional) slight fever which accompanies it, 
with at times acceleration of the pulse may precede the petechiae several 544 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
days, making positive diagnosis impossible. The subjective symptoms fade 
in from 3 to 7 days; the hemorrhagic spots show the characteristic changes 
in color after from 4 to 8 days and appear ecchymotic during two weeks 
or more. Often these “black and blue” spots persist longer. Purpura 
simplex bears all of the earmarks of a mild infection from which recovery 
without complication is the rule without sequelae. 
The blood picture in most simple purpuras is not materially changed. 
Occasionally there is a reduction of eosinophils—with convalescence these 
are promptly increased to the normal. Diarrhea, which is an occasional 
symptom is easily controlled and is never severe. 
Purpura fulminans is a malignant type of simple purpura which devel- 
ops in young infants (3 to 6 weeks old) without known cause, without 
hemorrhages from the mucous surfaces but with large hemorrhages into 
the skin, either limited to one extremity or both, or universally spread, 
with swelling of the parts, deep sepsis and death in from 2 to 7 days. 
(6) Purpura rheumatica 
Schoenleins Disease 
We have found purpura rheumatica, 
ls£, with symptoms referable to one or more joints (usually the ankles) 
during several days, without known cause, with but little constitutional 
disturbance, followed usually on the third or fourth day, sometimes ear- 
lier, at times later, by petechiae confined as a rule to the skin below the 
knees, either few or many. In six to ten days the disease ends favorably. 
The pain is likely to be more or less relieved as the eruption appears. 
Recovery is complete and without incident. 
2nd: Cases in which with the joint tenderness there are evidences of 
mild tonsillitis, more or less febrile movement and finally the same behav- 
ior of the petechiae as in the preceding cases. These patients do not con- 
valesce as rapidly as do those without tonsillar symptoms, and there is 
often a strong suspicion of an underlying grave infection. Cases with 
exactly parallel early histories have been found to develop endocarditis 
and in rare cases the petechiae have proved to be due to malignant endo- 
carditis. The majority of these cases, however, are benign and recover 
without permanent damage. 
3rd: There is a variety of purpura rheumatica which so closely resem- 
bles erythema nodosum as to lead us to the conclusion that the latter con- 
dition is but another form of purpura, dependent upon some unknown in- 
fection. In these cases the nodes—tender and erythematous—with in 
some, limited evidences of petechiae follow. A few days of tender or stiff 
joints, or without joint symptoms; only the pains due to the presence of 
the nodes and “stiff legs” follow. The ecchymosis persists several weeks, 
the nodes gradually disappear with full return to health. In children PURPURA 
545 
(2 to 8 years or older) the course is shorter than in the adult. There is a 
tendency to recurrence or a subacute course in some of the adult cases. 
Life is never threatened and full recovery may be expected. 
Recurrence is more likely with all forms of “rheumatic” than with the 
simple purpura. 
(c) Purpura hemorrhagica 
(Morbus maculosus Werlhofi) 
Werlhofs Disease is associated with hemorrhages from one or more 
mucous membranes with the usual dermal bleeding of purpura simplex in 
most cases. This is the gravest form of purpura, for in individual cases 
bleeding from many surfaces or into vital organs (brain) may threaten 
life. Hemorrhages from the nose, kidney, intestine, bladder, or bronchial 
mucosa may promptly deplete the weak subjects who are most predisposed 
to the disease. It occasionally happens that hemorrhage into the brain 
substance causes hemiplegia; into the brain membranes hemorrhagic men- 
ingitis. The purpura fulminans of the adult is an example of this form of 
so-called primary purpura. In such cases previously healthy subjects are 
suddenly seized, hemorrhages from several mucous membranes are coin- 
cident, septic symptoms promptly develop and death may follow within 
the first or second week. I have elsewhere in this chapter mentioned the 
purpura fulminans of early life, in which the symptoms as a rule, do not 
include bleeding from the mucous surfaces and justify its classification 
as a malignant type of purpura simplex of early life. 
The blood picture of Werlhof’s disease is that of secondary anemia. 
In the graver cases the blood clot does not contract, if it does, the coagu- 
lation is slow, and the blood platelets are markedly diminished (normal 
250,000 to 400,000 per c. mm.). The lower the red count and color 
index the longer the convalescence and the graver the prognosis. The 
prognosis of Werlhof’s disease is now materially and favorably influenced 
by the prompt use of the animal serum after the method which prevents 
anaphylaxis and which we have recommended (Eisner and Header) for 
the treatment of the chronic forms of' the disease. In the adult fulminat- 
ing purpura, the prognosis has been materially improved by the intro- 
duction of animal serum (preferably rabbit serum). Morbus Werlhofi 
may, because of hemorrhage into the appendix cause symptoms of appen- 
dicitis. One such case I had in my practice where the appendicular 
symptoms were the first and simulated appendicitis; the appendix was 
removed, was hemorrhagic, in two days other hemorrhages followed from 
mucous surfaces, and the significance of the hemorrhagic appendix was 
cleared. The patient made a perfect recovery without recurrence of 
symptoms. Uncomplicated Werlhof’s disease which is not of the ful- 
minating type usually leads, after slow convalescence to permanent re< 546 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
covery. Our experiences with the graver types of the disease with mod- 
ern treatment have been exceedingly encouraging. 
In offering the forecast in any case of threatening purpura it is safe 
to conclude that the changes from hemorrhage, barring cerebral apoplexy, 
are insignificant compared with those of complicating nephritis. 
(d) Chronic Purpura 
Chronic purpura has received but scant attention from writers on 
internal medicine, yet it is a complex which is not infrequent. The clin- 
ical picture is kaleidoscopic and the cycles of the disease include repeated 
recurrences of all classified types of the disease in the individual case. 
In the chronic cases, with a simple purpura, there may be a prompt 
addition of the rheumatic form, and while this seems in the ascendency, 
the hemorrhagic nature of the disease may be emphasized by drains 
from one or more mucous surfaces, occasionally hemorrhage into the 
brain or into hollow or solid viscera. Besides this, chronic purpura 
may alternate with erythema multiforme as we found in one of our cases 
(Eisner and Meader). Two or more forms of purpura may be present 
and persist with varying intensity during limited periods at the same 
time. 
In rare cases (one of which we have reported) whether because of 
embolic infarct, thrombosis or necrobiosis, due to some other unknown 
pathologic cause, death of the hemorrhagic skin results. 
Chronic purpura is exceedingly rebellious to ordinary treatment— 
repeated relapse is the fate of almost all. Two of our cases cover a 
period of twelve and fourteen years respectively. Osier mentions a case 
which was purpuric 36 years and Ilalsted operated on a case of cancer in 
which the patient had been purpuric since childhood. Bensaud and 
Rivet give the most complete resume of this subject. They report cases 
“with periods of quiescence, during which the return to apparent health 
seemed complete, but the phenomena recurred on extreme fatigue.” 
There are two forms: 
(1) the continuous and (2) the intermittent. 
1. The continuous form is associated with general debility, rheuma- 
tism and gastro-intestinal symptoms. Ecchymoses come and go during 
many years; the individual petechial spot disappears promptly. Epistaxis 
and gingival hemorrhages are frequent. There are always some evidences 
of purpura present but without the greater accidents which characterize 
the free crises of other forms of purpura hemorrhagica. 
2. The intermittent form of chronic purpura is more frequent than 
the continuous. In the crises there are “abortive and anomalous phenom- 
ena.” Crises may be preceded for months or years by frequent isolated PUKPURA 
547 
hemorrhages, nasal and gastric. The exacerbations are in no way distin- 
guishable from Werlhof’s disease. Slight fever may be present. Be- 
tween attacks the patient usually appears absolutely normal. Slight cause 
produces prodromal symptoms which are promptly followed by hemor- 
rhages. Recurrences have been observed covering periods of over 20 
years. Intermediary periods may be long—seven—eight and in one case 
seventeen years. 
The mode of termination is variable. Long latent periods do not jus- 
tify the conclusion that the patient is cured. Patients may die during a 
crisis. The disease cannot be considered benign. Hemorrhage is the 
cardinal symptom of all types of chronic purpura. 
The blood picture shows secondary anemia while the blood clot does 
not contract, the coagulation time is normal and the blood platelets are 
diminished. The increase of blood platelets is favorable. The results 
of treatment with rabbit serum (pi'eventing anaphylaxis) is encourag- 
ing, and while not all are permanently cured, symptoms are promptly con- 
trolled and long periods of latency may be expected to follow. The im- 
provement is often surprisingly prompt. In the chronic cases the animal 
serum is a life saving remedy. (Eisner & Meader.) In all grave pur- 
puras the absence of regenerative forms (nucleated red corpuscles) 
nrgues against a favorable prognosis. Thayer holds that hypoleukocytosis 
in the acute anemia is unfavorable as is also “the greatly increased per- 
centage of small mononuclear elements.” 
(e) Henoch*s Purpura (1874) 
Henoch’s purpura is a variety which may he associated with urticaria 
or erythema, with symptoms referable to the gastro-intestinal tract more 
or less toxemia and albuminuria very often. This variety was originally 
described by Henoch and considered clinically by Osier. The visceral 
symptoms include gastric, splenic and nephritic disturbance. The gas- 
tric and intestinal symptoms often arise suddenly, are suggestive of appen- 
dicitis, intestinal hemorrhage may be present and due to intussusception, 
vomiting and colic are frequent. My most serious cases have shown posi- 
tive evidences in the urine of nephritis. The spleen is enlarged and edema 
is not unusual. It is a doubtful question whether Henoch’s purpura is a 
primary disease, whether it is not due to intestinal infection or whether 
uremia is not responsible at times. When the complex is associated with 
chronic nephritis it usually leads to death. 
Henoch’s purpura is in reality erythematous although with increas- 
ing intestinal and visceral symptoms there may be petechiae. The com- 
plex is liable to recur and is usually found in children. The prognosis is 
good in almost all cases which are not burdened by serious complications 
(nephritis, etc.). 548 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
(f) Hemophilia 
Hemophilia is an expression of the hemorrhagic diathesis which is 
congenital, hereditary and permanent. It attacks the male members of 
families of “bleeders” and is transmitted by the female offspring of 
these to following generations. Females remain unaffected. They do 
not bleed, though their male offspring shows the classic features of the dis- 
ease early in life. These “bleeders” continue to bleed during abnormally 
long periods when they prick or cut themselves or after any mechan- 
ical insult. The cutting of the umbilical cord, circumcision, the eruption 
of a tooth or extraction may prove the hemorrhagic diathesis. In some, 
the bleeding may not occur until varying periods following birth. There 
are enormous variations in the symptomatology of hemophilia. Some 
“bleeders” may never bleed hut once, others bleed on slight cause, learn 
their tendency and with caution live to ripe old age. If the hemophilic 
lives beyond puberty the chances are that his life will not be shortened. 
With increasing years the chances of bleeding are reduced. The serious 
cases are likely to die during early childhood. There are no clinical 
anomalies which are characteristic of hemophilics. Those whom we have 
seen, who continued to bleed during adult life were anemic (chloranemia). 
The blood picture offers nothing characteristic. The coagulation time 
is reduced in hemophylics and is deficient. There is no organ which may 
not bleed; bleeding from mucous membranes is the most frequent cause 
of depletion. These include epistaxis, hematemesis, hemoptysis, intesti- 
nal hemorrhage, renal, vesical, and bleeding from ulcerated gums (ulcer- 
ative stomatitis and gingivitis). 
Pyorrhea alveolaris frequently retards the progress of hemophilics. 
Petecliiae or large surface hemorrhages may arise suddenly hut are more 
limited usually than with other forms of purpura. Joint hemorrhages 
are usually absorbed, permanent damage may occasionally follow (Ero- 
sion, anchylosis and contracture) usually there are no permanent lesions. 
The knee is the most frequent seat of hemorrhage. 
In individual cases the bleeding may continue during exacerbations 
from only one organ, as the kidney or bladder, nose, stomach or intes- 
tines. Senator’s case has become famous in which a bleeding kidney re- 
moved from a hemophilic, girl, aged 19 years, was found normal, but she 
never had recurrence of hemorrhage. 
Hemophilia is not limited to any one portion of the world, it is rare 
hut is universally distributed. Grandidier gathered the records of 93 
hemophilic families in Germany with 258 bleeders of which 22 were 
women. Bullock and Fildes in their report give a full bibliography of 
the subject. Morawitz reports the family Mampel which has been ob- 
served at Kirchheim near Heidelberg since 1827 and since that time has 
never been free from bleeders. ERYTHREMIA 
549 
References 
Bensaud & Rivet. Arch. General de Med., Jan. 24, 1905. 
Bullock & Fildes. Eugenic Laboratory Memoirs, xii, London, 1911 (Excellent bibliog- 
raphy). 
Eisner & Meader. Chronic purpura and its treatment by animal serum. Am. J. Med. 
Sci., Feb. 1913, 178. 
Grandidier. Die Hemophilia. Leipzig, 1877. 
Henoch. Vorles. u. Kinderkrankh., 10. Aufl., 839. 
Morawitz. Mohr & Staehelin, Handb. d. Inner. Med., Bd. iv, Berlin, 1912 
Naegeli. Bluterk. and Blutdiagnos. Leipzig, 1912. 
Osier. Am. J. Med. Sci., Jan., 1904. 
Practice of medicine. New York, 1914. 
Pratt. Osier’s Modern medicine, iv, Philadelphia. 
Schoenlein (J. L.). Pathol, u. Therapie. 5. Aufl., 1841. 
Senator. Berl. klin. Wchnschr., 1891, No. 1. 
Deutsch. med. Wchnschr., 1902, No. 8. 
Thayer (W. S.). Pratt [Z. c.], 697. 
Werlhof (1699-1767). Opera Medica, Hannover, 1775. 
E. Erythremia 
1. Primary Erythremia 
(Osier’s Disease, Vaquez Disease, Polycythemia vera, Plethora vera) 
Osier’s Disease is characterized by an excess of red blood corpuscles, 
an increase in the volume of the blood, the subjective appearances of ple- 
thora, with enlargement of the spleen and in all likelihood a lesion of the 
bone marrow in which the erythroblastic elements are primarily involved. 
With primary polycythemia there may or may not be cyanosis. True 
erythremia exists without known cause. It is a disease of adult life (SO- 
SO years). The prominent and cardinal symptoms of plethora vera, as 
the disease is sometimes named, are the increased number of red blood cor- 
puscles, increased volume of the blood, increased viscosity, the plethoric 
appearance of the patient and the enlargement of the spleen. Barring the 
enlargement of the spleen, the blood features of primary and secondary 
erythremia are practically identical. The striking appearance of the 
patient at once creates the suspicion of the disease; the blood count is 
confirmatory, the cautious physical examination must decide whether the 
condition is primary or secondary. 
In my last case I never found the red count below 8,000,000 per c. 
mm. Much higher counts are recorded. The characteristic color of the 
face is not materially changed in these subjects by any known treatment. 550 
DISEASES OF BLOOD A1ND HEMOPOIETIC ORGANS 
After venesection there may be less plethora but soon the regenerative 
process is stimulated and the features of the disease return. 
The enlargement of the spleen is never so great as in leukocytic leu- 
kemia. When the spleen is enormously enlarged it may he positively con- 
cluded that there is some complication. In a few authentic cases the 
liver has been found slightly enlarged. 
Destruction of large numbers of red blood corpuscles may lead to hemo- 
globinuria—a dark urine with urobilin. The disease is progressive, there 
is marked tendency to arterial degeneration (arteriosclerosis) and in 
some cases hypertension is prominent. Polycythemia as it advances may 
finally lead to dilatation of the heart and degenerative changes of the myo- 
cardium. These conditions with dropsies (edema, ascites, hydrothorax) 
are associated with albuminuria and are evidences of the terminal stage 
of the disease. 
UhthofF has reported purpuric symptoms in some of his cases. He 
found bleeding from the gums, stomach and intestines after which his 
patients were materially relieved. 
Erythromelalgia has been noted by several continental observers 
(Turk, Weintraud and others). When subjective symptoms are in the 
ascendency and persist, it may be assumed that the disease is progressing. 
The most unfavorable subjective symptoms are extreme fatigue, vertigo 
of the Meniere type (Naegeli), vomiting, somnolence and dyspnea on 
slight exertion. Albuminuria per se, without positive evidences of nephri- 
tis is usual and without decided prognostic significance. 
Persistent abdominal pain is an early symptom, usually recurrent 
and not of importance. These patients are usually obstinately constipated. 
There are atypical cases, in all of which, however, there is erythrocytosis. 
Geisbock’s polycythemia hypertonica is without perceptible enlargement 
of the spleen but with abnormally high systolic blood pressure. Morris has 
reported cases in which there was slight enlargement of the spleen but no 
polycythemia. Naegeli does not accept these as true erythremia. 
Blood Picture.—Erythrocytes.—The average count in plethora vera 
ought not to be below 7,000,000 per c. mm. and may reach to 10 millions 
or higher. Osier reports 11,600,000, Stern 13,800,000 per c. mm. 
Hemoglobin averages between 100-140. Rosengart reports 190-200. 
Color index is surprising low. The individual cells are pale. The rela- 
tive leukocytic count is not materially disturbed. There is usually a 
slight leukocytosis. In severe cases the leukocytes may suddenly or grad- 
ually increasec Osier reports one case in which there were 91,000 with 
93.2 per cent of neutrophilic leukocytes. 
Eosinophilia is present in most cases, while mast cells are according 
to most observers constantly present and strikingly increased (Morris, 
Muller). The entire quantity of circulating blood is increased as is its 
viscosity and specific gravity. The disease is insidious in its onset, is ERYTHREMIA 
551 
progressive, exceedingly chronic, the patient living many years in fair 
health. It is practically uninfluenced by medicines, save free catharsis. 
Diet has a Avholesome effect in relieving some temporarily Avliile repeated 
venesection often relieves subjective symptoms. Osier’s disease is incur- 
able, death may result from secondary complications, usually from dilated 
and insufficient heart Avith general dropsy including ascites. Hemorrhage 
into the brain or its membranes; thrombosis and infarct, invading the 
spleen are causes of death. Polycythemic patients Avhen they contract in- 
fection or are subjected to extra strain are found below par and without 
the resistance to withstand serious disease. Convalescence from insignifi- 
cant complications is abnormally slow.* 
2. Secondary Erythremia 
{Symptomatic Polycythemia) 
Secondary polycythemia may be symptomatic of any disease in which 
the blood is concentrated, in which there may be stasis due to circulatory 
obstruction or in which the lungs have not accommodated themselves to 
changed altitude or in which, because of poisoning, coal gas or drugs, as 
potassium chlorate, phosphorus, coal tar products, sulphuretted hydrogen, 
(methemoglobinemia and sulphemoglobinemia) blood changes follow. 
The leading primary diseases which lead to symptomatic plethora are 
chronic heart diseases, congenital heart defects, emphysema with right 
heart involvement, obstructive lung, laryngeal and bronchial disease, any 
disease causing chronic dyspnea, diabetes mellitus and insipidus, Asiatic 
cholera, depleting diarrhea and high altitude, besides the poisons men- 
tioned in the preceding paragraph. 
The prognosis of all of these conditions must be separately considered; 
polycythemia—the symptom—is an expression of added gravity in most 
chronic heart diseases and congenital defects and influences prognosis as 
such. It is surprising on the other hand to find with congenital heart 
lesions and many chronic diseases how comfortable the cyanosed and poly- 
cythemic subject remains during years, but how ready he is to yield to 
slight cause. In such cases the primary lesion is the cause of death, the 
erythremia is a condition which can never be credited with paramount 
significance. 
Parkes Weber in an interesting article on the Prognostic Significance 
of Secondary Polycythemia in Cardiopulmonary Cases makes the follow- 
ing statement: 
“Just as hypertrophy of the Avails of the heart is useful in so far as it 
* (Besides Osier’s classic article which placed the disease upon a scientific 
basis and gave it the name it now bears, Senator’s monograph is most instructive.) 
(See References.) 552 
DISEASES OF BLOOD AND HEMOPOIETIC ORGANS 
compensates for mechanical defects in the valvular apparatus, so also is 
polycythemia useful in so far as it compensates for difficulties in the 
proper oxygenation of the blood and tissues of the body; but just as in 
cardiac valvular disease great hypertrophy of the heart indicates some 
grave defect in the valvular mechanism, so also an extreme increase in 
the number of erythrocytes in the blood points to there being great im- 
pairment of the normal process of oxygenation of the body.” With the 
“cardiopulmonary cases,” however, with which I am chiefly concerned in 
the present paper, the prognostic significance of the polycythemia is, I 
believe, somewhat different, or rather, as I would prefer to put it, the 
outlook is exceedingly grave at the stage of the disease when cyanosis and 
a great degree of polycythemia become striking clinical features. 
With diabetes we have noted the secondary polycythemia in the more 
serious forms of the disease, usually most marked in advanced cases (See 
Diabetes Mellitus). 
The 'polycythemia following change to a high altitude is transitory in 
normal subjects and usually yields without permanent damage. Poly- 
cythemia due to chronic poisoning yields in most cases to discontinuance, 
though with acute poisoning it is always an expression of the gravity of 
its cause. The blood picture of secondary polycythemia is much like that 
of Osier’s disease, unless as sometimes happens the primary lesions may 
produce changes. Thus with pneumonia or acute infections, with Asiatic 
cholera, the leukocytic count will he markedly influenced. The poly- 
cythemia neonatorum is physiologic and transitory. 
References 
Cautley. Lancet, London, 1908. 
Geisbock. Kongress f. inner. Med., 1904, 47; also 1912. 
Morris. Johns Hopkins Hosp. Bull., 1910. 
Muller. Fol. Hemat., ix, Arch. 288. 
Naegeli. Blutkrankh. u. Blutdiagnos, 2. Aufl., Leipzig. 
Osier. Proc. of Royal Soc. of Med., 1908, 8, I. 
Am. J. Med. Sci., 1903. 
Brit. Med. J., 1904. 
Rosengart. Mittheil. Grenzgeb. Med. etc., 1903, Bd. xi, 495. 
Senator. Polyzythraemie u. Plethora. Berlin, 1911. 
Stern. Med. klin., 1908, Nos. 2 & 3; also No. 27. 
Turk. Wien. klin. Wochnschr., 1902, 163, 372; idem, 1904, Nos. 6 & 7. 
Uhthotf. Kl. Monatschr. f. Augenheilk., 1906, Bd. xliv. 
Vaquez. Soc. de Biolog., 1895, 2, v. 
Vaquez & Quiserne. Soc. de Biolog., 1902, 12, vii. 
Weber (Parkes F.). Lancet, London, May 10, 1913, 1307. 
Weintraud. Ztschr.f. klin. Med., 1904, Bd. Iv. Section V 
Diseases of the Digestive Apparatus 
A. Diseases of the Mouth 
Stomatitis * 
(a) Simple Catarrhal or Erythematous Stomatitis 
Stomatitis or acute inflammation of the mouth may be due to: 
1. “Chemical or mechanical irritation including acids, alkalis, tobacco 
and highly seasoned food.” 
2. “Chronic poisoning by mercury, arsenic or lead.” 
3. “Extension of inflammation from the neighboring parts, e. g., 
teeth, nose, nasopharynx.” 
4. “Gastro-intestinal disturbances.” 
5. “Constitutional disturbances, e. g., measles, variola, scurvy.” 
(Woodwark.) 
In mild cases the affection is limited to the gums; in the more severe 
to the buccal mucosa, the tongue and the lips. There are no marked 
general disturbances though children and susceptible adults have slight 
elevation of temperature. The sublingual and submaxillary glands are 
often swollen. The course of the disease is short, cure follows in the 
average uncomplicated case soon after the removal of the cause. With 
the infections the dryness of the mouth and salivation with local swelling 
of the mucosa and glands promptly disappear with recovery. 
(6) Aphthous Stomatitis 
Aphthous stomatitis is more severe than the simple, there is a patchy 
(gray) deposit on the lips, gums and tongue, with considerable glandular 
swelling and with the disappearance of the grayish, fibrinous deposit, 
* The surgical conditions are not treated in this work, neither are the surgical 
diseases of the nares, postnasal space or tongue. 
553 554 
DISEASES OF THE DIGESTIVE APPARATUS 
superficial but painful ulcers remain, which with cautious cleanliness 
heal in the course of four to seven or ten days. The aphthous deposit 
may cause multiple ulcerations of the buccal mucosa, the tongue, lips, 
and gums; the glands may be tender, suppuration is exceedingly rare. 
With added gingivitis, the teeth are at times loosened but are not lost. 
The inability to take food, particularly in young children, who are 
oftenest afflicted, may lead to weakness but to nothing more serious. We 
have seen children and adults in whom the disease has extended to the 
pharynx, the tonsils and tonsillar pillars who have finally shown few 
superficial deposits and ulcerations, which have promptly healed, though 
progress has been retarded by the extension. 
The epidemic form of aphthous stomatitis is separately considered 
(See Toot and Mouth Disease). 
(c) Ulcerative Stomatitis 
Ulcerative stomatitis may be either primary or secondary. The sec- 
ondary forms are associated with the diseases of childhood, including 
scarlet fever and other infections elsewhere considered. The prognosis 
depends on the virulence of the primary infection. 
Primary ulcerative stomatitis is unquestionably of infectious char- 
acter. In the severe forms fever and rapid, at times erratic, pulse 
(arhythmia) may accompany ulcerations of the buccal mucosa, the gums, 
lips and tongue. There is a characteristic odor, glandular enlargement. 
In children and adults many may contract the disease from the same 
drinking cup. In adults there is always a justified suspicion of mercury 
as the cause which demands investigation. 
The month may infect itself from the neglect of the teeth. In rare 
eases, the infection causes an erythematous eruption which creates the 
suspicion of scarlatina. The ulceration and swelling with foul breath 
not only rob the patient of appetite but make swallowing and mastication 
exceedingly painful. We have never known of a death in our experience, 
though young and feeble children (infants) are reported to have died 
of the disease. The duration averages two weeks. Hon-inf ectious (?) 
and limited ulcerations of the mouth in both children and adults heal 
readily. In some there is a strong tendency to recurrence. Cankers of 
the mouth may often prove exceedingly painful and their recurrence at 
short periods or the constant presence of one or more may make the 
patient wretched. Such cases are dependent upon an underlying cause 
which demands close investigation. When discovered (often difficult) 
recovery follows. 
Jacobi described an herpetiform stomatitis which he has found in neu- 
rotic individuals and characterized it stomatitis neurotica chronica. It is DISEASES OF THE MOUTH 
555 
exceedingly rebellious to treatment. Osier says “it may precede or accom- 
pany the fatal forms of pemphigus vegetans ” 
The Plaut-Yincent angina, infection from the fusiform bacillus, 
may limit its ravages to the gums. It is not without danger when wide- 
spread. (See Vincent’s Angina.) 
Leukoplakia Buccalis, buccal psoriasis—leukokeratosis mucosae oris 
is a condition of “patchy tongue”—the roof of the mouth, gums, lips 
and cheeks may be spotted, with whitish, grayish thickenings in patches, 
the tongue may be uneven or “wrinkled”; the tissue involved may become 
fissured. Epithelioma may develop after long periods of chronicity. 
The condition is always secondary, found in smokers usually; it is of 
syphilitic origin with but few exceptions. We have never seen a case 
in adult life which could not be traced to syphilis. Cure of the local 
lesion is the exception. It does not interfere with life save as cancer 
develops. 
Oral Sepsis (Hunter).—See Pernicious Anemia. 
Foul or fetid breath is always secondary, due either to disease of the 
teeth, pyorrhea alveolaris, tonsillar deposits, usually millet-seed sized, 
in the crypts of the tonsils, diseases of the stomach, sudden inhibition of 
digestion after emotion or shock or nasal disease. Foul breath is often 
rebellious to treatment but persistence after the recognition of the cause 
leads to cure. 
The causative relations of stomatitis—gingivitis—and pyorrhea alve- 
olaris to the arthritides and other infections are separately considered 
(See Rheumatoid Arthritis—Chronic Rheumatism, etc.). 
(d) Noma—Cancrum oris—Gangrenous Stomatitis, 
Wasserkrebs (German) 
IsToma was described by tbe older writers on medicine as afflicting 
many and after rapid progress with gangrenous destruction of the cheek 
(one or both) with all of the features of overpowering sepsis, these unfor- 
tunates usually died. At present we rarely see characteristic noma or 
cancrum oris. Our entire experience is limited to two cases. One of a 
young lady aged about 28 years who developed the disease after biting 
her cheek, the constitutional evidences of sepsis were present early, the 
gangrenous destruction was prompt and death followed in ten days in 
coma with albuminuria and casts. The odor was characteristic of gan- 
grene and the suffering intense until she became unconscious. As a 
rule there is little pain. Our second case was in a child in whom the 
process was rapid with deep sloughing of one cheek within three days and 
death with all of the earmarks of general sepsis about the sixth day. 
Kindborg reports aspiration pneumonia as a cause of death and he be- 
lieves that noma never develops in a normal mucosa. 556 
DISEASES OF THE DIGESTIVE APPARATUS 
The milder cases recover; those with deep sepsis, far-reaching gam 
grene without resistance and of tender age die. Adults may develop the 
more malignant type and die before the end of the tenth day. 
High temperature, rapid erratic and small pulse with evidences of 
toxic nephritis are all unfavorable, when together recovery is not to be 
expected. 
(e) Stomatitis Parasitica—Thrush-Soor—Muguet 
Thrush in healthy children and adults is an insignificant infection, 
dependent upon the oidium albicans. Its favorite seat is in the changed 
or diseased mucosa. Most cases may be traced to carelessness, uncleanli- 
ness of bottles, nipples or utensils. The disease is preventable. In chil- 
dren and healthy adults recovery is prompt. There are cases of tuber- 
culosis, carcinoma of the stomach, pernicious anemia and diabetes (the 
latter very often in the terminal stage) which are unfavorably influenced 
by the development of this form of stomatitis. There is always in neg- 
lected or cachectic cases danger of spread to the esophagus, stomach and 
intestines. When there is extension to the intestines obstinate diarrhea 
is often depleting. 
(0 Mercurial Stomatitis—Ptyalism 
Stomatitis with salivation following the administration of mercury 
or the use of mercury in the various occupations offers a favorable prog- 
nosis, though it often resists treatment during many weeks and may 
cause ulcerative changes from which recovery is also slow. Even small 
doses of mercury in some in whom the usual cautions have been neglected 
may lead to ptyalism. We have seen patients much reduced "by uncon- 
trollable salivation and extreme weakness has followed in some cases, but 
recovery in the average case is the rule in from two to three weeks. 
Marked anemia and slight albuminuria disappear with the relief of local 
symptoms and convalescence is rapid. In children the development of 
the teeth or the decay of those already erupted is not unusual. 
References 
Hunter (Wm.). The severest anemias. London, 1909. 
Jacobi (A.)- Tr. Ass. Am. Phys., 1894, ix. 
Kindborg. Innere Medizin. Bd. II. Berlin, 1912. 
Osier (TFm.). Practice of medicine. 8th ed. New York, 1914. 
Woodward. Manual of medicine. Oxford Med. Pub. London, 1912. DISEASES OF THE SALIVARY GLANDS 
557 
B. Diseases of the Salivary Glands 
1. Mumps 
Epidemic Parotitis 
(See Section I, The Infectious Diseases.) 
2. Parotitis 
The symptomatic parotitides are considered with the primary diseases 
which they complicate. (See Typhoid, Pyemia and other Infections.) 
Chronic parotitis is almost always a secondary disease associated with 
nephritis, syphilis or it is due to chronic poisoning, lead, mercury or iodin. 
3. Mikulicz’s Disease 
(.Bilateral Salivary Swellings) 
Mikulicz’s Disease (1888 and 1892) is a coincident enlargement of 
the parotid, lacrimal and buccal glands which is chronic, continuing 
many years and is of uncertain origin. In America the disease is rare, 
though several cases have been reported. The organic changes in the 
glands usually persist in spite of treatment. Osier reports the case of a 
girl of eleven, with enlarged spleen, death resulted from chronic tuber- 
culosis and “before death the enlargement of the salivary glands had 
disappeared—the lacrimal glands were completely sclerotic.” 
A recent article by Thursfield calls attention to the cases “which 
illustrate all stages of gradation between the strict type (cases with in- 
volvement of the lacrimal and salivary glands without changes in the 
lymphatic glands and in the blood) and those in which there is a positive 
picture of leukemia or lymphosarcoma. 
It is possible for cases which originally show the characteristic coin- 
cident enlargement of the parotid, lacrimal and buccal glands, to develop 
grave blood changes and present in the terminal stages, with grave 
anemias, more particularly leukemia. In these cases many lymph nodes 
are enlarged throughout the body and there are organic changes in the 
spleen. Most of these cases retain the bilateral swelling of the salivary 
glands. 
Brunn’s classification, in which the “Mikulicz symptom complex” 
was the leading feature and which must serve to prove the association 
of grave blood changes in a number of cases also corroborate the con- 
clusions of Senator, Stock, Dunn and Thursfield, that the complex may 
be a phenomenon of leukemia. 558 
DISEASES OF THE DIGESTIVE APPAKATUS 
Brun’s classification follows: 
“I. Cases without alterations in the blood. 
A. Without swelling of the spleen or lymphatic glands. 
(a) Symmetrical swelling of the lacrimal and 
salivary glands. 
(b) Symmetrical swelling of the lacrimal glands 
alone. 
(c) Symmetrical swelling of the salivary glands alone. 
B. With swelling of the spleen or lymphatic glands. 
(a) Symmetrical swelling of the lacrimal and 
salivary glands. 
(b) The same with infiltrations of the skin. 
II. Cases with alterations in the blood. 
A. Severe anemia with lymphatic pseudoleukemia and 
aplasia of the bone marrow. 
B. Leukemia.” 
Occasional cases of the complex show a marked hereditary influence. 
Quincke reports the case of a man, aet. 45, with congenital enlargement 
of both parotids whose father, two uncles, five brothers and two sisters 
showed the same anomaly. 
Tuberculosis, gout and syphilis may he coincident with the complex 
and influence prognosis materially. Thursfield, whose observations are 
exceedingly valuable, makes the following statement: 
“When there is no involvement of the lymphatic glands or spleen 
and no alteration in the blood, the disabilities of the affection seem to 
be confined to the disfigurement, and to a certain degree of discomfort 
from both of which the lapse of time, one to five years as a rule, releases 
the patient. When the lymphatic glands or the spleen are enlarged the 
outlook is more uncertain; of Howard’s twenty “pseudoleukemic” cases, 
six died; and of the definite leukemic cases, Stock’s patient alone sur- 
vived more than six months.” 
The removal of the enlarged lacrimal glands (Elliott) influenced 
the salivary enlargements in one case. 
References 
Osier. Practice of medicine. 7th ed. 
von Brunn. Beitrage zur ldin. Chirurgie. Tubingen, 1905, xlv, 225. 
Dunn. Howard, Transactions, College of Phys. Philadelphia, 1893. 3d series. 
Elliott & Ingram. Ophthalmoscope. 1911. 
Howard. Transactions, College of Phys. Philadelphia, 1893. 
Osier. Practice of medicine. 7th ed. DISEASES OF THE PHARYNX 
559 
Quincke. Munch, med. Wchnschr., 1906, liii, i, 1213. 
Senator. See Thursfield & Howard [l. c.]. 
Stock. Klin. Monatsbl. fur Augenheil., Stuttgart, 1906. 
Thursfield. Quart. J. of Med., Oxford, April, 1914, p. 237. 
C. Diseases of the Pharynx 
(The infectious diseases of the pharynx, including the tonsils, are 
considered in Section I, Infectious Diseases.) 
1. Circulatory Anomalies 
(a) Hyperemia of the Pharynx.—Congestion of the pharynx may 
depend upon primary disease, results from local irritation or it may he 
secondary; it may be either acute or chronic. Acute hyperemia accom- 
panies the eruptive diseases of childhood, hence its sudden appearance 
suggests vigilance and search for infection. In the adult irritating 
chemicals, highly seasoned or abnormally hot foods, colds, nasal irrita- 
tion, prolonged or abnormal use of the voice may cause transitory 
hyperemia. 
Chronic hyperemia is due to circulatory, obstructive, chronic local 
disease or other factors which continually act as irritants. The circu- 
latory disturbances which are paramount are chronic heart lesions, aneu- 
rismal pressure, emphysema with heart changes and bronchitis, tumors 
of the neck or mediastinum. Chronic pharyngitis and nasal diseases cause 
continuous hyperemia. Tobacco and alcohol are the most frequent fac- 
tors in causing chronic pharyngeal hyperemia. 
(b) Hemorrhagic symptoms may be due to the hemorrhagic diathesis, 
purpura, local disease, traumatism and occasionally to vicarious men- 
struation. 
(c) Edema of the pharynx (uvula and soft palate, peritonsillar tissue) 
is usually of inflammatory origin with tonsillitis or peritonsillitis, when 
the prognosis is good. It may be an evidence of stasis (circulatory), 
pressure, or with nephritis and general edema it may prove threatening. 
2. Pharyngitis 
(a) Acute Pharyngitis. 
Acute catarrhal pharyngitis is a common disease, which almost always 
gets well within a few days. It is an accompaniment of many infections 
which latter, when it remains limited, are not affected by it. With 
rhinitis and tonsillitis it is rarely absent. It is often the earliest symp- 560 
DISEASES OF THE DIGESTIVE APPARATUS 
tom of the infectious diseases of early life (exanthemata) though it may 
be primary and due to any of the causes mentioned in connection with 
acute hyperemia. The inhalation of all kinds of dust frequently pro- 
vokes it. 
(6) Chronic Pharyngitis 
Preceding acute neglected pharyngitis, tobacco and alcohol, nasal and 
postnasal diseases, the prolonged use of the voice (clergymen, lecturers, 
etc.) are the leading causes of chronic pharyngitis. The prognosis is 
favorable before the changes in the mucosa are not too far advanced for 
relief of symptoms. 
Pharyngitis sicca is never cured until its cause, usually in the nose 
or postnasal space, has been removed. 
(c) Ulcerative Pharyngitis 
(See Syphilis, Tuberculosis, Foot and Mouth Disease and the various 
infections which it complicates.) The prognosis depends upon the ability 
to remove its cause. 
(d) Phlegmonous Pharyngitis and Retropharyngeal Abscess 
Phlegmonous pharyngitis and retropharyngeal abscess are always 
secondary, often threaten life by local swelling—edema and associated 
involvement of the larynx (edema of the glottis). Phlegmonous tonsil- 
litis and peritonsillitis involve the pharynx and postnasal space. Sepsis, 
meningitis, otitis media and mastoiditis are among the dangerous sequelae, 
also toxic nephritis. In rare cases mediastinitis and pneumonia have 
ended life. 
Phlegmonous pharyngitis with erysipelas or any other infection is 
never to be lightly regarded. Retropharyngeal abscess may follow injury 
of the mucosa from foreign bodies; its greatest dangers are descending 
extension, associated compression, edema and pneumonia. It is always 
a surgical affection, the favorable outcome depends on the nature of its 
cause, early recognition and radical treatment. Disease of the cervical 
vertrebrae, usually tuberculosis, fracture or other bone changes, when 
associated with retropharyngeal abscess, make the outlook bad. 
(e) Ludwig’s Angina 
(Angina Ludovici) 
Ludwig’s Angina (first described by Ludwig in 1836) is a phleg- 
monous inflammation of the connective tissue of the neck, involving, as 
a rule, the deep and superficial tissue on one side in the submaxillary DISEASES OF THE PHARYNX 
561 
region, though in severe cases it may extend downward and to the oppo- 
site side. It is always of infectious origin, is a sequel of streptococcus 
infection, scarlet fever, infection from contaminated milk (epidemic 
streptococcus), typhoid and diphtheria. There are cases which are with- 
out known primary cause, others which follow injury and infection. The 
history of these cases prove that with deep constitutional infection, wast- 
ing disease and lowered vitality, there may he and often is a prompt 
sepsis, phlegmonous and gangrenous breakdown of tissue and deep in- 
volvement of the sensorium, rapid and feeble pulse, with albuminuria. 
In such cases the prognosis is grave and life may be in danger for several 
days. The phlegmonous periparotitis and involvement of the deep fascia 
of the neck with septic scarlet fever prolongs convalescence and with 
feeble pulse, nephritis and uremia present a serious complex. Edema 
of the fauces or glottis or both is always alarming. Idiopathic cases if 
treated radically early, as a rule, recover slowly after varying periods 
of sloughing and repair. Ludwig’s angina shows marked tendency to 
gangrene within the phlegmonous area. Sepsis and nephritis cause the 
death of a large proportion of such cases. The mortality of the disease 
is high—the danger period follows several days of slight febrile move- 
ment without cerebral symptoms. In unfavorable cases there is a sudden 
exacerbation of symptoms, collapse, dyspnea, 'cyanosis, pharyngeal and 
laryngeal edema, unconsciousness and cardiac insufficiency. Ludwig 
reported such cases which died before there was time to offer assistance. 
Dyspnea (asphyxia) is the prominent and threatening symptom. Unless 
these cases can be reached by surgical means they promptly die. A rally 
should not deceive the clinician, for relapse and sudden death may fol- 
low it. Aspiration bronchopneumonia, pleurisy, edema of the larynx, 
sepsis, and cardiac toxemia are the leading causes of death. 
In pure Ludwig’s angina the mouth is always infiltrated and Thomas 
bases his differential diagnosis on this fact. This is not the case with 
other forms of cellulitis (scarlet fever) which are considered by many 
(Osier, etc.) as Ludwig’s angina. 
Broad of Syracuse has partially reviewed the history and literature 
of this subject in a paper not yet published and has fully reported a 
case which terminated favorably. We have taken the following data 
from Broad’s paper: 
Davis reported 10 cases with a mortality of 40 per cent. 
Sharkey’s mortality w7as per cent. 
Thomas reported 106 cases with 43 deaths—40 per cent mortality. 
Naturally the percentage of recoveries varies materially if we include 
the neck infections which are phlegmonous following scarlet fever and 
other infections, many of which recover. These are not included in the 
above figures. 562 
DISEASES OF THE DIGESTIVE APPARATUS 
References 
Broad (G. B .). Not yet 'published. 
Davis. Am. J. Med. Sci., Feb., 1904. Annals of Surgery, 1906. 
Ludwig. Med. Cor. Bl. d. Wurtemb. artl. Ver., Stuttgart, 1836, vi, 21-25. 
Nelaton. Bull, et mem. Soc. Chirurg., 1892. 
Osier. Practice of medicine. 8th ed., 1914, p. 466. 
Parker. Lancet, London, 1879, ii, 572. 
Schwartz. Bull. Soc. de Med. Prat, de Paris, 1889, 314-321. 
Semon. Brooklyn Med. J., 1905. 
Sharkey. St. Thomas’s Hosp. Reports, 1890-91. London, 1892. (New Series) xx, 247— 
256. 
Thomas. University of Pennsylvania Med. Bull., March, 1908, p. 2. (Good bibliography, 
but incomplete.) 
D. Diseases of the Tonsils 
{Suppurative Peritonsillitis, Quinsy, Acute Streptococcus Tonsillitis, 
Vincent's Angina, Chronic Tonsillitis) 
(See Section I, Infectious Diseases.) 
E. Diseases of the Esophagus 
1. Acute Esophagitis 
Inflammatory or ulcerative changes of the esophagus are: 
(a) Catarrhal (i. Acute or ii. Chronic). 
(b) Pustular. 
(c) Phlegmonous. 
(d) Croupous. 
(e) Diphtheritic. 
(f) Ulcerative. 
(g) Corrosive. 
(h) Varices. 
The majority of inflammatory or ulcerative changes in the esophageal 
mucosa are due to thermic insults, chemical irritants, foreign bodies or 
inflammatory conditions accompanying other diseases. 
(a) Catarrhal Esophagitis 
i. Acute.—The acute catarrhal inflammation of the esophagus is usu- 
ally so mild as to give rise to no symptoms. When extensive and deep, as DISEASES OF THE ESOPHAGUS 
563 
it is at times with catarrhal bronchitis, tracheitis, pharyngitis, and acute 
nasopharyngeal infections and tonsillitis, the membrane is congested, 
there is epithelial desquamation and some dysphagia. The pathologic 
process follows the stages of acute catarrhal inflammation and unless 
there is some serious underlying disturbance it runs its course in a few 
days and leaves the tube intact. 
ii. Chronic Esophagitis.—Chronic esophagitis (catarrhal) leads to 
thickening of the mucosa and submucous tissue with hypertrophy of the 
muscularis. With alcoholic gastritis it may prove an annoying compli- 
cation, particularly if limited to the cardiac end when with productive 
change, stricture may develop. In rare cases polypi form. 
After acute esophagitis due to corrosive poisons, carbolic and mineral 
acids, caustic potash, arsenic and other destructive lesions, chronic 
esophagitis may develop with final narrowing of the tube. The evidences 
(subjective) may be long postponed in such cases. The obstructive symp- 
toms and physical signs (obstruction to the passing of the sound into the 
stomach) are often in evidence when the patient presents. Only surgical 
interference helps these cases. Many are not threatening and live with 
moderate narrowing of the tube many years. In some cases after caustic 
poisons have been swallowed, esophageal and aural lesions develop late 
and are persistent. One of our cases is living over 30 years after swal- 
lowing ammonia with deafness and chronic esophagitis. 
(6) Pustular Esophagitis 
Pustular esophagitis is secondary to grave infection, as a rule, and 
is often part of serious constitutional disturbance. Smallpox with which 
pustules form in the esophagus is usually of the malignant type, though 
not always, and the complication is by no means always fatal. Pustular 
esophagitis may develop with other infections. The prognosis is not 
materially influenced by the complication in the majority of cases. It is 
the primary process upon which the forecast rests. In smallpox the 
eruption may be present in the mouth, fauces and esophagus at the same 
time. In most of these ulceration and cure follow. 
(c) Phlegmonous Esophagitis 
This may follow from descending extension of phlegmon of the 
pharynx; it may be associated with poisoning or infection which disrupts 
the esophagus—usually septic processes. Sepsis and pyemia often cause 
infiltration, change in the superficial and deep structures of the esoph- 
agus. Phlegmonous disease associated with any constitutional infection 
is always grave, at the same time exceedingly painful. 564 
DISEASES OF THE DIGESTIVE APPARATUS 
(d) Croupous Esophagitis 
Croupous disease of the esophagus may be associated with croupous 
inflammation in other organs, as croupous pneumonia, croupous laryn- 
gitis and rarely there are membranous deposits which are primary— 
independent entirely so far as we are able to conclude of deposit elsewhere. 
Croupous esophagitis is usually of streptococcus origin and may be sec- 
ondary to streptococcus tonsillitis. With most of these conditions the 
prognosis is good, though as in other forms, most depends upon the nature 
of the primary infection. 
(e) Diphtheritic Esophagitis 
This form of esophagitis is less frequent since the introduction of 
the antitoxin for diphtheria, though occasionally in neglected or malignant 
cases, we find the membranous deposit in the esophagus. 
The prognosis depends on the nature and extent of the infection as 
well as on its virulence and the patient’s resistance (See Diphtheria, 
Section I, Infectious Diseases). 
(f) Ulcerative Esophagitis 
Ulcerative esophagitis may be cancerous. It may develop in infants 
while nursing; with long continued disease decubitus ulceration may 
prove painful and serious. Decubitus ulcers usually form in the depleted 
who are emaciated from chronic disease (nervous, tuberculous, chronic 
and subacute infections of all kinds) and are usually located hack of the 
cricoid cartilage which by pressure against the esophagus causes the “bed 
sore,” for it is that in reality. 
Peptic ulcers of the lower end of the esophagus are rare but may 
form and in the process of healing may cause cicatricial contraction. 
Perforation is exceedingly rare from ulcer, it is a fatal complication 
(See Rupture of Esophagus). Esophageal ulcers are often tuberculous 
or syphilitic (See Tuberculosis and Syphilis). 
The .prognosis of all ulcerative esophagitis depends on the primary 
cause—the corrosive ulcer often heals but stricture is to be feared. 
(g) Corrosive Esophagitis 
The corrosive may be associated with the phlegmonous form or it 
may exist alone, it is usually grave. The shock which follows the taking 
of a corrosive poison is always great. The changes are usually deep and 
in children and weak adults the prognosis is often bad. Naturally the 
extent of the corrosion and shock depends upon the kind of poison and 
dose. In very young children with chronic stricture after swallowing DISEASES OF THE ESOPHAGUS 
565 
corrosive poison the prognosis is unfavorable. We have seen one life 
saved by the establishing of a gastric fistula in the case of a girl not older 
than four years with a closed esophagus following the taking of caustic 
potash. She has lived, so far as we know, now over 20 years, feeding 
herself through the fistulous opening. If the stricture is fortunately lo- 
cated modern surgery offers some hope. 
(h) Varices .of the Esophagus 
Varices of the esophagus often form from long continued circulatory 
obstruction with chronic heart lesions, pressure, Banti’s Disease and with 
liver cirrhosis. Their presence can only he suspected during life when 
there is rupture and consecutive hemorrhage or when seen, through the 
esophagoscope. The dangers are rupture and depleting hemorrhage. I 
lost one Banti from erosion of a good sized varix. 
2. Spasm and Paralysis of the Esophagus 
(a) Spasm of the Esophagus 
(Esophagismus) 
Esophagismus or spasm of the esophagus is of rare occurrence. It is 
usually of neurotic—hysterical—origin, alarming to the patient hut 
without danger and, as a rule, of short duration. The patients are usu- 
ally robust and young. The spasm is sudden in its onset and at once 
closes the esophagus to solid food, often to liquids as well. In women 
the associated fear and ungeared nervous condition are, with the spasm, 
the leading features. Reassurance and suggestion are sufficient in most 
cases to quiet the patient and overcome the spasm. Any psychic impres- 
sion in some, as the passing of the stomach tube, particularly in young 
hysterical subjects, proves sufficient to overcome the symptom. There is, 
in most cases, recurrence on slight cause and occasionally esophagismus 
may alternate with spasm of the glottis (laryngismus stridulus), or both 
may he present together. The element of suggestion proves a powerful 
factor in the production and the relief of symptoms. 
Kindborg mentions incipient cancer as a cause of esophageal spasm. 
We have never met with a like case. 
Paralysis of the esophagus is likely to he associated with diphtheritic 
paralysis in children, occasionally in the adult (see Diphtheritic Paral- 
ysis). Its prognosis when not a part of extensive paralysis of other 
organs, is not bad. Esophageal paralysis with brain {tumor') and spincu 
(b) Paralysis of the Esophagus 566 
DISEASES OF THE DIGESTIVE APPARATUS 
lesions, lesions of the spinal bones, remains unchanged, simply one of 
many symptoms. The same is true of ascending paralysis (Landry’s Dis- 
ease). 
3. Stricture of the Esophagus 
Stenosis or stricture of the esophagus may be either (a) extra- or 
(b) intra-esophageal. 
Extra-esophageal stricture is due to compression from without; tumors 
of the neck, enlarged glands, cystic growths, aneurismal dilatations, medi- 
astinal pressure; tumors (malignant or non-malignant) of the lung and 
pleura, diseases of the spinal vertebrae associated with tumor formation, 
abscess, caries or malignant disease of the spine itself, diverticulum of 
the esophagus, peri- and para-esophageal abscesses, malignant masses 
springing from the sternum or ribs, pericardial and pleural effusion are 
among the leading causes which by pressure or torsion narrow the lumen 
of the tube. Only the removal of the cause, which is almost always im- 
possible, can overcome the stricture. 
(a) Extra-esophageal Stricture 
(6) Intra-esophageal Stenosis 
Over 60 per cent of all strictures of the esophagus are malignant— 
carcinomatous—and lead to death unless recognized early. Even the 
early recognition offers practically no hope though surgeons are extend- 
ing their knowledge and improving their technic and a few are recom- 
mending radical interference (See Willy Meyer’s Report of Cases, etc.). 
There are benign growths of the esophagus which cause narrowing of its 
lumen—these are usually cicatricial following causes which have been 
mentioned in connection with the various diseases of the esophagus and 
the productive changes which may follow. Some of these live many 
years, comparatively comfortable, when constriction is not too great. 
Most strictures are at or near the cardia, some hack of the cricoid car- 
tilage. Stricture of the esophagus when it has existed even a limited 
time, if very narrow, leads to dilatation above the point of constriction. 
The presence or absence of Meltzer’s 'phenomenon (Schluck and 
Spritzgerausch) is of no value in prognosis, though of considerable diag- 
nostic value in individual cases when correctly interpreted. The phe- 
nomenon is not present in all cases and according to our experience may 
in the same case be heard at one time and not at another. The greater 
the dilatation, as shown by the x-ray or by the amount of fluid or food 
which it holds, the greater is the obstruction and the more difficult will 
it be to nourish the patient. We rarely find malignant stricture mul- DISEASES OF THE ESOPHAGUS 
567 
tiple. The dilatation above the stricture is at once associated with nar- 
rowing below and collapse of the intestines with, in chronic cases, atrophy 
of the muscular coat of the stomach and intestines also atrophic changes 
in the glandular structures. The cachexia, and secondary anemia are in 
direct proportion to the primary and secondary lesions and the consecutive 
failure to nourish the patient. 
Symptoms of esophageal stricture after 40, without previous history 
of esophagitis or ulcer always creates a strong and justified suspicion of 
cancer. The prognosis of stricture from whatever cause is promptly 
given, for we have but to consider its pathology. In cases of doubtful 
origin, non-malignant—the ability to get sufficient food into the stomach 
either through the esophagus or gastric fistula will soon solve the problem. 
Progressive malnutrition, heart weakness and exhaustion is the fate 
of all of these patients in whom the constriction is extreme. 
Congenital stricture leads to death wdien complete during the early 
days of life. In other rare strictures though more frequent than the 
complete occlusion, the lower part of the esophagus opens into the trachea 
or into a bronchus. We have never met a case in our practice. Thomas 
(William) has collected 19 cases from medical literature. 
4. Cancer of the Esophagus 
Neoplasms of the esophagus are, as a rule, cancerous—epithelioma. 
The lower end of the tube is usually invaded and the growth is annular 
and constricting. At times the esophagus infiltration is limited and the 
progress is slow and during a considerable period the stricture may be only 
partial. We have seen cases in which the growth was so exceedingly slow 
as to make the diagnosis doubtful. If the cancerous mass is large, the 
wall of the esophagus and the surrounding structures (glands, etc.) are 
infiltrated. Metastases may or may not be numerous. Pressure symptoms 
under such conditions are not relieved and may lead to prompt death. 
In some cases there is sufficient growth to lead to pressure on the left 
recurrent laryngeal nerve with paralysis which persists until death. 
Slight improvement in swallowing may at times prove misleading as may 
also the vagaries of the disease. With extreme constriction the patient 
may be able to take solid food during limited periods and be almost com- 
pletely “closed” in the intervals. Ulcerative changes in the growth may 
make it possible to get more food into the stomach than had previously 
entered. Alcoholics are subject to cancer of the esophagus; the disease is 
more frequent in men than women; it is a disease of middle life and is 
usually primary. 
Osier reports 38 cases of cancer in the medical wards of the Johns 
Hopkins Hospital in 23 years. During the past six years we have seen 
8 cases of cancer of the esophagus in 6,300 cases of internal disease. 568 
DISEASES OF THE DIGESTIVE APPARATUS 
We refer the reader to our consideration of cancer as a cause of 
stricture of the esophagus in this section and repeat what we emphasized, 
that x-ray examination will lead to localization and will reveal the extent 
of secondary esophageal changes in most cases. The esophagoscope is a 
valuable adjunct in the hands of the expert. 
Fibrous thickening of the esophagus is secondary to conditions men- 
tioned in this section. 
Lipomata and polypi are rare—with newer methods these are recog- 
nized. We have never met either in our practice. 
There can be but one conclusion—the prognosis of esophageal cancer 
is bad, patients die of starvation usually, though complications, as with 
cancer elsewhere, may end life. The average duration of life in our 
cases has been between 12 and 18 months after the beginning of subjective 
symptoms. Unquestionably most cancers of the esophagus are tolerated 
during long periods before their presence is suspected or cause symptoms. 
Metastases may never follow esophageal cancer, on the other hand, a 
small carcinoma may have multiple metastases—often more than the 
larger growths. Metastases to the mediastinal glands, also enlargement 
compressing the thoracic duct (Gerhardt) hasten death. Secondary nod- 
ules may form in the esophagus itself. 
Gerhardt also calls attention to the relative frequency of the associa- 
tion of esophageal cancer and pulmonary tuberculosis. 
5. Rupture of the Esophagus 
Rupture of the esophagus is exceedingly rare. The wall of the esoph- 
agus may rupture as the result of softening (Zenker). Emphysema 
promptly follows whenever there is esophageal rupture from whatever 
cause. Traumatism—gunshot wounds, stab wounds, and the ulcerative 
and infiltrating conditions associated with esophagitis, ulceration and can- 
cer mentioned in this section may occasionally lead to rupture. Death 
follows rupture promptly in almost all cases from collapse with marked 
dyspnea, and widespread emphysema. Perforation or rupture of the 
esophagus may cause periesophageal suppuration. Aspiration pneumonia 
may follow fistulous openings into the trachea or into a bronchus. Per- 
foration into the pleura or pericardium leads to death from effusion and 
added pressure. Pneumothorax has complicated perforation. 
6. Dilatation—Diverticulum 
(a) Dilatation 
In connection with esophageal stricture we called attention to the 
dilatation of the esophagus above the point of closure. This is the in- DISEASES OF THE ESOPHAGUS 
569 
variable result in almost all cases which live any length of time. The 
extent of the dilatation is a safe guide in deciding upon the degree of 
narrowing. Rontgen pictures and the stomach tube will prove of mate- 
rial assistance. 
(b) Diverticula 
Diverticula of the esophagus may he acquired or congenital. Some 
forms are multiple, giving rise to small dilatations here and there, causing 
but few symptoms. Particles of food are likely to fall into the diverticula 
and cause symptoms. Weakness of the esophageal wall is one cause of 
dilatation (local) or diverticulum formation. This is the “pressure diver- 
ticulum” or e<Pulsionsdiverticulum.,> The local dilatation increases be- 
cause of the pressure and retention of food and is most likely to form at 
the junction of the esophagus and pharynx. Pulsionsdiverticulum may 
dilate to such an extent as to cause pressure symptoms, indeed constrict 
the esophagus itself when food is held without entering the stomach. The 
condition is purely surgical. Food is often regurgitated, emptying the sac 
with temporary relief. 
Traction diverticula are not, as a rule, of great clinicial significance. 
They result either from congenital defects—“embryonal preformed con- 
nective tissue strands” which form because of incomplete separation of 
the trachea and esophagus (Ribbert) or they are secondary to inflammatory 
changes in the lymphatics, which cause adhesions and consecutive con- 
nective tissue contraction which draw upon the esophageal wall causing 
the localized dilatation. Their presence may not be suspected until a 
foreign body is caught, ulcerates, causing perforation with consecutive 
suppuration, mediastinitis and death. Uncomplicated and limited, the 
presence of the traction diverticulum may never be suspected and is found 
post mortem. 
References 
Aschoff. Path. Anatomic. Jena, 1913. 
Gerhardt. von Mehring and Krehl. 8. Aufl. Jena, 1913. 
Kindborg. Innere Med. Bd. II, Berlin, 1912. 
Meltzer (S. J.). Berl. klin. Wchnschr., p. 361,1884, xxi, 1888, xxv. 
Meyer (Willy). Transact. Am. Gastro-enterve Ass., 1914. 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Ribbert. Virchow's Arch., etc. Bd. 184, anfl preceding volumes. 
Lehrbuch, Patho. u. path. Anat. Leipzig, 1908. 
Thomas (Wm.). On Congenital occlusion of the esophagus. Lancet, London, 1904. 
Zenker. Krankheiten der Speiserohre. In: v. Ziemssen Handb., p. 143. 570 
DISEASES OF THE DIGESTIVE APPARATUS 
F. Diseases of the Stomach 
1. Acute Gastritis 
Gastritis may be either (1) acute or (2) chronic. There are several 
forms of acute gastritis, as follows: 
(a) Acute Catarrh of the Stomach 
Acute catarrhal inflammation of the stomach is one of the most fre- 
quent of all internal diseases. It is, when uncomplicated, a benign catar- 
rhal inflammation which produces symptoms only of acute indigestion 
(gastricismus) which yield in the course of two to four days without leav- 
ing a remnant. It follows dietetic errors, the taking of excessively hot or 
cold foods, may result from exposure, sudden atmospheric changes, is an 
accompaniment of anemia and debility. The acute alcoholic 'gastritis is 
toxic and is considered elsewhere. The association of catarrhal gastritis 
with duodenitis may cause jaundice (See Catarrhal Jaundice) and post- 
pone recovery. The stomach contents in most cases of catarrhal gastritis 
offers nothing of value. In aggravated cases the free hydrochloric acid 
may be reduced, the digestion is tardy; there may be acetic and butyric 
acid, a few blood corpuscles and increased mucuSi 
(6) Infectious Gastritis 
The infectious type of gastritis follows the ingestion of contaminated 
food or may be due to an endemic in which many are attacked at the 
same time (probably streptococcus). Catarrhal grip may also be pres- 
ent at such times. During epidemics of true grip the influenzal type of 
gastritis or infectious gastritis is frequently met. Such cases include 
symptoms which make the patient uncomfortable (localized pain, localized 
tenderness, vomiting, nausea, hypersecretion, “bilious” vomitus, with the 
usual malaise and weakness of influenza). 
Infectious catarrhal conditions of the nasal and upper respiratory 
passages as well as the pneumonias may be associated with gastritis. With 
all of these conditions the localized stomach infection is not usually of 
paramount importance but the primary disease and the patient’s resist- 
ance are most important in offering a forecast. In old people and in the 
weak the added infection of the stomach may help to undermine resistance 
but such influence is exceedingly rare as the stomach changes are few 
and superficial. 
(c) Phlegmonous Gastritis 
Phlegmonous gastritis is exceedingly rare. Associated with the grave 
infections as typhoid fever, smallpox, pyemia, sepsis and abscess, it com- DISEASES OF THE STOMACH 
571 
plicates already existing serious disease, and adds to the dangers. With 
puerperal fever and with caustic poisons or erysipelas, the complication is. 
extremely grave. 
id) Membranous Gastritis 
Membranous gastritis is almost always of diphtheritic origin, there- 
fore, secondary and is exceedingly rare. There may be no subjective symp- 
toms of stomach invasion or there is pain, tenderness, vomiting, tense abdo- 
men, particularly in the epigastrium. The heart is rapid and offers the 
leading prognostic data. The temperature cannot be relied upon because 
it may not be materially influenced by the complication. The malignancy 
of the primary infection and general condition of the patient, including 
the heart, make prognosis certain. In the favorable cases convalescence be- 
gins with the third week. 
(e) Toxic Gastritis—Corrosive Gastritis 
Acute alcoholic gastritis is one of the most frequent of all the diseases 
of the stomach mucosa. It is simply one of several changes wrought by 
the poison and with proper care promptly yields to treatment. Most alco- 
holic toxic gastritis is superficial and catarrhal, is associated with great 
nervousness—unrest and insomnia—at times albuminuria—but all of these 
symptoms, unless there are marked depression, heart and other nervous 
symptoms and lesions, yield. The persistent use of alcohol leads to chronic 
changes (chronic gastritis). Other poisons which cause gastritis include 
the mineral acids, alkalis, lead, mercury, phosphorus and arsenic fre- 
quently. 
The caustic and corrosive effect of these poisons with the associated 
shock and kidney involvement often promptly lead to death. In these cases 
there are deep changes in the mucosa and prompt degeneration of the heart. 
The decomposition of albuminous substances, either directly or through 
the circulation, may cause threatening symptoms of toxic gastritis. Alt has 
attributed gastritis to the excretion of toxalbumins by the stomach in chol- 
era and Lauder Brunton and Favrer suggested its production by the ex- 
cretion of the cobra venom. Alt confirmed their suspicion. The vomiting 
in many general infections may be traced to primary toxemia and secondary 
gastritis (Brunton). 
(/) Acute Gastritis with Organic Diseases of the Stomach 
The presence of acute gastritis with organic diseases of the stomach: 
during exacerbation is among the possibilities and may account for some 
of the symptoms which are evanescent. The permanent symptoms are often 
%n expression of final chronic changes in the mucosa. 572 
DISEASES OF THE DIGESTIVE APPARATUS 
(;g) Acute Gastritis of Fungus Origin 
Acute gastritis of fungus origin (yeast, anthrax, favus and the Oidium 
albicans) is only persistent when neglected. The same may be said of 
gastritis due to the presence of animal parasites. 
(h) Acute Suppurative Gastritis 
There are rare cases of acute suppurative gastritis in which there is 
perigastritis with abscess formation in the'wall of the stomach. The evi- 
dences of profound pyemia—sepsis—are prominent and death is the rule. 
With the suppurative there may also he phlegmonous gastritis. 
Children often suffer from recurring acute gastritis with fever which 
continues only during a few hours or from one to two days. These attacks 
are due to faulty diet or other trivial causes in those who are said .to have 
“weak stomachs” or “poor digestion.” With the advent of the 6th or 8th 
year the intervals between the attacks grow longer and cease entirely usu- 
ally after the tenth year. There are adults who are subject to the same 
acute exacerbations of short duration at long intervals. Cautious differen- 
tiation is necessary as some of these are due to chronic appendicitis, gall- 
stones, are of central or spinal origin (cerebral syphilis, tabes dorsalis, etc.). 
The diagnosis of acute gastritis is not always easy, and prognosis there- 
fore becomes fallacious. The experiences of the past two decades prove 
the frequent presence of stomach symptoms “gastritis”—“acute dyspep- 
sia” in a surprisingly large number of abdominal and other conditions, in 
which the stomach is absolutely normal. 
2. Chronic Gastritis 
(Chronic Catarrh of the Stomach, Chronic Dyspepsia) 
Chronic catarrh of the stomach is an inflammation of the mucosa char- 
acterized by marked increase of mucus, changes in the gastric juice and 
in the advanced cases hypertrophy of the muscular coat; increasing thick- 
ening and proliferative change in the mucosa, atrophy of the gastric fol- 
licles and decided proliferation of the submucous tissue. Polypoid and 
cystic growth may develop. In some cases there is no hypertrophy of the 
muscularis but a weakening and dilatation of the wall. In a minority of 
cases the productive change leads to cirrhosis of the stomach. 
Cirrhotic Gastritis 
(Brintons Disease, Linitis cirrhotica) 
In this form of the disease the interstitial overgrowth predominates, 
the stomach is abnormally small and there are atrophic changes in the 
infiltrated mucosa upon which in individual cases multiple polypi may rest. DISEASES OF THE STOMACH 
573 
Productive change in cases of stomach cirrhosis may cause pyloric obstruc- 
tion and simulate carcinoma; the cirrhotic stomach may also simulate in- 
filtrating cancer. 
The forms of chronic gastritis which we consider are either parenchym- 
atous, interstitial or there may he mixed types in which lesions are irreg- 
ularly disseminated and are both parenchymatous and interstitial. There 
are but few cases of long continued gastritis in which the interstitial 
changes do not largely predominate and with the advance of the process 
there is loss of tone, motor insufficiency with final dilatation. We have 
seen cases in which after years of insult to the stomach the atrophy has 
been so extensive as'to leave but little remnant of the original mucous 
membrane (anadenia gastrica). Gastritis may be (a) primary or (b) 
secondary. 
(a) Primary gastritis is usually attributable to the patient’s own fault; 
alcohol, excessive drinking and eating are the leading etiologic factors. 
Poisons and irritants, improperly prepared food, faulty preparation of 
the food in the mouth for the stomach (faulty mastication, fast eating) 
irregularity in eating are also sufficient to start and continue primary gas- 
tritis. 
(b) Secondary gastritis depends upon other and primary organic dis- 
ease of the stomach, cancer, pyloric obstruction and dilatation, long con- 
tinued atony of the stomach wall and circulatory faults causing chronic 
enlargement of the mucosa from valvular diseases of the heart, pulmonary 
diseases (emphysema, chronic pneumonoconiosis, asthma, malignant 
growth or pressure, etc.). Kidney lesions with chronic uremia (chronic 
nephritis, etc.), obstruction within the portal circuit, syphilis, pernicious 
anemia and many other grave primary diseases. In the secondary gas- 
tritides the added stomach invasion is weakening, often an important 
factor, though the primary disease usually causes general stasis hence prog- 
nosis becomes a complex problem but always rests on the paramount influ- 
ence of the initial and responsible lesion. Often secondary gastritis de- 
pending on primary incurable disease may improve materially; there may 
with heart lesions be long periods without symptoms. The gastric features 
vary as do physical signs and symptoms when the primary condition is in- 
fluenced by rest and treatment. Cases in which chronic gastritis is associ- 
ated with or secondary to cirrhosis of the liver may be far advanced in or- 
ganic change and yet with latency of the latter disease and proper care, 
life may be made comfortable and indefinitely prolonged. We often find 
post mortem evidences of both conditions in subjects who had, during 
many years discontinued alcohol. 
In chronic gastritis there is usually subacidity though there are cases 
with normal acidity and as Boas has demonstrated there is a characteristic 
type in which there is hyperacidity {gastritis acida or hyperpeptica) or 
hyperacidity may be present temporarily. 574 
DISEASES OF TIIE DIGESTIVE APPARATUS 
The symptoms which predominate comprise the complex of chronic dys- 
pepsia. I do not consider chronic dyspepsia a disease per se hut always 
a complex of either primary or secondary gastritis or an accompaniment of 
other disease with complicating gastritis or faulty gastric function. (The 
Nervous Dyspepsia of Leube.) The symptoms of chronic catarrhal gas- 
tritis, including the excessive production and morning vomiting of mucus, 
anorexia, pyrosis, epigastric pressure, at times pain, persistent nausea, with 
irregular bowels, coated tongue, all aggravated and continued by the pa- 
tient’s indiscretions (alcohol, faulty eating, etc.) even in advanced cases, 
may yield to rational treatment and temperance. It is surprising to note 
how promptly these symptoms yield. The change does not indicate a 
return of the gastric mucosa to normal but the insult discontinued, the 
remnant of tissue with the assistance of the intestinal digestion proves 
sufficient. The mucus secretion in such cases, particularly the alocholic, 
will be fairly well controlled. Such cases are always ready to relapse on 
slight provocation particularly on the return of the original cause. 
The nervous manifestations in the above mentioned cases are usually 
as readily controlled as are the other symptoms. 
The examination of the stomach contents in chronic gastritis is of con- 
siderable value in deciding upon the type of gastritis present, but for 
prognosis it offers hut few data save in those forms in which it establishes 
the advanced atrophy of the gastric follicles and complete anadenia gastrica 
or achylia gastrica with or without primary constitutional disease (per- 
nicious anemia, diabetes mellitus). In all of these cases the microscopic 
examination is important. The presence of nuclei in the epithelial cells is 
suggestive of acid gastritis (Stockton). The presence of large quantities 
of mucus in the vomitus or expressed content is not per se unfavorable for 
the relief of symptoms. The majority of such cases are dependent upon 
removable causes (alcohol, etc.). 
Hyperacidity with gastritis acida is at times rebellious to treatment and 
when relieved tends to recur on cause but in the end it is controlled but 
only with the assistance of the patient. 
During the early stage of alcoholic gastritis hyperacidity is frequent. 
Unless conditions are improved there is progression with gradual reduction 
of free hydrochloric acid and other evidences of disturbed function, par- 
ticularly motor insufficiency. The presence of free HCl in the empty stom- 
ach in these cases often persists during long periods until with the advanc- 
ing atrophy the acidity falls and there is increase of organic acids (lactic, 
butyric and acetic). 
Anadenia or Achylia Gastrica.—The anadenia gastrica of Ewald or 
achylia gastrica offers evidences of far reaching atrophy with, in most 
cases, normal motor function. Anacidity in chronic gastritis does not 
Stomach Contents DISEASES OF THE STOMACH 
575 
always indicate atrophy of the mucosa for it may he due to gastric neu- 
roses. 
Pepsin and rennin are usually present and vary with the free HC1. 
Single examinations of the stomach contents are not always depend- 
able. The secretion often varies from day to day and faulty conclusions 
are reached unless repeated examinations are made. In many, psychic 
factors are potent in influencing stomach function. There is usually a 
large psychic element which demands consideration in connection with the 
examination of the stomach contents in the alcoholic as well as in some 
cases of gastritis which are of secondary origin. 
Chronic Gastritis.—The extreme nervous state of the alcoholic with 
acute exacerbations of chronic gastritis is often controlled with great dif- 
ficulty. Such patients are usually steady drinkers and not a few develop, 
wet brain (Alcoholic Meningitis). With the nervous symptoms there may 
be “stomachal vertigo,” a condition which Trousseau described, patients, 
fear the “sinking into an abyss” ; vertigo may be of the labyrinthine type; 
melancholia, hypochondriasis, changed disposition, erratic heart, 
morning cough, hiccough, dysphagia and asthma with cyanosis may all 
yield with the improvement following proper diet and abstinence in pri- 
mary cases and improvement of underlying conditions in secondary gas- 
tritis. 
Remissions and exacerbations are to be expected in all forms of primary 
gastritis depending largely on the habits of the patient. Many alcoholics 
live for years without subjective symptoms, who finally develop them. 
Such cases are controlled with great difficulty. The blood picture in those 
forms of anadenia or complete atrophy may resemble pernicious anemia 
or with cirrhosis of the stomach and thickening of its coats, with palpable 
small stomach there may be a strong suspicion of carcinoma. Such cases 
may, with proper treatment, improve materially for as with all gastritides, 
however far advanced, the digestive function of the intestinal tract may 
prove sufficient to supplement the gastric. It will be noted in all organic 
diseases of the stomach that symptoms are long tolerated without revolt, 
that digestion proves sufficient to carry the patient along without loss of 
flesh or many subjective symptoms during long periods while the organic 
changes are advancing insidiously. 
The changed and degenerated or infiltrated mucosa in chronic gastritis 
never becomes normal. It may be so little changed as to cause no serious 
disturbances. Symptoms may disappear during interminable periods, peri- 
ods of remission may be short, permanent cure, i. e., regeneration of peptic 
glands, removal of new connective tissue is not to be expected. Once the 
subjective symptoms are present they may, in spite of improvement or re- 
mission be expected to recur on slight cause. 
Alcoholic Gastritis.—Alcoholic gastritis which has existed during long 
periods may, after only short abstinence, show marked improvement and 576 
DISEASES OE THE DIGESTIVE APPARATUS 
with continued abstinence may never again give rise to symptoms. The 
improvement following treatment is promptly manifest in many cases. 
With motor and absorptive faults and pyloric obstruction from interstitial 
thickening the dilatation which follows is likely to remain; the general con- 
dition depends upon the ability of the intestines to supplement the work of 
the stomach and the direct result of the gastrectasia. The duration of 
uncomplicated primary gastritis in which the atrophy of the follicles is 
not too far advanced, and does not progress may be many years. Gastritis 
without other organic diseases without advanced atrophy, detected early 
and properly treated, may never give rise to symptoms, in spite of the 
changed mucosa. 
The complications of primary gastritis are few and of no prognostic 
import. The many primary conditions which lead to secondary gastritis 
are each likely to be associated with conditions which must naturally influ- 
ence prognosis independent of the existing gastritis. Severe secondary gas- 
tritis, uncontrollable vomiting, and toxic symptoms sometimes threaten 
cases in which resistance has been reduced. We have never known death 
to be due to chronic gastritis alone though the general condition is often 
below par and efficiency is reduced. 
I know of no other chronic disease in which rational treatment and 
the cooperation of the patient in primary cases so promptly and thoroughly 
control symptoms. Symptoms of "chronic dyspepsia” without stomach 
lesions may remain uncontrolled and lead to faulty diagnosis in a large 
number of cases unless great caution is used. Most of these are due to 
chronic appendicitis, gall-stones, cirrhosis of the liver, or spinal lesions, 
mainly tabes dorsalis. 
References 
Alt. Berl. klin. Wchnschr., 1889. Munch, med. Wchnschr., 1892, 89-41. 
Boas. Wien. med. Wchnschr., 1895, 1 and 2. 
Brunton-Lauder. Allbutt & Rolleston, System of Medicine. Vol. III. London, 1907. 
Fayrer. Proc. Royal Soc., London, 1872-73, xxi, 358; 1873-4, xxii, 68. 
Stockton. Diseases of the stomach. New York, 1914. 
Trousseau. Clinical medicine. Paris. 
3. Dilatation of the Stomach—Gastrectasia 
According to Ewald the stomach which continually holds more than 
1,600 c.c. of fluid is abnormally dilated. Such stomachs are found to hold 
food longer than seven hours. 
Dilatation of the stomach may be either (a) acute or (b) chronic. 
(a) Acute Dilatation of the Stomach 
My experience with acute distention of the stomach beyond its nor- 
mal capacity has been limited to its occurrence with chronic disease, acute DISEASES OF THE STOMACH 
577 
infections and following anesthesia, usually for abdominal conditions. 
The gastrectasia in all of these cases has been sudden in its onset, has at 
once been associated with symptoms of failing heart and collapse, vomiting 
of large quantities of fluid, pinched features and—unless the condition was 
at once correctly interpreted and treated—death followed. 
I have found acute dilatation of the stomach an occasional serious 
complication of pneumonia. If it arises suddenly during the height of 
the disease it may promptly lead to death. 
Sudden gastrectasia with pneumonia and chronic valvular disease is 
usually fatal. Fussell has recently reported his experiences with this dan- 
gerous complication. In all of Fussell’s cases the autopsy showed con- 
striction of the duodenum at the root of the mesentery. 
There is in all probability involvement of the innervation leading to 
dilatation, this in itself causing by traction a constriction of the duodenum. 
Fagge’s original description of these cases was based upon his observa- 
tions in a case in which the patient had overeaten, and with classic symp- 
toms died in collapse. Connor of Cincinnati reported 102 cases of which 
42 followed anesthesia. In the midst of typhoid fever, as in pneumonia 
or with chronic heart lesions, without added infection, blows upon the 
abdomen or from any other cause unless the symptoms are promptly re- 
lieved by lavage of the stomach and stimulation, recovery is exceedingly 
rare. It is possible for patients convalescing from acute infections to sud- 
denly fall into collapse from dilatation of the stomach, when with peristaltic 
unrest, marked splashing and collapse with all of the usual physical signs, 
their lives are threatened. Relief must be prompt, for unrelieved, death 
follows in a few hours. We have had no experience with suddenly arising 
dilatation in spinal disease. Connor’s cases showed the usual high mor- 
tality, practically 75 per cent. The prognosis is favorably influenced by 
the early lavage and turning the patient on the side to encourage the 
emptying of the stomach. The latter maneuver alone (without lavage) 
is of little value. Of 31 patients treated with medicine alone without 
posture or tube, 29 died; in 142 cases after operation the mortality was 
54.9 per cent according to Borchgrevink, who found that in 70 cases treated 
with the tube and following Moynihan’s advice to turn the patient on the 
right side, the mortality was 26.9 per cent. Meltzer suggests that the 
dyspnea with frequent swallowing of air without saliva may be a factor in 
the production of the dilatation. 
(6) Chronic Dilatation 
Chronic dilatation of the stomach is rarely primary; when it is, it may 
he characterized as myasthenic or atonic, and according to Boas represents 
“motor insufficiency of the first degree Primary myasthenic dilatation 
is usually due to the patient’s own fault—errors of diet, fast and in- 578 
DISEASES OF THE DIGESTIVE APPARATUS 
ordinate eating, the excessive drinking of fluids (alcohol, beer, tea, coffee 
and water). There are primary myasthenic dilatations which are con- 
genital; families are found in whom all members are afflicted. Dilata- 
tion which is chronic and due to myasthenia or atony, may be materially 
improved by treatment, but it is likely to recur and often leads to continu- 
ous ill health and persistent dyspepsia. When due to nervous influences 
which can be controlled unless the stomach wall is abnormally thin and the 
condition of long duration, the prognosis is good for the relief of symptoms 
but more or less dilatation usually remains. Enormous and unexplained 
gastrectasia is often found in the insane, with wasting diseases, diabetes, 
and in tabetics. 
Atonic dilatation which can only be explained on the theory of myasthe- 
nia without organic change, is often associated with nervous symptoms 
which are persistent and exceedingly annoying. They often include the 
complex of neurasthenia and in women, oftener than in men, continue un- 
influenced by any treatment. In both there is a large element of sugges- 
tion which continues and is responsible for many of the subjective features. 
Stomachal vertigo (Trousseau-Friedenwald) is exceedingly annoying 
in this form of dilatation as it is in chronic gastritis. It is unquestionably 
of toxic origin. Boerhave recognized it; Trousseau first described its 
leading features; Boas, Eriedenwald and Pick have all insisted on its toxic 
origin. 
The observers mentioned in the preceding paragraph found atony of 
the stomach and intestine the leading cause of stomachal vertigo. Enor- 
mously large stomachs—gastromegaly—may continue unchanged through- 
out life, without causing symptoms. The motor and digestive functions 
remain undisturbed. 
Secondary Chronic Dilatation 
Dilatation of the stomach which is secondary and chronic is dependent 
upon obstruction. The obstruction is either benign or malignant. There 
are a number of extragastric lesions which by compression or traction lead 
to secondary dilatation of the stomach. Whenever from any cause there 
is constriction of the pylorus, the stomach wall makes an extra effort to 
empty the organ and hypertrophy of the muscularis results, and with 
moderate non-malignant disease, may, during unlimited periods prove 
sufficient, giving rise to no or few symptoms. When the stomach is forced 
to overcome increasing obstruction, its musculature suffers; degenerative 
changes may follow in its wall; there is increasing consecutive dilatation. 
The degree and amount of secondary change depend entirely upon the 
extent and nature of the obstruction. If the obstruction cannot be over- 
come by mechanical or surgical means, complete insufficiency follows, and 
the stomach is continuously distended with undigested and irritating solid DISEASES OF THE STOMACH 
579 
and liquid food. With these cases the toxic and nervous symptoms are in 
the ascendency and long periods of ill health and the neurasthenic complex 
are thereby explained, though not always relieved. 
In all of these cases lavage is likely to relieve the subjective complaints; 
unless the primary cause can be removed or overcome, subjective and 
objective manifestations can only be treated symptomatically. These cases 
when neglected may develop tetany which is always threatening, demand- 
ing immediate care. Lavage may prevent the spasms during unlimited 
periods (See Tetany). There are chronic cases in which changes of a 
degenerative character or inflammation secondary to serious constitutional 
anomalies lead to muscular insufficiencies and consecutive dilatation. 
Such cases are not materially influenced by treatment. 
The organic constriction at the pylorus, either intra- or extragastric, 
produces motor insufficiency of the second degree and provokes persistent 
symptoms of dyspepsia. 
The prognosis of secondary dilatation of the stomach can only be of- 
fered with the separate consideration of the responsible lesions. The 
chapters which follow (Benign and Malignant Stenosis of the Pylorus, 
Ulcer of the Stomach, etc.) offer the necessary data which justify the 
forecast. 
Boas. Diseases of the stomach. (Translated by Bernheim.) Philadelphia, 1908. 
Connors (Lewis 4.) Am. J. Med. Sci., Philadelphia, 1906, xxi, 579-617. 
Ewald. Eulenberg Realencykl. 3. Aufl., Bd. 14; also his work on diseases of the stomach. 
Fagge. Guy's Hospital Reports, 1873, vol. 18. 
Friedenwald (/.). Med. News, New York, Dec. 23, 1892. 
Fussell. Am. J. Med. Sci., Dec., 1911, p. 794- 
Pick 04.)* Wien. klin. Wchnschr., 1892, 46-47. 
Stockton. Diseases of the stomach. New York, 1914. 
Trousseau. Gaz. des Hopitaux, 1862. Med. Clin, des Hotel Dieu, 1868. 
References 
4. Gastroptosis—Enteroptosis 
(Glenard’s Disease, Visceroptosis) 
Glenard’s disease is a condition in which there is ptosis of the abdom- 
inal viscera, gastrectasia, gastroptosis, enteroptosis, often prolapse of the 
liver and spleen, with—in a large number of cases—mobile kidney. There 
is, in most cases a train of prominent nervous manifestations, often but 
few gastro-intestinal symptoms. The neurasthenic complex is always in 
the ascendency and is the leading feature, besides the physical signs of the 
disease. While incorrect dress (lacing, etc.) may increase prolapse 
in individual cases, there is, as a rule, a predisposition to Glenard’s dis- 
ease and this is greatest in the children of neurotic parents, themselves 580 
DISEASES OF THE DIGESTIVE APPARATUS 
nervously overwrought. Any anomaly which removes the normal support 
of the abdominal organs—child-bearing, laceration of the perineum, injury 
to the abdominal wall, ventral hernia following laparotomy, abnormal 
“ligamentous and cartilaginous support” (Stockton)—may lead to pro- 
lapse of the abdominal viscera. The congenital loose attachments of the 
mesenteric and peritoneal supports are leading features. 
Stiller has demonstrated the absence of the tenth costal cartilage in 
a large number of cases of Glenard’s disease. We have been surprised 
by the frequency of this anomaly, the marked and persistent neurasthenia 
in such cases. The absence of the normal dorsolumbar curve is considered 
by R. R. Smith as a leading feature of enteroptosis, and both Smith and 
Goldthwait agree that the condition is of hereditary origin. Great caution 
in diagnosis is necessary, for Rontgen pictures have proved the fact that 
most adults have more or less enteroptosis and we are of the opinion that 
too many x-ray pictures are faultily interpreted to the injury of the patient 
(Holzknecht-Groedel). We are fully agreed with Stockton who in his 
recently published works says “ . . . insufficient value is attributed to the 
effect of gravity in dragging down viscera weighted with bismuth.” 
We are fully convinced that cautious physical examination of the 
abdominal viscera offers the most valuable data for diagnosis and prog- 
nosis which should in doubtful cases be confirmed by the Rontgen rays, 
but the latter need interpretation by the specialist who is not biased by 
preconceived notions or uncertain theories. We have, in lean subjects, 
frequently obtained valuable data from inflation of the stomach and rectum 
with carbonic acid gas or air. Auscultatory percussion is also of great 
value. 
Splashing is a symptom of value only as it is considered with other 
physical methods and x-ray in doubtful cases. The most difficult cases 
are those in which without cause, save inherent defects, we find the fully 
developed Glenard’s process with overpowering neurasthenia, at times 
psychoses, which are borderline; in all an overpowering autosuggestion 
which holds the patient without thought of anything but self. Often there 
are imperative conceptions which make life almost unbearable. Mobile 
kidney is as a rule a permanent defect and in most cases causes no symp- 
toms ; its presence when disregarded or unrecognized by the patient will 
be well borne during years, often forever. 
Treves, with others, has found that the larger number of “anchored” 
kidneys finally loosen from their moorings and are, after a few years, as 
movable as before. There are exceptions but they are few, and the con- 
sensus of opinion today favors support without operation. 
DietVs crises are exceedingly painful and when frequent may interfere 
with the general health of the patient besides leading to morphinism. 
These cases are favorably influenced by mechanical treatment or radical 
surgical operation. DISEASES OF THE STOMACH 
581 
The twisting of the ureter may cause repeated intermittent hydro- 
nephrosis, not a serious complication, for with positive diagnosis and 
surgical treatment, after scientific differentiation (cystoscopy, uretero- 
scopy) the condition may be overcome. The functional tests should in- 
clude the consideration of both kidneys. The circulation is often erratic 
and functional disturbances are not unusual; there may be palpitation and 
arhythmia with, in some cases venous engorgement. Many of these 
symptoms are promptly relieved by support or postural treatment. They 
return on slight cause. 
Chronic constipation is the bane of these cases and cathartics are taken 
by the majority. Support, diet and rational treatment improve many 
of these. 
The prognosis so far as life is concerned is always good ; the neuras- 
thenic symptoms in uncontrolled cases (usually in women, though men are 
frequently included) are likely to persist unchanged until after the years 
of greatest sexual activity, after which we have found enormous improve- 
ment. The element of suggestion with proper support, right living and 
occupation, are the paramount factors which influence the lives of these 
patients (See Neurasthenia). 
Glenard (F.). Les ptoses viscerates. Paris, 1885. Lyon Med., 1885, xlviii, 449. 
Groedel (Franz). Grundriss Atlas der Rontgendiagn. Munich, 1909. 
Holzknecht. Wien. med. Wchnschr., Jg. 63, Nr. 32. 
Stiller. Archiv f. Verdauungskr., 1896, ii, 285. 
Stockton. Diseases of the stomach. New York, 1914. 
Treves (Sir Frederick). Allbutt’s System of medicine, 1897, iii, 587; also London Prac- 
titioner, Jan., 1905. 
References 
5. Pyloric Obstruction 
Stenosis of the Pylorus.—Pyloric obstruction, or stenosis, may he either 
benign or malignant. The malignant stenoses of the pylorus are consid- 
ered with cancer of the stomach. 
Benign Stenosis of the Pylorus 
Benign stenosis of the pylorus may he either (a) functional or (b) 
organic. The latter may be (I) congenital or (II) acquired. 
Functional stenoses are found in the highly neurotic, and are transi- 
tory. Pyloric spasm may be chronic and lead to gastrectasia with intol- 
(a) Functional Stenosis 582 
DISEASES OF THE DIGESTIVE APPARATUS 
erant stomach, peristaltic unrest and hyperacidity. These patients are 
made worse by mental distress; they are often neurasthenic. While the 
spasm does not continue indefinitely, the gastrectasia may persist and the 
spasm is likely to recur on slight cause. 
Intermittent hyperchlorhydria without ulcer may cause pyloric spasm 
and temporary obstruction; in such cases the pains (always present), large 
fluid hyperacid vomitus, severe headache and other cerebral symptoms, 
yield to proper treatment. The symptoms persist until the hyperacidity 
is overcome. 
Acute dilatation depending on transitory causes (obstruction due to 
traction) has been separately considered (See Gastrectasia). 
Pyloric spasm may be safely considered secondary in most cases, and 
its presence should lead to a strong suspicion of organic disease. In young 
neurotic girls pyloric spasm may be associated with moderate gastrectasia, 
and there may he peristaltic unrest, painful cramping of the stomach, with 
or without vomiting. With increasing methods of precision, functional 
stenosis of the pylorus will be found less frequent. 
(b) Organic Stenosis 
(1) Congenital Stenosis of the Pylorus 
If congenital stenosis is of moderate degree, manhood may be reached 
in comparatively good health; nature may compensate for the defect, 
the stomach musculature increasing and digestion continuing practically 
normal (compensatory hypertrophy). 
Serious congenital stenosis proves its presence in symptoms before 
the fourteenth day—never after the ninth week—and death follows before 
the fourth month unless the infants are relieved by surgical interference. 
Cases which appear extreme may (rarely) yield unexpectedly. One of 
our cases, with symptoms beginning at birth, in which the child during 
the first two years of life presented all of the symptoms of congenital 
stenosis (before the days of the x-ray), has grown to manhood, perfectly 
well. When this boy was one year old he weighed less than he did at birth. 
Persistent vomiting in children beginning after the ninth or tenth 
week of life, is not due to congenital narrowing of the pylorus, and offers 
a better prognosis than does the vomiting of stenotic origin. 
Most children with congenital stenosis die before the end of the third 
or fourth month. 
No possible modification of the food relieves the symptoms when the 
stenosis is of high degree. Congenital incomplete stenosis of the pylorus 
causes chronic disturbances which continue throughout life. 
Stagnant food is always present in the stomachs of these patients. 
Dilated stomach persists in spite of well regulated treatment, lavage, etc. 
Gastric fibrosis of Ilanot or the hypertrophic pylorus of Cruveilhier DISEASES OF THE STOMACH 
583 
and Andral are sequelae which materially influence the size and position 
of the organ. 
(II) Acquired Stenosis—Intrapyloric 
1. Chronic Cicatricial Stenosis.—The majority of benign stenoses are 
due to ulcerative processes invading the pylorus. Ulcers may exist with- 
out causing symptoms; usually the history is direct and convincing. 
Cicatricial contraction follows slowly; in many there is the history of 
hemorrhage. The stomach contents, the x-ray and the tube confirm the 
dilatation and primary lesion. 
Phlegmonous sloughing due to corrosive poisoning and contraction 
cause dilatation. The prognosis in otherwise normal adults is excellent 
following surgical interference. 
2. Fibrotic Stenosis.—(a) General Stenosis.—General stenosis was de- 
scribed by Brinton and Hanot (See also Brintons Disease or linitis 
plastica or cirrhosa). The change is far-reaching in the mucous and sub- 
mucous coats of the stomach, invading the pylorus as the process advances, 
leading to marked contraction and thickening of the entire organ with al- 
most complete closure of the stomach outlet. Pernicious anemia may be 
simulated—also cancer. Surgery offers the only hope of relief in extreme 
cases. 
(b) Localized Stenosis. Localized fibrous thickening of the pylorus 
is likely to be annular. Previous limited ulceration may be the cause. 
Ring-shaped constriction causes consecutive dilatation. These cases are 
also favorably influenced by radical treatment. 
3. Hypertrophic Stenosis of Cruveilhier.—Hypertrophic stenosis of 
Cruveilhier fully described by Boas, follows chronic gastritis; there is 
ultimate dilatation. The prognosis depends upon the general condition 
of the patient and the ability, if the symptoms are threatening, to with- 
stand surgical interference. Most cases are not so extreme that they 
demand radical treatment and may live for years without it. 
4. Stenosis Dependent upon Active Ulcer.—Ulcer at or near the 
pylorus and in the first part of the duodenum with associated spasm, 
marked swelling which may be acute or due to secondary inflammation, 
is an occasional cause of pyloric constriction and offers a good prognosis. 
5. Acute Inflammatory Stenosis.—Acute inflammatory stenosis asso- 
ciated with infection, deep seated gastritis and acute poisoning may sub- 
side unless the changes are sufficiently deep to give rise to permanent 
lesions (Eisner). 
6. Syphilitic Stenosis.—Syphilitic stenosis is occasionally found; when 
extreme and the treatment radical, improvement may follow. Syphilis is 
a frequent cause of stomach symptoms which are transitory, disappearing 
on treatment, but if secondary dilatation follows it remains but little 
influenced. 584 
DISEASES OF THE DIGESTIVE APPARATUS 
7. Tuberculous Stenosis.—Tuberculous stenosis is rare and is not lim- 
ited. The process is far-reaching and involves the entire stomach. 
8. Stenosis dependent upon non-malignant growths, fibromyoma, ade- 
noma and polypi may prove puzzling; they are rare and are diagnosticated 
either during surgical interference or post mortem. 
9. Stenosis due to distortion or traction causing acute pyloric ob- 
struction (Kussmaul, Aufrecht and Riegel), dragging at a point in the 
horizontal part of the duodenum, is practically identical with acute dila- 
tation already considered. These cases are always serious (mortality 75 
per cent). (See Acute Dilatation of Stomach.) 
Extrapyloric Stenosis 
“It is difficult to divine all of the unusual and unexpected conditions 
which may lead to extrapyloric organic stenosis” (Eisner). The leading 
extrapyloric lesions which constrict the pylorus are: perigastritis, gall- 
stones, adhesions to neighboring organs—particularly to the liver and gall- 
bladder—distortions due to innumerable anomalies and pathologic changes 
invading the organs already mentioned, also the pancreas and kidney. The 
pylorus is constricted, and motor insufficiency with dilatation results. 
We have reported monstrous gall-stones which by pressure and adhe- 
sions caused stricture with symptoms of cancer (Eisner). It is at times 
exceedingly difficult to recognize the cause of extrapyloric stenosis; in 
the majority of cases diagnosis and prognosis are possible and with modern 
surgical technique the cause is often removed. Each case demands sepa- 
rate consideration that the underlying cause may be discovered and con- 
sidered. 
In the prognosis of pyloric stenosis we must cautiously differentiate 
benign and malignant disease. The diagnosis of constriction must always 
be suspected when the fasting stomach is distended and contains food. 
Food remnants after seven hours prove motor insufficiency and suggest 
obstruction. The obstruction creates a decided disproportion between the 
stomach's taste and its ability to perform its duty (Riegel). 
Dangers from tetany are separately considered (See Tetany). 
With advancing disease the heart may become ungeared; it influences 
the length of life in cases which are not amenable to surgical treatment. 
The stomach content which shows gradual loss of HC1 from time to time 
with the addition of organic acids as the free ITC1 disappears, evidences of 
fermentation must lead to a strong suspicion of malignancy and argues 
against benign disease. Large quantities of indican in the urine and an 
abnormally high urea output are suggestive of malignancy, and argue 
against benign constriction. 
X-ray examination proves exceedingly valuable, for it localizes lesions, 
outlines the stomach, and with the results of thorough physical examination DISEASES OF THE STOMACH 
585 
and the chemical analysis of the stomach contents makes a forecast reason- 
ably certain. 
With incomplete obstruction, persistence, prophylactic treatment and 
diet, will often hold the disease without advance. Diet requires special 
care, because of the weakened motor function and obstruction, that food 
may be forwarded beyond the point of resistance for further digestion. 
If this can be accomplished, life may be prolonged many years in the 
absence of complications. 
The prognosis is improved in proportion to the ability of the attendant 
to prevent stagnation and the formation of organic acids. This means 
that the distended stomach must be assisted, so far as it is possible, to 
empty itself. In no other disease of the stomach will detail and clear 
judgment with the full appreciation of the primary cause of the stenosis 
accomplish so much. 
References 
Andral. Clinique Medical, Paris, 1823-7. 
Aufrecht. Centralbl. f. klin. Med., Leipzig, 1893, xiv, 478. 
Boas. Deut. med. Wchnschr., Berlin, 1894, xx. Diagnosis u. Therapie der Magenkrank. 
Leipzig, 1890-93. (Translated Philadelphia, 1907.) 
Brinton. Brit. & For. M. Chir., London, 1857, xix, 212-470. 
Diseases of the stomach. 1872. (German Transl., Wurzburg, 1872.) 
Cruveilhier. Atlas of Pathol. Anat., 1838; also vol. i, 1829-1835. 
Eisner. Clinical features of the benign stenoses of the pylorus. New York Medical News, 
July 22, 1905. 
Kussmaul. Archiv f. Verd. Krankh., 1902; also vol. viii, 2d series, Index Catal. Surg. 
Gen.’s Office. 
Riegel. Erkrank. des Magens. Vienna, 1908; also Philadelphia, 1903. 
Deutsche med. Wchnschr., 1894, xx, 383. 
Deutsche Klinik, 1901, v, 85-120. 
Ztschr. f. klin. Med., 1886, Bd. ii. 
6. Gastric and Duodenal Ulcer 
(Ulcer of the Stomach, Peptic Ulcer, Round Ulcer of the Stomach') 
Symptoms.—Round ulcer of the stomach is characterized by circum- 
scribed loss of the mucosa, which when it becomes chronic shows but slight 
tendency to heat. 
History.—Our first conception of the disease dates from 1829 when 
Cruveilhier fully described it. The early literature is most interesting and 
proves how full was the knowledge which the clinicians possessed before 
our modern refinements of diagnosis were introduced. Following Cruveil- 
hier, Rokitansky, the great pathologist at Vienna (1804-1874), wrote a 
classic treatise on ulcus ventriculi. Virchow in 1853 advanced the theory 
that the break in continuity of the mucosa depended upon a quantita- 586 
DISEASES OF THE DIGESTIVE APPARATUS 
tive anomaly in the elaboration of free hydrochloric acid caused by 
vagus disturbance and that the circumscribed ulcer (limited) was associ- 
ated with a local anomaly with the choking of the circulation. 
In 1858 Brinton’s work appeared; Trousseau in 1860 followed and 
prepared the foundation for rational medical treatment; the same year L. 
Miller, a practicing physician in Minden, published as Leube says, the 
best treatise which we possess on the disease; 1864 brought Bamberger’s 
work, 1878 Lebert’s. Later Leube proved the overpowering influence of 
rest, diet, and rational treatment in the majority of cases, since which 
time the works of Riegel, Ewald, Boas, in Germany, in the domain of 
medicine, the Mayos, Rodman, Musser, Stockton, Jacobi in America, 
Robson and Moynihan in England, stand out in bold relief among the 
thousands of contributions dealing with the surgical and medical prob- 
lems, many of which are still unsettled. All of this activity has led to 
many positive conclusions—better than all else, to the saving of human life 
because of our appreciation of the dangers of complications and sequelae, 
and their conservative, often radical attack. 
General Considerations.—The forecast of stomach ulcer depends upon 
its type and depth, the local secondary changes, the resistance, the blood 
state, the complications, and the time when treatment (dietetic, medical or 
surgical) is instituted. 
Aschoff’s hemorrhagic erosions cause small multiform tissue loss; the 
erosions are round and sharply defined, usually located in the fundus; 
there are but few or no lesions at the pylorus. These hemorrhagic ulcers 
were supposed to be of embolic origin, but in the light of recent experiences 
this theory has been questioned. Septic and fat emboli may certainly cause 
hemorrhagic infarct, and venous emboli (Aschoff) have been considered. 
Hemorrhagic erosions are rarely found in adults, almost always in in- 
fants. When found in the adult they follow abdominal operations; they 
may cause subjective symptoms during a short time preceding death. 
Their formation is usually a terminal feature. The loss of blood connected 
with hemorrhagic ulceration is not large and is not a factor in prognosis. 
The infection or toxemia in these cases remains the prominent feature. 
Large hemorrhage into the mucosa may in the adult lead to acute mul- 
tiple ulcers in the fundus and at the pylorus. The posterior wall is their 
favorite seat. Fatal hemorrhage even from small ulcers is possible; the 
stomach is filled with blood and the ulceration is found to be deep, not 
simple as in the cases considered in the previous paragraph. These cases 
jare in all likelihood mycotic; they may follow traumatism, thrombosis 
(secondary to coronary thrombosis, to gall-bladder infection, thrombosis 
of the cystic vessels or embolic closure of the artery). With arteriosclerosis 
and nephritis, acute ulcer of the stomach has formed (Hauser, Ophuls). 
Whatever the method of formation, the majority of acute ulcers heal leav- 
ing sufficient evidences to prove that possibility in the light colored cica- DISEASES OF THE STOMACH 
587 
trix, usually superficial, which rarely causes secondary motor insufficiency 
or stenosis. In a 'proportion of cases the chronic round ulcer results from 
the acute. 
Aschoff makes the positive statement that “the chronic ulcer almost 
always originates after an acute defect.” The question, therefore, is not 
how does a chronic ulcer originate but under what conditions is the “acute 
defect” transformed to produce it. 
Between 85 and 90 per cent of chronic ulcers are found at or near 
the pylorus. The duodenal ulcers are near the pylorus in the first and 
second portion of the duodenum. Twenty per cent of Mayo’s cases in- 
volved the margin of the pyloric ring. 
The thorough observations and recorded experiences of surgeons dur- 
ing the past decade, particularly those of the Mayos, Moynihan, Deaver, 
Robson and others, who have had control of an enormous material which 
has been scientifically examined and treated, have revolutionized our ideas 
concerning many points bearing on diagnosis, prognosis, and rational treat- 
ment of all necrobiotic processes leading to gastric or duodenal ulcer. 
Facts Which Influence Prognosis.—The theories which have been en- 
tertained in the past concerning the formation of the ulcer have received a 
severe shock from the experimental work of Rosenow, Rosenau and Ander- 
son, which tend to prove that ulcer is of infectious origin. For our pur- 
poses in considering the prognosis of both gastric and duodenal ulcer it 
would be a work of supererogation to consider the many theories which 
have been advanced. We can only base our prognostic data on incon- 
trovertible facts and these prove that: 
(а) Ulcer of the stomach is most frequent in anemic or chlorotic 
women, between the ages of 20 and 40. Sixty per cent of all stomach 
ulcers are found in women. In these young subjects the stomach mucosa 
heals readily after injury or abrasion and simple uncomplicated ulcer is 
likely to heal. The older subjects are much more liable to relapse as the 
reparative powers are more feeble. 
(б) While the experiments of Rosenow point strongly to the infectious 
origin of ulcer, we are not yet ready to accept that theory without ques- 
tion—neither is he—but agree that ulcer of the stomach is always asso- 
ciated with an acid condition, usually hyperacidity (Ewald). There may 
be subacidity. 
(c) Ulcer of the stomach is a condition which may exist without caus- 
ing subjective symptoms; such ulcers may heal and the cicatrices are found 
post mortem in which death was due to some other disease. This fact has 
been fully corroborated by the observations of Welch who in a large mate- 
rial found that in at least 5 per cent of all deaths there are evidences of 
ulcers or cicatrices of old and healed ulcers. 
(d) The relative frequency of gastric and duodenal ulcers has only 
recently been recognized. Gastric ulcer is more frequent in females. The 588 
DISEASES OF THE DIGESTIVE APPARATUS 
Mayo material and that of Moynihan and other observers proves that 
relatively duodenal is more frequent than is gastric ulcer, and that 
duodenal ulcer is more frequent in males—77 and 23 per cent respec- 
tively. 
(e) Exceedingly important for diagnosis and prognosis is the estab- 
lished fact that a surprisingly large number of hyperchlorhydrias are 
symptomatic (possibly provocative) of peptic and duodenal ulcer. 
(/) Large surface burns may he followed by duodenal ulcer. Our ex- 
perience proves that this is more frequent in children than in adults, that 
burns with such complications are almost always fatal, that perforation 
is not frequent but possible. 
(g) Duodenal ulcer is a relatively frequent complication of chronic 
nephritis, and in two of our cases perforation offered the first evidence of 
its existence. In some cases the symptoms of duodenal ulcer are in evi- 
dence during long periods preceding death from the primary disease, with 
or without uremia. One of our cases, a physician, with chronic interstitial 
nephritis, died of perforation with consecutive subphrenic abscess over 
three years after his initial symptoms of ulcer. 
(h) Indicanuria does not influence the prognosis. In some cases of 
duodenal, occasionally with gastric ulcer, we have found it; with perfora- 
tion indicanuria is usually positive and is simply one of many symptoms, 
which, if taken alone does not materially influence the forecast. 
(i) Peptic ulcer may cause proliferative changes, induration simulat- 
ing carcinoma—life may he but little influenced unless there is pyloric 
constriction or other complications. 
(/) Periods of remissions of symptoms without the healing of the ulcer 
are to he expected in most chronic cases. The presence of an unhealed 
ulcer, either of the stomach or duodenum, is always a menace. Such a life 
is subjected to a number of dangers which without warning may, within 
a limited period, end it, though the proportion of deaths due to such possi- 
bilities is comparatively small. About one-half of all cases will either 
suffer from recurring attacks or have continuous symptoms. Between 6 
,and 10 per cent will remain in an uncertain state between recovery and 
more or less ill health. 
(Jc) The chances of chronicily and marked resistance to medical treat- 
ment are almost certain if two or more relapses have been experienced. 
Our material demonstrates the fact that while the large majority of these 
do not die directly as the result of the ulcer, they continue unhealed, and' 
with such a history many finally face some one or more of the leading 
dangers as mentioned below. 
(1) Freedom from symptoms during long periods does not by any means 
signify cured or healed ulcer. Failure to recognize this fact with result- 
ing carelessness may provoke one of the grave complications. 
So long as occult blood is present in the stool, the ulcer is not healed DISEASES OF THE STOMACH 
589 
and the dangers of complications exist. A single examination is insuffi- 
cient, for blood may be absent during limited periods from the stool. 
(m) Vomiting.—The majority of our cases have had irritable stomachs 
and have often presented with vomiting that has been neglected; most 
of these cases are relieved by treatment. We do not include a single in- 
stance in our series in which life has been lost as the direct result of pro- 
longed vomiting. Cases in which there has been a long period of vomiting 
with sudden serious complications have had lowered resistance, and re- 
covery was slower than it would otherwise have been. Vomiting is less 
frequent than one would expect; when it does occur it is likely to recur 
and continue several days. The vomiting is often paroxysmal; with stric- 
ture and dilatation large quantities are vomited at one time at varying 
intervals. 
(n) Examination of Stomach Contents.—The examination of the stom- 
ach contents and the influence of diet and treatment upon hyperacidity 
where it exists, have an important bearing on the clinical history. Cases 
in which the excessive production of HC1 persists, in which there is almost 
continuous hyperacidity, often hypersecretion, do not heal as a rule. The 
more favorable cases for relief of symptoms are those in which there is but 
slight hyperacidity or in which the symptoms yield to diet and treatment. 
It will require great caution to interpret the results of chemical analysis 
of the stomach content in anomalous cases. There are peptic and duodenal 
ulcers in which there is normal or slightly reduced acidity; cases in 
which there are exacerbations and both hyperacidity and hypersecretion, 
and a small class in which with loss of flesh and gradually increasing evi- 
dences of cachexia, the acidity falls and lactic acid appears. In this class 
of cases the development of cancer in the base of the ulcer should be 
strongly suspected (ulcus carcinomatosus). 
Gastrosuccorrhea {Reichman’s disease) should always excite the suspi- 
cion of ulcer. Usually it will be found at the pylorus; it may be anomal- 
ously located. It is a question whether with reduced resistance and chloro- 
sis, long continued hyperacidity and hypersecretion may not cause ulcer. 
(o) X-ray Pictures.—Rontgen rays are of value for diagnosis; 
for prognosis they offer but little. Both diagnosis and prognosis 
can be placed on a solid foundation without the aid of the x-rays, but in 
doubtful cases, as well as in those cases in which the examination can be 
made without risk to the patient (transportation, etc.) it should be 
included in the scientific examination of the patient. X-rays will estab- 
lish the presence of the hour glass stomach, will make clear secondary gas- 
trectasia, may aid in the early diagnosis (should not be depended 
upon without other clinical data), will often show hypermobility with 
ulcer; but hypermobility is not a constant attendant. With duodenal 
ulcer there is likely to be pyloric insufficiency (Bergman, Friedenwald and 
Baetjer), causing a prompt discharge of the bismuth into the duodenum 590 
DISEASES OF THE DIGESTIVE APPARATUS 
and the ulcer showing as a small clear spot. Others, including Cole, re- 
port the duodenal cap in position, more or less contracted, a “wormeaten” 
appearance with the duodenal surface of the pyloric sphincter irregular. 
Stockton in his recent works says “the radiographic evidence of duode- 
nal ulcer has not yet reached sufficient perfection to. warrant making a 
diagnosis on it alone.” 
Complications 
The leading complications and dangers are: 
1. Perforation 
2. Hemorrhage 
3. Degenerative changes leading to cancer of the stomach 
4. Cicatricial distortion and stenosis 
5. Perigastric adhesions 
6. Exhaustion 
.7. Parotitis (metastatic). 
8. Tetany 
9. Acidosis. 
1. Perforation. Perforation at once makes the case surgical. The 
full appreciation of this fact will save many lives. The prognosis of per- 
foration depends upon many conditions. While perforation is the most 
fatal of all the complications of ulcer of stomach and duodenum, it is a 
fact that in occasional and rare instances nature’s protective processes, the 
unusual resistance of the patient or some factor unknown, may lead to 
recovery. The busy internist may have two or three such experiences in 
a life time; they are indeed so rare and unusual as not to he expected 
and ought not to encourage the attendant in unwarranted delay. One- 
half of all perforations in women occur between the fifteenth and thirty- 
fifth year, one-third about the time of puberty (14 to 20). In men there 
is no time of predilection up to the fiftieth year (Craemer). Perforation 
is more frequent in men than in women, particularly with duodenal ulcer. 
Musser in his collective investigation found 28.1 per cent of 1,871 cases 
with perforation. This is much higher than our statistics from private 
practice. The German average is in the neighborhood of 13, Lebert and 
Welch 3 to 6, Leube in 1.2 per cent. 
Perforation may be either partial or complete. The perforation may 
be prevented or be incomplete leading to localized perigastritis or limited 
peritonitis if the adhesions are sufficiently firm to protect the free perito- 
neum. Brinton in 1858 called attention to the fact which has since been 
confirmed that most perforations are found in the anterior wall (70 per 
cent) ; they are unprotected and complete, and there is resulting general 
peritonitis. This is particularly true of the acute ulcer. The chronic ulcer DISEASES OE TIIE STOMACH 
591 
(Dreschfeld) usually perforates in the region of the pylorus, “on the 
posterior wall and near the lesser curvature.” 
The prognosis of perforation of the stomach wall will always be favor- 
ably influenced by the physician’s ability to make the correct diagnosis suf- 
ficiently early (during the first five hours preferably) to lead to imme- 
diate surgical action. Here we have the “acute abdomen” in which there 
is but scant hope of saving life without radical interference. The opera- 
tion within the first five hours offers enormous advantages and in the 
hands of most surgeons, unless there are associated conditions which in- 
terfere, recovery may be expected. The forecast is quite different in cases 
in which diagnosis and operation are delayed beyond the fifth hour. When 
the abdomen is tense and hard, the pain severe, vomiting persistent, hic- 
cough, rapid and feeble pulse, reduced urine, blood pressure low after an 
initial slight rise which usually follows perforation, the prognosis is ex- 
ceedingly grave and such cases are rarely saved. When the perforation 
has existed beyond the time mentioned (10 hours) the features are pinched, 
the heart rapid, vomiting often fecal, symptoms of extreme toxemia are 
prominent; neither surgical nor medical treatment offer much chance of 
recovery. 
In apparently perfectly healthy individuals, without a single warning 
of existing ulcer, perforation may occur and in those above fifty years 
of age, death may follow within the first few hours, with collapse, before 
peritonitis develops. If the perforation is small or incomplete and pro- 
tective localized peritonitis seals the opening, recovery will be likely to 
follow. Such cases are unquestionably more frequent than is generally 
supposed and post mortems have demonstrated that fact in those who 
finally died of other disease. 
Adhesive perigastritis agglutinating the transverse colon to the stom- 
ach wall may serve to protect the peritoneum when perforation takes place, 
and gastrocolic fistula may result. This is always a serious, but not neces- 
sarily fatal, complication and may be relieved by plastic operation. 
With duodenal ulcer, subphrenic abscess may form, and this without 
general peritonitis. Perforation from subphrenic abscess into the pleura, 
lung, or surrounding organs is a serious complication—the early recogni- 
tion of which may save life. Only rarely does the condition yield with- 
out surgical intervention. We have seen two cases. One was associated 
with metastatic parotitis and finally made a slow recovery. The other 
lived through peritonitis and is now perfectly well so far as we know. In 
this case, the dense adhesions due to perigastritis saved the man’s life. 
The operation for subphrenic abscess dependent upon perforation is en- 
couraging. Elsberg reports 13 cases—51 were operated and 40 recovered, 
18 of 22 not operated died. 
Perforation into the pleural cavity or heart sac, into the lung or after 
long burrowing through the abdominal wall may lead to long periods of 592 
DISEASES OF THE DIGESTIVE APPARATUS 
convalescence, or the patient may, after weeks of symptoms die of sepsis. 
The heart wall (left ventricle) has been perforated after burrowing, in 
which the pericardium was naturally first perforated. 
The recognition of perforation is not difficult in cases which have 
offered preceding symptoms of indigestion or ulcer. 
The "acute abdomen” should be suspected to be due to perforation of 
the stomach in all cases in which there has been hematemesis, localized 
pain or other symptoms of ulcer, with the characteristic behavior of the 
stomach contents (hyperacidity, etc.). 
There is no abdominal condition which causes such intense pain, none 
in which the collapse is more prompt, none in which the physical signs of 
peritonitis during the early hours are more prominent, and none in which 
the heart muscle yields more promptly to the resulting toxemia. All of 
these conditions which mean death, are fortunately less frequently met 
because of unanimity of opinion by which such cases are immediately re- 
ferred to the surgeon. Musser agrees that “the best percentage of cures was 
noted when operation was between one to twelve hours after perforation.” 
Statistics concerning the results of the medical and surgical treatment 
of perforation are of little value, and are best omitted because they cannot 
possibly be based upon premises which are the same in all cases. We do 
know that almost all die who are not surgically treated. We conclude 
as we commenced the consideration of this accident that perforation is at 
once a surgical affair, that delay, failure to recognize the cause of the 
suddenly arising and severe symptoms causes death; correct and early 
diagnosis, other factors being favorable, is very likely to save life. 
Recovery after operation for perforation of either gastric or duodenal 
ulcer is less favorable in cases with long existing dyspepsia than with a 
short history of digestive disturbances. The chronic cases with repeated 
acute exacerbations are found with annoying and complicating adhesions 
and often troublesome thickening. The “acute abdomen” from whatever 
cause, is serious; the future clinician will meet fewer cases, for experi- 
ence has grown and the causes which produce it are recognized by the 
acute diagnostician to receive timely treatment. Mayo (W.) places the 
conditions which lead to the acute abdomen in the vast majority of cases 
in the following order of their occurrence: 
1st. The appendix. 
2d. The duodenum. 
3d. Acute pancreatic fermentation. 
4th. Perforation of the stomach and of the gall-bladder. 
5th. Pelvic conditions which simulate thrombosis of the mesen- 
teric vessels. 
2. Hemorrhage.—My experience has brought the usual proportion of 
ulcers of the stomach but I have lost surprisingly few patients from hemor- DISEASES OF THE STOMACH 
593 
rhage. Small hemorrhages, or vomitus mixed with blood, are frequent; 
large hemorrhages are rare, occult blood is practically a constant feature; 
bloody stools wfith duodenal, at times with gastric ulcer are to be expected. 
Statistics are again fallacious because there is no standard of comparison, 
and those who offer high percentages probably include blood streaks, etc. 
Welch reported death from hemorrhage in 3 to 5 per cent; Miller in 10 
per cent; Muller (L.) in 29 per cent; Ewald and Leube in 1 per cent; 
and Jacobi’s experiences correspond closely with the latter figure. The 
frequence of hemorrhage is in the neighborhood of 50 per cent. 
Leube reports 46 per cent. 
Fenwick reports 75 “ “ 
Rutimeyer reports 71 “ “ 
Brinton reports 29 “ “ 
Beyond 50, with high arterial blood pressure and degenerated arteries 
and gastric ulcer, there may be uncontrollable and fatal hemorrhage. The 
average mortality from hemorrhage in private practice will not he found 
above 2 per cent; in hospital practice it may approach a higher figure— 
6 to 8 per cent. 
Repeated hemorrhages with acute exacerbations in chronic cases are 
ominous. We have seen a number of cases in which there were long 
periods of remission of all symptoms, in which with recurrence there was 
the usual localized pain and immediately profuse hemorrhage. Such 
cases (rare) are likely if they are not treated surgically, during the inter- 
val, to bleed to death ultimately. In the hemophilic the prognosis is 
naturally worse. We cannot too forcibly impress our readers with the 
great importance of appreciating the prognostic meaning of hemorrhage in 
this class of cases. Hemorrhage in some chronic cases may prove persist- 
ent and causes profound secondary anemia; such cases ultimately prove 
to he surgical and after a period of reconstruction during a favorable inter- 
val, are usually saved by surgical interference. It does not often happen 
that the initial hemorrhage is sufficiently profuse to deplete and cause 
death. Such an experience we had only once in a woman of thirty who, 
after a few days of localized pain and overeating, died within twelve 
hours following a profuse hemorrhage. 
3. Degenerative Changes Leading to Cancer of the Stomach.— 
When we consider the different opinions and statistics of able clinicians 
and pathologists relating to degenerative changes, we are forcibly re- 
minded of the fact that the study of gastric and duodenal ulcer offers a 
series of contradictions. 
Zenker in 1882 held that all cases of cancer of the stomach had their 
origin in simple ulcer. Hauser in 1883 first pointed out histologically the 
transition of ulceration into carcinomatous proliferation. Haberlin found 594 
DISEASES OF THE DIGESTIVE APPARATUS 
evidences of carcinomatous degeneration in 7 per cent of all ulcers; 
Miculisz in 7 per cent; Lebert 9 per cent; Rosenheim 6 per cent; Fenwick 
3 per cent; Osier 26 per cent; Moynihan 60 per cent; Mayo 54 per cent; 
Graham 62 per cent; Wilson and MacCarty 71 per cent. Rosenheim came 
to the conclusion that about one in 15 cases of stomach ulcer develops 
cancer. Einhorn holds that no one who has had a large experience has 
found it a frequent occurrence. “This coincidence is so small, cancer 
being such a frequent malady, that it is doubtful whether ulcer plays a 
part at all in the development of cancer.” 
Payr’s material of excised ulcers showed cancerous infiltration in 26 
per cent. Borrman in a very exhaustive article on the method of growth 
and dissemination of cancer of the stomach found in 63 cases of ulcer 
but one in which cancerous degeneration was proved to be present. Reim- 
ers, Haberlin, Sonnischen, Haberfeld and Dittrich offer figures between 
6 and 22 per cent. Futterer has seen 52 cases in which ulcer led to 
cancer. Rippert quotes Hirshfeld as saying “the processes are mere coin- 
cidence.” Borst believes the ocmirrence is overestimated—he found 5.6 
per cent. Wilson, at the Mayo Clinic, in 258 cases of cancer of the 
stomach found 109 to proceed from ulcers. Friedenwald has made an 
exhaustive study on the frequency of the transition of ulcer of the stom- 
ach into cancer in 1,000 cases of cancer, in 232 of which (23.2 per cent) 
there was a previous history of digestive disturbance; 73 cases gave a 
definite history of former gastric ulcer. “It is evident therefore that in 
the 1,000 cases, but 23 per cent present a history of any previous diges- 
tive disturbance whatever, and that but 7.3 per cent give a direct history 
of ulcer.” “If, therefore, all of the former digestive disturbances be 
considered as due to ulcer, the formation of gastric cancer from ulcer 
could not have taken place in more than 23 per cent.” 
Aschoff says that a large number of chronic gastric ulcers, considered 
callous ulcer by the surgeon, and which have been interpreted as cancer, 
microscopically are not ulcers degenerated into cancer but cancers in 
which typical ulcers have formed. 
The material which was submitted to MacCarty at the Mayo Clinic 
was frequently examined within two minutes after its removal from two 
hundred and sixteen resections of the stomach for ulcer, ulcer and car- 
cinoma, or carcinoma. This material divides itself into three groups— 
58 ulcers, 125 ulcers and carcinoma, and 33 carcinoma without any good 
evidence of ulcer. MacCarty under head cf “Ulcer and Malignancy” 
says: “The question, do ulcers become malignant as one of their sequelae 
seems, from my material at least, to be answered in the affirmative. 
What percentage heal, perforate, or become malignant is impossible to 
determine. The close association of carcinoma with ulcer may be strik- 
ingly seen in the fact that 71 per cent of all our resected specimens of 
the stomach for carcinoma were associated with definite ulcers (Wilson DISEASES OF THE STOMACH 
595 
and MacCarty) and that 68 per cent of the resected ulcers of the stomach, 
including the duodenal ulcer, which rarely becomes malignant, were asso- 
ciated with carcinoma.” 
Finally Rippert, who is probably the leading authority on human 
cancer, in his great work says that he has seen three cases of positive can- 
cerous development in ulcer of the stomach, and pictures one of these in 
his work. 
Our own material does not justify the presentation of statistics. We 
have, because of the great importance of this subject from the diagnostic, 
prognostic and therapeutic standpoint, presented the most recent data 
available. For our purposes it may be concluded that on the whole, in 
spite of the great differences of opinion which exist with regard to the 
frequency of the degeneration or transition, we must admit that ulcer of 
the stomach is a positive factor in the production of cancer, and prognosis 
and treatment should be framed accordingly. 
In our experience we have never seen a case of duodenal cancer 
resulting from ulcer. 
4. Cicatricial Distortion and Stenosis.—In the process of heal- 
ing and proliferation the two conditions which are most frequently faced 
are pyloric obstruction and hourglass contraction of the stomach. The 
first condition, pyloric stricture, we consider fully in connection with the 
benign stenoses of the pylorus (See Pyloric Obstruction). 
Without complications the prognosis, unless the patient has been ex- 
hausted by inability to nourish himself as the result of extreme stenosis, 
surgery offers an excellent prognosis. Medical treatment is of no avail 
in extreme cases; with moderate narrowing, life may be prolonged indefi- 
nitely with careful regulation of diet. The x-ray picture will prove of 
material assistance. 
The diagnosis of hourglass contraction can only be suspected; it can 
be positively confirmed by x-ray examination in most cases. Consecutive 
dilatation of the proximal part of the stomach may give rise to all of 
the symptoms of gastrectasia. The complication is rare. Medicine offers 
nothing to relieve the symptoms; most cases are not extreme and remain 
fairly comfortable. Without complication in extreme narrowing, the 
prognosis for life is good, for surgical interference also good. 
5. Perigastric Adhesions.—Most adhesions resulting from ulcer of 
the stomach do not lead to serious complications or annoying symptoms. 
Brinton demonstrated their presence in 40 per cent of ulcers. Perigas- 
tritis is likely to accompany acute exacerbations of chronic ulcers. With 
each acute exacerbation adhesions or localized thickening over the ulcer 
may be expected. This process is at times conservative and salutary, for 
the local thickening may prevent perforation or limit its ravage. 
The adhesions which result to the liver, spleen and intestines lead to 
pain on movement, particularly bending and stretching. When the new 596 
DISEASES OF THE DIGESTIVE APPARATUS 
tissue is dense and thick there may be tumor formation—at times puzzling 
for diagnosis. 
In rare cases the adhesions may lead to pyloric obstruction with 
symptoms of motor insufficiency. Adhesions which distort the duodenum 
may cause regurgitation of bile into the stomach with consecutive symp- 
toms. Most perigastric adhesions require little or no treatment; the 
deforming, constricting perigastritis demands surgical treatment which 
offers only reasonable chances of relief. Reformation of adhesions with 
extensive perigastritis is the rule. 
6. Exhaustion.—Exhaustion due to causes other than the serious 
complications mentioned is at times the cause of death (but rarely). 
Long continued, uncontrolled vomiting, associated chlorosis and extreme 
chloranemia, excessive menstruation, irritable or diseased heart, tuber- 
culosis or other diseases may prove factors in causing alarming exhaustion. 
The blood picture often during considerable periods shows all of the 
evidences of grave anemia which is associated with ulcer symptoms and 
great exhaustion. This is the complex which exists in young girls very 
often. Barring accident in spite of the fact that the heart often shows 
marked muscular enfeeblement and there be slight albuminuria, almost 
all of these patients recover. It is often surprising to note the extreme 
exhaustion and anemia even after hemorrhages, and the final restoration 
of blood elements and strength. 
It must not be forgotten that ulcers of the stomach and duodenum 
are often associated with other diseases which powerfully influence 
prognosis (nephritis, chronic heart and lung disease, etc.) (Rossle), in 
which there may he extreme exhaustion. 
1. Parotitis (Metastatic?).—In several of our cases we have seen 
parotitis during the height of the symptoms. Most of these have been 
found during or after hemorrhage. The swelling is painful; there is 
the usual rise of temperature and acceleration of the pulse. Hone have 
suppurated; all have recovered. 
8. Tetany.—We have elsewhere in this volume called attention to 
the association of tetany with stomach and duodenal ulcer. It is always 
a serious complication and when it recurs demands surgical treatment, 
which offers a good chance of relief. In some cases in which the ulcer 
is healed but there is secondary stenosis (incomplete) and motor insuffi- 
ciency, tetany is prevented by repeated lavage and diet. 
9. Acidosis.—There are occasional cases of peptic and duodenal 
ulcer in which alarming and threatening acidosis develops. Acetonuria 
and acetonemia are easily recognized; with acetone there is diacetic acid, 
and with persistent vomiting and other evidences of poisoning, charac- 
teristic breath, small pulse, thready and rapid, features pinched and eyes 
sunken, respiration is increased and death may follow. This is not the 
fate of all ulcers with acidosis, for in some during periods of exacerba- DISEASES OF THE STOMACH 
597 
tion, there is only moderate poisoning. The fact remains that cases of 
extreme hyperacidity and hypersecretion in which there is uncontrollable 
vomiting are most likely to develop acidosis. 
Contrary to the usually accepted theory of destruction of the liver 
cells and excess of ammonia in the urine, it has been suggested by Under- 
hill and Hand that the excess of ammonia ought not to be attributed to 
the degeneration of liver cells but to the direct results of starvation 
dependent upon uncontrolled vomiting. 
Dreschfeld has called attention to attacks of fainting with acetone 
and diacetic acid. We have had such cases in which threatening acidosis 
never developed. Rational treatment influences the majority of mod- 
erate acetonemies favorably and promptly. The deep involvement of 
the sensorium, rapid respiration, extreme weakness and small pulse are 
serious—not necessarily fatal. We have had a number of satisfactory 
recoveries. 
Important Considerations 
We have in private practice found ulcer of the stomach in 1.4 per 
cent of our cases of internal disease with a mortality of less than 2 per 
cent. The mortality of simple and complicated gastric ulcer with sur- 
gical treatment would naturally be high, as the average would be lifted 
by emergency operation for perforation or for any complication. Musser 
compiled reports from literature and various private sources; his results 
include a large number of operations during the pioneer days; they varied 
between 10 and 25.9 per cent. 
It is unfair to offer an opinion in the individual case based on sta- 
tistics which cannot possibly be considered to include parallel conditions 
nor equal skill or resourcefulness of the various operators. Hence sta- 
tistics bearing on this subject will probably never be of great value, save 
as they prove the possibilities in the hands of the expert and the average 
results of all operators. The mortality for simple ulcer after surgical 
operation varies from less than 2 per cent (Mayo-Moynihan) to 10 per 
cent and more, and it has been demonstrated that operations for duodenal 
ulcers present a higher average of cures than operations for gastric ulcers. 
Prognostic Significance of Age and Surgical Treatment 
Petren has demonstrated, in an investigation of 243 operated cases 
collected, that it appeared that younger subjects did not show as favor- 
able late results as did older individuals. In 33 women under 30 years 
who had been operated, 42 per cent had subsequent gastric disturbances. 
In 33 women over 50 years of age, only 24 per cent had subsequent trouble; 
and out of 41 men over 50, only 17 per cent had any annoying symptoms. 598 
DISEASES OF THE DIGESTIVE APPARATUS 
It is exceedingly difficult to offer any statistics of value which hear 
upon the relative frequency of the complications of simple peptic or 
duodenal ulcer. Much must depend upon early treatment and care. The 
average statistics of ten years ago are of no value today, for medical 
dietetic and surgical treatment have all been improved and it is as unjust 
to the physician as it is to the surgeon to make comparisons which are 
not based upon conditions which exist at the present time. 
The mortality based on surgical treatment will always be higher than 
that offered by the internist, but in all fairness to the surgeon we must 
admit that this is so because the average surgical material even of simple 
uncomplicated ulcer includes only the more serious and chronic, oft- 
relapsing cases which have during long periods postponed treatment and 
operation, or the acute cases with symptoms of sufficient severity to de- 
mand an emergency operation. Musser’s analysis of cases from medical 
literature and a collective investigation of private cases (1,871 and 586 
respectively) shows that in simple ulcer the death rate under surgical 
treatment was 20 per cent and under medical treatment 12.4 per cent 
(reported in 1907 from literature). The private cases showed a surgical 
mortality of 11.4 per cent and a medical mortality of 3.1 per cent. After 
my full rehearsal of the prognostic features of gastric and duodenal 
ulcers I feel safe in advising the clinician to consider the majority of 
these cases to he purely medical offering a good prognosis for life and 
cicatrization. 
There never is a time when the patient with an unhealed chronic or 
acute ulcer is not standing on the edge of a precipice ready to fall, never 
a moment when without warning his condition may not become sur- 
gical, though the large majority escape serious complications. Ulcers 
which are chronic and which prove their chronicity by repeated remissions 
and exacerbations with or without hemorrhage do not heal—the complica- 
tions which threaten life will complicate a small proportion of these but 
chronic invalidism is their positive fate, and as the exacerbations mul- 
tiply, adhesions and secondary changes (perigastritis, stricture of the 
pylorus, dilatation of the stomach) ivill prove increasingly annoying—at 
times threatening. 
Death resulting from ulcer during its incipient stage (acute ulcer) 
occurs in about 1 to 2 per cent. These figures approximately correspond 
with those of Russell. 
Duodenal ulcers rarely heal; they do not cause cancer. The question 
of surgical interference to prevent cancer from ulcer will need to be 
decided in the individual case. 
Gastric ulcer •may cause cancer but the incidence is not as frequent 
as the statistics of some clinics appear to prove; sufficiently frequent, 
however, to influence prognosis and treatment. The prognosis of com- 
plications has been favorably influenced by the growth of physiologic DISEASES OF THE STOMACH 
599 
and pathologic knowledge and the enormous improvement of surgical 
technic. 
In threatening complications, perforation particularly, life often de- 
pends on prompt diagnosis and immediate surgical treatment. 
Rest, diet and medical treatment are the paramount factors which 
the physician possesses to aid him in the cure of most cases or the control 
of symptoms. 
We must once more accent the fact that all threatening acute cases 
and all chronic relapsing cases, as well as life threatening complications 
demand the concerted action and ripe judgment of both the physician and 
surgeon—and this without delay. These facts accepted and acted upon, 
the mortality of gastric and duodenal ulcer will be enormously influenced 
and will be found to be surprisingly low (below 1.5 per cent). 
Aschoff. Patholog. Anatom. Jena, 1913. 
Bamberger. Virchow’s Path. u. Therapie (Chylopoetic system). 1864. 
Borrman. Mitth. d. Grenzgeb. Supplement I, 1901. 
Borst. Wurzburg. Abhandlungen. 1906. 
Brinton. Ulcer of the stomach. London, 1857. 
Cole. J. Am. Med. Ass., 1913, Ixi, p. 762. 
New York Med. J., 1913, xcvii, p. 960. 
Craemer. Das runde Magengeschwur. Munich, 1910. 
Cruveilhier. Atlas of pathol. anat., vol. i, Paris, 1829-1835. 
Denver. J. Am. Med. Ass., July 12, 1913, p. 77, etc. 
Dittrich. Prager Vierteljahrsch. 1847. 
Dreschfeld. Allbutt & Rolleston’s System of medicine. Vol. Hi, London, 1907. 
Einhorn {M.). New York Med. Rec., July 13, 1912, p. 48. 
Elsberg {C. A.)* Annals of Surgery, 1901, xxxiv, 729. 
Ewald. Erk. d. Magens. Berlin, 1893. 
Fenwick. Lancet, London, 1897, ii, p. 388. 
Friedenwald. Boston Med. & Surg. J., May 29,1913, vol. clxviii, No- .ft, p. 797. 
Futterer. Die Aetiologie des Karzinoms. Wiesbaden, 1901. 
Graham. J. Am. Med. Ass., 1908, li, p. 651. 
Illinois Med. J., 1909, xvi, p. 137. 
Haberfeld. Ztschr.f. Krebsforschung {quoted by Rippert). 
Haberlin. Arch, de Med. Exper., 1889. 
Habeshon. Med. Chirurg. Transact., London, 1907. 
Hauser. Das Magengeschwur, 1883. 
Hirshfeld. See Rippert, l. c. 
Jacobi. Transact. Congress of Am. Phys. & Surgeons, Triennial Session, 1907. 
Lebert. Ueber Magenkrankheiten. 1878. 
Leube. Deutsche med. Wchnschr., 1909, xxxv. S. 961-964- 
Ziemssen’s Handbuch {Magenkrankheiten). Bd. vii. 
MacCarty. J. Surgery, Gyn. & Obstetrics, May 10,1910, p. 449-462. 
References 600 
DISEASES OF THE DIGESTIVE APPARATUS 
Mayo (W. J.). Boston Med. & Surg. J., 1911, clxiv, 477-482. 
(See also reports Mayo Clinic), Annals of Surgery, Sept., 1911, p. 313 
J. Am. Med. Ass., July 12,1913; Discussion of Denver's Paper, p. 77-78. 
Mickulicz. Arch.f. klin. Chir., Berlin, 1888, xxxvii, 1895-6, li; 1897, Iv. 
Miller (J. M.). Ulcer of the stomach. Tr. Path. Soc., Philadelphia, 1889-91, xv, p. 102. 
Miller (L.). Corrosiv. Geschwiire des Magens, etc. Erlangen, 1860. 
Moynihan. Brit. Med. J., 1900, ii, p. 1631. 
Lancet, London, 1903, ii,. p. 603. 
Dublin J. Med. Sci., 1910, cxxxi, 15. 
Ophuls. J.Exper. Med., vol. viii, p. 182. 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Payr. Verhandl. path. Gesellsch., Bd. xiv. 
Petren. Bruns' Beitr. z. klin. Chir., Bd. Ixxvi, Hft. 2, p. 205. 
Reimers & Sonnischen. Rippert [Z. c.]. 
Rippert. Das Karzinom des Menschen. Bonn, 1911. 
Robson {Mayo). Brit. Med. J., 1906, ii, 1345. 
Robson & Moynihan. Diseases of the stomach. 2d ed. 1904. 
Rodman. Tr. Am. Surg. Society, 1900, xviii, p. 38; also p. 804, roZ. rvi, 2. 
Index Catal. Surg.-Gen.’s Office. 
Rokitansky. Handb. der allgem. Path. Wien, 1855. 
Rosenheim. Krankh. des Magens, etc. Wien, 1891. 
Rosenow. Tr. Med. Sect. Am. Med. Ass., 1914. 
Rosenau & Anderson. U. S. Hygienic Laboratory. 
Rossle. Mitth. d. Grenzgeb. Med. u. Chir., vol. xxv, p. 766. 
Russell. Lancet, London, 1904, i. 
Stockton. Int. Clinic, Philadelphia, 1893, 2d ser., p. 55. 
Diseases of the stomach. New York, 1914. 
Trousseau. Clin. Med., Paris. 
Underhill & Rand. Arch. Int. Med., 1910, Ixi. 
Virchow. Virchow's Arch. 1853. 
Welch {W. H.). Syst. Pract. Med. {Pepper), Philadelphia, 1885, ii, p. 480-529. 
Wilson & MacCarty. Am. J. Med. Sci., Dec., 1909. 
7. Cancer of the Stomach 
(Carcinoma ventriculi) 
General Considerations.—On. the basis of past statistics Hoffman 
concluded that during 1913, 30,105 would die of cancer of the stomach 
and liver; and his forecast was practically corroborated. 
The annual mortality in the United States from cancer, Hoffman 
places at 75,000; 500,000 in the civilized world. Cancer death rate is 
increasing at the rate of per cent per annum, and this holds through- 
out the civilized world. The average age of death from cancer is 60.4 
years for males, and 58.2 years for females. 
The male cancer death rate in the United States at ages 25 and over 
has increased 29 per cent during the last decade, and the female cancer DISEASES OF THE STOMACH 
601 
death rate has increased 23 per cent. The cancer mortality in Japan 
ranges from 83 to 95 per 100,000 inhabitants; Moscow 56 to 103; St. 
Petersburg 78 to 98; Southern Italy 6 to 70; Northern Italy 51 to 68; 
in the Netherlands 75 to 105; Germany 33.5 to 35. In the United States 
in 1907 it was 79.6 per cent in the cities, 73.9 per cent in the country. 
Rosenfeld reports the interesting coincidence brought out by his figures 
that the mortality from cancer is unusually high in the district of 
Joachimsthal, the source of the radium supply. The study of “cancer- 
free islands” is of great interest; there are no “cancer-free islands” in 
countries in which cancer is prevalent. Kosenfeld accents the fact that 
“there are numerous cancer islands in countries which are generally free 
from it.” 
The rule may be accepted without modification that cancer of the 
stomach is always a fatal malady unless detected in its very incipiency 
before marked infiltration has resulted, before adhesions have formed, 
before neighboring glands have been involved, and before there are evi- 
dences of changes in the blood. 
There is no reason for considering the majority of stomach cancers 
to be other than primary, therefore, no valid reason for concluding that 
cancer of that organ, if radically treated, during its early days differs 
from primary cancer, elsewhere which offers a favorable prognosis only 
under the conditions mentioned in the preceding paragraph. 
There are powerful factors, however, which make the early recogni- 
tion of stomach cancer exceedingly difficult and usually impossible save 
by exploration. The stomach is a tolerant organ; it continues to perform 
its functions during relatively long periods in the presence of organic 
disease which it continues to tolerate without creating a suspicion of its 
presence. The intestinal and pancreatic functions compensate for the 
failure of full gastric digestion, while the patient, in most cases, in the 
presence of few symptoms of “dyspepsia” is but little disturbed by these, 
and usually fails to seek medical assistance; when he does, in the very 
early days of the disease, the diagnosis remains, as already said, difficult 
and uncertain. 
We are reminded that the consideration of these tests, together with 
clinical history, should make early diagnosis easy: the analysis of the 
stomach contents, the testing of the motor function, the x-ray examina- 
tion, the Solomon test (determination of the amount of nitrogen contained 
in a known quantity of water with which the stomach is washed out— 
because with cancer there should be an increased amount of serous fluid 
discharged—more than normal, hence an abnormally high nitrogen con- 
tent), the Graefe-Rohmer hemolytic test, and the Oppenheimer test. 
Unfortunately all of these do not accomplish the desired end. 
The thorough investigation of the Solomon, Graefe-Rohmer and 
Oppenheimer tests by Leitner prove that all of these have inherent 602 
DISEASES OF THE DIGESTIVE APPARATUS 
sources of error which make the results uncertain and unreliable (Leit- 
ner). The early diagnosis of cancer by the Rontgen rays is uncertain 
and according to the most reliable authority (Haudek), carcinoma aris- 
ing from a callous ulcer, a fungus carcinoma which has invaded the 
normal stomach outline, a diffusely infiltrating cancer, may make it pos- 
sible to determine the character of a cancer with tolerable accuracy. 
These are all advanced conditions and have nothing in common with 
incipient carcinoma ventriculi; in all of these, the revelations of the 
x-rays are tardy and can only corroborate, when made, an unfavorable 
outlook because of the advanced changes. 
The repeated examinations of the stomach contents may make us 
suspicious, but they offer during the earliest stage but little upon which 
we can rely. Billroth in a personal communication to the author on this 
subject shortly before his death wrote: “It is true that free HC1 is more 
often absent from gastric juice in gastric cancer than' in ulcer; but this 
phenomenon is not sufficiently constant and may be physiological. It 
is not sufficiently definite to be of practical value.” Billroth added: 
“I consider the differential diagnosis of an ulcer of the stomach with 
cicatrization and beginning carcinomatous infiltration from primary can- 
cer as very difficult and usually impossible, ofttimes impossible when 
the fresh specimen is before us and cut into, only possible after many 
and large sections have been made and examined microscopically.” We 
have mentioned these facts as a preface to what follows because they 
demonstrate the problems which confront the clinician if he would im- 
prove the forecast of the disease under consideration. The patient, if he 
be saved, must consider his symptoms with his attendant early 
and the physician must learn to associate these symptoms with possible 
malignant disease of the stomach. Patients will never learn to present 
for early diagnosis until we have made clear to them, as we have to the 
incipient tuberculous, the facts relating to carcinoma which make prog- 
nosis favorable. Therefore, we repeat, early diagnosis is the only hope 
of the patient who has stomach cancer. Depend upon laboratory methods 
or any one symptom for diagnosis and your patient’s death warrant has 
been signed. The pyloric portion of the stomach is the seat of cancer in 
over 70, Mayo says 80 per cent of stomach cancers—therefore in the 
majority. The earliest evidences of motor insufficiency and stagnation 
(at the cancer age or earlier), food remnants after seven hours with 
pyloric resistance, and tumor, are the most dependable of all symptoms; 
all other data are of secondary import. In over 90 per cent of our cases 
there was a palpable tumor at the time of the first consultation. This 
fact proves that symptoms are absent or insignificant and treatment is 
not demanded until the process is well advanced. 
To the above we add the Leube rule, which should be indelibly im- 
pressed on every diagnostician: DISEASES OF THE STOMACH 
603 
“Cancer of the stomach is 'present in all probability if a questionable 
stomach disease has attacked a patient between 50 and 60 years of age 
who formerly digested all food well. If such a person becomes dyspeptic 
without an evident etiological factor, it may be assumed with considerable 
certainty that he is developing gastric cancer.” 
uCancer during early life is by no means exceptional, and this fact 
cannot be ignored in either diagnosis nor prognosis. The average per- 
centage of stomach carcinoma in early life is between 2.5 and 4 per cent. 
Osier reports in 3,257 cases of stomach cancer 2.5 per cent below the age 
of 30 years. Welch in 2,028 cases found 2.5 per cent below 30. 
Stomach cancers in early childhood are exceedingly rare. Rolleston 
and Hague report 17 cases collected from medical literature. One was 
an infant 10 days old, reported by Cullingsworth; Welch considered the 
growth to be congenital. 
Between 10 and 20 years of age cancer of the stomach is likely to be 
more acute than in the adult and usually runs a rapid course. After 
20 until 30, reported cases show rapid progress to death. Mathieu in a 
series of 19 cases in young subjects, also quoted by Osier and McCrae, 
estimated the duration at three months. Eleven of Mathieu’s cases lived 
months; 6 lived 6 months and 2 one year. Latent periods are not to 
be expected in the cancer of early life. 
The scirrhus cancer is the most frequent; colloid second; encephaloid 
third, and always of rapid growth; epithelial fourth; and adenoid fifth. 
Welch in 1,885 reported that “it is probably fair to conclude that in 
Hew York not over 1 in 200 of the deaths occurring at all ages from all 
causes is due to cancer of the stomach, and that about 1 in 100 of the 
deaths from 20 years of age upward is due to this cause.” 
Our statistics show the larger number of stomach cancers in male 
subjects. Welch believes the liability of the sexes is the same. Heredity 
is certainly a factor—less frequent than has been supposed (15 to 20 
per cent). It is not uncommon to find several members of a family with 
cancer of the stomach, a fact which is confirmed by the experience of the 
average busy clinician. It is an interesting fact that in most of these 
the symptoms appear at about corresponding ages. 
Secondary stomach cancer is rare, but possible. Welch’s material 
included 17 secondary to cancer of the breast. We have seen similar 
cases, and in one woman we found first uterine cancer for which she 
was successfully operated, later breast cancer also successfully operated, 
and finally stomach and liver metastases. 
The negro is rarely afflicted in his native country (Africa), while in 
the United States the proportion of deaths—as determined by Welch in 
an analysis of “7,518 deaths among this race in Hew York”—was about 
one-third less than among white persons. 604 
DISEASES OF TIIE DIGESTIVE APPARATUS 
Prognostic Significance of Leading Symptoms 
Pain.—Pain usually present, is not a symptom of great prognostic 
value; the rule may be accepted that pain is not, as a rule, an early symp- 
tom, that its persistence is evidence of advanced disease. 
Vomiting.—Vomiting is absent from one-eighth to one-fifth of can- 
cers of the stomach (Lebert and Brinton). In such cases there is no 
consecutive constriction at either end of the stomach. When the cancer 
is located at the cardia, it may lead to all of the symptoms of esophageal 
stricture, the vomiting or regurgitation follows promptly after taking 
of food. Dilatation, pocketing of the esophagus, with contraction of the 
stomach follow after a few months of symptoms and progression. Vomit- 
ing is present in practically all cases in which the pylorus is the seat of 
disease (80 per cent). The greater the quantity vomited at one time, the 
more dilated will the stomach be found and the greater the obstruction. 
Vomiting of blood, hematemesis, is not an early symptom except in cases 
in which there is infiltration of the base (ulcus carcinomatosum) of an 
old ulcer. These cases, often run a chronic course and are often slow to 
develop metastases. The “coffee ground” vomitus is evidence of advanced 
change in the growth (degeneration and ulceration) ; usually there is 
marked emaciation, cachexia, anemia, and muscular enfeeblement at the 
same time, with a failing heart (small pulse) and evidences of distant 
metastases. Under these conditions life is not prolonged. 
Once there has been marked emaciation there is but small chance of 
improvement; progression is manifest in the daily loss of strength and 
the increase of stomach symptoms. 
Stomach Function.—Stomach function is always disturbed in the 
presence of cancer. In the latent cases the reduction may be so slight as 
to remain unnoticed—no symptoms or but few; the tolerant stomach is 
relieved at the same time by the compensatory action of the pancreas and 
intestines. This ability of the stomach, when the pylorus has been re- 
moved to regain sufficient motor ability that the duodenum may carry on 
digestion, is the prime factor in the prognosis of early radical treatment 
of pyloric cancer. Miculicz and Rosenheim found that in three months 
motor function was sufficiently restored after removal of the pylorus to 
empty the stomach of its contents in five hours and a half; the duodenum 
and small intestines assume the stomach’s work. Ninety per cent of our 
cases show a reduction of free HC1. In average cases pepsin will be pres- 
ent, but reduced in accordance with the destruction of the peptic glands. 
Lactic acid is likely to be present; it is not pathognomonic. Lactic and 
other organic acid with reduced HC1, the Boas-Oppler bacillus, blood and 
mucus are presumptive evidence of gastric cancer. The yeast fungus is 
present in advanced carcinoma. When bits of cancer tissue are vomited 
the disease is advanced, and ulceration or breakdown is progressive. When DISEASES OF THE STOMACH 
605 
the vomitus has a gangrenous odor, sloughing and sepsis go hand in hand. 
Such cases often have fever and may show marked toxic symptoms (cere- 
bral) as the end approaches. 
The condition of the bowels is of no great significance unless there is 
persistent diarrhea, when the effect is weakening; usually constipation is 
troublesome. 
Stomach Contents.—The diagnosis of cancer of the stomach once 
established the condition of the contents, whether there is absence or 
presence of HC1, is only of slight prognostic value. The cases in which 
there is subacidity (not complete absence) do sometimes run a longer 
course than do those with complete anacidity (absence of the HCl), par- 
ticularly if there be achylia gastnca, which with carcinoma is indicative of 
far reaching infiltrating disease and atrophy of the gastric follicles. The 
cases with persistence of free HC1 are usually, not always, ulcus carcino- 
matosum. and these are likely to be chronic with latent periods to be men- 
tioned later. The presence of lactic and other organic acids (butyric, 
acetic), with the Boas-Oppler bacillus and yeast, is usually significant 
of advanced carcinoma and probable motor insufficiency (stagnation). 
Golding Bird in 1843 demonstrated the absence of free HC1 in pyloric 
cancer with dilatation but his communication was ignored until von den 
Velden at the Kussmaul Klinik systematically investigated the subject 
and established its diagnostic value. Free HC1 is the remnant which is 
left after all affinities have been satisfied. With “the constant presence 
of free HCl made positive after repeated examinations and a normal 
peptic strength” it will rarely be necessary to consider cancer of the 
stomach. Riegel would not consider the diagnosis of cancer under such 
conditions “however strongly they (the symptoms) point to it.” The 
greater the infiltration the more likely are we to have reduced HCl and 
the worse is the prognosis—this is particularly true when at the same 
time there is little pepsin and no peptones. 
Cancer of the pylorus may be limited, always fatal when advanced 
and yet free HCl is usually present, “its absence is the exception” (Cahn 
and von Mehring). This ought not to be accepted as a rule. Free hydro- 
chloric acid was absent in 92.7 per cent of my cases; present, but markedly 
reduced, in 7.3 per cent. 
The Glycyltryptophan and the tryptophan tests have been fully con- 
sidered by Smithies who reports on 1,400 cases of diseases of the stomach 
examined at the Mayo clinic. From these we can draw no data which 
influence prognosis or make positive the early diagnosis of cancer of the 
stomach.* 
* The tests are known as the Fischer-Neubauer glycyl tryptophan test for the 
presence of polypeptid splitting ferments and the Weinstein tryptophan test for 
the presence of free amino-acids. 606 
DISEASES OF THE DIGESTIVE APPARATUS 
Smithies found the first mentioned test present in 31 of 81 stomach 
cancers, the tryptophan test was positive in 7; with 35 ulcers 9 showed 
Fisher-Neubauer test and 3 the Weinstein; with 87 duodenal ulcers 3 and 
3 respectively. Other diseases—benign pyloric stenosis hypoacid anacid- 
ity, gastritis, neuroses and achylia gastrica, also gall-stones, cancer of 
liver, appendicitis, and pernicious anemia—gave positive results. No 
other disease gives so many positive reactions as does cancer of the stomach 
but in the absence of other suggestive or classic symptoms and positive 
Fischer-Neubauer and Weinstein with the knowledge that other diseases 
with similar symptoms give the same results, we are left without any 
material assistance from these tests. Feurer says “We can only consider 
the tests (including the Salowski—colloidal nitrogen, the hemolytic bodies, 
the Graefe—Rohmer and the Neubauer-Fischer tests) of value when the 
clinical features are corroborative”, and when these are, the disease is 
advanced far beyond the period of incipiency or even the first stage. 
Blood Picture.—The blood picture is of value in giving a fair esti- 
mate of the ability to nourish the patient. With progressive loss of 
strength, weight, and increasing secondary anemia and cachexia, life is 
threatened. With average infiltration the cachexia will always he out 
of proportion to the anemia—of diagnostic as well as prognostic value. 
My average red count at the time of positive diagnosis has been 3,500,000 
per c. mm.; hemoglobin 50 with leukocytic range between 10,000 and 15,- 
000. In some cases, where there is excessive vomiting the count may tem- 
porarily approach a polycythemia. This is rare, however. 
Fever.—Persistent fever, usually F. is not infrequent; 
it is almost always evidence of the terminal stage of the disease. But 
few cases die without rise of temperature at some time during the course 
of the disease. When fever persists it is an evidence of absorption of 
toxins and it is an unfavorable symptom. Chills and fever are always 
suspicious of sloughing and consecutive sepsis. 
The behavior of the heart and circulatory organs is of value in giving 
an index of the patient’s resistance as well as deciding in conjunction 
with physical signs and subjective complaints on the probable duration 
of life. 
The Urine.—The urine offers but few data. The chlorids are re- 
duced; there is usually, particularly in the advanced stage, indicanuria; 
there may be nephritis or albuminuria. 
I examined the urea content in all of my cases and have learned that 
advancing cases, during limited periods, often show very high urea loss. 
The urea estimation in all suspected cases is valuable for diagnosis and 
prognosis. When the disease is advanced the amount of urea is diminished. 
Acetonuria, if slight is not, per se, of great significance, it may cause no 
symptoms; when it does and the symptoms of acidosis are prominent the 
danger is great. DISEASES OF THE STOMACH 
607 
Dropsy.—Most cases are either edematous before they die, or there 
are evidences of dropsies of the serous cavities, or both. Dropsy is always 
an evidence of the approaching end. With dropsy there is usually marked 
cachexia and anemia; most dropsical patients have died with symptoms of 
toxemia, more or less delirium, and final coma. 
Ulcerative Stomatitis and Dry, Red, Glazed, Cracked Tongue.— 
Ulcerative stomatitis and the dry, red, glazed, cracked tongue are among 
the terminal conditions. I have never seen a case fall into a period of 
latency or remission after the tongue shows decided change. 
Perforation.—I have had no death in my practice due directly 
to perforation of the stomach wall. In one case there was perforation 
into the adherent transverse colon (gastrocolic fistula) which was at first 
unrecognized because, as the stomach was inflated, the distension of the 
colon simulated dilatation of the stomach. This patient lived a number 
of months after the perforation. There are a number of cases of peri- 
tonitis on record following perforation, but this combination is rela- 
tively rare. 
Latency of Gastric Cancer 
In 1893 I called attention to a series of cases which justified the 
conclusion that latency of stomach cancer is not unusual. There may he 
after symptoms strongly suggestive and sufficient for tentative diagnosis, 
marked improvement during varying periods, gain of strength and flesh, 
improvement of stomach function, approximate return of normal gastric 
juice, favorable change in the blood picture—all sufficient to create the 
suspicion of faulty original diagnosis. In some cases the motor func- 
tion as shown by tests has increased. In these cases it may be as- 
sumed that stenosis does not exist to any high degree and that the 
intestines, and the duodenum particularly, are sufficient to nourish the 
patient. These cases are therefore without much constriction at the py- 
lorus or secondary dilatation, or there is infiltration with only moderate 
thickening at the pylorus. The length of the periods of latency varies, 
the longest period in my experience being 6 years; during the early stage 
there were characteristic symptoms. This was not a case of cancer upon 
the base of an old ulcer as was proved by the post mortem. Death followed 
12 months of continuous symptoms. There are cases in which cancer 
remains latent, never causing subjective symptoms and is detected post 
mortem, death having been due either to accident or intercurrent disease. 
The blood picture of stomach cancer is not characteristic, but in this 
class of cases there may be less cachexia than is usual. As the process 
advances and the powers wane the cachexia is relatively greater than the 
anemia. The unfavorable features which show progression and presage 
an early ending are those of increasing stagnation, dilatation with periodic 
vomiting, progressive loss of flesh, increasing cachexia, and secondary 608 
DISEASES OF THE DIGESTIVE APPARATUS 
anemia. In these cases after the long period of latency, the tumor is 
usually palpable. 
Infiltrating cancer without palpable tumor, cases in which the stomach 
wall is evenly invaded, may not cause stagnation. The pylorus may not 
be constricted; if it finally is, then there will be stagnation with moderate 
dilatation and progressive, often rapid emaciation. 
With infiltrating cancer which may be mistaken for non-malignant 
atrophy of the gastric follicles, there will be remnants of the previous 
days’ food, usually absence of IIC1; lactic acid will be present; there will 
be progression of the disease, never improvement of functional activity 
cf the stomach. Whenever the cancerous growth fails to cause stagnation, 
the prominent symptoms may mask the primary disease. Such patients 
often die with the secondary manifestations in the ascendency. In some 
cases death may follow with the secondary lesions of liver cancer promi- 
nent, but few or no stomach symptoms. 
Both latent and infiltrating carcinoma may present symptoms of metas- 
tases before local evidences or subjective symptoms of existing disease. The 
most frequent metastases are to the lymphatic glands (in of all cases), 
to the liver in an almost equal number, and to the peritoneum, omentum 
and intestines in approximately £ of all cases, the pancreas in -J, the pleura 
and lung in 1-15. We have called attention to metastasis to the nervous 
system from cancer of the stomach and intestines. The secondary growths 
may be more conspicuous in causing symptoms than the primary. There 
may be invasion of any part of the nervous system, peripheral, spinal, or 
cerebral. Welch reported 9 metastases to the brain and meninges in 
1,514 cancers of the stomach. Pinatelle and Cavaillon report 2 cases of 
gastric cancer with secondary deposits in the cranial bones. 
Metastases 
Additional Considerations 
Long periods of latency or remission of symptoms alone can justify 
the belief during limited periods, that gastric cancer is curable. If the 
disease is carcinoma, relapse and death are sure to follow. The cases of 
so-called “self-cure of cancer ’ are usually ulcer with thickened or fibroid 
base—never cancer. I fully agree with Mayo when he makes the follow- 
ing positive statements: “In all the history of disease there is no 
authenticated case in which a cancer of the stomach has been cured by 
medical means.” Accepting this view, as absolutely true, we once more 
find ourselves face to face with the problem of early diagnosis and prompt 
surgical interference if we would save the lives of these patients. It is 
not within the province of this work to deal with surgical questions, but 
only benefit can result from the presentation of a few data taken from the DISEASES OF THE STOMACH 
609 
material of those in whom we may place reliance that the prognosis of the 
disease may be improved and cancer of the stomach may from the very 
beginning of observation of the individual case demand the attention of 
the diagnostician and the surgeon. Mayo reports: “Cancer of the stomach, 
when still localized, gives operative results as good as those after operation 
for cancer in any other part of the body; it has no higher grade of malig- 
nancy nor is the operation for its removal more difficult than operation for 
the cure of cancer in other organs of the gastro-intestinal tract.” 
It is obviously unfair to compare results today with those of even five 
or ten years ago—so great has been the improvement of technic—and so 
much better educated is the public that results are growing more and 
more favorable; the mortality is steadily diminishing. I was present 
at the Billroth clinic during the early days of the work in which he was 
the pioneer, and I have recently had opportunity to compare it with 
modern surgical methods in this country and abroad. The revelations are 
encouraging and prove the courage of the master who paved the way as 
well as the fact that the mortality of all plastic operations on the stomach 
depends not only on the early diagnosis but upon the cool judgment and 
superior skill of the surgeon. In no field of medicine does prognosis 
depend more upon the experience—the most valuable asset of the oper- 
ator. Mayo reports a mortality of 7 per cent in his last 100 cases; in 
the last 50 of these, 4 per cent. He modestly adds: “nor are these figures 
exceptional.” In this latter conclusion we differ from him; he under- 
estimates the value of his experience in the cases preceding his last 50. 
Xo patient can be considered cured who has not remained well five years. 
“Of 307 resections of the stomach for known carcinoma 150 of the 
patients were operated more than three years ago; 20 died from the 
results of the operation, and we were unable to trace 40. This gives 90 
patients who recovered from the operation and whose present condition 
we have been able to trace. Of this number 33 or 36.6 per cent are alive. 
Of the 93 patients operated more than five years ago, 15 died and 20 have 
not been heard from as to their present condition. Of the remaining 58, 
13, or 22 per cent, are known to be alive and well over five years. Every 
death occurring within the five year period has been classed as a death 
from return of the cancer without regard to the actual cause; this is an 
injustice to the statistics, since the normal death rate for five years of 
people the age of these patients is at least 8 per cent.” These results 
prove that “in the operated cases 90 per cent chance of recovery from 
the operation exists, a 36 per cent chance of 3 years of life, and 25 per 
cent of 5 years.” 
Faroy reports as follows on his surgical experiences with cancer of the stomach: 
Exploratory laparotomy was done on 8 cases, 6 of which died soon after opera- 
tion (3, 19, 23 and 30 days) from postoperative complications; 2 survived, 1 six 610 
DISEASES OF THE DIGESTIVE APPARATUS 
months, the other 1 year, in spite of the presence of ganglia, adhesions and infil- 
tration of the gastric wall and gastrohepatic ligament. 
Gastro-enterostomy—39 cases; 
8 survived only from a few hours to several days. 
11 “ up to 6 months (2, 3, 4 and 6 months). 
9 “ more than 6 months (7, 9, 10, 11 and 12 months). 
9 “ from 1 to 2 years. 
3 “ for 1 year 3 months. 
2 “ “ 1 " “ 5 “ 
2 “ “ 1 “ 10 “ 
1 “ “ 1 “ 11 
1 “ “2 years. 
1 “ more than 2 years (2 years 6 months). 
1 u u iC 3 iC 3 u 4 il 
Of these patients 9 had pyloric or prepyloric cancer, and survived as follows: 
Several hours 2 
3, 6 and 7 months 3 
1 year, 1 month 1 
1 year, 10 months 1 
1 year, 11 months 1 
3 years, 4 months 1 
Fifty per cent did not live one year; 45 per cent lived more than one year. 
Of 30 other cases of pyloric and prepyloric cancer and cancer of the lesser curva- 
ture, 77 per cent did not live one year, 23 per cent more than one year. 
In 12 cases the neoplasm was extensive, had infiltrated the glands or contracted 
adhesions with the liver and pancreas: 
2 died after several hours. 
2 u “ “ days. 
5 “ before 1 year (7, 8, 10 and 12 months). 
2 “ “2 years (13 and 23 months). 
1 lived 3 years and 4 months in spite of pancreatic adhesions. 
25 per cent did not live 1 year; 30 per cent not more than 1 year. 
Pylorectomy.—Simple pylorectomy (Billroth’s method No. 1) shows different 
figures from gastro-enterostomy. 
Of 10 patients, 5 died soon after operation from complications: 3, 7, 15 and 
30 days. 
5 survived: 1 year 6 months. 
1 “ 9 “ 
2 “ 2 “ 
3 “4 “ 
4 “ 6 « 
One patient in whom a total gastrectomy was done survived 3 years in spite of 
extensive lesions. 
Billroth’s method No. 2 gave similar results. DISEASES OF THE STOMACH 
611 
Of 6 patients, 2 died 10 and 15 days after. 
4 survived: 10 months. 
1 year 1 month. 
1 “ 4J months. 
1 “ 10 “ 
If we combine the figures of these two groups we find 7 deaths out of 16—a 
postoperative mortality of 45 per cent. The mortality in the cases operated accord- 
ing to Billroth’s method No. 1 was 50 per cent, that of method No. 2, 33 per cent. 
Temoin reports that the following results were obtained in 11 years, from 1898 
to 1909, on 168 tumors of the pyloric region. Of this number, 91 were operated 
before 1908, and 77 in 1908 and 1909. Of the first 91 cases, 38 are dead, 24 dying 
within 5 days after operation and 14 within 15 days. Of those operated in 1908, 
44 cases, 4 died within the first 5 days and 3 within 15 days. Of those operated in 
1909, 33 cases, 2 died within the first 5 days and 3 within 15 days. 
The figures show a uniform decrease in the immediate results of the operation, 
due to the ability of the operator and improved technic. 
Of the 119 that survived operation, 47 are still living and in good health: 
1 operated in 1898 13 years. 
1 “ “ 1899 12 ‘ “ 
1 “ “ 1901 10 “ 
4 “ “ 1902 9 “ 
5 “ “ 1904 7 “ 
3 “ “ 1905 6 “ 
4 “ “ 1906 5 “ 
5 “ “ 1907 4 “ 
8 “ “ 1908 3 “ 
15 “ “ 1909 2 “ 
“Setting aside the 15 survivals since 1909, that is 2 years ago, a sufficient 
length of time for recurrence, we still have 32 without any symptoms of relapse.” 
The oldest living case was one in which the tumor had so far advanced that 
exploratory7 laparotomy was done, and in spite of the objections of the attending 
physician Temoin removed the growth. This was 13 years ago and the man is 
living, works and eats everything. Examination showed the growth to be a car- 
cinoma. 
The greatest number of the cases operated were between 45 and 55 years; the 
youngest, 22 years, died 2 years later from metastases in the liver; the eldest, 71 
years, died 27 months later from generalized cancer of the peritoneum. 
Federman offers the conclusions of the Germans; they are: 
Resection is justified so long as the growth has not extended beyond 
the stomach or has not invaded the liver or pancreas. The size or seat 
of the limited growth are no contraindications. The author contends that 
the pessimistic views entertained are not justified, for from 20 to 30 per 
cent of operated cases are permanently cured. 
Complications 
Among the complications besides metastases are thrombotic 'processes, 
not due to the secondary deposits in the liver, i. e., catarrhal jaun- 612 
DISEASES OF THE DIGESTIVE APPARATUS 
dice, gall-stones, pancreatic invasion by continuity, pressure on tlie bile 
duct, pancreatic duct, the portal lymphatic glands and the liver itself 
(Welch). Chronic gastritis, non-malignant peritonitis, enteritis, colitis, 
nephritis, pericarditis and after perforation pyopneumo-thorax, abscess or 
gangrene of the lung. 
Hypostatic congestion of the lung was found at post mortem in a num- 
ber of the more chronic cases. 
Tuberculosis may accompany cancer; it is not a frequent complication. 
Healed tubercle nodules are not at all infrequent. Purpuric and embolic 
conditions are always terminal manifestations of malnutrition. 
Barring cases with latent periods, the average duration of life was 
fourteen months. Schweppe reports an acute case of twenty weeks’ dura- 
tion. Encephaloid cancer has run its course in less than three months. 
Boas reports five weeks’ duration of an acute, probably encaphaloid growth. 
Much depends on the extent, rapidity and location of the growth as 
well as the dissemination of the metastases, the individuality and the re- 
sistance of the patient as well as the complications. Hemorrhages are 
rarely sufficiently profuse to shorten life though they have a depressing 
effect on the patient. The mortality of cancer of the stomach will be 
reduced and life prolonged when we have educated the layman and the 
profession to appreciate that in all doubtful cases which justify the sus- 
picion, exploratory incision is imperative and radical surgical intervention 
is demanded when the infiltration is found to be limited, is without distant 
metastases or more than local glandular invasion. It must be remembered 
that a small and symptomless nodule in the stomach may cause metastasis 
to a distant organ. 
“Cancer of the stomach is the most frequent and the most hopeful form 
of cancer in the human body. Early operation affords the victim the only 
chance of cure” (Mayo). 
References 
Bird (Golding). Contributions to the Chemical Pathology of Some Forms of Morbid 
Digestion. 1843. 
Boas. Diseases of the stomach. Translated by Bernheim, Philadelphia, 1908. 
Brinton. Diseases of the stomach. London, 1857. 
Calm & Von Mehring. Deutsches Arch. f. klin. Med., No. 34, 3 & 4, P- 218. 
Cullingsworth. Brit. Med. J., 1877, vol. ii, p. 253. 
Eisner. N. Y. Med. J., May 6 and 20. 1893. 
N. Y. Med. J., Jan. 21, 1911. 
Faroy (G.). Results of operative treatment of 69 cases of carcinoma of the stomach. Arch, 
d. mat. I’appareil dig. et nutrit., Paris, 1913, vii, 61. 
Federman. Berl. klin. Wchnschr., No. 49, 1912, p. 164- 
Feurer. Mitth. a. d. Grenzgeb. der Med. u. Chirurg., vol. xxiv, 1912, p. 870-884- 
Haudek. Progressive medicine. June, 1912, p. 71-72. DISEASES OF THE STOMACH 
613 
Hoffman. Johns Hopkins Bulletin, 1913; also separate reprints. 
J. Am. Med. Ass., editorial, 1913. 
Lebert. Ueber Magenkrankheiten. 1878. 
Leitner. Wien. klin. Wchnschr., Sept. 18, xxvi, No. 38, p. 14-85-1520. 
Leube. Specille Diagnose der inneren Krankheiten. 3d ed. 
Mathieu. Semaine Med., 1895, p. 225. 
Mayo (Wm. J.). Surgery, Gynec. & Obst., Feb., 1912. 
Collected papers by the staff of St. Mary's Hasp., Rochester, Minn., 1911. 
p. 95. 
Mikulicz. Deutsche med. Wchnschr., No. 49, 1892. 
Osier. Practice of medicine. 8th ed., 1914. 
Am. J. Med. Sci., April, 1886. 
Osier & McCrae. Cancer of the stomach. Philadelphia, 1900. 
Pinatelle & Caivaillon. Progres Med., April 14, 1906. 
Riegel. Ztschr. f. klin. Med., 1887. 
Volkmann’s Samml., No. 289. Innere Med. 
Rolleston & Hague. Brit. Med. J., 1898, vol. i, p. 1070. 
Rosenfeld. Geographic distribution of cancer. Wien. klin. Wchnschr., Sept. 11 and lb 
1913, Nos. 37-38. 
Rosenheim. Krankh. der Speisirohe u. Magen. 1st ed. 
Deutsche med. Wchnschr., 1894, No. 49. 
Ztschr. f. klin. Med., Bd. xvii. 
Schweppe. Inaugural dissertation. Goettingen, 1890. 
Smithies (Frank). Arch, of Int. Med., 1912,10, p. 387. 
Temoin. Resection of 168 cases of carcinoma of the stomach. 
Bull, de I’Acad. de Med., Par., 1911, Ixvi, 151. 
von den Velden. Volkmann’s Samml. klin. Vortrdge. No. 280. 
Welch (IF. II.). System of medicine (Pepper). Philadelphia, vol. ii, p. 480-529. 
8. Hematemesis—Gastrorrhagia 
Hematemesis (or vomiting of blood) and gastrorrhagia (or hemorrhage 
from the stomach) are not absolutely synonymous. A patient with gas- 
trorrhagia may have hematemesis, or vomit blood, -while the patient with 
hematemesis may vomit blood which does not come directly from the 
stomach. 
Extragastric Bleeding.—Extragastric bleeding which leads to hema- 
temesis is, as are all bleedings, purely symptomatic and may be due to a 
variety of causes. It not infrequently happens that the tuberculous patient 
with a profuse bronchial hemorrhage swallows considerable blood and 
finally vomits it; the same is true of profuse epistaxis. 
I mention hemorrhage from esophageal varix with Bantis disease, 
also with other esophageal lesions (ulceration, etc.). Decubitus esophageal 
ulcer may lead to hematemesis also specific, tuberculous and esophageal 
peptic idcer, low down. With chronic valvular lesions and portal de- 
struction, varices or profound engorgement of the esophagus may cause 
extragastric bleeding. 614 
DISEASES OF THE DIGESTIVE APPARATUS 
Aneurismal ulceration, usually aortic, with final rupture into the 
esophagus is a cause of death. The bleeding may at first be slight, but 
suddenly it becomes profuse and is promptly fatal. Tumors within the 
thorax or abdomen may by pressure cause hemorrhage. 
Intragastric Hemorrhage.—With splenomegaly due either to leuko- 
cytic leukemia, splenic anemia, pernicious malaria, pernicious anemia, 
or other grave diseases there may be gastrorrhagia; it is always threaten- 
ing and may either deplete the patient if profuse and cause death or it may 
materially shorten life. 
Banti’s disease without esophageal varices may cause profuse gastric 
hemorrhage due to profound engorgement of the vessels of the stomach, 
gastric varix or hemorrhagic diathesis (purpura). 
Cirrhosis of the liver is one of the most frequent causes of hematemesis. 
Amyloid degeneration of the mucosa, acute yellow atrophy of the liver and 
surgical lesions are also included as causes of hematemesis. 
Chronic hyperemia of the gastric mucosa from whatever cause, circula- 
tory disturbances as a rule, including chronic valvular and myocardial 
lesions, may cause gastric bleeding. 
Hemorrhage from ulcer and cancer of the stomach is separately con- 
sidered. The former may threaten, occasionally does destroy life; the 
latter is rarely sufficiently profuse to interfere materially with the course 
of the disease; it is, however, an expression of disorganization and ad- 
vanced disease (See Cancer and llcer of the Stomach). 
With the infections, gastric hemorrhage is experienced. These in- 
clude smallpox, measles, typhus and typhoid fever, relapsing fever, acute 
yellow atrophy, embolic infarct with sepsis—indeed, any infection with 
purpuric or embolic processes or profound and disorganizing constitu- 
tional disturbances may be responsible for hematemesis. 
Various poisons, metallic and vegetable, food poisoning (phosphorus, 
etc.) may lead to moderate, at times, profuse stomach bleeding. 
Hemophilia, the severer purpuras, at times chronic purpura, are fac- 
tors, the recognition of which for rational treatment is all important. 
Following abdominal operations, more frequently than others, particu- 
larly if the omentum is injured, gastric hemorrhage may follow. With 
such complication there is usually peritonitis, and the prognosis is grave. 
I have seen gastrorrhagia with intestinal obstruction. 
Hysterical hematemesis. is not frequent ; it may occur but is never 
serious. Simulation in unexplainable cases should be considered; its de- 
tection has often proved exceedingly difficult. 
Hematemesis or gastrorrhagia, always symptomatic, the influence can 
only be considered with the underlying cause in the individual case. The 
intragastric hemorrhages rarely lead to death directly; they are not usu- 
ally profuse unless a large vessel has been eroded. The extragastric con- 
ditions are more likely to cause profuse and fatal hemorrhages (aneurismal DISEASES OF THE STOMACH 
615 
rupture, traumatism, large varices, etc.). Epilepsy may occasionally 
cause transitory insignificant gastrorrbagia. 
Hemorrhage from the stomach with the infections is usually an evi- 
dence of malignancy of the infection, and is of grave import. Septic con- 
ditions with multiple hemorrhages including gastrorrhagia are generally 
fatal. 
Occasionally there is oozing from the gastric mucosa without known 
cause; this condition occurs in girls near puberty, without pain or other 
subjective symptoms. The condition is not often serious though it may, 
if persistent, lead to secondary anemia. It is known as gastrostaxis. 
Purpuric or hemorrhagic conditions in the newborn with hemorrhages from 
mucous membranes is almost always fatal. We have seen petechiae and 
cord infection with these cases. 
9. Gastric Neuroses 
(Nervous Dyspepsia, Dyspepsia nervosa (Leube) 
General Consideration.—The consideration of dyspepsia is now lim- 
ited entirely to those forms of (1) sensory, (2) motor, and (3) secretory 
anomalies in which no anatomical change in the stomach can be diagnosti- 
cated or detected post mortem. All of the neuroses are characterized by 
poor and deranged digestion, in which the leading symptoms and general 
character of the disease point to the ungeared nervous system as the 
seat of the trouble. I consider with neurasthenia and hysteria many 
of the features of nervous dyspepsia (See separate chapters on Neuras- 
thenia and Hysteria), and must here again accent the facts that in all 
there is an unstable nervous system, a strong neuropathic habit; the ego 
is usually in the ascendency, and the patient is so self-centered that he 
is unable without powerful assistance to divorce himself from himself. He 
is eager to will but he cannot ; his symptoms are almost continually before 
his mental vision, and with all forms of the disease the importance of each 
feature is enormously exaggerated. There is no other organ of the body 
which is so often the seat of symptoms of a functional character as the 
stomach. 
With all of the neuroses there may be psychoses which include manic- 
depressive types, hypochondriasis or other anomalies. The 'phobias 
(fears) or imperative conceptions (obsessions) are often in the foreground 
and there is a strong tendency on the part of the patient to become more 
and more inefficient with the severe complex. There are but few patients 
who suffer from nervous dyspepsia who are not neurasthenic. In some 
cases there is organic disease with which dyspepsia is associated. Base- 
dow’s disease, anemia, malaria, uterine and ovarian anomalies in women, 
genito-urinarv disturbances in man, suprarenal disease and spinal lesions 616 
DISEASES OF THE DIGESTIVE APPAKATUS 
are often burdened with nervous dyspepsia. Ocular anomalies unques- 
tionably prove provoking factors. Often the graver disease is forgotten 
in the presence of symptoms referable to the stomach. 
1. Sensory Dyspepsia—Hyperesthesia 
The leading features of the sensory neuroses are subjective. With nor- 
mal, perverted or lost appetite, at times a craving for unusual foods, the 
marked general hyper esthetic condition of the patient stands out in bold 
relief. Often the fear of eating, causes loss of flesh and strength. The 
gastric mucosa revolts as soon as food enters in some cases. The resulting 
pain is described as unbearable, usually burning, boring, lancinating, or 
there may be complaint when the stomach is empty. These patients react 
peculiarly to medicines and foods. At times they show great tolerance 
for indigestible foods, while at the same time they complain of the acute 
pain which follows the simplest diet. 
Gastralgia, so called “neuralgia of the stomach” in my experience is 
rarely of functional character. I do not agree with Cohnheim that the 
neuroses of the stomach are not associated with pain or “neuralgia,” but 
1 hold that gastralgia is so rarely of functional origin that the diagnosis 
should not be accepted until all of the features of the case have been thor- 
oughly considered. The diagnosis should be made with a “loop hole” 
attached, through which the diagnostician will usually be forced to escape. 
Recurring gastralgia should always create the suspicion of gall-stones, tabes 
dorsalis, ulcer of the stomach or duodenum, chronic appendicitis, bone or 
other pressure (spinal or aneurismal). 
The mental condition of the dypeptic with this form of the disease is 
out of all proportion to the importance of his neurosis. As in all other 
forms of nervous dyspepsia the majority of patients are women. In some 
of these cases hyperacidity has been demonstrated; in the majority of 
cases the examination of the stomach contents offers nothing. 
Psychic influences, distant irritation, eye strain, a general condition 
below par, sexual anomalies, long continued worry, lack of occupation or 
overwork, occupation which is not suited to the individual, are all factors 
which make it impossible, unless relieved, to throw off the load which 
overwhelms the patient. The outlook in the cases which can be removed to 
the needed environment, with the relief of the neurasthenic and irritating 
factors, the added strong personality and overpowering suggestion of the 
attendant who is not wedded to polypharmacy, but who takes advantage 
of rational and natural methods of treating these unfortunates, is rela- 
tively good. These factors are important and influence the forecast of 
all types of gastric neuroses. DISEASES OF THE STOMACH 
617 
2. Motor Gastric Neuroses 
Motor disturbances may be due to (a) hyper motility or (b) hypomo- 
tility. 
(a) Hypermotility (Supermotility—Hyperkinesis). The prompt and 
premature expulsion of the food from the stomach may cause no subjec- 
tive symptoms, may be associated with the neurasthenic accompaniment, 
and can only be recognized by the use of the stomach tube or x-ray. 
The peristaltic unrest of Kussmaul is due to the contraction and re- 
laxation of the stomach musculature following the taking of food. In 
these cases there may be hypersecretion and hyperacidity. The attending 
nervous symptoms are prominent; vomiting is not infrequent; migraine 
is at times annoying; belching of gas, splashing noises, abnormal rapid 
emptying of the stomach, at times pylorospasm, all are without pain. 
In all of these cases the suspicion of organic disease should not be sur- 
rendered until there has been a thorough and satisfactory differentiation. 
Stockton and others have called attention to the possibility of pyloric and 
cardiac spasm in the same patient. Pyloric spasm long continued, as well 
as cardiospasms may lead to serious malnutrition. 
With hypermotility, the loud and annoying belching of gas (aero- 
phagia) is often uncontrollable during days at a time. In most of these, 
positively without organic fundament, the noisy and active belching ceases 
during conversation or distraction. We have seen a number of cases in 
which the symptom yielded to hypnotic suggestion; in occasional cases 
a sudden shock or intercurrent illness had a salutary effect. The expelled 
air has been aspirated or swallowed. 
Nervous Vomiting.—ITypermotility may cause so called "nervous 
vomiting.” In most of these cases there is a powerful hysterical or 
neurasthenic element which is materially aggravated by the persistent 
emesis. Between the separate emeses there may be peristaltic unrest or 
almost continuous belching of gas. The element of suggestion is prom- 
inent. The stomach, as shown by x-rays, is often filled with gas; the 
stomach content is found normal—occasionally there may be hyperacidity. 
There is never in uncomplicated cases the presence of organic acids. 
Rumination—Merycismus.—Rumination in the human being is ex- 
ceedingly rare. In my practice it occurred only twice. In both instances 
the patients were neurasthenic during long periods with ultimate perma- 
nent psychasthenia. Cases in the hysterical and insane, epileptic and 
idiotic, are occasionally recorded. When it becomes a habit, as it does very 
rarely, it is exceedingly rebellious to suggestion and is probably a stigma 
of degeneracy. 
(b) Hypomotility.—With atony of the stomach wall (musculature) 
the organ does not empty itself normally; there is stagnation, with final 
dilatation, and in some cases tetany (See Tetany). These patients are 618 
DISEASES OF THE DIGESTIVE APPARATUS 
highly neurotic; their splashing stomachs and eructations are to them 
enormously significant; they develop all manner of nervous symptoms; 
are exceedingly unhappy and often suffer from insomnia, and as most 
patients with gastric neuroses, they are subject to the cardiac neuroses, 
jjalpitation, precordial distress and abnormal fullness. 
Insufficiency of the Pylorus.—In some of these cases the pylorus is 
insufficient—a condition which is not usually recognized. When gastric 
atony persists unrelieved, the general condition suffers and there is always 
justification for the belief that it is dependent upon an organic fundament. 
3. Secretory Anomalies—Reichmann’s Disease 
Hypersecretion and hyperacidity may be of functional character, 
lleichmann first called attention to this combination which is now recog- 
nized by the use of the tube and examination of the stomach contents. 
The presence of abundant hyperacid gastric juice in the stomach, when 
it should be empty, is characteristic. Long continued Reichmanns dis- 
ease leads to motor insufficiency, in some to complete gastric atony. Gas- 
tralgia is a prominent symptom after great excitement or emotion. In all 
of these cases organic disease of the nervous system, ulcer, or other 
anomalies should be considered and strongly suspected. 
Hyperacidity (Ilyperchlorhydria).—Hyperacidity may be diagnosti- 
cated when the total acidity of the stomach contents is continuously above 
60. Hot all who have a total acidity of 60 or slightly above show symp- 
toms, but with neurasthenic symptoms and stomach distress such figures 
do justify the diagnosis. I am always suspicious in the absence of 
organic stomach disease and hyperchlorhydria of gall-stones or cholecystitis, 
and such suspicions have often been confirmed by the subsequent history. 
The presence of hyperacidity continuously not dependent upon organic 
disease, besides a train of nervous manifestations which are common to all 
the gastric neuroses, is likely to cause sensory disturbances, pain, gas- 
tralgia and (as the condition is found in young girls at puberty) often 
there is marked chlorosis. Epigastric pressure, pyrosis, eructation of some 
fluid and vertigo are the leading symptoms besides the marked neurasthenic 
features. 
Anacidity or Reduced Total Acidity (Hypochlorhydria).—Anacidity 
is characterized by the abnormal lowering of free ITC1 in the stomach 
contents. This condition is exceedingly rare in functional disease. There 
is an achylia gastrica nervosa. Riegel says: “It cannot be denied that 
occasionally achylia gastrica may be merely a perversion of function.” 
Long continued achylia or hypoacidity unless recognized and compen- 
sated by diet and treatment leads to loss of weight and strength. In some 
cases which have been originally considered functional, the advent of 
pernicious anemia has cleared the horizon. DISEASES OF THE INTESTINES 
619 
In presenting the leading clinical features of the various gastric neu- 
roses the psychic element has remained prominently in the foreground. 
Dreyfus has, after a thorough consideration of his material concluded that 
practically all forms of nervous dyspepsia depend upon psychic changes, 
and that the stomach symptoms are of “secondary nature.” Pawlow’s 
observations prove conclusively the close relationshop of the psychic and 
nervous element with gastric function. What is said in connection Avith 
the prognosis of neurasthenia and hysteria is equally applicable in offer- 
ing the forecast of all gastric neuroses. The prognosis of most of these 
functional anomalies is good A\Then \ve have gained an insight into the 
prime factor which has caused and is continuing the symptom complex. 
This means the thorough analysis of each case, the differentiation Avhich 
when complete Avill materially reduce the number of these cases, and the 
regulation of the lives of these patients that gladness may displace the 
gloom which surrounds them. Besides the strong personality of the at- 
tendant to lead the patient, the healthy occupation of the mind will do 
more than anything else to bring relief and cure. Uncomplicated gastric 
neuroses do not lead to death. Recurrence in all forms is the rule. 
References 
Cohnheim. Verdauung u. Erndhrung. Berlin, 1908. 
Dreyfus (L. Georges). Ueber Nerv. Dyspepsie. Jena, 1908. 
Kussmaul. Volkmann’s Samml. klin. Vort., No. 181. 
Deutsche Arch. f. klin. Med., Bd. vi. 
Leube. Specielle Diagnose d. inner. Krankh. 7. Aufl. Leipzig, 1904, Bd. i. 
Pawlow. Arbeit d. Verdauungsdriisen. 1898. 
Ergebnisse d. Physiologie. 1902, Biochemie, 266. 
Reichman. Berl. klin. Wchnschr., 1882, p. 606; 1884, p. 768; 1886, Nos. 32, 33; 1887, 
p. 12. 
Riegel. Volkmann’s Klin. Samml. No. 286 & 289. 
Nothnagel’s Spec. Path. u. Therap., 1908, Bd. xvi. ii. Halfte. 
Ztschr. f. klin. Med., Bd. xii. 
Stockton. Diseases of the stomach. New York, 1914. 
G. Diseases of the Intestines 
1. Acute Enteritis—Acute Diarrhea 
(a) Acute Catarrhal Enteritis 
Acute catarrhal enteritis—catarrh of the bowels—is one of the most 
frequent of all acute diseases; it is most frequent in young subjects, 
oftener during the first two years of life. The disease may be either 
'primary or secondary. 620 
DISEASES OF THE DIGESTIVE APPARATUS 
When acute diarrhea is primary, it is due to some error of diet, pol- 
luted food—ptomain poisoning—impure drinking water, epidemic condi- 
tions, excessive heat, with at the same time the eating of spoiled or tainted 
food (milk usually) toxic agents, drugs, such as arsenic, phosphorus, cor- 
rosive sublimate, purgatives, mental emotion, particularly fright. 
The secondary causes are the infections, heart diseases in which there 
is acute congestion of the mucosa, disease of the lung, acute or chronic 
congestion or obstruction in the liver, trichinosis, intestinal parasites, dis- 
eases of adjacent organs, extensive surface burns, nephritis, malaria, and 
the various cachexias. 
Acute duodenitis, or catarrhal inflammation which limits itself to the 
duodenum, which may or may not be associated with gastritis usually 
causes jaundice (See Catarrhal Jaundice). The latter condition is also 
known as gastro-duodenitis. 
Diarrhea is not necessarily an attendant of all catarrhal enteritides. 
It may be absent with duodenitis or inflammation of limited portions of 
the small intestine; such conditions may cause constipation. The more 
severe forms may involve not only the lower half of the small intestine 
but include the large intestines and provoke painful and weakening diar- 
rhea with tenesmus and heart weakness. Most of these recover after from 
ten to twelve days. 
The simple uncomplicated primary form of the disease without jaun- 
dice is easily controlled, and without more than a few days of weakness 
after the control of the diarrhea leads to full recovery without sequel. In 
some cases the recovery may be protracted, particularly when the cause 
is not at once evident or the intestinal tract has not been freed. When 
the mesenteric glands are involved, recovery is slow. If there are catar- 
rhal ulcers there may be a subacute course, but such cases are exceptional. 
Only rarely in average treated cases does chronic enteritis follow. 
Idiosyncrasies cause some to develop diarrhea (acute enteritis) when 
certain foods are taken which have no influence on normal individuals. 
These cases are easily controlled by diet. Food poisoning is elsewhere 
considered in this work. Enteritis due to ptomain poisoning is often 
severe and weakening, and when the patient is overwhelmed may prove 
very serious. Naturally the prognosis depends on the quantity and viru- 
lence of the poison, the prompt relief by vomiting early or late, and the 
ejection of the poison before it has been absorbed. The more unfavorable 
cases are those in which symptoms are postponed from twenty-four to 
forty-eight hours after the taking of the poison (See Food-poisoning). 
The prognosis of the secondary enteritides depends entirely upon the 
ability to influence the underlying causes; if these are remediable, as in 
malaria, some forms of acute nephritis, circulatory faults, intestinal para- 
sites, relief is possible. DISEASES OF THE INTESTINES 
621 
(6) Croupous Enteritis—Diphtheritic Enteritis 
Diphtheria may cause croupous enteritis with characteristic diph- 
theritic sloughs and ulcerations, and in rare cases perforation may result. 
The ulcerations are most frequent in the large intestine. 
Croupous enteritis may follow or he associated with mercury poison- 
ing, profound uremia, chronic nephritis, and dysentery, and may develop 
upon specific tuberculous or septic idcers (Mattlies). 
Riedel has reported diphtheritic necroses in the jejunum and ileum 
after laparotomy in weakened individuals. These conditions are all asso- 
ciated with weakening and uncontrollable diarrhea besides tenesmus and 
tormina. When croupous ulcerations of the intestines complicate the in- 
fections (pneumonia, pyemia, typhoid, smallpox and sepsis) chronic 
nephritis, cirrhosis of the liver, cancer or the other primary infections 
mentioned in the preceding paragraph, enteritis may be only superficial, 
without serious moment; on the other hand, it may prove to be among 
the terminal symptoms. 
(c) Phlegmonous Enteritis 
Phlegmonous enteritis with ulceration is not frequent. It may be 
associated with streptococcus infection {erysipelas), surgical lesions of the 
intestines, such as intussusception, volvulus, strangulated hernia, trauma- 
tism, or any of the mechanical obstructions. Unless the primary source 
of infection is relieved death will surely follow. These cases present a 
dark outlook. 
(d) Ulcerative Enteritis 
Ulcerative enteritis is usually secondary to the infections, including 
syphilis, tuberculosis, typhoid fever, dysentery, splenic fever; to the con- 
stitutional diseases including leukemia, purpura, amyloid disease, arterio- 
sclerotic changes, and infarct; also to neoplasms and conditions which 
originate outside the intestines, which by continuity lead to ulceration and 
perforation; decubitus ulceration is occasional. 
Acute and chronic catarrhal follicular ulcers may form after acute or 
subacute uncomplicated catarrhal enteritis has existed for some time; this 
is more likely to happen in children than adults and may prove rebellious 
to treatment, though the majority heal, leaving recognizable cicatrices. 
Ulcers may exist in adults during long periods without causing symptoms. 
Multiple ulcers of the intestine due to enteritis or infection may in the 
process of repair and final cicatrization lead to single or multiple constric- 
tion of the intestine, usually incomplete, but sufficient to cause symptoms 
of partial obstruction and chronic invalidism. The differentiation of this 
form of ulceration and tuberculosis is often exceedingly difficult. I have 
in such cases found the patient incapacitated during many years with 622 
DISEASES OF THE DIGESTIVE APPARATUS 
almost continuous symptoms. In one such case following typhoid fever, 
an exploratory laparotomy disclosed multiple constrictions with collapse 
of intestines below the first narrowing in the jejunum and marked pocket- 
ing above. There were eight separate constrictions. This patient lived 
unrelieved during four years after the exploration, and died of asthenia. 
When the ulcerations are in the large intestine (rectum, sigmoid, etc.) 
of specific catarrhal or dysenteric origin, they are amenable to treatment 
and many make very satisfactory recoveries (See Syphilis, Dysentery, 
also Actinomycosis). 
(e) Mucous Colitis—Membranous Enteritis 
The prognosis of mucous colitis depends entirely upon its cause- All 
cases may he divided according to their etiology into: 
(I) Nervous or hysterical colitis 
(II) Infectious mucous colitis 
(III) Infantile mucous colitis 
(IV) Secondary mucous colitis. 
(I) Nervous or Hysterical Colitis.—I have elsewhere considered 
mucous colitis of hysterical or nervous origin (See Hysteria, Neuras- 
thenia). The condition is most frequent in women but is not infrequent 
in men. It is usually one of many symptoms which are evanescent, and 
its importance is almost always enormously exaggerated by the patient. 
The passage of mucous casts always has a depressing and discomforting 
effect on the patient, though in truth the strength or resistance of the 
'patient is not disturbed by it. The disease is chronic; it does not as a 
rule yield to medical treatment but is materially influenced by psychic 
impressions, rest and changed environment; it may disappear suddenly 
and permanently without known cause, or relapses may be frequent. In 
some cases there is associated and weakening pain. We have never 
known of serious complications or death from hysterical or nervous mem- 
branous enteritis—a fact which it is necessary to suggest repeatedly to 
these patients; once indelibly impressed, the result is wholesome. 
(II) Infectious Mucous Colitis.—In children with intestinal infec- 
tion, casts or membranes occasionally form in severe summer diarrheas, 
vdiich are weakening and threatening. This complication is not fre- 
quent. In some of these cases the Shiga organism is present. With 
croupous enteritis in adults, without diphtheria bacilli, casts may form; 
unless the constitutional symptoms are severe or the enteritis deep with 
ulceration the prognosis is good. With acute infectious enteritis mucous 
casts may form, and are found in the stools. The prognosis in these cases 
is good. Catarrhal and infectious enteritis in hysterical subjects may 
be complicated by membrane formation, without materially influencing 
the progress of the acute inflammation. DISEASES OF THE INTESTINES 
623 
(III) Infantile Mucous Colitis.—The infectious infantile colitis, at 
times enterocolitis, has been mentioned in the previous paragraph; it may 
complicate cholera infantum or it may be due to faulty feeding and per- 
sisting intestinal catarrh and indigestion. In young children, colic and 
membrane formation may occur without known cause, though as a rule 
there are evidences in fever, rapid pulse, and constitutional symptoms of 
acute infection. The association of membranous colitis with the diarrheal 
diseases of childhood, in weakened rachitic and underfed children may 
prove serious. Most of my cases have made full recoveries, and a similar 
experience in over 95 per cent of all uncomplicated cases may be presaged. 
(IV) Secondary Mucous Colitis.—In grave organic diseases such as 
the deep ulceration of carcinoma, tuberculosis, syphilis or decubitus ulcers, 
membranes may form, are cast off in the stools with pain—at times tenes- 
mus—characteristic of the primary disease. The prognosis of the under- 
lying condition is almost always unfavorable, the addition of membranous 
enteritis is not of grave import. 
(/) Cholera morbus—Cholera nostras 
During the summer months sudden, acute, severe abdominal colic 
associated with diarrhea and vomiting, some fever, acceleration of the 
pulse dependent upon the eating of unripe fruits, bob veal or other errors 
of diet is frequent, but in the previously healthy is promptly relieved by 
simple means, often without medical treatment and without sequelae. 
In the very weak and sick, severe cholera morbus may, during collapse 
cause ominous heart weakness, but death very rarely. In previously nor- 
mal adults I have never known of a death. From twenty-four to sixty 
hours finds the patient fully restored, barring a slight remnant of weak- 
ness. 
I do not classify the infections due to the Gaertner bacillus (bacillus 
enteritides) as cholera nostras (See Food Poisoning) neither can we in 
this country accept the statistics of Eumpf (quoted by Matthes) that 
10 per cent of cholera morbus patients die in collapse. If we include the 
food poisonings above mentioned, we might possibly approach that mortal- 
ity. In all doubtful cases the diagnosis will require the differentiation of 
Asiatic cholera (during epidemics), acute poisoning (arsenic, phosphorus, 
strophanthus, etc.), intestinal obstruction, gall-stones, appendicitis, per- 
forative peritonitis from stomach more likely duodenal ulcer, and nephritis 
with uremia. 
2. Chronic Enteritis—Chronic Diarrhea 
Neglected or severe acute catarrhal euteritis may occasionally cause 
chronic changes in the intestinal mucosa and mesenteric glands. The 624 
DISEASES OF THE DIGESTIVE APPARATUS 
changes may he atrophic, or there may be cystic degeneration of the intes- 
tinal follicles as described by Aschoff (colitis cystica). Chronic hyper- 
emia of the intestinal mucosa, dependent upon circulatory or respiratory 
disease, chronic nephritis (uremia) or constitutional disturbances, may 
cause chronic diarrhea. In children, chronic diarrhea with wasting, may 
he associated with tabes mesenterica (tuberculosis of the • mesenteric, 
glands), or in earliest life to what was formerly supposed to be an atrophy 
of the intestinal glands, but which has been found to present no struc- 
tural changes (Aschoff, Huebner, Schelbe and others) and is now char- 
acterized as enteropathia dyspepiica chronica. In the foregoing condi- 
tions the prognosis depends entirely upon the ability to nourish the pa- 
tient and compensate by proper diet for the loss of normal intestinal 
digestion. 
The classification of the chronic diarrheas of the adult is, thanks to the 
thorough study by modern methods of the stool and the association of 
symptoms with microscopic finds made possible, and the prognosis there- 
fore rests on a solid foundation (Schmidt and Strassburger). 
Intestinal dyspepsia, dependent upon fermentation, in which there 
are symptoms of catarrhal enteritis, persists until the fault (usu- 
ally faulty starch digestion) is corrected by diet and other treatment. 
The diagnosis and prognosis of these cases may be cleared by the exami- 
nation of the stools which are light yellow, contain gas bubbles, are mushy, 
have a sour odor, and give an acid reaction. Macroscopically there are 
abundant remnants of undigested potato ; microscopically after staining 
with iodin the starch cells are in the ascendency undisturbed, surrounded 
by microorganisms. Schmidt and Strassburger found fermentation of the 
stools in the incubator. These patients digest albumin and fat well. Un- 
less the condition has been present during a long time, with a suitable 
diet, these patients may be freed of their intestinal indigestion and chronic 
diarrhea. 
The second variety of chronic diarrhea which Schmidt classifies is the 
gastrogenic diarrhea. In these cases it may be assumed that stomach 
digestion is at fault. The stools on a meat diet show by the presence of 
the meat and connective tissues, shreds particularly, that gastric function 
is impaired. With these diarrheas, anacidity, atrophy of the gastric folli- 
cles or functional indigestion may be paramount (achylia). The entire 
failure of stomach digestion in these cases to supply the intestine with its 
normal stimulant is largely responsible for the symptoms. In some of 
these cases the hypermobility of the stomach is a factor, for not all pa- 
tients with achylia have diarrhea. These gastrogenic diarrheas may be 
dependent upon a variety of causes and may include at the same time 
intestinal anomalies. Matthes suggests that in the absence of a single 
fault in the stomach which accounts for all cases, it might be wise to 
characterize them as chronic gastro-intestinal dyspepsia. DISEASES OF THE INTESTINES 
625 
Chronic diarrhea may he of nervous origin and it is not uncommon in 
such cases to find alternation of constipation and loose bowels. Schmidt 
relegates a few of these to faulty pancreatic function, functional pancreas- 
achylia. 
Most of the nervous diarrheas are largely dependent upon psychic 
influences, are not easily influenced by diet or medicine, and are favorably 
affected by travel, environment and agreeable occupation. 
I mentioned the prognostic significance of chronic or persistent diar- 
rhea with exophthalmic goiter and Addison’s disease (See Diseases of 
the Ductless Glands). With both, weakening diarrhea contraindicates sur- 
gical interference and influences the case unfavorably. Often the symp- 
tom improves with the other manifestations, and gain of flesh is phenom- 
enal. There are individuals, usually of nervous organization, who are 
unable without resulting diarrhea to take certain foods, milk particularly. 
Such idiosyncrasy does not make wholesome diet impossible, and with 
compensation for the loss of one or two articles of food, weight is improved 
and enteric symptoms are relieved. 
Chronic enteritis may result from previous typhoid infection, from dys- 
entery, paratyphoid infections, chronic malaria, and any disease which 
causes atrophic or productive changes in the intestines. Such cases are 
favorably influenced by diet; death rarely results as the direct effect of 
the enteritis. 
There are veterans of the Civil War still living with chronic diar- 
rhea which resulted from acute infections of the small and large intes- 
tines during service. In these chronic cases there is always danger of the 
opium habit; among some of the veterans above mentioned the “black drop” 
is still taken. 
Habitues of opium are often the victims of secondary diarrhea, and 
paresis of the intestinal musculature may cause symptoms of obstruction•. 
Chronic ulceration of the intestines, from whatever cause, may continue 
diarrhea. 
Secondary Chronic Diarrhea 
Chronic nephritis, uremia, cirrhosis of the liver, heart lesions, tumor 
pressure, secondary chronic hyperemia, and amyloid disease, may all con- 
tinue diarrhea during periods of varying length, according to the nature of 
the primary disease and the ability of the patient to resist. 
Chronic lesions within reach of the eye (rectal, sigmoid) which are 
non-malignant, with modern methods of recognition and local treatment, 
offer a good prognosis if not too far advanced. 
Productive changes and distortions secondary to dysentery are purely 
surgical affections; strictures of the rectum or sigmoid may continue 
chronic diarrhea, as may also chronic constipation and malignant constric- 
tions. Frequent, small stools, often unsatisfactory stools, should always 626 
DISEASES OF THE DIGESTIVE APPARATUS 
create the suspicion of an unrelieved bowel, just as frequent unsatisfac- 
tory urination, is evidence of retained urine. 
Diagnosis and prognosis of all forms of chronic diarrhea are materially 
advanced by the repeated consideration of the general condition of the 
patient, for in unexplained diarrhea suspicion should fall upon several 
vital organs, including kidney, liver, heart and nervous system. 
{Chronic Enteritis of Warm Countries, Aphthae tropical, Aphthae 
orientates, Psilosis linguae et mucosae intestini) 
Sprue 
With sprue the entire mucosa of the intestinal tract is involved in a 
chronic and remitting inflammation which seems to attack Europeans 
mainly, living in tropical or subtropical climates. The tongue and 
mouth are mainly involved in superficial ulceration; the mucosa is hyper- 
sensitive, Avhile the intestinal lesions cause diarrhea. The disease is occa- 
sionally brought to our country; in the tropics it may complicate other 
forms of enteritis. Thin has suggested the name of “psilosis” because 
of the raw appearance of the tongue and intestinal mucosa. Manson says: 
“Of all the chronic diseases the European has to contend against (in 
South China), sprue, in its various forms and degrees is by far the most 
frequent as well as the most formidable.” 
The bacterial cause of sprue is uncertain. Whatever its cause finally 
proves to be, the peculiar history of the disease, its chronicity, long periods 
of latency and recurrence (patients without returning to the source of 
infections years after the initial symptoms, developing anew the symp- 
toms) will require consideration. Unless relieved, the loss of flesh and 
strength with anemia and heart weakness associated with the “primary 
and secondary effects of starvation” (Manson) may cause death. The 
organic changes in the intestines, gastric mucosa, as Avell as in the upper 
portions of the alimentary tract, may be deep and variable. They include 
follicular changes, ulcerations, atrophy, infiltration of the mucous mem- 
brane (leukocytic), and in the more chronic types, fibrotic or productive 
deposits throughout the small and large intestines. 
When the disease is limited to catarrhal changes, full recovery is 
possible. The deeper changes above mentioned are secondary in all prob- 
ability to long continued and unrelieved catarrhal processes, and while 
symptoms may be partially overcome, the organic changes remain. In 
all the cases seen in this country, the tongue lesions have been prominent 
and painful. These cases, unless relieved, progress; emaciation advances 
and is excessive; the patients resemble the reconcentrados of the Cuban 
War; the urine is albuminous, edemas and general dropsy follow with 
increasing uncontrolled diarrhea, death results from starvation. The 
prognosis depends entirely upon removal to proper quarters and proper DISEASES OF THE INTESTINES 
627 
food during the early stage of the disease—before the mucous membrane of 
the alimentary canal has been destroyed. The clinician should not be 
deceived by periods of marked improvement or latency; he must guard 
his prognosis because of the tendency of relapse even after years of free- 
dom as already suggested (See references for history and literature). 
3. Diarrheal Diseases of Early Childhood 
I have repeatedly in the preceding pages referred to the infections 
of the infant which lead to diarrheal diseases, and have considered their 
prognosis. The campaign of education which has led to clean and pure 
milk has done much to reduce infant mortality. He who practiced during 
the days when ignorant of the causes of intestinal diseases thousands of 
infants were annually sacrificed, and who is privileged to note the change 
which has followed the dissemination of knowledge among the masses 
and the medical profession, is deeply impressed by the favorable advance. 
Prophylaxis is possible in all communities and in all families wher- 
ever concerted action of the profession and responsible head of the house 
obtains. The reduction of mfant mortality from diarrheal diseases is the 
problem of the state and the municipality. Infant mortality will be re- 
duced to an almost negligible factor when ideal conditions prevail. What 
they are, the profession understands; it remains only for the profession 
to demonstrate these to the lawmakers that competent health officers may co- 
operate with every household. 
Besides the prophylactic factors which can be easily controlled, the 
baneful effect of humidity and high temperature on infant mortality due 
to diarrheal diseases must be considered; to these factors must always be 
added bacterial contamination (the Shiga bacillus usually). The change 
which has resulted in infant mortality is best understood when the mortu- 
ary records of large cities are considered. Naturally the death rate is 
lower from cholera infantum and other diarrheal diseases of early life 
during favorable summers. In London, as in all cities, the science of 
infant feeding has progressed and the mortality during all years since 
1906 has been materially reduced. The last (1910) census of the United 
States shows for the registration area as a whole, the general death rate 
was 15 per 1,000 population for 1910, including an element due to 
infant mortality amounting to 2.9 deaths of infants under 1 year, and 
4 deaths of children under 5 years per 10,000. There were 44,695 
deaths of infants under 1 year of age from diarrhea and enteritis. The 
previous census, 1905, published in 1907, shows that in 1905 the death 
rate from diarrheal diseases was higher than during the preceding four 
years. 628 
DISEASES OF THE DIGESTIVE APPARATUS 
CENSUS OF 1905. 
Age 
Number of Deaths from Diarrhea and Enteritis 
Annual Average 
1900-1904 
1901 
1902 
1903 
1904 
1905 
Aggregate deaths 
Under 2 years 
2 years and over 
36,021 
35,596 
33,627 
33,035 
36,864 
39,399 
29,183 
6,838 
28,523 
7,073 
26,903 
6,724 
26,697 
6,338 
30,315 
6,549 
33,032 
6,367 
Number of Deaths per 100,000 of Population 
Annual Average 
1900-1904 
1901 
1902 
1903 
1904 
1905 
Under 2 years 
2 years and over 
112.8 
91.4 
21.4 
113.8 
91.2 
22.6 
105.4 
84.3 
21.1 
101.6 
82.1 
19.5 
111.3 
91.5 
19.8 
116.7 
97.8 
18.9 
The census of 1910 shows that over 90 per cent of all deaths from 
diarrhea and enteritis were in children under 5 years, and 70 per cent 
were of children under 1 year of age. The total number of deaths of 
infants under 1 year for 1910 was 154,373—one-fifth of all deaths (19.2 
per cent). During the second year 33,080, or 4.1 per cent of the total. 
Of 58,089 deaths of infants under one month 5,901 were due to diar- 
rhea and enteritis. Beginning with the second month of life diarrhea 
is the most serious cause of infant mortality. Of 15,223 deaths of in- 
fants 1 month of age and under 2 months, 4,692 were from diarrhea and 
enteritis. Infants 2 months of age and under 3 showed 4,980 deaths 
from diarrhea and enteritis. 
DIARRHEA AND ENTERITIS (Under 2 Years of Age). 
1909 
No. of 
Deaths 
Death 
rate per 
100,000 
Population 
1910 
No. of 
Deaths 
Death rate 
per 100,000 
Population 
The registration area 
44,648 
87.8 
54,216 
100.8 
Registration cities 
30,504 
102.9 
36,781 
117.8 
Registration states 
38,033 
85.9 
47,197 
98.7 
Cities in registration states 
23,889 
103.6 
29,712 
118.0 
Rural part of registration states 
14,144 
66.7 
17,485 
77.3 
Registration cities in other states.... 
6,615 
100.4 
7,069 
117.1 DISEASES OF THE INTESTINES 
629 
The above statistics make reliable comparisons from year to year im- 
possible because the registration of births in the United States is defective. 
The rate of infant mortality as given by English and continental cities 
where the registration is practically correct are encouraging. The fob- 
lowing from the annual summary of the Registrar-General of England : 
The decrease per cent between 1881-1885 and 1906-1910: in Lon- 
don 24.0, Edinburgh 6.3, Paris 34.6, Amsterdam 55.7, St. Petersburg 6.8, 
Berlin 41.3, Hamburg 32.4, Munich 42.6. 
The features which make the prognosis of cholera infantum had are 
weakness and lack of resistance, collapse, high temperature, rapid pulse, 
profuse watery depleting stools, convulsions, great restlessness, dry to7igue, 
reduced quantity of urine, tenesmus and uncontrollable vomiting. With 
irregular respiration and opisthotonos the prognosis is also bad; also with 
bronchopneumonia or other complications. 
Enterocolitis, ulcerative enteritis and membranous enteritis of child- 
hood are considered in the preceding pages of this chapter. The mortal- 
ity of summer diarrhea is always higher when the Shiga bacillus and 
streptococcus are present. The mortality in the presence of the gas bacilli, 
averages between 40 and 60 per cent in large cities. When acid move- 
ments are improved by proteid food the prognosis is accordingly better. 
Schmidt’s bile test in the summer diarrhea of infants has been thor- 
oughly tested for its prognostic value by Pearson. It has been established 
that zymotic enteritis (infectious) is associated with a marked diminution 
in the secretion of bile; in the cases which come to the post mortem room, 
according to Pearson, the tests for bile remain negative throughout the 
intestines. In a series of 500 cases with the “proper secretion of bile 
restored, and no other complication—such as bronchopneumonia—the cases 
invariably recover.” In Pearson’s latest publication he says: “The point 
I wish to lay stress on is that in over 2,000 cases of acute summer diar- 
rhea (of infants) I have never lost one in which the Schmidt test * con- 
tinued, or after treatment became positive. With as much emphasis I 
may say that I never managed to cure one case in which the test con- 
tinued negative.” 
4. Celiac Disease—Diarrhea alba—Diarrhea chylosa 
In children between the first and third year without the appearance 
of organic change, there may be numerous large, foul-odored, light col- 
* Schmidt test: A teaspoonful of fecal matter is placed in a wide test tube, a 
little sterilized water added, and well stirred with a glass rod. The tube is then 
filled to four to six times the volume with a saturated solution of corrosive subli- 
mate, the mixture well shaken and allowed to stand twelve hours. By this time 
feces if normal becomes colored bright red, showing the presence of hydrobilirubin 
or stero-bilin, but if unchanged, bile pigments are present and the color becomes 
green. If no change occurs bile is absent. 630 
DISEASES OE THE DIGESTIVE APPARATUS 
ored stools, resembling porridge. These children lose flesh and strength 
progressively; there is marked muscular weakness; in some there is threat- 
ening, at times, fatal tetany, and a number of writers have found infantil- 
ism, result. This type is exceedingly chronic, and improvement is often 
followed by repeated relapse and death. The fault lies in the failure of 
the child to digest fat and starch, and unchanged fat is found in the 
stools. These cases may be so severe as to suggest tuberculous enteritis and 
tabes mesenterica. In rare cases there have been ulcers. The substitution 
of raw minced meat or meat juice, improves most cases. 
References 
Aschoff. Pathol. Anatomie. Jena, 1913. 
Hillary. Diseases of the Island of Barbadoes. London, 1776. 
Manson. Tropical medicine. Allbutt & Rolleston’s System of medicine. London, 1907, 
vol. ii, part ii. 
Notes on sprue. Shanghai, 1880. 
Matthes. von Mehring, Lehrbuch d. inner. Med. Jena, 1913, 8 Aufl. 
Pearson. Med. J. of Australia, Sidney, Nov. 21,1914, p. 491. 
Zymotic enteritis. Cambridge, England, 1908. 
Riedel. Quoted by Matthes [l. c.]. 
Rumpff. Aschoff [l. c.]. 
Schmidt Diagnose u. Therapie chron. Diarrh. Halle, 1909; also English translation, 
Philadelphia, 1909. 
Schmidt & Strassburger. Die Faeces des Menschen. Berlin, 1905. 
Thin (G.). Practitioner, 1883, xxxi, 84,‘ 1887, xxxv. 
Psilosis or sprue, etc. London, 1897. 
5. Enteroptosis 
(Glenard’s Disease) 
See Diseases of the Stomach—Section V, F-4. 
6. Constipation—Obstipation 
Constipation is as a rule a functional disorder, for which the patient 
is largely responsible. It is a.physiologic fact that different people differ 
as to the frequency of bowel movement. There are women (rarely men) 
who continue perfectly well with one movement every two to four days. 
In most cases chronic constipation leads to or is associated with more 
or less disagreeable symptoms, mental depression, languor, drowsiness, in- 
ertia, anorexia, foul tongue and breath—and in young girls particularly— 
anemia, with other toxic symptoms. Individual predisposition is an im- 
portant etiologic factor, as is also heredity. 
Habits and diet are paramount and their correction, almost at once re- DISEASES OF THE INTESTINES 
631 
lieves the atony which continues constipation. Sedentary habits are pro- 
ductive of intestinal inertia. 
Faulty diet includes an excess of one article to the exclusion of many 
others. Sweets (candy), starches in excess, are leading faults which 
cause constipation. Insufficient fluids (water) and fats will often con- 
tinue constipation until the deficiency is supplied. 
Procrastination is one of the prominent causes of constipation. The 
habit of moving the bowels at the same time each day is easily and 
promptly formed even in chronic cases. 
Mental emotion, long continued worry, circulatory diseases, gastro- 
intestinal diseases including the neuroses, also central nervous diseases, 
as brain tumor, spinal lesions, compression of the spine (caries and tumor), 
are all provocative. 
The mechanical obstruction of the intestine at one or more points is 
not true constipation, but is considered with intestinal obstruction—either 
partial or complete. Pregnancy is a frequent cause of constipation. 
Chronic constipation may be diagnosticated when the bowels refuse to 
move without assistance, either by medicines or mechanical means. 
In all forms of obstipation in which correction of existing faults fail 
to overcome the symptoms, organic disease should be strongly suspected. 
Thorough search will usually reveal either a rectal anomaly, uterine or 
other pressure, or some positive cause, either intestinal or remote. Among 
the conditions which are often overlooked as causes of obstipation are 
chronic intestinal catarrh, lead poisoning, general asthenia and the func- 
tional gastric neuroses. Secretory anomalies, without organic change, 
when corrected, either in the stomach or intestines, cure constipation de- 
pendent upon them. 
The atonic form of constipation is dependent upon (a) reduced intes- 
tinal peristaltic activity, or (b) there is insufficient expulsive strength 
which includes enfeebled action of the diaphragm and abdominal walls. 
(a) Reduced Intestinal Peristaltic Activity. — Reduced intestinal 
peristaltic activity may follow long continued fevers or non-infectious 
diseases. It depends largely upon neural disturbances. It is frequently 
an expression of the neurasthenic complex—hysteria, inertia, central dis- 
ease—and in the majority of cases is due to improper stimulation of the 
intestinal mucosa because of the faults mentioned in the preceding para- 
graphs. In most cases in which reduced intestinal peristaltic activity is 
the paramount factor the regulation of the life of the patient, including 
proper exercise, diet and regularity in the attempt to move the bowels 
at the same time each day, though not at once successful, will always 
in the end prove efficient and if continued cure the bad habit. Neglect 
will provolce recurrence. Rectal torpor is a frequent and unrecognized 
cause. 
(b) Insufficient Expulsive‘ Strength.—Many causes of insufficient 632 
DISEASES OF THE DIGESTIVE APPARATUS 
expulsive strength are finally overcome. They include pregnancy, inherent 
weakness of the abdominal wall, asthenic conditions which include ven- 
tral and diaphragmatic weakness, malnutrition, obesity, abdominal 
growths, faulty exercise, organic disease of the heart, lacerations of the 
perineum, and constitutional diseases such as diabetes, gout, leukemia, 
etc. Painful affections of any kind, fissure in ano, hemorrhoids, neuritis, 
in which the pain is increased by pressure, lead the patient to procrasti- 
nate. Masturbation and sexual excesses may provoke both intestinal 
atony and insufficient expulsive force. Travel is another important factor. 
In children there may be idiopathic dilatation of the colon with en- 
feebled expulsive force, at times rectal torpor to keep up constipation 
(Hirschsprung’s disease). 
Spastic constipation is due to a spasmodic contraction of the intes- 
tine over separate fecal masses, usually found in nervous patients and 
first described by Fleiner, in which there are functional intestinal stenoses. 
The peristaltic unrest of the intestinal coils is recognizable. The move- 
ments are preceded, often accompanied with colic. The sphincter mus- 
cle of the rectum is also tense. Many of these cases are due to toxic 
influences (tobacco, excessive use of alcohol) and often the neurasthenic 
character is demonstrated by the association of membranous enteritis. 
Of late attention has been called to a condition in which there is 
claimed to be abnormal movement of the cecum (cecum mobile). Wilms 
first called attention to this condition. The leading features are consti- 
pation and pain in the right ileocecal region. The acceptance of mobile 
cecum as a cause of the symptoms mentioned has not yet followed, and I 
have seen several cases in which operative interference, in no way influ- 
enced the complaints; indeed the cecum is usually found abnormally mo- 
bile without causing any symptoms. 
Schmidt does not believe that the cecum mobile represents a clinical 
entity; the normal cecum is more or less mobile. The pathologic condi- 
tion which causes abnormal mobility depends upon an abnormal mesen- 
tery and changes in the walls of the cecum. There are congenital anom- 
alies of the ileocecal mesentery, diseases of the appendix, fcnteroptosis, 
obstipation, which may cause typhlatonia, also known as typhlectasia. 
These cases are both medical and surgical and offer a good prognosis. 
Spastic conditions may be assumed to be due to insufficient moisture 
and too great hardness of the feces; old adhesions should always be con- 
sidered possible as should other and graver lesions. We are fully con- 
vinced that the majority of constipations will yield after the correction 
of their removable causes, though often exceedingly rebellious. The 
individual case, in order to make the prognosis good and to prevent re- 
lapse, will demand thorough study and the greater success will always 
follow natural methods of treatment. Constipation may be considered a 
bad habit when not due to organic disease of which the patient can be DISEASES OF THE INTESTINES 
633 
relieved; the condition is never dangerous hut it often makes the victim 
wretched and unhappy, handicaps him physically and mentally and often 
keeps up a continuous autosuggestion which tends to exaggerate the im- 
portance of the symptom enormously. The habitual use of cathartics 
never cures constipation. 
Reference 
Schmidt. Zur Frage d. Coecum Mobile. Bruns Beitr. z. klin. Chir., 1913, Bd. Ixxxiii, p. 
639-43. 
7. Intestinal Obstruction 
(Ileus) 
While intestinal obstruction—a condition in which the intestinal con- 
tent cannot be forced beyond an existing narrowing, usually mechan- 
ical, and of organic origin—is a surgical affection, it is almost invariably 
presented to the physician first for diagnosis. 
Obstruction may be (a) partial or (b) complete. In all, x-ray exami- 
nation may prove of inestimable diagnostic and prognostic value. 
(a) Partial Obstruction 
When partial obstruction causes but moderate stenosis (narrowing 
of the lumen of the intestine), the symptoms do not threaten life, con- 
stipation is prominent, persistent, and is only temporarily overcome with 
considerable difficulty until the prime cause is removed. There are a 
variety of causes of partial intestinal obstruction; some of these may 
never lead to complete occlusion, others may. 
During the early days or months of grave intestinal disease, as carci- 
noma or extra-intestinal pressure, there may be only partial obstruction 
which as the disease progresses may lead to increasing obstruction and 
final occlusion. Most growths do not lead to complete intestinal obstruc- 
tion. 
The symptoms produced by partial intestinal obstruction depend much 
upon its location, cause, and the degree of constriction. It may be assumed 
that any narrowing of the small intestine is more likely to produce serious 
and threatening symptoms than is stricture of the large intestine. It is 
not at, all uncommon to find intestinal lesions post mortem, with narrow- 
ing of the small intestine distant from the pylorus or ileocecal valve, with- 
out having caused symptoms during life. This would hardly be possible 
with obstruction within the duodenum or at the ileocecal valve. The 
partial narrowing of the large intestine at any point above the sigmoid 
flexure may be present, even due to malignant disease without symptoms 
and without threatening life during long periods (See Intestinal Cancer). 634 
DISEASES OF THE DIGESTIVE APPARATUS 
Partial obstruction may be due to removable pressure—such as pelvic 
growths or tumors elsewhere in the abdomen—which may by pressure, ad- 
hesions or transitory causes narrow the intestinal lumen. The most fre- 
quent cause of partial as well as complete obstruction to the emptying 
of the intestines is fecal accumulation (40 per cent), which may follow 
obstipation, or adynamia (enfeebled intestinal peristalsis) from a vari- 
ety of causes. Gall-stones within the intestines or by adhesions of the 
gall-bladder may cause incomplete obstruction. 
Chronic adynamic partial obstruction may be an expression of general 
enfeeblement; it may be an accompaniment of central disease of the 
nervous system (tabes dorsalis, brain tumor, chronic meningitis, cerebral 
apoplexy, or other serious organic lesion). Chronic morphinism has in 
two of my cases caused fatal adynamia. Following abdominal surgical 
operations, intestinal obstruction due to acute adynamia is a serious and 
at times fatal combination. In such cases all of the symptoms of com- 
plete and organic obstruction may precede death. The prognosis of these 
adynamic cases following abdominal operation is grave. Most partial 
intestinal obstructions are amenable to treatment; life is not threatened, 
as a rule. The organic causes are purely surgical and demand radical 
treatment, for most of them are progressive. Large fecal accwmulatmis 
and most gall-stone obstructions within the intestines yield without rad- 
ical surgical treatment (See also later paragraphs). Partial intestinal 
obstruction may exist with continuance of unsatisfactory, at times, fre- 
quent movements; this is an important diagnostic as well as prognostic 
fact. 
(b) Complete Intestinal Obstruction 
The majority of all organic obstructions are found in the male (65 
to T5 per cent) and almost one-half between the ages of 15 and 30. Be- 
tween 85 and 95 per cent are in the small intestine, and as Fitz, Treves, 
Leichtenstein, Wiggins and others have demonstrated, two-thirds are in 
the ileocecal region and four-fifths in the lower abdominal regions. The 
various forms of intestinal obstruction are found at different ages; 
strangulation by bands is most frequent in advanced life and with the 
preceding history of peritonitis. Hernial obstruction does not often hap- 
pen early in life. Intussusception or invagination is a complicaton of 
early childhood. 
Complete intestinal obstruction is always a life-threatening condi- 
tion. It demands immediate diagnosis and prompt radical treatment in 
almost all cases. This is true of all cases within the small intestines 
which arise suddenly; the gradually increasing obstructions and final 
complete occlusion are less malignant, but they too when located in the 
small intestines offer the same doleful prognosis, though the septic condi- 
tion may be less virulent. Complete obstruction of the large intestine Q,t DISEASES OF THE INTESTINES 
635 
the sigmoid may exist during weeks without causing the symptoms which 
promptly follow occlusion of the small intestine. Enormous dilatation 
of the large intestine above the stricture and surprising tolerance has 
characterized some of my cases. 
Sepsis, peritonitis, and final cardiac toxemia are the leading dangers 
of complete intestinal obstruction. 
Complete intestinal obstruction may be acute, without preceding symp- 
toms. There is no warning, but suddenly the “acute abdomen” is devel- 
oped with associated subjective and objective features at once suggestive 
of a grave intra-abdominal (intestinal) lesion. Acute obstruction may 
suddenly develop in cases in which during a variable period there have 
been evidences of chronic partial obstruction; and finally chronic intes- 
tinal partial obstruction may gradually increase stenosis until it becomes 
complete. The features of complete occlusion which influence prognosis 
unfavorably are suddenness of onset, shock, prompt peritonitis, profound 
sepsis, fecal vomiting with increasing abdominal distension, strangury, 
pinched and characteristic facies, cold extremities with cyanosis, and 
rapid small and thready pulse with hypotension after a short initial period 
of rise of blood pressure. 
Hiccough is an exhausting symptom and is not relieved while the 
obstruction continues. Indicanuria is always present when the small in- 
testine is obstructed, often with constriction of the large gut. Albumi- 
nuria is not constant but is unfavorable when present with casts. Com- 
plete intestinal obstruction may be due to: 
(I) Strangulation by bands or adhesions and incarceration (hernia) 
(II) Volvulus 
(III) Intussusception 
(IV) Stricture 
(V) Tumors or foreign bodies in the bowel 
(VI) Extra-intestinal pressure (from tumors, etc.) 
(VII) Eecal accumulation. 
In order of frequency following fecal accumulation the leading or- 
ganic causes are: 
1st. Strangulation by bands or adhesions and incarceration 
2d. Intussusception 
3d. Stricture within the intestine 
4th. Extra-intestinal causes 
5th. Tumors or foreign bodies in the bowel 
6th. Volvulus. 
The typhlitis stercoralis of the Germans is a condition in which there 
is impaction of feces in the colon wfith tumor formation and localized 636 
DISEASES OF THE DIGESTIVE APPARATUS 
symptoms, with features simulating obstruction and appendicitis. The 
prognosis of this condition is good. 
Multiple growths or tumors within the abdomen may cause symptoms 
simulating fecal impaction, and require cautious differentiation* 
Causes of Complete Intestinal Obstruction 
(1) Strangulation.—Strangulation or obstruction by bands and in- 
carceration (hernia) through apertures was found- in 35 per cent of 295 
cases of organic obstruction by Fitz. 
Treves includes 
(a) Ligaments (false) following peritonitis 
(b) Omental cords 
(c) Meckel’s diverticulum 
(d) Normal structures abnormally attached (ovarian, etc.) 
(e) Incarceration through slits and apertures (herniae) 
(f) Isolated bands and adhesions. 
(a) False ligaments following cured peritonitis may suddenly cause 
obstruction, or obstruction may be sudden after a long period of increas- 
ing symptoms, particularly “ballooning” or “sausaging” of the intestine 
above the constriction. The intestinal wave and distention with gurgle 
and collapse are easily recognized by watching the abdominal wall. The 
sudden and repeated ballooning of the intestine is a symptom of great 
value. It is always indicative of partial obstruction and should be 
heeded; when it is properly interpreted in time, and treatment in operable 
cases is not postponed in the absence of complications, the prognosis is 
excellent. 
A small short or a long slender band may exist a long time without 
causing symptoms until a loop of intestine slips under it, and once held, 
the occlusion is complete. All die unless relieved surgically. The excep- 
tions to this rule are so few as not to deserve consideration. 
(b) Omental cords may cause strangulation with all of the symptoms 
of concealed hernia. A loop of intestine may rest in a hernial opening 
unobstructed, but above it a thin omental cord with adherent omentum 
may continue the strangulation after the hernial sac has been emptied. 
Unrecognized, such a complication is fatal. Omental strings and cords 
with fixed omentum should always be suspected when obstruction is not 
otherwise explained. 
(c) Mechel’s diverticulum.—My experience with Meckel’s diverticu- 
lum proves that when it throws itself around the intestine and forms a 
knot, only radical treatment can save the patient. Diverticulum strangu- 
lating the gut leads to prompt collapse, usually a profound septic state, 
and strangury or scanty urine with enormous indicanw'm in the little 
urine voided. DISEASES OF THE INTESTINES 
637 
(d) Normal structures abnormally attached by adhesions, organs ad- 
herent to each other, "balling” of intestines, after repeated peritonitis, at 
times adhesions to the abdominal wall, may by traction or compression 
cause obstruction. I have before the days of improved abdominal sur- 
gery seen tumor formation due to the agglutination described, with sud- 
den acute or chronic partial obstruction gradually followed by complete 
closure. The prognosis of these conditions is not favorable when a part 
of general chronic peritonitis; when limited, recovery may be expected 
to follow surgical treatment in a large proportion of cases if instituted 
early. 
(e) Incarceration Through Slits and Apertures' {Hernia).—Isolated 
bands may form slits or apertures which intestines enter to be strangu- 
lated. When in the neighborhood of the appendix, appendicitis is simu- 
lated, the McBurney point is included, and procrastination will surely 
cause death. Experience with early operation in such cases has been favor- 
able. I had one tabetic woman who had previously repeated gastric crises; 
I mistook the incarceration of a loop of the ileum into the ischiatic notch 
for a crisis—the symptoms were identical; when the correct diagnosis was 
made, the gut was found gangrenous and I lost my patient. Such a com- 
bination is exceedingly rare but with the warning and experience, the 
error ought not to be repeated. I have seen large and small intestines 
agglutinated with resulting obstruction and relief from operation. 
The herniae belong entirely -within the domain of the surgeon and 
rarely come to the internist. If the majority of intestinal obstructions are 
to be saved, the inguinal, femoral, and umbilical openings should be sus- 
pected and examined, in spite of a. negative previous history. 
(f) Isolated Bands and Adhesions.—I have considered these cases 
in connection with (e) incarceration through slits and apertures, for iso- 
lated bands may hold a loop of intestine, or adhesions with or without 
isolated bands may cause obstruction. 
(II) Volvulus.—The gut sometimes circles or twists on itself in 
such a way as to narrow its lumen or completely occlude it. Fitz found 
42 cases of volvulus (twists) in his 295 cases. About 70 per cent were 
males. One-half were sigmoidal, and in most there was an axial twist 
of the gut. The average age was between 30 and 40. The cecum is fre- 
quently the seat of volvulus; the ascending colon and small intestine less 
frequently. The prognosis of complete obstruction due to volvulus is 
good when operated early. If the large intestine is involved, the shock 
is less; the urine is not likely to be entirely suppressed and indicanuria 
is slight or absent. 
(III) Intussusception (Invagination).—Intussusception is a com- 
plication of early life. The telescoping brings the six layers of the in- 
vaginated gut together (layer to layer) peritoneum to peritoneum, and 
if held long enough, strangulation leads to gangrene, at times to slough-  DISEASES OF THE DIGESTIVE APPARATUS 
638 
ing and passage of the slough. In these cases it occasionally happens that 
nature’s processes coapt the intestine and life is thus saved. In one of 
my cases twelve inches of gut was passed and the child lived. Osier 
reports one case in which 17 inches sloughed with recovery. Fitz’s cases 
(295) were due to invagination. Lichtenstein found 52 per cent of his 
cases ileocecal or ileocolic, 30 per cent enteric, and 18 per cent rectal and 
colico-rectal. 
In children invagination may be without known cause; it may com- 
plicate infections (measles), constipation, or diarrhea. Wiggins reported 
103 cases in early life of which 50 per cent were between four and six 
months of age. 
Nature’s method (sloughing) and surgery, offer the only hope of sav- 
ing life. 
(IV) Stricture.—Stricture leading to complete occlusion and intes- 
tinal obstruction may be due to 
(a) cicatrization 
(b) carcinoma 
(c) congenital defect. 
(a) Among the causes of stenosing cicatrization are hernia, typhoid 
fever, dysentery, catarrhal ulcers, syphilis, and tuberculosis. In all of 
these there is a characteristic previous history of chronicity with long 
periods of gradually increasing symptoms (ballooning and collapse of 
intestine after gurgling), and when these symptoms are unheeded com- 
plete obstruction may follow. 
(b) Carcinoma and other neoplasms are not often causes of complete 
obstruction because their favorite seat is in the large intestine, in the sig- 
moid flexure, or descending colon. When there are annular constrictions, 
benign or malignant, near the ileocecal valve they may cause complete 
obstruction. Cancerous infiltration of the ileocecal valve and appendix 
are proved to be increasingly frequent as removed specimens are being 
microscopically examined. When carcinoma or other neoplasm causes 
obstruction, surgery must be invoked. The diagnosis can, in almost all 
cases, be made with sufficient accuracy to justify exploration long before 
occlusion. 
(c) Congenital defects are usually found in the rectum (imperforate 
anus or union of the pylorus and duodenum has failed). Almost all of 
these infants die. 
(V) Tumors or Foreign Bodies in the Bowel.—Among the 
tumors of sufficient size to cause obstruction are polypi, fibroma, lipoma, 
sarcoma and carcinoma. The foreign bodies are gall-stones, indigestible 
food, foreign substances swallowed (glass, metal and a large variety of 
material) and enteritis. When gall-stones are of sufficient size to obstruct 
the intestine, they gain entrance after adhesive and localized peritonitis DISEASES OF THE INTESTINES 
639 
has been protective during the process of ulceration. The vagaries of 
gall-stones are many and Courvoisier and Eisner have reported interest- 
ing experiences which hear on this subject. The majority of large gall- 
stone masses which obstruct the intestine pass per rectum. Obstruction 
may, with gall-stones, continue during many days and yet recovery may 
follow. There is danger of subsequent perforation and peritonitis, but 
that is comparatively small. I have never been forced to resort to sur- 
gery after the stone has entered the intestine, though extra-intestinal 
adhesions of the gall-bladder filled with gall-stones causing obstruction 
almost always in the presence of threatening symptoms demands radical 
treatment. 
Enteroliths may occasionally demand surgery to save life. Obstruc- 
tion due to foreign bodies offers a favorable forecast; those dependent upon 
the tumors above mentioned when non-malignant, are favorable for surgi- 
cal treatment. The malignant growths within the intestine when suffi- 
ciently advanced to cause obstruction are likely to have metastases and 
adhesions which darken the outlook. 
In 44 of Eitz’s cases of obstruction due to foreign bodies 23 wTere 
gall-stones, 19 were fecal masses, and 2 were enteroliths. 
(VI) Extra-intestinal Pressure (Tumors, etc.).—Pelvic growths, 
tumors of the uterus and ovaries, pelvic abscess, retroperitoneal growths, 
large malignant masses connected with one or more of the abdominal or- 
gans—kidney, spleen, liver and suprarenal tissue (hypernephroma), tuber- 
culous masses and associated adhesions—may each by pressure or trac- 
tion cause obstruction. The prognosis must depend upon the operability 
and the complications of the individual case. 
(VII) Fecal Accumulations.—We have in several of the previous 
paragraphs mentioned fecal accumulation as a cause of incomplete and 
complete obstruction, in all of which when uncomplicated, the prognosis 
is good. We once more call attention to adynamic or 'paralytic ileus when 
neglected with fecal accumulation, in which the prognosis is always seri- 
ous. With infarct involving the mesenteries and the abdominal wall as a 
cause of adynamic obstruction, the prognosis is exceedingly grave. 
Whenever there is organic, complete, acute, intestinal obstruction, the 
life of the patient depends upon the diagnostic ability of the physician, 
and the full appreciation of his responsibility which must lead to imme- 
diate surgical consultation and radical surgical treatment. I offer no 
statistics because they are valueless, owing to the faulty classification of 
the included material. 
References 
Courvoisier. Causuistische statistisch Beitrage z. Path. u. Chir. d. Oallenwege. Leipzig, 
1890. 
Eisner. The vagaries and wanderings of gall-stones. New York Med. News, 1898, i. 
Transact. Med. Soc. State of New York, 1898. 640 
DISEASES OF THE DIGESTIVE APPARATUS 
Fitz. Transact. Congress of Am. Phys. & Surg., 1899. 
Lichtenstein. Ziemssen’s Cycl. Prod. med. New York 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Treves. Intestinal obstruction. London, 1884. 
Wiggins. New York Med. Rec., 1896. xli, 78-86. 
8. Dilatation of the Colon 
Hall White divides dilatation of the colon into four groups, in all of 
which Rontgen rays may prove of great assistance: 
(I) Distention Due Entirely to Gas.—There is no obstruction or 
organic lesion. It may be an accompaniment of acute infection (typhoid 
fever, peritonitis, tuberculous peritonitis, traumatism, or severe nervous 
diseases). The result of pressure may be exceedingly troublesome, in some 
cases causing heart and lung symptoms, and there is extreme distention 
of the abdomen. When with pneumonia or chronic heart disease there is 
dilatation of the colon and stomach, the combination is exceedingly grave, 
and unless relieved may cause death. (See Pneumonia, also Acute Dila- 
tation of the Stomach.) 
(II) Distention of the Colon With Solid Matter Within It.—This 
may be due to faulty diet, coarse food, hard fecal matter, hair and other 
foreign substances. In the insane the swallowing of foreign bodies is a 
frequent cause of dilated colon; enormous gall-stone masses which have 
ulcerated through the intestinal wall may prove causative. 
Excess of lime phosphate in the stool,insufficient water, typhilitis ster- 
coralis, are among the causes. 
Treatment and careful attention to the diet, watching the patient, 
thus preventing the swallowing of foreign bodies usually overcome the 
condition. 
(III) Organic stricture, or compression of the large intestine beyond 
the dilatation, leads to hypertrophy of the muscularis when chronic and 
secondary changes (catarrhal colitis, ulceration, etc.) follow. The prog- 
nosis of these cases depends entirely upon the ability of the surgeon to 
remove the cause. 
(IV) Hirschsprung’s disease, or idiopathic dilatation of the colon 
—a congenital defect—is also mentioned in this section in connection 
with constipation (Section V, G. 6, Constipation). The dilatation, if 
the children live, is marked and nearly fills the abdomen. The dilata- 
tion is often progressive. There is great danger from tetany; obstipation 
is severe. The children are otherwise imperfectly developed and often 
show infantilism. Acute intestinal obstruction is a fatal complication in 
occasional cases, and is the most serious complication. I have occasion- 
ally met idiopathic dilatation of the colon in the adult, usually between DISEASES OF THE INTESTINES 
641 
25 and 30, without known cause, exceedingly rebellious to treatment with 
neurasthenic symptoms and cardiac neuroses. Life was not threatened. 
Crozer Griffith reported 24 cases from medical literature of idiopathic 
colon dilatation. Osier reported a case of a boy aged 10 years with enor- 
mously distended abdomen in which there was diarrhea, vomiting, and 
visible intestinal peristalsis. Medical and mechanical treatment were of 
no avail. When the abdomen was opened, no stricture was found; “the 
sigmoid was 18 inches in circumference, the cecum was half this size, 
and the bowel progressively increased in size from the cecum to 
the sigmoid which was folded on itself, but not so as to cause any ob- 
struction.” An artificial anus was made. There was improvement; he 
gained in weight; he lost his tympany but the artificial opening was 
never closed. But few of the congenital cases reach adult life; Kredel 
believes if they do, they may reach old age. I am fully satisfied that 
idiopathic dilatations of the colon occurs in the adult without congenital 
anomaly, and when it does, unless great caution in diet and exercise is 
practiced, it remains a chronic and annoying condition, uninfluenced by 
medicine but with many subjective and positive objective manifestations. 
Surgery offers hope of relief. 
References 
Bristowe. Brit. Med. J., 1885, i, 1085. 
Crozer (Griffith W.). Am. J. Med. Sci., 1897, cxviii. 
Kredel (L.). Ztschr.f. klin. Med., 1904, liii. 
Nothnagel. Diseases of the intest. & perit. Encyl. Pract. Med. London & Philadelphia, 
1904. 
Osier. Johns Hopkins Hosp. Bull., iv, 30. 
Virchow. Berl. klin. Wchnschr., 1887, No. 50. 
White (W. Hale). Allbutt & Rolleston’s System of medicine. London, 1907, vol. Hi. 
9. Diverticulum of the Intestine 
Diverticulum—a circumscribed dilatation of the intestine—may be 
either congenital or acquired. Aschoff classifies diverticulum as either 
true or false. The false diverticulum is characterized by coves in the 
intestinal wall in which the hollow opens into the muscularis and causes 
prolapse of the mucosa. The true diverticulum is characterized by a 
localized excavation of a part of the intestinal wall in which the mucosa 
is included. The one (false) is a mural, the other (true) is a diverticu- 
lum of the mucous membrane. The false is included between the mucosa 
and peritoneal covering of the gut. The true diverticulum is usually 
congenital. The intestinal surface has the appearance of partial perfo- 
ration and the coves are most abundant and usual at the sigmoid flexure. 642 
DISEASES OF THE DIGESTIVE APPARATUS 
The appendix may be involved, and unquestionably appendicular diver- 
ticulum is a cause of appendicitis. 
Diverticulum may be single or multiple. The acquired diverticula 
are found in advanced life. 
Diverticula may lead to obstipation, pocketing, inflammatory condi- 
tions (diverticulitis and perisigmoiditis), giving rise to serious symptoms. 
Intestinal obstruction may be caused by Meckel’s diverticulum (See 
Intestinal Obstruction), or the smaller multiple or single diverticula may 
lead to stricture with consecutive dilatation, gangrene, ulceration, per- 
foration, fistula formation (vesico-colic fistula) and distant suppuration, 
also thrombosis (phlebitis). In elderly subjects carcinoma is simulated. 
A surprisingly large number of physicians have recently suffered from 
the disease and have been successfully operated (resection). The results 
at the Mayo and other clinics where a large number of cases have been 
detected, have been surprisingly satisfactory. Unfortunately the diag- 
nosis is not usually easy. Where there are persisting and increasing 
symptoms the condition should at least be suspected; Rontgen rays should 
be used to assist in diagnosis. As a rule, sufficient time for radical treat- 
ment precedes the graver complications. 
References 
Aschoff. Pathol. Anal. Jena, 1913. 
Matthes. von Mehring <fc Krehl’s Lehrbueh der inner. Med. Jena, 1913. 
10. Intestinal Cancer and Other Growths 
In connection with stricture, intestinal obstruction, dilatation, and 
other organic diseases of the intestinal wall I have repeatedly called 
attention to intestinal carcinoma in this work. 
New growths may be either in the intestinal wall, or malignant 
nodules (good-sized masses) may by pressure (extra-intestinal) be the 
cause of symptoms. For prognosis, the rule may be accepted that unless 
localized at the ileocecal valve, within the duodenum, at the sigmoid 
flexure, in the rectum low down, or at a point the function of which 
approximates a sphincter action, the subjective symptoms of the disease 
may be entirely absent during periods of sufficient length to give ample 
time for progression, infiltration, and even metastasis before the diag- 
nosis is possible. When there are evidences of cancer in obstruction or 
in changed stools early, the diagnosis is made and the chances of the 
patient are consequently improved. 
The intestines, both large and small, are tolerant of malignant and 
non-malignant infiltration during relatively long periods; only increasing 
obstruction, characteristic stools (blood and mucus), x-ray pictures, and DISEASES OF THE INTESTINES 
643 
progressive weakness make tlie diagnostician suspicious. When the dis- 
ease has advanced sufficiently to cause glandular invasion, near and dis- 
tant, the chances of rescue are lost. There is no malignant disease which 
offers such surprises as cancer of the intestines. I have seen physicians 
with advanced sigmoid and rectal cancer who continued practice until 
the growth was so far advanced as to be inoperable without having created 
a suspicion of its presence. 
Suddenly arising symptoms of intestinal flatulence and indigestion, 
more or less abdominal discomfort, increasing constipation and blood- 
streaked stools or mucus in the stools of patients at or beyond middle life, 
should create a strong suspicion of possible cancer and should lead to the 
necessary physical examination and x-ray picture to clear the horizon. 1 
have seen brilliant results follow early diagnosis and prompt surgical 
treatment. 
Cachexia and profound blood changes are not likely to be early mani- 
festations; metastasis to the spine may precede the local symptoms. We 
have in suspicious cases gained considerable assistance from watching the 
abdominal wall for peristaltic unrest—gurgling after ballooning of the 
intestines. This is always suspicious. Most intestinal carcinomata are 
“adenocarcinomatous”; the scirrhus and encephaloid are relatively rare. 
Over 95 per cent of my cases have been primary, and the rectum and 
sigmoid have been their most frequent seat (over 95 per cent). The 
statistics furnished by Brill of 3,563 cases of intestinal cancer (probably 
including sarcoma) showed 89, or 2.5 per cent, in the small intestine. 
Rolleston collected 54 cases of primary cancer of the duodenum and 19 
of the ileum jejunum. My material demonstrates the further fact that 
over 90 per cent of cases presented with palpable masses. It is the excep- 
tion to find a case of rectal or ileocecal cancer in practice before careful 
examination at least creates the suspicion of its presence. The late diag- 
nosis is the discouraging feature. 
Chronic cases with progressive ulceration may lead to perforation and 
adhesions as well as multiple glandular (metastatic and distant) infiltrar 
tion. The metastases to the liver and peritoneum, particularly the for- 
mer, may cause symptoms in some cases which overshadow those of the 
primary growth. 
I have never seen a case of rectal cancer in a child; Matthes reports 
its possibility. Most cases have been in male adults in middle life. My 
results wfith rectal carcinomata surgically treated immediately after recog- 
nition have been most encouraging. I have patients living who were 
operated over 14 years ago. Cases of rectal cancer unoperated rarely live 
beyond the second year. My results have been encouraging after the early 
diagnosis of cancer of the ascending colon and ileocecal valve following 
resection. No case of cancer of the small or large intestine recovers -with- 
out surgical intervention. 644 
DISEASES OF THE DIGESTIVE APPARATUS 
My experience with sarcoma of the intestine is limited. I gather 
from it and the study of its literature that it is a rare condition; Libman 
has collected 15 cases of primary sarcoma. It may cause stenosis; the 
growth is primary and, in most cases, causes death in less than 12 months 
after its detection. Skin metastases are relatively frequent. With stom- 
ach sarcoma, secondary intestinal masses have been found. 
Polypoid growths are benign and offer a good prognosis. Their 
favorite seat is in the rectum; they are also found in the duodenum. 
The location of these, naturally influences the symptoms and prognosis. 
There are a few recorded cases of duodenal obstruction from innocent 
growths (myxofibromatous polyps). 
Myoma, fibroma, and fibromyomata may cause intussusception. 
References 
Allbutt & Rolleston. System of medicine. London, 1907, vol. in. 
Aschoff. Pathol. Anatom. 3 Aufl. Jena, 1913. 
Brill. Am. J. Med. Sci., 1904, cxxviii, 824; atso has excellent bibliography. 
Libman. Am. J. Med. Sci., Philadelphia, 1900, exx, p. 309. 
Nothnagel. Diseases of the intestines and peritoneum. English translation, 1907. 
Matthes. von Mehring u. Krehl,Lehrb. d. Inner. Krankh. Jena, 1913. 
H. Diseases of the Appendix 
1. Appendicitis 
(Inflammation of the Vermiform Appendix, Typhlitis, 
Paratyphlitis, Perityphlitis) 
One of the most encouraging messages which this work has to offer 
is that acute appendicitis, recognized during the early hours of its ex- 
istence, in the absence of complications, immediately treated surgically, 
offers a favorable forecast in all cases. 
“The fate of the patient, the victim of an abdominal emergency, 
depends almost entirely upon the skill and promptitude of his doctor, 
and any special surgical skill has very little to do with his recovery” 
(Morrison). 
I mention these facts at the very outset of the consideration of this 
subject for there are still those who, because of their doubt, are sacrificing 
valuable life. 
History.—It is not within the province of this work to go into the 
history of appendicitis. The most complete and authentic data are 
offered by Kelly in his monumental work on appendicitis and his paper 
dealing on this subject. It is strange that the graphic description of the DISEASES OF THE APPENDIX 
645 
disease as we see it today published by Addison and Bright * in the first 
and only volume of their incomplete practice had received no attention. 
It was overlooked and it became the privilege of the American, physician, 
Fitz, and our surgeons, Willard Parker, Hall, Sands, Weir, Bull and 
others, to demonstrate the surgical nature of the disease, its dangers, the 
fact that it was the most important of all the acute abdominal disorders, 
that it was the most frequent cause of what had formerly been consid- 
ered “idiopathic peritonitis,” and that it demanded early surgical relief 
that the mortality might be entirely effaced as above suggested in uncom- 
plicated cases. 
Special Considerations.—Appendicitis is a disease characterized by 
infection and inflammation of the appendix, deep changes in the sub- 
stance of the organ with tendency to gangrene, leading to perforation 
and early peritonitis in the more acute cases. Beginning with the demon- 
stration of Chauveau, who in 1882 proved that the injection of micro- 
organisms into the peritoneal cavity might cause peritonitis, until the 
present day, with a growing literature to corroborate the theory of the 
infectious nature of appendicitis, we have learned that not one but any 
one of many microorganisms may be responsible for the disease. The 
most frequent is the Bacillus coli communis. Streptococci are at times 
* Six pages are devoted to a classic consideration of “Inflammation of the 
cecum and appendix vermiformis.,, The clinical history is clear; no work of today 
presents morbid appearances more graphically: 
“From numerous dissections it is proved that the fecal abscess thus formed in 
the right iliac region arises, in a large majority of cases, from disease set up in the 
appendix ceci. It is found that this organ is very subject to inflammation, to 
ulceration, and even to gangrene, and moreover, that it is occasionally thickened 
and ulcerated from tuberculous deposits if the peculiar diathesis favors the change. 
So that this little wormlike body is often detected in the midst of the abscess, 
with a perforation at its extremity, or by ulceration higher up in its parietes. A 
considerable portion of it, nearly or entirely separated, is found in a disorganized 
condition amongst the pus and feces which fill the abscess. In other cases the 
appendix is truncated within a short distance of its origin from the cecum. In a 
small number of instances the cecum itself is found inflamed and ulcerated and 
extensively implicated in the abscess, in a way which shows that the appendix had 
little to do with the disease.” 
“Our prognosis will depend very much on the general health of the individual, 
and the time of life; and if both be favorable, the disease, though always of a 
most doubtful and dangerous character, will often slowly yield to cautious treat- 
ment. In the individual case the more favorable indications will be found in the 
mildness of the general symptoms and the absence of peritoneal inflammation; 
whereas if the contrary should be the case the abdominal tenderness becomes ex- 
treme, the prostration great, and sickness, purging, and hiccup supervene. Our 
hopes of recovery will of course diminish; and whatever fecal abscess has estab- 
lished itself, we are certain that the patient has to undergo a tedious process in 
which the strength may gradually give way or many casualties may arise to give 
a more sudden unfavorable turn to the disease.” 646 
DISEASES OF THE DIGESTIVE ADPAKATI'S 
found without other germs or with them. The other germs are the 
Bacillus lactis aerogenes, the Bacillus capsulatus aerogenes the Bacillus 
pyocyaneus, the Pfeiffer influenza bacillus, the bacillus of Friedldnder 
and FraenkeL Stengel contends that most cases “represent a mixed in- 
fection, the most important organisms being the Bacillus coli communis, 
the Streptococcus pyogenes, and the anaerobic forms.” All are agreed 
that the milder cases, with limited peritonitis and favorable symptoms 
are associated with colon infection; the more severe are of streptococcus 
and anaerobic origin. 
The absence of muscular fibers which make it impossible for the 
appendix to expel infectious material, fecal, or other bodies, once they 
gain entrance, adds to the dangers of infection and consequent progres- 
sion of destructive changes. The greatest pathologic factor in appendi- 
citis is its obstruction, either from fecal concretions, other foreign bodies, 
or organic change (stricture, inflammation, ulceration). 
Twenty-four per cent of all cases show occlusion of the lumen. 
Treves found fecal concretions in 80 per cent of his cases; Deaver in 
16 per cent. In 146 adult cases there were 63 with fecal concretions, 
9 foreign bodies, in 74 nothing positive could be found. In children, in 
49 cases, 27 showed fecal concretions, 3 foreign bodies, and 29 failed to 
reveal a cause. Toft in 300 examinations found evidences of appendicitis 
in one-third of all subjects. But few go through life without either 
insignificant and unrecognized catarrhal inflammation or the fully devel- 
oped disease. 
The irregular and anomalous course of the disease is characteristic, 
and often misleads patient and attendant. If the clinical histories of 
many cases are carefully compared, it will he found that while all have 
some symptoms which are alike and almost always present, there are 
features in the individual cases which stand out in bold relief upon which 
the unguarded diagnostician places undue importance, losing valuable 
time before reaching a correct conclusion. 
The abnormal position of the appendix in many cases is responsible 
for anomalous symptoms, both subjective and objective. Kraussold has 
demonstrated the changed relations of the appendix and cecum in these 
cases, and it is easy to understand how the physical signs may differ 
from those of the majority of cases in which the location and origin of 
the appendix does not approach the normal. This fact is of enormous 
diagnostic and prognostic value, for because of it irregular and unusual 
subjective and objective symptoms are often incorrectly interpreted. 
The inexperienced should be warned against concluding that in the ab- 
sence of the “McBumey point” in its usual location appendicitis may be 
excluded, its presence is not always pathognomonic of appendicitis. The 
appendix may arise from either side of the cecum, it may be a little 
anterior or posterior, a little nearer the head of the colon than normal; DISEASES OE THE APPENDIX 
647 
it may arise from the very edge of the cecum, higher than normal; indeed 
I have found it so high as to lead to the conclusion that an appendicular 
abscess was the distended gall-bladder. Kelly and Hurdon report the 
appendix placed horizontally toward the promontory, or pointing laterally 
in 32 per cent; oblique toward the spleen in 10 per cent; ascending in 34 
per cent; descending in 24 per cent. 
Another cause of misleading and anomalous distribution of pains and 
other features are the reflex symptoms which lead to distant symptoms 
in both acute and chronic cases during dangerously long periods. Thus 
I have seen renal colic simulated by appendicitis during the first twenty- 
four hours of its existence, and only the dependence upon the partially 
developed physical signs of the disease with a suggestive leukocytosis 
saved the patients’ lives—the appendix was so placed as to occlude tem- 
porarily the right ureter. 
The radiation and localization of all pains from the epigastrium or 
hypochondriac regions may prove misleading and expensive. Left-sided 
pain with anomalous location of the appendix demands cautious exami- 
nation and consideration of separate symptoms and blood counts. 
The frequency of appendicitis fully appreciated, will often lead to 
safe conclusions in the absence of typical pictures, but with a few symp- 
toms which are suggestive. 
The age of the patient is of great prognostic significance. Treves’ 
statistics bearing on the incidence of the disease shows it most frequent 
between the tenth and twentieth year. He offers the following, showing 
the percentages: 
5 to 10 10.8 per cent. 
10 to 20 40.7 “ “ 
20 to 30 29.0 “ “ 
30 to 40 11.5 “ “ 
40 to 50 4.6 “ “ 
50 and over 3.4 “ “ 
Children between 5 and 10 years of age in unoperated cases show a 
high mortality. In 1906 in Prussia, the mortality in the first fifteen 
years of life in one thousand cases was 14 to 16 per cent; from 15 to 30, 
6 to 7 per cent. Heubner had a mortality of 15 per cent; only 3 were 
operated. Heuberg claimed the mortality following operations about 
23.4 per cent, unquestionably due to late operation. Riedel reported a 
mortality of 16.4 per cent in 310 children operated. He reduced the 
mortality in the adult during 21 months to 2.9 per cent, while the death 
rate among the children during the same period was 13 per cent. In 
Germany there has been great objection by parents to the early opera- 
tion of children so that the statistics compare unfavorably with our own. 648 
DISEASES OE THE DIGESTIVE APPARATUS 
The mortality in the adult during the active period of life has been 
reduced in America to an almost negligible figure when operation is early. 
In patients beyond middle or in advanced life the mortality rises with 
increasing age. The character of the lesion is of paramount prognostic 
value. 
Catarrhal Appendicitis 
Unquestionably the majority of catarrhal appendicitides escape the 
physician, because they are so insignificant as to demand no treatment 
and the patient may remain without subjective or objective symptoms. 
Simple catarrhal appendicitis may remain subacute, give rise to dys- 
peptic symptoms without recognizable fever or local physical signs, and 
recover fully. Recurrence is likely. There are a large number of mild, 
acute cases which make early diagnosis possible in which there are no 
evidences of localized peritonitis, no rigidity, no changed percussion note, 
insignificant tenderness, but slight elevation of temperature and mod- 
erate leukocytosis, pulse practically normal, in which after from two to 
four days all subjective symptoms are overcome. The large proportion 
of cases which demand our close study are those of catarrhal character in 
which the diagnosis is possible and positive before the end of twenty-four 
to forty-eight hours, in which there is slight rigidity, some fever, at times 
slight chill, and slightly accelerated pulse. There may or may not be 
vomiting. Many of these cases do offer a good prognosis without opera- 
tion. Many of these, considered favorable, suddenly change their features 
and present evidences of extension, increased rigidity, increasing dis- 
tension, obstipation, with or without rise of temperature. Most of these 
vomit more or less. These cases are serious; they may perforate. Ulcera- 
tion without perforation may cause peritonitis—toxemia—overpowering 
and fatal. 
There are no criteria which make it possible for the clinician to tell 
whether the simple catarrhal type of the disease is to remain so, whether 
an ulcer which results from the infection is to perforate or cause local or 
diffuse peritonitis, whether there will finally be abscess formation or other 
complication. The catarrhal form, of the disease with physical signs 
sufficient to make the diagnosis positive with leukocytosis and rigidity 
{it matters little ivhat other symptoms are present) is positively a sur- 
gical disease, the prognosis of which is enormously improved by early 
operation. Spreading symptoms after a period including the clinical 
picture described in the preceding paragraph are evidence of increasing 
infection from which the majority die unless saved by radical treatment 
Catarrhal cases may present -with increased pain and fever, when a 
short period of relief may follow. The temperature in such cases may 
fall; the pulse may or may not show improvement—usually it does not 
vary much. Under such conditions I have frequently met patients and DISEASES OF THE APPENDIX 
649 
physicians who opposed operation. Such relief of pain, is insignificant 
if the local physical signs (rigidity particularly, and slight dullness) 
persist. The chances are that there is either perforation or deep ulcera- 
tion which will ultimately perforate, and within from twelve to twenty- 
four hours increasing distension and rapid heart will indicate the presence 
of peritonitis. In one case seen in consultation in which there were the 
initial symptoms of catarrhal appendicitis, later exacerbation of symptoms, 
vomiting and localized rigidity, there was fall of temperature; the rigidity 
remained though the pulse was slower; leukocytosis continued. I insisted 
on operation, and found the appendix with three perforations. Fortunately 
protective peritonitis prevented diffuse inflammation and the boy (aet. 20) 
recovered. Failure to interpret the meaning of the apparent improvement 
of subjective symptoms may lead the attendant and patient to false conclu- 
sions with disastrous results. 
A large number of mild or catarrhal cases recover from the acute 
symptoms, but slight tenderness remains and dyspeptic symptoms are 
likely to develop. Some of these show hyperacidity and with slight acute 
exacerbations of pain, no marked increase of local physical signs or fever, 
they gradually merge into chronic appendicitis. 
Not' a few during the first twenty-four hours are apparently mild 
catarrhal cases, when in truth they have been ulcerative and gangrenous 
from the beginning. These are often fulminating, and unless promptly 
relieved by operation they are almost always fatal. 
In the process of repair and “cure,” the possibility of thickening of 
the organ, constriction, distortion, dilatation below the occlusion and late 
abscess formation, as well as suddenly arising localized or diffuse peri- 
tonitis are to be considered. In some cases the thickened appendix 
remains tender, may never cause acute symptoms, but is sufficient to 
limit the efficiency of the patient. 
Purpuric Appendicitis 
Occasionally there are cases in which the earliest evidence of pur- 
pura hemorrhagica is hemorrhage into the substance of the appendix 
causing all of the symptoms of acute appendicitis. I have had two such 
experiences; in both operation proved the hemorrhagic nature of the 
disease and hemorrhages from various sources (mucous membranes and 
into the skin) followed. Both recovered. 
Fibrinoplastic Appendicitis 
The appendix infected, the fibrinoplastic deposit may he prominent. 
The exudate may not limit itself to the appendix hut there may also he 
either localized, or moderately diffuse, or general fibrinous peritonitis. 
Catarrhal inflammation, primarily with or without ulcer or necrosis, may 650 
DISEASES OE THE DIGESTIVE APPARATUS 
cause plastic exudate. It may happen that in such cases the peritoneum 
is protected by localized fibrinous deposit which organizes later, and leaves 
a thickened appendix with or without adhesions. These are among the 
chronic appendicitides, which when they cause subjective symptoms are 
never relieved permanently save by operation. 
The prognosis of uncomplicated fibrinoplastic appendicitis for life 
is favorable without operation; the tendency to relapse is great, and a 
large number of chronic cases are easily traced by the pathologic lesions 
to this form of the disease. 
Fibrinoplastic appendicitis may finally be complicated by ulceration 
of the mucosa, diffuse peritonitis or abscess formation, due to perforation. 
Perforation is the result of infection and necrosis; it is at once the 
most serious of all appendicular lesions associated with its acute inflam- 
mation. Catarrhal ulcers, as suggested in the preceding paragraphs, may 
perforate or the infection may cause early deep and destructive changes 
leading to death of tissue at one or more points. 
Three per cent of typhoid appendix ulcers perforate. Perforative 
peritonitis unoperated and advanced beyond the first twenty-four hours, 
offers an unfavorable forecast. 
The perforation, when preceded by nature’s protective exudate (pro- 
tective peritonitis) may not open into the free peritoneum but into a 
sac; an abscess is likely to form, which may or may not perforate in one 
of many organs. 
The sac may perforate into the peritoneal cavity with resulting gen- 
eral septic peritonitis. Almost all of these cases when advanced to this 
stage die. There are in most cases of perforative peritonitis which are 
not fulminating, “factors of safety” which seek to prevent extension by 
protective and localized peritonitis during the early hours of the process. 
The gravest of all cases are those which without tumor or protective 
exudate, adhesions, or localized peritonitis, open directly into the cavity 
of the peritoneum, causing diffuse acute peritonitis. These patients show 
early the overpowering and deadly influence of toxemia, which includes 
the symptoms whose prognostic significance will be separately considered 
General diffuse peritonitis due to perforation is separately considered 
(See Acute Diffuse Peritonitis) ; it offers, when due to perforation, only 
the gravest outlook. 
General diffuse peritonitis may he caused by infection from deep 
ulceration of the appendix without perforation. The anatomic location 
of the appendix is an important factor in determining the point of per- 
foration, the location of the appendicular abscess and the nature and 
extent of the resulting peritonitis. 
Perforative Appendicitis DISEASES OF THE APPENDIX 
651 
Rupture into a hollow viscus is naturally much more favorable than 
is perforation into the free abdomen. 
Retroperitoneal abscesses are within easy reacli, and offer a good 
prognosis; these may rupture into the ileum, cecum, duodenum, dia- 
phragm, colon, bladder, acetabulum, externally, through sinuses, or 
directly into the peritoneal cavity. 
The ultimate fate of pus accumulation is of great importance. It is 
difficult to give a forecast. The presence of pus remains a menace; it may 
cause sudden diffuse peritonitis by perforation; it may open in any one of 
the directions above mentioned. While there will always he cases which 
empty without threatening life, the large majority left untreated lead 
either to subacute or chronic pyemia or to fatal peritonitis. The prognosis 
of appendicitis has been enormously improved by the prompt evacuation of 
the abscess cavity. Other secondary complications are thus prevented, such 
as liver and kidney abscess, pylephlebitis, occasionally meningitis and other 
grave organic changes. 
The presence of previous disease (particularly chronic nephritis and 
heart lesions) always handicaps the patient. Chronic nephritis with 
appendicitis invites infection and deep-seated ulceration, perforation, and 
rapidly spreading peritonitis. The same is true of diabetes mellitus 
and other metabolic diseases. 
Tonsillar streptococcus infection as well as the Streptococcus rheu- 
maticus of Poynton and Paine may precede appendicitis, which may 
then be considered metastatic. Jores and Aschoff have also reported 
metastatic appendicitis with scarlet fever. The latter cases are always 
serious because of the primary sepsis. 
Influencing Factors 
Leukocytosis.—Increase of polymorphonuclear leukocytes is prac- 
tically constant. There are exceptions, but they are so few as to demand 
but little consideration. My average count at the first visit is rarely 
below 12,000. usually nearer 15,000. Counts above 15,000 early, are 
indicative of pus accumulation. Fully developed appendicitis shows an 
average of 85 to 90 per cent of polynuclear leukocytes and white counts 
between 20,000 and 25,000. Symptoms of increasing peritonitis with 
increase of leukocytosis are suggestive of perforation. The white count 
is of much greater diagnostic than prognostic value. 
Heart.—The condition of the heart and the study of the pulse offer 
data for prognosis of the greatest value. 
In fulminating cases, the sudden toxemia finds expression in marked 
cardiac asthenia. It is always unfavorable to find children with rapid 
pulse and erratic systolic action during the early hours of the disease. 
In adults, grave local lesions may he associated with a tense, not of neces- 652 
DISEASES OF TIIE DIGESTIVE APPARATUS 
sity rapid pulse, and slight rise of temperature during the first hours; 
but with advancing disease (if perforative), the pulse grows progres- 
sively more rapid and weaker, while the blood pressure falls. The 
pulse may not be materially accelerated; indeed we have found it 
surprisingly slow, in the presence of perforation or ulceration without 
perforation. In such rare cases the diagnosis and prognosis must depend 
upon the physical signs and other subjective symptoms. 
Perforative peritonitis may in its early stage, as I have already 
suggested, show an unchanged pulse, a decided drop of temperature and 
relief of pain. The recognition of such possibility means much to the 
patient; failure seals his fate within twelve to twenty-four hours. 
The rule may be accepted that in the adult a rapid pulse from the 
beginning is unfavorable and indicates profound toxemia and deep tissue 
changes. Rapid pulse with septic symptoms in patients with good re- 
sistance does not argue against the possibility of recovery. Such cases 
frequently recover after operation. Unchanged and rapid pulse after 
operation (within 24 to 36 hours) considered alone or with other symp- 
toms, is evidence of a severe condition. 
Improved systolic force within the first twenty-four hours following 
operation is always reassuring. The pulse is slower and fuller and usually 
the general appearance of the patient and other symptoms show decided 
change also. 
Intermittent hearty arising at any time during the course of the dis- 
ease, must be considered among the grave symptoms if the frequency is 
materially increased and the heart sounds are feeble. 
Sudden heart dilatation is possible and should be anticipated by the 
attendant in cases wThere the previous history leads to the suspicion of 
a diseased myocardium. Thrombosis of the pulmonary artery or one of 
its branches may cause sudden death. 
Temperature.—Initial chill is not the rule; “chilly sensations” are 
frequent with rise of temperature during the first twenty-four hours. 
The temperature during the first twenty-four hours does not offer any- 
thing upon which the prognosis of the individual case can be based. The 
rise of temperature may be so insignificant in serious cases as to deceive 
the attendant and lead away from the correct diagnosis. Taken alone, 
temperature therefore is of little value for our purposes. There are those 
who hold that there is always rise of temperature early; this is probably 
true, but failure to detect it with other suggestive symptoms must not 
overthrow the diagnosis. 
Cbradual rise of temperature in spite of surgical treatment and rapid 
heart, with or without change in the local symptoms, justify only an 
uncertain prognosis not necessarily unfavorable; the general picture of 
the case as seen after giving all of the symptoms their relative value will 
usually lead to safe conclusions. DISEASES OF THE APPENDIX 
653 
Repeated chills and fever after operation indicate pus accumulation 
and sepsis. Repeated chills, rapid pulse, jaundice or icteroid appearance, 
are suggestive of pylephlebitis, thrombosis, secondary abscess of the liver, 
involvement of the gall-bladder or bile passages. 
The reappearance of fever after fall, following operation, is indica- 
tive of some complication which in most cases is not serious. 
Vomiting.—Early persistent vomiting is characteristic of the more 
severe cases; when distension rapidly follows or rigidity increases, there 
is usually a serious underlying ulceration, perforation, or a severe type 
of catarrhal appendicitis. Fecal vomiting early, indicates perforation; 
fecal vomiting later attends perforative peritonitis and adynamic intes- 
tinal paralysis. 
When vomiting is controlled by the operation and suddenly returns, 
it demands the thorough consideration of possible intestinal obstruction 
(either mechanical or paralytic) and makes the outlook grave. The 
prognosis depends on the ability of the surgeon to remove the cause. 1 
have seen a number of fatal cases in adults operated late; there was 
beginning perforative peritonitis—death followed after two or three days 
of vomiting which finally became fecal, the distension increasing, hic- 
cough was uncontrolled; these cases represent the adynamic intestinal 
paresis above mentioned. 
It may be concluded that the prognosis is always bad when vomiting 
does not yield promptly to surgery or medical treatment. 
Hiccough.—Early or late hiccough is always an ominous symptom. 
When early, it is usually associated with the fulminating type of the 
disease; when late, it is very likely to be a symptom of diffuse peritonitis 
with intestinal paresis; when it follows surgical operation, it may be 
due to one of several conditions (obstruction, band formation, adynamia, 
uremia, acidosis, diffuse and increasing peritonitis, etc.). 
Obstipation.—I mean by “obstipation” obstinate constipation with- 
out positive organic obstruction of the intestine. But few cases of 
appendicitis are of serious moment in which the bowels are open and 
free. I do not remember to have lost such a case. The cases with obstipa- 
tion from the beginning are very likely to include those with the deepest 
appendicular and peritoneal changes. 
Pain.—Severe pain with prompt distention and early rigidity is sug- 
gestive of the graver types of the disease. 
The milder forms are less painful than are the severer during the 
early hours, and as a rule it is possible for the patient to get into a 
position which makes him fairly comfortable most of the time. 
The McBurney point is tender and present in those cases in which 
the origin of the appendix is normal or nearly so (about 60-70 per cent). 
Tenderness over an abnormally large area is indicative of peritonitis, 
either local or diffuse. 654 
DISEASES OE THE DIGESTIVE APPARATUS 
Cessation of pain during a limited period following perforation is 
not infrequent, and is of great prognostic significance. 
The location and radiation of pain offers some indication of the rela- 
tive position of the appendix. Severe backache may characterize pain 
with abscess or appendicitis in which the origin is posterior. These cases 
offer a good prognosis and with pus are easily drained, without opening 
the peritoneal cavity. It would lead to unsafe conclusions if pain as a 
symptoms were depended upon for prognosis. It should not be forgotten 
that severe and fatal cases may begin with but few sensory symptoms. 
Hyperalgesic areas (Head zones) are of diagnostic, and not of prog- 
nostic value. 
Albuminuria and Indicanuria.—Most perforative and ulcerative cases 
in which there is toxemia show evidences of toxic nephritis if the urine 
is cautiously watched. A faint trace of albumin with free secretion is 
not serious. Marked reduction in quantity, albuminuria and casts (blood, 
hyalin, granular) is always grave. Cases in which albuminuria depends 
upon previous nephritis with any form of appendicitis are serious—not 
of necessity fatal. These cases early recognized, in the absence of heart 
lesions, offer a fairly good prognosis. 
Sudden strangury, following preexisting albuminuria whether early 
or late, is of grave moment. 
Indicanuria is present in most cases. Its presence taken alone is of 
no prognostic value. Bacilluria and albuminuria per se are not of neces- 
sity serious. 
Facies and General Appearance.—The facies with the “acute abdo- 
men” are characteristic; the pinched appearance, sunken eye, anxious 
expression with clear mind, as a rule, are not easily forgotten. Hip- 
pocrates described the facies of acute peritonitis (facies hippocraticus). 
The experienced eye sees in the facies, the general appearance and posi- 
tion of the patient in bed, much that is either encouraging or discourag- 
ing. In no other disease are the facies more expressive. In extreme 
danger, the facies hippocraticus with cold extremities, congested con- 
junctiva, hiccough and fecal vomiting and small rapid pulse, tell of 
approaching death. 
Physical Signs.—Increased abdominal resistance—rigidity—is the 
most important physical sign of acute appendicitis. The clinician who 
appreciates the significance of rigidity early and treats his cases secundern 
artem will reduce his mortality to a negligible figure. There are hut few 
cases in which cautious examination will fail to show some increased 
resistance in the region of the appendix. Light percussion will show 
some dullness, and palpation in many cases makes it possible to palpate 
a mass of varying size. Rigidity is the more dependable of all of these 
signs; the one which should lead the attendants whenever present. Its 
presence justifies the disregard of most other symptoms. It always means DISEASES Oh TI1E APPENDIX 
655 
something; it should never be ignored for safe prognosis and treatment. 
The size of the tumor with its attending physical signs is also im- 
portant. Palpable tumor ivithout physical signs of general peritonitis 
proves pus accumulation in almost all cases. The circumscribed tumor 
is evidence of the success of nature to limit the disease, and offers an 
excellent prognosis. Increasing distention, tympany, is always suggestive 
of peritonitis or adynamic paresis and is usually serious. Perforation 
or deep ulceration, with diffuse peritonitis is usually found. 
Effacement of liver dullness appearing suddenly, is symptomatic, but 
by no means pathognomic of perforation. I have met it in cases with- 
out perforation; at times after operation, or even before, in which re- 
covery followed. As a rule, however, marked tympany with effacement 
liver dullness is a combination which justifies a doleful forecast. 
Haturally other symptoms show the danger also. 
Relapse—Recurring Appendicitis 
Forty per cent of unoperated cases relapse. Some of these merge 
into chronic appendicitis, others after one or more relapses cause perfo- 
ration; a proportion of these form abscesses, others have fulminating 
peritonitis, some localized peritonitis, while with the majority of perfo- 
rations the dangers of acute diffuse peritonitis are faced. Some of these 
cases which appear to be mild during one relapse may in the next, or 
one of the subsequent attacks, perforate unexpectedly. 
Saviaraud found that in children the mortality in the cases which 
followed procrastination was 32 per cent. Sahli found in 7,213 cases 
of which number 6,740 were not operated, recurrence followed in 4,593. 
Of these he claims 3,635 recovered without further recurrence. 
Chronic Appendicitis 
Any form of acute appendicitis which lives after the initial attack 
may leave remnants of the infection which finally cause persisting symp- 
toms, or without an original acute attack, chronic appendicitis may 
gradually develop. Chronic appendicitis is subject to acute exacerbations 
of both local and distant symptoms. I have considered chronic appen- 
dicitis as a cause of dyspeptic, gastric, and gastro-intestinal symptoms 
in connection with a number of diseases, which the reader will find 
included in this section. In all chronic unexplained dyspepsias, chronic 
appendicitis should be suspected. 
Adhesions and thickening, distortion, retained foreign bodies (fecal 
concretions), pus accumulation, may continue symptoms during unlimited 
periods. The symptoms once present with a chronic underlying change 
do not often yield; they do not threaten life unless there are acute ex- 
acerbations, perforation, intestinal obstruction from extensive adhesions 656 
DISEASES OF TIIE DIGESTIVE APPARATUS 
or other grave complications; but the majority continue with dyspeptic 
symptoms, chronic constipation, pain varying in severity from time to 
time, often inefficiency in many directions, including mental lethargy. 
The prognosis of these cases when operated is excellent. A large material 
during the past twelve years has been without a single death following 
interval operation; most have made full and satisfactory recoveries. 
With extensive adhesions some symptoms may persist, but in practically 
all, the patients were markedly relieved. 
There is danger of intestinal obstruction in cases in which symptoms 
of chronic appendicitis persist with adhesions of the ileum and at times 
tumor formation. Such cases demand early attention to prevent strangu- 
lation of the intestine (See Intestinal Obstruction). The symptomatology 
and prognostic significance of Jackson’s veil and the conditions which 
Lane in England and Bainbridge in this country have described undef* 
“intestinal stasis,” and upon which the latter place great stress as pro- 
ducing the symptoms of many diseases, are all surgical. I am fully satis- 
fied that the Jackson membrane causes persistent symptoms which may be 
relieved by surgical interference in individual cases, for I had telling 
experiences. Adami has fully and well answered many of the conten- 
tions of Lane, to which the profession has not subscribed; there may be 
justification in isolated cases to assume that the conditions which Lane 
describes cause some symptoms, but the galaxy of diseases to which he 
refers in his recent publications will never be included. 
Cancer of the Appendix 
Cancer and carcinoid of the appendix are more frequent than is gen- 
erally supposed. Rogg reports 58 in 11,000 cases of appendicitis, and 
reports 200 cases taken from medical literature. The microscopic exam- 
ination of appendices removed by operation is showing an increasing 
number of cases. Most of these are found early in life—in the third 
decade. They may be.either intramucous, submucous, or subserous (car- 
cinoid). Their favorite seat is the tip. Some involve the entire appendix 
by infiltration, and in some there is a distinct history of preceding acute 
and final chronic appendicitis. In these cases in young subjects there are 
few or no metastases; the course seems to be benign, and early operation 
offers a good prognosis. With the valve and cecum involved, I have not 
had brilliant results from resection. All cases in subjects after fifty 
promptly recurred and died within twelve months. The growth is rapid 
after fifty and metastasis is the rule. 
Tuberculosis of the Appendix 
See Intestinal Tuberculosis, Section I. 
Primary tuberculosis of the appendix is possible, but rare. Tuber- DISEASES OF THE APPENDIX 
657 
culous ulceration and appendicitis are usually secondary to similar disease 
of the lung, intestine, and peritoneum. The prognosis of the primary 
disease is not bad.* 
Appendicitis and Typhoid Fever 
Appendicitis is not frequent with typhoid fever. Typhoid ulcers of 
the appendix are relatively frequent. Rolleston found the appendix 
altered in Id of 60 cases; in 5 it was swollen, in 7 ulcerated, and in 2 
perforated. Fitz found in 167 typhoid perforations that 5 were situated 
in the appendix; Curling found 20 typhoid perforations with 2 in the 
appendix; Church 3 of 21; Morin 12 of 64; and Heschl reports 56, in 
8 of which the appendix was perforated. Kelly finds that appendicitis 
with typhoid may be purely accidental—the two conditions are concur- 
rent, or latent appendicitis is lighted into activity by typhoid fever. 
Appendicitis, either mild or severe, may arise during typhoid from 
lymphatic infection or from an appendicular typhoid ulcer. These latter 
cases often perforate. Typhoid fever may be followed by appendicitis, 
following so soon as to suggest typhoid infection of the appendix. 
Naturally the prognosis is more grave with typhoid appendicitis than 
without such complication or when the patient has been in perfect health. 
Surgeons are agreed that “the symptoms to justify operation must be of 
a more urgent character than would be necessary in the case of a person 
in perfect health suddenly affected in a similar manner, as the greater 
gravity of an operation in the height of typhoid fever warrants the sur- 
geon’s assuming greater risks in waiting to make sure that an operation 
is inevitable” (Kelly). Of seven typhoid perforated appendices operated, 
only one recovered. 
Cushing believes that the prognosis of appendicular perforation with 
typhoid is better than perforation of the ileum. The toxemia and typhoid 
lesions with added appendicitis present a complication of extreme gravity. 
No surgical complication will demand more judicious care. Richardson 
has accented the great danger of operations during typhoid fever. In 
the absence of perforation which demands operation, the prognosis is 
good without operation. This has been the experience of most clinicians 
and surgeons (Murphy, quoted by Kelly). 
Complications 
I have recently referred to the dangers of nephritis—usually toxic 
—as a complication of appendicitis and peritoneal infection. Preceding 
chronic nephritis until or without uremia is always of grave import. 
* Sehnitzler considers this subject fully in an able article, to which the reader 
is referred for further information. 658 
DISEASES OF THE DIGESTIVE APPARATUS 
Toxemia is invited by this complication and in many of my cases the 
course has been surprisingly rapid and fatal. 
The cardiac complications have been mentioned in considering the 
pulse. Preceding myocardial disease, valvular lesions with faulty com- 
pensation in the presence of added toxemia, often lead to cardiac asthenia 
during the early days of the disease. Pylephlebitis with or without pus 
deposits (abscess of the liver) is a grave complication; when extensive, 
death usually follows after a period of pyemic septic symptoms. 
Septic phlebitis—thrombosis—may, according to location and consti- 
tutional involvement, cause grave symptoms during only a short period, 
or chronic phlebitis may develop and lead to weeks of invalidism. The 
septic type of thrombosis with marked toxemia and involvement of the 
sensorium is usually fatal. 
Pneumonia, empyema, non-purulent pleurisy are occasional compli- 
cations. The first, in severe cases, is exceedingly grave; the second dur- 
ing convalescence after operation usually yields to operation; the third 
offers the same prognosis when a late complication as when the disease 
is primary. In all, the resistance of the patient is paramount. Typhoid 
fever may follow appendicitis when the prognostic features are materially 
influenced by lack of resistance following the original disease. 
References 
Adami. Brit. Med. J., 1914, vol. i. 
Bainbridge. Brit. Med. J., London, 1913, ii, p. 1129. 
Bright (Richard) & Addison (Thomas). Practice, etc. London, 1839, vol. i, p. 498. 
Bull (W. T.). New York Med. J., 1895, vol. xviii, p. 248. 
Chaveau. Lyon Medicale, 1882, vol. xli, p. 272. 
Eisner (H. L.). New York Med. J., Apr. 9, 1893. 
Fitz. Am. J. Med. Sci., 1886, vol. xcii. 
Hall (R. J.). New York Med. J., May 8, 1886. 
Huebner. Deutsch. Ztschr. f. Chir., 1907, vol. 89, p. 874- 
Illoway. New York Med. J., vol. xcriii, No. 4, V■ 162-168. 
Jores & Aschoff. Verhand. d. Deutsch. path. Gesellsch., Marburg, 1913. 
Kelly & Hurdon, Kelly (H. A.). Diseases of the appendix, etc. Philadelphia, 1909. 
Kraussold. Volkmann’s Sammlung klin. Vortrage innere Medizin, No. 191. 
Lane. Brit. Med. J., London, 1913, ii, 1125-1128. 
Lockwood. Brit. Med. J., 1882, ii. 
J. Anat. & Phys., London, 1883-4, vol. xviii. 
Lockwood. Allbutt & Rolleston’s System of medicine. London, 1907, vol. in. 
McBurney (Chas.). N. Y. Med. J., Dec. 21,1889. 
Morrison. Brit. Med. J., Jan. 8, 1914. 
Parker (Willard). Quoted by Kelly & Hurdon; also Bull, Sands, etc. 
Poynton & Paine. Researches on rheumatism. London, 1913. 
Riedel. Munch, med. Wchnschr., 1907, Nov. 26. No. 48, p. 2367. DISEASES OF THE PERITONEUM 
659 
Rogg. Ztschr.f. Krebsforsch., 1913; Bd. xiii, H. I, p. 12-41- 
Sahli. Stengel’s article. In: Osier’s Modern med., vol. v, p. 428-9. 
Sands (Henry B.). New York Med. J., Feb., 1888, vol. xlvii, p. 197. 
Savariaud. Annal. de Med. et Chir. Jg. 17, No. 12, p. 401. 
Schnitzler (J.). Med. Klinik, Jg. 9,1913, No. 88, p. 1538, No. 39, p. 1584 
Stengel. Osier’s Modem medicine, 1914. Article: “Appendicitis,” vol. Hi. 
Toft. Cited by Kraussold. In: Samrnl. klin. Vortrage Inner. Med. No. 191. 
Weir (R. F.). New York Med. Neivs, Jan. 15, 1887. 
New York Med. J., June 11, 1887. 
Additional Monographs 
Church. Records of St. Bartholomew's Hosp., 1881, vol. xvii, p. 97. 
Cushing. Records of Johns Hopkins Hosp., 1899-1900. 
Denver (John B.). Treatise on appendicitis. Philadelphia, 1900. 
Fowler (G. R.)< Treatise on appendicitis. Philadelphia, 1894. 
Heschl. Schmidt’s Jahrb. 1853, vol. Ixxx, p. Jf2. 
Morin. These de Paris, 1867. 
Mynter (Herman). Appendicitis and its surgical treatment. Philadelphia, 1897. 
Richardson. Boston Med. & Surg. J., Jan. 9, 1903. 
Rolleston. Lancet, London, May 29, 1898. 
Sonnenberg. Path. u. Ther. d. Perityphlitis. 7 Aufl. Leipzig, 1913. 
Treves. Perityphlitis. Allbutt’s System, etc., vol. Hi, p. 879. 
I. Diseases of the Peritoneum 
1. Acute Diffuse Peritonitis 
(Inflammation of the Bowels) 
General Considerations.—Peritonitis may be either circumscribed or 
diffuse. It is almost always of bacterial origin and practically always 
secondary. “Idiopathic peritonitis” has fallen into oblivion. Those 
cases of nephritis, tonsillitis and other diseases which were closely asso- 
ciated by the older clinicians wTith unexplained peritonitides are now 
known to be of bacterial origin, or to have an added infection which ex- 
plains the inflammation of the peritoneum. 
The cases which Flexner has characterized as primary “are those 
originating apart from disease of any neighboring organ, or in other 
words cases due to metastasis by way of the blood or lymph stream” ; hence 
these, too, may safely be considered secondary. Peritonitis with rheu- 
matic infection, formerly considered “rheumatic peritonitis” depends 
upon bacterial invasion, is rare, never primary, and offers a high mor- 
tality. Osier mentions acute peritonitis “as a terminal event” in 
nephritis, gout, and arteriosclerosis; 12 were found in 102 cases of acute 660 
DISEASES OF THE DIGESTIVE APPAKATUS 
peritonitis at the Johns Hopkins Hospital. My material reduces the 
number of such incidents far below these figures. Flexner includes among 
the secondary cases those infections of the peritoneum due to injury or 
disease of an organ in direct contact with the peritoneum. The infecting 
agent may enter from without the body (exogenous), or it is endogenous 
when it comes from within (Allchin). 
Flexner’s 106 cases included only 2 in which he was unable to de> 
termine the variety of the bacterial infection. Bacterial virulence and 
proliferation are invited by the inability of the peritoneum to take ad- 
vantage of its “factors of safety,” or normal protecting power. Thus in 
the presence of fluid in the cavity (injury or disease) with ascites, as in 
nephritis or other lesions, with perforation, and foul and other foreign 
matter, the protective agencies are reduced, and proliferation is invited; 
virulence, as suggested, is increased. These facts are sufficient to explain 
the rapid development of acute peritonitis following injury to the abdom 
inal wall, the breaking of adhesions, perforations, uterine lesions, salpin- 
gitis and the many other primary diseases which promptly cause the second- 
ary disease. In the preceding chapter I considered the association 
of peritonitis with appendicitis—the most frequent of all of the causes. 
I have also considered peritonitis as it complicates the various intestinal 
obstructions, including hernia and constriction due to intraintestinal les- 
ions, with the perforation of typhoid, stomach and duodenal ulcer, also 
malignant ulceration and perforation, gonorrheal and puerperal infection 
of the genitalia, and their dependencies. It would be a work of superero- 
gation to again dilate on each of these. The resulting peritonitis offers 
the same general picture; its gravity is always the same though the viru- 
lence and malignancy of the infection does influence the resistance of the 
individual, but with all the rule holds that it is the rare exception for a 
case of general peritonitis, in which the cause has not been promptly re- 
moved, to recover. Once peritonitis is general from whatever cause, the 
chances of saving life are exceedingly small. Septic (streptococcus) peri- 
tonitis leads to such profound toxemia as promptly to rob the patient of 
heart strength. 
Localized and protective peritonitis is often a life saving process, for 
by the throwing out of plastic material and its organization it protects 
against general and septic peritonitis. This is often true of ulcerative 
intestinal diseases (appendicitis, intestinal, gastric, duodenal ulcer, and 
gall-bladder disease). 
Subphrenic abscess is considered with ulcer of the stomach and duo- 
denum ; for its clinical study Maydl’s monograph is a classic. 
It may he assumed that the sudden development of general peritonitis 
following perforation of a hollow viscus, without preceding protective 
peritonitis, is among the most serious forms—almost always fatal unless de- 
tected at once and relieved by surgical treatment (perforative peritonitis). DISEASES OF THE PERITONEUM 
661 
In these cases the Streptococcus pyogenes is usually found, the albus is 
less virulent. In children the pneumococcus is among the more malignant 
of the bacteria present (Rischbieth). The gonococcus in my experience 
is less virulent than the streptococcus and often leads to a subacute or 
chronic course. Prognosis is materially influenced by the resistance 
which rugged health and the normal previous conditions offer. Young 
children particularly offer a bad prognosis in acute peritonitis from any 
cause. 
Acute Diffuse Peritonitis with Appendicitis.—With appendicitis (the 
usual cause) diffuse peritonitis once developed is almost uniformly fatal. 
The unfavorable features are pronounced abdominal distention, obstipa- 
tion, fecal vomiting, hiccough, pinched features, reduced and albuminous 
indican-laden urine, small pulse, rapid heart, hippocratic facies, and cold 
extremities. Never have I seen but two patients recover with this 
symptom complex. 
The Temperature.—The temperature in the midst of fully formed 
symptoms is not to be depended upon as a prognostic index. Prompt 
collapse with subnormal temperature in the early hours of peritonitis is 
only occasionally followed by a happy result. High temperature is un- 
favorable in the presence of other advancing symptoms. Extreme rest- 
lessness and insomnia, are always unfavorable. The average duration of 
fulminating or perforative appendicitis is rarely beyond forty hours. 
Treves mentions cases in which the peritoneal symptoms are less 
prominent than is the typhoid condition. These are in aged and previ- 
ously reduced individuals. 
Kidney and Liver.—Among the serious secondary lesions are those 
which involve the kidney and liver. The rapid advance to the liver 
through the portal circulation of toxins from the abdominal cavity and 
to the kidney lead to parenchymatous changes. These add factors of 
enormous danger. 
Puerperal Peritonitis.—Puerperal peritonitis is fortunately rare when 
modern methods are used during labor; it is a streptococcus infection, is 
probably of lymphatic origin, and spreads from the uterus to the peri- 
toneum. Continuous fever with rapid pulse is less favorable than re- 
mission with profuse sweat, following chill and fever. It is a true 
septicemia. The mortality is rarely below 50 per cent in developed cases. 
Further Considerations.—In all forms of the disease the more favor- 
able cases are those in which the intestinal paresis is not complete, and 
there are occasional movements with fair quantity of urine and a heart 
which is without the asthenia of extreme toxemia. When the pulse is 
persistently at 120 and above, the condition of the patient is threatening, 
■whether before or after operation. The conclusions offered in considering 
the blood picture and appendicitis, are equally true of peritonitis. High 
leukocytic counts are not encouraging—low counts are equally unfavorable. 662 
DISEASES OF THE DIGESTIVE APPARATUS 
Diffuse peritonitis as a rule, when it is not controlled within the first 
30 hours, is fatal. 
I have learned to place great reliance in prognosis on the facies of 
the patient. Changed facies, pinched appearance, means death. Of 
Treves’ 70 fatal cases 14 per cent died within 36 hours, 6 per cent be- 
tween 36 and 48 hours, 20 per cent between the third and fifth day, 33 
per cent between the fifth and seventh day, and 27 per cent after a week. 
References 
Allchin. Allbutt & Rolleston’s System, of medicine. London, 1907, vol. in. 
Cushing. Johns Hopkins Hosp. Bull., 1899, x. 
Eisner. Protective peritonitis. (See Second Series Index Catal., Library of the Surgeon- 
General’s Office, vol. xiii, 2d Series, 1908. 
Flexner (S.). Philadelphia Med. J., 1898, ii, 1019. 
Hunner. Pneumococcus peritonitis. Quart. J. of Med., 1902, xiii. 
Maydl. Uber Sulphr. Abscesse. Wien, 1894. 
Nothnagel. Diseases of the intestine and peritoneum. Philadelphia, 1904. 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Rischbieth. Pneumococcus peritonitis. Quart. J. of Med., Oxford, 1911, iv. 
Romberg & Paessler. Deutsch. Archivf. klin. Med.,Bd. Ixiv. 
Treves. Allbutt & Rolleston’s System of Medicine. 1897, vol. in. 
2. Chronic Peritonitis 
After acute localized peritonitis there is organization of tissue (produc- 
tive peritonitis) which leads to thickening and adhesions (periuterine, 
perigastric, perisplenic, periappendicular). In occasional cases there may 
be pus accumulation between the layers of new tissue. Such abscesses 
are naturally encapsulated and usually operable, and offer a good prog- 
nosis. These include appendicular and subplirenic as well as other ab- 
dominal abscesses. 
Deforming and obliterating peritonitis or adhesive peritonitis follow' 
in those cases of agglutination in which after acute or subacute peritonitis 
or the tuberculous variety, the coils of intestine or organs are so firmly 
united as to make separation impossible. The peritoneum is obliterated, 
and <(deformed.” Such complications are also likely to follow extensive 
abdominal operations. 
Periserositis (See Pick’s Disease and Periserositis) may also b© in- 
cluded among the chronic types. In these cases besides the spleen, the 
liver, general peritoneum and pericardium are included. 
The great dangers of localized and obliterating chronic peritonitis, are 
possible intestinal obstruction and chronic invalidism, due to the effect 
of adhesions, bands, distortions, and the changed relations of organs. In- DISEASES OF THE PERITONEUM 
663 
testinal obstruction due to fibrous bands and adhesions is fully considered 
elsewhere (See Intestinal Obstruction). 
Chronic Nodular Proliferative Peritonitis.—Pathologists and 
clinicians are familiar with a form of productive chronic peritonitis with 
nodular growths of the peritoneum and thickening, which so closely re- 
semble tubercle, as to be differentiated intra vitam (at the time of oper- 
ation) with the greatest difficulty. Welch calls attention to such cases in 
his section on the pathology of peritonitis in Flint’s “Practice of Medi- 
cine,” also in his discussion of Nicholl’s paper. Such cases are undoubt- 
edly at times included among the tuberculous, and are favorably influenced 
by surgical interference. Fitz and Wood also mention such possibility. 
The thickening and agglutination in these cases may lead to tumor forma- 
tion, either single or multiple; the viscera are covered with tense and thick 
peritoneum; circulatory embarrassment and ascites, at times obstruction, 
cause of death. I have found the productive (proliferative) peritonitis 
with alcoholic cirrhosis. In children I have occasionally seen chronic 
nodular non-tuberulous peritonitis with ascites and chronic invalidism. 
Some of these cases yield after operation; a few have made satisfactory 
recoveries without. Most of these children recover. 
General Conclusions.—Chronic peritonitis may complicate malignant 
and echinococcus involvement of the peritoneum when hemorrhagic ascites 
is likely. Whether “hemorrhagic peritonitis” is ever prinlary is ques- 
tionable. 
References 
Fitz & Wood. Practice of medicine. Philadelphia, 1897. 
Nicholls. J. Am. Med. ylss., March 14,1903, vol. xl, p. 701. 
Welch (W. H.). Flint’s Principles & practice of medicine. 6th ed., p. 583. 
3. Tuberculous Peritonitis 
See Tuberculosis, Section I. 
4. New Growths of the Peritoneum 
I have never in practice seen a case of primary cancer of the peri- 
toneum. Neoplasms (malignant) of the peritoneum are practically 
always secondary. Fatty deposits {lipoma), fibroma, and neurofibroma 
are occasional benign growths which do not materially interfere with the 
patients’ comfort as a rule, and are operable if large and troublesome. 
Innocent cysts and echinococcus of the peritoneum offer a good prog- 
nosis (See Echinococcus Disease). 
Aschoff calls attention to a diffuse endothelial degeneration of the peri- 664 
DISEASES OF THE DIGESTIVE APPARATUS 
toneum which he considers primary and malignant (endothelioma). The 
prognosis is bad. 
The secondary carcinomata, usually multiple and disseminated, are 
found with stomach, gall-bladder, bile passage, pancreatic, intestinal 
(rectal often), ovarian, uterine, and renal (hypernephroma) growths. 
The mesenteric glands are involved; ascites is prominent—usually bloody 
—and after varying periods with characteristic facies and marasmus, 
death follows. 
References 
Aschoff. Path. Anatomic. Jena, 1913. 
Rippert. Das Karzinom des Menschen. Bonn, 1911. 
J. Diseases of the Liver 
1. Jaundice 
(Icterus) 
Surcharged fluids and tissues of the body with bile coloring matter 
cause a yellowish coloration of the skin, mucous membranes, and con- 
junctivae, easily recognized and known as jaundice. 
Jaundice is never a disease per se; it is always a symptom and is due 
to obstruction of the flow of bile, which may be either complete or in- 
complete, in almost all cases. 
(a) Hepatogenous jaundice is always obstructive and is due to the 
resorption of bile manufactured in the liver which fails to escape from 
that organ, wholly or in part. 
(b) Hematogenous or hemo-hepatogenous jaundice is due to the 
change of hemaglobin into hematoidin, identical with bilirubin. In these 
cases there is rapid destruction of large numbers of red blood corpuscles— 
hemolysis, causing hemolytic jaundice; the hemoglobin is converted into 
bilirubin in the liver in most instances. Recent experimentation tends to 
prove the possibility of such conversion in the blood stream. 
(a) Hepatogenous Jaundice 
(Obstructive Jaundice) 
Causes.—The larger number of cases are due to mechanical obstruction 
in which there is reabsorption of bile which cannot escape into the intes- 
tine through the common duct. The most frequent causes of obstructive 
jaundice are (1) catarrhal inflammation of the duodenum and common 
duct with consecutive closure at the opening of the ampulla of Vater 
(catarrhal jaundice). Among the other causes of mechanical obstruc- DISEASES 0? THE LIVER 
665 
tion leading to jaundice are (2) the impaction of gall-stones in either the 
hepatic or common ducts; (3) stricture of the common duct, complete or 
incomplete, due to either ulcerative or inflammatory disease; (4) pressure 
of growths within the intestine or ducts causing sufficient obstruction to 
prevent the onward flow of bile; (5) extra-hepatic pressure from tumors 
of the liver itself or growths in the surrounding organs including cancer of 
the stomach or pancreas, or both at the same time, kidney growths, malig- 
nant disease of the omentum, glandular enlargements in the portal fissure 
of the liver, enlargement, either benign or malignant of the gall-bladder, 
mobile kidney, abdominal aneurism, either aortic or celiac, perihepatitis or 
any pressure from whatever cause which is sufficient to obstruct the free 
flow of bile. 
Bile is normally secreted at very low pressure; relatively insignificant 
increase of this pressure makes absorption of bile pigment into the blood 
easy and jaundice results. 
Catarrhal Jaundice (Gastroduodenocholangitis).—In consid- 
ering the diseases of the stomach we mention j aundice as one of the symp- 
toms of catarrhal gastro-duodenitis. In most cases in which jaundice 
develops there is more or less cholangitis, the larger ducts are involved by 
extension from the duodenum. The majority of these cases are found in 
young subjects in whom the jaundice follows error of diet, and a short 
period of gastro-intestinal symptoms. The features are characteristic of 
obstruction and include besides the yellow-tinged skin, discoloration of the 
internal organs and secretions, the conjunctivae and mucous membranes, 
with a slow pulse and respiration, subnormal temperature, clay colored 
stools and constipation; bile laden urine, pruritus; in obstinate and severe 
cases petechiae and cerebral symptoms. Simple uncomplicated catarrhal 
jaundice or gastroduodenocholangitis is usually a self-limited process which 
runs its course in from a few days to several months. In but few cases 
does jaundice persist beyond three or four weeks, but it may happen that 
the obstruction remains and continues the symptom beyond the average 
time. Such cases are associated with more or less stomach and intestinal 
symptoms and loss of weight with weakness. Convalescence is slow, but 
complete restoration to health is the rule. 
Influencing Factors 
Urine.—The urine offers evidences of value for prognosis. With ob- 
structive jaundice scanty and high colored urine is evidence of an active 
process; with increase of urine and the usual change to a lighter color from 
day to day, the prognosis for prompt recovery is good. The persistence of 
jaundice (usually fading) after the urine has cleared, is not unfavorable. 
Leucin and tyrosin are always unfavorable, they indicate grave and de- 
structive disease. 666 
DISEASES OF THE DIGESTIVE APPARATUS 
Indicanuria is not unfavorable. Casts and albuminuria are frequent, 
and with the positive diagnosis of catarrhal obstruction—uncomplicated—- 
do not as a rule influence prognosis unfavorably. Transitory glucosuria 
in catarrhal jaundice is frequent and of no great significance. 
Feces 
The feces when “clay colored” prove the absence of bile from the 
intestine. The return of normal color is coincident with the removal of 
the obstruction. 
When jaundice is due to congestion of the liver secondary to disease 
of the mitral valve or to infections, as pneumonia or typhoid fever, the 
prognosis depends almost entirely upon the gravity of the primary disease. 
The infections and organic diseases in which jaundice may be a 
prominent symptom are separately considered. The presence of jaundice 
with any infection proves extension to the liver or bile passages and is of 
great prognostic significance. 
Jaundice with puerperal eclampsia is almost always fatal. With 
malarial infection (See Section I) it is significant but not always grave; 
with relapsing fever it is ominous; following or associated with acute 
abdominal lesions as appendicitis—it is unfavorable in 55 per cent of 
cases (Reichel). In a relatively large number of cases swelling spreads 
from the small intestine (duodenum) to the head of the pancreas sufficient 
to obstruct the common bile duct; the j aundice disappears as the pressure 
is relieved. 
In a few cases the infection causes chronic catarrhal jaundice; the bile 
passages, including the gall-bladder, are involved. Free drainage may be 
necessary to effect a complete cure. 
Deep jaundice, with or without cerebral symptoms, severe itching and 
petechiae are symptoms of the more severe types of the disease and in 
diagnosis should lead to the suspicion and differentiation of malignancy or 
other organic change. It is not impossible, however, to find these symp- 
toms in uncomplicated and severe catarrhal jaundice which recovers after 
a varying period and slow convalescence. 
Jaundice with marked liver insufficiency and evidences of toxemia. 
including marked nervous manifestations (delirium, somnolence, and 
deep coma) and hemorrhagic diathesis offers an unfavorable forecast; 
cholemia is the paramount factor in this syndrome. Nervous symptoms 
and jaundice usually indicate some grave underlying condition. There 
are cases of infectious jaundice with meningeal symptoms during a few 
days, with final full recovery wfithout disagreeable or persisting sequelae 
(Guillian and Richet). Rolleston has called attention to the similarity 
of these cases to epidemic cerebrospinal meningitis. 
Slow pulse with lowered arterial tension, subnormal temperature, 667 
DISEASES OF THE LIVER 
slight albuminuria, yellow vision and slightly enlarged liver, or palpable 
gall-bladder, are not unfavorable in the absence of complications. Un- 
changing jaundice with loss of flesh and evidences of increasing weak- 
ness, whatever the initial symptoms, justify the conclusion that the ob- 
struction is likely to be of malignant or organic nature and demands 
thorough differentiation before prognosis is given. With cancer of the 
liver, jaundice once present persists and is not modified by any treatment. 
It only rarely happens that catarrhal jaundice complicates malignant 
diseases of the liver or pancreas; it is safe to cling to the rule that with 
malignancy the jaundice is persistent and deepens as the primary disease 
advances. 
I elsewhere consider the infectious type of jaundice known as Weil’s 
disease (See Section I). 
The occurrence of epidemic catarrhal jaundice is possible. Large 
numbers may be infected within a limited area at the same time; the 
prognosis of such infection is almost uniformly good; recovery follows 
in from seven to ten days in average cases. 
The jaundice associated with impacted gall-stone, either in the hepatic 
or common ducts, usually offers a good prognosis. In the majority of 
cases the obstruction is overcome either by nature’s process or by surgical 
interference. There is under such conditions, always danger of ulcera- 
tion, infection and suppuration; these complications are elsewhere con- 
sidered (See Gall-stones). 
Jaundice due to organic stricture of the common duct, complete or 
incomplete, following ulceration or inflammatory disease, pressure of 
growths within the intestines or ducts, can only be overcome by surgical 
interference unless of specific origin. 
Tumors of the liver itself, or growths in the surrounding organs 
including cancer of the stomach or pancreas, or both, and pressure from 
other sources already mentioned as causes of jaundice, only offer a favor- 
able prognosis when the growth is removable. The larger number of 
these conditions are not operable. 
Chronic jaundice may lead to multiple xanthoma (xanthelasma or 
vitilligoidea). In these cases the cause is not removable. Xanthoma 
may occur without jaundice. Xanthoma is evidence of chronicity and 
non-malignancy as a rule. Chauffard considers xanthoma due to excess 
of cholesterin in the blood. 
Chronic jaundice offers a grave prognosis. Surgical interference is 
not well borne. Hemorrhage is likely to occur and is not easily con- 
trolled. In chronic jaundice the functional activity of the kidney is an 
important factor; when sustained, the prognosis is thereby improved. 
Deep jaundice, also chronic, known as black jaundice, due to the 
presence of biliverdin is usually of malignant origin. In occasional cases 
leukoderma complicates chronic jaundice due to carcinoma (Warthin 668 
DISEASES OF THE DIGESTIVE APPARATUS 
and Rolleston). Deep jaundice persisting from any cause is always 
ominous. 
(6) Hemolytic Jaundice—Toxic Jaundice 
(Hemo-hepatogenous Jaundice) 
It is now assumed that all forms of jaundice whether “obstructive” 
or “non-obstructive” as the older writers characterized them, are in truth 
hepatogenous. It has been abundantly demonstrated that the formation 
of bile pigment from the blood coloring matter of destroyed (fragmented) 
corpuscles outside the liver is usually limited to the liver cells, and accord- 
ing to most authorities does not take place in any other organ of the body; 
hence all forms of hemolytic jaundice are in reality hemo-hepatogenous 
(Moleschott, Stern, Minkowski, JSTaunyn and Stadelman). 
Hemolytic jaundice according to Eppinger is obstructive, because 
with the destruction of the red blood corpuscles there is an excessive 
amount of hemoglobin which in the end provides for increase of bili- 
rubin ; there is plugging of the smallest bile ducts and change in the 
epithelial cells with increased viscosity of the bile. Thrombi in the bile 
passages and in the capillaries of the liver are common. The intrahepatic 
bile stasis and rupture of intralobular biliary capillaries, with entrance 
of bile through the lymphatics, are the changes which follow hemolysis 
which leads to jaundice. 
Ogata has demonstrated the possibility of jaundice before the rupture 
of the intralobular capillaries, and he believes that it is possible to con- 
vert hemoglobin into bile coloring matter in the blood current or in the 
spleen; this view has not been generally accepted, though Whipple and 
Hooper have experimentally demonstrated the rapid transformation of 
hemoglobin into bilirubin in the blood current outside the liver. Ep- 
pinger claims to have demonstrated the production of lymphatic tissue 
at the peripheral end of the common duct in these cases of hemolytic 
jaundice, which prevents the free exit of bile. 
It is exceedingly difficult to offer positive evidence which explains 
the method or seat of blood corpuscle destruction. It has been estab- 
lished by Chauffard (1907) that the red blood corpuscle undergoes hemol- 
ysis in an abnormal manner when exposed to hypotonic saline solution; 
“normally hemolysis of the red blood corpuscle begins in 0.42 per cent 
HaCl solution and is complete in 0.3 per cent”; in hemolytic jaundice 
“it begins at 0.6 per cent and is complete at 0.42” (Rolleston). This 
fragility of the blood corpuscles is characteristic of hemolytic jaundice 
when a disease sui generis, and is not present with hemolysis of pernicious 
anemia nor the intoxications including lead poisoning. 
The influence of the spleen on hemolytic jaundice has received care- 
ful consideration in connection with splenectomy. It has been demon- DISEASES OF THE LIVER 
669 
strated that removal of the spleen in Banti’s disease and in the familial 
types of jaundice has overcome all symptoms with restoration of normal 
blood conditions (Kahn, McPhedren, Fletcher and Harold Orr). 
Hemo-hepatogenous jaundice may be a symptom of: 
1. Infectious disease 
2. Poisons and drugs 
3. Cerebral disturbance 
4. Sudden hemolysis, non-infectious or toxic 
5. Splenomegaly. 
Causes of Hemo-hepatogenous Jaundice.—1. Infectious Disease.— 
The prognosis of jaundice of hemolytic origin with the infections is always 
exceedingly grave, for it is idicative of malignancy. The infections which 
hemolytic jaundice may accompany are yellow fever, typhoid, typhus, 
malarial, relapsing fevers, septicemia, pyemia, scarlet fever, pneumonia, 
Weil’s disease, and acute yellow atrophy of the liver. 
2. Poisons and Drugs.—These include snake bites—exceedingly 
grave; phosphorous antimony and other mineral poisons, chloroform and 
ether, potassium chlorate, coal tar products, chloral, santonin, male fern, 
toadstools, copper sulphate, carbolic acid, pyrogallic acid and ptomain 
poisoning. The prognosis of these poisonings varies in the individual 
cases depending upon prompt detection of the poison and its treatment, 
the size of the dose, the resistance of the patient and many associated 
factors, each requiring separate consideration. 
3. Cerebral Disturbances.—In the reduced and predisposed, sudden 
mental emotion or cerebral injury may be promptly associated with 
hemolysis and jaundice. The prognosis depends entirely upon the sever- 
ity of the brain lesion when this exists, and the constitutional disturbance; 
with mental emotion as a cause, the prognosis is usually good when 
uncomplicated. 
4. Sudden Hem,olysis (Non-infectious or Non-toxic).—There are 
cases in which after periodic hemoglobinuria following exposure to cold, 
jaundice develops. When without nephritis, usually tubular, or the 
hemorrhagic diathesis, the outcome is favorable. The majority of these 
hemaglobinurias are due to existing, often latent nephritis, and it is not 
unusual to find hemolysis recurring after each exposure, until finally the 
symptoms of chronic nephritis are fully developed and death results from 
the usual causes which end the lives of nephritics. 
Jaundice following transfusion of blood is of no great prognostic 
value; the outcome will always depend upon the nature of the disease 
demanding the added blood elements. 
5. Splenomegaly.—Splenomegaly with hemolytic jaundice include 
familial and hereditary types, and according to Rolleston the chronic 
infective jaundice of Hay era. The general features of obstructive jaun- 670 
DISEASES OF THE DIGESTIVE APPARATUS 
dice are missing; there is absence of bile from the urine (acholuria) and 
the feces are normal colored. Rolleston insists that the familial types 
of jaundice are an exception to the rule which insists on obstruction as 
the cause of all jaundice, for the evidence, he holds, is conclusive, which 
proves the production of bilirubin in the blood current. The fragility 
of the red blood corpuscles as shown by hypotonic salt solutions is char- 
acteristic. 
Chronic splenomegalic hemolytic jaundice may be either hereditary, 
congenital or familial, or in occasional cases it may prove to be acquired 
(Rolleston). Benjamin and Sulka have reported family jaundice which 
appeared after birth in one generation and congenital in subsequent 
generations. The disease may be hereditary and congenital or hereditary 
without being congenital. In occasional cases there is no enlargement 
of the spleen. 
The acquired hemolytic jaundice may follow infection; it is usually 
syphilitic. This represents the type described by Hayem who unhesi- 
tatingly declares in favor of the specific origin of the disease in spite of 
repeated negative IVassermann reactions. The prognosis of the acquired 
or Hayem infections type—usually specific—is favorable. The prognosis 
of the congenital, hereditary and familial type, is not unfavorable for 
life; these subjects may live to old age without subjective complaints 
though they are without resistance to disease or traumatism and they 
never lose their jaundice. 
(c) Hereditary Splenomegalic Jaundice 
Jaundice in the newly horn may be either (1) physiologic, (2) in- 
fectious, (3) of the grave familial type, (4) obstructive due to organic 
lesions in the ducts or liver. 
1. Physiologic Icterus.—Physiologic icterus, or the usual icterus 
neonatorum, also known as yellow gum, is found in the majority of babes 
soon after birth; it is hemo-hepatogenous and offers an excellent prog- 
nosis, for in a few (2 to 3) days without annoying complications the skin 
clears and all evidences of icterus disappear. From 40 to 85 per cent of 
all infants become jaundiced during the first, four days of life. 
At the Sloane Maternity Hospital in Hew York City, 300 of 900 
births showed jaundice; 88 were intense, and 212 mild (Holt). Stevens 
made a collective investigation of 2,086 children of which 1,212 were 
icteroid—58.1 per cent. Jorak in 248 newly born babies found icterus 
neonatorum in 80 per cent. The important point to decide in offering 
the prognosis of icterus of the new born babe is whether the process is 
id) Icterus neonatorum DISEASES OF THE LIVER 
671 
physiologic or infectious, and in occasional cases two or more days may 
elapse before differentiation is possible. 
2. Infectious Icterus neonatorum.—Infectious icterus neona- 
torum is rarely of the catarrhal variety or what Rolleston has character- 
ized as “mild infectious jaundice.” Skormin found but three recorded 
sases. Thompson says that new born infants may be very ill with catar- 
rhal jaundice and yet they recover as a rule. 
The severe infectious jaundice of the new born is usually of umbilical 
origin—suppurative umbilical phlebitis. The complication is prevent- 
able, is often conveyed from the mother—when it is likely to be strepto- 
coccic and has a very high mortality. 
Unfavorable features are high fever, rapid pulse, evidences of suppu- 
ration, gastro-intestinal symptoms, cyanosis, great unrest, and infection 
of several organs. There are at long intervals epidemic forms of infec- 
tious jaundice among the new born in which there are marked hemor- 
rhagic symptoms. In these epidemics almost all die. Winckel reports 
24 cases with 23 deaths. In most severe and malignant jaundice of the 
new born the infection is associated with the symptoms of septicemia 
and purpura, multiple embolic infarct, and acute fatty degeneration of 
the liver and other organs (Buhl's disease, also Winckel’s disease). 
3. Grave Familial Type of Icterus neonatorum.—Grave fa- 
milial type of icterus neonatorum, attacks successive infants of the same 
mother—all of these die. I had four consecutive cases, children of 
one mother all of whom died within four days of birth. The first child 
born to this mother was perfectly well, never jaundiced and grew to man- 
hood. There was no history of similar disease in the ancestors of these 
parents nor among the brothers or sisters. 
Arkwright reports a series of 14 cases in one family—the mother of 
these infants had jaundice when four years of age. 
Glaister reports that all of Morgagni’s children, 15 consecutive 
births, had icterus neonatorum. 
4. Obstructive Icterus neonatorum Due to Organic Lesions 
in the Ducts or Liver.—Congenital obliteration of the bile ducts has 
been fully described by John Thomson who reported 50 cases; and How- 
ard and Wolbach gathered the reports of 76 post mortems. Rolleston 
offers two explanations: (I) “that there is in the first place a develop- 
mental aplasia or a narrowdng of the duct which gives rise by obstruction 
to cirrhosis; (II) that there is first a mixed cirrhosis of the liver which 
gives rise to a descending obliterative cholangitis.” 
In practically all cases examined microscopically by Thomson and 
Rolleston, cirrhosis ivcis present. Rolleston says: “To sum up it is reason- 
able to believe that the disease is primarily started by poisons derived 
from the mother and conveyed to the liver of the fetus, and that a mixed 
cirrhosis and cholangitis are thus set up. The cholangitis accounts for DISEASES OF THE DIGESTIVE APPARATUS 
672 
the jaundice and by descending to the larger extrahepatic bile-ducts, 
induces an obliterative cholangitis analogous to obliterating appendi- 
citis.” In the unfavorable cases the occlusion of the ducts is absent, as 
death takes place early in life from congenital cirrhosis—if such cases 
live occlusion finally results. 
Death may result during the first week of life from either umbilical 
or other hemorrhage. Of Thomson’s 49 cases, 30 lived beyond the first 
month and of these 16 lived more than four months; 2 lived “into the 
eighth month.” Laveson collected 62 cases; of these hut three lived 8 
months, and of these 1 lived 11 months. 
Infection and hemorrhage claim most infants. Only the gloomiest 
prognosis is justified. There are, as Treves and Ashley have demon- 
strated, cases with only limited changes which remain latent for years, 
finally there is gradual cicatricial inflammatory occlusion. 
Hereditary syphilis of the liver and hile passages is a cause of icterus 
neonatorum. Many of these children die; a large proportion recover if 
radical treatment is promptly instituted. It rarely happens that gall- 
stones cause jaundice in the new horn (See Gall-stones). 
References 
Arkwright. Edinburgh Med. J., 1902, New Ser., xii, p. 156. 
Benjamin & Sulka. Berl. klin. Wchnschr., 1907, xliv, p. 1065. 
Chauffard. Jubile du Prof.Lepine. Rev. de Med., Paris, 1911, xxxi, p. 177. 
Eppinger. Ergebn. d. inner. Med. u. Kinderh., 1908, i, 107. 
Glaister. Lancet, London, March, 1879. 
Guillian. Paris Medicate, 1912, No. 27, p. 9. 
Guillian & Richet. Bull, et Mem. Soc. Med. des Hop. de Paris, 1910, 3d Ser., xxviii, p. 289. 
Hayem. Bull, et Mem. Soc. Med. des Hop. de Paris, 1908, 3. Ser., xxv, p. 122. 
Holt. Quoted by Rolleston [Z. c.]. 
Howard & Wolbach. Arch. Int. Med., Chicago, 1911, viii. 
Kahn. Kong. f. inner. Med., Wiesbaden, 1913. 
Leveson. J. Med. Research, Boston, 1908, xviii, p. 61. 
McPhedren, Fletcher & Orr. Canad. Med. Ass. J., vol. Hi, No. 1, p. 14-20, 1913. 
Meyer-Betz. Die Lehre d. Urobilin. 1913, Bd. xii. Ergeb. inn. Med. u. Kinderheilk., 
p. 733. 
Minkowski. Verhand. d. Congress, f. inner. Med., Wiesbaden, 1900, xviii. 
Minkowski & Naunyn. Archivf. exp. Path. u. Pharmakol., 1886, xxi, 1. 
Molleschott. Archivf. physical. Heilkunde, 1852, xi, p. 479. 
Ogata. Ziegler's Beitrag. z. pathol. Anat. u. allgem. Path. Bd. Iv, p. 315-321; also Bd. Iv, p. 
236-314. 
Pearce, Austin & Musser. The relations of the spleen to blood destruction and regeneration 
and to hemolytic jaundice. J .Exp. Med., 1912,16, p. 758. 
Porak. Rev. Mens, de Med. et Chirurg., Paris, 1878, ii, 342. 
Reichel. Deutsche Ztschr. f. Chir., Leipzig, 1907, Ixxviii. DISEASES OF THE LIVER 
673 
Rolleston. Proceed. Royal Soc. Med., London, 1910, Hi {Clinical Section). 
Diseases of the liver, gall-bladder, etc. London, 1912. 
Roth. Korrespond. Blatt f. Schweizer Aertze, 1913, Jg. 43, No. 22. 
Skormin. Jahrbuch f. Kinderheilkunde, 1902, Ivi, p. 200. 
Stadelman. Icterus. Stuttgart, 1891. 
Stern. Arch. f. Exp. Path. u. Pharmak., 1885, xix, p. 39. 
Stevens {J. L.). Glasgow Med. J., 1897, xlvii, 4- 
Thompson. Allbutt & Rolleston’s System of Medicine. 1908, vol. iv, part i, 98; also 
Congen. obliter. of the bile ducts. 1892, p. 38. 
Treves & Ashby. Med. Chron., Manchester, 1898-9, x, 28. 
Warthin. Philadelphia Med. J., 1900, vi, p. 38. 
Wenckel. Deutsche med. Wchnschr., 1879, v, 303. 
Whipple & Hooper. J .Exp. Med., 1913, vol. xvii, No. 6, p. 612-635. 
2. Acute Yellow Atrophy of the Liver 
Malignant Jaundice 
General Statements.—Acute yellow atrophy of the liver is an infec- 
tious disease of adult life, occurring oftener in women than in men; the 
relative frequency with which it attacks pregnant women is surprising. 
It is characterized by atrophy and degeneration of the liver cells, prob- 
ably autolytic (Flexner) and is usually fatal. 
Legg found that Baillon (Ballonius) reported a case in 1616; Bright 
in 1836 described and illustrated the disease, and in 184-2 Rokitansky 
gave it its present name. 
Acute atrophy of the liver is a very rare disease; in an active hos- 
pital experience I have during the past thirty years seen hut 2 cases, and 
in private practice during an equal time I do not recall more than 3 cases. 
Among my last 6,300 internal diseases tabulated in private practice I 
failed to find a single case of malignant jaundice. In 21,682 medical 
cases at the Johns Hopkins Hospital, Thayer reports but 3 cases. 
Rolleston has seen 11 cases post mortem in twenty-seven years. 
Symptoms.—With the rapid destruction—degeneration of liver cells 
—-the evidences of overpowering toxemia are prominent early, and the 
symptoms referable to the nervous system—delirium and coma, in young 
subjects convulsions—with jaundice, are suggestive with the physical 
signs of decreasing liver dullness of the gravity and nature of the 
process. There are cases in children, though these are exceedingly rare. 
The usual age is between twenty and forty years—my last case was six- 
teen years of age. 
The symptoms which brand the disease and which make prognosis 
possible before the end of the first twenty-four hours in the majority of 
cases, are early obstinate vomiting, greenish skin and conjunctiva, hemor- 
rhagic symptoms—hematemesis, melena, petechiae—followed by the 674 
DISEASES OE THE DIGESTIVE APPARATUS 
prompt invasion of the sensorium and rapid wasting, weak heart, and 
urinary changes, including leucin, tyrosin and albuminuria with scanty 
urine, tinged bile, and in some, almost complete suppression. Some 
enlargement of the spleen is the rule; the heart and kidneys show the 
degenerative changes of malignant infection. 
Origin.—The atrophic and degenerative congenital liver changes are 
probably without exception of luetic origin. The acute syphilitic liver 
changes are considered elsewhere (See Syphilis of the Liver, Section I). 
Weber in 1909 found 53 cases of acute yellow atrophy of syphilitic origin 
in medical literature, and Fischer reports 50 collected cases of which 
four-fifths were females. These cases are not true cases of acute yellow 
atrophy, they may run a long course and occasionally recover and should 
he classified as icterus gravis. Unquestionably preceding infection and 
worry or mental emotion, as well as alcoholic excess, invite acute liver 
atrophy. 
Ballin and Torek both report fatal cases of the disease after surgical 
operation and anesthesia. Torek reports its occurrence after the use of 
anesthol, a combination of chloroform, ethyl chlorid and ether. 
Fatal acute atrophy of the liver may develop after chloroform anes- 
thesia ; evidences of degeneration are not immediate. These cases are 
exceedingly puzzling. One such with complete yellow atrophy Fischer 
of Frankfurt demonstrated in 1914 which followed an operation for 
appendicitis in a boy. Brackel’s experiences are also worthy of study in 
this connection (See References). 
Atrophy, acute and fatal, may develop in occasional cases of cirrhosis 
of the liver, catarrhal jaundice, hyperemia and gall-stones. The inci- 
dence is exceedingly rare. 
Acute phosphorous poisoning is not identical with acute yellow atrophy 
though the subjective features are strikingly similar. Pathologically the 
differences are positive. With phosphorous poisoning the fat in the liver 
reaches 30 per cent and more, the size of the liver is increased; with 
acute atrophy there is but five per cent of fat in the organ and atrophy 
is its fate (Rolleston). The blood shows abnormal concentration with a 
high red count and moderate leukocytosis. Grawitz reports 5,150,000 
red blood corpuscles and 16,000 leukocytes, while at the Massachusetts 
General Hospital the count averaged 5,520,000 reds and 12,000 whites 
with 60 per cent hemoglobin. Blood cultures have thus far failed to 
enlighten the clinician. Libman and White report negative culture, and 
Vincent found the colon bacillus in his case. 
There is marked acidosis and fixation of ammonia by the organic 
acids, the liver being unable to transform the ammonia into urea. Urea 
is reduced and the percentage of ammonia is increased in the urine. 
The total nitrogen loss is increased because of the autolysis of the 
liver cells, and the ammonia accounts for at least twenty per cent of the DISEASES OF THE LIVER 
675 
total nitrogen, whereas normally it accounts for only five per cent. I 
have not seen the cases of prolonged and subacute liver atrophy described 
by some writers (MacDonald and Milne). These are likely to be due to 
cirrhosis with enormous destruction of liver cells or to subacute hepatitis, 
and ought not to be considered acute yellow atrophy. 
Forecast.—Cases with positive symptoms lifting the diagnosis above 
doubt offer an unfavorable forecast. My experience does not include a 
single recovery. I agree with Rolleston who says: “Some doubt would 
always arise as to the nature of cases that recover completely.” The 
regenerative power of the liver which is certainly paramount when there 
is a remnant of liver cells to proliferate, may in rare instances make 
recovery possible. In these cases there is a compensatory hyperplasia 
which may save life, but recurrence and advancing degeneration may 
ultimately lead to death. 
The prognosis, bad at all ages,, is slightly better in children than in 
adults. Pregnant women offer only the gloomiest prognosis. Once the 
kidney function is seriously disturbed—and this is a part of the toxic 
and degenerative process—in most cases the outlook becomes correspond- 
ingly bad. Legg’s list includes 28 cases, 4 reported recoveries; and 
Wirsing collected 15 non-syphilitic cases of recovery. 
Duration.—The duration of the average case of yellow atrophy is 
less than four days. Some live into the second week; only a few become 
subacute. The chronic course casts doubt on the diagnosis as already 
suggested. 
Ballin. Annals of Surgery, 1903, xxxvii. 
Bracket. Samml. klin. Vortrdge, 674, P• 539-564- 
Bright. Guy's Hosp. Reports, 1836, i, p. 613. 
Cabot. Guide to clin. exam, of the blood. New York, 1897. 
Fischer. Berl. klin. Wchnschr., 1908, xlv. 
Flexner. Am. J. Med. Sci., 1903, cxxvi, p. 202. 
Grawitz. Klin. Pathol, d. Blutes. Leipzig, 1906. 
Legg. Bile, jaundice, and bilious disease. London, 1880. 
Libman. Johns Hopkins Bulletin, 1908, xvii, p. 222. 
MacDonald & Milne. J. Path. & Bact., Cambridge, 1907, ix, 577: idem, 1909, xiii, p. 161. 
Rokitansky. Lehrbuch d. path. Anat. Wien, 1861. 
Rolleston. Diseases of the liver, etc. London, 1912. 
Thayer (W. S.). Johns Hopkins Hosp. Bulletin, 1908, xix. 
Torek. Annals of Surgery, 1910, lii, 489. 
Vincent. Semaine Med., Paris, 1893, xiii, 228. 
Weber. Proc. Royal Soc. Med., Path. Section, London, 1909, ii. 
White. Boston Med. & Surg. J., 1908, clviii, p. 729. 
Wirsing. Inaug. Dissert., Wurzburg; also quoted by Albu, Deutsche med, Wchnschr., 1901, 
xxvii, p. 216. 
References 676 
DISEASES OF THE DIGESTIVE APPARATUS 
3. Circulatory Disturbances of the Liver 
(a) Congestion of the Liver 
(.Hyperemia) 
In all forms of congestion of the liver the prognosis must be based 
on its cause. 
i. Active Hyperemia 
Active hyperemia is purely physiological during the process of diges- 
tion, and is pathological in such conditions as cause increased supply of 
blood to the liver, either as the result of vascular paralysis or true ple- 
thora, i. e., polycythemia. The prognosis of this condition as it occurs 
with the various infections (diphtheria, malaria, typhoid and typhus 
fever, etc.) has been separately considered. 
There are in all probability a limited number of active hyperemias 
arising from faulty diet and improper living in which judicious and 
temperate habits with proper exercise lead to prompt recovery without 
remnant of organic change. 
ii. Passive Hyperemia 
Passive hyperemia is always a secondary process; it is rarely recog- 
nized during its incipiency, but in the advanced stage presents charac- 
teristic changes which prove the obstruction in the portal system. The 
leading primary lesions are cardiac and pulmonary. There are other 
factors which may lead to chronic congestion of the liver, including 
aneurismal pressure, growths, which cause pressure on the inferior vena 
cava, occlusion of the hepatic veins, obstruction of the portal vein, or 
thrombosis. Rolleston includes malignant growths or hyatid cysts, 
pleural and pericardial effusion, pericardial and mediastinal adhesions.' 
The prognosis of hyperemia in these conditions naturally depends on 
the ability to remove the cause. 
The cardiac lesions which cause secondary hyperemia of the liver are 
usually valvular, in which compensation is faulty. 
Mitral obstruction and regurgitation and diseased myocardium are 
the leading lesions which cause backward pressure, with consecutive 
tricuspid insufficiency and chronic liver engorgement. Tricuspid stenosis 
may cause marked secondary hyperemia; it almost always follows mitral 
obstruction. With mitral stenosis there is, after a varying period, per- 
sistent venous engorgement, with characteristic enlargement of the liver 
which persists and leads to consecutive organic changes. Mitral stenosis 
is probably the most powerful cause of the “cardiac liver.” 
The acute infections may also cause liver congestion depending upon DISEASES OF THE LIVER 
677 
myocardial degeneration and sudden dilatation. The pulmonary lesions 
which cause chronic hyperemia of the liver are chronic emphysema and 
asthma, chronic bronchitis, interstitial pneumonia, the pneumonokoni- 
oses, and occasionally pulmonary tuberculosis. The damage to the liver 
depends entirely upon the degree and duration of the venous stasis. 
Early, the liver is enlarged and the capsule tense; as the condition re- 
mains and becomes chronic there is more or less productive change, final 
atrophy and shrinking, with the usual symptoms of portal obstruction. 
With heart lesions, the hyperemia may always be considered to he per- 
manent, and if the patient lives, the secondary changes in liver tissue are 
sure to follow. The prognosis of cardiac and pulmonary conditions is 
unquestionably unfavorably influenced by the secondary changes in the 
liver, hut it depends more upon the ability of the heart to compensate 
for the primary anomaly than upon any other factor. 
Secondary hyperemia with persistent gastro-intestinal symptoms, 
which are proof of engorgement of the entire portal system, offers an 
unfavorable prognosis for life; with cardiac dyspnea and associated 
dropsies there is usually congested kidney and evidences of overpowering 
toxemia and weakness. Ascites is an unfavorable symptom, though in 
some cases, under treatment, the tone of the heart may be sufficiently 
improved to prolong the lives of these patients. 
With mitral obstruction and insufficiency it is not at all uncommon 
to follow patients during many years who live in comparative comfort 
with chronic painless enlargement of the liver. 
Persisting jaundice with passive congestion of the liver is always 
unfavorable, and is found in the most severe cases. The deeper the 
coloring the more threatening is the complication. Jaundice with cya- 
nosis is always unfavorable. 
The urine gives valuable data for prognosis in all primary heart, lung, 
and other conditions associated with congested liver. 
Concentrated, scanty, albuminous, bile-laden urine with casts or with- 
out, urobilinuria, acidosis, leucin and tyrosin, is always ominous and 
justifies the conclusion that death is imminent in most cases. W ith the 
gradual increase of hyperemia and consecutive organic changes in the 
fiver substance, a degree of tolerance may be established with regenerative 
and compensatory changes sufficient to prolong life during indefinite 
periods until the right heart finally yields. 
When the organic changes are sufficiently advanced in the liver as to 
cause marked cirrhosis and atrophy, conditions exist which, according 
to Hunter, amay be said to have an independent existence, and such 
advanced changes make the prognosis exceedingly grave. It is often 
surprising how many years patients with chronic heart and lung lesions 
(emphysema, asthma, chronic bronchitis) live without change in the size 
of the enlarged and engorged liver. With enlarged and pulsating liver 678 
DISEASES OF TIIE DIGESTIVE APPARATUS 
associated with tricuspid insufficiency, improvement of secondary symp- 
toms is not to he expected. The pulsation remains to the end (Mackenzie). 
Infection (pneumonia, pleurisy, malignant endocarditis) is a frequent 
cause of death. In a number of my cases the infection has followed 
along the bile passages from the intestine; icterus gravis has resulted, and 
death has promptly followed. 
The association of purpuric or hemorrhagic symptoms with or with- 
out jaundice, delirium, coma, convulsions, the typhoid state with increas- 
ing myocardial weakness, are among the most unfavorable features. 
References 
Aschoff. Path. Anat., Jena, 1913. 
Hanot. Bull. Soc. med. d. Hop. de Paris, 1895, p. 409. 
Hunter (Wm.). Congestion of the liver. In: Allbutt & Rolleston’s System of medicine 
London, 1908, vol. iv. 
Mackenzie. Diseases of the heart. London, J.908. 
Rolleston. Diseases of the liver, gall-bladder and bile ducts. London, 1912. 
(6) Diseases of the Portal Vein 
Pylephlebitis 
(Pylethrombosis, Adhesive Pylephlebitis; 
when suppurative: 
Suppurative Pylephlebitis, Portal Pyemia, Multiple Abscesses of the 
Liver) 
Pylephlebitis is an inflammation of tlie wall of the portal vein or 
one or more of its branches with thrombosis or final suppuration. The 
majority of all cases are associated with primary systemic infection in 
which the blood shows characteristic changes. 
Thrombosis of the portal vein may follow long continued inflamma- 
tion of the vein, change in its coats, calcification, phlebitis, or syphilitic 
deposit. Thrombosis may be due to extension of inflammation, i. e., 
infection from neighboring or distant organs. Thus with ulcer of the 
stomach or intestine, cancer of the stomach or pancreas, cholecystitis— 
with or without gall-stone—cholangitis, liver abscess, pancreatic inflam- 
mation, appendicitis, pelvic abscess, puerperal or pneumococcus infection, 
diphtheria, distant or near thrombosis, there may be extension to the 
portal vein. Following surgical operation for infectious processes, portal 
thrombosis is a relatively frequent complication. If the causes of all 
portal thromboses were cautiously tabulated, the seat of the primary 
disease in the individual case would be found in one of many organs, 
and with innumerable infections. There is scarcely an organ from which DISEASES OF THE LIVER 
679 
portal infection may not spread. Portal thrombosis is frequent with 
splenic infarct and other lesions of the spleen, including abscess, trauma, 
infection and perisplenitis. With many grave forms, the spleen is mark- 
edly enlarged. 
The thrombosis of marasmus is of infectious origin, and always sec- 
ondary. Herringliam says: “To sum up, it may therefore be stated that 
the great majority of the cases depend upon local conditions; that, 
whether of local or general origin, infection is the most probable cause 
in all but those in which the vein is invaded by new growth, or by mul- 
tiple adenoma, and is not excluded even in these; and that in a few cases 
no explanation can be given.” 
The underlying infection is usually so malignant or serious as to 
threaten life; the added thrombosis increases the dangers, making recov- 
ery exceedingly rare. With thrombosis and liver cirrhosis the course is 
often subacute, the duration varying from several weeks to as many 
months. The same course is found with malignant disease of the liver. 
Cases in which there are peritoneal adhesions may persist during a num- 
ber of months. A number of recoveries have been reported. In some 
of these reported by Lyons, Osier and Rogers, it is difficult to controvert 
the diagnosis, but a strong element of doubt is justified and I am fully 
in accord with Herringham when he insists that “where diagnosis is so 
certain, no case of recovery can be admitted which is not proved by sub- 
sequent dissection.” The prognosis, however, is better than in pylephle- 
bitis. Compensation of the circulation is possible in cases in which portal 
thrombosis is limited and progresses gradually. 
Suppurative Pylephlebitis—Portal Pyemia—Multiple Abscess of the Liver 
This condition, always infectious, is fully considered in this section 
with Abscess of the Liver, to which the reader is referred. 
(c) Diseases of the Hepatic Vein 
Complete occlusion of the hepatic vein is exceedingly rare; its only 
interest is pathologic, for it cannot be diagnosticated intra vitam. The 
symptoms of hepatic occlusion, thrombosis, or phlebitis, are rather indefi- 
nite but usually include pain, abdominal and epigastric, gastro-intestinal 
symptoms, vomiting; in the subacute cases, ascites with enlargement of 
the liver, which continues more or less tender; jaundice is ndt usual. 
All are supposed to die. 
Thrombosis of the hepatic vein may be due to new growths of the 
liver, cirrhosis, stricture, or it may be a part of a widespread thrombosis, 
including portal thrombosis. Growths by pressure (carcinoma, hydatids, 
gummata) causing stasis lead to thrombosis. Rolleston includes oblitera- 680 
DISEASES OF THE DIGESTIVE APPARATUS 
tive endophlebitis of the hepatic veins as a cause. Embolism of the 
hepatic vein is rare. Welch reported fragments of new growth in the 
hepatic vein in cases of primary carcinoma of the thyroid and abdom- 
inal organs. 
(d) Diseases of the Hepatic Artery 
The anomalies of the hepatic artery include: 
Aneurism 
Embolism 
Thrornbosis 
Arteriosclerosis 
and according to Rolleston: Enlargement of the vessel. 
Aneurism.—Rolland reported (1907) 41 cases in medical literature 
of aneurism. The average age of Holland’s cases was 37 years, and the 
extremes were 83 and 14 years. The proportion of males to females was 
3 to 1, and the average age in women was 10 years higher than in men— 
45 to 35 years. 
Ulceration in the gall-bladder or bile ducts may erode the wall of the 
artery and cause aneurism; the rupture is usual into the biliary tract in 
such cases. Gall-stones are potent factors in causing these ulcerations. 
ISTaunyn and Schmidt have reported cases in which impacted gall-stones 
have finally opened into aneurism of the hepatic artery. Jaundice is 
usually a late symptom, and is due to pressure on the ducts. Ascites is 
not a symptom of hepatic aneurism. 
Aneurismal dilatation of the artery is always fatal; death is usually 
due to perforation. Perforation may take place into the peritoneum, 
the bile passages, the gall-bladder, the portal vein, or into the stomach, 
or (rarely) into the intestine or pancreas. Infection of the bile passages 
and pancreas is an occasional complication. Ross and Osier reported a 
case of infected aneurismal sac, multiple emboli, and many secondary 
liver abscesses. Fully formed hepatic aneurism is incurable; not all die 
from it directly, but most do. Rupture and perforation into the sur- 
rounding organs are the leading causes of death. Hans Kehr has suc- 
cessfully removed an aneurism after ligating the hepatic artery. 
Embolism.—Embolic infarcts may cause multiple abscesses. They 
are always fatal, are secondary to malignant endocarditis, carcinoma, 
sarcoma—the melanotic type particularly—and are occasionally present 
with tuberculosis. 
Thrombosis.—Thrombosis of the hepatic artery is considered a 
“pathological curiosity” (Rolleston). I have never met a case. Lance- 
reaux found a clot in an arteriosclerotic hepatic artery in a patient, aged 
65, who had general atheroma and died of gangrene of the feet. 
Arteriosclerosis.—Arteriosclerosis of the hepatic artery is a part DISEASES OF THE LIVEK 
681 
of a widely disseminated process. Secondary atrophy of the liver results 
in some cases—fibrosis of the liver is not usual with hepatic arterio- 
sclerosis. 
Endarteritis obliterans may accompany cirrhosis of the liver; Kol- 
leston holds that endarteritis deformans is more frequent. 
Enlargement of the Hepatic Artery (Eolleston).—With carci- 
noma and other new growths the hepatic artery is at times enlarged; the 
same is occasionally true of advanced cirrhosis and chronic portal 
thrombosis. 
In all vascular lesions of the liver, both the underlying causes and 
the vessel changes are so grave and far-reaching as to make the forecast 
bad. The length of life in the individual case depends upon the nature 
of the primary lesion and the local changes caused by the altered vessels 
and disturbed circulation. 
References 
Herringham. Allbutt & Rolleston’s System of medicine. Vol. iv, part i. 
Kehr (Hans). Munch, med. Wchnschr., 1903, xl, p. 1861. 
Lancereaux. Traite des mal. dufoie et du pancreas. 1899, p. 541. 
Lyons. Dublin J. Med. Sci., 1877, Ixiv, 457. 
Naunyn. Cholelithiasis. Leipzig, 1892. 
Osier. J. Anat. & Physiol., 1882, xvi, p. 268. 
Rogers. Brit. Med. Chir. J., 1899, xvii, 107. 
Holland. Glasgow Med. J., 1908, Ixix, p. 342. 
Ross & Osier. Canada Med. & Surg. J., 1877, vi. 
Schmidt. Deutsch. Archiv f. klin. Med., 1893-4, lii, p. 536. 
Welch (W. H.). Allbutt’s System of medicine. Vol. vi, 1st ed., 1899. 
4. Cirrhosis of the Liver 
(a) Multilobular Cirrhosis 
(■Chronic Interstitial Hepatitis, Laennecs Cirrhosis) 
(b) Unilobular Cirrhosis 
{Hanot’s Cirrhosis) 
(c) Pericellular or Syphilitic Cirrhosis 
(d) Capsular Cirrhosis 
(.Perihepatitis) 
All forms of liver cirrhosis are characterized by connective tissue 
proliferation and changes in the liver substance. In all there is, in spite 
of destructive changes, marked tendency to regeneration of the liver 
cells. Another favorable factor is the fact that the connective tissue, 
contrary to the rule, holds capillary vessels which permit of the passage 682 
DISEASES OF THE DIGESTIVE APPARATUS 
of blood to the intralobular veins by way of the hepatic artery, which 
(in alcoholic cirrhosis particularly) continues liver function, including 
bile formation. 
(a) Multilobular Cirrhosis 
(Laennecs Atrophic Cirrhosis, Portal Cirrhosis, Chronic Interstitial 
Hepatitis, Contracted Liver, Hobnailed Liver, Drunkard’s 
Liver, Alcoholic Cirrhosis) 
Factors Which Influence Prognosis.—Alcohol is unquestionably the 
most frequent poison which causes cirrhosis of the liver taken in the 
form of whiskey, gin, and brandy. Beer may cause mixed forms of 
cirrhosis, but it is less likely to produce the multilobular type of cirrhosis 
than are the stronger spirits. It is rare to find Laennec’s cirrhosis with- 
out the history of alcohol abuse; it is possible however—a fact of diag- 
nostic as well as prognostic value. 
The study of my material justifies the conclusion that the majority of 
atrophic cirrhoses were found with an alcoholic history. Whether the 
changes in the liver are primary or secondary, we cannot ignore the 
positive history of the habit and I cannot agree that there is danger of 
exaggerating the “importance of alcoholism” as a pathogenic factor. 
There are other factors besides alcohol which cause cirrhosis, and there 
are many ingested poisons, besides alcohol, as well as congenital and 
acquired factors which lower liver resistance and predispose the organ to 
degenerative and productive changes. 
The spleen is under suspicion as a poison-producing organ of trans- 
cendent importance in causing productive changes in the liver. The 
telling results which follow splenectomy in Banti’s disease in which there 
is co-existing cirrhosis of the liver, and the early enlargement of the 
spleen in some forms of hypertrophic biliary cirrhosis justify the strong 
suspicion and the hope that ultimately we may find that through the 
spleen the liver changes are invited or provoked, and that early splenec- 
tomy in cirrhosis may abort these. This entire question is still sub 
judice—no authoritative statement is justified. There are some facts 
connected with the spleen which are of importance and are positive. 
The spleen is enlarged in 80 per cent of all cases of portal cirrhosis of 
the liver (Klopstock). The spleen is small in the more rapidly pro- 
gressive cases, with profuse hematemesis, also with those in which ascites 
develops early. To some of these facts I again refer in considering 
individual symptoms. 
Faulty Diet.—There are unquestioned cirrhoses in which faulty diet 
and consequent dyspeptic conditions, long continued, are causative fac- 
tors. Ingested poisons by irritation, as well as those due to fermentation 
in the intestinal tract, may lead to “dyspeptic cirrhosis.” The early DISEASES OF THE LIVER 
683 
detection of such cases is by no means easy; the changes are insidious 
and are advanced before marked subjective or objective manifestations 
cause the patient to seek medical advice. Most of these cases run an 
exceedingly chronic course and are favorably influenced by rational treat- 
ment and proper living. 
Etiology.—The question of etiology of cirrhosis as it influences 
'prognosis is still uncertain, but it is positive that there are many poisons 
which may cause liver changes parallel with cirrhosis. The lesions may 
be limited or widespread. There is a growing belief that cirrhosis of the 
liver in man is always of toxic origin. Rolleston’s conclusions in this 
connection are as follows: “Poisons may be absorbed either from the 
alimentary canal and reach the liver in a comparatively concentrated 
form, or they may travel to the liver by the hepatic artery and are then 
comparatively diluted. Ordinary cirrhosis in man is generally due to 
poisons traveling by the portal vein. Alcoholism is rather an antecedent 
condition than a true cause, and acts indirectly or in an accessory man- 
ner. The possibility that cirrhosis is definitely due to microorganisms 
must be faced; from analogy it is most probable, but at present it has 
not been certainly established. It is also highly probable that poisons, 
or perhaps microorganisms, reaching the liver by the hepatic artery, may 
give rise to cirrhotic changes.” “As a result of destruction of the hepatic 
cells and absorption of their proteins into the circulation, hepatic anti- 
bodies, or cytolvsins, are produced. These destroy the liver cells and 
thus a vicious circle is produced” (Fiesinger). 
The disease may be found during childhood, this is rare; it is most 
frequent during and after middle life, in the male oftener than the female. 
Mortality.—Hawkins’ statistics show that “the annual death rate from 
cirrhosis of the liver in England and Wales rose considerably from 1871- 
1900, reaching 134.6 in the last year, but in the quinquenium, 1901-5, 
a fall of 121.2 occurred. In 1905 there were 4,008 deaths registered in 
England and Wales as due to this disease.” 
The mortality from cirrhosis of the liver in the rural districts of 
Hew York State, as shown by Hoffman’s statistics, is lower than in the 
cities of the State. “The rates have not been subject to a wide range, 
for the minimum rate per 100,000 of population in the cities of Hew 
York State was only 19.3 in 1909, while the maximum rate was 22.2 in 
1907. The minimum rate for the rural territory was 10.1 in 1900 and 
the maximum rate was 15.1 in 1907. In 1909 the rural mortality from 
cirrhosis of the liver was 69.9 per cent of the urban.” 
Of 91 male white cases of cirrhosis of the liver admitted to the Johns 
Hopkins Hospital at Baltimore, 16 died in the hospital—17.6 per cent. 
During the same period (1902-1911) 16 white females were admitted 
with one death in the hospital—6.3 per cent. During the same period 
15 colored males with cirrhosis were admitted with 2 deaths while in the 684 
DISEASES OF THE DIGESTIVE APPARATUS 
hospital—13.3 per cent, and 4 females with no deaths. The total num- 
ber of white medical cases was 7,299 males, from 1892 to 1901, and 
3,209 females, from 1902-1911, 8,213 males, and 4,186 females. Col- 
ored medical cases included 1,678 males from 1892-1901 and 442 
females; from 1902-1911 there were 2,109 colored males and 650 females 
(Hoffman). 
The average age of individuals who die with the lesions of cirrhosis 
but without symptoms during life is according to Hilton Fagge “five years 
higher than of persons dying of the disease.” This fact is a strong argu- 
ment in favor of the success of the “compensatory processes.” Rolleston 
on the other hand says: “In my own figures there is very little difference 
between these two classes.” 
Rolleston’s statistics gathered from 78 cases dying from cirrhosis 
show an average of 48.3 years; whereas in 87 patients who died from 
independent causes but whose livers were cirrhotic, the average age was 
49.1 years. 
In alcoholic women especially, death from cirrhosis is much earlier 
than in those cases in which there is no history of alcoholic excess. Natu- 
rally the prognosis of all portal cirrhosis depends upon the extent of the 
liver changes, including the destruction of the liver cells, the extent of 
connective tissue production, the changes in the capsule, the obliterative 
changes in the portal vein, and its branches, the secondary changes in 
the ducts, the amount of amyloid and fatty degeneration of the organ, the 
accompanying lesions in other organs—kidney, heart and blood vessels 
particularly—the habits of the patient and his resistance, besides the 
regenerative power and tolerance of the liver itself. 
Additional Prognostic Factors.—Latency.—It is often surprising to 
find how long after initial symptoms and positive physical signs the dis- 
ease may remain latent. The duration of these periods of latency depends 
upon compensation which results from the collateral circulation estab- 
lished between the branches of the portal veins and the systemic veins 
and the regeneration of the liver cells. I have followed cases which 
finally died of intercurrent disease or accident during many years, in 
which the cirrhosis was advanced as shown at post mortem, the patients 
having lived with but few or no symptom's of the liver lesions. Hanot 
and Gilbert believe that the compensatory changes during latency cause 
enlargement of the liver in the majority of cases. All agree that cirrhosis 
is oftener latent in men than in women. Rolleston does not believe that 
this is due to the greater frequency of the diseases in men than in women, 
“for the ratio of women to men is lower among the cases dying inde- 
pendently of cirrhosis than among the cases fatal from the direct effects 
of cirrhosis.” 
The latency of the disease is an important prognostic factor. If the 
diagnosis is made early, before the various processes are advanced and PISEASES OE THE LIVEK 
685 
the habits of the patient are controlled, without complication or toxemia, 
the chances for long periods of latency are exceedingly good; limited 
changes in the organ under such conditions may not materially interfere 
with the general health or length of life. 
Patients with advanced latent cirrhosis are subject to complications-— 
pneumococcus and tuberculous infections particularly—which often end 
their lives. Such subjects do not offer normal or average resistance to 
disease or trauma. Cirrhosis of the liver in the majority of cases, because 
of the tolerance of the organ and long periods of latency, often the care- 
lessness of the patient and faulty diagnosis, due to the prominence of 
gastric symptoms, is not diagnosticated, until the disease is far advanced 
and pernicious habits are thoroughly fastened. 
Lesions in Other Organs.—The lesions in other organs than the liver 
have an important bearing on prognosis. Cirrhosis of the liver is often 
associated with far-reaching changes in the digestive tract with organic 
lesions of the esophagus, stomach, intestines and pancreas, besides the 
spleen, already considered. Advanced pancreatitis is frequent; the fibrosis 
of the organ is often so advanced as to be out of proportion to the changes 
in the liver. 
Esophageal lesions include changes in the mucosa, epithelial thicken- 
ing, dilatation and varicose veins, and ulceration. The rupture of an 
esophageal varix or ulceration may cause profuse and threatening hem- 
orrhage. 
The stomach lesions include chronic gastritis (alcoholic) varicosities of 
the gastric veins at the cardia, continuous with the esophageal dilatation 
or separate. These may rupture or ulcerate and prove life-threatening. 
Single or multiple gastric ulcers are occasional complications. The 
multiple ulcers are usually superficial, the single gastric ulcer is not fre- 
quent. Intestinal lesions which are associated with cirrhosis include 
chronic enteritis with productive changes causing marked thickening of 
the mucosa and atrophic changes in the glandular structures. There is 
with these atrophic changes in the chronic cases diminution in the length 
of the intestinal tract. The venous system of the intestine is likely to be 
engorged and the rectal veins dilated with hemorrhoidal swellings. Rec- 
tal ulceration and bleeding‘ may prove depleting. 
Kidney lesions complicated the majority of our cases. In over 50 
per cent of. all cases the kidney is enlarged. Milian and Bassnet in 89 
fatal cases of cirrhosis found the kidneys normal in 19; in 53, or 59.5 
per cent, they were healthy or more or less hypertrophied. Pitt’s sta- 
tistics show that when otherwise healthy, the kidneys were hypertrophied 
in 50 per cent of liver cirrhosis. 
Arteriosclerotic interstitial nephritis is present in at least one-fourth 
of all cases and with the general invasion of the arterial tree, and toxemia 
is serious. Sears and Lord in this series of 78 fatal cases of cirrhosis 686 
DISEASES OF THE DIGESTIVE APPARATUS 
report chronic nephritis (interstitial or tubular) in 23—or 29.4 per cent, 
fatty change in 15, and lardaceous change in 2. Rolleston compiled 
440 cases of cirrhosis of the liver from the statistics of Pitt, Kellynack, 
Yeld, Cheadle and his own, in which he found 110 “with distinct fibrosis 
of the kidneys (25 per cent).” 
Non-tuberculous Chronic Peritonitis.—Sears and Lord in their series 
of 78 cases found chronic peritonitis in 19 per cent. In most cases this 
peritonitis is mild and insignificant; indeed by causing agglutination of 
peritoneal layers or folds it may often prove salutary. Severe or advanced 
and threatening chronic peritonitis is comparatively rare with liver cir- 
rhosis. The peritoneum, according to Rolleston, may with ascites be 
irritated by the “toxic bodies or bacteria in the ascitic fluid”; . . . “and 
it is conceivable that occasionally they are both related to alcoholism.” 
Ascites with chronic peritonitis may require repeated tapping, and re- 
covery may at times follow. The prognosis following tapping without 
chronic peritonitis is less favorable than with it and death is more prompt. 
The latter cases rarely live to be tapped more than two or three times. 
Chronic peritonitis has complicated a few of my cases. In some of 
these ascites was an early symptom, in others late. From 8 to 10 per 
cent of all liver cirrhosis show tuberculous peritonitis. Nineteen per 
cent of Sears’ and Lord’s cases of cirrhosis had chronic peritonitis. 
Kellynack’s material included 121 cases of cirrhosis, of which 12 had 
active peritoneal tuberculosis. Only one-third of these failed to show 
tuberculous disease elsewhere in the body. 
Pulmonary Tuberculosis.—Cirrhosis of the liver predisposes to tuber- 
culosis and the lungs are the usual seat of disease. Not all cases of 
pulmonary tuberculosis associated with cirrhosis are active. There may 
be but few or no symptoms; the process may be latent during long periods. 
In a small number of .cases there is an acute and rapidly fatal course 
with all of the lesions and symptoms of miliary tuberculosis. 
Tuberculous lesions are found in the lungs of over 22 per cent of 
patients dying of liver cirrhosis as proved by the statistics obtained from 
584 cases (Lancereaux, Kellynack, and Yeld). The addition of acute 
pulmonary peritoneal or intestinal tuberculosis is promptly fatal with 
fever, emaciation, and deep toxemia. Chronic tuhercxdosis with cirrhosis 
may cover a long history and if the latter is limited and the former not 
far advanced, under favorable conditions life may be materially pro- 
longed (See also separate symptoms, etc.). 
Arteriosclerosis, etc.—Syphilis, alcoholism and cirrhosis of the liver, 
coincident during middle life, naturally include arteriosclerosis. Prob- 
ably arteriosclerosis and liver cirrhosis bear but little relation to each 
other, and cirrhosis per se is not likely to produce arterial degeneration. 
Most cases of cirrhosis unless complicated with coincident nephritis 
and arteriosclerosis are without suggestive arterial hypertension. Mixed DISEASES OF THE LIVER 
687 
cases of alcoholic and syphilitic cirrhosis may include specific arteritis 
(<endarteritis). 
Arteriosclerosis is unquestionably present in the bodies of most cir- 
rhotics but it is by no means essential; in many it does not directly 
influence prognosis. When advanced, involving the heart and kidney or 
mesenteric vessels, or when there are evidences of cerebral or spinal 
arterial degeneration, the prognosis is correspondingly bad. 
The Heart.—The heart in the average cirrhotic during the early 
stages may remain uninfluenced. With increasing toxemia or neglect 
and advance of the process, renal invasion or other complications, such 
as tuberculosis or portal obstruction with ascites, the myocardium suffers 
and the prognosis is correspondingly bad. The frequent association of 
syphilis clouds the prognosis because of specific aortitis, coronary endar- 
teritis, and degenerative changes in the heart muscle in many. Malignant 
endocarditis, always fatal, may be grafted upon the previously diseased 
endocardium, for valvular lesions due to chronic cardiopathies are not 
infrequent. 
Calcified adherent pericardium is rarely found without cirrhosis of 
the liver. If extensive it may interfere very materially with the com- 
fort of the patient and cause secondary and severe complications (Diemar, 
Wells, Mitchell). 
Cancerous Infiltration.—The prognosis of cirrhosis promptly becomes 
bad when there is cancerous infiltration of the liver or other organs. The 
cases reported as primary cancer of the liver with cirrhosis• are (accord- 
ing to modern pathologists), cirrhosis primarily, with ultimate secondary 
proliferation—“hyperplasia of the liver cells.” These conditions have 
been variously described as “primary carcinoma with cirrhosis,” “malig- 
nant adenoma,” “cirrhosis maligna,” and “cirrhosis carcinomatosa” (See 
Sabourin, Hanot and Gilbert). Rolleston says that since the malig- 
nant change follows the cirrhosis, as carcinoma of the breast follows 
chronic mastitis, “or on the analogy of carcinoma supervening on gastric 
ulcer,” it would be better to speak of the condition as “cirrhosis car- 
cinomatosa.” 
Individual Symptoms.—I have purposely considered the complica- 
tions and secondary changes associated with Laennec’s cirrhosis before 
dilating on the prognostic significance of individual symptoms because 
it is a striking fact that the disease may exist during! long periods with- 
out causing the slightest, or but few, subjective complaints; patients often 
die of intercurrent disease in whom cirrhosis was never suspected, in 
whom advanced lesions are found post mortem, while the symptoms of 
secondary changes or complications are prominent. 
Cirrhosis of the liver, per se, barring secondary changes and compli- 
cations is a disease with but few well-defined symptoms. Patients usually 
continue comfortable and are without threatening symptoms so long as 688 
DISEASES OF THE DIGESTIVE APPAKATUS 
the compensatory circulation is upheld and the regenerative processes are 
maintained. In no other disease is the compensatory influence of col- 
lateral circulation with pathologic changes more important than in liver 
cirrhosis. With the compression of the branches of the portal vein and 
resulting portal stasis, symptoms appear. The gravity of the condition 
depends upon the extent of the obstruction and the associated toxemia and 
the lesions in distant organs. 
Weight.—Progressive loss of weight, with or without evident com- 
plication, is always unfavorable. The subjects of advanced cirrhosis are 
not likely to regain lost weight. As a rule some complication of grave 
import is added when with loss of weight, the general condition and 
resistance suffer. In the advanced cases, loss of weight is always indica- 
tive of progression toward the end. Tuberculosis and malignant disease 
or chronic toxemia may be responsible for the loss of weight. Obese 
patients with latent cirrhosis may develop acute tuberculosis which 
promptly becomes disseminated, in the presence of an eplarged liver. In 
some of these, cirrhosis may not be suspected. Loss of weight at any 
time in the course of cirrhosis is unfavorable and demands thorough 
investigation. 
Facies.—Just as with ovarian tumor there is often a characteristic 
facial change and a striking expression (ovarian facies), so I have 
noted in cirrhosis of the liver, often before the disease is far advanced, 
facies exceedingly suggestive but difficult to describe. The face is thin, 
the eyes somewhat sunken, the conjunctiva congested, superficial vessels 
prominent—particularly about the nose—the lips dry, often cracked, the 
teeth are abnormally dry and often with little sordes; the expression, as 
the disease advances, appears anxious. 
Venous obstruction.—When there are positive symptoms of obstruc- 
tion of the branches of the portal vein it may be concluded that the 
fibrous changes in the liver are advanced and the outcome will be largely 
dependent upon the factors of safety already mentioned in this chapter. 
The tolerance of the liver and its compensatory changes may often pro- 
long the lives of these patients during indefinite periods. I have seen 
life prolonged in comparative comfort after positive physical signs and 
subjective symptoms of liver cirrhosis—over twenty years in one case—- 
in which the post mortem verified the original diagnosis; the patient died 
of stomach cancer. 
Gastro-intestinal Symptoms.—The gastro-intestinal symptoms may be 
due either to primary gastritis or enteritis, or to circulatory obstruction. 
Persistence of passive gastro-intestinal hyperemia is usually associated 
with marked disturbance of hepatic function; stomach intolerance and 
frequent vomiting are weakening. Such cases are rarely free from tox- 
emia and other circulatory symptoms which, unless promptly relieved, 
are likely to prove fatal. In the majority of cases the secondary gastro- DISEASES OF THE LIVEK 
689 
intestinal hyperemia is well borne during long periods and is as a rule 
only a part of a symptom complex which includes changes in other organs 
of serious import. Persistent diarrhea in advanced cases is suggestive of 
ulcerative or tuberculous disease. In incipient cases diarrhea may he 
due to associated catarrhal enteritis and is amenable to treatment. Diar- 
rhea alternating with constipation is always suggestive of tuberculous 
peritonitis. 
Spleen.—The enlarged spleen is found in the majority of cases. It 
cannot be definitely asserted that it is always the result of secondary 
congestion for it is not at all unusual to find the spleen enlarged during 
the early stages of the disease before there have been sufficient primary 
changes to cause obstruction. The spleen is most likely to be prominent 
with advancing cirrhosis; during periods of latency it often recedes. 
When during latency the spleen increases in size other evidences of pro- 
gression are not long postponed; these include ascites, gastro-intestinal 
symptoms, hematemesis, a toxic state often, which is associated with pro- 
found nervous symptoms, and albuminuria with few or abundant casts. 
Persistent enlargement of the spleen after hematemesis is unfavorable; 
recurrence of hemorrhage, toxemia or ascites may be expected. With 
obstruction there is, as a rule, obstinate constipation and the associated 
subjective symptoms including languor, anorexia, and often toxemia. 
Unless the disease is advanced, diet and rational treatment are fairly 
effective. With toxemia, ascites, intolerant stomach and obstipation, 
there are usually cardiovascular symptoms (myocardial insufficiency), 
characteristic facies, and death in coma is not unusual. In this class of 
cases paracentesis of the abdomen for the relief of ascites is often promptly 
followed by the deep invasion of the sensorium and death. 
Caput medusae.—With closure of the collateral circulation the com- 
pensation of portal obstruction is reduced. As portal obstruction advances 
every collateral avenue is employed to return the blood to the right heart. 
The dilatation of the superficial abdominal veins is indicative of marked 
portal obstruction and failure of the collateral circulation to compensate. 
Blocking of the communication between the epigastric and internal mam- 
mary veins, usual with marked portal stasis, causes dilatation of the 
superficial veins around the umbilicus (wreath-shaped), and is known to 
clinicians as the Ucaput medusae.” 
With marked ascites, there is obstruction in the portal circuit, stasis 
in the vessels of the lower extremities with consecutive distension of the 
inferior epigastric and internal mammary veins with consecutive super- 
ficial stasis. 
Hematemesis.—The prognostic significance of hematemesis depends 
upon the stage of cirrhosis in which the bleeding occurs. When hema- 
temesis is an early symptom it is not at all unusual, under favorable 
conditions, for the patient to live many years. Such histories are com- 690 
DISEASES OF TIIE DIGESTIVE APPARATUS 
paratively frequent even in the presence of marked cirrhosis followed by- 
latency. Early bleeding may prove a wholesome warning, which when 
heeded may prolong life. Hematemesis in late cases, with other evidences 
of obstruction, is unfavorable. 
In advanced cirrhosis the first hematemesis may be profuse and fatal. 
Hematemesis due to esophageal varix may be fatal at once or there may 
be repeated small bleeding which with the co-existing toxemia finally 
deplete the patient. The prognosis of bleeding due to varices is worse 
than ordinary uncomplicated hematemesis. 
Hematemesis with ascites or other circulatory embarrassment is 
always unfavorable. 
Hemoptysis.—Hemoptysis has never in my experience been profuse 
in uncomplicated liver cirrhosis. When a symptom of the purpuric con- 
dition with advanced cirrhosis, it is unfavorable. 
With hemoptysis due to disease of the nasal mucosa it is insignifi- 
cant, per se. 
When due to associated tuberculosis, the forecast depends on asso- 
ciated conditions and the amount of blood lost, and is easily made. The 
majority who raise blood with cirrhosis are tuberculous. 
Hematuria with cirrhosis is either dependent upon purpura and a 
deep toxic state or nephritis. In either event there are likely to be hemor- 
rhages from other sources particularly with purpura. Acute nephritis 
occasionally complicates cirrhosis and adds an element of danger. 
Epistaxis.—Nose-bleed is frequent with cirrhosis. It may be one 
evidence of the purpura dependent upon hepatic insufficiency or infec- 
tion, and is often counted among the symptoms of the terminal toxemia. 
Uncontrolled epistaxis may prove depleting. In the purpuric and pro- 
foundly toxic it alternates with bleeding from other surfaces—the kid- 
neys, intestines (melena), or bladder. 
Helena.—Intestinal bleeding early may be transitory and without 
significance. With advanced cirrhosis melena is always of serious import. 
When it follows hematemesis its significance is measured by the quantity 
of blood lost and associated eonditions. Gastric and duodenal ulcers with 
cirrhosis may cause intestinal without gastric hemorrhage. Extensive 
rectal ulceration with profuse bleeding may cause death. 
Hemorrhoidal bleeding is not, as a rule, of grave significance. 
Purpuric conditions are evidences of profound toxemia and malnu- 
trition, and with cirrhosis are promptly followed by death. In some cases 
bleeding from the gums or nose with small patches of necrobiosis may 
continue with chronic toxemia during a number of weeks before the end. 
Change in the Size of the Liver.—It is exceedingly difficult to offer a 
forecast based upon the change in the size of the liver. Possibly it is safe 
to conclude that in the majority of cases the smaller the organ (the more 
advanced the contraction) the more unfavorable is the forecast. With DISEASES OE THE LIVER 
691 
latency, the prognosis is usually more favorable when the liver shows 
some enlargement, but its enlargement during this period may be the 
precursor of serious complication or advancing disease. Rolleston says: 
“But this is not a hard and fast rule, since enlargement may be tempo- 
rary and due to alcoholic excess, to absorption of poisonous products 
from the alimentary canal, or to complications such as cardiac failure 
and backward venous pressure.” llie outlook is, however, always bettei 
with a large than with a small liver and most of my cases which fell into 
long latent periods or improved after tapping for early ascites had large 
livers. 
Ascites.—Ascites should always he regarded as one of the gravest 
results of portal obstruction and unless it is an early symptom with an 
enlarged liver, without toxemia in a well nurtured and resistant patient 
in whom early paracentesis is followed by improvement, without recur- 
rence, it offers an unfavorable prognosis. 
With previous symptoms making the diagnosis of liver cirrhosis posi- 
tive, and the development of ascites, the prognosis is absolutely bad and 
but few cases survive more than one or two tappings. Hale White makes 
the unqualified statement that cases of uncomplicated cirrhosis—without 
chronic peritonitis—never survive more than one paracentesis abdominis. 
This has not been my average experience. There are cases of advanced 
cirrhosis in which tapping is promptly followed by a toxic condition and 
death within three or four days. No advanced case should be tapped 
without having this possibility in mind. 
It may be positively stated that by tapping in individual cases, m 
which ascites is an early complication, in which the liver is large, periods 
of latency or apparent recovery may follow. Cures have been reported by 
competent clinicians under similar conditions. 
Ascites with cirrhosis due to mitral disease or chronic peritonitis offers 
a much better prognosis than does the dropsy which is entirely due to 
portal obstruction of productive origin. Hemorrhagic ascites is always 
less favorable than ascites with a relatively clear fluid. It may be evi- 
dence of chronic hemorrhagic peritonitis, rarely tuberculosis, or added 
malignant disease within the abdomen. 
General Dropsy.—General dropsy (edema of the legs, general anar 
sarca) is a terminal complication of cirrhosis and offers only the most 
unfavorable outlook. These patients are usually profoundly anemic and 
toxic with myocardial insufficiency and often show kidney invasion. 
Urinary secretion.-— So long as the urinary secretion remains suffi- 
cient to allow of free elimination and there is no serious or deep invasion 
of the parenchyma of the kidney, the prognosis is favorable, for it is a 
fact that with serious obstruction, profound toxemia or threatening com- 
plications, the urine is promptly changed and excretion proves insuffi- 
cient. With rapid destruction of liver cells, acute exacerbation or serious 692 
DISEASES OF THE DIGESTIVE APPARATUS 
interference with hepatic function, the urine is a valuable prognostic 
index. 
Acidosis with fully developed cirrhosis is often acute and grave; 
chronic acidosis is less threatening, but is a part of the toxic process 
which is always of serious import. A large increase in ammonia (nitro- 
gen in the form of ammonia) is often due to the destruction of liver cells 
and is unfavorable. Marked increase in ammonia and decided decrease 
in urea are ominous. 
The presence of leucin and tyrosin in the urine indicates advanced 
liver cell degeneration and is therefore serious. 
In the majority of uncomplicated cases there is but little jaundice; 
hence the urine is not surcharged with bile, as with the hypertrophic 
disease. The urine in the graver cases, usually in the advanced stage 
with obstruction, is concentrated; the quantity is decreased; there is 
increase of urates and uric acid; urobilinuria is almost constant. 
Evidences of passive congestion of the kidney (albuminuria: few casts, 
red blood corpuscles) marks the period of portal stasis and is coincident 
with other secondary changes unlikely to yield to treatment. Marked 
urea reduction with albuminuria and myocardial weakness justify only 
the gravest forecast. Occasional glucosuria with limited liver changes 
during the early stage is not serious; it usually proves to be transitory. 
With diabetes bronze (See Diabetes) the prognosis is always had. Per- 
sistent glycosuria with marked stasis during the advanced stage is always 
ominous. 
The combination of diabetes mellitus and liver cirrhosis in the alco- 
holic is serious, though with rigorous and rational treatment, without 
grave complications and in the absence of toxemia of any kind such lives 
may often be prolonged and made comfortable during long periods. Ali- 
mentary levulosuria is of some value in determining the extent or degree 
of liver insufficiency. The increased, toxicity of the urine is a factor of 
considerable value in determining hepatic inadequacy (Roger). 
Albumosuria may prove to be evidence of hepatic insufficiency; asso- 
ciated conditions demand serious consideration before its importance as 
a symptom is interpreted. 
Uremia with cirrhosis and advanced stasis make a dangerous complex. 
Such patients die within a few days in coma, though chronic uremia may 
be present during a number of weeks or even months before coma or 
other complications end life; some of these patients yield to infection. 
Jaundice.—Slight icteroid tint is frequent. Deep jaundice is the 
exception in uncomplicated cirrhosis. Moderate jaundice is found in 
about one-third of all cases (Rolleston). Slight or even marked jaundice 
may depend upon transitory cause, and disappear. With acute exacer- 
bation of g astro duodenitis jaundice becomes prominent, to fade as the 
mucosa returns to its chronic condition. When with cirrhosis iaundice DISEASES OF THE LIVER 
693 
persists and is deep, it is an unfavorable feature, more particularly 
when with acute exacerbations liver cells degenerate and icterus gravis 
results. 
Jaundice due to gall-stone impaction in the common duct may com- 
plicate cirrhosis. The prognosis, unless relieved by nature is less favor- 
able than without cirrhosis, as cirrhotics do not tolerate radical surgical 
interference so well as do normal subjects. With such complication there 
is always great danger of added infection. 
The Blood.—The blood picture offers a fair index of the general 
result of the liver changes and included toxemia. The latent and early 
cases which are favorable show but slight or no blood changes. 
Progressive cirrhosis runs parallel with increasing secondary anemia. 
There is decrease in the hemoglobin and a lowering red blood count. 
Emerson reports counts between 3,100,000 and 5,000,000 in 32 cases 
with an average of 4,500,000; the hemoglobin average was 68. The 
hemorrhagic diathesis increases anemia very suddenly at times. When 
the secondary anemia becomes grave, normoblasts are found. I have 
records of a number of cases in which with depleting factors and toxemia 
the count fell to 2,000,000—in one case lowTer. Cabot reports a case with 
1,200,000 reds and 22 per cent hemoglobin. Limbeck saw a case with 
1,500,000 reds, while Grawitz offers no such low counts but agrees that 
with the secondary anemia there is moderate leukocytosis and that the 
specific gravity of the blood never falls below 1,040. 
Leukocytosis is characteristic of cirrhosis; marked leukocytosis in- 
variably makes the prognosis bad (Rogers). Marked reduction of the 
alkalinity of the blood indicates acidosis, and is unfavorable. This con- 
dition is frequent in advanced cases. 
Tuberculosis.—I have elsewhere referred to the frequent association 
of pulmonary tuberculosis and liver cirrhosis and its baneful influence. 
Acute miliary tuberculosis with cirrhosis is rapidly progressive; with high 
fever, rapid pulse and emaciation, death may follow in from four to twelve 
weeks. In several cases in men of middle life the average duration was 
less than six weeks. 
Chronic tuberculosis and cirrhosis may cover a long period. Latency 
of both processes under favorable conditions is not impossible. This is 
particularly true of chronic fibroid phthisis as well as of those forms in 
which there was previous latent phthisis with fibrosis, in which liver 
degeneration is not far advanced and in which environment and habits 
are favorable. 
Active tuberculosis with cirrhosis of the liver always justifies a 
guarded prognosis and as a rule it is unfavorable. From 10 to 15 per 
cent of all cirrhotics die of pulmonary tuberculosis; 22 per cent of all 
cirrhotics show lesions of pulmonary tuberculosis on post mortem exam- 
ination. 694 
DISEASES OE TIIE DIGESTIVE APPARATUS 
Bronchitis.—The chronic 'pharyngitis and bronchitis of the alcoholic 
with cirrhosis are not of importance in prognosis, though often annoying. 
These conditions are likely to yield to treatment and abstinence. The 
uncontrolled cough or persistent bronchitis of the cirrhotic patient should 
always arouse the suspicion of coincident tuberculosis. 
Pneumonia.—Pneumococcus infection is frequent; alcoholic cirrhosis 
invites it. Either croupous or catarrhal infection of the lung offer an 
ominous outlook. Pneumonia is likely to complicate streptococcus infec- 
tion such as erysipelas in the subjects of Laennec’s cirrhosis, and with 
delirium, often meningismus or meningitis; these patients die. Occa- 
sionally an alcoholic recovers from pneumonia in the presence of an 
incipient cirrhosis (See Pneumococcemia). 
Pleurisy.—Fibrinous pleurisy is not frequent; it offers a good prog- 
nosis. Pleurisy with effusion is often tuberculous in cirrhotic subjects. 
Pleurisy with effusion is more frequent on the right side, due to the 
spread of inflammation from the liver through the diaphragm (Villain). 
Such effusion is likely to be bloody. In advanced cases the addition of 
pleural effusion or hydrothorax due to cardiac failure are serious, and 
never to be lightly regarded. 
Invasion of Nervous System.—Most symptoms and complications 
referable to the nervous system are of toxic origin. Profound invasion 
of the nervous system—the brain particularly—is always grave and in 
most cases presages early death. During acute exacerbations there may 
be some evidences of mental hebetude which often yields with the relief 
of the toxic state. 
Acute or chronic alcoholic poisoning, with exacerbations including 
mental disturbances, delirium tremens, stupor or coma is always serious 
in the course of an active cirrhosis. The milder evidences of toxemia, 
frequently present during the early stage of cirrhosis, including head- 
ache, lassitude, mental laziness, vertigo, tremor, and a variety of sub- 
jective complaints, yield to treatment and abstinence from alcohol. 
Mental symptoms due to uremia and renal insufficiency are always 
grave. Renal insufficiency with cirrhosis of the liver promptly increases 
all nervous symptoms due to the resulting toxemia. Coma suddenly or 
gradually developed at any stage of cirrhosis is a symptom of the gravest 
significance, and never justifies any other than a grave prognosis. 
There are occasional cases, as already suggested, in which coma proves 
transitory; these are exceptional, particularly when the cirrhosis is in 
an advanced stage. Coma is largely dependent upon renal and hepatic 
insufficiency. The prognosis depends therefore on the extent of the liver 
degeneration and the ability of the kidney to relieve the surcharged blood 
of its toxins. 
Delirium tremens with alcoholic meningitis and cirrhosis of the liver 
usually ends fatally. I have in my service met cases of delirium tremens DISEASES OE THE LIVER 
695 
with wet brain which slowly mended. In a few of these I have found 
peripheral neuritis a sequel, from which recovery was usually slow. 
It occasionally happens that a fully developed, or even incipient, 
cirrhosis is complicated by fully developed peripheral neuritis in which 
the prognosis of the latter complication has been fairly good when with- 
out associated depressing factors. 
Convulsions during any stage of cirrhosis are serious. They usually 
depend upon grave underlying conditions; toxemia or pressure may pre- 
cede meningitis or coma from which recovery is the rare exception. 
Delirium with cirrhosis and active delirium tremens often includes 
pneumonia—a bad but frequent combination in hospital practice. Any 
form of meningitis complicating cirrhosis is serious and with increasing 
stupor and final coma leads to death. 
Gowers, Wilson and ISTammack have described cases of “progressive 
lenticular degeneration” in which there is mixed cirrhosis of the liver 
and symmetrical degeneration of the lenticular nuclei. The course may 
be chronic; the prognosis is bad. Gowers characterized the disease, 
which is usually familial, as “tetanoid chorea ” The disease is not 
hereditary. There is bilateral tremor and spasticity when the disease is 
advanced, dysphagia and anarthria without true paralysis. The disease 
is not syphilitic and probably not of alcoholic origin but is due to a 
toxin; it is probably not microbic and possibly a lipoid; it exerts a 
selective action on the lenticular nuclei, comparable to the selective bile- 
staining of the lenticular nuclei in “kernicterus” (Rolleston). 
Cerebral thrombosis, embolism and cerebral hemorrhage are all 
without encouragement for the future of the cirrhotic patient. These 
complications may occur during the latent or active periods of the 
disease. 
Gout with its symptoms may materially influence the comfort and 
general health, and with associated heart lesions or kidney changes often 
proves a formidable complication. In but few cases does gout, per se, 
cause the death of patients with liver cirrhosis. The influence of trau- 
matism and resulting infection on the lives of these patients is paramount. 
As we have already said the average cirrhotic offers but little resistance 
to surgical interference ; the same is true of trauma of any Jcind. Surface 
injuries and fractures are likely to be followed by streptococcus infection 
(erysipelas often) and pneumonia. 
Terminal infections are easily acquired and demand the greatest 
vigilance. Besides erysipelas and pneumonia, malignant endocarditis, 
pericarditis, pachymeningitis, and hidney infection are among the causes 
of death. 
Temperature,—Slight elevation of temperature during the early stage 
of the disease is usually transitory and not significant. Persistent ele- 
vation of temperature is always worthy of investigation; its cause will 696 
DISEASES OF THE DIGESTIVE APPARATUS 
at once make its significance clear and prognosis possible. With unex- 
plained fever, tuberculosis should be suspected. 
Pulse.—The pulse is always a valuable prognostic index with cir- 
rhosis. Persistently rapid heart is indicative of some complication or 
degenerative change of the myocardium. 
Heart.—Heart failure in cirrhosis is rarely sudden; the heart con- 
tinues tolerant with a rapid pulse during surprisingly long periods. 
Rapid pulse with coma is almost always the precursor of the end. Marked 
hypotension with associated evidences of venous stasis and feeble pulse 
not infrequently continues during several weeks before death. The prog- 
nostic significance of hypertension depends upon associated conditions. 
Alone it is of but little value. 
Respiration.—Hurried respiration may persist during weeks with 
advanced cirrhosis and ascites, or there may be tuberculous infection, 
pleurisy, or heart weakness. Abnormally sloiv respiration may be due 
to toxemia or to some central lesion. 
Skin Lesions.—The skin lesions do not materially influence prog- 
nosis. Obstinate pruritus with or without icterus may prove annoying, 
but does not as a rule do more than cause insomnia and aggravate the 
other nervous symptoms. Pain is not sufficiently severe to depress or 
influence the patient seriously. 
Pigmented Cirrhotic Livers.—Cirrhotic livers occasionally show char- 
acteristic pigmentation in which particles of carbon, metals, or stone find 
their way through the blood stream to the organ (cirrhosis anthracotica) ; 
hemorrhage during the course of cirrhosis may leave sufficient blood 
coloring matter to cause moderate pigmentation; with hemochromatosis 
and diabetes bronze and with chronic malarial poisoning with associated 
cirrhosis, pigmentation is found (See Malaria and Diabetes Bronze). 
The prognosis of hemochromatosis with pigmented cirrhosis and diar 
betes bronze is uniformly bad. The former patients may live during 
long periods but they die as a rule of gastro-intestinal hemorrhage, while 
in the latter the course of the disease is much shorter and death is rarely 
postponed beyond eight to twelve months. 
The malarial cases are chronic as a rule. It is questionable whether 
malaria per se causes cicatricial change in the liver. Barker claims that 
existing conditions with severe malarial infection (the degenerative and 
necrotic changes in the liver parenchyma) are favorable for the pro- 
liferation of connective tissue in the liver. Osier has failed to find 
malaria causative of cirrhosis and the post mortem table strengthens 
Osier’s contentions. Probably in these cases alcohol is the factor and 
the prognosis Of portal cirrhosis must hold for that of the pigmented 
cirrhotic liver with the history of malaria. 
The Influence of Surgical Treatment.—It occasionally happens that 
after repeated paracentesis abdominis ascites does not return and patients DISEASES OF THE LIVER 
697 
remain fairly comfortable during comparatively long periods. The re- 
peated tapping or possibly wounding the liver may have caused adhesions 
around the liver. 
The history of the surgical treatment of cirrhosis of the liver is inter- 
esting. The operation most popular is known as the “Talma-Morrison 
operation.” Drummond and Morrison (1896) attempted to establish and 
increase the collateral circulation between the portal and the general 
systemic veins. Talma had originally planned the operation in 1889, 
and Van der Muelin in 1889 did the operation. He was followed by 
Schelkley in 1891 and by Lens in 1892. The operation ha,s for its 
object an examination of the peritoneum to determine whether the exist- 
ing ascites is due to chronic peritonitis; if it is, the operation is useless. 
Then the peritoneal surface over the liver is scraped to provoke adhesive 
inflammation and the surfaces are brought together by stitching the 
round ligament to the abdominal wall or by running the stitches through 
the liver. In some cases the greater omentum is used to increase the 
vascular adhesions, and it is held between the diaphragm and the convex 
surface of the liver. Pathologists hold that the improvement in the 
condition of the patient is not due entirely to the increased collateral 
circulation, for it has been shown that this may cause deep toxemia 
experimentally; but that there must be some other explanation. 
Thomson has contended that the improvement is due to the oblitera- 
tion of the peritoneal cavity by adhesions, and Rolleston and Turner 
held that the benefit of a collateral circulation following adhesions around 
the liver “might be beneficial to the economy ...” “(1) By some- 
what diminishing the flow of blood through the liver it may enable that 
organ to deal more satisfactorily with the blood passing through it and 
so reduce the toxemia, which is probably the important factor in inducing 
ascites. (2) That the presence of vascular adhesions over the surface 
of the liver would relieve venous engorgement and so allow a freer sup- 
ply of arterial blood to the liver. The nutrition of the liver cells would 
thus be improved and they would be under better condition to undergo 
compensatory hyperplasia. The compensatory hypertrophy of the liver 
will enable the organ to perform more efficiently its important antitoxic 
function, and so lead to a latency of the symptoms” (See Rolleston and 
Turner, Weber and Rolleston, references appended). 
Late operation can only end disastrously. If the Talma-Morrison 
operation is to accomplish its purposes it must be performed before there 
is overpowering debility and advanced degeneration of the liver paren- 
chyma. It can offer no advantages in the presence of deep jaundice or 
marked cardiovascular lesions. 
Sinclair White’s material collected by him includes 221 cases of 
cirrhosis operated, of which 87—or 13 per cent—were improved; in 15 
per cent the operation failed, and in 33 death followed. The French 698 
DISEASES OF THE DIGESTIVE APPARATUS 
(Monprofit) report the recovery of 35 per cent of 224 operated cases. 
Willems reported only 4 per cent of successes in 250 operated cases. 
Bunge in Germany presents in his work 288 operations, of -which 70 per 
cent proved to be cirrhosis, with 30 per cent of cures and improvement 
in 14 per cent. 
American physicians and surgeons have not become enthusiastic sup- 
porters of the operation; they interpret their results and those of foreign 
surgeons as rather discouraging. The efficacy of the operation cannot 
he fairly judged because in most cases it is postponed until the latest 
possible moment. It appears that the early operation does materially 
improve the chances of inducing latency of the disease and in some cases 
its comjjlete arrest. 
Duration of Laennec’s Cirrhosis.—It is difficult to give any data of 
value which justify any conclusion concerning the duration of Laennec’s 
cirrhosis. As already emphasized, early diagnosis is the exception; long 
periods of latency are frequent without subjective symptoms; compen- 
satory changes often take place while the disease remains unnoticed. 
Years may lapse without progression after the positive diagnosis. There 
are acute cases which run a rapid course, particularly in young subjects. 
The duration of the average case depends largely upon secondary changes 
due to portal stasis and toxemia. There are but few chronic cases which 
die before the end of the second year following diagnosis. The majority 
live longer. The duration of cases detected early with good resistance 
depends upon the patient’s ability to free himself from the slavery which 
holds him. Limited liver changes of ‘productive character may remain 
stationary, and because of compensation, such patients may for all prac- 
tical purposes be considered cured. Patients with mixed cirrhosis, with 
syphilitic liver lesions, and improvement following the intensive treatment 
with the iodids, may live many years and may die of other disease. 
Experience teaches that but few patients die directly from cirrhosis; 
most deaths are due to secondary changes in distant organs or to compli- 
cations—infection and toxemia—invited by the primary disease. 
(b) Unilobular Cirrhosis 
(Hanot’s Cirrhosis, Biliary Cirrhosis, Cirrhose Hypertrophique avec 
Ictere Chronique, Hypertrophic Biliary Cirrhosis, Obstructive Bil- 
iary Cirrhosis) 
General Statements.—Hypertrophic biliary cirrhosis and obstructive 
biliary cirrhosis are not exactly synonymous; both may be considered 
biliary cirrhosis but they differ from each other. In the former there is 
no gross obstruction in the larger bile duct, while in the latter (obstruc- 
tive biliary cirrhosis) there is positive evidence of obstruction, to the out- DISEASES OF THE LIVER 
699 
flow of bile, which is followed by dilatation of the biliary ducts, destruc- 
tion of liver cells, pigment deposit, and connective tissue proliferation. 
Obstructive biliary cirrhosis can be experimentally produced in animals 
by tying or obstructing the common duct. Biliary cirrhosis of Ilanot is 
unilobular, involving one lobule of the liver tissue at a time; it may be 
complicated with true portal cirrhosis, and is characterized by marked 
enlargement of the liver and spleen, jaundice which is persistent, febrile 
attacks which recur, and the absence of ascites in uncomplicated cases. 
Men are more subject to the disease than women, and it shows a decided 
preference for young subjects (20 to 30 years—rarely after 40). The 
juvenile type of the disease is occasionally found, and this has been de- 
scribed by Gilbert and Fournier. Requin in 1846 was the first to men- 
tion the disease, Todd in 1857 again called attention to it, but Hayem 
in 1875 succeeded in giving a classic description of its clinical and patho- 
logical features, and Kiener in 1893 named it Hanot’s disease. 
Causes.—It is exceedingly difficult in the average case to give a 
cause for the far-reaching liver changes; neither alcohol nor syphilis 
account for the lesions. In the obstructive biliary cirrhosis the etiology is 
clearer, though pathologists are not entirely agreed; the fact remains 
that in a number of cases obstruction of the common duct by gall-stones 
or other pressure occurs. Rolleston assumes that when the symptoms of 
cirrhosis follow obstruction, “due to gall-stones or other causes, the cirrho- 
sis is reasonably explained as the result of poisons manufactured in the 
intestines and carried to the liver by the portal vein.” Haunyn says 
the association of gall-stones and biliary cirrhosis is rare but possible, and 
that gall-stones secondary and not the cause of the biliary cirrhosis. 
Complications.—Attacks of pain in the region of the liver with the 
physical changes mentioned and increase of the jaundice, sometimes acute 
enlargement of the already enlarged liver are depressing, and tend when 
associated with fever to weaken the patient and increase the tendency to 
myasthenia. Marked change in the pancreas is characteristic of some 
cases (See Chronic Pancreatitis) and interferes with digestion, and often 
proves a serious handicap—patients emaciate rapidly or they fall into a 
chronic condition of enfeeblement from which they do not lift themselves. 
The renal and cardiovascidar complications of portal cirrhosis may ac- 
company the biliary type. Purpura (petechiae) has been noted in some 
of our cases, particularly with other toxic symptoms and has proved to be 
a difficult complication to treat; usually it is present in the terminal stage. 
Nose-bleed is at times profuse. 
Hemorrhages from the intestine are rare, as are hemoptysis, hematuria 
and hematemesis save in the terminal stage, and then are not frequent. 
Gastrointestinal symptoms are often persistent. The complete anorexia 
in some cases with nausea, at times diarrhea, depleting the patient, lead 
to marked marasmus, cerebral anemia, mental confusion and death. 700 
DISEASES OF THE DIGESTIVE APPARATUS 
Course of the Disease.—The size of the spleen is variable. Ordinarily 
the spleen is enlarged and palpable; in some cases the enlargement of 
the spleen is greater than the liver (splenomegaly), in other cases the 
liver is enlarged out of all proportion to the size of the spleen and it may 
happen that the spleen is miniature in size, in the presence of a good 
sized liver—or the liver in some forms of atrophic biliary cirrhosis may 
ultimately be small and the spleen enlarged. 
Jaundice is a permanent feature, it may show variations in depth, 
and may be so deep as to give a brownish cast to the skin. 
Joint changes do not materially influence prognosis; they are occasion- 
ally found. Clubbing of the fingers is evidence of advanced disease but 
slowly progressive. Deep invasion of the nervous system is always unfa- 
vorable. The chronic cholemia often causes mental hebetude and with 
depression there may be acute exacerbations of an emotional nature. 
Many cases terminate in a condition of profound toxemia. Delirium 
may persist during several weeks or days, hiccough Avith delirium, convul- 
sions and coma are all possible; all are terminal. 
With progression there is myocardial insufficiency—often hemic and 
mitral systolic murmurs. During the chronic stage the pulse continues 
reasurring without marked change in tension. As the end approaches or 
as the chronic toxemia begins to show its ravages, the pulse becomes more 
rapid, feeble and small; there are often symptoms of cardiac insufficiency 
and dilatation. 
Blood.—The blood picture varies with the stage of the disease and 
associated conditions. In the plethoric adult polycythemia is not un- 
usual. Emerson has reported counts as high as 7,800,000 and 8,500,000 
in 2 of 5 cases; while the same writer reports the other extreme showing 
the usual characteristic secondary anemia of the disease—1,504,000. 
Hemoglobin may be increased in the individual cell or decreased, depend- 
ing largely on the stage of the disease and complications. Moderate 
leukocytosis is the rule. Marked leukocytosis as in portal cirrhosis is 
not, as a rule, favorable. 
Urine.—The quantity of urine in the average case is increased. Mil- 
ian holds that polyuria is the rule and is characteristic. There are always 
evidences of jaundice (bile pigment) in the highly colored urine. Uro- 
bilinuria is frequent as is indicanuria. Albuminuria is less likely to be 
found with biliary than with portal cirrhosis. When present, its cause 
must be determined; it is often transitory. Persistent albuminuria is un- 
favorable. A moderate shower of casts with jaundice is not of grave im~ 
port; with albuminuria and casts and evidences in the heart and arteries 
as well as the nervous system of added nephritis the prognosis becomes 
more serious. 
Diabetes mellitus or glucosuria with hypertrophic cirrhosis is exceed- 
ingly rare. Sugar tolerance may be increased. Incipient obstructive bit- DISEASES OF THE LIVER 
701 
iary cirrhosis in which the cause may be removed surgically or yields to 
nature’s processes, may remain stationary. 
Conclusions.—Hypertrophic cirrhosis of Hanot is an insidiously 
progressive disease which, as already indicated, finally causes overpower- 
ing toxemia and death. The acute infections, gastro-intestinal compli- 
cations, hemorrhage from the stomach or intestines, carcinoma, myocardial 
degeneration, nephritis, cerebral anemia, or meningitis, are among the 
most frequent causes of death. This variety of cirrhosis, as portal cirrho- 
sis, invites erysipelas, pneumonia and peritonitis. The duration is from 
one to twelve years. One of my cases died in the twelfth month; the 
average of my cases has been two and a half years after positive symp- 
toms. Goluboff reports cases of twelve years’ duration. Rolleston gives 
the average as five years. Much can be done to prolong life by proper 
attention to diet and to detail. Environment and habits are potent prog- 
nostic factors. I know of no authentic cure. 
In rare cases ascites may finally prove to be a terminal symptom; 
these are cases of the mixed type. Other individual symptoms not men- 
tioned in connection with biliary cirrhosis, but fully considered in con- 
nection with portal cirrhosis, are of equal prognostic value in both vari- 
eties of the disease. 
(c) Pericellular or Syphilitic Cirrhosis 
Syphilitic cirrhosis is considered in the section on syphilis (See Syphi- 
lis of the Liver). 
Unexpected disappearance of liver masses due to syphilitic cirrhosis 
and large tumor formations (gummata) follow antisyphilitic treatment 
very often. The enlarged or uneven livers of unknown origin given the 
benefit of antisyphilitic treatment are also frequently and favorably influ- 
enced. Liver syphilis is surprisingly frequent; under rigorous treatment, 
even with productive changes, it offers a fairly good prognosis. I have 
experienced so many successes that specific treatment is now commended 
in all cases of enlarged or nodular liver. 
With congenital syphilis pericellular cirrhosis or diffuse intralobular 
fibrosis may develop. The clinical and pathologic picture of acute diffuse 
hepatitis may be present early with congenital syphilis, from which recov- 
ery is often possible and with which pericellular cirrhosis is finally 
closely related. Many of these children recover when the luetic character 
is recognized and leads to prompt and rigorous treatment. With jaun- 
dice, the prognosis is less favorable than without it. 
(d) Capsular Cirrhosis 
(.Perihepatitis) 
Associated Symptoms.—Perihepatitis is often of syphilitic origin, both 
in adult and in early life, and is associated with other liver changes due 702 
DISEASES OF THE DIGESTIVE APPARATUS 
to the same cause. In these cases there may be proliferation of con- 
nective tissue sufficient to compress branches (large and small) of the 
portal vein causing obstruction, ascites, and the other usual symptoms. 
These cases are examples of peripylephlebitis syphilitica. Jaundice is 
present according to Leube in one-third of all cases and enlarged spleen is 
the rule. Specific perihepatitis may with advanced liver syphilis be asso- 
ciated with amyloid degeneration of the liver, and in some cases one or 
many gummata may be present in the organ. Fever and pain in the re- 
gions of the liver are characteristic, and are aggravated by pressure. The 
therapeutic test applied to cases in which amyloid change is not general 
or diffuse in the liver, proves the prognosis of many of these cases 
(usually with limited productive changes in the liver) to be relatively 
favorable (See also Syphilis of the Liver). 
Chronic hyperplastic hepatitis (Pick’s disease, periserositis—Zucker* 
gussleber) is separately considered (See Periserositis in connection with 
pericarditis and peritonitis, etc.). These cases live for years with chronic 
obstructive symptoms and obliterating pericarditis, enormous capsular 
thickening of the liver and spleen with ascites. After years, during which 
these patients are tapped at short intervals, complications are likely to de- 
velop including the toxic state, marasmus, at times pneumonia or other 
infection; no case ever recovers. 
Another class of cases includes besides the chronic proliferative peri- 
tonitis, chronic perisplenitis without any marked cirrhosis; but according 
to Hale White there is always preceding chronic interstitial nephritis. 
Ascites in these cases is a terminal complication; death usually follows 
before a second tapping is demanded. 
Hale White found 14 of his cases demanding tapping. The average 
duration of life after the tapping was only 8 weeks. Of 10 cases which 
were tapped more than once the post mortem in 4 proved the diagnosis to 
be wrong. “Each of the other three had chronic peritonitis and perihepa- 
titis; the remaining six had peritonitis, more or less chronic, associated 
with the cirrhosis.” 
Ascites with chronic perihepatitis is of extreme gravity. Fagge found 
“one fatal case of ascites from perihepatitis to every five fatal cases of 
ascites from cirrhosis.” 
Hale White offers statistics based on 22 cases of which number 14 
had perisplenitis. He believes that perihepatitis and perisplenitis in this 
variety of the disease are a part of the general chronic peritonitis. In 
19 of the 22 cases there was chronic interstitial nephritis. In 19 of the 
cases, there were “evidences of failure of the heart or lungs and conse- 
quently sometimes the liver was “nutmeg”; in one case in which the car- 
diac failure was extreme there was jaundice, but this was the only instance 
of jaundice in perihepatitis.” The average age of White’s cases was 
years; the youngest was 29 and the oldest 68. There were 13 males and 
8 females. DISEASES OF TIIE LIVER 
703 
Evidences of the fatal termination include ascites, general edema, 
increasing myasthenia, the toxic state, increasing heart weakness, the gen- 
eral features of amyloid disease and often cerebral manifestations. 
References 
Barker. Johns Hopkins Hosp. Rep., 1895, v, 221. 
Bunge. Die Talma Drummondsche Operation. 1905. 
Cabot. Examination of the blood. New York, 1897, p. 586. 
Cheadle. Some cirrhoses of the liver. London, 1900, p. 47. 
Diemar. Ztschr. f. Heilk., 1899, xx, 257. 
Drummond & Morrison. Brit. Med. J., 1896, ii, 728. 
Emerson. Clinical diagnosis. 1906, p. 586. 
Fagge (Hilton). Guy’s Hosp. Reports, 1874, i, xx, 193. 
Fiesinger. J. physiol, et path, gener., Paris, 1908, x, 671. 
Gilbert & Fournier. Semaine Med. Paris, 1900, xx, p. 154. 
Goluboff. Ztschr. f. klin. Med., Berlin, 1894, xxiv, 353. 
Gowers. Rev. Neurol. & Psychiatrie, Edinburgh, 1906, iv, 249. 
Grawitz. Klin. Path, des Blutes. Leipzig, 1906. 
Hanot. These de Paris, 1875. 
Hanot & Gilbert. Etudes sur les maladies dufoie. 1888, p. 63. 
Hawkins. Allbutt & Rolleston’s System of medicine. London, 1908, vol. iv. 
Hayem. Arch, de physiol, normal et pathol., Paris, 1874. 
La cirrhose hypertroph. Paris, 1892. 
Hoffman. Statistical experiences, etc., of the Johns Hopkins Hospital, Baltimore, Md., 
1892-1911. The Johns Hopkins Hosp. Reports, Monographs, Balti- 
more, 1913, New Series, No. 4- 
The Rural Death Rate of the State of New York. Albany, N. Y., 1913. 
Rural Health & Welfare, etc. Newark, New Jersey, 1912. 
Kellynack. Medical Chronicle, 1897, vi. 
Birmingham Med. Rev., 1897, xli. 
Kiener. Semaine Medical, Paris, 1893, xiii, p. 345. 
Klopstock. Virchow’s Archiv. 1907, clxxxvii, Hi. 
Lancereaux. Traite des malad. du foie et du pancreas. 1899, p. 302. 
Limbeck. Pathol, des Blutes. Transl. New Sydem. Soc., 1901. 
Milian. Bull. Soc. Anat., Paris, 1903, 6, ser. v, 13. 
Milian & Bassunet. Bull. Soc. Anat., Paris, 1903, Ixxviii. 
Mitchell. Transact. Chicago Path. Soc., 1911, viii, 109. 
Monprofit. Rev. de Chir., 1904, xxiv, 602. 
Nammack. New York Med. Rec., 1914, vol. Ixxxvi, p. 997. 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Pkt. Transact. Path. Soc., London, 1889, xl. 
Requin. Path. Med. Tome II, p. 748. 
Roger. Presse Medical, 1897, i, p. 293. 
Rogers. Lancet, London, Aug. 10, 1912, p. 355. 
Rolleston. Diseases of the liver, etc. London, 1912. 
Transact. Path. Soc., London, 1901, lii, 203. 704 
DISEASES OF THE DIGESTIVE APPARATUS 
Rolleston. Diseases of the liver, etc. London, 1912. 
Rolleston & Turner. Lancet, London, 1898, ii, 1660. 
Sabourin. These de Paris, 1881. 
Rev. de Med., Paris, 1884, iv, 321. 
Sears & Lord. Boston Med. & Surg. J., 1902, cxlvii, 285. 
Talma. Berl. klin. Wchnschr., 1898, xxxv, 833. 
Thomson (H. Campbell). Med. Chir. Trans., London, 1901, Ixxxiv, 265. 
Todd. Med. Times & Gazette, 1857, xv, 571. 
Villiani. Riforma. Med., Napoli, 1895, ix, pt. 1, 686. 
Weber (F. P.). St.Barthol. Hosp. Rep., 1898, xxxiv, 321. 
Wells. Am. J. Med. Sci., 1902, cxxiii, 259. 
White (Hale). Guy’s Hosp. Rep., 1892, xlix. 
White (Sinclair). Brit. Med. J., 1906, ii, 1287. 
Willens. Rev. de chir., 1904, xxiv, 606. 
Wilson (Sak). Brain. London, 1912, xxxiv. 
Yeld. St. Barth. Hosp. Report, 1898, xxxiv. 
Fagge. Guy's Hosp. Reports, xxxv, 196-202. 
Leube. Diagn. d. inner. Krankh. Leipzig, 1911, I. Band, 8. Aufl. 
White (Hale). Guy’s Hosp. Report, 1893, xlix, i. 
Transact. Clin. Soc., London, 1888, xxi, 219. 
Allbutt & Rolleston’s System of medicine. London, 1908, vol. iv, p. 163- 
168. 
See references also—Peritonitis and Pericarditis. 
Perihepatitis—Capsular Cirrhosis 
5. Abscess of the Liver 
{Suppurative Hepatitis, Tropical Abscess of the Liver, 
Suppurative Pylephlebitis) 
General Considerations.—Abscess of the liver is either single or mul- 
tiple. The single or solitary abscess is the more favorable for prognosis. 
Tropical abscess is usually single and is frequent among continental in- 
habitants in India after exposure to heat and alcohol excess, with infec- 
tion. I have elsewhere considered the relation and prognosis of liver 
abscess to amebic dysentery (See Dysentery). 
Small and hidden single abscess of the liver buried deeply in the sub- 
stance of the organ offers a less favorable prognosis than does the large 
and superficial abscess. It is unusual for liver abscess to follow direct 
trauma, though this is possible. 
The majority of all abscesses in the liver are due to infection through 
the blood stream or bile passages—hence they are secotxdary to distant or 
coincident disease. The portal vein is the usual avenue through which 
pus-pi'oducing germs enter. These include among others the strepto- and 
staphylococcus, the pneumococcus and the coli commune. I have else- DISEASES OF THE LIVER 
705 
where considered abscess due to actinomycosis and the infection of the 
liver following or associated with amebic dysentery. 
The most frequent causes of liver abscess dependent upon hematogen- 
ous infection are appendicitis, dysentery, typhoid fever, tuberculosis, 
cancerous ulceration, pyogenic disease of the spleen and pancreas. 
Infection through the bile passages causing liver abscess results from 
infectious cholangitis and cholecystitis; gall-stones are the most frequent 
cause. Foreign bodies including worms are also among the infecting pos- 
sibilities. It is possible for suppuration within an encapsuled echino- 
coccus to cause liver abscess (See Echinococcus Disease). 
(a) Single or Tropical Abscess 
Most tropical abscesses are secondary to dysentery (See Amebic Dys- 
entery). Sodre’s statistics (1907) show that in autopsies of dysenteric 
subjects 20 per cent had liver abscess. Kelch and Kiener found that in 
314 cases of liver abscesses, 268—or 75 per cent—had dysentery. 
Statistics bearing on the incidence of tropical abscess are not entirely 
reliable, as European subjects in India show a much larger percentage 
of liver abscess than do the natives, while the latter, when they contract 
dysentery, are more profoundly affected by the disease than are the former. 
Rolleston reports 79,723 cases of dysentery among the natives, with 
but 127 liver abscesses—1 in 628; “while in the European army during 
four years (1893-96) there were 7,972 cases of dysentery and 441 cases 
of abscess, or 1 in 18.” 
Liver abscess in the tropics may be secondary to typhoid fever; occa- 
sionally influenzal infection is a cause. Malta fever, yellow fever, and 
erysipelas (streptococcus) infection are among the primary diseases. Al- 
coholic excess predisposes to liver abscess. It has been found that teetotal- 
ers are less likely to develop tropical abscess than are the native alcoholics; 
indeed abscess is rare in non-alcoholics (Rolleston). Uncomplicated ma- 
laria is not considered to be a cause of liver abscess. 
Duration.—Tropical abscess may be present in the liver without giv- 
ing rise to symptoms; hence it is impossible to be certain of its duration 
in many cases. When single abscesses rupture, either into the lung or 
into the alimentary tract, a fistulous opening may persist during long 
periods. 
Spontaneous cure of abscess is an occasional occurrence. The abscess 
becomes encapsuled and “dries.” Waring reported that in 25 cases 
which recovered, 2 “underwent spontaneous cure.” The possibility of mis- 
taking gummata for liver abscess, in some of these cases, must be consid- 
ered. Unrelieved tropical abscess may lead to secondary abscesses in the 
lung; in other cases general pyemia may result. Most patients die of 
exhaustion with all of the constitutional symptoms of pyemia. 706 
DISEASES OF THE DIGESTIVE APPARATUS 
Rupture.—Neglected or undetected cases may rupture in one of many 
directions. The frequency of rupture naturally depends upon the diag- 
nosis as well as the treatment. Prompt surgical treatment reduces the 
percentage of ruptures. Most cases rupture upward and through the dia- 
phragm. We quote Cyr’s and Thierfelder’s statistics as given by Rolles- 
ton: 
Cyr—159 Cases 
Thierfelder—170 Cases 
Pleura 31 i57 per cent. 
Pericardium 1J 
Periotoneum 39 
Stomach 8 
Intestines 13 
Kidney 2 
Inferior vena cava 3 
Bile passages 4 
External 2 
74] 
26 p9 per cent. 
4J 
23 
13 
32 
1 
Complications.—Among the complications which may lead to death are 
abscess of the brain, purulent pleurisy and pericarditis, pneumonia, adhe- 
sions of the intestines causing obstruction, thrombosis of the inferior vena 
cava, and amyloid degeneration of the liver and other vital organs in the 
more chronic cases. 
Blood.—The blood count is of greater diagnostic than prognostic value. 
Leukocytosis is the rule; there are exceptions, however, as was demon- 
strated by Osier. 
Mortality.—Naturally the prognosis of tropical or single abscess de- 
pends upon the early diagnosis and the result of timely surgical interfer- 
ence. Solonoff collected 1,094 cases with a mortality of 30 per cent. 
This mortality is being reduced by improved surgical technic and greater 
diagnostic accuracy. Osier gives the mortality as 50 per cent. 
Lafleur and Manson do not agree entirely in their conclusions. The 
former holds that the prognosis of amebic abscess is more unfavorable than 
other forms of liver abscess, while Manson has not had a similar experi- 
ence. It may be concluded that the prognoses of single liver abscess is 
good in cases which are superficial and operated early. The prognosis of 
cases which rupture externally is also good. Internal rupture is less favor- 
able, the course of such cases is often exceedingly chronic, and death from 
exhaustion and pyemia is to rule.. Here too statistics differ. 
DeCastro reports 76 per cent of recoveries after rupture into the lung; 
others offer much lower figures: Manson 50 per cent, Lafleur considers the 
prognosis of the complications unfavorable. Rupture into the intestine 
offers a favorable forecast. DISEASES OF THE LIVER 
707 
Course of the Disease.—Rupture into the peritoneal cavity is promptly 
followed by general peritonitis and death. Amebic abscess in the presence 
of an active and persisting dysentery offers an unfavorable prognosis. 
Single liver abscess may cause multiple deposit in the organ finally; 
these cases are always fatal. With chronic abscess, increasing anemia, 
albuminuria, circulatory weakness and obstruction (edema), intestinal 
symptoms, invasion of the sensorium, and amyloid disease are of the 
gravest import. 
(6) Multiple Abscesses of the Liver 
{Suppurative Pylephlebitis, Pyemic Abscesses of the Liver, Portal 
Pyemia) 
Causes.—Whether multiple abscesses of the liver are due to infection 
through the hepatic artery or portal vein, to suppurative cholangitis, or to 
the single tropical abscess, the prognosis is bad and death is the rule. 
Most multiple liver abscesses are due to gastro-intestinal lesions. 
Appendicitis is unquestionably the most frequent cause of purulent 
pylephlebitis. The incidence of suppurative pylephlebitis with appendi- 
citis is only 0.5 per cent. 
Langdon Brown collected 64 cases of suppurative pylephlebitis of 
which 27 were due to appendicitis—42.2 per cent. Fitz found 11 cases 
in 257 of perforative appendicitis. Kelly and Hurdon report 10 with 
pylephlebitis among 86 fatal cases. Gerster found only 9 cases among 
1,189 operated at Mt. Sinai—0.75 per cent. 
Among the causes of multiple abscesses of the liver are gastric 
and duodenal ulcer, cancer of the stomach and intestines, infection follow- 
ing foreign bodies, pelvic infection, rectal fistula and carcinoma, infected 
hemorrhoids, gall-stone disease with cholangitis, infected spleen and pan- 
creas and as already mentioned (See Tropical Abscess) single liver 
abscess may cause portal pyemia (multiple abscesses). 
Course of the Disease.—The clinical history is synonymous with sep- 
ticemia and pyemia. Death is preceded by a limited period which in- 
cludes repeated chills, intermittent fever, abdominal pain and distention. 
As the disease progresses the nervous system is profoundly affected, and 
death in coma is the rule. Langdon Brown gives the average duration 
forty-seven days. There may be a much shorter or longer duration, vary- 
ing, as we conclude from our own reported cases, from 3 to over 200 days. 
In all cases there is first the history of the underlying disease, second, the 
development of the septic state, and third, the evidences of liver abscesses 
(Taylor). 
Accompanying Symptoms.—Jaundice is not a symptom of prognostic 
value. It may or may not be present. Liver enlargement characterizes 
most cases. Splenic enlargement may be expected in about 20 per cent 708 
DISEASES OF THE DIGESTIVE APPARATUS 
of cases. Hiccough is an annoying and persistent symptom when present 
—often uncontrollable. 
Secondary anemia and leukocytosis are usual (10,000 to 28,000). 
Libman reports 15 cases in which he cultured the blood with negative 
results in 14. In the one case which was consecutive to calculous cholan- 
gitis pneumococcus infection was present. I know of no well-authenti- 
cated case of recovery. Once the portal vein and its branches are included 
in a pyemic process, death is certain to follow. In those cases which are 
reported as having recovered, the correctness of the diagnosis may he 
doubted. Rolleston says: “Conceivably this verdict may require some 
modification in the light of more frequent observations of the state of the 
liver as seen in the course of exploratory laparotomies. In isolated cases 
recovery has occurred in which multiple abscesses were thought to exist, 
hut some question must arise if suppurative inflammation of the portal 
vein was present.” Evidences of healed suppurative pylephlebitis were 
found in cases reported by Goodhart and Moschowitz. 
Quenn and Mathieu report 13 cases wdiich recovered after operation, 
all due to appendicitis. Treves and West have recorded two cases. 
References 
Brown (Langdon). St. Bartholomew's Hosp. Rep., 1901, xxxvii, 95; also 1901, xxxvii, 128. 
Cyr. Traite pratique des malad. du foie. 1887, 
Fitz. Tr. Ass. Am. Physicians, 1886, i, 110. 
Gerster. New York Med. Rec., 1903, Ixiii, 1005. 
Goodhardt. Transact. Path. Soc., London, 1882, xxxii, p. 137. 
Kelch & Kiener. Traits des malad. des pays chaud. Paris, 1889. 
Kelly & Hurdon. The vermiform appendix. 1905, p. 225. 
Lafleur. Allbutt’s System of medicine, 1897, iv, 168. 
Libman. Amer. J. Med. Sd., Philadelphia, 1908, cxxxvi, p. 5J+8. 
Manson (P.). Tropical diseases. London, 1903, p. J+57. 
Lane Lectures on Tropical Med. 1905. 
Quenn & Mathieu. Rev. de Chir., Paris, 1911, xliv, 519. 
Rolleston. Diseases of the liver, etc. London, 1912, p. 118. 
Sodre. Twentieth century practice of medicine. 1899, xvi, 253. 
Solonoff. Brit. Med. J., 1903, l, 262. 
Taylor. Guy’s Hosp. Rep., 1902, Ivi. 
Thierfelder. v. Ziemssen’s Cycl. of the practice of medicine. 1880, vol. ix. 
Treves. Allbutt’s Syst. of med. 1897, Hi, p. 927. 
Lancet, London, 1894, i. 
Waring. Abscess of the liver. 1854, p. 195. 
West (S.). Tr. Clin. Soc., London, xvii, 126. DISEASES OF THE LIVER 
709 
6. Neoplasms of the Liver—Cancer of the Liver 
General Statements.—Cancel' of the liver should always make the 
clinician suspicious of a primary growth in another organ, and search 
should he made in all directions to determine the location of such growth. 
The diagnosis of primary cancer of the liver should always he omitted until 
confirmed post mortem. 
Hale White found in 18,500 autopsies at Guy’s Hospital 24 cases of 
'primary cancer of the liver (0.13 per ce"nt.). Eggel places the percentage 
at 0.05. Rolleston places the numerical relation of primary and secondary 
cancer of the liver between 1 to 20 and 1 to 40. Hale White, 1 to 21— 
Hansemann, 1 to 40. 
The majority of liver cancers are epitheliomata of the cylindrical vari- 
ety or medullary; sarcoma of the liver is exceedingly rare, either as a 
primary or secondary disease. Melanosarcoma is a frequent form of sar- 
coma of the liver. When it attacks that organ it may he secondary to 
choroidal growths or melanotic degeneration of pigmented skin (Jacobi). 
Secondary cancer of the liver is, as a rule, multiple. The organ is en- 
larged, the nodules are usually scattered throughout the organ, there may 
be hut one nodule; occasionally there is diffuse carcinomatous infiltration. 
The liver is large, the nodules are prominent and umbilicated, the edge 
of the liver is irregular and nodular, the gall-bladder is often distended, 
may also be carcinomatous, and may contain gall-stones. The portal 
current carries the disease to the liver from either the stomach, intes- 
tine, esophagus, pancreas, or the growth may come from some other unsus- 
pected organ, as the prostate, uterus, kidney and rectum, or occasionally 
it happens that there is direct extension of the growth from one of the 
neighboring organs. In doubtful cases the stomach is the most likely 
primary source of the disease often there are also metastases to the supra- 
clavicular glands. 
Primary cancer of the liver may he either diffuse or there may be hut 
a good sized nodule. The large nodule may ultimately he surrounded by 
few smaller growths; there are often glandular infiltrations in the hilus 
without distant metastases. 
Factors Which Influence Prognosis.—Jaundice.—With persistent 
j aundice of unknown cause, Avhich remains uninfluenced by treatment, usu- 
ally accompanied by progressive loss of weight, cancer of the liver should 
be suspected and prognosis accordingly given. Jaundice is present in 50 
per cent of all cases. Deep jaundice is indicative of obstruction by can- 
cer nodules of the hepatic or common ducts. Jaundice is rare with pri- 
mary cancer of the liver. 
Edema of the extremities is a terminal symptom. Thrombosis of the 
femoral or saphenous veins may be responsible for edema of the left leg 
and is usually a late complication. 710 
DISEASES OF THE DIGESTIVE APPARATUS 
Ascites is less marked than in alcoholic cirrhosis; the fluid is likely 
to be bloody; ascites is present in most cases and is a late complication— 
it is usually associated with far-reaching infiltration, cachexia, and heart 
weakness. Life is not prolonged after its appearance for any considerable 
period. Diffuse cancerous peritonitis may be the cause of ascites in some 
of these cases. While the fluid, as already stated, may be bloody, it may 
be clear or cloudy or bile-tinged in some cases; the clear or cloudy fluid 
may later become bloody. 
Spleen.—With uneven liver and suspected carcinoma, the presence of 
an enlarged spleen argues against cancer, for the spleen is rarely enlarged 
in liver cancer. There are but few exceptions. 
Fever is usually a late symptom and may be due to toxemia, or 
in occasional cases to associated cholangitis. 
Mortality.—The prognosis of cancer of the liver is absolutely bad. 
Surgical treatment offers nothing for secondary or multiple liver cancer. 
There are references in medical literature to supposed successful excisions 
of a part of the liver, where the disease was primary, detected early and 
limited to a constricted lobe. Some success has been claimed to follow the 
removal of the cancerous gall-bladder and adjacent infiltrated liver tissue. 
Keen’s statistics include 76 cases of liver tumor of which 63 recovered, 
but of the 76, 18 were carcinoma and 5 sarcoma. Neither the operations 
for carcinomata nor sarcomata when thoroughly analyzed offer much 
that is encouraging. 
Mayo Kobson’s case—in which a small secondary liver nodule was re- 
moved at the time of the resection of the primary stomach cancer—is re- 
ported to have recovered. 
Practically all liver carcinomata operated have been followed by recur- 
rence and multiple deposit; indeed it may be assumed that in most of 
these there was already dissemination at the time of the operation. Kol- 
leston says: “But even in these cases, which can hardly be diagnosed with 
any certainy before the abdomen is opened, the disease usually returns 
and kills the patients. Operation for removal of malignant growths from 
the liver, whether from its substance or when starting in the gall-bladder, 
is the only means at one’s disposal at present of mitigating the otherwise 
fatal prognosis.” 
Spontaneous Recovery.—It is true that occasionally cases of liver 
tumor diagnosticated as malignant have recovered spontaneously. The 
majority of these cases were specific and not malignant. The experiences, 
however, of reliable observers, who report cases of spontaneous recovery 
which they insist were malignant and cancerous, including Greig Smith, 
Gould, and Hopendyl, cannot be entirely ignored. 
But few eases live beyond twelve months and most die in a much 
shorter time. As a rule, the course of the disease is comparatively rapidv 
and death may follow within from three to six months after the diagnosis DISEASES OE THE LIVER 
711 
has been made. Encephaloid cancer of the liver usually grows with sur- 
prising rapidity. In one of my cases the growth almost filled the abdo- 
men in less than five weeks and caused death by rupture with consecutive 
sudden hemorrhage into the peritoneal cavity. A rent in medullary 
growths has suddenly ended the lives of a number of cases. 
Hale White holds that the course of primary cancer of the liver is 
practically acute, and life is rarely prolonged beyond four months. Lat- 
ency is possible; death may follow a short period of activity. Exceptional 
cases covering long periods are recorded. Christian had one case in which 
liver cancer was secondary to a rectal growth in which the liver was enor- 
mously enlarged for thirty-five months before death, and Taylor reports 
a case which lived three years. Increasing weakness and toxemia includ- 
ing final coma during several days end most lives. There is always with 
cancer of the liver the hope that the diagnosis is wrong and that the nod- 
ules may prove to be specific gummata or other benign growths as hyda- 
tids or angioma. 
Heredity.—My statistics showed heredity in from 15 to 20 per cent 
of all cases. The sexes were almost equally afflicted with the preference 
favoring men with primary cancer, and women with secondary disease. 
The average age was between 40 and 60 years. 
I have seen several primary sarcomata of the liver in early life and 
have records of one congenital case. Eolleston collected 32 cases of pri- 
mary sarcoma of the liver under 10 years of age. Picot in 424 cases of 
malignant disease under 17 years of age found 13 of primary malignant 
disease of the liver. EToeggerath and Jacobi each report a case of con- 
genital liver malignancy. 
General Conclusions.—Sarcoma of the liver offers an unfavorable 
prognosis; as already stated, it is rarely met. 
Benign growths of the liver include fibroma, angioma and cysts. Liver 
cysts and cystic degeneration of the kidney are almost always coincident 
(Bristowe). Many of these are operable and favorable. I have sepa- 
rately considered the leukemic infiltration of the liver (See Leukemia). 
Multiple adenomata of the liver are, as a rule, found with cirrhosis. 
In these cases there is usually ascites and hematemesis, portal thrombosis, 
and advanced asthenia. The prognosis under such conditions is naturally 
bad. 
References 
Bristowe. Tr. Clin. Soc., London, 1856, vol. vii. 
Christian. Am. Med., Philadelphia, 1903, v, p. 131. 
Eg gel. Beitr. z. path. Anat. z. allgem. Path., Jena, 1901, xxx, 506. 
Gould. Clin. J., London, 1902, xx, p. 96. 
Hansemann. Berl. klin. Wchnschr., 1890, xxvii, 353. 
Hopendyl. Med. Rec., New York, 1910, Ixxviii, p. 359. 712 
DISEASES OF THE DIGESTIVE APPARATUS 
Jacobi (/!.). Therap. of infancy and childhood, p. 371, 3d ed. 1903. 
Keen. Annals of Surgery, 1899, xxx, 276. 
Noeggerath. Deutsche Klin., 1854, vi, p. 496. 
Picot. Rev. Med. de la Suisse Rom., 1883, Hi, p. 660. 
Robson (Mayo). Med. Chir. Tr., London, 1896, Ixxix, p. 159. 
Rolleston. Diseases of the liver, etc. London, 1912. 
Smith (Greig). Med. Chir. Tr., London, 1894, Ixxvii, p. 139. 
Taylor. Clin. J., London, 1912, xl, p. 17. 
White (Hale). Allbutt & Rolleston’s System of medicine. 1908, iv, Part I. 
Guy’s Hospital Reports, 1890, xlvii, 59. 
7. Fatty Liver 
Fatty infiltration and fatty degeneration of the liver are secondary 
processes. 
Fatty Infiltration.—Fatty infiltration may be physiological. It is 
not unusual to have an excessive accumulation of fat in the liver in young 
children. It has been found in normal pregnant women who die acciden- 
tally, and in the obese. 
Fatty Degeneration—Fatty Liver.—The liver is uniformly and 
evenly enlarged, rather soft, the border is smooth and rounded, there is 
no jaundice neither is there pain nor enlarged spleen. Advanced fatty de- 
generation of the liver in chronic alcoholics is common. It may accom- 
pany cirrhosis and it is unfavorable under such conditions. It may result 
from acute or chronic poisoning among which phosphorus is most promi- 
nent. The other poisons which may cause fatty degeneration are arsenic, 
antimony, copper, chloroform and the various acids. 
Fatty liver is frequent with infectious diseases, dependent upon the 
destructive influence of the toxins (typhoid fever, pneumonia, puerperal 
fever, smallpox, diphtheria, scarlet fever, cholera, erysipelas, and the other 
malignant infections. (Roger and Gamier, also Rolleston.) 
In connection with appendicitis, I mentioned the danger of acute 
fatty degeneration of the liver with appendicitis. It is sometimes in 
such cases difficult, when death follows operation to determine whether 
the liver destruction is due to the anesthetic or to the infection. Such a 
case I recently saw in Frankfort, Germany. The death of the boy aged 
14 years followed within three or four days after appendectomy; the liver 
was found with universal fatty degeneration. 
Fatty degeneration and enlargement of the liver with pernicious ane- 
mia is a late manifestation of the primary and progressive disease. With 
cancer, tuberculosis, chronic respiratory and heart lesions, the prognosis of 
fatty liver must of necessity be that of the primary disease. It has been 
observed that alcoholics with fatty livers bear infection and surgical inter- 
ference badly—they develop toxemia and cardiac asthenia on slight cause. DISEASES OF THE LIVER 
713 
Acidosis is very likely to follow any operation of importance; even slight 
insult is badly borne. 
Pneumonia is a frequent cause of death. 
References 
Roger & Gamier. Rev. de med., 1901, xxi, p. 97. 
Rolleston. Diseases of the liver, etc. London, 1912, p. 426. 
8. Amyloid Liver 
(Waxy Liver, Lardaceous Liver, Chondroid (Wells) Liver) 
General Statements.—Amyloid degeneration of the liver is always 
secondary and when advanced is associated with progressive and fatal dis- 
ease. The diseases which usually precede waxy change in the liver are 
chronic tuberculosis, syphilis, prolonged suppuration, and chronic bone 
disease. The degeneration shows its earliest changes within the arterial 
zone of the hepatic lobules; the minute vessels—arteries, capillaries—are 
involved. The degenerative changes in the vessels extend to the central 
and peripheral vessels. The liver is enormously increased in size, is hard, 
its surface is even, its border rounded, there is no jaundice, but anemia 
and ascites are present; the enlargement is painless, and the spleen is en- 
larged. 
Amyloid degeneration in other organs—the spleen, kidney, gall-blad- 
der, and the glands in the portal fissure—is common. With advanced 
waxy liver, the anemia of the patient, his color and general dropsy are 
characteristic. The experienced clinician recognizes these features of the 
disease which forecast early death. Albuminuria is a constant attendant 
of advanced lardaceous disease. 
Limited amyloid changes in the liver, without marked enlargement 
with acquired or congenital syphilis, radically treated, may recover. 
Limited amyloid changes of syphilitic origin with cirrhosis, not far 
advanced, are amenable to intensive treatment. Amyloid degeneration 
with the essential anemias—leukemia particularly—has been found a 
terminal complication in my experience. 
I have never failed to find evidences of widespread amyloid degen- 
eration, post mortem, in other organs besides the liver; it is this fact which 
makes the prognosis bad besides the usually fatal primary disease. In 
practice it will be found that enlarged livers which are diagnosticated as 
waxy, which recede under treatment are positively syphilitic. I have 
never known of recovery from a supposedly amyloid liver in which the 
diagnosis of syphilis was not justified and the therapeutic test was not con- 
vincing. 714 
DISEASES OF THE DIGESTIVE APPARATUS 
9. Echinococcus of the Liver 
See Section I—D (Internal Parasites). 
10. Syphilis of the Liver 
'See Section I (Syphilis). 
11. Tuberculosis of the Liver 
See Section I (Tuberculosis). 
K. Diseases of the Bile Passages and the 
Gall-Bladder 
1. Acute Cholangitis 
(Acute Catarrh of the Bile Passages, Acute Duodenocholangitis) (See 
Catarrhal Jaundice) 
When acute cholangitis is a part of a general infection, secondary to 
some one of many infectious diseases, it ends an element of danger, but 
the prognosis always depends upon the malignancy and nature of the pri- 
mary infection. Infection of the common duct and gall-bladder with 
typhoid fever, pneumonia, or other diseases may lead to chronic changes 
and is often responsible for subsequent gall-stone disease (See Cholelithi- 
asis). 
2. Chronic Cholangitis 
In rare cases an acute inflammation of the bile passages persists and 
becomes chronic. I have seen such cases in which several months of jaun- 
dice, uninfluenced by treatment, created the suspicion of serious organic 
(malignant) disease; the obstruction finally yielded and there was full 
recovery. In such cases there may be suggestive loss of weight, but the 
other serious manifestations of grave icterus are absent, including ascites, 
hemorrhage, petechiae, mental torpor and cachexia. 
Chronic cholangitis is a frequent complication of liver cancer and can- 
cer of the bile passages, and as elsewhere suggested, may under such con- 
ditions be somewhat influenced by treatment; but in the majority of cases 
the icterus of malignant disease, abscess of the liver, hydatids or other 
organic changes is due to mechanical pressure mainly, is persistent, and 
remains unchanged to the end. DISEASES OF THE BILE PASSAGES 
715 
Gall-stones are provocative of chronic cholangitis by occlusion and in- 
fection; they continue symptoms until relieved either by nature’s proc- 
esses or surgical interference. In these cases there is likely to be associ- 
ated chronic pancreatitis of the productive type (chronic interstitial or 
fibroid pancreatitis). With persisting obstruction, the liver substance 
may undergo organic changes, the organ enlarges, and chronic invalidism 
with great loss of weight results. 
When there is persisting complete obstruction of the common duct or 
of the larger ducts, dilatation of the bile passages follows and jaundice 
remains. Occlusion of the common duct may be due to one of many 
causes and may be either complete or incomplete. Gall-stones are a fre- 
quent cause of such occlusion. Pressure from growths in the liver or sur- 
rounding organs, ulcerative processes of the duodenum at the ampulla of 
Vater, or in the duct itself, with final cicatricial contraction have been 
found in my cases. Surgical interference in non-malignant cases offers a 
favorable forecast. 
3. Suppurative Cholangitis 
Suppurative cholangitis is always secondary; usually impacted gall- 
stones with infection are responsible; abscess of the liver (pylephlebitis), 
pyemia, erysipelas, puerperal infection, pneumococcus or influenzal infec- 
tion, dysentery, and many other infections are causative. The condition 
is always serious; when far-reaching, is usually fatal. There is danger of 
perforation. The gall-bladder is often involved and filled with pus; there 
may he multiple small abscesses of the liver and enlarged spleen. The 
symptoms are those of deep infection, pyemia with intermittent fever, 
and in occasional cases there are associated metastases in other organs. 
The parotid gland is occasionally involved in metastatic parotitis. With 
multiple metastases the prognosis is always bad. Naturally the prognosis 
must depend upon the ability to remove the primary focus and drain the 
infected and suppurating area. The duration of suppurative cholangitis 
in fatal cases may he only a few days. 
4. Acute Inflammation of the Gall-bladder 
Cholecystitis 
Acute infection of the gall bladder may be due to gall-stones, or it 
may depend upon direct infection of the organ with or without the inva- 
sion of other organs. The majority of cases are associated with cholelithi- 
asis. The gravity of the disease depends upon the character of the infec- 
tion and the depth of the gall-bladder change. 
Uncomplicated acute catarrhal cholecystitis is rarely diagnosticated, 
and leads to recovery without leaving a remnant. 716 
DISEASES OF THE DIGESTIVE APPAKATUS 
5. Chronic Cholecystitis 
With gall-stones in the gall-bladder, catarrhal changes may lead to 
chronic cholecystitis, thickening, increase of mucus in the gall-bladder, and 
all without symptoms, or there may he an indefinite train of symptoms 
which suggest mild infection—all of which disappear with the drainage 
of the gall-bladder. If untreated, constitutional disturbances gradually 
develop, due to general infection and toxemia with loss of strength, fever, 
and kidney involvement; death may result. Once diagnosticated or sus- 
pected in the absence of complications with modem radical treatment, 
recovery is the rule. Chronic cholecystitis leads to dilatation of the gall- 
bladder besides the changes already mentioned; with pyemic infection, 
to empyema of the gall-bladder. 
Hydrops, or dropsy of the gall-bladder is also the result of cholecys- 
titis. The prognosis of empyema and hydrops of the gall-bladder is good 
with drainage in most cases. 
Infections of the gall-bladder leading to empyema may result from 
cholangitis, hut gall-stones are the most frequent cause. 
6. Obliterative Cholecystitis and Cholangitis 
Any organic disease of the bile passages which causes ulceration or 
productive change or pressure which is sufficient, may cause occlusion 
with consecutive changes and chronic jaundice. 
Duodenal ulcers may involve the ampulla, and cause stricture of the, 
common duct; gall-stones in their passage or hy ulceration may in the 
process of healing lead to stricture or complete occlusion. 
Following the ulceration of gall-stones into the intestine or surround- 
ing organs, adhesions often form which occlude the bile passage and the 
surrounding viscerae may he bound to each other. 
With partial obstruction of either the gall-bladder or larger duct, re- 
peated attacks of pain may simulate gall-stone colic; fever, loss of 
strength and flesh with jaundice persist until surgery comes to the rescue. 
Obliterating cholangitis of the common or hepatic ducts in which there 
is complete obstruction leads to permanent jaundice, which can be overcome 
only by surgical intervention. Without complication, the prognosis of this 
condition is relatively favorable. 
Unrelieved obstruction of the bile passages leads to enlargement and 
chronic liver changes, weakening intermittent fever, jaundice, and death. 
The prognosis of obstruction of the bile passages dependent upon con- 
ditions other than gall-stones or cicatricial contraction following ulcera- 
tion, is not good because the responsible lesions in the liver or in the 
surrounding organs are usually malignant or exceedingly grave. DISEASES OF THE BILE PASSAGES 
717 
Congenital obliteration of the bile ducts is considered in the chapter 
on icterus neonatorum. 
7. Gangrene and Phlegmonous Cholecystitis 
Gangrene of the gall-bladder is rarely found without gall-stones. With 
biliary colic, associated septic fever, and persisting local symptoms, chole- 
cystitis should be suspected. Radical surgical treatment early, will save 
the majority with phlegmonous or gangrenous gall-bladder. My material 
includes patients beyond the age of seventy who were successfully oper- 
ated without subsequent symptoms. 
Acute phlegmonous cholecystitis with the infections, typhoid fever, 
pneumonia, or septicemia is exceedingly grave, most of these patients die. 
Perforation of the galVbladder is always a grave complication, and 
leads to peritonitis and death unless operated immediately. 
Phlegmonous cholecystitis is a more common complication than has 
been heretofore supposed, as is demonstrated by the operative statistics of 
Mayo Robson and others. 
8. Cancer of the Gall-bladder 
Cancer of the gall bladder is not frequent and when found is usually 
secondary. The most frequent cause is the long continued irritation of 
gall-stones or extension from the neighboring organs. Futterer collected 
248 cases of gall-bladder cancer. There are, according to Mayo Robson, 
only 10 cases of sarcoma on record. Mayo Robson found gall-stones in 
73.2 per cent of his cases of cancer of the gall-bladder and bile ducts. 
Zenker found gall-stones in 85 per cent, Musser in 69 per cent, and Cour- 
voisier in 88 per cent. 
Early removal of the gall-bladder offers the only hope. When limited, 
the prognosis with early operation offers great encouragement; the results 
of surgeons who have had a large experience justify this conclusion. Au- 
thentic cases are recorded by Mayo Robson, Kehr, and others in which 
patients were alive and well years after cholecystectomy. 
With metastases or when secondary to neighboring growths, the prog- 
nosis is absolutely bad. 
The metastases are larger, as a rule, than the primary growth; the 
growths when primary in the gall-bladder are surprisingly small. 
Primary cancer is occasional in the bile passages, usually in the open- 
ing of the common duct. 
Courvoisier. Pathol, u. Chir. d. Gallenwege. Leipzig, 1890. 
Futterer. Ueber d. Aetiol. d. Carcinoms. 1901. 
J. Am. Med. J.ss., Oct. 15, 1904. 
References 718 
DISEASES OF THE DIGESTIVE APPARATUS 
Kehr (Hans). Gallensteinkrankheit. Berlin, 1899. 
Berl. Klinik, 1894, Hft. 78. 
Path. Wirk. der Stein in d. Gallenwege. 
Langenbuch. Chir. d. Leber u. Gallenwege. Stuttgart, 1897. 
Musser. Boston Med. & Surg. J., Oct. 15, 1889. 
Robson (Mayo). Allbutt & Rolleston’s System of medicine. London, 1908, vol. iv. 
Tr. Clin. Soc., London, 1905, Ixxxviii, p. 229. 
Brit. Med. J., 1906, i, p. 430. 
Zenker. Deutsches Arch. f. klin. Med., 1889, xliv, 159. 
9. Cholelithiasis 
(Gall-stones, Hepatic Calculus, Biliary Calculus) 
General Considerations.—The vagaries of gall-stones are numerous; 
the clinical history proves this and establishes the further fact that one or 
more gall-stones may often be tolerated in the gall-bladder or bile passages 
during unlimited periods without creating a suspicion of their presence 
and without causing secondary changes, and that the same gall-stones with- 
out the slightest warning may suddenly cause life-threatening complica- 
tions. There is no other condition associated with disease of the digestive 
system in which such a variety of clinical pictures may be presented; none 
in which tolerance to an anomaly is longer borne; none in which the dan- 
ger may arise more suddenly; none which may so promptly change from 
an apparently benign to a serious disease; none which may so insidiously 
produce organic changes in the organ which holds it, including the liver 
substance as well; none in which distant and constitutional changes and 
infection may prove more damaging; and none which offers so many inter- 
esting features for study as does cholelithiasis. In the consideration of 
the conditions which lead to the formation of gall-stones, we are practically 
agreed that infection is a sine qua non, whatever theory we adopt. 
Haunyn holds that cholesterin, the main constituent of gall-stones, is 
not a product of metabolism nor a specific secretion of the liver cell, but 
that it is found in the secretion of all inflamed or infected mucous mem- 
branes. In cholelithiasis, he contends, it originates not in the bile but in 
the mucous membranes of the bile passages and the destroyed or broken 
down epithelia. The normal cholesterin content of the bile is made innocu- 
ous by the protoplasmic poison which it holds. The lime salts are held to 
be of similar origin. Without primary change in the mucosa and its 
infection, these substances are not aggregated and gall-stones are never 
formed. Aschotf and Backmeister represent a new school. They hold that 
cholesterin is precipitated from the bile itself; that it is not necessary to 
have inflammatory changes of the mucosa of the gall-bladder or any mu- 
cous surface in order to form the stone; but that obstruction to the outflow 
of bile is sufficient. Further they hold that cholesterin may be precipi- DISEASES OF THE BILE PASSAGES 
719 
tated in the presence of aseptic conditions, and that inflammatory change 
is unnecessary. The process is dependent upon a change in the concentra- 
tion of the separate bile constituents, upon an increase of cliolesterin con- 
centration, and a reduction in solubility and resorption. Pure cholesterin 
stones may be formed in this way. Most authorities agree that fixed 
stones are unquestionably dependent upon associated infection. With in- 
fection there is (1) stasis of the bile; (2) precipitation of cholesterin; 
(3) cleavage of albumin content, and (4) epithelial degeneration. In 
pregnant women who are particularly prone to the formation of gall-stones, 
Hofbauer has demonstrated the presence of all of these conditions. 
Women are more frequently afflicted than men, the proportion being 
4 to 1. jSTaunyn found that 90 per cent of women with gall-stones have 
had children. The favorite age is between 40 and 50; infants and the 
newborn are occasionally found with gall-stones. 
The association of gall-stones with metabolic faults is said to be fre- 
quent. Diabetes, gout, and rheumatoid arthritis are among these, but sta- 
tistics concerning diabetics recently collected are not absolutely convincing. 
With malignant disease the occurrence is strikingly frequent. The 
search made by gynecologists at the time of abdominal operations un- 
earthed the presence of a large number of gall-stones with other condi- 
tions in which there are often disturbances of the internal secretions. 
My material proves gall-stones to be present in 2.5 per cent of all 
internal diseases. Ten per cent of all autopsied bodies show gall-stones,, 
and of this number 95 per cent never had symptoms which suggested their' 
presence. My experience justifies the conclusion that gall-stones while' 
they give rise to no symptoms in many cases, are never to be considered 
harmless. The prognosis is always materially influenced in those who are 
predisposed to metabolic faults by sedentary habits or any condition which; 
leads to stagnation, also such diseases as prevent sufficient exercise—as; 
chronic heart disease. The deposition of cholesterin is increased by lack 
of muscular movement. 
Diet is also an important factor in the formation of gall-stones. The 
bile requires the presence of its normal solvents, sodium glycochocolate 
and taurocholate, which are provided by the nitrogenous foods in the proc- 
ess of metabolism. The absence of nitrogenous food encourages the precip- 
itation of cholesterin. Mayo Robson says: “This may serve to explain the 
presence of gall-stones in gouty persons who on account of the lithic diath- 
esis limit their intake of nitrogen.” 
Gall-stones, once formed, are not likely to dissolve spontaneously; nei- 
ther have we any remedy which dissolves them in the gall-bladder or in 
the liver. Aschoff and Backmeister question the possibility of their solu- 
tion; if possible at all, it is exceedingly rare. Haunyn contends that 
spontaneous solution is hardly probable, and that for cure we are never 
to depend upon such a possibility. 720 
DISEASES OF THE DIGESTIVE APPARATUS 
Ilanseman has recently apparently proved by experiment in vitro, 
and by transferring gall-stones from human beings to dogs, that gall- 
stones are soluble in normal bile, particularly stones composed largely of 
cholesterin. ITanseman’s contentions hold that if the catarrhal conditions 
of the bile passages can be cured, inflammatory products removed, and 
the bile restored to its normal condition, the stones will be dissolved spon- 
taneously—“normal bile under normal conditions does not permit concre- 
ment to develop and will dissolve in time those already formed. He fur- 
ther holds that the peculiar shape of the gall-stones found at the operation 
in many cases is due to their being partly dissolved.” In practice we can- 
not subscribe to ITanseman’s conclusions. It would be exceedingly diffi- 
cult to obtain normal conditions of the bile passages and the bile, which he 
considers necessary in the presence of gall-stones. 
I consider the prognosis of the 
(a) Acute biliary colic 
(b) Chronic cholelithiasis 
(c) Obstruction of the common duct 
(d) Obstruction of the cystic duct 
(e) Obstruction of the hepatic duct and intrahepatic ducts 
(f) Complications and remote results. 
(a) Acute Biliary Colic 
In patients otherwise normal, the gall-stone colic, while painful and 
depressing is well borne; the shock in most cases is not severe; the heart 
function remains uninfluenced and without remnant; recovery from the 
colic is complete after a few days of hypogastric and epigastric tender- 
ness, associated fatigue, and anorexia. 
I have had but one death during the acute attach—a woman nearly 
seventy years of age, with myocardial degeneration. This patient had 
a solitary stone, and she died of rupture of the heart, within one-half 
hour after the onset of the colic. Courvoisier has collected 41 deaths 
during acute biliary colic, and fSTaunyn 9 cases. Collapse is at times 
profound but the majority of patients react with the relief of pain. 
Associated Symptoms.—With a weak myocardium and recurring colic 
at short intervals, death may result during the acute attack. Perfora- 
tion may occur during the attack, may cause sudden death, or may 
promptly lead to peritonitis. Relative mitral insufficiency is not infre- 
quent during acute exacerbation and colic. Riesman has called attention 
to this complication and I have found it present in a number of cases. 
With relief of the colic, usually within 24 hours, often sooner, if a true 
relative insufficiency, the murmur disappears. Riesman reports 56 cases 
of chlolelithiasis, 6 of which had a mitral systolic murmur. DISEASES OF THE BTLE PASSAGES 
721 
In weakened subjects an acute gall-stone colic may be followed by sev- 
eral days of depression, rapid pulse, and unsettled digestion. 
The tender epigastrium and right hypochondrium are not followed by 
general tenderness or extensive peritonitis. It may however be safely 
assumed that with each gall-stone colic there is more or less local inflam- 
mation which causes adhesions; consequently each exacerbation increases 
these inflammatoi'y changes. With repeated gall-stone colic the local 
changes, including thickening and adhesions increase, and unless the 
stones are removed, such lesions may sooner or later cause traction, pres- 
sure, obstruction, or other changes in accordance with the extent and 
location of the stone. 
The initial attach is usually the most severe, for with repeated attacks 
the gall-bladder loses its elasticity, and the expulsive efforts are conse- 
quently more feeble; the duration is shorter, and with increasing adhe- 
sions, the pains and other symptoms of the colic are less severe and there- 
fore more easily borne. 
Jaundice is not always to be expected. There may be early or late 
jaundice depending upon the location of the stone and secondary changes. 
Less than one-third of all patients with biliary colic are jaundiced. Jaun- 
dice never develops when gall-stones remain in the gall-bladder or cystic 
ducts, but when during the acute colic the stone is held in the common 
duct, obstruction to the outflow of bile immediately follows with jaun- 
dice. Such jaundice persists until the stone is removed either by 
nature’s process or by surgery. 
Ball valve action of stones in the common duct may cause gall-stone 
colic with intermittent jaundice—often with fever. The persistence of 
jaundice after colic positively dependent upon gall-stones is a prognostic 
sign of great significance for it is positive proof of obstruction, usually 
in the common duct, though obstruction of the hepatic ducts, one or both, 
may also lead to jaundice. 
Jaundice due to occlusion of the common duct by gall-stones may be 
present without colic. In such cases a stone of small size may find its 
way into the duct, be caught there, grow by aggregation until the occlu- 
sion is complete. 
Fever is not always a symptom of great prognostic value with gall- 
stone colic. It is very likely to follow a well-defined early chill. Hyper- 
pyrexia with gall-stone colic is as a rule evidence of purulent cholecystitis, 
cholangitis, or it may be an expression of hysteria or idiosyncrasy. 
When, following a classic colic, intermittent fever persists after 24 
or 48 hours, empyema of the gall-bladder or purulent cholangitis should 
be suspected. 
The intermittent hepatic fever of Charcot—“intermittent biliary 
fever”—is due to the associated infection and the irritat>ion of the mucosa 
by the stone. Kehr has found that the most frequent cause of intermittent 722 
DISEASES OF THE DIGESTIVE APPARATUS 
fever is the impaction of the gall-stone in the common duct. When there 
are repeated acute attacks with intermittent fever, or if after one or more 
attacks, the fever continues to observe a characteristic periodicity, the 
stone is usually impacted or complication due to infection—ulceration, 
abscess, suppurative cholangitis, destructive cholecystitis, or other lesions 
are the cause and these are but rarely overcome without surgical interven- 
tion. 
Vomiting.—Vomiting during the attack may have a salutary effect, 
for not infrequently the colic ceases when the stomach, which may be 
overloaded or still holds remnants of a previous meal, is unloaded. Vom- 
iting or attempts to empty the stomach with but little or no food, may be- 
cause of the pain added by the effort, increase collapse; perforation dur- 
ing vomiting has been reported but is a rare complication. When the 
vomitus contains bile, the common duct is not completely occluded. 
Enlargement of the liver may be demonstrated during some acute at- 
tacks—by no means the majority. The palpable liver is tender, the 
symptom is not of serious import, and disappears after a few days. When 
present it outlasts the pain by several days. The more severe the attacks 
the more likely is the liver to he enlarged. The liver is usually tender to 
pressure because of the peritoneal irritation without evident enlargement. 
Marked acute enlargement of the liver with acute biliary colic is not of 
serious significance. The rule is that such enlargement disappears 
promptly but recurs with subsequent attacks. 
Enlargement of the gall-bladder during the attack may or may not be 
evident. During severe attacks the abdominal wall is so tense and tender 
that deep palpation is impossible. It is often possible to demonstrate the 
enlarged organ by directing the patient to take a deep breath, holding it 
long enough to percuss gently over the liver and gall-bladder, marking 
the outlines and comparing these with the result of percussion during the 
normal respiratory movement. In thin subjects this may not be neces- 
sary ; gentle palpation may suffice. With repeated acute attacks the possi- 
bility of adhesions must be considered. The enlargement is likely to dis- 
appear suddenly and, without evidences of persisting acute infection, does 
not add to the dangers of cholelithiasis. 
Slight enlargement of the spleen is common, but of no prognostic influ- 
ence. The urine may be almost completely suppressed during a severe 
colic; as a rule, it is concentrated and materially reduced in quantity. Its 
color depends largely upon the degree of obstruction. The presence of 
albumin and an occasional hyaline cast are usual and not serious; the same 
is true of transitory glycosuria. 
The severity of the colic is not in proportion to the size of the stone, 
but depends more upon the extent and depth of the inflammation. Small 
calculi often provoke greater local changes than do the larger. There is no 
rule. DISEASES OF THE BILE PASSAGES 
723 
Eolleston holds “The prognosis in some degree depends on the pres- 
ence or absence of facets on a calculus found in the stools. If, after a first 
attack, a smooth gall-stone without facets is found in the feces, it may 
reasonably he hoped that no further attack will follow. If, on the other 
hand, the calculus is faceted, there are more calculi in the gall-bladder 
and the probability of fresh attacks must be faced.” 
It is 'possible for small stones to find their way from the hepatic and 
cystic ducts through the common duct into the intestine. The size of the 
stone which may be passed directly through these passages varies in the 
individual cases, but it is rarely larger than a hazel nut, according to 
the experience of most clinicians (Grube and Graff). When larger 
stones during acute attacks or at any time enter the intestines or are found 
in anomalous locations it is the result of ulceration and protective adhe- 
sions. 
The Blood.—With acute attacks and intermittent fever the blood has 
been found contaminated; Netter found Staphylococcus pyogenes aureus, 
and Sittman, Gilbert and Girode demonstrated staphylococci also. The 
frequency of typhoid infection is striking and is of enormous etiologic and 
prognostic value. 
Leukocytosis with fever and gall-stone colic as a diagnostic and prog- 
nostic feature is of but little value, for it is not constant. Pick claims 
that the intermittent fever of gall-stone colic is always due to a purulent 
infection in which he claims the presence of leukocytosis, while Grawitz 
and others have failed to confirm his observations. My experience seems 
to justify the conclusion that with gall-stone colic and persisting leukocy- 
tosis , there is as a rule complicating infection, usually cholecystitis or 
cholangitis, or both; with a high leukocytosis and repeated chills and in- 
termittent fever, suppurative cholangitis should be suspected or empyema 
of the gall-bladder. 
X-Ray Examination.—I have failed to receive aid in the diagnosis 
or prognosis of gall-stones from x-ray examination. The shadow can only 
be present when the stone contains considerable lime. Negative results 
are valueless, positive results are rare. X-ray examination can but rarely 
be relied upon. 
(b) Chronic Cholelithiasis 
The presence of gall-stones in the bile passages during long periods 
without biliary colic or only occasional acute exacerbation is possible. In 
the majority of these there are insidious changes in the tissues which sur- 
round the stone, without marked symptoms. A large proportion of such 
patients are chronic invalids; they may never appear very sick, neither 
do they ever feel perfectly well. Over one-half of all gall-stones are in 
the bladder (55.5 per cent) ; 12.5 per cent in the gall-bladder and cystic 724 
DISEASES OF THE DIGESTIVE APPARATUS 
duct; 10.5 per cent in the gall-bladder and common duct; 6.6 per cent in 
the common duct alone, and 6 per cent in the cystic duct alone (Kelly). 
The prognosis of chronic cholelithiasis depends entirely upon added 
infection, mechanical influences, and secondary changes. Chronic chole- 
lithiasis is in the overwhelming number of cases a latent condition; this 
simply means that subjective and objective symptoms may be absent 
during long periods, hut does not preclude the possibility of local changes, 
which in the end may add to the dangers or may prove conservative, with 
or without complications. 
Adhesions.—Cases of chronic cholelithiasis which during life may 
give but few or no symptoms are often found on postmortem to have 
caused extensive adhesions. In a proportion of cases adhesions prove pro- 
tective and prepare the way for the safe delivery of the stones into the 
intestines or other organs. Adhesions may materially influence symp- 
toms ; these may prove the cause of acute or chronic conditions in accord- 
ance with the organs included and the resulting distortion or occlusion. 
The organs included are the liver, stomach, duodenum, transverse colon, 
omentum, pancreas, and right kidney. The gall-stones with such compli- 
cations may be entirely overlooked in the presence of the grave secondary 
lesions. 
Pyloric obstruction, without the history of previous acute attacks or 
chronic symptoms sufficient to create the suspicion of gall-stones as the 
primary and causative condition, may develop and threaten life. Such 
cases and other mechanical defects due to adhesions which cause symptoms 
can only be saved by surgical interference. 
Cholelithiasis without colic may lead to secondary changes near or dis- 
tant which demand attention that life may be saved. The accompanying 
infection of the bile passages and gall-bladder may be either acute or 
chronic; in some cases subjective symptoms may yield during limited 
periods. Exacerbations are reasonably certain and unless there is free 
drainage one of many dangers must be faced. The recognition of the 
true condition is often difficult, and many are found septic with the heart 
and kidney deeply involved or there may be, as was recently found in the 
case of a colleague, advanced amyloid disease with disseminated liver 
infection. Such conditions are fatal; they can be prevented; and life 
may be saved by reasonably early vigorous and radical treatment. The 
further results of chronic cholelithiasis are considered in this section un- 
der the head of “Complications and Remote Results.” It is safe to con- 
clude that in latent cases which are made active by added infection, symp- 
toms will persist—are either continuous or intermittent—and the resist- 
ance of the patient will be taxed in accordance with the virulence and 
extent of the secondary changes, whether acute or chronic. The prognosis 
will, under such conditions, depend entirely upon the ability to remove 
the focus of infection and drain the bile passages. In the chronic cases DISEASES OF THE BILE PASSAGES 
725 
with acute or chronic infection, the dangers of feeble resistance, hemor- 
rhage, shock, nephritis, myocardial insufficiency, eholemia, and a variety 
of other complications materially influence the outcome. 
(c) Obstruction of the Common Duct 
Courvoisier considers gall-stones in the common duct dependent upon 
one of three possibilities: their passage to the duct from the gall-bladder, 
their entrance through the hepatic ducts, or their formation in situ. 
The majority of stones in the common duct cause only partial obstruc- 
tion. The symptoms and changes produced are dependent upon the size 
and the situation of the stone in the duct. Untreated stone in the common 
duct finally produces changes not only in the duct, but also in the gall- 
bladder, the smaller bile passages, and in the liver tissue. In the duct, 
when the passage of bile is prevented there is dilatation, and infection is 
invited. Cholangitis is usual. With small gall-stones plugging the pas- 
sage, bile may find its way into the duodenum; with a single large stone 
and secondary changes it is not uncommon to find the obstruction partial 
and bile entering the intestine. If the obstruction is complete, the jaun- 
dice is deep and unyielding. In these cases the surprising feature is the 
effect of the occlusion on the gall-bladder which is evident in most but not 
in all cases. This has been formulated and is known as the Courvoisier’s 
law: 
With obstruction of the common duct by gall-stones the gall-bladder 
does not enlarge. It is atrophied and if it holds gall-stones it is con- 
tracted upon them, while with cancer and obstruction, either within or 
without the duct, (usually there is invasion of the pancreas) the gall- 
bladder is enlarged and palpable, and atrophy results in only one-twelfth 
of the latter obstructions (Courvoisier s Law). Dilatation of the bile 
ducts behind the stone is the rule; the hepatic and intrahepatic ducts are 
often so dilated as to admit the index finger (Bland-Sutton). 
Long continued pressure of an incarcerated stone in the common duct 
or associated infection often causes ulceration with the discharge of the 
stone into the duodenum. Such outcome is favorable and in most uncom- 
plicated cases is followed by recovery and the passage of the stone. 
Nature seeks to establish “adventitious outlets’ for the bile with com- 
plete obstruction of the common duct, and thus saves life. The resulting 
fistulae afford drainage into the intestine and make the prognosis of un- 
complicated jaundice due to gall-stones favorable (ISTaunyn, Bland-Sut- 
ton). Among the more serious complications are liver abscess, suppura- 
tive cholangitis, thrombosis of the portal or other large veins, aneurism of 
the hepatic artery, septic pneumonia, empyema, and acute or chronic pan- 
creatitis. In a number of cases chronic sepsis ends life unless the cause is 
removed. 726 
DISEASES OF THE DIGESTIVE APPARATUS 
Erom the preceding statements it is apparent that gall-stones in the 
common duct may induce local changes and distant serious disturbances. 
Liver abscess due to occlusion by stone of the common duct is more likely 
to occur than with any other obstruction, and ulcerative perforation is 
comparatively frequent. With the ball valve action of a stone in the com- 
mon duct the symptoms are intermittent including the hepatic fever of 
Charcot, jaundice, and recurring biliary colic. The prognosis of such 
cases is not bad; the symptoms may recur during many years without 
materially lowering the resistance of the patient, but unless nature over- 
comes the.recurring obstruction or it is relieved by radical means, the 
prognosis for cure is unfavorable and local or distant complications may 
end life. The absence of added infection in these chronic cases for many 
years is often striking and favorable. 
(d) Obstruction ot the Cystic Duct 
Gall-stones held in the cystic duct originate in the gall-bladder; they 
may increase in size by aggregation. In 255 post mortems of gall-stone 
disease in Basel,. 17—6.7 per cent—were in the cystic duct, and in Er- 
langen there were 16 of 343—4.6 per cent (Courvoisier) 
Lawson Tait taught that the acute symptoms due to stone in the cystic 
duct were more violent than when in the common duct. This is so, Tait 
held, because of the difference in the caliber of the two tubes in most 
cases. Courvoisier and others deny the anatomic cause given by Tait 
and contend that Oehme’s measurements do not justify the former’s con- 
clusions. 
When the stone is held in the duct, dilatation of the gall-bladder usu- 
ally results. Gradual obstruction of the cystic duct by gall-stones may 
cause but few or no symptoms during considerable periods, and without 
dilatation or colic and atrophy of the gall-bladder may escape detection. 
Courvoisier reports 30 of 97 cases in which the stone was held in the cystic 
duct in which atrophy of the gall-bladder resulted. The frequency of 
atrophy of the gall-bladder (in 1/3 of all cases of stone in the cystic duct) 
has been overlooked by clinicians. 
The dilatation of the gall-bladder due to stone in the cystic duct is 
known as “dropsy of the gall-bladder“hydrops vesicae felleae” and “ec- 
tasiaIt offers an excellent prognosis when the diagnosis is followed by 
free drainage and the removal of the offender. Dilated gall-bladder re- 
sulting from cystic obstruction may reach enormous size and may simu- 
late cystic kidney, hydro- and pyo-nephrosis, and ovarian cyst. “Riedel’s 
lobe,” a tongue-shaped bit of liver connected with the right lobe, may 
project from the anterior margin and present over the enlarged gall-blad- 
der. Obstruction of the cystic duct may be borne during long periods even DISEASES OF THE BILE PASSAGES 
727 
with dilated gall-bladder. The dangers are due to infection, perforation, 
peritonitis, liver abscess, cholangitis, and acute or subacute pancreatitis. 
Small gall-stones in the cystic duct may cause enormous enlargement 
of the gall-bladder, and often larger stones may be associated with less 
dilatation. With these—one or more—the duct may dilate, adhesions re- 
sult, and because of ulceration, fistulous openings may follow into the 
stomach (cystogastric fistula), into the duodenum (cystoduodenal fistula) 
or into the transverse colon (cystocolic fistula). 
(e) Obstruction of the Hepatic Duct and Intrahepatic 
Ducts 
Gall-stones in one of the hepatic ducts, in the smaller ducts or in the 
liver substance, are almost always coincident with gall-stones in other 
passages—usually in the common duct. In 56 of 59 collected cases of 
gall-stones in the hepatic ducts there were stones in other parts of the 
liver, and in 51 cases of gall-stones in the hepatic duct there were 45 in 
which the common duct was obstructed and displaced, or there had been 
previous operations (Courvoisier). These statistics show further that in 
24 of 45 cases of hepatic duct calculi there was stone in the common duct, 
or dilatation due to previously incarcerated calculi; in 6 cases there was 
narrow constriction, and in 2 compression of the duct due to hydatid in 
one, and cancer of the pancreas in the other. 
Unquestionably the impeded flow of bile, usually because of occlusion 
of the common duct, is the powerful factor in the causation of cholelithi- 
asis, within the hepatic tree (Courvoisier). 
The prophylaxis of hepatic calculi must depend almost entirely upon 
the radical and early removal of gall-stones within the common duct and 
the prompt relief of all organic constriction. Rupture of the hepatic duct 
due to stone is not frequent, hut there are recorded cases in which death 
was prompt and in most of these there was septic peritonitis with pus ancfj 
blood in the abdominal cavity. 
Multiple or single stones are found at times in the liver substance (iru 
trahepatic ducts'), usually of the bilirubin-calcium variety (Bland-Sutton). 
This condition when multiple and disseminated, offers but little hope of 
relief by surgical means. In many cases these gall-stones cause no symp- 
toms and are recognized post mortem. In framing the prognosis of all 
gall-bladder disease it must be conceded that the long continued presence 
of gall-stones in the gall-bladder and the continuous excretion of irritating 
and poisonous products through the bile current provoke precipitation and 
gall-stone formation in the intrahepatic bile passages (William Hunter). 728 
DISEASES OF THE DIGESTIVE APPARATUS 
(f) Complications and Remote Results 
The presence of gall-stones in the bile passages is always a menace. 
Ten per cent of all autopsied bodies have gall-stones, and of this number 
95 per cent never had symptoms which suggested their presence. In 
those cases which cause symptoms, the complications and remote results 
are so numerous and far-reaching as to make their full consideration im- 
possible within the space available in this volume. Reference has been 
made to the many results of associated infection and their dangers, the 
frequency of gall-stones with or following the graver infections—typhoid 
fever, pneumonia, etc. 
In the prognosis the insidious changes which are produced in the im- 
mediate surroundings of the stone are of importance, as already shown 
in the preceding pages. These changes always depend upon a number of 
factors, the most important of which is infection. The number of stones 
held in the gall-bladder is not the important factor, for in the presence of 
hundreds of faceted gall-stones, closely packed within the thickened wall, 
there may be no subjective symptoms and no complications; on the 
other hand, with an equal number or but few stones and added infection, 
or as the result of pressure, adhesions, or from a variety of causes, life 
may be threatened by one or more of almost countless complications. The 
leading complications besides those already mentioned are referable to 
the 'peritoneum, intestines, stomach, liver, pancreas, kidney, and cardio- 
vascular system; while the vagaries and wanderings of gall-stones in indi- 
vidual cases may lead to the invasion of other organs, unsuspected, be- 
cause of their distance from the original seat of the stone. 
One fact of enormous prognostic value stands out prominently and 
that is that the protective powers—the factors of safety—are almost 
always stimulated by the presence of gall-stones by which subsequent 
complications are anticipated, and their dangers are reduced, so far 
it is possible. Such conservative effort is prominent with perfora- 
tion by gall-stones, with ulceration, with fistulous openings through 
long or short avenues. In cases of perforation or ulceration without 
protective adhesions, general or local peritonitis may often prove promptly 
fatal. 
Perforation of the gall-bladder is not frequent in spite of its enormous 
dilatation. The distended and inflamed gall-bladder may cause peritonitis 
without perforating. With such complication the acute manifestations of 
peritonitis may be absent; the course may be subacute; ascites finally de- 
velops. 
The gangrenous gall-bladder, without perforation, may at first cause 
localized peritonitis which may become diffuse unless radical surgical treat- 
ment is promptly instituted. DISEASES OF THE BILE PASSAGES 
729 
Fistulae.—Perforation into the duodenum is a frequent result of 
chronic cholelithiasis and if the stone is not too large, it passes without 
further incident; the local changes may never again cause symptoms. 
Adhesions of the gall-bladder and duodenum or pylorus may form a 
mass with symptoms of obstruction and stagnation simulating cancer of 
the stomach during indefinite periods. In one of my cases after repeated 
gall-stone colic there was a tumor simulating cancer of the stomach with 
symptoms of pyloric obstruction during 15 months; the disappearance of 
the tumor was promptly followed by intestinal obstruction, the passage per 
rectum of an enormous gall-stone weighing 15 grams (240 grains) 5 cm. 
(2 inches) long and 7.5 cm. (3 inches) in circumference (Eisner). The 
simulation of pyloric cancer by gall-stones is not without parallel; in most 
reported cases the prognosis proved to be good. Life was saved either by 
surgical interference or by ulceration, as in our case, and the passage of 
the stone (Pepper, Miles, Fiedler, Ross, Hale White, Ogle and Cour- 
voisier). 
The wanderings of gall-stones, their vagaries, and the protection offered 
by adhesions are often surprising. The distance to which stones may 
travel is often remarkable. I have accumulated a large number of his- 
tories with post mortem examinations which prove the remarkable toler- 
ance of the aberrant gall-stones in new locations (Eisner). 
The route from the gall-bladder into the duodenum by protective adhe- 
sions first, and then ulceration, is almost as frequent as the external or 
cutaneous fistula. 
fSTaunyn’s material offers the following figures: 
/ 
Cutaneous fistulae, usually opening near the umbilicus 184 
Gastrointestinal fistulae 108 
Fistulae between the common duct and duodenum 15 
Courvoisier found perforation directly into the peritoneum in 70 of 
119 cases, and in 49 the free peritoneum was protected by an encapsulated 
abscess. 
My material included the case above mentioned of enormous stone 
which for 15 months caused symptoms of pyloric obstruction and final 
intestinal obstruction after it traveled down the intestine. In this case 
the symptoms of intestinal obstruction were complete, operation was de- 
cided upon, and while the preparations were being made the stone passed 
spontaneously per rectum. The patient made a full recovery after passing 
a second larger stone several weeks after the first. 
Infectious cholecystitis, cholangitis, empyema of the gall-bladder due 
to gall-stones in another case, were associated with complete obliteration 
of the cystic and common ducts with probable primary duodenal ulcer in 
which there was burrowing of the stone into a bed of fibrous tissue pro- 730 
DISEASES OF THE DIGESTIVE APPARATUS 
vided by nature. This patient made a full recovery after cholecystotomy 
and final choledochoduodenostomy. 
Another experience less favorable was the wandering of a larger gall- 
stone through a fistulous opening with numerous dilatations into the retro- 
peritoneal space lodging finally in pancreatic tissue. Pancreatic cancer 
was simulated during several months. The post mortem cleared the 
horizon. 
Migration of gall-stones with or without abscess formation into the 
right lcidney, with repeated attacks of renal colic, in one of my cases ended 
in the death of the patient. Courvoisier collected seven cases of urinary 
fistulae associated with gall-stones; six of these were in women. Pelleton 
and Barraud report two hundred gall-stones passed by a woman per ure- 
thram in eight days. The last stone was caught in the urethra, but was 
easily pushed on from the vagina. The patient recovered. 
The histories of similar cases are included in Langenbuch’s material, 
and prove the tolerance and protective methods of nature and the rela- 
tively good prognosis. Patients with biliary (cutaneous) fistulae may 
live during many years and finally die of intercurrent disease or infection. 
In some of these cases the fistula may close during varying periods, finally 
open to allow the escape of one or more stones, or remain permanently 
closed. The long continued presence of gall-stones may lead to such enor- 
mous dilatation, distortion, and adhesions with aberrance of gall-stones as 
to preclude the possibility of operation. Such patients may live during 
long periods barring accident due to the gall-stone disease, but with added 
infection the prognosis is bad. 
Bronchobiliary Fistulae.—Gall-stones may cause fistulous opening into 
a bronchus through an abscess following infectious cholangitis, adhesions 
of the diaphragm and the lung and rupture into the latter, or as Rolleston 
suggests the perforation may be into the pleura primarily, and then into 
the lung. Subphrenic abscess may result from perforation of the gall- 
bladder and from this opening into the diaphragm, and finally into the 
lung results. Mandard reports the perforation of the gall-bladder directly 
through the diaphragm into the lung. Recovery from hronchobiliary fis- 
tula is often spontaneous; once healed the tract is not likely to reopen, but 
relapse may occur. The removal of the primary focus where possible is 
likely to lead to cure. 
Ulceration into the portal vein and into the hepatic artery are rare 
accidents, but it does occasionally happen and with fatal results. Ivehr’s 
case mentioned in connection with aneurism of the hepatic artery was an 
exception. 
Chronic cholelithiasis with added chronic infection, continuous or in- 
termittent, is unquestionably instrumental in inviting arterial and rerml 
degeneration. 
The frequency of arteriosclerosis and interstitial nephritis with gall- DISEASES OF THE BILE PASSAGES 
731 
stones is striking and not accidental. Mosher found that of 115 cases of 
cholelithiasis, 50 or 43 per cent had arteriosclerosis. Moore has shown 
that interstitial nephritis increases the liability to cholelithiasis in women. 
Moore’s statistics are exceedingly valuable and we quote them: 
“In 261 cases of granular kidney with an average age of 56 years, 
there were gall-stones in 56, or 21.4 per cent (average age, 59 years). In 
49 cases of large white kidney, with an average age of 40, there were 
gall-stones in 2, or 4 per cent; and in 47 cases of small white kidney, with 
an average age of 34 years, gall-stones were present in 1, or 2 per cent. 
The greater incidence among the cases of granular kidney does not, as 
might at first sight appear, depend on the greater average age alone; for 
among the 261 cases of granular kidney there were 36 between the ages of 
32 and 42 (thus including with a margin the average ages of the large 
white and small white kidneys), in 6 of which, or 16.7 per cent, there 
were gall-stones. Of these 36 cases, 11 were women, 4 of whom had 
gall-stones—or 36 per cent—and 25 men, 2 of whom—8 per cent—had 
gall-stones. Of the remaining 225 cases of granular kidney there were 
138 men, 21 of whom—15.2 per cent—had calculi, and 87 women, 29 
of whom-—33.3 per cent—had calculi. The increased incidence of gall- 
stones in granular kidney therefore appears to he due to the high inci- 
dence of cholelithiasis in women with granular kidney. In the 261 cases 
of granular kidney the women were to the men as 3 to 5. The incidence 
of gall-stones in the 98 women was 33 per cent, and in 100 consecutive 
women over 40, dying in St. George’s Hospital from all kinds of diseases, 
the incidence of gall-stones was 25 per cent.” 
In all of these cases the prognosis is darkened by the associated and 
progressive myocarditis. Endocarditis is a frequent association. The 
association of pancreatic disease with cholelithiasis is fully considered 
with the prognosis of pancreatitis (See Pancreatic Diseases). 
The long continued irritation due to gall-stones unquestionably leads 
to cancerous degeneration of the organ harboring it, but it cannot be 
assumed that malignant disease in distant organs is stimulated by the 
presence of gall-stones. Cancer will be found associated with gall-stones 
in 2.25 per cent of operated cases. 
Intestinal Obstruction.—Obstruction by gall-stones may be either 
complete or partial. In most cases with a stone of sufficient size to cause 
intestinal obstruction there is a palpable tumor which disappears from 
its original habitat and wanders on until it is caught in the intestine, 
causing during varying periods depending upon the degree of obstruction 
and the acuteness of its onset, a train of characteristic symptoms with 
visible peristaltic unrest, particularly if the obstruction is partial. Sud- 
den acute complete occlusion is at once life-threatening, and can only be 
relieved as a rule by prompt surgical treatment. There are exceptions to 
this statement, but in the light of the experiences of the present day, 732 
DISEASES OF THE DIGESTIVE APPARATUS 
including the results of surgical operation, it is unfair to the patient to 
reach a conclusion which would justify procrastination in these cases. 
When large stones pass from the gall-hladder into the intestines, 
ileus or obstruction is to he expected in almost 40 per cent of such cases. 
Courvoisier reports ileus in 28 of 73 cases—38.3 per cent. The majority 
of stones are dislodged and pass per rectum. The prognosis is more seri- 
ous when ileus follows gall-bladder duodenal fistulae than when the open- 
ing is into the colon. Of 30 fatal cases 22 were due to gall-bladder 
duodenal fistula, and only 2 to gall-bladder colon perforation (Haunyn). 
If a gall-stone finds its way into the duodenum through the common duct 
there is but little danger of intestinal obstruction. Symptoms of intes- 
tinal obstruction with changing position of the mass prove that the stone 
is being pushed by peristalsis; in such cases the prognosis is good. 
Robson says: “If it were possible to be certain that a gall-stone was the 
cause of the block, the expectant form of treatment would be fully jus- 
tified, since the probability, arguing from published cases, is that the 
gall-stone would eventually pass.” 
Cases in which there are “diagnostic difficulties” throw an enormous 
responsibility on the surgeon if he waits for nature’s cure. It is true 
that 50 per cent at least of the cases recover without operation, that the 
obstruction may not yield for several days; Gray reports one case in 
which the stone was dislodged after 12 days, with full recovery. The 
encouragement which such experiences strengthen leaves the remaining 
50 per cent seriously handicapped and the majority of these are therefore 
operated after necrosis of the intestinal wall, and circumscribed or dif- 
fuse peritonitis are fully developed. Langenbuch takes the extreme view 
which seems justified in these days of splendid technic and early opera- 
tion and makes the unqualified statement that “gall-stone obstruction is 
a surgical disease, the treatment of which is to be entrusted to the physi- 
cian only during a very short period,” if the prognosis is to be favorable. 
A diverticulum containing a stone may be associated with mechanical 
obstruction of the intestine. Gangrene may follow. Gall-stones may find 
their way into Meckel’s diverticulum and into the appendix. In both 
infection is invited, and unless relieved serious results are likely to follow. 
Hemorrhage.—In many cases of prolonged obstruction of the common 
duct with jaundice, the blood condition invites hemorrhage and often 
makes operation hazardous. The prognosis of gall-stone operations on 
such patients as show the hemorrhagic tendency is often favorably influ- 
enced by preparatory treatment, including the injection (secundum 
artem) of blood serum—preferably rabbit serum—after the question of 
possible anaphylaxis has been thoroughly considered. 
Symptoms referable to the nervous system usually yield with the 
removal of the stone, but persistent jaundice due to long continued gall- 
stone impaction may cause alarming brain symptoms and occasionally DISEASES OF THE BILE PASSAGES 
733 
insanity. One of my patients, an old man, became violently insane, but 
was relieved after a cholecystotomy. In another case prolonged cholemia 
due to obstruction of the common duct caused confusional insanity. 
Surgery and Cholelithiasis 
In considering the prognosis of gall-stone disease our conclusions must 
he materially influenced hy the brilliant results of surgery in the radical 
treatment of diseases of the gall-bladder and biliary passages. Early 
operations in uncomplicated cases “is an innocent and simple operative 
procedure” (Jacobson). W. J. Mayo giving his experiences in 4,000 
operations on the gall-bladder and biliary passages which he and his 
brother have performed, found the average mortality 2.75 per cent; 11 
per cent of the total number of deaths occurred in patients with cancer. 
The Mayo experience proves that “simple operation for uncomplicated 
gall-stones has had a mortality of less than 0.5 per cent, and this might 
he called accidental, since it was due to the condition of the patient rather 
than to the operation.” 
“Fatalities can be traced in almost every instance to delay.” My 
conclusions justify the accentuation of the fact in spite of the escape of 
the majority who harbor gall-stones that in the bile passages they are 
always a menace, not only to the organ which harbors them, hut they may 
suddenly or gradually lead to pathological processes, benign or malignant, 
near or distant, giving rise to unexpected and serious conditions. As 
I have elsewhere in this section remarked, a large number of patients 
with indefinite symptoms are suffering from chronic infection with gall- 
stones. In almost all radical treament- is followed by a return to health. 
References 
Aschoff & Backmeister. Die Cholelithiasis. Jena, 1909. 
Bland (Sutton). Gall-stone and bile ducts. New York, 1907. 
Courvoisier. Path. u. Chir. d. Gallenwege Leipzig, 1890. 
Eisner (Henry L.). The vagaries and wanderings of gall-stones. 
Tr. Med. Soc. State of New York, 1898; Medical News, 1898, i. 
Fiedler. Wiener Med. Blatter, 1880, No. 49. 
Gilbert & Girode. Le Semain Medicale, 1890, No. 58. 
Grawitz. Klin. Path, des Blutes. Leipzig, 1906. 3. Aufl. 
Gray. Tr. London Clinical Soc., vol. iv, p. 194- 
Grube & Graff. Die Gallensteinkrank. Jena, 1912. 
Hansemann. Virchow's Archiv f. Path. Anat. etc., Bd. ccxii, H. I, p. 139. 
Hofbauer. Med. Klinik, 1909, p. 239. 
Ztschr. f. Geburtsh. u. Gynak., 1998, Bd. Ixi. 
Hunter (Wm.). Brit. Med. J., 1897, ii. 
Jacobson (N.). Am. J. Med. Sd., July, 1914. 734 
DISEASES OF THE DIGESTIVE APPARATUS 
Kehr. 3. Jahre Gallensteinchirurgie. 1908, p. 574. 
Kelly {A. O. J.). System of medicine {Osier and M’Crae), 1908, vol. v, p. 831. 
Langenbuch. Chir. d. Leber u. Gallenblase. Stuttgart, 1897. 
Mandard. These de Paris, 1854. Quoted by Naunyn & Rolleston. 
Mayo {W. J.). Collected papers by the Staff of St. Mary’s Hosp., Mayo Clinic, Philadelphia, 
1911, p. 148 & 144- 
Miles. Lancet, London, 1861, vol. i. 
Moore {A. W.). Quoted by Rolleston [Z. c.]. 
Unpublished Thesis for M. B. Cantab. 1906. 
Mosher. Johns Hopkins Hospital Bull., Baltimore, 1901, xii, p. 253. 
Naunyn. Cholelithiasis. Leipzig, 1892. 
Grenzgeb. d. Med. u. Chir., 1905, Bd. xiv. 
Netter. Progres Medical, 1886, No. 46. 
Oehme. Quoted by Courvoisier [Z. c.], p. 27. 
Ogle. St. George’s Hosp. Reports, 1868. 
Pelleton & Barraud. J. de Chemie Med. de Pharm. et de Toxic, II. Ser., T. 2., 1836, pp. 
593-600, 653-669. 
Pepper. Am. J. Med. Sci., 1857, vol. xxx, p. 18. 
Pick. Beitr. z. inner. Med., Leipzig, 1900. 
Riesman. Am. J. Med. Sci., Nov., 1911. 
Robson {Mayo). Diseases of the gall-bladder. 3d ed. 1904. 
Ross. Brit. Med. J., 1885, vol. i, p. 25. 
Sittman. Deutsch. Arch. f. Iclin. Med., 1894, Bd. liii, p. 323. 
White {Hale). Tr. Path. Soc., London, 1886, vol. xxxvii, p. 280. 
L. Diseases of the Pancreas 
1. Pancreatitis 
Pancreatitis may be either (a) acute or (b) chronic. 
(a) Acute Pancreatitis 
Acute pancreatitis is almost always hemorrhagic, and the varieties 
which are characterized as gangrenous and suppurative pancreatitis are 
not independent conditions—ab initio—but represent the advanced stage 
of hemorrhagic pancreatitis. Gall-stone disease is the leading provoking 
factor; traumatism and alcoholic excess with local lesions are also etio- 
logic factors. Most cases are in men above the ages of fifty years. 
Deaver says: “The common bile duct is the crucial point of the whole 
biliary system, as it is the outlet for the biliary secretion and by its 
anatomic relations wields an important influence over the pancreatic func- 
tion. The pancreatic portion (of the common bile duct) lies in a groove 
in the posterior surface of the head of the pancreas and extends from 
the inferior border of the first portion of the duodenum to a point where DISEASES OF THE PANCREAS 
735 
the duct enters the wall of the descending or second portion of the 
duodenum. In two-thirds of the subjects this portion of the bile duct is 
completely surrounded by pancreatic tissue.” “The opening of the com- 
mon duct is usually above that of the duct of Wirsung.” The two are 
separated by a thin layer of mucous membrane. The duct of Santorini 
is “always present and anastomosis with the duct of Wirsung within the 
pancreas is about 90 per cent of cases.” In 50 per cent of all cases the 
duct of Santorini is obliterated or constricted; hence when the duct of 
Wirsung is closed, it cannot under such conditions assume its functions. 
Usually the common bile duct and the duct of Wirsung open at the am- 
pulla of Vater. “The apex is situated at the summit of the diverticulum 
and is their common duodenal orifice.” It is easy therefore under 
anomalous conditions of the mucosa for the bile and intestinal content to 
find its way to the pancreas. Occlusion of the ampulla (papilla) of 
Vater by a gall-stone, a plug of mucus, or because of catarrhal swelling 
or cicatricial change following ulcer, may turn the bile into the pan- 
creatic duct and lead to pancreatitis. Unless the duct of Santorini is 
patent there is no means of escape; Opie found this to obtain in less than 
50 per cent of his cases. 
Traumatism may cause the sudden development of acute hemorrhagic 
'pancreatitis. In these cases the evidence of shock and collapse with 
symptoms which simulate acute peritonitis, with great abdominal pain—• 
at times symptoms of intestinal obstruction—without fecal vomiting, and 
hut little or no fever and rapid pulse, at once prove the gravity of the 
condition. When there is a large loss of blood the patient may not rally. 
The average duration of life is between 2 and 3 days. I had one case 
in which there was arteriosclerosis with advanced disease of the abdom- 
inal aorta and rupture of the pancreatic vessel; the hemorrhage was large, 
the symptoms simulated intestinal obstruction during the first 24 hours; 
the patient lived between 12 and 13 days. The diagnosis of hemorrhagic 
pancreatitis was corroborated post mortem. In cases of gastroduodenal 
catarrh usually recurrent, which may or may not be associated with gall- 
stones or cholangitis, pancreatitis may develop. These cases at times 
show gangrene of circumscribed portions of the gland. The bleeding is 
not always limited to the pancreas but the surrounding tissues may he 
infiltrated, particularly the fat tissue including the mesentery, mesocolon 
and omentum, also the regions of the left kidney (Fitz and Wood). 
With hemorrhagic gangrenous pancreatitis there may he localized 
peritonitis; diffuse peritonitis is the exception. Disseminated fat necrosis 
is a frequent complication of pancreatitis. Fat necrosis which is con- 
sidered pathognomonic of acute pancreatitis depends upon the ferment 
action upon the gland and its secretion (trypsin) when there is obstruc- 
tion to its outflow. The fat necroses may be widely spread throughout 
the omentum, mesentery and the fat tissue of the body. 736 
DISEASES OF THE DIGESTIVE APPARATUS 
Suppurative pancreatitis may follow the hemorrhagic, complicate it, 
and involve the adjoining tissues, thus converting the lesser omentum into 
an abscess cavity. This may rupture in one of several directions, usually 
into the stomach or duodenum, or form a suhphrenic abscess. 
Secondary infection may involve the veins, causing purulent throm- 
bosis or abscess of the liver; the pleura and pericardium are occasionally 
involved; perforative peritonitis is rare. 
Hemorrhagic gangrenous pancreatitis is always a grave disease, and 
usually causes death from shock within 24 to 60 hours. If patients with 
hemorrhagic pancreatitis live and develop gangrene they become pro- 
foundly septic, and die within 4 to 8 weeks. 
Suppurative pancreatitis may become chronic, the patients living 
several months or longer with evidences of sepsis and diabetes. Fitz 
feels that his experience justifies the statement that “the prognosis is 
not absolutely hopeless however, since evidences of antecedent pancreatitis 
have been found repeatedly at post mortem examination.” The self- 
digestion of the gland (by trypsin) is an important factor. The value of 
the Cammidge test is questionable for diagnosis and prognosis. Cam- 
midge holds that the reaction is positive in acute pancreatitis and that it 
makes the differentiation of intestinal obstruction possible and that 
chronic pancreatitis can he differentiated from gall-stones. Osier says 
“the reaction is negative in about three-fourths of malignant disease.” 
Reports from the Mayo clinic offered by Wilson led him to the conclusion 
that without the clinical histories and other factors “the end results 
judged by Cammidge’s own criterion must he considered as a means of 
diagnosing disease of the pancreas, as both valueless and misleading.” 
T do not recommend its consideration for prognostic purposes. (The 
method of carrying out the test is fully given by Latham and Torrens. 
See References at end of chapter.) 
The prognosis of the acute cases depends largely upon the ability of 
the surgeon to remove or overcome the primary cause. Where this can 
be accomplished the early operation offers considerable hope. Much will 
depend on the discriminating sense of the surgeon in deciding upon the 
opportune time for operation. Concerted action of the physician and 
surgeon will always be necessary from the moment of diagnosis or sus- 
picion of pancreatitis. 
Deaver has called attention to the importance of pancreatic and peri- 
pancreatic lymphangitis, and believes that certain cases of acute hemor- 
rhagic pancreatitis are due to infection of lymphatic origin. 
(6) Chronic Pancreatitis 
There are a variety of causes of chronic pancreatitis. Among these 
are chronic or recurrent gastro-intestinal catarrh, gall-stones, chronic DISEASES OF THE PANCREAS 
737 
alcoholism, obstruction to the pancreatic duct from pressure without, or 
organic change within, calculi, neoplasms, cicatricial change and adhe- 
sions due to ulcers of the stomach or duodenum; Fitz mentions caries of 
the spine and aneurism, and in infants congenital syphilis. Typhoid, 
colon and streptococcus infection have also been responsible. 
Sclerosis of the head of the 'pancreas resembling cancer is not un- 
common. The disease may be either interlobular or interacinar. In the 
former, the sclerotic change rarely includes the islands of Langerhans, 
in the latter (interacinar) there is productive change between the acini 
without much inclusion of the interlobular tissue. Arteriosclerosis may 
also cause interstitial chronic changes in the pancreas. 
Diabetes mellitus is often due to fibrosis of the pancreas (See Dia- 
betes Mellitus and the Pancreas). Chronic pancreatitis often causes 
indefinite symptoms of ill health with faulty digestion and anorexia, fat 
stools (not pathognomonic), some jaundice, abdominal pain during long 
periods. In another class of cases there are persistent symptoms of 
chronic gastritis. If the disease advances, diabetes is fairly certain to 
develop; it may develop early. There are cases which remain stationary. 
The productive changes cannot be overcome; if the atrophy is advanced 
and the islands of Langerhans are included, life as a rule is threatened. 
Fitz holds that permanent glycosuria and chronic pancreatitis is a fatal 
combination (See Diabetes Mellitus). 
2. Hemorrhage 
(.Pancreatic Apoplexy) 
It is exceedingly difficult to differentiate hemorrhage and hemorrhagic 
pancreatitis. There are cases in which, without warning, there is a 
sudden and depleting hemorrhage into the pancreas with prompt death. 
With the purpuras we occasionally meet such an accident, also with 
arteriosclerosis, the acute infections, with chronic alcoholism, and cir- 
rhosis of the liver. Fatal hemorrhage may occur during the early hours 
of acute pancreatitis; it may develop suddenly with gangrene during the 
terminal stage of hemorrhagic pancreatitis. The prognosis of hemor- 
rhage depends upon the extent of the bleeding, the damage to the gland, 
the resistance of the patient, and the cause. There are probably many 
small hemorrhages into the pancreas which cause no symptoms, but gen- 
erally the prognosis of pancreatic hemorrhage may be considered grave 
and the majority die before the end of 48 hours. In one of my cases 
the patient died within 3 hours. His initial symptom was severe epi- 
gastric pain, sudden collapse; there was no radial pulse palpable for over 
2 hours before death. Those who live beyond the period of collapse face 
the dangers of acute pancreatitis. 738 
DISEASES OF THE DIGESTIVE APPARATUS 
3. Necrosis of the Pancreas 
We have referred to fat necrosis in connection with acute pancreatitis. 
Eat necrosis may accompany any of the diseases of the pancreas because 
of self-digestion. Fat necrosis is comparatively frequent after trau- 
matism. The condition is said by Minkowski to be more frequent in 
advanced life. Its leading clinical features are sudden and progressive 
symptoms which are suggestive of perforative peritonitis which lead to 
death in from 24 to 72 hours. 
When fat necrosis is limited, patients may live during several weeks, 
but this is the exception. Large necrotic foci or destruction of the entire 
'pancreatic tissue are uniformly fatal. Recrosis may precede suppura- 
tion (abscess). In the mild and circumscribed cases, the tolerance for 
sugar is found reduced—a symptom of diagnostic and prognostic value. 
Pancreatic necrosis is never to be lightly regarded. Recovery from 
the initial collapse should not delude the attendant to believe that an 
absolutely favorable prognosis is justified, for following this there may 
be fever, deep toxemia, and finally cardiac asthenia. Surgery offers the 
only hope in most cases. 
4. Pancreatic Calculi 
We rarely see pancreatic calculi. Medical literature gives compara- 
tively few histories of the disease. The chemical constituents are car- 
bonate and phosphate of lime. The origin of these stones (they are 
usually multiple) is due to stasis and infection. A number of the cases 
will be accidentally discovered post mortem. Some have escaped during 
severe colic. When they remain in situ they may cause secondary changes 
characteristic of chronic fibrotic pancreatitis, cysts, and abscesses; some 
hold that their continued irritation may cause carcinoma ( ?). With 
symptoms justifying the suspicion of their presence and continuous ill 
health, surgery offers hope of successful removal. 
5. Pancreatic Cysts 
The clinical experiences of Korte who reported 121 cases operated, 
60 males and 56 females, showed over half beyond 40 years of age. 
Pancreatic cysts have been found in early life—no age is exempt. 
Cysts which arise suddenly after traumatism, promptly recognized 
and operated early, offer, in the absence of complications, an excellent 
prognosis. Cystic tumors developing in the midst or as a sequel of infec- 
tion, or with evidences of active inflammatory change, are less favorable, 
but many of these yield to radical treatment. There are cases with the 
history of surprising chronicity in which the cause is unknown which DISEASES OF THE PANCREAS 
739 
live during many years. Korte classifies pancreatic cysts as (a) reten- 
tion (due to occlusion of the main duct), (b) proliferation (cysto- 
adenoina), (c) retention cysts (alveolar and smaller duct obstruction), 
and (d) false cysts. 
The anatomic location of the cyst between the stomach and transverse 
colon may be demonstrated by means of the Rontgen rays in most cases, 
and by physical examination. It is possible when there is not complete 
occlusion that the cyst may empty itself from time to time. The dangers 
are pressure symptoms, hemorrhagic or chronic pancreatitis, with fat 
necrosis, exhaustion, and final permanent glycosuria. Surgery saves over 
90 per cent of cysts. The possibility of self-cure in the presence of a 
positive diagnosis ought not to exclude radical treatment. 
6. Pancreatic Neoplasms 
Cancer of the head of the pancreas is the most frequent neoplasm, 
and develops after the age of 40. In these cases jaundice, loss of flesh, 
palpable tumor, at times inordinate appetite and ascites, are the lead- 
ing features. Diabetes has complicated some. In {5,300 cases of in- 
ternal disease I have had three pancreatic cancers. At the Allgemeine 
Krankenhaus in Vienna among 18,069 post mortems, 22 cases of cancer 
of the pancreas were found. Hale White found 20 cases in 6,000 autop- 
sies. Osier reports in 1,500 autopsies at the Johns Hopkins Hospital 
6 adeno-carcinoma, and one doubtful case, with 8 cases of secondary 
malignant deposits in the pancreas. 
Prominent among the symptoms was persistent salivation with a dry 
glazed tongue and, as above suggested, an inordinate appetite. Food, 
however much is taken, does not prevent the progressive loss of flesh and 
increasing enfeeblement. Jaundice remains, “does not disappear at any 
time”; deep jaundice and petechiae are terminal symptoms. 
I have never in my practice seen a sarcoma of the pancreas. 
Tuberculosis of the pancreas is considered among the infections (See 
Section I). 
Syphilis of the pancreas is also considered with visceral syphilis 
(Section I). 
Prognosis of cancer is clouded by the fact that in almost all cases 
the diagnosis is not made until the disease has advanced. Early recogni- 
tion and prompt operation offers the only hope. 
References 
Deaver. Archives of Diagnosis. 1912, No. 5, p. 1-13. 
Fitz. Boston Med. & Surg. J., 1889, cxx. 
Fitz & Wood. The practice of medicine. Philadelphia, 1897. 740 
DISEASES OF THE DIGESTIVE APPARATUS 
Korte. Injuries and diseases of the pancreas. In: Bergman's System of practical surgery. 
1904, iv, p. 718-739. 
Latham & Torrens. Medical diagnosis. New York, 1915. 
Minkowski, von Mehring u. Krehl’s Lehrbuch der Inneren Medizin. Jena, 1913. 
Opie. Etiology of acute hemorrhagic pancreatitis. Baltimore, 1901. Am. J. Med. Sci., 
1901, cxxi. 
Diseases of the pancreas, Philadelphia, 1903. 
Osier. Practice of medicine. 8th ed. 1914. 
White {Hale). Diseases of the pancreas. Guy's Hosp. Reports, 1897, London, 1900, liv, 
p. 17-63. 
Wilson. Mayo Clinic Report, 1911. Section VI 
Diseases of the Kidney 
Anomalies of the Urinary Secretion 
The Prognostic Significance of : 
(a) Albuminuria 
General Considerations.—Scarcely a chapter in this work fails to 
impress the reader with the fact that albuminuria is frequent and symp- 
tomatic; to understand its clinical significance fully demands close inves- 
tigation of all that the individual case offers. Its prognostic significance 
cannot be determined without a full consideration of the associated 
urinary changes; indeed, the microscopic picture is always more impor- 
tant than is the chemical, and with many acute and chronic diseases in 
the presence of albuminuria, the functionating ability of the kidneys 
and heart, the ability to prevent renal insufficiency and other complica- 
tions are among the leading and most important factors. 
Albuminuria is the 'presence of serum albumin in the urine. With 
serum albumin there is always an admixture of serum globulin; the latter 
is of but little prognostic significance in most cases. No attempt has yet 
been successful to take advantage of the varying ratio of serum albumin 
to globulin as an aid in the prognosis of disease. The quotient is so 
variable according to Paton—from 0.6 to 39—“as to deprive it of much 
prognostic value” (Dixon Mann). 
There are surprising variations in cases of benign nephritis without 
clinical evidences of increase of symptoms, without evidences in the 
clinical history of increasing change in the glomerular apparatus; while 
occasionally it has been found that during the terminal stage of nephritis 
there is a striking and continuous increase of globulin in the urine. 
Mann believes that this is due to “denudation of some of the tubular 
walls. Under these conditions the excess of globulin usually indicates 
that the end is near.” With amyloid kidney there is often a preponder- 
ance of globulin over serum albumin (Senator, Joachim) ; there are cases 
741 742 
DISEASES OF THE KIDNEY 
in which the opposite is true (Noel Patou, Petri). In all of these the 
process is secondary and fatal. 
Nicholas Cotugno toward the end of the eighteenth century (1770) 
called attention to the coagulation of the urine in certain forms of dropsy. 
Early in the nineteenth century Richard Bright, one of the three geniuses 
of Guy’s Hospital (the others were Addison and Hodgkins, 1827 ) clearly 
demonstrated to the profession, the clinical and prognostic significance 
of albumin loss with the urine in certain conditions, associated more par- 
ticularly with the dropsies. Normal urine contains an unrecognizable 
infinitesimal trace of albumin. 
Eor diagnostic purposes it is sufficient to recognize two varieties of 
albuminuria: 
(1) False Albuminuria. 
(2) True Albuminuria. 
When albumin is demonstrated by the, usual tests it should be core- 
si dered abnormal. 
(1) False Albuminuria.—With false albuminuria the albumin finds 
entrance to the urine outside the tubular apparatus of the kidney; it is 
therefore proper to consider it to be of extra-renal origin. The leading 
sources of extra-renal or false albuminuria are from the genito-urinary 
tract, including the kidney pelvis to the meatus urinarius. The majority 
of such albuminurias are surgical, due to stone (pyelitis calculosa), blad- 
der and ureteral lesions, including cystitis, gonorrhea and leukorrhea, 
menstrual discharge, etc. 
(2) True Albuminuria.—True albuminuria may be either (a) 
hematogenous, (b) parenchymatous or (c) vascular. 
(a) Hematogenous albuminuria is due to alterations in the diffusi- 
bility of the blood, more particularly the blood albuminoids, owing to 
changes in the salts of the blood or the alkalinity of the serum; it is 
never due to the excretion of undigested or partly digested albumin from 
the food. 
(b) Parenchymatous albuminuria is due to changes in the glomerular 
and tubular apparatus of the kidney. 
(c) Vascular albuminuria is due to changes in the walls of the renal 
vessels (glomerular apparatus) which may be affected by toxic agents, 
inflammatory conditions, vasomotor changes, or altered blood pressure. 
Physiological Albuminuria 
The statement is above made that albumin is always present in normal 
urine, but I must again accent the fact that ivhen its presence is madet 
clear by the ordinary tests used in the laboratory of the clinician it should 
be considered abnormal if it is persistent or recurs on slight cause. For 
prognosis it should be remembered that the diagnosis of physiological ANOMALIES OF THE URINARY SECRETION 
743 
albuminuria is not justified except with moderate albuminuria without 
symptoms of disease, without dropsy, without heart changes and without 
arterial lesions (Leube’s rule). 
Albuminuria in normal newborn infants is of common occurrence. 
Heller found it at least once in each of 31 normal infants. Franz and 
von Reuss have graphically demonstrated the frequency of albumin dur- 
ing the first few days of life. 
The acute clinical observer may at long intervals feel justified in 
diagnosticating “physiological albuminuria” and prognosticate accord- 
ingly, but experience will prove exceptional in which close observation 
with recurring albuminuria finally justifies the diagnosis, for in the end 
the majority of such diagnoses are changed to chronic nephritis. Even 
the occasional presence of albumin in the urine, in suspected cases, which 
has been voided before the patient arises, never justifies the diagnosis of 
physiological albuminuria; such cases are, when of renal origin, an ex- 
pression of true nephritis. Granger Stewart wrote: “Led by the con- 
tradictory results I experimented anew and concluded if albumin is 
present in healthy people it was barely discernible after delicate tests, 
even after concentration of the urine; if present it is accounted for by 
transudation with the urine, or from epithelia or other cellular elements 
from the genito-urinary tract.” 
It cannot be denied that active exercise in otherwise healthy indi- 
viduals may cause transitory albuminuria, bid even such cases should be 
carefully studied before a prognosis is justified which has its basis on 
the diagnosis of physiological albuminuria. Leube, it is true, found of 
119 soldiers 4 per cent with albuminuria on arising in the morning, and 
16 per cent of these showed albuminuria after a morning march. These 
figures—4 per cent of albuminurias—correspond very closely with the 
results of the urine analysis of life insurance applicants which we have 
made and in which as a rule true albuminuria was finally found to be of 
renal (nephritic) origin. 
For diagnostic as well as prognostic purposes, “physiologic albu- 
minuria” may well be considered a misnomer. Crofton agrees and says: 
“I consider this term a misnomer, for a biologic phenomenon because it 
is innocent need not therefore be physiological. It is better always to 
regard the excretion of serum albumin as a pathological phenomenon.” 
In the end, in the prognosis of these unexplained and supposedly innocent 
albuminurias in which positive evidences of kidney lesion are absent, 
some toxic or nutritional fault should be suspected if the urine repeat- 
edly shows the presence of albumin. 
Albuminuria following exercise, cold bathing, emotion, chilling of the 
surface, epileptic seizures, or indigestion will rarely prove to be “physi- 
ologic” but will be found to depend upon transitory circulatory disturb- 
ances or metabolic faults which are usually toxic. For the purposes of 744 
DISEASES OF THE KIDNEY 
prognosis in these cases the results of experience prove the reliability of 
Osier’s conclusion that “the cause must be something unusual and exces- 
sive—as a very hard tramp, a football match, a race, etc.” When albumi- 
nuria without other evidences of renal change recurs at long or short inter- 
vals even without casts, for which no extra-renal cause exists, it is always 
suggestive of change in the kidney and in the majority of such cases asso- 
ciated conditions finally make the diagnosis positive. 
Renal albuminuria without casts is most frequent in young adults. 
It is not a symptom always of incipient nephritis but often evidence of 
lowered resistance and predisposition to infection (tuberculosis). The 
death rate is higher than among normal subjects (Barringer, Jr., and 
Warren). It should be remembered that the most severe forms of neph- 
ritis are those with but little or no albuminuria and few or no casts (See 
Casts and Interstitial Nephritis). The quantitative loss of albumin is 
not, as a rule, in proportion to the severity of the underlying disease— 
large loss often offers a better prognosis than does the small trace with 
evidences of arteriosclerotic disease. Young subjects with albuminuria 
of indefinite origin are less likely to develop chronic nephritis ultimately 
than are those beyond twenty-five. At middle life the possibility of 
nephritis is increased with recurring albuminuria with or without casts. 
With casts the diagnosis of nephritis is materially strengthened. We 
are not referring to cases in which, for instance, in the course of an ex- 
amination for life insurance, on a single occasion, or during a day or 
two, transient causes provoked temporary albuminuria, nor to the albu- 
minurias which have resulted from acute poisoning or febrile disturbances, 
but to those albuminurias for which there seems to be no adequate cause 
but which recur on slight provocation. Before any albuminuria can be 
interpreted as being insignificant, the blood state, the arterial tree and 
heart, including the blood pressure, demand full consideration. There 
are functional or so-called physiological albuminurias, but they are ex- 
ceedingly rare. 
Cyclic Albuminuria. 
Orthostatic-Postural Albuminuria 
With orthostatic or postural albuminuria the albumin presence is 
dependent upon changes in the position of the body—the upright posture 
of the trunk or muscular fatigue. 
In these cases the albuminuria is more or less “cyclic.” The urine 
voided before or on arising in the morning is albumin free; after even 
moderate exercise during the morning hours albumin is present and the 
loss is likely to be greater during the early afternoon hours, in some cases 
gradually disappearing toward night. 
Nicholson reports “that 7.5 per cent of English school boys among 
189 healthy lads studied, showed albumin on arising, 7 per cent after ANOMALIES OF THE URINARY SECRETION 
745 
breakfast, 10.7 per cent after football, and 18 per cent after a three mile 
run.” Twenty-eight per cent showed albumin at some time. Bugge found 
orthostatic albuminuria in 14.9 per cent of 1,076 school children in Chris- 
tiania. Bass and Wessler found “that children with orthostatic albu- 
minuria who showed marked cardiovascular symptoms could not be 
differentiated by means of blood pressure tests from the remainder of 
the group.” 
I have not found orthostatic albuminuria frequent among tubercu- 
lous children; some claim that orthostatic albuminuria is usually, if not 
always, a sign of tuberculous infection somewhere in the body. 
Reyher collected 20 cases of orthostatic albuminuria in all of which 
he found tuberculosis. Arnold does not believe that orthostatic albu- 
minuria is pathognomic of tuberculosis. Orthostatic albuminuria should 
always be considered as suggesting tuberculosis but it is not pathognomic. 
Sturm found 12 of 20 cases of tuberculosis with orthostatic albuminuria. 
It is unsafe to conclude that a urine which is albumin free on arising and 
becomes albuminous and remains so during most of the day, and shows 
variations in the quantity of albumin, is always an example of cyclic or 
orthostatic albuminuria. I have under observation at the present time 
a boy, aet. 12, who was supposed to have an innocent orthostatic albu- 
minuria because of its characteristic cyclic behavior, who now shows renal 
epithelia and casts, heart and blood pressure changes which are dependent 
upon tubal nephritis. 
Cyclic albuminuria (orthostatic) which may not depend upon serious 
renal changes in young and growing children (10 to 20 years of age) 
usually boys, is in most cases nucleo-albumin; in some there may be serum 
albumin and occasionally both are combined. 
Persistent orthostatic albuminuria should be considered to be dependent 
upon a relative circulatory insufficiency (Crofton). 
When so-called “orthostatic albuminuria” continues beyond puberty, 
though casts may be absent during long periods, organic kidney change 
should be suspected and such subjects, unless they die of intercurrent 
disease, finally develop nephritis. Such cases are not true orthostatic 
albuminurias. The favorable cases of orthostatic albuminuria are with- 
out hypertension, accented second aortic sound and hypertrophy, and void 
the normal quantity of urine without nocturnal urination. 
It has been amply demonstrated that spinal curvature, particularly 
lumbar curve, may provoke orthostatic albuminuria which disappears with 
the correction of the deformity. Erl anger and Hooker found that under 
such conditions the albnmin is excreted during periods of low pulse pres- 
sure. Erlanger and Hooker, and Jehle—who has recently published an 
interesting monograph on albuminuria of lordotic—orthostatic origin—• 
offer a good prognosis when the curvature is amenable to treatment. 
I agree with Luthje who says: “I believe that for practical thera- 746 
DISEASES OF THE KIDNEY 
peutic purposes it is safest to treat these cases (of persistent orthostatic 
or cyclic albuminuria) as if they were mild forms of nephritis, at any 
rate so long as the albuminuria persists; though it is unnecessary to 
limit the activities of these subjects by interdicting all arduous occupa- 
tions and the pleasures of life.” These conclusions prove that the prog- 
nosis is not to be given without reservation in the persistent cases; the 
possibilities of grave organic disease cannot be ignored. Senator insists 
on the close relationship of cyclic albuminuria and nephritis, while 
Huebner acknowledges “a constitutional weakness of the kidney filter” 
which bears no relation to nephritis. 
Albuminuria in the Aged and Young 
Albuminuria in the aged and young with occasional casts and without 
other evidences of advancing nephritis, may persist during many years 
without final evidences in dropsy, uremia, or circulatory changes of serious 
disease. Such patients may reach old age or die of intercurrent disease; 
probably hut limited portions of the kidney are involved (circumscribed 
nephritis). 
The occasional trace of albumin and few hyaline casts in men beyond 
fifty has been interpreted by Osier as of “positive advantage.” Such 
men are thereby warned, mend their method of living, prevent further 
insult to the kidney, and thus prolong their lives. 
The persistent presence of albumin in men beyond fifty years of age 
with or without hyaline or granular casts takes such subjects out of the 
insurable class. 
Febrile Albuminuria 
With the separate infections I have fully considered the significance 
of albuminuria. It cannot be denied that the milder infections are less 
likely to have albuminuria than are the severer types, hut in the majority 
of bacterial toxemias there is usually more or less albumin excreted, and 
this runs parallel with the fever. ITayashi holds that “acute infections 
predispose to alimentary albuminuria,” and concludes that “not infre- 
quently in cases of albuminuria there can appear in the urine unchanged 
albumin from the food ingested.” (?) 
Febrile albuminuria with non-vialiquant infections in which the quan- 
tity of the urine is not materially reduced and profound toxic symptoms 
are absent, does not as a rule materially influence the prognosis. Deep 
toxemia is made more serious by kidney invasion in which there are evi- 
dences of toxic nephritis, reduced quantity of urine, abundant albumin, 
many casts, low urea output, and invasion of the sensorium. 
The albuminuria of the first week of scarlet fever is in no way related 
to the acute nephritis which follows the febrile period. 
With cholera, albuminuria may depend upon nephritis and toxemia; ANOMALIES OF THE URINARY SECRETION 
747 
in the severe cases anuria and uremia are threatening. If the patient 
withstands the acute infection the kidney lesion with associated symp- 
tomatic albuminuria yields completely, leaving no remnant. The albu- 
minuria and nephritis of pneumonia, epidemic cerebrospinal meningitis, 
whooping-cough and other acute infections, are not associated with uremia, 
edema or hypertension, and recover fully if the primary disease does not 
prove fatal. The same holds true of typhoid fever. The danger in all 
of these is primarily due to the virulence of the infection and secondarily 
to the lack of resistance of the patient. The prognosis of influenza albu- 
minuria (nephritis) in which there may he large albumin loss, hematuria, 
and slight hypertension, is good. 
With diphtheria and scarlet fever, suddenly arising albuminuria, deep 
toxemia, scanty urine, and many casts make an unfavorable complex. 
With streptococcus tonsillitis, albuminuria may occasionally prove to 
he the first symptom of a progressive nephritis which remains uninflu- 
enced by treatment. Such behavior is infrequent, hut possible. As a 
rule the slight albuminuria of tonsillar infection yields during the con- 
valescence of the patient. The malignant infections which from the 
beginning offer an unfavorable prognosis, always show albuminuria— 
usually septic nephritis. 
Toxic Albuminuria 
Albuminuria due to the poisons has been separately considered (See 
Intoxications). Albuminuria following anesthesia, ether or chloroform, 
is transient and without danger in normal subjects. 
Albuminuria with glycosuria is separately considered (See Diabetes 
Mellitus) ; it is always of very serious significance. 
Albuminuria associated with the constitutional diseases, (the anemias, 
purpuras, and malignant diseases) is a part of a grave process as a rule; 
the albumin loss per se is not paramount—the albuminuria is but a single 
symptom of the fatal primary disease. 
The albuminuria of pregnancy, not dependent upon nephritis, demands 
close observation and a guarded prognosis; as a rule it is favorable and 
transient. The nephritis of pregnancy is separately considered (See 
ISTephritis of Pregnancy). 
I have separately considered the prognostic significance of albu- 
minuria with diseases of the nervous system, not of infectious origin. 
These include epilepsy (during and after convulsions), delirium tremens 
cerebral apoplexy, neurasthenia, migraine, and at times hyperthyroidea. 
With each of these, differentiation is demanded for in some, there are 
likely to be arterial and renal changes of organic nature which influence 
Albuminuria with Functional and Organic Nervous Diseases 748 
DISEASES OF TIIE KIDNEY 
prognosis unfavorably. Without such changes as a cause of albuminuria, 
the latter—usually transitory—is without marked influence. 
Sudden albuminuria with intestinal obstruction and promptly devel- 
oping anuria following in a few hours, is a complex, associated with 
collapse as a rule, and death. 
Albuminuria following surgical operations in those previously albu- 
min free is not infrequent, but always demands close investigation. If 
due to the anesthetic it promptly disappears; if due to transitory circu- 
latory disturbance it is evanescent; if with casts, lowered secretion, and 
toxic symptoms—an expression of general infection—the prognosis is 
unfavorably influenced by the complication. Albuminuria, casts and deep 
nervous symptoms following operation are always of grave import. Ex- 
acerbation of nephritis following operation is infrequent. 
For the insurance examiner a conclusion based upon albuminuria 
alone is valueless. Those assuming the risk have learned that the cellular 
elements in the urine—the presence or absence of casts, at times cylin- 
droids—the general condition, the blood pressure and the condition of 
the cardiovascular system, the evidences of changes in the fundus of the 
eye, and the blood picture, are the paramount factors in deciding upon 
the insurability of the individual. 
For further data bearing on the prognosis of albuminuria the reader 
is referred to the parts of this section dealing with the nephritides and 
other kidney lesions, as well as the separate diseases of which albuminuria 
is a symptom. This will lead to the consideration of the circulatory, 
nervous, digestive, hemopoietic and most other systems, as already sug- 
gested in the beginning of this chapter. 
While the prognostic importance and seriousness of albuminuria has 
unquestionably been overestimated in the past, because of faulty diag- 
nostic methods and hasty conclusions, the relative value of the symptom 
must always rest on thorough differentiation. 
References 
Arnold. Munch: med. Wchnschr., 1913, lx, No. 9. 
Barringer, Jr., & Warren. Report Sect, of Pract. of Med. of Am. M. ass., 1912, p. 314. 
Bass & Wessler. Arch. int. Med., 1914, xiii, 39. 
Bright (Richard). On renal disease accompanied with the secretion of albuminous urine. 
Guy's Hosp. Rep., London, 1836, i. 
Observations on 24 cases, etc. Memoirs II. Report of medical cases, 1827. 
Bugge. Norsk Mag. Laegervidensk, 1913, Ixxiv, No. 12. 
Cotugno (Nicholas) (1736-1822). Neuburger u. Pagel Handb. d. Geschichte d. Med. 
Jena, 1903. 
Crofton. Clinical urinology. New York, 1904. 
Engel. Deutsch. med. Wchnschr., 1914, xl, 1963. 
Erlanger & Hooker. Johns Hopkins Hosp. Rep., 1904. 
Franz & von Reuss. Ztschr. f. Kinderheilk., 1914, xi, 193. ANOMALIES OF THE URINARY SECRETION 
749 
Hayashi. Monatschr.f. Kinderheilk., 1913, xii, 101. 
Heller. Ztschr. f. Kinderheilk., 1913, vii, 303. 
Jehle. Die Albuminurie orthost. lordot. u. d. neph. Albuminurie. Berlin, 1914. 
Joachim. Pfliiger’s Archiv, 1903, Bd. 93, 558. 
Leube. Ueber phys. Albumin., Ztschr. f. klin. Med., xiii. 
Luthje. Von Mehring u. Krehl's Lehrb. d. inner. Med., Jena, 1913, i. 
Mann (Dixon). Phys. and path, of the urine. London, 1904. 
Neubauer. Huppert’s Lehrb. Analyse d. Hams. Wiesbaden, 1913. 
Nicholson. Practitioner, 1914, xciii, 113. 
Osier (Sir William). Practice of medicine. 8th ed. New York, 1914. 
Paton. Brit. Med. J., July 26, 1890, ii. 
Petri. Dissert. Berlin, 1876. 
Higher. Pediatra, 1914, vi, No. 1; also Monatschr. f. Kinderheilk., 1913, orig., xii, 82. 
Senator. Die Albuminurie, etc. Berlin, 1890. 
Virchow's Archiv, 1874, Bd. 60, 4-76. 
Stewart (Granger). Lectures on albuminuria. New York, 1888. 
Sturm. Munch, med. Wchnschr., 1913, lx, 763. 
(b) Casts 
Tube Casts 
Casts are not always indicative of true nephritis. Casts are frequently 
found to be transitory and of no pathological significance. Healthy indi- 
viduals, after excessive exercise, fatigue, or functional disturbance of the 
kidney, due to improper diet or long continued strain, may show the 
presence of hyaline casts during only a limited period without further 
impairment of the general health or permanent kidney change. The per- 
sistence of casts—hyaline or granular, or both, with or without albu- 
minuria, should always lead to thorough search and in the majority of 
cases will be found dependent upon organic disease of the kidney (neph- 
ritis). Promptly disappearing casts are of no grave importance. The 
use of salicylic acid preparations and other urinary irritants is often 
associated or followed by a shower or the presence of casts which may 
continue one or two days after discontinuance of the drug. 
Casts are molds of the renal tubules and when persistently present 
they are, as a rule, evidence of kidney disease. Their prognostic signifi- 
cance is as easily over- as underestimated, unless the many data which 
make diagnosis and prognosis positive are gathered from a thorough study 
of all that the urine offers wfith a detailed consideration of the other sub- 
jective and objective features of the individual case. There are three 
leading varieties: 
1. Blood Casts 
2. Epithelial Casts 
3. Hyaline Casts. 750 
DISEASES OF THE KIDNEY 
Pus casts are simply pus cells plastered on a basement substance, either 
hyaline or hyaline and epithelial. The fatty or oily casts are varieties 
of epithelial casts which have undergone fatty degeneration. Waxy or 
amyloid casts are like hyaline casts but show the amyloid reaction, are 
highly refractive, and are characteristic of amyloid disease; they are 
always secondary and when not specific, are as a rule associated with fatal 
disease (See Amyloid Nephritis). 
Granular casts are degenerated or changed epithelial casts. Cylindroids 
are composed largely of mucus with added elements held together by a 
basement substance. They are formed in the tubule or at times in the 
pelvis of the kidney and are expressive of more or less irritation of the 
part in which they are formed; they are less serious than are casts and 
are often dependent upon transitory causes, though they may be found 
with other casts in the more serious organic diseases of the parenchyma 
of the kidney. 
1. Blood Casts 
Blood casts show the seat of existing hemorrhage to be in the tubules 
of the kidney, including the glomeruli. When the microscope shows the 
presence of blood casts, the prognostic significance must depend upon 
a number of factors, the most important of which include the nature of 
the primary lesion which has caused the bleeding. In young subjects 
tuberculosis, calculosis, occasionally malignant growths and acute neph- 
ritis, are among the leading causes (See Hematuria). During middle 
life tuberculosis, calculosis, malignancy, renal and circulatory disturb- 
ances (secondary to heart, vascular, and liver disease) are among the 
underlying anomalies. In advanced life, arteriosclerotic, cardiovascular 
disease, nephritis, varicosities, malignancy (cancer and papilloma) cal- 
culosis, and other causes are among the possibilities. The blood casts of 
acute nephritis in young subjects are often abundant (scarlatinal neph- 
ritis, etc.). The prognosis is not bad so long as profound uremia is pre- 
vented and the associated conditions are not threatening. 
Blood casts in young subjects with anuria and uremic symptoms are 
always ominous and demand a guarded prognosis. The prognosis is not 
necessarily unfavorable in cases which appear serious and threatening 
under rigorous and rational treatment (See Acute Nephritis). The length 
of the threatening period is short in the majority of these cases. An 
occasional blood cast in adult nephritis is not of serious moment. Often 
with acute exacerbations the urine of subacute and chronic nephritics may 
become bloody—in the majority it clears after a few days of rest and 
treatment. Occasionally the presence of a few blood cells and blood casts 
precedes a free hemorrhage and serious uremic symptoms. 
2. Epithellvl Casts 
Epithelial cells plastered on a hyaline basement substance are char- ANOMALIES OF THE VRINAKV SECRETION 
751 
acteristic of acute tubal nephritis. Epithelial casts are positive evidence 
of tubular involvement ; considered alone they offer little of prognostic 
value, their diagnostic significance is more important. Abundant epi- 
thelial cells and casts with progressive reduction of the urine secretion, 
with or without blood casts or blood corpuscles, with dropsy and increas- 
ing nervous symptoms are always ominous, though not of necessity fatal 
(See Acute Nephritis). 
When epithelial casts become fatty and granular they indicate a degen- 
erative process, characteristic of the more advanced forms of nephritis. 
The persistence or even occasional presence of epithelial casts with albu- 
minuria, with at times the addition of a hyaline cast, in a urine which 
shows progressive lowering of its specific gravity, is indicative of either 
secondary contraction of the kidney following tubal nephritis or chronic 
interstitial nephritis, and the prognosis should be accordingly given (See 
Chronic Tubal Nephritis and Interstitial Nephritis). 
It is an established fact that subjects with granular casts and albu- 
minuria are bad risks, and show a mortality far above that of the normal 
individual. They are below par and yield to infection readily when 
exposed. The more acute the nephritis, the better is the epithelium 
preserved; hence degenerated epithelium as plastered upon hyaline sub- 
stance to form granular and fatty casts is always an expression of ad- 
vanced tubular change. 
3. Hyaline Casts 
Hyaline casts are homogeneous, glassy, are regularly outlined, and are 
not highly refractile, in contradistinction to waxy casts which are highly 
refractile. 
I considered the association of an occasional hyaline cast with mod- 
erate or transitory albuminuria in men beyond fifty years of age (see 
Albuminuria) and called attention to the salutary influence of such 
occurrence (Osier). The diagnostic and prognostic significance of hyaline 
casts with or without albuminuria depends upon age, associated condi- 
tions, and a variety of factors which are numerous in individual cases. 
Hasty conclusions in the presence of hyaline casts and albuminuria are 
likely to prove erroneous and expensive. Hyaline casts may be found 
occasionally in the urine of normal subjects; persistent albuminuria with 
hyaline casts and an occasional granular cast indicates nephritis, and the 
forecast should be accordingly given. An occasional hyaline cast with 
albuminuria after excitement, exertion, overeating does not necessarily 
mean diseased Jcidney. 
When albumin is present on arising in the morning in large or small 
quantities with hyaline casts—many or few—but one safe conclusion is 
justified, and that is that we are dealing with an abnormal condition 
which demands the close study of the patient before reaching a conclusion; 752 
DISEASES OF TIIE KIDNEY 
further, it should be remembered that hyaline casts may be present with 
all forms of nephritis, with jaundice, diabetes mellitus, and insipidus, 
heart lesions, pregnancy, and after long walks or marches (soldiers) with 
gouty exacerbations and under various conditions which are especially 
influenced by excitement, mental emotion, and diet. 
My experience coincides with that of Barringer, Jr., and Warren 
who assert that “cases of albuminuria with a few hyaline casts have no 
particular age incidence. The mortality of this group is also above the 
normal.” 
The prognosis of febrile albuminuria, toxic albuminuria, and all forms 
of albuminuria due to infection with the presence of casts depends upon 
many factors which are considered in connection with the separate diseases 
(See Section I—The Infections). It may be safely assumed that deep 
kidney involvement—with or without casts complicating acute or chronic 
disease—always adds an enormous element of danger (See also Cardio- 
vascular Disease, Arteriosclerosis, etc.). 
Hyaline casts with congested kidney and blood casts, an occasional 
granular cast, scanty urine, and clouded sensorium are among the ter- 
minal features when compensation is broken, usually beyond repair. 
Casts often precede albuminuria during the early days of acute nephritis 
(Pick, Hecht and Koessler). The gravest types of nephritis may remain 
without demonstrable casts during weeks and months (See Interstitial 
Nephritis; also Secondary Contracted Kidney). 
In the presence of any form of nephritis with acute exacerbation, the 
gravity is often in direct proportion to the profusion of the urinary casts 
though there are abundant cases in which the number of urinary casts is 
in no way related to the gravity of the disease. Grave and threatening 
nephritis—often in the terminal stages—may show but few or no casts, 
but little or no albuminuria; chronic nephritis (usually interstitial) may 
remain “albumin and cast free” during days or months at a time, when 
suddenly symptoms of toxemia develop, uremia without warning, coma 
and death. 
Fischer after considering the mode of formation of casts, basing his 
conclusions upon the influence of acid, etc., says: “These simple facts 
regarding the origin of casts, and the conditions under which the one 
type may be converted into another, are not without some clinical sig- 
nificance.” . . . “It seems to me that the experiments that have just 
been detailed urge upon one the necessity of caution in drawing sweeping 
conclusions from such data. So far as mere numbers of casts are con- 
cerned, it requires no special emphasis to realize that great numbers of 
casts present in the urine at one time, while indicative of a more ex- 
tensive involvement of the kidney parenchyma, may not be as significant 
as a lesser number present over long periods of time. The aggregate 
destruction may in the latter case, of course, be much greater than in the ANOMALIES OF THE UKINARY SECRETION 
753 
former (a condition further modified in the living organism by the rate 
and quantity of the regeneration occurring in the kidney).” 
With septic and embolic nephritis, pyelonephritis, and other deep 
infections involving the kidney, bacterial casts are found in the urine 
composed of agglutinated masses of bacteria in the freshly voided urine. 
The presence of these masses of bacteria, probably agglutinated in the 
kidney, is one of many serious features of grave infection. Neubauer 
and Huppert and others call attention to the importance of examining the 
urine immediately upon its passage; otherwise the clinician may be de- 
ceived by the formation of conglomerate masses of bacteria into forms 
which resemble the renal bacterial casts. 
Barringer (Jr.) & Warren. The prognosis of albuminuria with or without casts. Section 
on Practice of Medicine, Am. M. Ass., 1912, 805. 
Eisner (Henry L.). Lectures delivered at College of Med., Syracuse University. 
Fischer. Nephritis. New York, 1912. 
Luthje, von Mehring & Krehl. Lehrb. d. inner. Kranlch. . Jena, 1913. 
Neubauer & Huppert. Analyse des Hams. Falk & Eppinger. Wiesbaden, 1913, 
Zweite Halfte, p. 1585. 
Osier (Sir William). Practice of medicine. 8th ed. New York, 1914. 
Pick, Hecht & Koessler. Clinical symptoms. New York & London, 1911. 
Stewart (G.). Lectures on albuminuria. New York, 1888. 
Tyson & Fussell. Practice of medicine. Philadelphia, 1914. 
von Leube (W7.). Diagnose der inner. Krankh. 8. Aufl. Leipzig, 1911. 
References 
(c) Hematuria 
Origin.—Visible blood in the urine—tbe symptom hematuria—may be 
either of renal or extra-renal origin. The determination of the cause of 
hematuria is often difficult because the bleeding may be without subjective 
symptoms or physical signs. 
Cystoscopic examination with catheterization of the ureters makes the 
localization of lesions more positive than ever before, though the major- 
ity of hematurias will for many years to come be diagnosticated by the 
average clinician without the aid of these refinements of diagnosis. When- 
ever possible, advantage should be taken of this new method of diagnosis. 
The methods suggested make possible the localization of lesions to one 
or both kidneys in renal hematuria but they fail in many cases to 
establish the true underlying pathologic condition. For prognosis and 
diagnosis it is fortunate that the overwhelming number of hematurias find 
their way to the diagnostician early, for blood in the urine rarely fails to 
alarm the patient who usually demands immediate treatment of the symp- 
tom. 
Blood may enter the urine from any one of many sources; beginning 754 
DISEASES OE THE KIDNEY 
with the malpighian tufts and ending with the meatus urinarius, there 
is not a surface which when disturbed may not add blood elements to the 
urine. Besides local lesions within the urogenital tract, hematuria may 
complicate the constitutional diseases with hemolysis when it is but one 
symptom of a grave and usually fatal malady. With grave local (renal) 
or constitutional diseases there are besides the hematuria, sufficient sub- 
jective and objective features to clear the diagnostic horizon and to lead 
to a safe forecast. 
There are but few conditions associated with hematuria in which the 
bleeding is so profuse (this is particularly true of bleeding from the 
kidney) as to threaten life. It does occasionallly happen that hematuria is 
profuse and depleting. Many cases become excessively anemic, but few 
of these die as the direct result of the hemorrhage. In the terminal stages 
of malignant disease of the kidney or bladder, at times with malignant 
purpura, pernicious anemia, Hodgkin’s disease, or with hemolysis due to 
other grave constitutional diseases, the bleeding may so weaken the pa- 
tient as to add an enormous element of danger (See also Malignant Jaun- 
dice and other grave liver infections). 
Renal hematuria is more frequent than is generally supposed without 
analyzing a large number of cases. The symptom may be continuous, 
or it may recur at irregular intervals. Hematuria due to organic change 
in the kidney which is permanent is likely to recur, and it is unwise for 
the physician or patient to believe that the organic disturbance has been 
overcome because of periods of latency or the insidious behavior of the 
underlying process, which adds but little to the clinical history during 
long periods. This sense of security after kidney hemorrhage even with- 
out associated symptoms, sufficient to make Its cause positive, is rarely 
justified, for it may be assumed that the bleeding must always be consid- 
ered an important symptom, demanding close surveillance during many 
months and years; such conclusion and consecutive action will do much 
to improve prognosis. 
I have in private practice tabulated the clinical histories of 4,832 
consecutively examined cases of internal disease. I found among this 
number 229 cases of chronic tubal nephritis, 14 cases of acute tubal nephri- 
tis, 17 cases of chronic interstitial nephritis, 8 cases of secondary con- 
gested kidney with the prominent symptoms of marked stasis, and 7 cases 
of tuberculous nephritis, in which no tuberculosis was demonstrable in 
other organs. Of the 229 cases of tubal nephritis, blood was found in the 
urine of 33 per cent. The 14 cases of acute nephritis all contained more 
or less blood. Of the 77 cases of chronic interstitial nephritis 14 per cent 
were found with blood in the urine. All of the 8 cases of secondary con- 
gested kidney contained blood. In only 12 of the 328 cases, was the 
hematuria profuse. In 4 of these there was chronic tubal nephritis with 
marked hypertension, arteriosclerosis and aortic disease, with, in one case, ANOMALIES OF THE URINARY SECRETION 
755 
a final malignant growth in the bladder. In 4 of the 12 profuse hemor- 
rhages there were evidences of gouty kidney with advanced interstitial 
change. The remaining 4 cases showed microscopic elements which jus- 
tified the diagnosis of chronic tubal nephritis. 
Rayer in 1844 called attention to the frequency of nephritis as a cause 
of hematuria, and Askanazv presents the results of the observation of 562 
cases of chronic nephritis, 35 per cent of which showed blood in the urine. 
Of these 126 showed moderate, 64 abundant red corpuscles. It is evident 
from the foregoing statistics that while bloody urine is a frequent symp- 
tom of all forms of nephritis—tubal nephritis particularly—it is rarely 
threatening or profuse. 
Hematuria may be a Symptom of: 
1. Acute Tubal Nephritis 
(Hemorrhagic (acute) Nephritis) 
2. Chronic Tubal Nephritis 
(a) painful 
(b) painless 
3. Chronic Interstitial Nephritis 
(Hematuria due to arteriosclerosis, change in blood pressure 
and localized degeneration) 
4. So-called “Essential Hematuria” or “Renal Epistaxis” 
5. Cases of Renal Hematuria with gouty diathesis in which there 
may be latent kidney disease without calculosis 
6. Paroxysmal Renal Hematuria following chilling of the surface 
7. Renal Infarct causing hematuria with septic fever, usually asso- 
ciated malignant endocarditis 
8. Acute and Chronic Primary Infections—pyelitis, non-calculous, 
with moderate hematuria. 
9. Stone in the Kidney 
10. Tuberculous Nephritis 
11. New Growths of the Kidney 
12. Traumatism causing rupture of the kidney 
13. Echinococcus 
Bilharzia Hematobia 
Filaria Sanguinis Hominis 
14. Constitutional Diseases 
(Purpura and the Anemias) 
15. Hemorrhagic Conditions with the Infections—scarlet fever, 
typhoid and typhus fever, measles, smallpox and diphtheria and 
following surgical operations 756 
DISEASES OF TIIE KIDNEY 
1. Acute Tubal Nephritis 
These cases are easily recognized: the urinary (microscopic) picture is 
characteristic in the preponderance of cellular elements, the hemorrhage is 
rarely profuse, blood in small quantity is usually present, in the hemor- 
rhagic form bleeding may be profuse with other serious symptoms, includ- 
ing scanty urine and uremia. Hematuria with acute nephritis is rarely of 
serious importance. 
2. Chronic Tubal Nephritis 
The hemorrhage may be (a) painful or (b) painless. It is rarely 
sufficiently profuse to materially add to the dangers of the case; in occa- 
sional cases with acute exacerbation of the already existing chronic nephri- 
tis the urine may show considerable admixture of blood. Most uncompli- 
cated cases are painless. The prognostic significance of hematuria with 
chronic tubal nephritis (uncomplicated) is not great. The process in the 
kidney is progressive and disseminated, of constitutional origin, and is not 
materially influenced by the hemorrhage. With chronic tubal nephritis but 
one kidney may bleed, though both organs are equally invaded; both may 
bleed at the same time or they may alternate in adding blood to the urine 
(For further data see Chronic Tubal Nephritis). In this form, of nephritis 
as in all others, the general condition of the patient, his resistance, the blood 
state, blood pressure, specific gravity of the urine, as well as the Junctional 
ability of the Icidney, demand consideration, that a safe forecast may be 
given when hematuria is a prominent symptom. 
3. Chronic Interstitial Nephritis 
Included is a class of hematurias in which there are advanced arterial 
lesions, the blood pressure is abnormally high, and there are localized 
degenerative changes—particularly in the walls of the arteries, at times 
in the veins—with possible rhexis. In these cases the hematuria, per se, 
is not threatening; active exercise or faulty diet, excitement, or emotion 
may cause relapse; chronic constipation aggravates or provokes the bleed- 
ing (straining at stool). 
In some of these cases there may be hemorrhage from other sources, as 
the urethra, bladder or pelvis, and it not infrequently happens that cere- 
bral hemorrhage ends the life of such nephritics. In one of my cases 
observed during many years, the original hemorrhage was profuse and 
from the urethra, the second from the nasal mucosa, the third from the 
kidney. Death followed from cerebral hemorrhage after a fishing trip 
on a hot summer day. In these cases hematuria may occur in conjunc- 
tion with transitory hemiplegia. 
In offering the prognosis of these cases the possibility of the complica- ANOMALIES OF THE URINARY SECRETION 
757 
tions suggested should be considered and the further fact remembered 
that profuse renal hemorrhage with chronic interstitial nephritis is more 
frequently due to changes in the pelvis of the kidney than to any other 
single cause; that the blood vessels may either rupture here or that there 
may be a sudden hyperemia, such as surgeons have found during surgical 
operations upon the kidney (Israel) and that as in the brain, increased 
arterial tension is an important factor in causing rupture of diseased 
arteries or veins (Eisner). 
4. So-called “Essential Hematuria” or “Renal Epistaxis” 
So-called “essential hematuria5’ or “renal epistaxis” is supposed to exist 
without organic change. Well authenticated cases are so rare as to cast 
doubt upon the correctness of this conclusion. Several years ago I re- 
viewed the literature of this subject and found but few well authenti- 
cated cases (Klemperer, Senator, Schede, Caspar, and Schenck). The 
kidneys in the cases of Klemperer, Schede, and Schenck were found normal 
after nephrectomy. Caspar reports 7 cases of so-called essential renal 
hematuria, or as he says “bleeding from healthy kidneys.” The consider- 
ation of his material strengthens him in the conclusion that the majority 
of these mysterious cases are due to nephritis, though clinical manifesta- 
tions may be entirely absent. In this connection, for purposes of prog- 
nosis, it should be remembered that nephritis may persist during many 
months without casts or albumin, and during long periods without hemor- 
rhage, 
Schenck’s case in which the cause of the hemorrhage after the removal 
of the kidney remained a complete mystery led him to conclude that it 
would seem far better to put these cases aside as yet unexplained, than to 
assert that an anatomically sound kidney could cause profuse hematuria, 
The majority of cases which are originally diagnosticated as “essential 
hematuria” prove ultimately to be either chronic, tubal, or interstitial 
nephritis with limited or punctiform change in the substance of the organ 
or its pelvis, often undiscoverable macroscopically but usually demonstrable 
microscopically, 
In a number of cases the final history leaves no room for doubt be’ 
cause of the development of the complete clinical history of nephritis. 
When the hemorrhages are profuse and recur at short intervals, secondary 
anemia may prove serious, and when the process is limited to one kidney 
(as shown by ureteral catheterization) surgical intervention may be needed 
to save life. 
Unexplained and supposed “renal epistaxis” may be slight and never 
recur—may leave no remnant of renal change. The pain is rarely severe; 
some cases are painless. 
The prognosis in the majority of cases, of the symptom itself is good 758 
DISEASES OF THE KIDNEY 
(Hale White). Probably the hematuria of pregnancy is due to varices of 
the renal pelvis. The prognosis is good. 
5. Cases of Renal Hematuria with Gouty Diathesis in Which There May 
Be Latent Kidney Diseases without Calculosis 
These cases usually advance after a number of years and show all of 
the changes of chronic interstitial nephritis, at times secondary contracted 
kidney. The hematuria does not materially interfere with the course of 
the disease in the majority of cases, though occasionally the progression 
dates from the bleeding. With acute exacerbation of gout in nephritics, 
hematuria may be a prominent symptom. The majority of these cases 
yield to rest and treatment. In occasional cases profuse hematuria asso- 
ciated with the gouty diathesis may be the first of a long train of symp- 
toms which characterize chronic interstitial nephritis. 
6. Paroxysmal Hematuria following Chilling of the Surface 
The history of these cases is interesting. Usually the patient is a mid- 
dle aged man, who had considered himself perfectly well; he is exposed to 
cold, a slight chill follows, with a desire to urinate. The urine is bloody 
at once and is voided without pain. The hematuria is profuse and con- 
tinues during twelve to twenty-four hours, to return whenever there has 
been exposure to cold. Usually these patients complain of cold feet before 
the chill and hemorrhage. During the summer months there are no renal 
hemorrhages. Finally the hematuria recurs on slight cause, evidences of 
nephritis (chronic tubal) are continuous, and death with all of the symp- 
toms of chronic nephritis, usually dropsy and uremia, with cardiovascular 
change follows. These cases may prove exceedingly chronic. One of my 
cases lived over 17 years after the first hematuria. He died of uremia 
preceded by a long period of renal dropsy. 
7. Renal Infarct Causing Hematuria with Septic Fever, Usually 
Associated Malignant Endocarditis 
A strong suspicion of malignant endocarditis and renal infarct is justi- 
fied when there is associated septic or pyemic fever (intermittent fever) 
in which there is no other clear cause for the bleeding. Renal hematuria 
may he an early or a late complication of infectious endocarditis. I have 
seen chronic malignant (Streptococcus viridans) endocarditis uninfluenced 
by the early renal infarct; as a rule, there is recurrence, with evidences 
of infarct in other organs (spleen, brain, lung, and skin). In one case 
hematuria recurred at varying intervals during six months preceding 
death. Hematuria is not the cause of death. The infection is malignant, ANOMALIES OF THE URINARY SECRETION 
759 
often chronic, and always offers a bad prognosis. I have no recovery to 
report (See Malignant Endocarditis). 
8. Acute and Chronic Primary Infections—Non-calculous Pyelitis with 
Moderate Hematuria 
These are the acute cases of primary infection of the pelvis of the 
kidney, in contradistinction to calculous pyelitis or ascending pyelitis due 
to gonococcus or other infection. There is a characteristic history, includ- 
ing temperature curve, most frequently found in women—often during 
pregnancy and at the menstrual period. 
The renal pelvis is directly infected, usually by the Bacillus coli com- 
mune, occasionally by other pathologic bacteria—pneumococci, paratyphoid 
bacilli, etc. Obstinate constipation is usual; bladder symptoms are absent. 
The temperature following the direct (non-ascending) infection is almost 
pathognomonic; high at first during from three to four days, then a 
period of remission, almost normal temperature for two to four days, then 
a series of chills and intermittent fever. These cases may be subacute 
or chronic—eight to fourteen days—some several weeks, others continue 
a number of months. The disease is usually right-sided; in thin subjects 
the kidney is palpable, tender and enlarged (Eisner). The sharp pains 
resemble renal colic; they radiate along the ureter; the hemorrhage is 
not often profuse. Leuhartz's resume of the subject is classic. 
My experience with these cases, without surgical intervention, has been 
favorable. Often the anemia becomes extreme. In those complicating 
pregnancy, the fever and local symptoms of infection and anemia usually 
disappear after delivery—recovery is complete as a rule. 
9. Stone in the Kidney 
Renal calculosis does not, as a rule, cause profuse hematuria. I have 
never met a case in which hematuria with calculous pyelitis threatened life 
in an otherwise healthy subject. The prognosis of kidney stone is sepa- 
rately considered (See Pyelitis Calculosa—Kidney Calculosis). 
10. Tuberculous Nephritis 
(See Tuberculosis of the Kidney—Section I) 
Most hematurias due to tuberculous disease of the kidney are finally 
controlled; I have never experienced death from hematuria per se. 
Hematuria with tuberculous nephritis is often the first symptom of 
renal infection. My experience does not include many cases of profuse 
hematuria after the tuberculous process was far advanced. With radical 
treatment the prognosis in threatening cases is good. The early recogni- 760 
DISEASES OF THE KIDNEY 
lion of the pathologic cause of the hematuria in tuberculous nephritis and 
prompt surgical treatment offers an excellent outlook for the complete resto- 
ration to health in cases in which the process is not disseminated or double. 
11. New Growths of the Kidney 
(See Neoplasms of the Kidney) 
Early hemorrhage witli cancer—papilloma of the kidney or other renal 
growths, when the cause is clear and radical treatment not too long post- 
poned, offers a good prognosis. 
12. Traumatism—Rupture of the Kidney 
In otherwise healthy subjects without injury of other organs and 
prompt surgical treatment, the prognosis is relatively good. There are 
naturally many factors associated with the accident which influence the 
outcome, but it may be safely concluded that unless the ruptured kidney 
is surgically treated the prognosis is absolutely had in practically all cases. 
There are hut few exceptions. 
13. Echinococcus Disease, Bilharzia hematohia, Filomia sanguinis 
liominis 
(See Section I—Parasitic Diseases, etc.) 
14. Constitutional Diseases 
(Purpura, Hemorrhagic Diathesis, the Anemias, Hemophilia, etc.) 
(See separate chapters dealing with individual primary diseases) 
Hematuria, petechiae and other evidences of the hemorrhagic diath- 
esis with constitutional disease, are usually terminal. The prognosis of 
the primary disease is of paramount importance in reaching a safe 
conclusion. With purpura (uncomplicated and benign) the prognosis 
is good. With the other constitutional diseases, pernicious anemia, 
Hodgkin s disease, the leukemias, the prognosis is always bad. 
15. Hemorrhagic Conditions with the Infections 
(,Scarlet Fever, Typhoid and Typhus Fevers, Measles, Smallpox, 
Diphtheria and following Surgical Operations) 
We have separately considered hematuria and the hemorrhagic com- 
plications of the infections. They are always of serious significance, 
always evidence of malignancy of the primary infection, and often fatal. ANOMALIES OF THE URINARY SECRETION 
761 
Hematuria is usually but one symptom of the complicating diathesis 
and profound constitutional disturbances. Following major surgical oper- 
ations the hemorrhagic symptoms are, as a rule, evidence of grave infec- 
tion and are always discouraging. With measles, hematuria may not 
always prove to be a serious complication—it is often transitory and may 
leave no remnant of kidney change. 
Hemoglobinuria 
The presence of hemoglobin or niethemoglobin in the urine is evi- 
dence of a primary hemoglobinemia and hemolysis, in which the destruc- 
tion of red blood corpuscles has been extensive. Toxic hemoglobinuria 
may follow the ingestion of a number of poisons including potassium chlo- 
rate, arsenic, antimony, toluylendiamin, nitrobenzol, quinin, turpentine, 
carbolic acid, lysol, the anilin dyes, carbon monoxid and muscarin. 
In severe cases of infection—scarlet, typhoid, typhus, streptococcus 
infection—hemoglobinuria is an expression of blood destruction and ma- 
lignancy. I have seen hemoglobinuria after transfusion of blood and 
large surface burns. With the latter it is always ominous, usually fatal. 
Periodic hemoglobinuria is usually a chronic recurring condition which 
follows exposure to cold in susceptible individuals, usually males. As a 
rule if these patients escape without cold feet, hemoglobinuria is pre- 
vented, but in most cases exposure to cold and cold extremities promptly 
cause the symptom. In occasional cases of Raynaud’s disease during the 
winter months, paroxysmal hemoglobinuria is an annoying symptom. 
Osier reports one case in which his patient with Raynaud’s disease had 
paroxysmal hemoglobinuria and epileptic seizures at the same time. 
The prognosis of the toxic form of the symptom depends upon the 
constitutional effect of the poison; with the infections it is always grave. 
The prognosis of paroxysmal hemoglobinuria is favorably influenced by 
climatic treatment. I know of no fatal case directly due to the com- 
plication. One chronic case finally died of chronic tubal nephritis and 
uremia. 
Recent studies of the blood serum of these patients prove the pres- 
ence of a powerful toxin which causes the destruction of the erythrocytes. 
There is an “amboceptor component of the hemolysin” which at a low 
temperature in the presence of the complement unites with the erythrocyte 
and by autohemolysis dissolves the cells themselves. When due to syphi- 
lis, radical treatment may bring relief. 
Spontaneous cures are recorded. The duration of the separate attach 
varies from a few hours to several days. 
The graver attacks may include hemolytic jaundice, striking anemia, 
muscular enfeeblement and finally splenomegaly. 762 
DISEASES OF THE KIDNEY 
References 
Casper. Handb. d. Cystoscop. Leipzig, 1905. 
Donath & Landsteiner. Centralb. f. Bakteriol. 1 Abt., Jena, 1907, xlv, orig., 205-213. 
Eisner (Henry L.). N. Y. State J. of Med., March, 1913. 
Hoover & Stone. Arch. int. Med., Chicago, 1908, ii, 392-404- 
Israel. Arch. f. klin. Chir., xlvii, 2. 
Millh. a. d. Grenzgeb. d. Med. u. Chir., 1889, v. 
Klemperer. Deutsch. med. Wchnschr., 1897, xx, Hi, 129-155. 
Lenhartz (H.). Munch, med. Wchnschr., 1907, No. 16. 
Lenhartz & von Rost horn. Deutsch. med. Wchnschr., 1908, xxxiv, 761. 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Rayer. Traite des Malad. des Reins. 1839-1851. 
Sabatier. Rev. de Chir., 1889, ix, 62. 
Schede. Eisner [l. c.]. 
Schenck. J. Surg. Gynec. & Obst., Chicago, 1911, xiii, 68-73. 
Senator. Berl. klin. Wchnschr., 1895, xxxii. 
Idem., 1891, xxviii. 
(d) Uremia 
Uremia, whatever theory we finally adopt to explain its production, 
is always evidence of faulty metabolism and auto-intoxication dependent 
upon the reduced functional ability of the kidney. It is a true poisoning 
in which blood changes are practically constant and the associated or 
consecutive symptoms are never to be lightly regarded. When acute, 
they are often life-threatening; when subacute or chronic and not over- 
whelming, they are often borne for long periods during w7hich the clinical 
picture may vary from time to time, the toxemia may yield, the central 
nervous system may resume its normal functions and the gastro-intestinal 
discomfort and cardiac complaints may disappear entirely if the primary 
cause has been removed. Relapse, with chronic kidney disease may be 
expected at any time. 
Uremia as a rule is more grave in direct proportion to the extent of 
the kidney lesion and the disorganization or degeneration of the organ. 
In the presence of disorganization or destruction of kidney tissue, it is 
certain that the functional ability of the organ is reduced, but besides 
this, it is probably equally true that a nephrolysin (a poison) is elabo- 
rated. In consequence secondary changes including toxemia (uremia), 
increased blood pressure, and nervous as well as gastro-intestinal symp- 
toms promptly develop. 
Uremia is a symptom complex. The leading features include reduced 
h-idney function, disturbances of the nervous and digestive systems. When- 
ever there are evidences of uremia, for diagnostic, prognostic, as well as 
therapeutic purposes, in the light of our present knowledge, the safest ANOMALIES OE THE URINARY SECRETION 
763 
conclusion to reach is that the symptoms are of toxic origin, that the 
blood stream is surcharged with effete matter (urea), and that the patient 
is never out of danger until the quantity and quality of the urine are 
within safe limits. See References for Armard Formula and importance 
of the increased urea content in the blood, also Renal Sufficiency tests. 
Every acute or chronic nephritic who develops nervous symptoms or who 
has gastro-intestinal disturbance which can be explained in no other way, 
should be considered uremic until proved otherwise. With acute nephritis 
reduction in the quantity of urine, with specific gravity suggesting reten- 
tion, the microscopic field often rich in casts and blood elements, the urine 
frequently concentrated and smoky, the onset of uremia is to be feared 
and treatment should be accordingly framed. 
Uremia may be (I) acute, (II) latent, or (III) chronic. It may 
present a variety of clinical pictures because of the character and extent 
of the lesions, the resistance and idiosyncracies of the patient. The lead- 
ing features upon which prognosis is founded are referable to the nervous, 
the cardiovascular and renal system, the stage of the disease and the 
extent of consecutive changes in the many organs, often invaded. 
I. Acute Uremia 
Acute uremia is always an expression of serious renal insufficiency. 
The prognosis of acute and overpowering uremia is less favorable than is 
that of most other forms, for as a rule the underlying kidney changes are 
likely to be serious, the nervous system is profoundly involved, the symp- 
toms are often apoplectiform, the mania may be active and promptly 
weakening, the gastro-intestinal tract intolerant, and the cardiovascular 
system not able to carry the patient beyond the critical period. 
In spite of these threatening symptoms the prognosis of acute uremia 
ought not to be made without considering the possibility of relief unless 
the parenchyma of the kidney is too far advanced in disease or renal func- 
tion cannot be stimulated. Uremic symptoms may be acute and exceed- 
ingly grave and yet—particularly in children with acute nephritis— 
rigorous treatment may often lead to recovery. 
With acute uremia the freer the subject is of cardiovascular changes 
the more acute the renal changes, and the more these are limited to the 
parenchyma the better is the prognosis. In some cases renal sufficiency 
tests give some assistance, but alone they are not dependable for in the 
presence of grave uremia I have found high readings, and vice versa. 
Acute uremia with the chronic nephropathies in which there has been 
a period of latent or chronic uremia does not offer an encouraging fore- 
cast. Even these cases are often amenable to treatment and may return 
to their former state. Chronic arteriosclerotic nephritics often have long 
periods of acute exacerbations of uremia, with profound involvement of 
the sensorium between which they may continue with the chronic to& 764 
DISEASES OE THE KIDNEY 
emia, Or they may clear mentally and return to their responsible positions 
with average judgment. Relapse in these eases is the rule. The acute 
Exacerbations are repeated, or after a number of these, the uremia be- 
comes Coiitinuous and chtonic, finally leading to coma and death. Other 
eottipiicatioiis (cerebtal apoplexy, cardiac insufficiency, etc.) may also 
cause the death of these patients. 
The increase of urine* and the improvement of the gastro-intestinal 
symptoms as the brain clears, are favorable; 
Sudden blindness just before a uremic convulsion, with acute uremia, 
is not as a rule evidence of retinal hemorrhage. In my experience the 
majority of such amauroses have not recurred. 
The persistence of vomiting and other gastro-intestinal symptoms after 
the acute manifestations yield, are not favorable. Such patients are likely 
to have convulsions, or because of the profound renal insufficiency they 
develop chronic uremia. Persistent or recurring drowsiness after an 
acute uremic convulsion, with either acute or chronic nephritis is proof 
of continuous toxemia and is unfavorable though relief is not uncommon 
after rigorous dietetic treatment and rest. 
Acute uremia with respiratory paralysis or irregular breathing— 
Cheyne-Stokes particularly—with chronic nephritis and arteriosclerosis is 
always dangerous. 
Pulmonary edema vTith acute uremia is often a fatal complication. 
This is not always true for in hospital practice with acute nephritis, acute 
uremia and pulmonary edema, results have at times been surprisingly 
favorable. 
Abnormally high temperature with acute uremia and cerebral symp- 
toms are unfavorable and suggestive of meningitis. 
Active mania may be a manifestation of acute uremia, With myocar- 
dial insufficiency it is serious; with advanced nephritis it is a grave com- 
plication ; with alcoholics and nephritis, pneumonia often complicates and 
usually death results. Mania may follow the acute convulsion or it may 
develop suddenly without preceding nervous manifestations. The mono- 
plegias which follow acute uremic convulsions are at times due to local- 
ized edema of the brain and yield in the course of a few hours or days. 
Hemiplegia is more likely to be due to rhexis of a cerebral vessel and 
does not offer the same favorable prognosis for restitution of motion as 
does the more limited paralysis. Cerebral paralyses of uremic origin are 
often exceedingly puzzling, and early prognosis is not always possible for 
the paralysis may be thrombotic, apoplectic, edematous, or of toxic origin 
and the prompt recognition of the true cause is impossible. 
Batty Shaw has recently written extensively on this subject and I 
quote from his article: “Turning now to the practical side of the question 
it is this; that we must not only think of a thrombotic hemiplegia in 
future, with all the elements of a wrong prognosis following in its w^ake, ANOMALIES OF THE URINARY SECRETION 
765 
if we find hemiplegia occurring in a case of uremia or hypertension.”— 
“We may say that the patient may get quite well of the hemiplegia, but 
we cannot say for certain. The same may be said of cases of recurrent 
loss of consciousness associated with uremia or hypertension.”—“What, 
then, is the explanation of such curious paralyses ? They are almost cer- 
tainly of toxic origin, and the toxin picks out motor areas in one indi- 
vidual and sensory areas in another.”—“The presence of a toxic 
‘pressor’ body, which appears to be so often the case in uremia, makes 
it easy to understand that such a body acting on the brain vessels would 
cause them to contract. If the arteries going to the particular area of 
the brain affected are small, then a moderate contraction of them will 
produce a relatively greater anemia of such parts than of other parts 
of the brain, and they suffer to the exclusion of the others.” 
Extreme dyspnea is always an unfavorable complication of any form 
of uremia. Acute uremic dyspnea without convulsions or other evidences 
of uremia is occasionally the only symptom; if relieved, when due to 
chronic nephropathy, it is likely to recur. With marked cardiovascular 
lesions it offers a gloomy outlook. 
Chronic nephritics with severe headaches and acute uremia usually 
have high blood pressure, secondary changes in the heart and cerebral 
arteries, and present a train of unfavorable symptoms in connection with 
the uremia and urine characteristics of disseminated renal disease. 
Acute uremic diarrhea with either chronic or acute nephritis in the 
absence of threatening symptoms, is not as a rule of serious import. Pa- 
tients are often relieved of annoying nervous and gastric symptoms after 
this depletion. 
Acute uremia in which the patient, immediately following the early 
symptoms, falls into the “typhoid state” is always gmve and demands a 
guarded prognosis. 
Retinal hemorrhages preceding any form of uremia “acute or chronic” 
are evidences of advanced arteriosclerosis and nephritis, and offer an 
unfavorable outlook for recovery. 
Hypertension long present with nephritis and final acute or chronic 
uremia is always proof of a grave primary lesion. 
A persistently rapid pulse, arhythmia, angina or other evidences of 
vascular spasm either before or after acute uremia, are unfavorable; most 
of these patients die within a limited time. Chronic nephropathies which 
have had one or more acute exacerbations of symptoms, including deep 
uremia always stand on the edge of a precipice—they may fall without a 
moment’s warning. 
II. Latent Uremia 
Anuria in the absence of nephritis may or may not give rise to uremia 
unless relieved within a reasonable time. Anuria with kidney lesions is 766 
DISEASES OF THE KIDNEY 
likely to he associated with uremic symptoms. Anuria with some forms 
of obstruction, or even with kidney lesions, may persist during several days 
without marked—at times without any—evidences of uremia; finally 
there are convulsions or uncontrollable vomiting, increasing heart weak- 
ness, air hunger and, unless the obstruction is relieved, death follows. 
Anuria due to non-obstructive suppression of the kidney function leads 
to death in most cases unless relieved in from three to five days; patients 
with anuria due to obstruction of the ureter or kidney pelvis by stone, 
growth, or other cause may live with but few symptoms as long as two 
weeks. 
With complete suppression of urine, without advanced or chronic kid- 
ney lesions, with obstruction to the outflow of urine due to stones in both 
ureters or other causes, I have seen life prolonged during periods of sur- 
prising length. In one of my cases (an old man) both ureters were 
plugged with stones. The patient lived two weeks without secreting urine, 
never had a uremic convulsion, vomited during the last few days of his 
life and died without uremic dyspnea. 
In children with nephritis, usually scarlatinal anuria may persist dur- 
ing three or four days—in some cases without marked evidences of 
uremia—and recovery, in my experiences, from such complication has 
been the rule. 
I have seen one case of renal sarcoma (a woman thirty years of 
age) removed surgically, which proved to be horseshoe shaped and her 
only kidney, in which death followed on the thirteenth day. There 
are recorded cases in which recovery followed long periods—com- 
paratively speaking—of anuria without marked uremic symptoms or in 
some with uremic manifestations in the absence of grave kidney change 
(the anuria usually dependent upon obstruction) ; the issue has been fa- 
vorable. 
Latent uremia is to be expected in most forms of obstructive anuria. 
Latent uremia with complete obstruction will finally lead to death unless 
such obstruction is removed. The condition is usually surgical. 
III. Chronic Uremia 
There are patients who are really suffering from chronic uremia, who 
are surcharged with urea and the products of faulty metabolism, who are 
without annoying or noticeable subjective symptoms but whose urines con- 
stantly give evidence of faulty elimination and advanced renal destruction. 
When these cases are thoroughly studied they prove the correctness of the 
preceding statement, for they are really chronic invalids; they have per- 
sistent indigestion, ocular disturbances, morning headaches; they have a 
pasty complexion, are always below par and many are with mental prom 
esses which are slow and not always dependable. ANOMALIES OF THE URINARY SECRETION 
767 
This chronic uremia, for that is what these symptoms mean, may 
suddenly light into an acute exacerbation, or the free and frank expression 
of the toxic condition may never develop. Most cases, however, either fall 
into a state in which there are continuous symptoms, or they develop acute 
uremia unless they die of intercurrent disease. All of the symptoms of 
acute uremia may be present with the chronic form though less stormy. 
From the preceding paragraphs it is clearly evident that it is often exceed- 
ingly difficult to determine the exact time when chronic uremia com- 
menced. 
Chronic uremia may be diagnosticated in the presence of symptoms 
referable to the nervous system or digestive tract when there are evi- 
dences of nephritis and no other cause for the persistent complaints. Oc- 
casional deep nervous symptoms, loss of consciousness, uremic dyspnea, 
transitory amaurosis, sudden emesis with associated cardiac weakness, may 
recur during varying periods. In most of these cases the evidences of 
chronic nephritis are positive in cardiovascular and urinary changes (also 
hypertension) and once established, such deep chronic uremia is not likely 
to yield, though it may persist during many months. 
In both acute and chronic uremia wakefulness is often one of the lead- 
ing symptoms of the toxemia. When with insomnia there is great unrest 
and a rapid pulse or evidences of cardiac arteriosclerosis (Stokes-Adams 
phenomenon, coronary symptoms), or the unrest and insomnia are asso- 
ciated with eye symptoms, convulsions may follow or after a number of 
days the patient, exhausted, falls into a coma, respiratory symptoms follow 
and but few escape death. It is the exception tor patients with any form 
of chronic nephritis to rally after a considerable period of insomnia fol- 
lowed by convulsions or coma. Children and young adults with acute 
nephritis may often suffer from sleeplessness during uremia without fall- 
ing into convulsions or coma. Much depends upon the associated symp- 
toms and stage of the disease in all cases of uremia with insomnia and 
unrest. With associated occasional delirium or visual anomalies the 
prognosis is not encouraging though not necessarily fatal. 
With non-albuminuric chronic nephritis, chronic uremia may be 
present and prove a determining factor in causing death. 
Repeated renal or cardiorenal asthma is often of uremic origin and is 
always serious. 
The uremic breath, with many or few symptoms, is always a warning 
and in most cases general improvement follows its disappearance. The 
uremic breath with chronic nephritis often precedes acute exacerbation of 
symptoms. Convulsions arising suddenly in the course of chronic uremia 
are always grave. 
With chronic uremia, skin lesions (pruritus, etc.) prove rebellious to 
treatment. 
Subnormal temperature is an occasional ominous symptom. Eleva- 768 
DISEASES OF THE KIDNEY 
tion of temperature above normal is never found in uncomplicated cases 
of chronic uremia. 
Bradycardia with other evidences of heart block and uremia is posi- 
tively unfavorable. Chronic uremia dependent upon renal lesions, which 
are also chronic, offers but scant hope of relief. There are chronic neph- 
ritics who live during many years with positive evidence of one or more 
symptoms of chronic uremia; these include headache, occasional vomiting, 
transitory visual disturbances, anorexia, pruritus, and insomnia. In such 
cases the prognosis depends upon possible complications of the nephritis, 
acute exacerbations of uremia, sudden vascular ruptures, heart insuffi- 
ciency and a variety of complications which are included in the study of 
the chronic nephropathies. These patients are always between Scylla 
and Charybdis; ultimately they must strike the rocks. 
References 
Armard. Journ. Am. Med. Ass., March 7, 1914, p. 813; idem, Nov. 27, 1915, p. 1958. 
Fischer. Nephritis. New York, 1912. 
Leube. Die Uremie. Diag. d. inner. Krankh. 8. Aufl. Leipzig, 1911. 
Roberts. Urinary and renal diseases. Philadelphia, 1885. 
Saundby. Renal and urinary diseases. Philadelphia, 1897. 
Senator. NothnageVs Spec. Path. u. Therap. Wien, 1896, xix, 1. 
Tyson. Bright's disease, etc. 2d ed. Philadelphia. 
Tyson & Fussell. Practice of medicine. 6th ed. Philadelphia, 1914. 
Vollard & Fahr. Die brightsche Nierenkr. Berlin, 1914. 
For full and recent literature see Index Medicus; also Bibliographic d. gesamt. inner. 
Med. u. ihrer Grenzgebiet. Berlin, 1913 and 1914. 
(e) Renal Sufficiency Tests 
The clinician will never be limited to any one test or symptom for 
the diagnosis or prognosis of the nephropathies or other organic diseases 
of the kidney. It will never be safe to pin onr faith to renal sufficiency 
tests alone for the prognosis of urogenital disease. Unwarranted enthu- 
siasm has unquestionably led some observers to place too great reliance 
upon the renal sufficiency tests to the exclusion of other features of para- 
mount importance. Rational diagnosis and ultimate safe prognosis 
should include, besides the careful clinical history, the microscopic and 
chemical picture of the urine, the blood pressure study, the cautious 
physical examination—indeed every detail bearing on the individual case 
and the modern renal sufficiency tests. However it should be fully under- 
stood that the prognosis of the nephropathies (nephritides) is scarcely 
justified from the determination of the diminution in total renal func- 
tion alone, for we have learned that the tests do not make absolutely clear 
the type of nephritis present in the individual case, nor does the fact tli^ ANOMALIES OF THE URINARY SECRETION 
769 
phenosulphonephthalein is mainly excreted by the tubules justify “the 
type of the pathological lesion in a case of nephritis” (Christian). The 
diagnostic and prognostic value of the functional renal tests is further 
weakened because of the failure of good observers to reach parallel results. 
The opinions as to the “locus of excretion of the several substances are 
not in accord” (Christian). 
Victor Blum says: “It has been shown that the results obtained by 
examination of the urine (quantity and chemical examination) are often 
insufficient to establish the proof of renal competency or incompetency. 
At the best, these results gave us an idea of the momentary functional 
condition of the kidney, of its effective work at the time.” 
“Our modern functional diagnosis, however, has a broader aim. We 
want not only to learn to recognize the work actually performed by an 
organ, but must attempt to gain an idea of its maximum capacity for 
work, its possible extent of function.” . . . “When renal impairment 
exists in company with satisfactory compensation, there will be no symp- 
tom whatever of renal incompetence as long as the store of latent reserve 
force is sufficient to guarantee the excretory function of the kidneys. In 
the pathology of the kidneys however, particularly in surgical treat- 
ment, the important question arises whether the organ will be adapted 
to increased demands (e. g., in cases where unilateral nephrectomy is 
intended).” Blum in his enthusiasm says: “The old clinical methods 
give us no information on this point; we can only designate a kidney as 
sound in a functional and anatomical sense when we have shown how it 
carries out the various departments of work forced upon it in experiment.” 
It may be assumed, further, that at present the results of accumulated 
experimentation do not establish a positive relation between kidney func- 
tion and pathological change basing these on the rapidity of excretion 
of lactose, (Schlayer) potassium iodid, salt and water. Schlayer’s pioneer 
work is based upon large clinical and experimental study. He contends 
that vascular nephritis—acute and chronic—is characterized by retarded 
lactose excretion, that the oliguria and polyuria depend upon the influ- 
ences of the vasodilators upon the renal vessels whether the latter are 
sensitive or insensitive to the former, and the normal excretion of the 
iodids and chlorids. Tubular nephritis, it is held, is characterized by 
delayed chlorid and iodid excretion, with the water and lactose output 
normal. 
Christian, considering the work of Schlayer and his associates in 
this field, says: “Still it is undoubtedly true that in functional studies 
of experimental toxic nephritis anatomical lesions do not parallel closely 
functional disturbances, and so from these studies it was to be anticipated 
that in man there would continue to be some discrepancies between clin- 
ical diagnosis, even though based on functional tests and demonstrable 
structural changes in the kidney. These particular functional tests have 770 
DISEASES OF THE KIDNEY 
yielded valuable information, but so far they have failed to serve as an 
adequate basis of diagnosis of type of renal lesion.” 
He further contends that toQ few cases examined functionally have 
been submitted to the subsequent histological examination of the kidneys 
to justify the complete acceptance of the significance of these tests. 
The tests of Schlayer are most valuable in establishing early renal 
change. They offer but little assistance in differentiating the vascular 
and tubular varieties of nephritis, and it is generally conceded that be- 
cause of the diffuse character of the lesion in chronic nephritis, they offer 
but little of value for diagnosis or prognosis (Piersol). 
“The most valuable single aid to the estimation of total renal func- 
tion which is known at present” is that devised by Rowntree and Geraghty 
which makes it possible to determine the total renal function in all forms 
of nephritis whether acute or chronic (Fitz). The phenolsulphoneph- 
tlialein test of Rowntree and Geraghty shows the quantity of the dye 
eliminated through the kidneys within a given time. It has been further 
demonstrated that the extent and severity of the kidney lesion is in direct 
proportion to the quantity of phthalein eliminated within that given time. 
The test is easily applied and is innocent, causing no local irritation 
nor constitutional disturbance. The object of the test is to give the 
clinician an approximate idea of the ability of the kidney to perform 
its function. Rowntree contends that the “phthalein test is of prognostic 
value in all pathological conditions, whereas certain cases of severe neph- 
ritis, even in uremia, show no marked increase in incoagulable nitrogen 
or urea.” Rowntree, who may be considered the leading authority on 
this subject, is absolutely fair in his statements, for he insists that “func- 
tional studies reveal only the excretory capacity of the kidney. By them- 
selves they do not make the diagnosis nor settle the prognosis. Just as 
routine blood examinations occasionally reveal an unsuspected leukemia, 
the routine use of functional tests bring latent kidney involvement to 
light.” It is not often that, as in a case reported by Rowntree, functional 
tests (phthalein) will be required to differentiate and prognosticate dia- 
betes insipidus, but it can be easily understood that such differentiation 
by the renal sufficiency test may promptly change our conception of the 
case and lead to accurate prognosis. 
To he of value for the prognosis of internal disease the extent of kid- 
ney invasion can only he determined hy adding to the careful clinical 
study of the case, the knowledge gamed hy repeated functional tests 
(phthalein). The regenerative power of the kidney cannot be ignored; 
the improvement of the cardiovascular condition and the relief from 
increased skin and bowel function are factors of great prognostic value, 
particularly in the chronic nephropathies, i. e., interstitial nephritis more 
particularly. In cases of the chronic nephropathies which show progres- 
sion, in which the clinical history is usually characteristic and suggestive, ANOMALIES OF THE URINARY SECRETION 
771 
the progressive lowering of renal function argues in favor of early uremia. 
With renal obstruction, calculosis—hydronephrosis, abscess—the prog- 
nosis is less grave with reduced elimination as demonstrated by the 
phthalein than with a similar find in the chronic or acute nephropathies. 
On general 'principles it may be concluded that whenever the kidney 
jails to eliminate phthalein it is proof of renal insufficiency, and the prog- 
nosis should be guardedly given—it is usually bad. 
In all nephropathies the prognosis based upon the tests can only in- 
clude a knowledge of the efficiency or inefficiency of the organ. “Death 
may occur from innumerable other factors concerning which (the tests) 
they give no information” (Rowntree). 
In acute uremia the impairment of function is clear without any 
functional test, though the test gives positive information. In fatal 
uremia there is practically no trace of the dye, or but little, during the 
two hours of observation. If in mild cases of nephritis with fair quan- 
tity of urinary secretion and nervous manifestations, repeated functional 
tests show normal or approximately normal output of the phthalein, the 
prognosis is good and the symptoms are not likely to be of uremic origin. 
With nephropathies and symptoms referable to the brain, the eyes, 
or the gastro-intestinal tract in which uremia is strongly suspected, the 
sufficiency test will give valuable information, making the diagnosis of 
uremia or threatening uremia possible in many cases without inconvenience 
to the patient, while the forecast is consequently strengthened. 
Clinical observations by trustworthy observers prove that with both 
chronic and acute nephropathies the functional tests may occasionally 
give figures which approach the normal (or they are normal) and yet 
uremia may promptly follow and may be fatal (Foster-Baetzer). I 
advise against relying upon functional tests alone in deciding upon the 
possibility of uremic poisoning in cases in which the clinical, including the 
urinary (chemical and microscopic) features, are strongly suggestive. 
When the nephropathies are associated with cardiovascular symptoms 
(failing heart and renal engorgement) the output of the dye is materially 
reduced. Under such conditions the increased and timely excretion of 
phthalein is encouraging and indicates improvement of the heart, relief 
of congestion and, for the time at least, danger reduced. When the heart 
symptoms improve and the functional test shows lowered excretory capacity 
persistent, the nephritis is grave and the prognosis correspondingly bad. 
The tests for the estimation of the incoagulable or nonprotein nitrogen 
of the blood are valuable, but are complex and cannot easily be used by 
the busy clinician without a well-trained laboratory assistant. The study 
of the retention of urea in the blood is of great prognostic value. The 
range easily computed by the Armard formula establishes 1.0 as the 
standard. High readings are found with advanced chronic nephritis and 
run parallel with increase of symptoms (See References for method, etc.). 772 
DISEASES OF THE KIDNEY 
These studies are of great prognostic value for they prove “the stage of 
accumulation of waste products, an accumulation that may vary from 
almost normal figures to enormous increase in uremia” (Elliott). 
The experimental observations of Frothingham, Fitz, Folin and Denis 
with uranium nephritis show that the non-protein index in the blood and 
the phthalein test run parallel as “indicators of renal function, varying 
from normal during the course of the nephritis and returning to normal 
as the nephritis heals” (Elliott). These observers hold that while the 
phenolsulphonephthalein excreted offers the index of the kidney function 
at the time tested, study of the non-protein nitrogen content of the blood 
shows the accumulated difference between manufactured effete or waste 
nitrogen bodies in metabolism and the quantity actually excreted. 
Cumulative symptoms follow, when excretion of the dye (phthalein) 
falls below 40 per cent in two hours (Agnew, Folin, Otto and Seymour). 
The reader is referred to Mosenthal’s article for the consideration of the 
prognostic value of renal function as measured by the estimation of fluids, 
salt and nitrogen, and the specific gravity of the urine; also Janeway’s 
recent paper (See References). 
Another important prognostic feature has been noted by Rowntree, 
Fitz and Geraghty in chronic secondary congestion of the kidney, in 
which the secretion of the phthalein in the urine is reduced, but the in- 
coagulable nitrogen of the blood is not materially increased. Agnew has 
thus succeeded in differentiating the cardiac from cases in which the kidney 
invasion is in the ascendency; Foster suggests that this holds for the 
milder circulatory obstruction but with graver circulatory lesions in which 
there is non-protein nitrogen excess, the criterion is not dependable. 
It seems to the author that the confirmatory evidences of anatomic 
lesions by Thayer and Snowden are among the strongest evidences of the 
value of the phenolsulphonephthalein test in prognosis. These observers 
compared the lesions found on autopsy with the previously made tests in 
54 cases of nephritis of varying types. In all cases of grave nephritis 
they found a decided reduction of excretion of the dye. They contend 
that their experience proves a progressive lowering in the excretion of 
the dye, and this they have learned to consider of considerable value in 
prognosis. They make the strong statement that during a period of fivf 
years they have never met with a severe case of chronic nephritis in 
which there was a satisfactory excretion of phenolsulphonephthalein. 
The observations of Thayer and Snowden were confirmatory of the 
conclusions offered by Rowntree and Fitz, that with chronic kidnev con- 
gestion and reduced dye excretion the normal may be reached as the heart 
compensation is established. The tolerance which is often established by 
the individual to uremic and toxic states becomes an important factor in 
prognosis, and under such conditions it will be found that the dye excre- 
tion may remain abnormally and surprisingly low during long periods; ANOMALIES OF TIIE URINARY SECRETION 
773 
OH the other hand., as has been demonstrated by Arnold, proper living 
(rational diet) in these cases often holds patients with marked renal 
insufficiency during months and years* 
The results of renal sufficiency tests are often contradictory* Serious 
clinical manifestations are often at variance with the functional test* and 
vice versa, mild clinical evidences of nephritis are associated with 
prisingly low values. Elliott expresses the opinion of the advanced dim 
ician. He says: “In view of the long recognized fact that it is impossible 
co predict accurately by clinical study alone what course the disease will 
take in development, it would appear that we should at least accept the 
results of function study as a qualifying factor in prognosis.” 
The early application of the sufficiency tests was largely limited to 
surgical cases by Rowntree and Geraghty. The most recent article deal- 
ing with the surgical aspect of this question is from the pen of Braasch 
and Thomas, of the Mayo Clinic. The material of these observers is 
large and has been carefully tabulated. It is not within the province of 
this work to consider the prognostic value of the tests from the surgical 
point of view, but it may be assumed that the authors mentioned are 
correct when they hold that “probably the greatest value of the functional 
tests will be as an aid to the diagnosis of doubtful lesions of the kidney.” 
The urologist has given us valuable diagnostic and prognostic data in 
obscure cases from ureteral catheterization and associated renal sufficiency 
tests of the separate kidneys. It can be easily understood that in cases 
where surgical interference is indicated such study may prove invaluable 
for prognosis and therapy. Braasch and Thomas in their concluding 
paragraph say, after acknowledging the scientific efforts of Rowntree and 
Geraghty: “The phenolsulphonephthalein test, because of the ease of 
application and rapidity of secretion, remains as probably the best func- 
tional test at our command. Hor is it our purpose to detract from the 
value of a careful examination of the character of ureteral secretion in 
surgical conditions of the upper urinary tract. It is our contention, how- 
ever, that the fundamental surgical principle and clinical data should 
determine whether or not an operation is indicated; and that renal func- 
tional tests are of practical value, largely as an aid to differential diag- 
nosis and only to a limited degree as a prognostic aid,” Clinicians are 
inclined to subscribe to the dictum of Christian as safe, in the light of our 
present knowledge and experience. 
“As in all forms of clinical diagnosis, not the single test, but many, 
yield the data on which diagnosis must be based. In this sense these 
functional tests have yielded new data, and a discriminating evaluation 
of this new data along with a consideration of data furnished by other 
methods of examining our patients already long in use, justify us in 
making diagnosis of renal condition with an increased certainty. We 
can expect few<w failures in renal diagnosis than before we had these 774 
DISEASES OF THE KIDNEY 
functional tests, but so long as microscopic study fails to yield a demon- 
strable anatomical change to correspond with all observed functional 
variations, so long will we remain unable to make in advance an exact 
anatomical diagnosis which in most cases will prove to be correct when the 
pathologist examines the kidneys.” 
Urinary cryoscopy—the determination of the freezing point by means 
of the Beckmann thermometer, an exceedingly delicate instrument—has 
not been accepted by the profession as a means of much value in determin- 
ing the total renal efficiency. 
References 
Agnew. Arch. Int. Med., March, 1914, 485. 
Arnold. Boston Med. & Surg. J., 1914, clxxi, 601. 
Armard. J. Am. Med. Ass., March 7. 1914, p. 813; also Nov. 27, 1915, p. 1958. 
Baetjer (Wm. A.). Arch. Int. Med., June, 1913, 593. 
Blum (Victor). Renal diagnosis. Translated by Christopherson, New York, 1914. 
Braasch & Thomas. J. Am. Med. >4ss., 1915, Ixiv, 104-108. 
Christian. Tr. Cong. Phys. & Surg., 1913, ix. 
Elliott. J. Am. Med. Ass., June 5, 1915, 1885. 
Fitz. Am. J. Med. Sc., cxlviii, No. 3, 330. 
Folin, Denis & Seymour. Arch. Int. Med., Feb., 1914, 224- 
Foster (Nellie B.). Functional tests of kidney in uremia. Arch. Int. Med., Oct., 1913, 452. 
Uremia—the non-protein nitrogen of the blood. Idem., March, 1915, 356. 
Frothingham (Jr.), Fitz & Denis. Arch. Int. Med., Sept., 1913, 245. 
Janeway (Theo.). N. Y. Med. Rec., Dec. 11.1915, p. 1026. 
Mosenthal. Arch, of Int. Med., Nov. 15, 1915, p. 733. 
Piersol. Interstate Med. J., 1914, 1172. 
Rowntree. Tr. Cong. Am. Phys. & Surg., 1913, ix. 
Rowntree & Fitz. Studies of renal function in renal, cardiorenal and cardiac disease. 
Arch. Int. Med., March, 1913, 258. 
Rowntree, Fitz & Geraghty. The effects of experimental passive congestion on renal 
function. Arch. Int. Med., Feb., 1913, 121. 
Rowntree & Geraghty. J. Phar. & Exper. Ther., 1910, i, 579. 
Ibid., 1911, ii, 393. Arch. Int. Med., March, 1912, 284- 
Schlayer. Deutsch. Arch. f. klin. Med., 1910, xcviii, 17. Idem., 1911, ci, 333; 1911, cii, 311. 
Thayer & Snowden. Am. J. Med. Sci., Dec., 1914, 781. 
(f) Bacilluria—Bacteriuria 
When the urine is laden with disease-producing germs, the condition 
is known as bacteriuria or bacilluria. 
Most cases of bacilluria are symptomatic—secondary to general infec- 
tion due to the Bacillus typhosus, the Bacillus coli commune, streptococcus 
or gonococcus—or they arise from foci either in the bladder or somewhere 
within the genito-urinary tract. It is often exceedingly difficult, in fact 
impossible, to decide whether the bacilluria is due to the entrance of ANOMALIES OF THE URINARY SECRETION 
775 
germs (as in typhoid fever) directly from the blood stream to proliferate 
in the kidney or urinary passages or whether there may not be a focus 
somewhere within the urinary passages, often giving rise to no symptoms, 
which surcharges fhe urine. When bacilluria is due to genito-urinary 
infection (local) the prognosis is almost always good and depends entirely 
upon the nature of the primary disease. 
With the bacteriuria of constitutional infection there is rarely a local 
lesion in the kidney. With the grave infections, or even some milder 
infections, there may be but slight evidence of bacilluria though nephritis 
often complicates the primary disease and materially influences the out- 
come. 
Pyuria (purulent urine) is an indication of bacteriuria. The prog- 
nosis depends on the ability to reach the focus responsible for the second- 
ary infection. Moderate and transitory bacteriuria may be normal and 
insignificant, for in over 50 per cent of normal individuals the urethra 
holds bacteria (Kelly and Burnham). (See also Lustgarten & Manna- 
berg, Rovsing, Savor, Hofmeister and Chvostek.) 
Cystitis is the cause of a large number of bacillurias. This is a 
surgical field, which offers an excellent prognosis when rationally treated. 
The reader is referred to the article of T. R. Brown dealing with the bac- 
teriuria of cystic origin. 
As a rule, the fresh urine of normal subjects does not show bacterial 
contamination. With true bacteriuria it is exceedingly difficult, even in 
the fresh specimen to overcome the turbidity of the urine entirely. 
Bacteriuria or bacilluria is frequent with diabetes mellitus, tubercu- 
losis of the genito-urinary tract, 'purulent kidney, embolic nephritis, 
scarlatinal nephritis and infectious jaundice (Weil’s disease). 
Spaeth includes among the pathologic bacteria causing bacteriuria; 
1. Bacillus Tuberculosis.—Every purulent urine which persists, 
should be suspected to be of tuberculous origin; only repeated examina- 
tions will clear the diagnostic and prognostic horizon (See Tuberculosis 
of the Kidney). 
2. Gonococcus (See Gonococcemia). 
3. Bacterium Coli Commune.—This bacilluria is likely to be resist- 
ant at times; the urine is persistently acid. 
4. Typhoid Bacillus.—The typhoid bacillus in the urine demands 
cautious attention; it is of greater danger to those who surround the 
carrier than to the host. 
5. Staphylococcus 
(a) Staphylococcus pyogenes aureus 
(b) Streptococcus pyogenes 
6. Streptococcus Pyogenes Ureae—The urine is alkaline as a rule. 
The process is usually rebellious. 776 
DISEASES OF THE KIDNEY 
1. Streptococcus with Acute Nephritis (See Acute Nephritis) 
8. Streptococcus Cystitidis 
9. Bacillus Septicus Vesicae 
10. Bacterium proteus fluorescens 
11. Proteus vulgaris Hauser. 
The actinomycotic or the ray fungus, the saccharomyces (particularly 
with diabetes), the mycelium, the Penicillium glaucum and with pregnant 
women the Oiduim albicans, may cloud the urine. 
Most fcacillurias offer a favorable prognosis; all demand the thorough 
consideration of the primary condition before any forecast is justified. 
References 
Brown (T. R.). Johns IIopkxns Hosp. Rep., 1005, 1 89* 
Chvostek. Zur Aetol. d. acuten Gelenkrheum. Leipzig, 1898. 
Hofmeister. Fortschr. d. Med., 1894, xii. 
Kelly & Burnham. Diseases of the kidney, ureters and bladder. New York, 1914. 
Lustgarten & Mannaberg. Vierteljahr. f. Dermat. u. Syphilis, 1887, xiv, 905. 
Savor. Beitrage z. Geburtskunde u. Gynaek., 1899, ii, 103. 
Spaeth. Untersuchung des Harnes. 3. Aufl. Leipzig, 1908. 
(g) Chyluria 
(a) Chyluria 
(b) Lipuria 
Prout named the condition “chylous urine,” a disease mainly of trop- 
ical climates. 
(a) Chyluria 
Chyluria is never normal—fat is not a normal ingredient of the urine. 
Chyluria may he either 'parasitic or non-parasitic. 
Parasitic chyluria is found in the tropics; the urine is characteristic 
for it contains the constituents of the chyle, fat, lymph cells, blood cor- 
puscles and soluble albumin. In some urines cholesterin and lecithin are 
present. In the milder cases the urine may be bloody and decomposes 
easily. 
The chyluria due to the Filaria sanguinis hominis is not directly 
dangerous, per se; it is chronic; causes considerable drain and weakness, 
often persistent anemia; it limits the activities of the patient and makes 
him wretched. 
In pregnant women the symptom when infected is markedly aggra- 
vated, probably because of the rupture of a lymphatic varix into the blad- 
der (See also Filaria Sanguinis Hominis). ANOMALIES OF THE URINARY SECRETION 
777 
(b) Lipukia 
(See also Lipuria in this Section, Subdivision b). 
Lipuria is not a true chyluria. With fatty degeneration of the kid- 
ney and marked parenchymatous breakdown and milky urine, lipuria 
may occasionally occur; the same condition may be associated with or 
follow phosphorous poisoning; it is also found in pregnant women. With 
kidney complications—chronic nephritis or acute nephritis—there may be 
abundant sediment on centrifuging including degenerated epithelia and 
casts. 
With obstruction of the thoracic duct due to the pressure of nodules, 
adhesions or large-sized growths, chyluria may be a symptom of the 
primary disease. In all forms of non-parasitic chyluria (not lipuria) the 
chyle must in some way gain entrance to the urine through a leaking 
chyle-carrying vessel. It happens occasionally after fractures that fat 
gains entrance to the urine and causes lipuria (See Lipuria). 
Contusion or compression of the liver or fatty growths may cause 
fatty urine. Lipuria may be a symptom of diabetes mellitus, tuberculosis 
or obesity. There is danger of fat emboli in some of these cases; for- 
tunately the complication is rare. Prognosis of uncomplicated lipuria 
depends upon its cause (See Lipuria). 
Non-parasitic chyluria may persist during many years; there may be 
latent periods long or short followed by exacerbations, until finally the 
symptom may disappear never to return. The attacks may last during 
varying periods—few weeks, months or years. Normal urine is voided 
during remissions (See also Filaria Sanguinis Ilominis). 
The majority of non-parasitic chylurias offer a favorable prognosis; 
though obstinately chronic, life is not often threatened. 
(h) Phosphaturia 
The deposition of the phosphatic content of the urine depends upon 
its reaction. The earthy phosphate of lime and magnesia are soluble in 
the acid urine; neutral and basic phosphates of lime and magnesium show 
strong tendency to be deposited in urine which is but slightly acid, neu- 
tral or alkaline. The phosphates are derived principally from the food 
but also from the tissues. Brain workers, nervous individuals, tubercu- 
lous subjects, patients with marked wasting, with the grave anemias and 
degenerative atrophic diseases of the liver show increased production of 
phosphoric tcid. 
During pregnancy and with many acute diseases the loss of phos- 
phates is reduced early, to increase with the advance of the infection. 
Normally the urine is alkaline after meals and the phosphates are appar- 
ently increased. The diminished acidity of the urine, or alkalinity, often 778 
DISEASES OF THE KIDNEY 
causes a turbid urine to be voided after eating—which is by no means to 
be interpreted as pathologic or significant. Only the quantitative esti- 
mation of the phosphates is of value for diagnostic or prognostic purposes. 
If the clinician wishes to reach conclusions he must estimate the loss 
of the earthy and triple phosphates, rather than depend upon the total 
amount of phosphates eliminated through the urine, and this during 
twenty-four hours. With ammoniacal fermentation of the urine there 
is a precipitation of amorphous phosphates without indicating an abnor- 
mal loss of phosphoric acid, hence not a true phosphaturia. In treating 
certain urinary conditions (uric-acidemia, calculosis, etc.), Roberts years 
ago called attention to the advantage of keeping the urine alkaline during 
the greater part of the day by eating small quantities at short intervals. 
In these cases the changed reaction shows marked phosphatic deposit, 
which means nothing prognostically. 
In nervous patients with marked neurasthenia, with diseases char- 
acterized by polyuria (diabetes insipidus, diabetes mellitus, diseases of 
the sexual organs) the voiding of a clouded alkaline or weak acid urine 
causing the “phosphate cloud” often leads to great fear on the part of 
the patient. Autosuggestion may follow, and it is with the greatest diffi- 
culty that the clinician is able to impress the patient with the insignifi- 
cance of the symptom. To the average patient’s mind, the clear urine is 
without danger, but the clouded or milky urine in which there is only a 
changed reaction to cause the deposit, as a rule, is associated with the 
gravest possible genito-urinary diseases. 
With a decreo.se of intestinal excretion in children, particularly with 
some forms of colitis, there is often an increase in the calcium phosphate 
in the urine. The prognosis of true phosphaturia dependent upon faulty 
diet, or functional disturbances, is positively favorable. With brain 
workers, the neurasthenic and hysterical patients who are physically and 
mentally fatigued, the element of rest is important and when fully appre- 
ciated and acted upon improvement of all symptoms is the rule. When 
in the neurotic it is found that calcium metabolism is at fault and that 
as a result there is an abnormally large calcium phosphate loss, diet, rest 
and rational treatment continued during a sufficiently long period, will 
lead to general improvement as well as normal metabolism. 
The 'presence of triple phosphates in the urine (ammonio-magnesium 
phosphates) is, as a rule, dependent upon bladder infection or organic dis- 
ease of that organ. It is only one of the conditions to be considered in 
offering the forecast—the primary disease alone makes prognosis possible. 
The normal amount of phosphoric acid excreted daily is from 1 to 
5 grams; the amount of earthy phosphates from 2 to 2.5 grams. 
Cases of so-called “phosphoric diabetes” or “essential phosphaturia” 
have been reported (Teissier) and are occasionally met in practice (rare 
-—but one in 6,500 cases of internal disease seen by the author) in which ANOMALIES OF THE URINARY SECRETION 
779 
the condition is chronic. There are many symptoms of diabetes, includ- 
ing polyuria, great thirst, progressive emaciation and enormous loss of 
phosphates, in some cases as high as 8 to 10 grams daily. These patients 
may die with symptoms of acidosis, just as diabetics die in spite of the 
fact that the carbohydrate output has been found normal with a high 
organic phosphorous percentage. According to Barker the leading feature 
in a case which he studied was an abnormally large amount of organic 
acids. 
References 
Barker. Quoted by Osier [l. c.]. 
Bradford. Allbutt & Rolleston’s System of medicine, iv, pt. i, 550. 
Osier. Practice-of medicine. 8th ed. New York, 1914, 690. 
Soetbeer. Ueber Phosphaturia. Jahrb.f. Kinderheilk., Berlin, 1902, Ivi, 1, 54- 
Teissier. Essential phosphaturia. Lyon, 1876. 
(i) Oxaluria 
Oxaluria per se has never in my practice threatened life, nor has 
it often required consideration except as the precipitation of calcium 
oxalate in the kidney or bladder, which because of its insolubility has 
led to the formation of calculi. 
The daily output of lime oxalate is largely dependent upon the food 
ingested, though a small amount is excreted on an absolutely oxalate free 
diet. Hence it may he safely assumed that the normal small oxalic acid 
output (1 to 2 mg.) daily is of exogenous origin (vegetable foods mainly) 
and the remainder is endogenous. The entire oxalic acid output daily in 
the normal urine is 10 milligrams. This is held in solution in the form 
of a salt by the acid phosphate of sodium normally present in the urine. 
The “oxalic acid diathesis’’ was introduced when Donne (1838) 
demonstrated lime oxalate crystals in the urine. In practice we fre- 
quently find acid dyspepsia associated with oxaluria. Garrod says: 
“The administration of hydrochloric acid has been shown to promote the 
absorption of calcium oxalate from the food and to increase the urinary 
output; and it is probable that in the cases described by Beghie and others 
as examples of an oxalic acid diathesis attended with neurasthenic symp- 
toms, the deposition of oxalate crystals in the urine was, as Dunlop sug- 
gested, largely due to such increased absorption as the result of the acid 
dyspepsia which was a prominent phenomenon of the condition.” 
Proper diet and the regulation of conditions which will best hold the 
oxalates in solution make prognosis favorable. The presence of free 
hydrochloric acid in the stomach contents and its administration when 
absent, besides the prevention of intestinal fermentation will do much 
to prevent oxaluria in individual cases. In some, there is no known 780 
DISEASES OF THE KIDNEY 
explanation of the tendency, and unless calculosis follows, these patients 
are fairly comfortable as a rule. These conditions are usually transitory, 
though in some subjects there is a marked tendency to the precipitation 
of lime oxalate. The calculi formed are hard and irritating, easily 
recognized by x-ray examination and usually amenable to surgical 
treatment. 
Crofton probably expresses the truth when he says: “The clinical 
significance of oxaluria in the light of our present knowledge is slight. 
When oxaluria is not alimentary, it presumably indicates some oxidative 
perversion, leading to incomplete metabolism of uric acid and of blood 
sugar, occasionally it may indicate derangement of the liver function.” 
In diabetes and in icterus, oxalic acid in large quantities is found in 
the urine in some cases. 
Crofton. Clinical urinology. New York, 1904. 
Garrod (A. E.). Anomalies of urinary secretion. Osier’s Modern Medicine, vi, 40. 
References 
(j) Indicanuria 
Indican—i. e., indoxyl sulphate of potassium—may be present in 
normal urine in small, but easily recognizable quantities. It is but one 
product of intestinal putrefaction; putrefaction may go on in the intes- 
tinal tract without indicanuria. 
E. E. Smith has called attention to marked gastrointestinal toxemia 
without excessive indol absorption. Brunon and Gibert have proved that 
the proportion of the ethereal sulphates to the total nitrogen of the urine 
is a nearly constant one in health, which rarely falls below 1 to 100 and 
never rises above 1.40 to 100. 
Indol which is resorbed from the intestinal canal is oxidized in the 
tissues of the body to indoxyl and is converted into indoxyl potassium 
sulphate in the urine where it is bound to potassium sulphate. The 
formation of indol in the intestinal tract depends upon bacterial action. 
The albumin content is decomposed in the presence of the bacteria. 
Indicanuria per se is not of great prognostic significance; it is often 
symptomatic of functional or organic disease and may in occasional cases 
prove of diagnostic importance. This is true of cases in which there are 
but scant or unsatisfactory symptoms of intestinal obstruction, also with 
peritonitis, Asiatic cholera, malignant and ulcerative diseases of the 
stomach and intestines. The depth of color with intestinal obstruction is 
of some prognostic and diagnostic value; considered alone it is valueless. 
Indicanuria—associated with gastro-intestinal indigestion and the 
evidences of auto-intoxication indicanuria—is not the principal disease, 
simply a symptom and as such it should be interpreted (Forchheimer). ANOMALIES OF THE URINARY SECRETION 
781 
Of 77 cases examined by Forchheimer, 68 showed indicanuria. The 
formation of intestinal toxins which are responsible for indicanuria takes 
place in the lower segment of the small intestine and in the colon. Mor- 
gan holds that the chief distributing center is the colon, and he asserts 
that “imperfect digestion of proteid foodstuffs in the small intestine is the 
leading cause.” He further holds that “depressed nerve action due to 
overwork or disease, amounts rather than quality of food taken in excess 
of the ability of the intestines promptly to take proper care of it, too 
great preponderance of one class of food taken over too long a period when 
at the same time there may be more or less nerve depression” are among 
the most frequent causes of disturbed intestinal digestion which are re- 
sponsible for indicanuria. 
There are indicanurias not easily influenced by treatment in which it 
is often exceedingly difficult to define a cause and in which, barring 
symptoms (usually insignificant, never threatening early) the condition 
persists during many years. These cases are characterized as “chronic 
intestinal toxemia,’’ and are unquestionably responsible with other toxic 
products for distant changes in heart, arteries and kidneys in a large 
number of cases. 
Lesions of the intestinal mucosa, however slight, continue indicanuria 
during unlimited periods. The greater the epithelial change the more 
persistent is the indicanuria. Formal epithelium offers a barrier to the 
formation of indol and its resorption from the intestinal tract (Herter 
and Wakeman). 
Constipation per se is not a cause of indicanuria (Jones, Houghton) ; 
Forchheimer’s experience does not agree with Jones’ conclusion. The 
former found indican in 39 of 44 cases of constipation. Baar in his 
recently published work enters minutely into all the possible factors which 
cause indicanuria. For purposes of prognosis I have considered the 
literature included by Baar and the diseases of which indicanuria may be 
a symptom. 2,037 patients examined and 8,406 tests for indican 
were made of which 4,039 were positive and 4,007 negative. 
There are but few diseases in which repeated examinations of the 
urine for indican will fail to give positive results at some time during 
their course. 
It is safe to conclude that the majority of indicanurias per se are of 
minor significance; that with chronic intestinal diseases, indicanuria is a 
prominent symptom and indicates intestinal putrefaction; that many 
grave diseases, cancer and ulcer of the intestine, large and small (particu- 
larly if causing obstruction), are associated with marked indicanuria; 
that indicanuria is often an expression of a chronic toxemia in which 
there are also other toxic substances which when neglected may after long 
periods invite distant degenerative changes in vital organs (heart, arteries 
and kidney). 782 
DISEASES OF THE KIDNEY 
. Bacterial action is required to produce putrefactive fermentation in 
connection with the production of indican (Senator, Porter). 
The toxins formed at the same time as indol are absorbed into the 
circulation from the alimentary canal and by their combined action cause 
a train of nervous symptoms. 
Conditions which favor the production of indican are improper diet, 
lack of exercise, mental strain and fatigue, perverted gastro-intestinal 
secretions and abnormal gastric and intestinal mucosae. 
In my last 6,510 cases of internal disease 50 per cent showed either 
a trace or considerable indicanuria some time during observation. 
References 
Baar. Die Indicanurie. Berlin & Wien, 1912. 
Brunon & Gibert. La Presse Medicate, Oct. 21, 1908. 
Forcliheimer. Am. J. Med. Sci., 1907, ii, 70. 
Herter & Wakeman. J. Exper. Med., iv, 307. 
Houghton (H. A.). Quoted by Baar P. c.]. 
Jones (Allen). New York Med. J., Ixxi, 637. 
Morgan. American medicine, Nov., 1908. 
Prout. Nature and treatment of stomach and urinary affections. 5th ed. London, 1840. 
Porter. New York Med. Rec., June 15, 1907. 
Smith (E. E.). American Medicine, July, 1908. 
(k) Urobilinuria 
The clinical significance of urobilin in the urine is often of consider- 
able importance. Meyer-Betz in his most exhaustive study of the subject 
holds that urobilin is produced from bilirubin, and he accepts the con- 
clusion of Friedrich Mueller that the transformation takes place in the 
intestinal tract (enterogenous, in contradistinction to the hepatogenous 
theory). Without bile in the intestine urobilinuria is impossible. Uro- 
bilinogen is the antecedent of urobilin and the two cannot be divorced. 
Urobilinogen is often present in normal urine in very small quantities, 
and gives the urobilin reaction only when exposed to air and light or by 
the action of acids (Wood). 
Whenever urobilin is present it may be concluded that the liver- 
parenchyma has suffered, that bile is finding its way into the intestinal 
tract. If the intestinal tract were absolutely free of bacterial contamina- 
tion, with bile in the intestine there would be no urobilinuria. In the 
newborn there is no urobilinuria; after the third or fourth day it may 
appear with the appearance of germ life. 
With stricture of the common duct sufficient to prevent the onward 
flow of bile, however grave the disease, urobilinuria does not appear. ANOMALIES OF THE URINARY SECRETION 
783 
Small quantities of urobilin in tbe urine are of no prognostic signifi- 
cance; large quantities are evidence of disease, except during the last 
days of pregnancy when its presence may be considered to be normal. 
For diagnostic and prognostic purposes it should be remembered that it is 
impossible to consider urobilin separate from urobilinogen, for the transi- 
tion of urobilinogen as already suggested to urobilin is' usually prompt 
and rarely fails to take place. 
Urobilinuria is frequent with scarlet fever (Jugendreich) particu- 
larly with the malignant or more severe types. The mild cases of measles 
may show moderate urobilinuria, the more severe are likely to give posi- 
tive reaction. The fact that urobilinuria has been demonstrated with 
German measles would prove that for the prognosis of the exanthemata 
it is unwise to consider its presence of great value. 
Urobilin may be present in the urine of typhoid patients during the 
active periods of the disease and is often found during convalescence. It 
is not expressive of the severity of the infection; it is, however, influenced 
by the extent of intestinal lesions and resulting diarrhea. 
With bacillary dysentery urobilin is absent from the urine; with the 
amebic variety it is only found when there are liver complications, i. e., 
abscess (Justi). 
Urobilinuria with acute polyarthritis is always indicative of severe 
infection. Ilildebrandt found it in 50 per cent of all cases. 
With septicemia urobilinuria is only present when there are liver or 
heart complications; wdth erysipelas it is usually present early and per- 
sists until convalescence has ended; the same is true of meningococcus 
erysipelas. With pneumonia urobilinuria is usual. When jaundice is 
present the prognosis is serious—otherwise it is not of moment. With 
pernicious malaria urobilinuria is present and reduces the effect of quinin 
(Simpson and Edie). The severe types of yellow fever and relapsing 
fever are rarely without urobilinuria. 
Urobilinuria with pulmonary tuberculosis is rarely present in mild or 
incipient cases; it is an accompaniment of advanced tuberculous, general 
infection. Hoppe-Seyler found but slight urobilinuria with acute miliary 
tuberculosis, and that urobilinuria followed the injection of tuberculin. 
With heart lesions it may be concluded that well compensated faults 
are without urobilinuria; that with an extra tax upon the heart, with 
broken compensation, it promptly appears to disappear with improvement 
in heart tone. With evidences of stasis (renal and hepatic) urobilinuria 
is to be expected. This is the more evident when organic disease of the 
liver coexists, and Jonas has demonstrated the greater frequency of uro- 
bilinuria with disease or failure of the right heart. 
Urobilinuria is not prominent with the nephritides or nephropathies 
unless there is associated infection or organic disease of the liver. With 
infectious pyelitis during pregnancy I have found urobilin in the urine. 784 
DISEASES OF THE KIDNEY 
The ease terminated favorably for mother and child and the grave anemia 
which was threatening yielded promptly. 
Ulcer of the stomach and cancer, when uncomplicated, are without 
urobilinuria. When there are metastases, or with added infections, the 
condition is reversed (Infectious gastritis) (Meyer-Betz). 
The presence or absence of urobilin from the urine with other intes- 
tinal diseases, including 'peritonitis, appendicitis, obstinate constipation, 
is of no prognostic value. 
With alcoholics persistent urobilinuria is at least suggestive of advanc- 
ing liver change. With acute alcohol poisoning urobilinuria is prominent. 
Discontinuance of alcohol, unless there are deep liver changes, is followed 
by disappearance of urobilin from the urine. 
Poisons, such as carbon monoxid, chloroform, antifebrin (Friedrich 
Mueller) sulphonal, trional and salvarsan may cause liver changes leading 
to urobilinuria. 
Urobilinuria with the diseases of the blood may be present; rarely 
with uncomplicated chlorosis; often with pernicious anemia and 
bothriocephalus anemia. The leukemias in the terminal stages and with 
acute leukemia often show urobilinuria, as do Hodgkins disease and 
purpura. 
Almost all diseases of the liver in which the bile finds its way into the 
intestinal tract are associated with urobilinuria. The most prominent of 
these is Laennecs cirrhosis. In this disease urobilinuria may precede 
other evidences of organic change. Meyer-Betz calls attention to the fre- 
quency of urobilin in the blood and ascitic fluid of these patients. 
Hypertrophic cirrhosis and Banti’s disease are almost always found 
with urobilinuria. I have, in connection with other grave diseases of 
the liver hemolytic jaundice and the degenerative diseases of the liver, 
called attention to urobilinuria as a symptom and have considered its 
prognostic significance (See Diseases of the Liver). It may be safely 
assumed that the more severe and deep the changes in the liver paren- 
chyma, the more marked is the urobilinuria. The presence of urobilin- 
uria will often prove of great value in deciding upon the functional ability 
of the liver; it should never, however, be given precedence over subjective 
symptoms or objective signs. Large cancer masses in the liver are usually 
found with urobilinuria, not so with small nodules always. It is safe to 
conclude that infectious processes when associated with urobilinuria are 
complicated with liver degeneration. Whatever the disease of the liver, 
if the common duct is occluded, urobilinuria is invariably absent. 
References 
Hildebrandt. Ztschr. f. klin. Med., 1906, lix, S51 {full literature Munch, med. Wchnschr., 
1909, 710). 
Ztschr. f. klin. Med., 1911, Bd. Ixxni, 189. ANOMALIES OF THE URINARY SECRETION 
785 
Uoppe-Seyler (G.). Virchow’s Arch., 124, H. 91, 80. Ueher d. Einwirkung d. Tuber- 
culose auf d. Gallenfarbstoffbildung. 
Jonas. Wien. klin. Wchnschr., 1912, xxv, 875-877. 
Jugendreich. Arch. f. Kinderheilk., 1904, xxxviii, 208. 
Justi. Arch. f. Schiffs- u. Tropenhyg., 1912, xvi, 443. 
Meyer-Betz. DieLehrevom Urobilin (with exhaustive literature). 
Ergebnisse d. inner. Med. u. Kinderheilk., 1913, xii, 733-808. 
Mueller (Friedrich). Ztschr.f. klin. Med., 1887, Bd. xii, 45. 
Kongr.f. inner. Med., 1892, xi, 118. 
Simpson & Edie. Annals of Trop. Med., 1912, vi, 443. 
Wood (Francis Carter). Chemical and microscopical diagnosis. 
(/) Other Substances 
Among the leading urinary anomalies which have not been considered 
in the preceding pages are: 
Lithuria 
Cystinuria 
Melanuria 
Alkaptonuria 
Pneumaturia 
Lipuria 
Lipaciduria 
HematoporpTiyrinuria 
Lithuria 
Lithuria and the uric acid diathesis are considered in connection with 
the study of the prognosis of gout and the consideration of urinary changes 
with many functional and organic diseases. 
Free uric acid is insoluble and is found only in hyperacid urine. 
Uric acid is held in normal urine in solution and as the ammonium, 
sodium and potassium salts, i. e., urates. When uric acid is precipitated 
it is present in increased and abnormally large quantity, the acidity is 
high, the mineral acid content is low as is also the pigment. The prog- 
nostic significance of uric acid in the urine has been enormously exag- 
gerated : excessive production and faulty elimination cause symptoms to 
which the proper significance has been given in the Section on Metabolic 
Faults. 
The precipitation of the amorphous urates causing the “brick dust 
deposit” (acid sodium urate) from the cool urine is of no great clinical 
or prognostic significance. Often the urine is excessively acid and con- 
centrated (specific gravity high). The underlying conditions, if there are 
any which are abnormal, offer their own prognosis. 
Cystinuria 
Usually cystin when found in the urine is indicative of calculosis 
either of the bladder or kidney pelvis. I have seen but few cases of 786 
DISEASES OF THE KIDHEY 
cystinuria in which there were no symptoms of stone. One of my cases of 
cystinuria, seen over twenty-five years ago, has never so far as I have been 
able to determine from x-ray or bladder search, formed a calculus, and 
has not been affected by the persistence of the symptom. Most cystinurias 
are congenital and hereditary. My case showed no hereditary predis- 
position. In the case of a babe, aged twelve months, I removed, over 
25 years ago, a cystin stone which was caught in the urethra; there never 
was return of cystinuria. How grown to manhood, there are no evidences 
of anything abnormal in the urogenital system. 
Melanuria 
Mel anuria or “black urine” may be due to one of several causes. 
True melanuria (melanin, phymatorhusin) is due to the presence of 
a pigment of unknown origin which is, in all probability, derived from 
blood pigment. It is not per se of prognostic value, but occurs with a grave 
condition (melanosis) in which there are multiple melanotic or sarcoma- 
tous growths. With marasmus and reduced (cachectic) patients melan- 
nria may persist without melanotic growths. It is not pathognomonic of 
melanotic cancer and is not always present with such growths, though it 
may be. 
With deep jaundice the bile salts and coloring matter are responsible 
for the “black urine.” Jaundice with black urine is usually grave, often 
of malignant origin. 
It is exceedingly rare to find benign indicanuria so deep as to cause 
black urine; the malignant intestinal obstructions may occasionally offer 
black urines due to excessive indicanuria. During the early days of anti- 
septic surgery when the spray .was used and open surfaces were long ex- 
posed, black urine with other evidences of carbolic acid poisoning was 
frequent. Such complications added an element of danger because of 
interference with renal function. The long and injudicious use of salol, 
salicylates, carbolic acid, resorcin and some coal tar preparations may be 
followed by black urine. The associated symptoms and general condition 
of the patient with the primary disease make prognosis easy. 
Alkaptonuria 
I have never in practice met a case of alkaptonuria. It is an exceed- 
ingly rare condition, usually found in males; it is always congenital and 
persists during life without interfering in any way with the general condi- 
tion or activities of the subject. There are a number of recorded cases in 
which several members of a family had alkaptonuria, some in which father 
and son showed it and in some consanguineous marriages seems to have 
been a factor. 
When alkaptonic urine is first voided it may appear normal, it 
promptly becomes brown and later black. ANOMALIES OF THE URINARY SECRETION 
787 
Pneumaturia 
Gas in the urine without trauma or mechanical insult is exceedingly 
rare unless there ha\re been ulcerative changes, such as cancer or pressure 
(vesicovaginal fistula, vesico-enteric fistula), or as the result of the 
growth of fungi or germ life (air producing bacillus, colon bacillus), or 
where, through instruments, air enters the bladder. I recently had a 
case of cancer of the bladder and prostate with pneumaturia in Avhich no 
perforation Avas found; neither Avas the Bacillus aerogenes capsulatus 
present. The prognosis of pneumaturia depends entirely upon the pri- 
mary cause. The condition is usually surgical. 
Lipuria 
The prognosis of lipuria (fat in the urine) when due to degenerative 
changes in the kidney parenchyma, fat embolism (usually after fractures), 
acute or subacute phosphorous poisoning, is always grave. These condi- 
tions are not true chylurias. 
When the excessive use of fat leads to lipuria it is of no prognostic 
significance. 
Tn one of my cases a tuberculous pyonephrosis Avas associated with 
fat in the urine. Ebstein reports pyonephrosis with lipuria. 
I have also seen lipuria with cases of amyloid disease in tuberculous 
subjects and with long continued suppuration. 
Lipacidueia 
von Jakseh and Rokitansky called attention to the presence of volatile 
fatty acids in the urine, including formic, acetic, butyric and propionic 
acids. Volatile acids in the urine have been found with grave febrile 
disturbances, profound involvement of the liver parenchyma and the 
severe type of diabetes mellitus. Lipaciduria when considered alone is 
of no prognostic value, von Jakseh says that the origin and course of 
lipaciduria follows the same laws which govern febrile acetonuria. 
H EMATOPOEPHYRIXTTRIA 
Hematoporphyrin is hematin without the iron element. Normal urine, 
according to Crofton, always “contains minimal quantities of this pig- 
ment.” When hematoporphyrinuria is excessive it is formed in the blood. 
Acute sulphonal, trional and tetronal poisoning shows excessively 
large quantities of the pigment. In Tyson’s case of sulphonal poisoning 
large quantities of hematoporphyrin were passed on three successive days 
(1.683, 1.013 and 0.098 grams). The author calculated that fully “one- 
seventeenth of the body hemoglobin was destroyed and wasted in the 
urine.” 
The leading grave diseases in which hematoporphyrin may be in- 788 
DISEASES OF THE KIDNEY 
creased are diseases of the ductless glands and the blood-producing organs. 
These include Addison’s disease, Graves’ disease, the primary anemias, 
pulmonary tuberculosis, acute polyarthritis, lead poisoning, and Osier 
mentions intestinal hemorrhages and pleuritic effusion. 
References 
Crofton. Clinical urinology. New York, 1904. 
Ebstein. Arch. f. klin. Med., 1879, xxiii, 115. 
von Jaksch. Ztschr. f. klin. Med., 1886, xi, 307. 
Ztschr. f. phys. Chemie., 1886, x, 536. 
Osier (Sir William). Practice of medicine. 8th ed. New York, 1914. 
Rokitansky. Wien. med. Jahrb., 1887, ii, No. 1, 205. 
Tyson. Tr. Ass. Am. Phys., 1902. 
Diseases of the Renal System 
The Nephropathies 
(a) Acute Parenchymatous Nephritis 
{Acute Tubal Nephritis, Acute Bright’s Disease, Acute Croupous 
Nephritis, Acute Catarrhal Nephritis, Acute Desquamative Nephri- 
tis, Acute Nephropathy, Acute Diffuse Nephropathy, Acute 
Glomerular Nephropathy) 
Origin.—Most kidney lesions which are characterized as nephritis are 
degenerative in the main and are of secondary origin (nephropathies). 
They are dependent upon toxic substances as a rule, brought to the kidney 
through the blood stream (hematogenous). These forms of nephropathies 
have been considered in connection with sepsis, scarlatina, diphtheria, 
pneumonia, tuberculosis, erysipelas, Asiatic cholera, typhoid and typhus 
fevers, streptococcus tonsillitis and many of the other acute and chronic 
infections. 
Determining Factors.—The complication (acute nephropathy of infec- 
tious character) with these diseases should never be lightly regarded, and 
I have with each considered the influence upon the forecast (See 
Infections, Section I). The resistance of the patient and the virulence 
of the infection, the depth of the toxemia resulting, are leading determin- 
ing factors for prognosis. 
It is surprising to note that with some epidemics the toxemia is malig- 
nant and overpowering, the nephropathy rapidly degenerative, the urinary 
secretion promptly reduced, the albumin loss in the concentrated urine 
large, the evidences of degeneration, at times inflammatory changes strik- DISEASES OF THE RENAL SYSTEM 
789 
ing, with abundant casts and epithelial desquamation, the uremic symp- 
toms prompt—all favoring an unfavorable termination. In spite of the 
presence of all of these unfavorable conditions and symptoms recovery is 
not impossible. There are, on the other hand, infections and epidemics 
in which there are but few evidences of degenerative changes, moderate 
albuminuria without marked change in renal sufficiency, no overpowering 
toxic symptoms, little influence on the cardiovascular condition, in which 
the prognosis of the primary infection is but slightly modified by the 
presence of the kidney complication. Mild infections may be complicated 
by alarmingly severe nephritis while it often happens that the graver 
infections may escape the complication and an insignificant albuminuria 
remains the only evidence of renal invasion. This is often true of scarlet 
fever. 
As a rule, the more malignant the primary infection the more likely 
is nephritis to develop and the more severe does it prove to he. As already 
suggested this is not always the case. While acute nephritis may he dif- 
fuse and the degenerative changes extensive, including vascular changes 
and abundant exudation, the disease is, as a rule, glomerular. With the 
malignant infections there is a strong tendency to grave degenerative 
changes, hemorrhage and exudation. This type of acute nephropathy is 
always serious, it may complicate diphtheria or other overpowering infec- 
tions with scanty urine, abundant casts (epithelial, granular, blood and 
hyaline), a profound primary toxemia, added uremia, great unrest and 
myocardial wealcness (rapid pulse). 
The Glomerular Type.—The glomerular type of acute nephritis which 
develops in young adults most frequently (less frequent after middle life, 
though not uncommon), is found in the male oftener than in the female 
(3-1), is usually a disease of the middle and lower classes, may develop 
after exposure to cold, after overheating, or the acide infections, after the 
rapid and sudden destruction of the shin (wounds and extensive burns), 
with syphilis; occasionally it proves to be an acute exacerbation of chronic 
nephritis; it is found with pregnancy, alcohol poisoning, Spanish fly 
(cantharides), turpentine, copaiba, phosphorus, salicylic acid, arsenic, 
antimony, potassium chlorate and other drugs. 
The Acute Non-suppurative Nephritis of Councilman 
This form of nephritis may be associated with acute infection. In 
these cases there is often a profound toxemia—particularly with the 
deeper and malignant infections—in which the lymphoid elements are 
numerous in the renal cortex. There are evidences of involvement of the 
spleen and bone marrow from which the cells, which correspond with the 
TJnna “plasma cells,” are carried to the kidney by the blood. Councilman 
holds that acute interstitial nephropathy “is the most common lesion of 
the kidney in the acute infectious diseases of children, particularly 790 
DISEASES OF THE KIDNEY 
scarlet fever and measles, less common in uncomplicated cases of diphthe- 
ria and in smallpox. 
This condition is rare in adults. The lesions most prominent are the 
“infiltration of the interstitial tissue with large mononuclear cells of an 
indefinite type often closely resembling or identical with the plasma cells, 
often closely resembling myelocytes.” The cortex and pyramids are also 
infiltrated; in the renal capillaries and veins these cells are found and the 
larger mononuclear cells are “actively ameboid.” With the more severe 
cases similar changes were found in the heart muscle, spleen, lymph nodes 
and other organs of the body. In these cases the prognosis must always 
he considered grave because the cell accumulation is dependent upon 
anomalies of the blood primarily. 
Nephritis Complicating Infections.—Careful consideration of the his- 
tories of the acute nephropathies establishes the fact that almost all are 
preceded by an acute infection. Many acute infections which lead to 
nephritis are so mild as to receive but little attention. No acute infec- 
tion, however mild or limited, is without the possibility of complicating 
nephritis. Many chronic nephropathies originate in neglected and undis- 
covered acute nephritides. 
Acute syphilitic nephritis has been separately considered (See Syphilis 
af the Kidney). It usually arises in the secondary stage and within the 
first year. My cases have usually yielded to treatment. In some of 
these, edema, dropsies of the serous cavities and urinary conditions have 
seemed threateyiing and unfavorable, but recovery though slow, is usually 
complete. One of my acute specific cases was water-logged and uremic, 
and demanded repeated paracentesis abdominis, yet he made a full re- 
covery without leaving a remnant of kidney disease discoverable by 
repeated tests and long surveillance. 
Outlook.—In grave cases of acute nephritis and primary infection the 
development of the former complication may cause sudden serious cardiac 
weakness after a distinct chill and almost complete anuria with or without 
evidences of uremia. Increase of the constitutional symptoms, particu- 
larly the nervous manifestations of the primary disease with acute 
nephritis, always demands the closest consideration, for the sudden abey-- 
ance of kidney function in such cases, continued twenty-fppr to forty-- 
eight hours, is among the leading dangers. 
Cases in which the added kidney infection is ivithout marked influence 
on the subjective or objective features of the primary disease, in which 
the quantity of urine is not markedly decreased, without dropsy of the 
serous cavities, though edema may be present, without uremia, offer a 
good prognosis. 
Acute nephritics who develop uremia early with convulsions, who fail 
to respond to treatment promptly, in whom the circulatory symptoms are 
prominent, with early changes in blood pressure, with or without persist- DISEASES OF THE RENAL SYSTEM 
791 
ent vomiting, offer a doubtful prognosis. The early invasion of the heart 
(hypertrophy) and vascular (arterial) changes, with bounding pulse and 
relatively high blood pressure, and high pulse pressure, are always evi- 
dences of far-reaching kidney invasion. 
Marked reduction in the quantity of the urine, large albumin loss, 
abundant evidences of desquamation in the presence of renal epithelial 
cells, casts and blood corpuscles with uremic symptoms always demand 
the most guarded prognosis. 
Bloody urine is not always of prognostic significance. Some cases, 
scarlatinal often, begin with hematuria or strongly blood-tinged urine. 
When hematuria is profuse, this is a rare complication of acute uncompli- 
cated nephritis and leads to profound anemia; the condition may become 
grave (See Hematuria, Section VI, III). 
In children compdete suppression of urine is much better borne during 
varying periods than in adults. This is particularly true of scarlatinal 
nephritis (See Uremia). 
An abundant urinary secretion is the most favorable prognostic fear 
ture of acute nephritis in the presence of a sufficient heart. It therefore 
follows that markedly reduced renal function and cardiac weakness are 
the leading unfavorable features of acute nephritis. 
Rapid heart early, with evidences of dilatation and edema, which is 
not favorably influenced by treatment within from three to seven days, is 
unfavorable. Rapid heart arising suddenly during the course of the 
complication with or without fall of systolic blood pressure, demands cau- 
tious watching and is often serious. If the pulse remains rapid and the 
systolic blood pressure is progressively lower and the pulse amplitude is 
low, myocardial weakness may be suspected and the prognosis should be 
guardedly offered. The condition is serious. 
Heart weakness which is not improved by treatment, including rest 
and persistence of dropsy with stomach symptoms (vomiting-uremia) is 
always unfavorable. 
The left heart is not likely to show marked hypertrophy during the 
early days of acute nephritis; rapidly developing enlargement of the heart 
with corresponding rise of systolic blood pressure demands close watching. 
Marked difference between systolic and diastolic pressure under such condi- 
tions, i. e., high pulse pressure, is suggestive of marked obstruction within 
the renal circuit. Marked and persistent hypotension is always serious. 
When with symptoms of acute nephritis there is within the first few days 
or weeks marked hypertension it may be safely concluded that the kidney 
lesion is not acute, that there is an acute exacerbation of a preceding 
chronic nephritis, and the prognosis must be shaped accordingly. 
Sudden acute dilatation of the heart is an occasional fatal complica- 
tion; this may follow with general edema and serous dropsies in cases 
with myocardial degeneration. 792 
DISEASES OF THE KIDNEY 
Pulmonary edema with weak heart, unless it yields promptly, is 
usually fatal. With heart weakness pulmonary edema is likely to recur; 
with endo- and pericarditis it is always grave. Deep and persisting 
cardiovascular changes with acute nephritis are so rare that when present 
they excite a strong suspicion of subacute or chronic nephritis and the 
prognosis should be made accordingly. 
Dropsy is by no means an expression of the severity of the acute 
nephropathy; it is the most constant symptom of acute nephritis. The 
pneumococcus, diphtheritic and typhoid nephropathies are rarely asso- 
ciated with dropsy, whereas the scarlatinal and syphilitic forms are likely 
to show dropsy. 
There are innumerable chronic cardiopathies which develop in the 
wake of acute and neglected nephropathies. 
Acute nephritis may complicate acute or subacute infections without 
causing symptoms of sufficient prominence to create a suspicion of its 
presence. Neglected, this may lead to chronic degenerative changes, i. e., 
chronic nephritis. Acute nephritis, in spite of the disappearance of 
albumin and casts from the urine, may insidiously lead to subacute disease 
which finally merges into chronic and incurable nephropathy. This is 
often true of the acute tubular nephritis of scarlatina, grip, diphtheria, 
tonsillitis, pneumonia and other infections. 
Uncontrollable vomiting with cardiac weakness is always suggestive of 
uremia and unfavorable. 
Vomiting during the early days of nephritis with or without febrile 
movement is not always serious; if it persists with reduced urine output 
and rapid pulse it is ominous. 
Peritonitis with complicating nephritis, whether surgically or medic- 
ally treated, is always exceedingly grave. Appendicitis complicated by 
acute nephritis early is usually deeply toxic; it is likely to be perforative 
and consequently grave. The sudden development of acute nephritis dur- 
ing appendicitis, whether medically or surgically treated, adds an 
enormous element of danger. 
An occasional trace of albumin with the infections without elements 
in the urine, which justify the diagnosis of an acute nephritis, demands 
close watching hut it is by no means of serious import (See Albuminuria). 
Uremia is always a grave complication of acute nephritis but of much 
less serious import than with the chronic types of the disease. Barring 
scarlatina and diphtheria, deaths from uremia in uncomplicated acute 
nephritis are exceedingly rare. In all cases the nitrogen content of the 
blood offers valuable prognostic data (See Section VI, Anomalies of 
Urinary Secretion [ 1 ] ). 
As already suggested children often hear uremic poisoning longer than 
do adults, and complete suppression in children with toxic and infectious 
nephritis may continue during several days without a fatal issue (See DISEASES OF THE RENAL SYSTEM 
793 
Uremia). The tolerance developed by adults and children which makes 
it possible for them to withstand long periods of urinary suppression or 
marked reduction is surprising and in cases which often appear threaten- 
ing the prognosis may justly include this encouraging feature. 
The persistence of albuminuria after the disappearance of acute symp- 
toms and dropsy, must lead to the suspicion of permanent renal damage— 
chronic nephritis. There are cases in the experience of all who watch 
their acute nephritics in which albuminuria in small quantities, without 
more than an occasional cast, persists during many months in which it 
occasionally happens that full recovery follows. The prognosis of such 
cases can be safely offered after thorough and repeated microscopic exam- 
ination of the urine, blood pressure study and the physical examination 
of the cardiovascular organs. 
The Blood.—Most cases present the blood picture of secondary anemia. 
The hemoglobin is markedly reduced; the erythrocyte count is low. The 
specific gravity of the blood is also reduced—in some cases to 1,020 or 
even lower. Increasing anemia with unfavorable urinary conditions and 
constitutional anomalies are often suggestive of subacute or chronic 
nephritis. 
Anemia which persists after the disappearance of dropsy and the other 
acute symptoms must lead to thorough watching of the case. 
If the specific gravity of the urine falls, the blood pressure rises and 
there is slight dyspnea on exertion and there is malaise in spite of the 
absence of albumin from the urine, subacute or chronic nephritis should 
be suspected. 
When there is persistence of elevated blood and pulse pressure, ac- 
cented second aortic sound after the disappearance of the dropsy and 
other acute symptoms, the patient has not been cured of nephritis; the 
case was either one of acute exacerbation of a preceding nephritis or con- 
secutive subacute or chronic nephritis resulted. 
Duration.—It is exceedingly difficult to give an accurate estimate of 
the duration of the acute nephropathies in favorable cases, for there is no 
assurance that there is return to a normal condition of the kidney tissue 
with the disappearance of all subjective and objective features. It often 
happens that months after the patient is supposed to be normal there are 
evidences of chronic nephritis which followed insidiously. The average 
case runs its course in from ten days to almost as many weeks. Cases in 
which many symptoms develop promptly—during the first week—are 
usually serious and likely to prove fatal. I agree with Tyson and Fus- 
sell that no cases which recover “do so in a few days.” Cases may drag 
during long periods and finally recover. 
Mortality.—Favorable cases show increased urinary secretion and de- 
creased cvlindrinuria usually after a period of concentrated and dark- 
colored cast- and epithelial-laden urine, with improvement or disappear- 794 
DISEASES OF THE KIDNEY 
ance of the dropsies and the return of stomach tolerance which indicates 
improved urea elimination. But comparatively few patients die as the 
direct result of acute nephritis; it is a curable disease; even the more 
severe types are likely to recover. It should be remembered and it cannot 
be too often repeated that following the acute symptoms a remnant of 
latent nephritis may lead to chronic changes (chronic tubal or parenchym- 
atous nephritis), which is incurable. The mortality is between 8 and 14 
per cent. 
Between 45 and 50 per cent of all acute nephropathies make a satis- 
factory and full recovery. The remaining 50 per cent pass into a subacute 
or chronic condition, markedly improve for a time or they die, usually of 
uremia (eclampsia), or cardiac insufficiency or some one of the complica- 
tions mentioned in this chapter during the height of the disease. 
The prognosis of the individual case depends more upon the cause of 
the nephritis—the underlying and primary disease—than upon the kid- 
ney complication itself; the toxemia of the former determines the malig- 
nancy or benign character of the latter. 
Complications.—With pneumonia, either in the adult or during early 
life, febrile albuminuria is not always serious. Acute nephritis fully 
developed with pneumonia during the height of the disease is a part of 
existing deep toxemia, and is serious. If in these cases there is active 
delirium, many casts, reduced secretion, or with cardiac weakness and 
even limited infiltration of lung—such complications exist—they are 
always alarming (See Pneumonia—Section I). 
Edema of the lungs has been considered in connection with the study 
of the prognostic significance of individual symptoms. It is always 
serious. It usually means cardiac insufficiency. 
Peritonitis complicating primary nephritis is always grave and usually 
fatal. 
High fever with correspondingly rapid pulse, which persists after the 
first six or seven days is usually due to some complication and is serious 
in accordance with its cause. The majority of acute nephritides are with- 
out marked elevation of temperature. 
Purulent serous effusions (empyema, pericarditis) are always grave 
and add an enormous element of danger. I have referred to the other 
possible complications—heart and vascular anomalies—hypertension, and 
gastro-intestinal lesions, in connection with the consideration of the prog- 
nostic significance of separate symptoms. 
Nephritis of Pregnancy 
Kidney of Pregnancy 
Albuminuria of Pregnancy.—As a rule, the albuminuria of preg- 
nancy, is an expression of a degenerative and inflammatory nephritis DISEASES OF THE RENAL SYSTEM 
795 
with varying albumin loss, abundant casts, at times but few constitutional 
symptoms, in most severe eases edema, reduced urine output, retained 
nitrogen—the quantity varying with the severity of the lesions—often 
circulatory and ocular symptoms; in threatening cases there is uremia 
and nervous manifestations, including convulsions, etc. 
With acute nephritis of pregnancy, I have relied upon the daily meas- 
ure of the urine secreted and the urea output to offer indications for treat- 
ment and prognosis; such observations are possible in practically all cases 
away from the larger laboratories where naturally the other refinements of 
diagnosis (nitrogen and ammonia coefficient) are made. 
The acute nephritis of pregnancy is much more likely to have asso- 
ciated uremia and ocular changes (retinitis) than does acute nephritis due 
to other causes. 
Modern methods of diet and treatment have reduced the mortality of 
puerperal nephritis. Cautious watching of the nitrogen output and the 
nitrogen content of the blood, a cautious observation of the specific gravity, 
urea loss and subjective symptoms as pregnancy advances, make it possible 
for the obstetrician to prevent uremia and consecutive convulsions in most 
cases. There are now but few cases (exceedingly rare) of uncomplicated 
nephritis of pregnancy (albuminuria) which are not safely piloted 
through confinement, for the prognosis without eclampsia (convulsions) 
is not bad, and this complicates less than 25 per cent. The mortality 
among those who develop convulsions depends largely upon the care given 
and prompt rational treatment. The mortality of mothers with convul- 
sions varies between 10 and 25 per cent. In some lying-in hospitals 
where these patients have received treatment (dietetic) during varying 
periods preceding confinement, convulsions are rare and the mortality 
among those who have them, because of prompt treatment, is low. Con- 
vulsions are alivays serious; for the fetus the mortality is higher than for 
the mother—reaching over 50 per cent. 
Eclampsia.—The prognosis of eclampsia is more favorable when it 
occurs after than before delivery. Some obstetricians, however, report a 
high mortality after confinement. Olshausen and Lichtenstein lost 2.) 
and 27 per cent of their cases respectively. Yeit in 002 cases found the 
mortality among primipara 11.3 per cent and 10.1 per cent among multi- 
para, while Goldberg and Lichtenstein claim that eclampsia is most 
dangerous in multipara, while Olshausen found no difference in the two 
groups. 
With persistently high systolic blood pressure and convulsions the out- 
come is serious. Anuria unrelieved after a reasonable period, inability of 
the patient to sweat in a hot pack (Williams), pulmonary edema, feeble, 
rapid and small pulse, are unfavorable. 
With the death of the fetus or its expulsion, the danger of further 
convulsions is materially reduced. With chronic nephritis and pregnancy 796 
DISEASES OF THE KIDNEY 
there is always great danger of recurring convulsions and uremia. The 
cases which offer a serious prognosis are those which develop suddenly— 
usually late—in which the toxemia is at once overpowering and uremic 
convulsions are the first indication of any disturbance. 
Eclampsia arising suddenly toward the end of pregnancy in untreated 
and unsuspected cases in which convulsions continue after delivery, often 
with suddenly arising dropsies, offers an unfavorable outlook. 
Suddenly arising general dropsy with marked reduction of the urinary 
secretion and lowered renal sufficiency toward the end of pregnancy, with 
or without convulsions, is always ominous. 
The prognosis is grave in those cases in which there are early retinal 
hemorrhages; in some of these the acute nephritis is grafted upon a 
chronic nephropathy. Retinal hemorrhage in all cases of puerperal 
nephritis is an unfavorable complication, particularly when associated 
with convulsions. Many recover fully after puerperal retinitis after 
supposed retinitis has proved to be uremic. 
Le Page after reviewing his experiences warns against the dangers of 
subsequent pregnancies and his statistics prove that the stricter medical 
advice is followed the more favorable will be the outcome. With syste- 
matic care, Le Page with others, agreed that later pregnancies can usually 
be carried to a successful termination. My experience is encouraging; 
warned by the original nephritis, subsequent pregnancies have, because of 
rigorous diet, rest and thorough surveillance, rarely, unless chronic 
nephritis was already fully established, given serious trouble; as a rule the 
unfortunate complication did not recur. With women who suffer from 
chronic nephritis, nephritic toxemia should be feared during pregnancy 
(Williams). 
Pregnancy aggravates existing nephritis. With symptoms of fully 
developed chronic nephropathy the dangers are multiplied; the blood 
changes are often prompt, the accumulation- of toxic material is increased; 
the added cardiovascular task invites insufficiency, and resistance is con- 
sequently reduced. 
In our experience the “kidney of pregnancy” occasionally serves as 
the cause of chronic nephritis. Such cases finally follow the clinical 
course of the ordinary parenchymatous disease. One of my cases lived 
over twenty years after her initial nephritis in which she had eclampsia 
and transitory blindness and died after a long period of hypertension, 
hypertrophied heart and arterial degeneration in coma. 
When face to face with the kidney of pregnancy the prognosis must 
be cautiously given and the case always demands the closest surveillance. 
Eclampsia is always to he feared; the time of occurrence cannot he fore- 
told in the individual case; it is the leading danger, and prognosis remains 
uncertain until the time of its possible occurrence has been safely passed. DISEASES OF THE RENAL SYSTEM 
797 
(6) Chronic Parenchymatous Nephritis 
{Chronic Bright’s Disease, Chronic Tubal Nephritis, Chronic Glomerulo- 
nephritis, Chronic Diffuse Nephritis, Chronic Catarrhal Nephritis, 
Chronic Nephropathy, Large White Kidney) 
General Considerations.—Chronic nephritis is a progressive and pro- 
ductive disease of the kidney most frequent between the ages of twenty- 
five and forty, in which the organ is at first enlarged (large white kidney) 
with a chronic diffuse hyperplasia involving the epithelium, the glomeruli 
and the interstitial tissue—always a grave condition—offering an abso- 
lutely bad prognosis for restitution to health. In all, there is a marked 
tendency with the productive changes to final atrophy (secondary con- 
tracted kidney). Besides these changes the cardiovascular system is in- 
volved early and the blood pressure is elevated to compensate for the renal 
obstruction that the tissues of the body may receive the needed food. 
There is never complete regeneration of destroyed kidney tissue; new 
tubules are never formed, neither are new glomerules reformed after their 
destruction. It is possible for epithelial cells to proliferate when neigh- 
boring single cells have been destroyed, provided always that the tubular 
structure has remained intact. 
With destructive changes in the kidney both glomerules and tubules 
may undergo compensatory hypertrophy in the organ involved. These 
compensatory changes in diseased kidneys, the same as is found with 
enlargement of the remaining kidney following the destruction or removal 
of its fellow, are among nature’s processes which make it possible for the 
kidney—when not too extensively diseased—to continue to perform suffi- 
cient function to maintain life during long periods in individual cases. 
Bor prognosis this fact is of transcendent value and is true of all forms of 
nephritis. With the chronic nephropathies life is often continued during 
many years in comparative comfort because of the reserve and compensa- 
tory power of these complex organs. We can easily spare, as Bradford 
contends, two-thirds or even more of our kidney substance without serious 
inconvenience. 
In practice I have never seen a true case of chronic tubal nephritis 
make a full recovery. Those cases which have been reported cured were 
either the extended form of acute nephritis, often syphilitic nephritis, or 
the diagnosis was not absolutely correct. 
The majority of all cases are far advanced when they present for 
treatment. The disease is insidious very often without offering many 
subjective or objective symptoms. In some cases there is from the begin- 
ning a combination of interstitial and glomerular nephritis, with prompt 
cardiovascular change, including high blood pressure. Such cases are 
likely to show dropsies and uremia, while myocardial degeneration and the 798 
DISEASES OF THE KIDNEY 
attending symptoms usual with broken compensation are in the fore- 
ground early; this combination is promptly threatening and fatal early. 
Origin.—It is often exceedingly difficult, almost impossible, to be 
sure of the cause of chronic nephritis. In considering the acute nephrop- 
athies, I mentioned the possibility of chronic nephritis as a cause; Tyson 
believes that “more frequently it originates de novo/’ 
Prognostic Features 
Cases which follow the nephritis of scarlatina and pregnancy never 
recover, though they may live many years with but few symptoms so long 
as there is compensation within the cardiovascular system and uremia or 
other complications (infections particularly) are prevented. 
Cases which owe their origin to cold or exposure in which the cause 
is repeated are likely to progress and are subject also to lung complica- 
tions. 
Malarial infection may lead to chronic and fatal nephritis, though 
in this country it is less frequent than in Germany and other countries. 
Thayer in his Johns Hopkins Hospital experience found that of 1,823 
cases of malaria 25 had nephritis. 
Prolonged surgical (pyemia, sepsis and tuberculous) conditions 
causing or associated with parenchymatous nephritis argue against the 
prolongation of life. 
Nephritis due to chronic lead poisoning is always associated with 
cardiovascular changes, usually marked arterial thickening and hyperten- 
sion. When the condition is discovered early, exposure to lead is pre- 
vented, the kidney lesions and arterial and heart anomalies are incipient, 
the process may remain latent during many years and never progress; 
such patients may ultimately die of intercurrent disease. Chronic or 
advanced lead poisoning in which the kidney is involved, in which the 
associated cardiovascular changes are also marked, offers an absolutely 
hopeless forecast and the length of life depends upon a number of factors 
—ability of the heart and arteries to compensate, the prevention of rup- 
ture of the changed arteries, the renal sufficiency, the prevention of 
uremia, the addition of complications referable to the lungs and brain, 
and a number of other conditions which may arise early, often without 
warning. 
Retinal hemorrhage with saturnine chronic nephritis, whether largely 
of the mixed type or interstitial, is always unfavorable—such patients 
usually die within twelve months; they rarely live more than from 
eighteen to twenty-four months. 
Persistent or recurring digestive derangement is always unfavorable 
—most of these are due to chronic uremia. 
Recurrent and uncontrolled vomiting is always grave. With reduced DISEASES OF THE RENAL SYSTEM 
799 
urinary secretion and digestive disturbance the prognosis is bad, whatever 
the renal sufficiency test may unfold. 
Progressive and unrelieved anemia is evidence of profound toxemia 
and is usually associated with edema, hypertrophied and Aveak heart and 
the usual blood pressure changes. Caution in prognosis is needed Avhen in 
spite of the relief of the dropsies the anemia persists, for such behavior is 
unfavorable for the prolongation of life during a long period. 
Marked myasthenia is always unfavorable; when this is associated 
with dyspnea or orthopnea the end may be expected at any time, though 
such symptoms with or without uremia may at times be relieved during 
limited periods, but they are likely to recur. 
Uremia.—I have fully considered the prognostic significance of 
uremia under Anomalies of Urinary Secretion (d) of this Section, to 
\\diich we refer the reader for a full consideration of the subject. 
It should be remembered by the clinician that many nephritics live 
during long periods without sufficient uremia to cause alarming symptoms. 
It is possible for uremia to become ovenvhelming suddenly, to cause deep 
disturbance of the central nervous system—convulsions or coma—by 
A\Thich the life of the patient is threatened. Many die without regaining 
consciousness. On the other hand the patient may rally from profound 
uremic poisoning, the sensorium may clear, the heart function may prove 
sufficient to assist the patient into a period of material improvement, 
making it possible for life to be prolonged and usefulness continued dur- 
ing limited periods. From the medicolegal point of view it is exceedingly 
important to remember that deep coma and clouded brain function may 
disappear and the patient may fall into a condition of chronic uremia in 
which the brain function continues to be normal. Chronic uremia in such 
cases includes gastro-intestinal symptoms and lethargy, but judgment is 
not clouded in the majority of cases. With chronic nephritis such occur- 
rence is not uncommon; sooner or later the symptoms of deep uremia re- 
turn unless the patient loses his life as the result of some complication, 
usually cardiac. 
There are chronic parenchymatous nephritics Avho live comparatively 
comfortable during years, avIio are almost continually slightly uremic. 
This condition in such subjects shows itself Avith gastro-intestinal symp- 
toms, often high blood pressure, in the stage of secondary contraction, 
abundant urine, increased nycturia, hypertrophied left ventricle and per- 
sistent but slight anemia. They usually remain sufficiently active 
mentally to attend to their business, and in many cases their executive 
ability has not been reduced. The coma of nephritis may recur after 
short intervals during which the patient may be either clouded mentally 
or he may return to full consciousness. 
Prolonged drowsiness, uncord roll able insomnia or other evidences of 
invasion of the nervous system are among the evidences of uremia which 800 
DISEASES OF TIIE KIDNEY 
are common in advanced nephritis, and with other symptoms of progres- 
sion argue against the prolongation of life. 
Once uremic, the chances are that recurrence will not be long post- 
poned in the majority of cases. This is not without many exceptions, for 
months and years may pass without toxemia after eclampsia and deep 
coma. 
Renal Sufficiency Test.—Where there are sufficient laboratory facilities 
in connection with the test for renal sufficiency the examinations for re- 
tained nitrogen by the Folin method or other methods, which are held by 
some laboratory workers to be more efficient, may be made (See Renal 
Sufficiency Tests, Section VI). 
In normal subjects the residual nitrogen in the blood amounts to 
about 50 mgms., while in uremia it may rise to 250 mgms. When 
150 mgms. are reached the prognosis is grave; from 50 to 75 mgms. has 
no prognostic significance; from 75 to 150 mgms. is not without hope 
(Strauss). 
Dropsy.—Dropsy is a leading symptom of chronic nephropathy, pres- 
ent in 90 per cent of cases. It is never to be lightly considered prognos- 
tically. With chronic tubal nephritis it is less likely to be a symptom of 
the terminal stage of the disease than with interstitial nephritis or the 
secondary contraction of the former. 
In the early stage of the disease the disappearance of dropsy under 
treatment is not unusual. Irregularly distributed dropsy, sometimes 
greater on one side or in one member than in the other, is quite character- 
istic. Marked edema of the genitals in both the male and female may 
be early or late. Any form of dropsy with chronic nephritis, particularly 
when associated with marked cardiac insufficiency, with reduced urinary 
secretion, retained urea and with fluid in the serous cavities, is unfavor- 
able for the prolongation of life. 
In the stage of secondary contraction and unfavorable urinary fear 
tures the conditions mentioned in the preceding paragraph are rarely 
relieved. 
In offering the prognosis of chronic nephritis in the presence of ex- 
tensive dropsy, insufficient cardiac force, hydremia and vascular changes 
are paramount. 
Many neglected hospital cases of chronic tubal nephritis with extensive 
dropsies have been successfully treated, i. e., the dropsy has been relieved 
and life has been prolonged—but sooner or later these patients returned 
with exacerbation of the original symptom. 
XJrine.—The urine of chronic nephritis offers positive prognostic data. 
Abundant urine with specific gravity at normal or slightly above, but 
moderate debris, occasionally hyaline, few granular, mainly epithelial casts 
and moderate epithelial desquamation with considerable albumin is not 
alarming. So long as the specific gravity and amount of secreted urine DISEASES OF THE RENAL SYSTEM 
801 
remain within normal limits, the number of casts is limited and without 
evidences of advancing degeneration in abundant granular and fatty casts, 
other symptoms (objective and subjective) are favorable, the prognosis 
for life is good. 
When the specific gravity begins to fall, the quantity of urine secreted 
is increased, the urea and nitrogen of the blood are also increased, the 
quantity of urine voided during the night equals or exceeds the quantity 
of the day, with or without dropsy, it is safe to conclude that the atrophic 
stage is fully established. Lowered urea output in this stage with pro- 
gressively increasing gastro-intestinal symptoms, hypertension and in- 
creasing heart changes (hypertrophy, dilatation, myocardial degeneration) 
and dropsy, offer the complex of the terminal stage of most chronic 
nephropathies. Marked lowering of the urinary secretion with general 
dropsy (anasarca), loss of functional ability of the kidney as shown by 
the phthalein test or urea estimation is unfavorable. Marked delay in 
the excretion of potassium iodid is unfavorable. 
The clinician should never depend on renal sufficiency tests alone for 
prognosis (See Renal Sufficiency Tests, Section VI, Anomalies of Urinary 
Secretion (e) ). 
Paroxysmal hematuria (See Hematuria) with chronic tubal nephri- 
tis is usually indicative of progression and vascular degeneration, though 
there are cases in which hemorrhage recurs after exposure to cold during 
many years. With such cases hematuria may not return more than once 
in two or three years. I recently saw an active lawyer, aged 43, who 
since his sixteenth year has had repeated attacks of hematuria (average 
of 3 or 4 each year) ; on one occasion, 12 months before the consulta- 
tion, he had uremic convulsions. All physical signs and urinary fea- 
tures are characteristic of chronic tubal nephritis. lie is mentally alert 
and has recently been elevated to the bench. Such cases usually show 
high systolic pressure, but this was not present in the case mentioned, for 
there were evidences of myocardial weakness with systolic blood pressure 
—120 mm. Hg. The urine showed both hyaline and granular casts with 
moderate albuminuria, specific gravity 1,017, acidity 20°. Such symp- 
toms are a continuous menace but the patient may live many years. The 
dangers are sudden uremia with anuria; chronic uremia ivith prompt in- 
crease of vascular disease, cerebral hemorrhage. Edema of the b?'ain or 
lung may end the scene. 
Blood Pressure.—The significance of blood pressure study and hyper- 
tension as prognostic features has been fully considered in Section III 
(See Section III—Arteriosclerosis). 
Hypertension is characteristic of chronic nephritis; it is not long post- 
poned after the symptoms of the nephropathy are positive and it may 
occasionally precede other diagnostic features of the disease. 
Once the hypertrophy of the left ventricle is advanced and hyperten- 802 
DISEASES OF THE KIDNEY 
sion is striking, the disease may be considered fully established and pro- 
gression is the rule. 
Hypertension and hypertrophy are compensatory and salutary, the 
fall of the former and the failure of the latter (dilatation) argue in favor 
of degenerative change in the myocardium, increasing weakness, and with 
other evidences of cardiac insufficiency (dyspnea, orthopnea, dropsies) 
a fatal termination may be presaged. Low systolic pressure with a high 
diastolic pressure, hence a small pulse pressure, is characteristic of the 
myocardial weakness of nephritis. High systolic pressure and low dias- 
tolic pressure, hence a large pulse amplitude, are characteristic of chronic 
nephritis before the break. In the study of advanced nephritis a small 
pulse amplitude is evidence of cardiac insufficiency. Gradual or sudden 
fall of systolic blood pressure after a period of hypertension is always 
significant of failing compensation and calls for an unfavorable or guarded 
prognosis. 
Coronary disease with chronic nephritis, repeated attacks of angina 
pectoris, makes the prognosis exceedingly grave (See Angina Pectoris, 
Section III). 
Pulse.—Changes in the character of the pulse and pulse rate to corre- 
spond with the fall of systolic blood pressure and lowered pulse amplitude 
offer valuable data for prognosis; in all stages of chronic nephritis—par- 
ticularly the atrophic—such changes are positively unfavorable. 
Alcohol, Proper Living, Etc.—The prognosis of chronic nephritis is 
clouded by the persistent use of alcohol and the failure of dietetic, medical 
and climatic treatment with cautious living to control the symptoms. It 
is surprising to note how fully established nephritis, often in the stage of 
secondary contraction, remains stationary during long periods under 
favorable conditions and scientific diet. 
Edema.—My experience is in accord with Francis Boyd’s who says 
that “edema may be due to salt retention; but salt retention may be com- 
bined with degenerative changes in the smaller vessels and with cardiac 
failure.” When the salt-free diet reduces existing edema and increases 
the urinary flow the prognosis for prolongation of life is favorable. The 
edema due to cardiovascular degeneration is rarely favorably influenced 
by the salt-free diet alone; in connection with digitalis and theobromin 
salicylate I have experienced satisfactory improvement during long 
periods. 
Arteriosclerosis and Faulty Living.—In active brain workers with as- 
sociated arteriosclerosis and faulty living, with unchecked activities the 
progression is often surprisingly rapid, and death may follow before the 
end of twelve months. 
Heavy responsibilities add enormously to the dangers, invite uremia 
and rapid cardiovascular failure, while rest under favorable surroundings 
often prolongs life during periods of surprising length. DISEASES OF THE RENAL SYSTEM 
803 
Retinal Changes.—Retinal changes in the subjects of chronic neph- 
ritis are of considerable prognostic significance. Patients with albuminu- 
ric retinitis (hemorrhage) rarely live beyond two years, often not so long. 
One-half of my cases died within one year of the diagnosis of the compli- 
cation. Nettleship found that in 42 cases “one-fifth only of the cases lived 
for more than two years, and no less than 25 died within the year from 
the time of the recognition of the ocular changes (Bradford quotation of 
ISTettleship statistics). 
Complications 
Most complications of all chronic nephropathies are due to added in- 
fection. Following surgical operations infection is frequent, while resist- 
ance to the operation itself is lowered and the prognosis is bad (See the 
Infections—Section I). 
I have called attention to the dangers of pericarditis, pleuritis, 
empyema, pneumonia, endocarditis, peritonitis, bronchitis and diseases 
of the stomach and intestinal tract in the various sections of this book (See 
the Infections, Section I, and Diseases of the Pericardium, Section III, 
etc.). 
With all of these complications, if the nephropathy is advanced or 
secondary contraction is established, the prognosis is grave and should be 
given with reserve. Pericarditis is particularly unfavorable as a compli- 
cation. Cerebral apoplexy with chronic nephritis is always serious; 
restoration of brain function is rare; death in coma has been the rule in 
my cases. 
Acute meningitis is usually preceded by a period of cerebral symptoms 
(headache and mental torpor) ; the course of the disease is progressive and 
death is the rule (See Meningitis). (The reader is referred to the Pneu- 
mococcemias and Pulmonary Edema, also the other respiratory diseases 
for further data concerning their prognostic significance when complicat- 
ing nephritis). 
The frequency of duodenal ulcer with chronic nephritis has been over- 
looked by most clinicians (See Ulcer of the Stomach and Duodenum, Sec- 
tion V). The dangers are perforation with final peritonitis, also sub- 
phrenic abscess (Barie et Delauney, Dickinson). 
Purpura, visceral symptoms with erythema and nephritis often prove 
serious complications (Henoch, Osier). 
Conclusions 
Conclusions based on the preceding data prove chronic parenchymatous 
nephritis to be a grave disease which is never cured. Cures and long 
latent periods have been reported but restitutio ad integrum has never 
been demonstrated. 804 
DISEASES OF THE KIDNEY 
The duration of the disease in comparative comfort during many 
years is often surprising and this may occasionally follow a period of 
threatening symptoms including uremia. Prompt, early recognition, ra- 
tional treatment and living, often prove of great importance in prolonging 
life and favorably influencing the course of the disease. 
Unfavorable features leading to death are sudden uremia, persistent 
dropsies and uremia with cardiovascular changes including myocardial 
degeneration, retinal hemorhage, the complications (surgical and infec- 
tious) mentioned in the preceding pages, recurring hematuria and pro- 
found anemia with myasthenia. Surprises are in store for the clinician; 
cases which at times seem to progress favorably are suddenly and unex- 
pectedly overwhelmed by uremia or some other complication; while with 
almost equal frequency a serious symptom complex may mend and life 
may be indefinitely prolonged. There are no set rules for the prognosis 
of any of the nephropathies; all require the close study of the individual 
case almost continuously. 
Surgical Treatment and Prognosis 
In spite of the rose-colored prognosis offered by Edebohls following 
his introduction of surgical interference in chronic parenchymatous and 
interstitial nephritis (decapsulation of the kidney) the profession of this 
country and of the continent of Europe found no justification for its rec- 
ommendation. Results have been unfavorable—at times immediately dis- 
astrous. There are a few cases in which pain is prominent with per- 
sistent anuria and dropsy, in which splitting the capsule may be indi- 
cated. In these the tension of the capsule is great and its splititng gives 
relief. 
(c) Chronic Interstitial Nephritis 
(■Contracted Granular Kidney, Fibrosis of the Kidney, Contracted Kidney, 
Red Granular Kidney, Gouty Kidney, Arteriosclerotic Kidney, 
Chronic Nephropathy, Renal Cirrhosis, Renal Sclerosis, Granular 
Kidney, Senile Kidney) 
Leading Features.—The leading features of chronic interstitial neph- 
ritis are progressive destruction of the tubular apparatus of the kidney, 
change in the arterioles of the organ, interstitial overgrowth and atrophy. 
Various Forms. 
First Variety.—The last stage of chronic parenchymatous nephritis 
leads to atrophy of the kidney or ‘‘secondary contracted kidney” in which 
there is marked productive change which has justified some to consider 
such kidneys as belonging to the chronic interstitial type (See Chronic 
Parenchymatous Nephritis). DISEASES OF THE RENAL SYSTEM 
805 
Second Variety.—There is a second variety of interstitial nephritis 
which may be considered primary, known as the “contracted kidney” or 
“red granular kidney.” This variety may be due to one of several causes, 
including gout, lead, alcohol, syphilis, errors of diet long continued, and 
very often, hereditary influences. 
Heredity.—With a strong hereditary taint the prognosis for life of the 
arteriosclerotic kidney is less favorable than without it. My histories 
show that with several members of a family (brothers and sisters) suffer- 
ing from nephritis the disease is almost always of the arteriosclerotic type, 
that grave vascular complications are frequent, including apoplexy, that 
cardiac stability is uncertain, metabolic faults—such as diabetes and gout 
—add to the dangers, and that angina pectoris is comparatively frequent 
and fatal. 
Third Variety.—The third variety of chronic interstitial nephritis 
is arteriosclerotic and is in all probability the most frequent type of the 
contracted kidney, for there are but few cases of chronic interstitial neph- 
ritis, in which the arterioles are not sclerosed. It is this form of chronic 
nephritis in which the kidney changes, so far as the arteries are concerned, 
are a part of a general degeneration and productive process involving the 
blood vessels throughout the body. 
Fourth Variety.—The fourth type has been characterized by Osier 
as the “senile form.” It is the contracted kidney of old age in which the 
organ is reduced in size, with thickened and adherent capsule, increased 
pelvic fat and marked atrophy of the pyramidal and cortical substance, 
with prominent arteries throughout the kidney (Osier). 
Outlook.—The prognosis of contracted kidney must be based upon the 
leading underlying pathologic condition, i. e., disease of the arterioles 
through the entire body, including the organ under consideration. 
The disease cannot be cured. Detected early it may by proper care 
be held in abeyance. Even this is doubtful, but is in accord with the 
observations of some excellent clinicians (Senator). While interstitial 
nephritis is an incurable disease, its presence is by no means inconsistent 
with long life in many cases when compensation of the cardiovascular tree is 
sufficient and renal function is but little disturbed. Such patients may 
live in comparative comfort during many years. All clinicians of experi- 
ence constantly number among their patients chronic nephritics who by 
practicing temperance, sobriety and abstinence, are without the knowl- 
edge of the dangers which surround them or the changes in heart and 
arteries which are necessary to compensate for existing faults. 
Prognostic Features . 
The prognosis therefore of all varieties of interstitial nephritis depends 
primarily jpon die ability of the heart to compensate for the resistance 806 
DISEASES OF THE KIDNEY 
within the renal circuit and periphery, the security of the arteries, and 
the ability of the kidney to functionate sufficient to prevent uremia. 
Much depends therefore upon the co-operation of the patient and his 
ability to regulate his daily life. 
Blood Pressure and Heart Changes.—Blood pressure study of chronic 
interstitial nephritis and changes in the heart have been fully considered 
in the treatment of hypertension, arteriosclerosis, myocardial disease and 
chronic nephritis (the latter in this section). 
Blood pressure must of necessity he elevated and the heart enlarged 
to overcome arterial resistance and renal block. The hypertension of 
interstitial nephritis and the pulse pressure are higher than with chronic 
tubular nephritis, but the prognostic data in both are practically iden- 
tical and do not require repetition, though apoplexy is more frequent 
with the interstitial disease. In both, sudden or gradual fall with attend- 
ing symptoms of increasing circulatory embarrassment is ominous. Many 
cases of chronic interstitial nephritis present for treatment only after 
there is a break of compensation with dropsy, dilatation of the heart, often 
pulmonary edema, orthopnea and other terminal symptoms. These pa- 
tients die of cardiac asthenia. 
Renal Insufficiency.—Another class of patients suddenly or gradually 
develops the positive symptoms of renal insufficiency. The kidney function 
materially reduced, toxic symptoms follow, uremia—either acute (eclamp- 
sia) or chronic—becomes life-threatening, persistent vertigo incapacitates 
the nephropath, and not infrequently cerebral hemorrhage or sudden car- 
diac dilatation add to the danger and end life. 
Persistent or recurrent headache with marked hypertension, thick 
artery (radial) and ocular disturbances may continue during several 
weeks or months, but when these symptoms are uncontrolled by treatment 
or rest, serious complications—either cerebral apoplexy or uremia—may 
be expected. It not infrequently happens that unrecognized nephritis 
ends without warning with cerebral apoplexy or sudden overpowering 
uremia. In some of these cases, particularly in the uremic, occipital head- 
ache may precede the end during several days (Seguiij). 
Marked hypertension with hypertrophy of the left ventricle may 
continue during many years with chronic interstitial nephritis and not 
materially interfere with the life of the patient. I have bad such a 
case under observation during almost ten years: a woman, aet. 52, who 
during that time has never had a blood pressure below 250 mm. Hg., 
with enormous hypertrophy of the heart, Avho until within the past month 
has been able to teach in a country school but who is now showing evi- 
dences of increasing peripheral resistance. The blood pressure is so high 
that it cannot be accurately measured by any instrument at our com- 
mand, the pulse amplitude is correspondingly high while evidences of 
chronic uremia and cerebral arteriosclerosis are increasing. DISEASES OF THE RENAL SYSTEM 
807 
Polyuria, nocturnal frequency, cerebral symptoms (headache, vertigo 
and visual disturbances) with hypertension in patients below fifty years 
of age always makes the prognosis serious; most of these nephritics die of 
uremia. 
Dyspnea—Orthopnea.—It matters little what the urinary picture is 
when with hypertension early, there is dyspnea or orthopnea; for these 
are evidences of cardiac insufficiency and make the outlook dark. Marked 
accentuation of the second aortic sound (almost constantly present) with 
increasing hypertension and irregular or arhythmic heart is a discourag- 
ing complex. 
Stasis.—The break in compensation often follows a period of increased 
tension; the artery is evenly thickened, like a “pipe stem” under the 
finger. The suddenly appearing irregularity, intermission or other anom- 
alies of the pulse when promptly associated with respiratory embarrass- 
ment or other symptoms of stasis are always unfavorable. 
Intermittent or irregular hearts which have become chronic and which 
are not due to advanced myocardial degeneration may not interfere with 
the comfort or the life of the patient during unlimited periods. Such 
hearts, however, when facing an added burden are likely to prove insuf- 
ficient. 
Sudden tachycardia is serious; when associated with dilatation there 
may be pulmonary edema with general anasarca. These paroxysmal at- 
tacks repeat themselves at short intervals in cases with myocardial degen- 
eration. 
Adams-Stokes phenomenon is a part of the far-reaching arteriosclerosis. 
Angina pectoris may complicate chronic nephritis and makes the tenure 
of life uncertain (See Angina Pectoris). 
Respiratory Symptoms.—Respiratory symptoms, particularly bron- 
chitis, with nocturnal dyspnea and occasional bloody or pinkish expec- 
toration are suggestive of final fatal edema of the lungs. 
Orthopnea with dropsy (a late complication) is soon followed by death. 
Cheyne-Stokes breathing is a terminal symptom. 
Dropsy.—Dropsy is not an early symptom of the average contracted 
kidney. There may be transitory edema of the ankles but fully devel- 
oped dropsy is a terminal complication and depends upon broken com- 
pensation. 
Dropsy with ocular symptoms does not continue long before death. 
The same general conclusions given in the consideration of chronic 
tubal nephritis in its advanced stages with dropsy may be accepted for 
the prognosis of contracted kidney (See Chronic Parenchymatous Neph- 
ritis). 
Edema of the glottis with all forms of nephritis is a serious complica- 
tion and demands immediate surgical treatment when it causes respira- 
tory embarrassment. 808 
DISEASES OF THE KIDNEY 
Digestive Symptoms.—Symptoms referable to the digestive system 
are always suggestive of uremia and should be so interpreted for our 
purposes. 
Vomiting not dependent upon error of diet is either of uremic or 
cerebral (arteriosclerotic) origin and demands cautious consideration, for 
it is usually unfavorable. 
Diarrhea is often salutory and should be so considered in most cases 
by the therapeutist for it may be an expression of existing uremia; occa- 
sionally it is profuse, weakening and unfavorable. 
Persistent constipation or obstipation may lead to threatening toxic 
symptoms and for safety demands rigorous treatment. 
Urine.—The urine offers prognostic data of considerable importance. 
During the stage of full compensation when conditions are favorable and 
the disease is not far-advanced, the quantity is decidedly increased, the 
specific gravity is low, the albumin loss may be slight or so small as to 
escape detection with ordinary tests; there may be no casts or only an 
occasional hyaline cast; the urea is decreased but not always strikingly 
so; nocturnal frequency is slightly increased but the quantity is not so 
great as in the advanced stage; the functional tests are favorable. The 
occasional red blood corpuscle, a few renal cells, an occasional leukocyte 
and squamous epithelia are frequent and not of great significance when 
there are no untoward complications or associated symptoms. 
When the nocturnal secretion of urine is greater than the diurnal and 
with this there are other evidences in increasing systolic pressure and 
heart changes of greater renal obstruction and the radial artery shows 
increasing arteriosclerotic change (thickening increasing), there are usu- 
ally gastro-intestinal and pulmonary anomalies—all of which argue in 
favor of an early break. 
Probably there are but few cases of chronic interstitial nephritis which 
are not n on-albuminuric during varying periods. There are many cases 
of non-albuminuric nephritis which are easily recognized, if the possibility 
of their existence is borne in mind. It is often possible to diagnosticate 
and prognosticate this anomalous form of the disease, months before 
albumin or the usual features are established. Many cases diagnosticated 
as hypertension without albuminuria have proved to be insidiously pro- 
gressive interstitial nephritis. 
Hypertension in which the symptom is not due to aortic disease, in 
which the urine may contain no albumin or only a trace, no matter what 
the other associated arterial lesions may be is as a rule due to chronic 
nephritis and is progressive. If in the advanced stages the blood pressure 
is excessively high, the urine begins to show increasing albumin loss, the 
quantity secreted grows less, the cylindruria increases and urea detention 
is increased, the eye symptoms are prominent and the heart shows increas- 
ing weakness, death is imminent. DISEASES OF THE RENAL SYSTEM 
809 
It is not impossible in chronic nephritis after periods of markedly 
reduced urine secretion—almost complete anuria—to find the kidney func- 
tion improved, and it may again prove sufficient during varying periods. 
Once the patient has lived through such a period he may be considered 
to be in constant danger of recurrence of renal insufficiency with attend- 
ing uremia. 
Anemia.—As a rule the anemia of chronic interstitial nephritis is 
less striking than with the other nephropathies. Persistent anemia, with 
myasthenia is unfavorable and is usually associated with renal insuffi- 
ciency—chronic uremia. In the terminal stage, with persistent dropsy 
and other threatening symptoms including increased urinary anomalies, 
the anemia is often profound. Anemia which has become chronic is unfa- 
vorable because it is an expression of one or more grave underlying con- 
ditions. 
Albuminuric Retinitis.—What I hold in connection with the retinitis 
of chronic tubal and glomerular nephritis is also true of contracted kid- 
ney. Diffuse opacity due to edema, hemorrhage and optic papillitis are 
common, and are evidences of advanced arteriosclerotic nephropathy. 
Once there is diffuse retinitis and hemorrhage the patient’s fate is seated 
and uremic or cardiac death may he expected at any time, though some of 
these patients live as long as two years after positive changes in the fundus 
of the eye. Albuminuric retinitis is among the most valuable of prognostic 
data and often serves to strengthen the forecast in the absence of other 
reliable features. It may be the first recognized symptom to lead to the 
diagnosis. 
Purpura is positive evidence of profound toxemia and lowered resist- 
ance and is usually a terminal complication. 
Repeated epistaxis is always suggestive of arterial degeneration, usu- 
ally advanced, and may be the first of a series of hemorrhages with final 
cerebral apoplexy. 
In one of my cases there was first epistaxis, then urethral hemorrhage; 
these alternated with each other. Death was due to cerebral hemorrhage 
after a fishing excursion on an unusually hot day. Such experiences 
are not unusual. 
Complications 
The complications of chronic interstitial nephritis are practically the 
same as are those of the chronic parenchymatous disease and offer the 
same prognosis (see Chronic Parenchymatous Nephritis) though the arte- 
rial anomalies (cerebral hemorrhage) are more frequent with interstitial 
disease. 
Surgical Operations and Infections 
Surgical operations and infections are not well borne by the subjects 
of chronic arteriosclerotic nephropathies. This is particularly true of 810 
DISEASES OF THE KIDNEY 
surgical operations on the genito-urinary organs and with pneumonococ- 
cemia. With pneumonia, the pulse is at first reassuring, often slow, the 
tension slowly falls, and after a few days the heart muscle is exhausted. 
After bladder and prostate operations there is often prompt and sudden 
suppression of urine which with a failing heart leads to death. 
Duration 
The duration of this form of nephropathy is always uncertain. The 
patient is doomed but yet, as contended in the beginning of this chapter, 
the disease is by no means inconsistent with long life and in many cases 
the regulation of the habits and life of the patient makes it possible to add 
years of comparative comfort. Early recognition is an important favor- 
able prognostic factor. I have had patients who have lived over twenty 
years with interstitial nephritis. 
References 
Allbutt. Diseases of the arteries, etc. London, 1915. 
Bamberger (H.). Ueber Morbus Brightii u. seine Beziehung zu anderen Krankh. 1879. 
Barie & Delaunay. Bull, et Mem. Soc. Med. d. Hop. de Paris, 1903, 45. 
Bond (Francis). Index of prognosis, etc. London & New York, 1915. 
Bradford. Allbutt & Rolleston’s Diseases of the kidney. London, 1908, iv, pt. 1. 
Croonian Lectures, Royal Coll., etc. London, 1904. 
Lancet, London, 1904, i. 
Bright (Richard). Reports of medical cases. London, 1827. 
Charcot. Lectures on Bright’s disease of the kidney. Translated by Millard. New York, 
1878. 
Dickinson (W. H.). Albuminuric ulceration of the bowels. Med. Chir. Tr., London, 1894. 
The pathology and treatment of albuminuria. London, 1876. 
Fischer (M. H.). Nephritis. New York, 1912. 
Furbringer. Krankh. d. Ham u. Gechlechtsorgane. Braunschweig, 1884. 
Gaucher & Sergent. Rev. de Med., Paris, 1901, xxi, 1. 
Goldberg. Arch. f. Gynak., 1891, xli, 295-329; also 1892, xlii, 87-102. 
Gull & Sutton. On the pathol., etc., of chronic Bright’s disease with contracted kidney. 
Med. Chir. Tr., 1872, Iv, 273. 
Henoch. Berlin, 1890. 
Herrick (J. B.). Modem medicine. Osier & McCrae. Philadelphia, 1909, vi. 
Johnson, George. On diseases of the kidneys. London, 1852. 
Lectures on Bright's disease. London, 1873. 
Jores. Anat. Grundlagen Wichtige Krankheiten. Berlin, 1913. 
Lepage. Ann. Gynec. et d’obst., Paris, xxxix, No. 11, 641. 
Leyden. Ztschr. f. klin. Med., ii, 186. 
Lichtenstein. Centralb. f. Gynak., 1909, 1813-1325. 
Luthje. Von Mehring & Krehl’s Lehrb. d. inner. Krankh. Jena, 1913. 
Millard. Bright’s disease, etc. New York, 1884. DISEASES OF THE RENAL SYSTEM 
811 
Nettleship (E.). Royal London Oph. Hosp. Rep., 1906, xvi. 
Brit. Med. J1903, ii, 722. 
Olshausen. Ueber Eklampsie. In: Volkmann’s Samml. klin. Vortrage. N. F. No. 89, 
1891. 
Osier (Sir William). On the visceral complications of erythema, etc. Am. J. Med. Sci., 
Philadelphia, 1895. N. S. CL. 
Ponfick. Exudative Nierenentzundung. Jena, 1914. 
Porter. Renal disease. New York, 1887. 
Prior. Krankh. Ham, etc. Leipzig, 1894. 
Purdy. Bright’s disease, etc. Philadelphia, 1886. 
Rayer. Traite d. malad. des reins, etc. Paris, 1839-44. 
Roberts (Sir W.). Urinary and renal diseases. 1885. 
Rosenstein. Path. u. Therap. Nierenkr. Berlin, 1894. 
Saundby. Lectures on renal and urinary diseases. Philadelphia, 1897. 
Seguin (E. C.). Arch, of Med., 1880, iv, No. 1. 
Senator. Die Erkr. d. Nieren. In: Nothnagel’s Spec. Path. u. Therap., Wien, 1896, xix. 
Stewart (Granger). Bright’s disease of the kidneys. Edinburgh, 1868. 2d ed., 1871. 
Strauss. Berl. klin. Wchnschr., Feb. 24, 1913. 
Med. Rec., New York, March 29, 1913. 
Thayer. Lectures on the malarial fevers. New York, 1897. (See also Johns Hopkins 
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Traube. Ueber d. Zusammenhang v. Herzu. Nierenkrank. (Classic). Berlin, 1856. 
Tyson. Treatise on Bright’s disease and diabetes. 
Tyson & Fussell. Practice of medicine. 6th ed. Philadelphia, 1914. 
Veit. Berl. klin. Wchnschr., 1902, xxxix, 512-540, Nos. 22 cfc 23. 
Volhard & Fahr. Die Brightsche Nierenkr. Berlin, 1914. 
Weigert. Die Bright. Nierenkrank. In: Volkmann’s Sammlung klin. Vort. Series vi, 162. 
West. Granular kidney and phys. alb. London. 
Williams. Obstetrics. New York, 1912. 
(d) Congested Kidney 
(Cyanosed Kidney, Hyperemia of the Kidney, Stauungsniere) 
(1) Acute Congested Kidney 
Whether acute or chronic, congested kidney is a secondary condition. 
Hyperemia of the kidney follows general stasis within the venous system; 
insufficient cardiac force, in which the kidney and other organs of the 
body are likely to be involved at the same time, or local pressure may 
cause this condition. 
Acute congestion of the kidney may be associated with the acute infec- 
tions. Whenever the circulation is impaired through the renal circuit 
or whenever cardiac weakness causes renal stasis from acute or suddenly 
arising complications, hyperemia results. Some have held that the kid- 
neys are not congested during the acute infections but that they are 812 
DISEASES OF THE KIDNEY 
anemic (Walter Mendelson). There is proof, however, that in most 
cases there is acute hyperemia. Turpentine, copaiba, cubebs, cantharides, 
arsenic, carbolic acid and other substances which also cause genito-urinary 
irritation may produce acute congestion of the kidney. Heart lesions with 
acute exacerbations or sudden cardiac insufficiency from any cause may 
provoke, among other evidences of general stasis, all of the urinary fea- 
tures of acute cyanosis of the kidneys. 
Unquestionably there is in most cases of acute nephritis a period of 
congestion in which the kidney shows the characteristic changes of hyper- 
emia. The prognosis of acute congestion of the kidney must always de- 
pend upon the nature of the primary cause and the ability of the thera- 
peutist to overcome its grave secondary effect. The majority of cases 
of infection in which the urine shows the results of renal hyperemia, in 
which toxemia is not overpowering and the resistance of the patient is 
normal, recover fully. It should be remembered in offering the prognosis 
of acute renal congestion with the infections that the noxious effect of the 
toxins on the kidney is more important than any direct circulatory em- 
barrassment (stasis). 
(2) Chronic Congested Kidney 
Causes.—The leading causes of chronic congested kidney are 
(a) Heart lesions 
(b) Pulmonary obstruction 
(c) Local obstruction 
(d) Venous stasis from whatever source. 
(a) Heart Lesions.—The leading heart lesions which cause renal 
stasis are valvular and myocardial. The valvular defects are usually 
mitral or tricuspid, or both may be present. With valvular disease or de- 
generation of the heart muscle (myocardial insufficiency)—usually during 
periods of broken compensation—the symptoms of renal cyanosis are 
added to the others which together complete the picture of cardiorenal 
obstruction. With all of these primary anomalies the condition of the 
heart muscle and the ability of the congested kidney to prove sufficient 
remain the paramount prognostic features. There are often long periods 
of congested kidney with chronic valvular lesions and myocardial weak- 
ness in which rest and rational treatment improve conditions with the 
relief of venous stasis. As a rule, with chronic heart lesions cyanosed 
kidney is an expression of failing heart strength, and consequently only 
a symptom of a grave condition. Many of these patients with chronic 
heart lesions live for years during which, with temporary recurring loss 
of heart strength, there are repeated periods of congestion of the kidney. 
Rest and rigorous scientific treatment of the underlying heart lesions (if 
amenable to treatment) are important factors in prolonging life. DISEASES OF THE RENAL SYSTEM 
813 
(b) Pulmonary Obstruction.—Acute and chronic pneumonia, 
tumors of the lung and mediastinum (aneurismal growths, etc.), emphy- 
sema, and chronic asthma, pleurisy and pulmonary tuberculosis may 
cause renal stasis. Here too the prognosis depends entirely on the nature 
and extent of the primary lesion. We have fully considered the renal 
complications and their prognostic significance with each one of the pri- 
mary diseases above mentioned. 
(c) Local Obstruction.—Local obstruction to the return of blood 
from the kidney associated with thrombosis, embolism—sometimes of the 
vena cava—compression of the renal vessels by abdominal growths, often 
cause stasis. Most of these conditions are serious. 
(d) Venous Stasis From Whatever Source.—Venous stasis from 
whatever source, not included in the preceding paragraph causing con- 
gested kidney is, as a rule, evidence of advanced disease. This is par- 
ticularly true of the numerous diseases of the liver associated with portal 
obstruction (See Diseases of the Liver, including Cirrhosis, etc.). 
General Statements 
Long continued cyanosis causes productive changes in the kidney lead- 
ing to connective tissue increase and consecutive contraction. These cases 
are associated with thickened renal vessels, and finally there are changes 
in all structure of the kidney (diffuse interstitial nephritis). 
The length of life depends upon the ability of heart and kidney to hear 
the strain. 
Congested kidney associated with other serious organic disease—malig- 
nant disease of the liver, Hodgkin’s disease, pernicious anemia, aneuris- 
mal dilatations within the abdomen or elsewhere, is usually among the 
terminal manifestations. The symptoms are mainly circulatory, respira- 
tory and renal. 
The prognostic significance of the symptoms of the primary disease 
need not he reconsidered in this section; the reader is referred to the 
separate chapters dealing fully with the primary diseases. 
The urine of the cyanosed kidney may be materially reduced in quan- 
tity, the specific gravity is high (1,025 to 1,035), dark colored, often 
cloudy. The amount of albumin is small. In the microscopic field there 
are red blood corpuscles, blood casts occasionally. 
With congested kidney, the disappearance of albumin and casts is coin- 
cident with returning heart strength—hence favorable. Improvement 
of the circulation often runs parallel with change in the concentration 
of the urine; the specific gravity falls with increase in the quantity of the 
urine at the same time. The higher the specific gravity the greater is the 
engorgement, hence the smaller the quantity of the urine secreted. 
Uremia is not to be dreaded in uncomplicated cyanosis of the kidney. 814 
DISEASES OF THE KIDNEY 
If present it may be assumed that there is coexisting nephritis. The 
solids of the urine continue to pass in uncomplicated cases because the 
tubules and the epithelia are not involved. 
Renal infarct and renal anemia are both considered separately; the 
first with the malignant endocardial infections, the latter with the Dis- 
eases of the Blood and Hemopoietic Organs. 
References 
Aschoff. Path. Anatomie. Jena, 1913. 
Luthje. Von Mehring & Krehl’sLehrbuch d. inner. Med. Jena, 1913, l.Band. 
Mendelson (Walter). Quoted by Osier; also Tyson (see below). 
Osier (Sir William). Practice of medicine. 8th ed. New York, 1914. 
Tyson & Fussell. Practice of medicine. Philadelphia, 1914. 
See also Literature and References at end of the preceding chapter. 
(e) Amyloid Kidney 
(Waxy Kidney, Lardaceous Disease) 
Origin.—Amyloid kidney, like amyloid liver, is a secondary degener- 
ative disease dependent upon prolonged suppuration, tuberculous disease, 
chronic bone lesions, syphilis, cancer, bronchiectasia, chronic bronchitis or 
various other chronic disorganizing diseases. Amyloid degeneration of 
the kidney is coincident with similar lesions in the liver, spleen, and often 
in the intestinal glands. I have never seen the kidneys involved alone. 
Naturally, as with all amyloid disease, far-reaching changes in the blood 
vessels are prominent in the organs involved. With chronic nephritis 
(parenchymatous) in the terminal stage, amyloid degeneration is common 
and unfavorable for life. 
Course of the Disease.—With the advance of degeneration with any 
one of the underlying processes, the heart muscle weakens and the blood 
pressure falls. Amyloid kidney is never hypertensine. 
Associated Diseases.—Syphilitic disease, is often associated wdth amy- 
loid degeneration. It is the only form of amyloid disease which offers 
any hope when advanced. Once chronic exhausting non-syphilitic disease 
is associated with amyloid degeneration the prognosis is absolutely bad. 
Characteristic Symptoms.—The prominent features of renal degen- 
eration (waxy) may not be in the foreground, but the waxy color of the 
patient and the anemia, the dropsies, the cardiac insufficiency, the low 
blood pressure and the urinary anomalies make clear the gravity of the 
complication. DISEASES OF THE RENAL SYSTEM 
815 
General Statements 
Urine.—The characteristic features of the urine include the presence 
of serum albumin and serum globulin with the characteristic chemical 
reaction, casts of all kinds—waxy predominating. The quantity is in- 
creased, the specific gravity is low. 
Amyloid kidney ivith operable diseases may, when the primary disease 
is surgically treated, lead to latency of the kidney changes but only when 
these are limited. In children with tuberculous hone disease there is 
often marked and suggestive anemia with symptoms of amyloid kidney, 
without marked dropsy in which the removal of the primary focus of 
tuberculous bone disease stays the onward march of the waxy degenera- 
tion. 
Restoration of organs to normal in which there are amyloid changes 
not due to syphilis is impossible; with limited changes in the kidney and 
cure of the primary disease the organs may continue to functionate satis- 
factorily. When with fully established amyloid disease diarrhea is per- 
sistent and exhaustive, often colliquative, the prognosis is bad. 
Persistent or uncontrollable vomiting is an unfavorable symptom. 
The nature of the primary disease, which, as a rule, is grave, makes the 
prognosis of degenerative changes in distant organs (spleen, liver, kid- 
ney and intestines) unfavorable. The development of amyloid degenera- 
tion with any chronic disease is unfavorable, and death follows within 
a short time as a rule. 
The larger number of amyloid diseases are associated with surgical 
affections and tuberculosis—diseases which if treated early offer a rea- 
sonably good prognosis and make the prevention of waxy change in the 
vital organs usually involved possible in a large proportion of cases. 
(f) Tuberculous Kidney—Tuberculous Nephritis 
See Section I—Tuberculosis 
Surgical Diseases of the Kidney 
(g) Hydronephrosis 
General Considerations.—Hydronephrosis, or the distention of the 
pelvis and calyces of the kidney with urine, always implies the presence 
of an obstruction to the free discharge from the renal pelvis into the blad- 
der. When there is infection and the dilated sac holds pus, it is spoken 
of as pyonephrosis (See Pyelitis). The majority of cases are right-sided. 
Numerous causes have been found by pathologists for hydronephrosis. 816 
DISEASES OF THE KIDNEY 
They may exist within the urinary organs or without—intrarenal and 
exlrarenal. The obstruction may be either congenital or acquired. It 
may be unilateral or bilateral. 
Prognostic Factors 
(1) The cause of the obstruction 
(2) Whether the lesion is unilateral or bilateral 
(3) If unilateral, the condition of the second kidney 
(4) The general condition of the patient and complications . 
(5) The time of recognition and the ability to treat the condition 
surgically. 
(1) The Cause of the Obstruction 
Congenital Hydronephrosis.—The prognosis of congenital hydroneph- 
rosis is not good. The dilatation is often bilateral; it is secondary to 
ureteral obstruction. In some cases the obstruction cannot he found; the 
child comes into the world with large dilated kidneys, or these gradually 
increase in size after birth. There are cases of unilateral congenital 
hydronephrosis. The congenital defect is often coincident with other anom- 
alies, including cleft palate, visceral abnormalities or other unique devel- 
opmental faults—such combinations lead to early death. When the con- 
genital obstruction is in the urethra, the dilatation of the pelvis and ure- 
ters may be (relatively) enormous. In other cases there is anomalous 
implantation of one or both ureters into the bladder, or the ureter may 
be placed at an abnormal angle, the ureter may be twisted on its own axis, 
there may be abnormal obliquity, the ureter may be completely occluded, 
converted into a fibrous strand. Anomalous distribution of the renal ves- 
sels has been observed in some cases. It is possible for hydronephrosis to 
be present at birth and of considerable size, secondary to congenital stone 
in the pelvis or ureter. Among some of the other anomalies are double 
ureters and double pelves on each side. In these cases the kidney sub- 
stance is atrophied and there is simply a sac left holding the retained fluid. 
Acquired Hydronephrosis.—Acquired hydronephrosis may be sec- 
ondary to one of many causes. Morris in his original work on the “Sur- 
gical Diseases of the Kidney” reports 142 cases of marked hydronephroses 
in his 2,612 post mortem examinations. 
Cancer of the pelvic organs, uterus, vagina, bladder or rectum was the 
leading cause of the obstruction, including 116 cases of the entire 142. 
This is an unusually large percentage and hardly corresponds with the 
experience of other observers. 
Malignancy of the primary obstruction usually bars operation and 
makes relief impossible. The majority of my cases were due to calculi 
caught either in the pelvis of the kidney or in the ureter, low down, often DISEASES OF THE RENAL SYSTEM 
817 
looking into the bladder. Tuberculous ulceration and thickening of the 
renal pelvis or ureter, compression of the ureter by benign or malignant 
abdominal growths, ovarian cyst, rectal cancer, cancer of the prostate or 
bladder and the pregnant uterus are among the causes in my material. 
Aschoff also calls attention to torsion of the ureter due to dislocation 
of the kidney. Stricture of the urethra, chronic cystitis with unrelieved 
residual urine during long periods have been observed by urologists. Fol- 
lowing acute and chronic peritonitis, occasionally after major abdominal 
operations, adhesions, bands of new connective tissue and consecutive 
continuous obstruction lead to hydronephrosis. I have seen two such 
cases in which the relief of tension overcame hydronephrosis. 
Cases have been reported by reliable observers (one quoted by Morris) 
in which the symptoms and characteristic urine of diabetes insipidus per- 
sisted with obstruction and hydronephrosis. 
Kelly and Burnham make the statement after considering most of the- 
possible causes of hydronephrosis that “abnormal movability of the kidney 
is undoubtedly the commonest single cause of hydronephrosis,” and they 
claim that the successful results of fixation of such kidneys is proof of their 
contentions. “It is not, however, movability alone, but an associated con- 
dition such as that afforded by bands, blood vessels and adhesions, which 
terminate the formation of the pathological distention” (Kelly and Burn- 
ham). 
(2) Whether the Lesion is Unilateral or Bilateral 
Bilateral hydronephrosis usually offers a more serious forecast than 
does the unilateral disease. Obstruction below the pelvis is most likely to 
cause bilateral hydronephrosis. The dangers of infection, atrophy and 
uremia, are greater than with unilateral obstruction. Stone in both pelves 
or in both ureters low down, as in one of my cases may after years, with 
but few symptoms, suddenly cause complete anuria (in a man over 80 
years of age) and death from uremia in less than one week. Considerably 
over 50 per cent of all cases are bilateral. 
Of 665 cases collected by Newman, 227 were unilateral and 448 bilat- 
eral. 
The cause of death with bilateral hydronephrosis is usually loss of renal 
function because of the atrophy, i. e., displacement by pressure of the kid- 
ney tissue. Some cases are enormously tolerant and the atrophy increases 
gradually; but in the end the fate of all is the same—uremia—unless 
death results from intercurrent disease. When bilateral hydronephrosis 
is due to obstruction which is operable, the dilatation is not abnormally 
large and the destruction of the renal parenchyma is not too far advanced 
(renal sufficiency fair) the prognosis for life is good. 818 
DISEASES OF THE KIDNEY 
(3) If Unilateral, the Condition of the Second Kidney is of 
Paramount Importance 
Life may be indefinitely prolonged in spite of unilateral hydronephro- 
sis, so far as the kidneys are concerned, if the second kidney continues 
to functionate sufficiently. With organic disease of the second kidney— 
nephritis, nephrolithiasis, pyelitis—or other anomalies the prognosis is 
clouded. 
(4) The General Condition of the Patient and Complications 
The general condition of the patient is important. With acquired 
hydronephrosis, heart lesions, arteriosclerosis, syphilis, constitutional dis- 
eases or metabolic faults, as well as added serious infections or other med- 
ical and surgical complications, at once lower the chances of prolonging 
life for any length of time. In old subjects with chronic hydronephrosis, 
intermittently emptying itself, even in the presence of advanced ather- 
oma, the patient may continue to live in comfort but such a subject stands 
on the edge of a precipice all the time. 
Acute infection (pneumonia, influenza, typhoid or diphtheria) finds the 
subject with resistance far below normal and makes prognosis uncertain. 
Infection of the diseased kidney, causing pyelonephrosig, is always seri- 
ous and can only be overcome by free drainage—ultimate nephrectomy. 
Such complication with the needed surgical interference is associated with 
a high mortality. 
There are hydronephroses which gradually become purulent without 
marked constitutional disturbance during long periods. 
In practice I do not recall a single case of rupture of the hydronephro- 
sis. Such cases have been occasionally reported, and when operate'd at 
once offer a fair chance of recovery—when uncomplicated. Most of my 
patients who yielded to the hydronephrosis (usually bilateral) finally 
developed uremia. I have, however, had some unique and happy experi- 
ences with both unilateral and bilateral hydronephrosis due to stone with 
added uremic poisoning. One of my cases, a woman over 60 years of age, 
with double hydronephrosis after a severe double renal colic became pro- 
foundly uremic after a short period of shock. For over forty-eight hours 
there was complete anuria and coma. She made a happy recovery, so far 
as her uremia is concerned, and is now 68-70 years of age, comparatively 
comfortable. Such experiences are rare. In most cases of anuria with 
uremia death follows within a few days. 
(5) The Time of Recognition and the Ability to Treat the 
Condition Surgically 
Early recognition in cases dependent upon operable conditions adds 
enormously to the chances of success. Bilateral (congenital) hydroneph- 
rosis, in which the dilated pelves are palpable at birth or which increase DISEASES OF THE RENAL SYSTEM 
819 
rapidly after birth, offers a bad prognosis. There are successfully oper- 
ated cases (nephrotomy) of congenital bilateral hydronephrosis on record 
but there are relatively few; surgeons have recommended plastic opera- 
tions of this kind preparatory for more radical interference. In infants 
any kidney operation is serious, and unless the obstruction is easily oper- 
able success need not be expected. Congenital cases may offer no symp- 
toms when the obstruction is slight or the hydronephrosis is small at birth 
and the condition under such circumstances is only discovered after much 
damage has resulted. Such cases are always serious. 
Cases of hydronephrosis which are unilateral and which present to the 
surgeon early offer, because of improved methods of diagnosis (cath- 
eterization with cystoscopy, pyelography, sufficiency tests and cautious 
physical examination), a much better prognosis than ever before. It is 
only by these refinements of diagnosis that the condition can be detected 
early—and that means much for the patient and surgeon. 
Advanced hydronephrosis is synonymous with destructive changes in 
kidney substance and a relatively had prognosis for the restoration of the 
diseased kidney. With the second kidney as already suggested free, the 
prognosis for life is good in the absence of complications, including con- 
stitutional anomalies. Such cases in resistant subjects offer a good prog- 
nosis after radical surgical interference. With the second kidney in- 
volved or with ascending infection in one or both kidneys, particularly 
the latter, the results of surgical interference are discouraging. It is 
often surprising to find prompt response from the surgical operation of 
bilateral hydronephrosis though only a small remnant of kidney tissue 
remains. 
Incising and draining the kidney sac (nephrostomy) leads to the estab- 
lishing of a urinary fistula which usually discharges during a long time. 
In almost 50 per cent of these cases the sac finally collapses completely 
and the fistula closes. In the remaining cases the fistula persists; the 
patients live during varying periods—sometimes for years; they die of 
intercurrent disease or they become infected, emaciated, develop amy- 
loid degeneration of several organs and die with the usual symptoms of 
amyloid kidney and liver (dropsies, anemia, etc.). 
The percentage of successes with nephrectomy for unilateral hydro- 
nephrosis and a healthy second kidney is most encouraging. Cases of 
uncomplicated unilateral hydronephrosis due to stone in the pelvis of the 
kidney or ureter on the same side in which the obstruction was removed 
by the extraperitoneal method have given almost uniformly favorable 
results. 
Conclusions 
The prognosis of hydronephrosis will grow more favorable as time 
advances, for the modern methods of diagnosis, already mentioned, now 820 
DISEASES OF THE KIDNEY 
practiced by urologists, will be more generally used in the future; technic 
will be improved and radical surgical treatment will not be postponed until 
life is threatened. In considering the prognosis of individual cases the 
secondary bladder and ureteral changes are not to be ignored. 
The prognosis of hydronephrosis following malignant growths either 
within or without the urinary tract is almost uniformly bad. The late 
recognition of the primary cause makes the forecast ominous. 
The surgical relief of fibrous bands or other operable ureteral obstruc- 
tion offers an encouraging prognosis. 
The great dangers are atrophy of kidney substance, final anuria and 
uremia, which may result from the unrelieved obstruction, also sepsis. 
It is possible for renal and ureteral obstruction to lead to moderate hydro- 
nephrosis ; the sac may collapse; finally there is atrophy of the kidney. 
Enormous dilatation may persist with intermittent discharge of the 
fluid {intermittent hydronephrosis'), the patient living during many years 
These cases are often operable and permit of successful plastic operations; 
they include sections of valves, ureteropyeloplasty, ureteropyeloneostomy, 
lateral ureteral anastomosis, plastic operations on the renal pelvis, pyelo- 
plication, orthopedic resection and combined operations. Schloffer has re- 
ported 86 such operations, with 7 deaths and 17 failures. There are occa- 
sional cases in which the sac may discharge and the fluid may never re- 
accumulate. The conversion of a sterile hydronephrosis into a pyonephro- 
sis is possible. These sacs often rupture externally or are surgically treated 
after they point. The rupture may take place in one of several directions 
(See Pyonephrosis and Pyelitis). Early surgical treatment offers great 
encouragement for these purulent accumulations. 
References 
Aschoff. Path. Anatomie. Jena, 1913. 
Guiteras. Urology. New York, 1912. 
Kelly & Burnham. Diseases of the kidneys, etc. New York, 1914. 
Kuster. Chir. Krankh. d. Nieren. Deutsch. Chir., Lief. 52. 
Morris [Henry). Diseases of the kidney. London & Philadelphia. 
Schoffer. Cited by Walker [2. c.]. 
Walker. Index of Prognosis. London, 1915. 
(h) Nephrolithiasis 
{Renal Calculus, Calculosis of the Kidney and TJreter, Nierenstein) 
Cause.—The deposition or precipitation of normal or abnormal solid 
constituents of the urine (often dependent upon marked diathesis) usu- 
ally layer upon layer around a nucleus, is the cause of calculus formation 
which, as a rule, is held in the pelvis of the kidney or in the substance of DISEASES OE THE REHAL SYSTEM 
821 
that organ. Stone may be caught in the ureter—either a prolongation 
from a pelvic stone or the calculus may find its way down the tube to be 
caught—usually below the brim of the pelvis, most frequently near the 
bladder. Calculi may fall into the bladder and there by aggregation 
grow, or they may be passed per urethram. In rare cases the stone may 
fall into a diverticulum of the bladder, either remain there without caus- 
ing serious mischief or, as often happens, it gradually increases in size 
ultimately becoming a formidable body in the bladder. Renal calculus 
may form in the substance of the kidney; several stones may plug the 
calices, or the kidney pelvis may hold one or more calculi during varying 
periods without materially influencing the health or comfort of the carrier. 
Varieties of Calculi.—When there are only small rough or gritty bits, 
these are spoken of as “sand” or “gravel” and such particles are often 
passed without pain or constitutional disturbance. Millet-seed-sized gravel 
or even larger calculi are often passed unnoticed and without symptoms. 
The most frequent calculi are uric acid and lime oxalate; in the bladder 
with decomposing urine a calculus which is hard (oxalate or uric acid) 
may be surrounded by phosphatic deposit precipitated from the urine. 
The reaction of the urine is the prominent factor in determining the char- 
acter of the precipitate. Cystin stones, also xanthin, are exceedingly rare 
(See Cystinuria). There are occasionally phosphate and carbonate of 
lime, also triple phosphate calculi. One or more stones may remain in the 
pelvis of the kidney without symptoms when suddenly there is a renal colic 
in which the pain and other accompanying symptoms are characteristic. 
The stone or a part of it may find its way into the bladder; it may remain 
unmoved; it may become caught in the ureter, or what rarely happens, 
it may, because of its size or other anomalies, wander from the urinary 
tract after perforation at some point either into the perinephric tissue ( See 
Perinephritic Abscess), into the peritoneal cavity or into one of the sur- 
rounding organs. 
Prognostic Features 
Single calculi without infection offer a good prognosis. In about 50 
per cent of all cases there is but one stone. Multiple calculi are frequent. 
Israel says that both kidneys are involved in 27 per cent of his cases of 
renal calculosis, while Lequen claims 50 per cent; Hugh Young holds 
that these figures are too high. The size and shape vary. Casts of the pel- 
vis in coral-shaped and large stones are not unusual. In some of these cases 
the pelvis is tightly drawn over the stone, in others, when infected, the 
concretion lies in pus. Large calculi with septic symptoms are unfavor- 
able. 
The x-ray has opened an important diagnostic field for the prompt 
and certain localization of calculi within the urinary tract; the x-ray 
shows calculi most distinctly which cast the deepest shadow. In order 822 
DISEASES OF THE KIDNEY 
of their density therefore, the denser calcium oxalate shows best, then 
the phosphatic, and finally uric-acid stones (gall-stones are less likely to 
show than are renal calculi). 
With ureteral stones it is wise to make repeated plates, and it should 
be remembered that if caught they are found below the brim of the 
pelvis at the junction of the ureter and bladder. The recognition of renal 
and ureteral calculi early by means of the rontgenogram has enormously 
improved the prognosis of ureteral and renal calculosis, for it leads to 
early radical treatment and therefore prevention of infection and sec- 
ondary local changes which must of necessity follow from the presence of 
the foreign body. The prognosis of those cases in which one or more 
calculi are held in the kidney, without causing more than a mild grade 
of pyelitis (See Pyelitis) is good, as a rule. These patients may live 
without any symptoms, and the presence of a pyelitis calculosas is only 
recognized by an examination of the urine, usually for life insurance; 
the stone is detected by x-ray examination or it may suddenly provoke 
renal colic, or without marked symptoms it falls into the ureter. If the 
clinician subjected his clients who show evidences of pyelitis or obstruction 
to x-ray examination he would very often detect renal stone in its incipi- 
ency or at a time when the secondary changes have not advanced or infec- 
tion, the greatest danger, has not occurred. A single plate which may 
prove negative is insufficient for diagnosis; a single positive picture is 
convincing and cannot be controverted. 
Stone in the ureter, usually below the brim of the pelvis (Tousey), if 
held for any length of time may lead to secondary changes, dilatation, 
hydronephrosis, infection (pyelonephrosis and septic fever). In these 
cases the prognosis must always depend upon the ability to overcome sec- 
ondary changes by removing the cause, also upon the resistance of the 
patient (See Pyelonephrosis). 
Stone in the pelvis of the hidney may cause no pain, but yet pyelitis 
may be sufficient to cause constitutional symptoms and materially reduce 
the patient during long periods. Here urine analysis and x-ray must aid 
in diagnosis and suggest treatment. In pregnant women I have diag- 
nosticated cases of previously unrecognized renal calculosis during Ba- 
cillus coli infection by x-ray examination. At times such complications 
may threaten life; the fetus may be prematurely expelled, after which the 
condition may become latent. The presence of the stone is almost forgot- 
ten until renal colic proves a sufficient reminder and the case is usually 
treated successfully by surgical means. 
A large stone in the pelvis of the kidney may not always cause marked 
subjective symptoms; urinary examination, cystoscopy and ureteral cath- 
eterization and examination of the segregated urine will, however, prove 
advancing encroachment on the parenchyma of the organ, and in most 
cases pyogenic infection follows. Such cases, when the second kidney DISEASES OF THE RENAL SYSTEM 
823 
is not infected or diseased and there are no other complications of mo- 
ment, offer a favorable forecast following the surgical treatment most 
indicated. 
It occasionally happens that a patient dies suddenly during a renal 
colic. Such subjects are usually arteriosclerotic, have myocardial in- 
sufficiency, or they suffer from some form of nephritis. The shock of 
renal colic does occasionally lead to anuria (calculous anuria), and uremia 
may develop. I have seen cases, in 'which after double renal colic and 
the passage of calculi, anuria and uremia persisted between two and three 
days in patients advanced in years, which finally recovered. 
It may he safely assumed that in patients with marked diatheses, 
hereditary tendency (several members of the same family often suffer 
from metabolic faults—diabetes, gout, cholelithiasis) and renal lithiasis 
at the same time, the prognosis is not encouraging, for with all of the 
above mentioned anomalies there is very often cardiovascular (arterioscle- 
rosis) disease, in some cases marked tendency to obesity. 
The majority of patients who during or after renal colic pass the 
offender, in whom, after such passage the urine appears normal during 
from six to nine months, in ivhom there is no remnant of symptoms either 
objective {x-ray) or subjective, rarely have recurrence. This has been 
my experience based upon many years of observation; with strong hered- 
itary tendencies the rule may need modification. I have rarely seen 
recurrence after the passage of a calculus of congenital origin. 
Calculi in both pelves are always a menace. Sudden complete anuria 
may cause overwhelming and fatal uremia (See Uremia). When renal 
calculi lead to suppuration the only hope of complete cure lies in prompt 
surgical interference. 
Renal or ureteral stone with nephritis, heart lesions, advanced arterio- 
sclerosis, constitutional or metabolic disease offers an unfavorable prog- 
nosis for life. While neglected nephrolithiasis is most likely to become 
infected, it not infrequently happens that sclerotic (interstitial) changes 
are produced in the kidney holding the stone, and secondary heart and 
arterial changes result. The pain of nephrolithiasis other than the renal 
colic is usually in the hack, is often constant and nagging on the affected 
side but does not materially interfere with the activities of the patient. 
The hematuria is less profuse than with cancer or tuberculosis and in 
my experience has never threatened life. 
The temperature may be elevated, the nausea and vomiting exceed- 
ingly troublesome and weakening, the pulse often rapid during the attack 
(renal colic) but unless there are associated conditions the patient rallies 
in a few days. It not infrequently happens that with one or more small 
stones, renal colic—severe and exhausting—recurs at short intervals ; some- 
times there are several seizures during a single day. In most of these 
the stone passes per urethram without being held after it enters the bladder. 824 
DISEASES OF THE KIDNEY 
The prognosis of pyelitis calculosa has been separately considered (see 
Pyelitis) ; when there is added infection (purulent) as repeatedly sug- 
gested, intermittent fever persists until radical treatment removes the focus. 
Blood counts showing marked leukocytosis in these cases offer valuable 
diagnostic and prognostic data coupled with x-ray pictures and pyelog- 
raphy. 
Persistent pyuria with or without renal colic which cannot be explained 
in any other way, particularly if the patients are of full habit, should make 
the clinician suspicious of renal calculus. 
An acid urine, pyuria (moderate), kite-shaped epithelia, shingle ar- 
rangement of the epithelia are characteristic of pyelitis; when with this 
picture we also find uneven crystals with irregular and ragged prolonga- 
tions, the diagnosis of pyelitis calculosa is justified and the prognosis 
should he framed accordingly. 
The surgical treatment of calculous anuria is unfavorable. The period 
of tolerance is often surprising and has justified procrastination. The 
cautious study of cases in which the obstruction is one-sided, with calculous 
anuria resulting in spite of the surprising tolerance, leads to the conclu- 
sion that the safest time to operate is before uremia supervenes—for the 
mortality increases with each day. Iluck found that before the fourth 
day the mortality is 25 per cent, before the fifth 30.7 per cent, and before 
the sixth 42.1 per cent (Walker). Watson (quoted by Walker) collected 
205 cases of calculous anuria and reports: 
“Treated without operation, 110; deaths 80; mortality 72.7 per cent. 
Treated by operation 95; deaths 44; mortality 46.3 per cent.” 
Walker adds: “These results are capable of improvement if the neces- 
sity for early and rapid operation is fully realized.” 
The mortality following operations for stone (nephrolithotomy) in 
healthy or slightly infected kidneys and in infected kidneys, as shown by 
collective investigation, is 8.8 per cent for the former and 23 per cent for 
the latter (Legueu). It may he concluded that the carrier of a stone in 
the kidney or ureter is not a safe risk; he is constantly in the midst of 
more or less danger though spontaneous cure is not impossible nor unusual. 
The dangers are infection, prolonged anuria, possible uremia, perforation 
into the peritoneal cavity, occasionally erosion of the renal artery, pyelo- 
nephrosis and cystitis (ascending infection), final sepsis, amyloid de- 
generation and paranephritic abscess, hydronephrosis and interstitial ne- 
phritis (Luthje). 
For further data relating to the prognosis (surgical) of renal and 
ureteral calculosis, the reader is referred to the well-known works of Israel, 
Henry Morris, Kiister, Kelly and Burnham, Guiteras, Rovsing, Keen and 
Harrison. (See Index Medicus and Index Catalogue—Surgeon General’s 
Office.) DISEASES OF THE REHAL SYSTEM 
825 
References 
Guiteras. Urology. New York, 1912. 
Huck. Cited by Walker. 
Israel. Chir. Klinik d. Nierenkrank. Berlin, 1901. 
Kelly & Burnham. Diseases of the kidneys, ureters and bladder. New York, 1914. 
Legueu. Ztschr. f. Gyndk., 1908. Also cited by Young [l. c.]. 
Rev. franc, de Med. et Chir., 1904. 
Luthje. von Mehring u. Krehl’s Lehrb. d. inner. Med. Jena, 1913. 
Osier (Sir William). Practice of medicine. New York, 1914. 
Tousey. Medical electricity and Rontgen rays. Philadelphia, 1915. 
Walker. Index of prognosis. London, 1915. 
Watson. Cited by Walker. 
Young (Hugh). Osier & McCrae’s modern medicine. Philadelphia, 1909, vi. 
(i) Neoplasm of the Kidney (including Hypernephroma) 
General Statements.—Renal growths may be primary or secondary, 
benign or malignant. They are not frequent, are difficult of recognition 
unless they produce symptoms, or are palpable. They are often palpable 
before they cause symptoms sufficient to bring the patient to the physician, 
because of the tolerance of the organ invaded and in many cases the slow 
growth. In some the superimposed panniculus is sufficient to make early 
recognition exceptional. 
Malignant Growths 
The majority of malignant growths of the Icidney (carcinoma) are 
secondary. Morris in 2,610 post mortem examinations (of kidney 
diseases) found 5 primary and 22 secondary cases of malignant disea-se 
of the kidney. Rolleston found but one primary renal growth in six and 
one-half years at St. George’s Hospital; in 10 years 5 cases were met in 
the pathological department (Kellynack). 
At Wurzburg Virchow found only 0.5 per cent of the malignant neo- 
plasms involving the kidney. Kellynack reports among 1,400 cases of 
kidney lesions while he was pathologist in the Manchester Royal In- 
firmary, 6 cases of primary renal growth. 
Sarcoma—Carcinoma.—In my experience sarcoma of the kidney is 
more common than carcinoma; many cases reported as cancer are unques- 
tionably sarcoma. The more frequent seat of the primary cancer is the 
alimentary canal. Kellynack says “that secondary deposits are met with 
in the kidney in about 8 per cent of all cases of cancer and nearly 
per cent of all cases of sarcoma.” 
It is the consensus of opinion among pathologists and clinicians that 826 
DISEASES OF THE KIDNEY 
the kidney is comparatively seldom involved in secondary growths and 
that primary growths are exceedingly rare. 
Congenital sarcoma is not uncommon; if small it may escape notice; 
it often grows to enormous size before it is detected—too late for an en- 
couraging forecast in most cases. It may be of enormous size at birth, a 
smooth globular mass tilling the abdomen. 
My experience with sarcoma in children has been unfortunate; 
operated on detection, they have recurred within less than twelve months 
in most cases in spite of what appeared to be a radical operation. 
Hypernephroma.—Grawitz in 1883 called attention to a growth since 
known as hypernephroma. The growth arises from “aberrant renal rests 
My observation of the material of Fischer, in Frankfurt on the Main, 
during almost an entire year convinced me that most renal growths were 
true hypernephromata and that in most of these the recognition of the 
disease was too late to anticipate metastases. In my experience the metas- 
tases to distant organs are comparatively early; in the most favorable cases 
recurrences or fatal metastases are not long postponed; in the more favor- 
able cases after comparatively early operations, with but few exceptions, 
there are positive evidences of return or metastasis within between two 
and three years. The metastases have frequently been to the spine and 
brain, in one case to the heart, to the lung in a number of cases, and to the 
bones of the extremities. There are but few cases on record with the diag- 
nosis positively established in which hypernephroma, unless operated very 
early, offered hope of permanent cure. Israel reports 2 cases alive after 
two years, 2 after six years and one after nine years. 
Prognosis of Malignant Diseases of the Kidney.—With the' data be- 
fore us concerning sarcoma and carcinoma, the fact that so many of these 
kidney tumors are secondary, that they are long tolerated, that the kidney 
mass is often a part of a general carcinomatosis or sarcomatosis, that most 
operations are late—the prognosis of both must be exceedingly grave. My 
cases secondary to growths in the testicle have been rapidly fatal, often 
with liver metastases at the same time. 
Renal tumors (malignant) may remain latent or increase insidiously 
over a very long time, the general condition may not be materially affected 
during many months; hemorrhage, a leading symptom may cease and lull 
patients into a false and unjustified feeling of security. The growth may 
be palpable during long periods before there is retrogression. 
With papilloma of the kidney, hematuria may be paroxysmal during 
many years (in one of my cases over twenty years) before there is pro- 
gression to a fatal termination. In the case above mentioned the bladder 
and kidney were both finally involved and there were metastases to distant 
parts. 
The entire consideration of the prognosis of the malignant diseases of 
the kidney may be summarized in a short paragraph: “All malignant DISEASES OF THE RENAL SYSTEM 
827 
groivths of the kidney are surgical affections in which the only hope of 
permanent relief lies in the early recognition of the growth when it is 
primary and its prompt and radical removal. Secondary groivths, which 
are numerically in the ascendency offer no hope of permanent relief by 
any means at our command at the present time 
The benign growths of the kidney include the fibroma, lipoma, 
angioma, lymphadenoma and myxoma. They are exceedingly rare, may 
cause no symptoms or hut few, and offer a good prognosis. The majority 
of benign growths are discovered on the post mortem table. 
The reader is referred to the authoritative surgical treatises mentioned 
at the end of the preceding chapter for fuller information on this subject 
than I am able to give in a medical work. 
Cysts of the Kidney.—With chronic nephritis, tubal and parenchy- 
matous, cysts of varying size are often found; they are usually small, due 
to dilatation of constricted tubules. They are not of sufficient size to be 
palpated and are not recognized intra vitam—are not of great prognostic 
significance. 
Polycystic Kidney.—Polycystic kidney is an interesting condition 
from the diagnostic and pathologic standpoint, but it is not amenable to 
cure though there are recorded cases in which death has been postponed 
during several years. The condition may continue during many years; 
indeed with recurring characteristic symptoms patients, may live to reach 
old age. The majority die between 40 and 60; of these the death rate 
between 40 and 50 is highest. 
The leading symptoms are paroxysmal hematuria and pain which recur 
at long or short intervals during many years with physical signs of a renal 
mass; in thin subjects its contour leaves little room for doubt in diagnosis. 
The size of the cyst varies—several may be small while in the same kidney 
one or two or more cysts are of considerable size. The lobulated appear- 
ance of the kidney is often recognized through the abdominal wall. The 
condition is almost always bilateral, though Trench observers have con- 
cluded from the study of a large material that almost one-fifth are uni- 
lateral. 
Morris’ statistics are quoted by those who favor surgical interference as 
encouraging. At best they cannot avert the fatal termination, for these 
patients die with symptoms of chronic nephritis, characteristic cardio- 
vascular changes and uremia. The urinary features include the low 
specific gravity, hyaline and granular casts and other features of inter- 
stitial or secondary contracted kidney. 
Osier has recently reported two interesting cases of polycystic kidney 
in the adult recognized intra vitam—one died while under observation, the 
post mortem confirmed the diagnosis. Whatever surgical operation is per- 
formed, the mortality is high and it is questionable whether life is ma- 
terially prolonged where there are bilateral cysts. With unilateral 828 
DISEASES OF THE KIDNEY 
polycystic Tcidney surgery offers greater hope—but a high mortality. 
There is a strong hereditary character; several members of the same 
family may be afflicted. 
When the cysts are large at birth, life is not prolonged and associated 
congenital anomalies are common. 
References 
Garceau. Renal, ureteral tumors, etc. New York, 1909. 
Grawitz. Verhandl. d. deutsch. Gesellsch. f. Chir., Berlin, 1894. 
Israel. Chir. Klin. d. Nierenkrank. Berlin, 1901. 
Kellynack. Renal growths. Edinburgh & London, 1898. 
Morris. Virchow's Arch., 1883, Bd. xciii. 
Surgical diseases of the kidney. London. 
Allbutt's System, 1897, iv. 
Osier (Sir William). Internat. Clin., Philadelphia, 1915, ser. 25, i. 
Rolleston. J. Path, and Bacteriol., London, 1893-4; also quoted by Kellynack. 
Virchow. Die krankhafte Grschwvlste. 1865, Bd. Hi. 
Young (Hugh H.). Osier & McCrae’s Modern medicine. Philadelphia & New York, 
1909, vi. 
(j) Movable Kidney 
(.Mobile Kidney, Nephroptosis, Floating Kidney, Renmohilis) 
This subject has been fully considered from the medical standpoint in 
Section V, F. 4, gastroptosis, also enteroptosis (Glenard’s disease in same 
section). 
Operation.—The operation of kidney fixation is less frequently per- 
formed than it was ten or fifteen years ago. Failures have been repeated 
and in many the subjective complaints have persisted after the operation. 
Mortality Following Operation.—The mortality following the opera- 
tion is between one and two per cent. I have considered the results 
obtained by Treves in Section V, to which reference is made above. In 
America, Edebohls collected 846 cases from the literature, with a mortality 
of 1.65 per cent. Billington operated on 575 patients with 4 deaths. 
Short says: “Probably the mortality is between 1 and 2 per cent.” 
For detailed surgical statistics the reader is referred to the works of Bill- 
ington, Morris, Rovsing, Keen, Mills of Birmingham, the reports of the 
London Hospitals, Bristol Hospitals, the Mayo Clinic, Kelly and Burn- 
ham and Guiteras (See Index Medicus). Statistics which are intended 
to prove the curability of the condition by operation are unreliable. Most 
patients with movable kidneys are neurasthenics and in many the mobility 
of the organ is only a part of a process which includes many organs (Glen- 
ard’s disease). 
Associated Symptoms.—Cases in which there are repeated Dietl’s DISEASES OE THE RENAL SYSTEM 
829 
crises, which are not relieved by mechanical support, in which there is 
repeated kinking of the pedicle, demand surgical interference. In my 
experience the crises were overcome by radical treatment, but many, indeed 
most of the neurasthenic symptoms persisted. 
Cases with hydronephrosis have given disappointing results; this is 
particularly true of intermittent hydronephrosis unless some radical 
measure was instituted to prevent kinking of the ureter because of the 
mobility of the kidney. 
The association of gastric ulcer with movable kidney is surprisingly 
frequent. 
Prognostic Factors.—The autosuggestion practiced by the subjects of 
this condition is overpowering and with many mental symptoms is often, 
but not always, relieved by surgical treatment. I have found over 50 
per cent of nervous patients in private practice and a large percentage in 
dispensary material the subjects of movable kidney. 
In my experience the regulation of the habits of the patient, well- 
timed and repeated suggestion, proper mechanical support and healthful 
occupation are more important and offer better results than does radical 
surgical treatment. Organic diseases of the stomach and intestines have 
often been suspected, when mobile kidney alone was responsible for such 
simulation. In some of these cases it requires the most cautious and long- 
continued personal supervision before positive differentiation is possible. 
In a small proportion of these cases the effect of surgical interference 
proves wholesome per se though failures are not unusual. 
In offering the prognosis in the average case of movable kidney with 
neurasthenic accompaniment the diagnostic ability, tact and discriminat- 
ing sense of the attendant are all taxed and upon his judgment and per- 
sonality the future welfare of the patient often depends. I have seen 
many cases in which the strong personality of the attendant has been 
sufficient with mechanical support to make the patient comfortable and 
keep her so. 
Suppurative Diseases oe the Kidney 
(k) Pyelitis 
(Pyelonephritis, Perinephritic Abscess, Nephritic Abscess, Suppurative 
Nephritis, Pyonephrosis) 
General Statements.—While the preceding terms are generally consid- 
ered to be synonymous, they are not really so. Pyelitis is literally an 
inflammation of the renal pelvis; pyelonephritis includes pyelitis and 
nephritis; perinephritic abscess is a pus accumulation about the kidney (in 
the perinephric tissue) ; nephritic abscess and suppurative nephritis are 
synonymous with abscess of the kidney. Pyonephrosis includes the break- 830 
DISEASES OF THE KIDNEY 
down of the parenchyma of the kidney substance (atrophy) in a process 
of suppuration. The organ is practically converted into a pus sac. 
Pyelitis as well as (e) perinephric abscess (g), hydronephrosis (h), 
nephrolithiasis (i), neoplasms of the kidney (including hypernephroma), 
and (j), mobile kidney—the conditions included in 2 of this Section VI— 
are all surgical affections which as a rule find their way to the internist 
for diagnosis, and I therefore feel justified in considering their prognosis 
without entering into the detail which has been given to the strictly medi- 
cal diseases included in this section (See also Section VI—Anomalies of 
Urinary Secretion— (c) Hematuria for the consideration of Acute and 
Chronic Primary Infections, non-calculous pyelitis with moderate hema- 
turia, usually found in pregnant women and at the menstrual period due 
to the Bacillus coli communis as a rule, though occasionally other patho- 
genic bacteria may he the cause. About 30 per cent of these cases abort. 
This condition is also known as pyelocystitis). 
Prognostic Factors.—Pyelocystitis may be acute or chronic. When the 
urinary tract has been normal the infection is usually ascending, oftener 
of Bacillus coli origin than of any other infection and secondary to some 
intestinal disturbance including appendicitis, colitis (acute or chronic), 
proctitis, hemorrhoids, dysentery or other grave intestinal disease (car- 
cinoma, ulcer, etc.). With the benign infections and pyelitis the course 
of the disease is favorable. In old men with intestinal lesions and consecu- 
tive pyelitis (pyelocystitis) septic symptoms may be prominent early and 
overpowering. Such subjects soon become thoroughly toxic, the kidney is 
tender, at times palpable and enlarged, and the prognosis is bad. 
When the symptoms are profoundly toxic, there may be repeated chills, 
high fever and rapid pulse. The prognosis depends upon the ability of the 
patient to offer sufficient resistance during the acute period to withstand 
the added infection. The course of the disease in old and enfeebled sub- 
jects is rarely more than seven to ten days when toxemia is deep. The 
infections, as already stated in considering the prognosis of cases in preg- 
nant women—to which Ave also refer above—is faAmrable in most cases. 
The condition in our experience has improved with the emptying of the 
uterus. 
Pyelitis in enfeebled subjects due to exposure to cold and wet with 
added infection is often associated with symptoms of grave constitutional 
disturbance, and may lead to abscess formation or a deep toxic condition 
from Avhich the patient does not rally. The majority of pyelitides, in 
which the etiology is obscure, in patients with normal or even slightly 
reduced resistance, recoAmr. 
Catarrhal pyelitis may become chronic when due to stricture of the 
urethra, cystitis, stone in the bladder, ureter or pelvis of the kidney, tuber- 
culous disease of the organ or the urinary tract below the pelvis. 
With tuberculosis of the genito-urinary tract there may be suppuration DISEASES OF THE EENAL SYSTEM 
831 
due to the degeneration of the tubercle and breakdown of included tissue 
in both the pelvis and kidney substance at the same time (See Tuberculosis 
of the Kidney—Section I). 
Surgical Interference, etc.—Pyelitis, upon whatever cause it depends, 
if unrelieved, is likely to encroach upon renal tissue causing breakdown 
and suppuration. When pyelitis is secondary to kidney infection, the 
disease beginning in the substance of the organ with abscess formation, 
surgical interference offers the only hope of saving the organ, or nephrec- 
tomy offers the only hope of saving life once the disease is far advanced. 
It is plain that the prognosis of pyelitis must often depend upon the 
ability of the surgeon to remove the primary cause, the extent of coexisting 
lesions, the resistance of the patient and the depth of the toxemia. The 
condition of the second kidney is of paramount importance and the exam- 
ination of the segregated urine with the assistance of the ureteral catheter 
and the cystoscope and its thorough study both chemically and bacterio- 
logically, beside x-ray pictures, will always supply data of great prognostic 
value which demand expert and cautious interpretation. 
With acute pyelonephritis the English have not had encouraging re- 
sults from nephrotomy. Walker reports 7 deaths among 20 operations (35 
per cent). He says: “In surviving cases, the late results are also unsatis- 
factory; the acute symptoms subside, but chronic pyelonephritis persists, 
and nephrectomy may be required later.” 
In America the results of nephrectomy in pyelonephritis have been 
most encouraging in the presence of a healthy second kidney. Almost all 
of these cases, when uncomplicated, recover. Walker reports 17 nephrec- 
tomies without a death for pyelonephritis. 
Symptoms of chronic cystitis with all forms of chronic pyelitis are 
persistent and never yield until the renal lesion has been successfully 
relieved. 
Catarrhal pyelitis is likely to recur after supposed relief. In all of 
these cases stone in the pelvis of the kidney should be strongly suspected. 
The x-ray will prove a valuable adjunct, not only for diagnosis but for 
prognosis as well. 
Calculous pyelitis may cause symptoms of acute pyelitis during a 
limited period; the urine may practically clear and the patient as well as 
the attendant are deluded to believe that complete cure has resulted. Un- 
less the stone is passed or in some way encysted—which is comparatively 
rare—the colic with hematuria recurs with other urinary and x-ray evi- 
dences which prove the presence of the offender (See Nephrolithiasis). 
The prognosis of these cases is good in resistant subjects who are without 
serious complications. 
One of the leading dangers of neglected pyelitis calculosa is ascending 
suppurative nephritis with consecutive renal insufficiency and uremia (See 
also Nephrolithiasis). 832 
DISEASES OF THE KIDNEY 
Ascending pyelitis from an infected prostate may be either acute or 
chronic. Most of these cases are chronic and yield only to the radical 
treatment of the primary disease. 
Gonorrheal pyelitis in spite of rigorous local treatment is exceedingly 
rebellious, and complete cure is exceptional though patients live for years 
unless there are complications, including (occasionally) gonococcus endo- 
carditis—always fatal. 
Neglected pus accumulation in the pelvis or kidney usually finds exit 
in one of several directions. It may lead to perinephric abscess or it may 
perforate into the free peritoneal cavity causing peritonitis and death. 
When the pus is encapsuled or there is a sinus which continues to dis- 
charge and the diseased kidney is not removed, the patient usually dies 
after months of suppuration and often amyloid disease in many vital 
organs (liver, spleen and kidney). I cannot accent with too great force 
the assistance in prognosis which may be received from the correct 
INTERPRETATION OF CYSTOSCOPIC EXAMINATION WITH URETERAL CATH- 
ETERIZATION, PYELOGRAPHY, X-RAY EXAMINATION, CHEMICAL AND BAC- 
TERIOLOGICAL METHODS AND BLOOD EXAMINATIONS. 
Most cases of pyelitis which to all appearances make full recoveries are 
not bacteriologically cured, for according to Scheidemandel, only 35 per 
cent of acute cases which are relieved of subjective symptoms in from five 
to six weeks are found with sterile urine. 30 per cent of the remaining 
cases fall into a chronic latent period which may persist during many years 
without advance of renal lesions. 
Acute pyelitis occasionally attacks babes during the first months of 
their existence, when it is likely to be due to the Bacillus coli communis. 
Most of these babes recover after an acute and threatening period in which 
there is high fever with evidences of profound toxemia, at times convul- 
sions. Older children may also become infected. The average duration 
of these forms of pyelitis in children is from seven to ten days. 
Chronic pyelitis is frequent in the urological clinics. Of 1,800 uro- 
logical cases Fritz found 161 cases without involvement of the parenchyma 
of the kidney. Of these 56 were males, and 105 females. The right side 
was involved in 87, the left in 32 and both sides in 42 cases—the right 
side therefore in 129 and the left in 74. 
Chronic pyelitis may exist during years without encroaching on the 
parenchyma of the kidney. The treatment of such cases, purely local 
(pelvic lavage), has in properly selected cases proved eminently success- 
ful (Geraglity). The uncomplicated cases of pyelitis are without reduc- 
tion of kidney function; pyelonephritis when advanced always shows de- 
creased function. 
Geraghty contends that the organism causing infection has very little 
influence on prognosis. Pyelography is of considerable prognostic value, 
for it shows the condition of the pelvis resulting from the infection. DISEASES OF THE RENAL SYSTEM 
833 
The prognosis after local treatment of the pelvis is particularly good 
in cases of “fairly active infection with a normal function and in which 
the collargol shows few changes in the pelvic outline.” 
In the chronic cases, i. e., “long standing pelvic infections, in which 
marked changes have occurred in the pelvic wall, as shown by pyelography, 
and in which one finds in the catheterized specimen very few lekocytes 
and only an occasional bacterium, the prognosis is not so favorable.” 
When with chronic pyelitis there is marked dilatation of the renal pelvis, 
residual urine and bacteriuria, the prognosis for restoration of the kidney 
is bad. 
Some of these chronic cases may develop renal calculosis or finally 
pyonephrosis (Lenhartz). 
Of 80 cases reported by Lenhartz, to whom we owe much of our knowl- 
edge concerning pyelitis, there were 5 deaths—one due to cancer, one 
tuberculosis, two pyonephrosis and one ended after acute and severe symp- 
toms of pyelitis with renal abscess due to the Friedlander bacillus. 
Suppurative nephritis or abscess of the kidney is a suppurative inflam- 
mation of the kidney substance dependent either on hematogenous or 
lymphogenous origin, to direct or indirect infection from traumatism or 
extension by contiguity from suppurating neighboring organs. The 
disease, when not part of a general pyemia, may be one-sided, but it is 
unually bilateral. When there is obstruction of one ureter or the suppura- 
tion spreads from the pelvis of the kidney, the abscess is likely to be uni- 
lateral. With fully developed suppurative nephritis the destructive process 
includes all of the renal structures and the abscess may be single or 
multiple. Multiple abscesses of the kidney may become confluent because 
of the destruction of intervening tissue and pyonephrosis (pyelitis with 
suppurative nephritis and atrophy of the kidney substance) results. The 
organ becomes a pus sac. With all forms of suppurative diseases of the 
kidney the symptoms, objective and subjective, are outspoken and usually 
make a reasonably positive forecast possible. With pyonephrosis Brown 
quotes Kiisler as offering “four favorable factors in the prognosis—the 
possibility of an early correction of the urinary stasis, youth, a strong 
constitution, and a unilateral lesion.” 
The urine always shows pus in varying quantity. With pocketing it 
may be intermittent, a large discharge may be unloaded but once daily, 
usually on arising in the morning. If the ureter is constricted there may 
be but little pus during part of the day and a free discharge at one time, 
or the pyuria may recur at longer intervals. Renal casts are not infre- 
quently found. With simple catarrhal pyelitis kite-shaped epithelia 
shingle-arranged with a few pus cells and moderate albuminuria are char- 
acteristic. The urine is usually acid but not necessarily so; the reaction 
depends upon a variety of causes and on the responsible micro-organism. 
IJrine with shreds of renal tissue, with the appearances mentioned, proves 834 
DISEASES OF THE KIDNEY 
advancing destruction of renal tissue; unless relieved surgically, the out- 
come is fatal. 
Repeated chills and fever are indicative of progression and toxemia. 
I have learned to recognize these symptoms with tuberculous nephritis and 
pyelonephritis as indicating invasion which can only be relieved by radical 
surgical means. With both tuberculous and pyemic conditions, if the 
patient lilves long enough, progressive anemia is finally associated with 
amyloid degeneration and death. 
In some chronic cases after a few days of chills and fever, there is a 
free discharge of pus and a return to a fairly comfortable condition during 
a long period. Recurrence of symptoms is the rule. Finally the chills 
and fever and pyuria become almost continuous; the fever is characteristic 
of pyemia; the pulse grows more and more rapid, and with symptoms of 
profound invasion of the nervous system these patients die (coma, etc.). 
It is often surprising to find on post mortem examination the presence of 
pyonephrosis, tuberculous or non-tuberculous, in subjects who have never 
complained of renal symptoms and in whom the development of acute 
symptoms, often suggestive of uremia or overwhelming toxemia (non- 
uremic), end life within a few hours or days. 
Pus in the kidney may become encapsuled, may pass through the 
ureter, may burrow and find a safe exit—all without destroying life. 
Nature’s reparative and conservative processes occasionally come to the 
rescue, hut the majority of cases must be saved by modern surgical 
methods. Permanent damage to the kidney with all forms of suppurative 
disease of that organ is best prevented by the full appreciation of the old 
surgical principle that pus accumulation is best treated by free drainage. 
References 
Brown (Thos. R.). Osier & McCrae’s Modem medicine. Philadelphia, 1909, vi. 
Fritz. Die Therapie d. Gegenwart, Aug. 1914. 
Geraghty. J. Am. Med. Ass., Dec. 19, 1914, 2212. 
Guiteras (R.). Urology. New York, 1912. 
Kelly & Burnham. Diseases of the kidney, etc. New York, 1914. 
Kiister. Die chirurg. Erk. d. Nieren, Deutsch. Chirurg. Lief. 52. 
.enhartz. Munch, med. Wchnschr., 1907, No. 16. 
Scheidemandel. Wurzburger Abhand., xiii, H. 7 & 8. 
Walker. Index of prognosis. London, 1915. 
(l) Perinephric Abscess 
(Perinephritis, Epinephritis, Paranephritis, Paranephritic Abscess) 
General Statements.—Brown, whose consideration of the suppurative 
diseases of the kidney is truly classical, in considering the nomenclature, 
says: “It is better to be more explicit, however, and to define perinephritis DISEASES OF THE RENAL SYSTEM 
835 
as inflammation of the fibrous capsule immediately surrounding the kid- 
ney, epinephritis, inflammation of the fatty capsule, and paranephritis, 
inflammation of the retroperitoneal fat.” The differentiation intra vitam 
is exceedingly difficult, unlikely, and for all practical purposes, unneces- 
sary. 
Origin.—Most perinephritic abscesses are unilateral, acute, and when 
developed the pus is collected around the kidney in the lumbar region. 
My experience agrees with that of Guiteras which he expressed ten years 
ago that nearly all cases of perinephritic abscess are due to kidney disease 
and “that those secondary to diseases of other organs are rare and not, 
properly speaking, perinephritic abscesses.” He found that 85 per cent of 
perinephritic abscesses were due to kidney disturbances; these he classified 
as follows, reporting 20 cases: 
Pyonephrosis: 
Calculous 3 
Tuberculous 5 
Obstructive 3 
Total .”lT 
Pyelonephritis: 
Calculous 1 
Tuberculous 2 
Obstructive 2 
Total 5 
Rupture of kidney 1 
Empyema 1 
Uecrosis of rib 1 
Unknown eause (probably retroperitoneal gland 
suppurating) 1 
Total 4 
Eull Total 20 
Prognostic Factors.—In my experience I have no death to record 
resulting from perinephritic abscess per se when the complication was 
recognized reasonably early and the abscess was freely drained. Cases 
not recognized, but neglected, have died of pyemia perforation (peri- 
tonitis) or from other causes. The prognosis of perinephritic pus accumu- 
lation rests largely upon the nature of the primary kidney lesion and timely 
recognition. 
When there is primary pyelonephritis or pyonephrosis with paraneph- 
ric suppuration, unless the primary abscess cavity is removed the chances 
are against full recovery, and one or more sinuses usually remain with 
annoying urine discharge. In unrecognized cases there may be burrowing, 836 
DISEASES OF THE KIDNEY 
depending upon the position of the abscess, the point of least resistance 
and the extent of the complications (adhesions, etc.). 
Perforation may be either visceral or ventral. Perforation or pointing 
in the lumbar region (ventral) is more favorable than rupture into the 
peritoneum, intestines, stomach or pleural cavity (visceral). In a fair 
number of cases fistulae in the lumbar or inguinal regions persist during 
considerable periods, and finally heal spontaneously. When the renal 
suppuration leads-to sepsis (acute and malignant) the organ breaks down 
rapidly, the sloughs show a gangrenous process, and the patient dies with 
symptoms of profound toxemia unless saved by timely surgical interfer- 
ence. Rosenberger’s statistics show 26 cases of perforation—6 were into 
the intestine, of these 2 died; 13 into the pleural cavity, with 8 deaths; 3 
into the free peritoneum, with 3 deaths. Early recognition, with prompt 
drainage overcomes the danger of the complication; the surgeon then has 
the primary lesion to combat. 
There are a number of cases in which pus accumulation is found about 
a kidney without evidence of any underlying renal lesion—so-called 
“primary cases”; these when recognized early, pointing outward, offer a 
good prognosis. When drained by surgical means they recover promptly. 
I have met a few cases in which perinephric abscess followed typhoid 
fever and pneumonia; in these recovery was complete. 
Perinephric abscess does not often present for diagnosis in the practice 
of the internist. In private practice I have seen but 5 cases among my 
last 6,600 cases. In hospital practice I occasionally find a case to be 
transferred to the surgical side. At the Johns Hopkins Hospital among 
the white surgical patients during the period from 1892 to 1911—18,448 
males and 6,934 females—there were 18 cases of perinephritic abscesses, 
all among the males, with 2 deaths (11.1 per cent). There were no cases 
among the females. We note that the statistician Hoffman includes 6 
cases of perinephritic abscess in his “white medical cases”—all in males, 
and without a death. 
Kiister reports 230 cases of paranephritis, of which 145 made a com- 
plete recovery; in 6 there were fistulae, 79 died (mortality 34 per cent). 
These cases prove neglect of early diagnosis or treatment, for it is not in 
accord with the experiences of the clinician at the present time, either in 
our own country or in Europe. 
References 
Brown (Thomas R.). Osier & McCrae’s Modern medicine. Philadelphia, 1909, vi. 
Fritz (M.). Die Therapie d. Gegenwart. Aug., 1914. 
Guiteras (R.). Urology. New York, 1912. 
Hoffman. Johns Hopkins Hosp. Rep. Monographs. N.S. iv. 
Kiister. Chirurg. Krank. d. Nieren, Deutsch. Chirurg. Liefer. 52. 
Lenhartz. Munch, med. Wchnschr., 1907, No. 16. 
Scheidemandel. Wiirzb. Abhandl., xiii, Hft. 748. Section VII 
Diseases of the Nervous System 
A. Diseases of the Peripheral Nerves 
I. Neuralgia 
General Considerations.—Neuralgia is a symptom, it is never a disease 
per se—a fact which must be kept before the mental vision of the clini- 
cian for all purposes of diagnosis, prognosis, and treatment. That there 
are many acutely arising paroxysmal pains which course along one or 
more single nerves or nerve trunks in which the true pathology escapes 
detection, which yield to treatment, must be admitted. 
Those “neuralgias” are dependent upon nerve pressure, perineuritis 
oftener than neuritis, true structural irritative disease of the nerve, or 
upon change of a nutritional character in which no structural change in 
the nerve can he demonstrated. 
The word “neuralgia” is carelessly used by the physician very often, 
and should be limited to the idiopathic nerve pains in which it may be 
assumed after thorough consideration of the individual case, that there is 
no pathologic change. 
The classification of Herter should be accepted which divides all 
neuralgias into either “idiopathic ” those without evident lesion, and 
“symptomatic,” those depending on structural disease, usually neuritis or 
perineuritis. 
Definition.—Neuralgia may be defined as a pain, arising suddenly, 
without prodomata, of a shooting, darting, pricking, burning or boring 
character, which radiates along the course of a single nerve and its 
branches, recurring in paroxysms at short intervals. 
To consider the significance of all neuralgic pains and their causes 
would lead through every department of internal medicine and of surgery. 
The first question to be decided is whether an existing neuralgia is symp- 
tomatic or idiopathic, i. e., whether it rests on a pathologic fundament (if 
so it is necessary to consider the nature of the primary lesion) or whether 
837 838 
DISEASES OF THE NERVOUS SYSTEM 
the neuralgia is idiopathic. There are also many other factors to be con- 
sidered in deciding upon the prognostic significance of neuralgia. The 
following are among the more important factors which influence the prog- 
nosis of idiopathic neuralgia: 
Neuropathic or Neuralgic Predisposition.—There are patients 
who after their childhood, which is usually characterized by marked 
asthenia, develop neuralgia in some part of the body on the slightest ex- 
posure to cold, sudden changes of climate, after insignificant effort or 
depressing conditions, or after slight strain or excitement. These patients 
are always below par. Women are oftener burdened than men with such 
neuropathic tendencies; with menstruation, pregnancy, and during the 
climacteric, they are made wretched by the recurring neuralgic pains 
which are not always limited to the same nerve. Unless the tendency is 
recognized early and corrected by such methods as lift the patients to the 
normal standard of health or above, they are likely to suffer throughout 
life. These subjects are almost always sensitive and emotional women of 
the better classes. 
The influence of climatic change and rational living on prognosis in 
these neuropaths is paramount. Following the climacteric, often puberty, 
under favorable conditions with an improvement of the general condition, 
the neuralgias in these subjects cease, but are likely to recur on slight cause. 
When this hyperesthesia which leads to neuralgia, is acquired, the 
prognosis as a rule is better than when there is a strong family history 
of neuralgia or other functional nervous diseases, for the acquired tend- 
ency is usually amenable to rational treatment. 
Age and Sex.—Neuralgia is unusual early in life—rare before the 
tenth or twelfth year. Males suffer oftener than do females; in the latter 
neuralgias are often idiopathic; in men they are as a rule of organic 
origin. There are occasional periods when women suffer oftener than 
men. The cause of this variation is difficult to understand. Dividing 
our cases into five year periods and drawing an average, we find that 
women suffer oftener than men. Oppenheim and Bernhard however, from 
their large experience claim the preponderance of cases in men. 
In young girls abdominal neuralgias and “neuralgic headaches" are 
favorably influenced by the establishing of normal menstruation. 
Neuralgias in the aged are often dependent upon degenerative and 
nutritional faults (arteriosclerosis) which do not admit of successful 
treatment. Such neuralgias are associated with other symptoms of the 
underlying fault which make the cause clear and the prognosis easy. 
In young and old, the prognosis of neuralgia is best in those cases in 
which the pain does not remain fixed. In both young and old, neuralgia 
in which there is evanescence of tenderness and acute pains in more than 
one nerve is not usually dependent on organic disease. 
Anemia and Constitutional Diseases.—-A frequent cause of all DISEASES OF THE PERIPHERAL NERVES 
839 
forms of neuralgia is simple anemia, or chlorosis which promptly yields 
to treatment. 
The graver forms of anemia are more likely to have anesthesias and 
paresthesias (Lichtheim symptoms) than the ordinary neuralgias, though 
occasionally grave anemias are associated with persistent neuralgic pains. 
The prognosis for complete relief depends on the nature of the anemia. 
Diabetes is often associated with pains of neuralgic character. Many 
of these are due to neuritis, and are persistent; others yield with the im- 
provement of the general condition and the reduction of sugar loss. 
Cachexias are at times associated with vague and irregularly dis- 
tributed neuralgias without showing pathologic change on post mortem; 
these are likely to persist, though at times they disappear without known 
cause and do not return. 
Infections, particularly influenza, pneumonia, typhoid fever, measles 
and smallpox during their early stages may have severe neuralgia which 
in most cases disappears with the full development of continuous symptoms. 
Epidemics of neuralgia, described by Reilly and others, are unques- 
tionably of influenzal origin; these yield to treatment. 
The neuralgic pains of syphilis are, as a rule, due to neuritis, though 
occasionally it would seem that the toxemia is sufficient to cause neuralgia 
without organic change. This question is sub judice. The pain promptly 
yields to treatment. 
Malaria may cause neuralgia in any part of the body; it observes 
some of the family tendencies of the disease including the periodicity of 
intermittent malaria. With acute malaria the pains yield promptly to 
treatment; with cachexia the course may be slower but unless malignant, 
complete recovery follows. 
The neuralgias due to poisons are relieved if not chronic, by removal 
of the cause. These poisons include lead, arsenic, copper, mercury, alco- 
hol, tobacco and phosphorus. 
The neuralgias due to masturbation, sexual excesses and other dissipa- 
tion, yield with the correction of the vice. 
Bad habits, overwork, faulty housing, improper ventilation and ex- 
posure to cold, are all factors which invite neuralgia, which when con- 
trolled prevent recurrence and lead to cure. 
In men, the larger nerves are involved (sciatic, etc.) more frequently, 
while in women the smaller trunks and their branches (intercostal, tri- 
facial, etc.) are the seat of the pain. 
When the nerve is tender to pressure during the first day or two of 
neuralgia, particularly during the paroxysms of pain, and the pain is 
limited to a single nerve, neuritis must be strongly suspected rather than 
simple neuralgia ; these do not recover so promptly as do the idiopathic 
cases. 
Pains (neuralgic) radiating along the intercostals and lumbar nerves 840 
DISEASES OF THE NERVOUS SYSTEM 
after the fortieth year, should not he interpreted as neuralgic without 
considering the possibilities of hone (caries), spinal, aortic or visceral 
disease. 
In adults, crural pains, continuous or paroxysmal, are rarely neu- 
ralgic ; they are dependent upon pressure on the lumbar plexus, with knee 
jerk reduced or absent; this conclusion is strengthened and prognosis 
should be accordingly given. 
The possibility of hone or other pressure should always be considered 
with “fixed” neuralgia which increases in severity from day to day, and 
the possibility of metastases from distant organs in which primary growths 
may exist without causing symptoms (prostate, stomach, large intestine, 
etc.) should he remembered. 
Mild paroxysms are always favorable to speedy cure when not asso- 
ciated with marked hyperesthesia or anesthesia. With the latter, there 
is usually neuritis though there are exceptions to this rule. 
Neuralgia with flabby and atrophic muscles is not as a rule idiopathic 
but of organic origin and the prognosis naturally depends on the cause 
and extent of the lesion. 
Transitory tenderness along the course of the nerve is frequent with 
idiopathic neuralgia; the exacerbations of pain are associated with increase 
of tenderness. 
Neuralgic pains about the head and jaw are usually dependent upon 
some discoverable cause which offers its own prognosis. The recognition 
of syphilis as a cause of neuralgia about the head with tender spots in 
the scalp leads to the relief of many. Caries of the teeth is the most fre- 
quent cause of pain about the face; to this I will again refer. 
Neuralgic pains during the period of incubation of meningitis and 
the radiation of pain along a single branch of the trigeminus during the 
early stage of brain tumor, when there are no other evidences of disease, 
are not infrequent. 
Nasal and frontal pains, neuralgic in character, can be correctly inter- 
preted only after the examination of the sinuses and nasal cavities. 
In deciding upon the significance of persistent or recurring neuralgic 
pains in the thorax, the abdomen, and the extremities, advantage must be 
taken of every possible aid, for after the thirty-fifth year the majority of 
these pains depend upon anatomic change. The reflexes are not to be 
ignored in prognosis, particularly in the unexplained neuralgias of women. 
Diseases of the heart, the lung, the abdominal viscera, the kidney, the 
genitals, associated with neuralgia, must be separately considered to make 
diagnosis and prognosis safe. 
The hyperesthetic areas of Head will often prove of value for differen- 
tiation and prognosis. 
The safe and scientific clinician will always brace himself against the 
diagnosis of idiopathic neuralgia, for he has learned that it is rarely jus- DISEASES OF THE PERIPHERAL NERVES 
841 
titled with increasing knowledge and refinement of diagnosis; its cause 
often exists within the nervous system itself and thorough search will 
reveal its presence. Tabes dorsalis, spinal and peripheral growths, 
syringomyelia, syphilis of the spine, single and multiple neuritis and 
chronic spinal meningitis, are among the causes of neuralgic pains with- 
out other developed symptoms. 
Relapses.—Relapses with long intervals of freedom from symptoms 
are characteristic of idiopathic neuralgia, and offer a favorable forecast 
if the patient is not burdened with neuropathic tendencies. 
Neuralgia which persists during long periods, in which paroxysms 
follow in rapid succession, are rebellious to treatment though cure often 
follows after years of symptoms. 
Hysterical patients with neuralgic pains, indefinite as to paroxysmal 
recurrence and in which there is as a rule no “fixed pain,” with marked 
development of the emotional element, “psychoalgia,” are often stubborn; 
the pains persist during long periods but finally yield to suggestion and 
rest. 
Trifacial Neuralgia 
(Tic Douloureux, Neuralgia of the Trigeminus) 
The majority of trigeminus neuralgias are acute, severe, and depend 
upon diseased teeth, diseases of the nasal passages, bone or mucous mem- 
brane, exostoses, neoplasms, periosteal thickening or malarial poisoning, 
or persist without known cause. 
In most cases but one branch of the fifth nerve is involved, though 
two may be painful at the same time depending on the location of the 
lesion. The fifth nerve is the most frequent seat of neuralgia. Conrad 
found it present 239 times in 717 cases of neuralgia. 
Besides the usual manifestations of neuralgia including “Valleix 
points,” in severe cases there are secretory disturbances, spasms of facial 
muscles or auditory symptoms; the taste is disturbed and the general 
condition suffers. 
Mastication in the chronic and many acute cases is impossible, and 
loss of weight is not unusual. 
The acute cases run a favorable but painful course. The removal of 
the cause leads to prompt cure. 
Neuralgia of the supra orbital branch is less obdurate than are the 
pains of the second and third branches of the nerve. When there is a 
neuropathic fundament the prognosis is materially influenced thereby. 
Supra-orbital Neuralgia 
Supra-orbital neuralgia due to ocular defects yields with the correc- 
tion of the fault. Two-thirds of all trigeminal neuralgias are supra- 
orbital. 842 
DISEASES OF THE NERVOUS SYSTEM 
With pain limited to the eye (ciliary neuralgia), search must be insti- 
tuted for possible existing glaucoma or optic neuritis, errors of accommo- 
dation or other diseases of the eye which may cause ciliary neuralgia. 
There is no more painful disease than neuralgia of the second and 
third branches of the trigeminus which becomes chronic (tic douloureux). 
It is almost impossible to determine the cause of this form of the disease; 
it may be idiopathic or symptomatic, it may be a symptom of grave dis- 
ease, tumor, aneurism, osteoma, chalky concretions, disease of the nerves 
or of the Gasserian ganglion (I)ana, Putnam, Horsely, Rose, Saenger, 
Krause, Keen, Spiller and Schwabe). 
Operative interference and injections now extensively practiced, have 
relieved some of my chronic cases of tic douloureux during varying 
periods; the large majority have relapsed. It may be safely contended 
that modern treatment offers longer periods of relief than were formerly 
possible and make the disease more bearable, but complete restitutio ad 
integrum is not frequently reached. Syphilitic cases yield to treatment. 
Chronic cases often continue during many years—twenty to thirty 
years, and longer. Senile and arteriosclerotic neuralgias select the tri- 
geminus oftener than any other nerve, and remain unrelieved or cease 
without known cause. 
There are cases of recurring trigeminal neuralgia in which the inter- 
vals are long and the cause remains unrecognized. These cases seem to 
run their course unrelieved by any known medical treatment and most 
recur in spite of surgical interference, though in some, the intervals have 
seemed to be lengthened thereby. 
Occipital Neuralgia 
Occipital neuralgia is, as a rule, symptomatic of either infectious 
disease, arthritis deformans (spinal), spondylitis, gout, caries of the cer- 
vical vertebrae, syphilis, uremia, cerebral or spinal tumor, or ocular error. 
With neurasthenia, hysteria and muscular asthenia, occipital neuralgia 
is frequent. The prognosis depends entirely on its cause. 
The pain in the fully developed cases is bilateral (one proof of its 
organic cause). The occipital major branch is usually involved. 
Intercostal Neuralgia 
Intercostal neuralgia may prove to be the forerunner and accompani- 
ment of herpes zoster; it is often of reflex origin in women with diseases 
of the uterus or its appendages (salpingitis, etc.) ; in young girls it is a 
symptom of anemia or chlorosis. Women suffer oftener than men. The 
left intercostals are oftener involved than the right. The Valleix points 
are present in most cases. 
With persistent intercostal neuralgia organic disease should he sus- DISEASES OF THE PERIPHERAL NERVES 
843 
pected; caries of the spinal vertebrae, locomotor ataxia, spinal syphilis, 
aneurism of the aorta, angina pectoris, tumor of the cord, metastases from 
breast, stomach or other viscera must be excluded. 
Hysterical women and oversensitive men often become self centered; 
they fear heart disease or other grave conditions. 
The prognosis in uncomplicated cases is good; the pain yields to the 
treatment of the removable cause. 
The symptomatic neuralgia depending on most of the conditions above 
mentioned makes the forecast unfavorable. Recovery of idiopathic cases 
is often slow. 
Mastodynia 
Sir Astley Cooper called attention to this painful neuralgic condition 
of the breasts in women—occasionally in men. The pain is aggravated 
during menstruation. Unbearable pain has been described by some of 
the sufferers. With the cure of the menstrual and uterine anomalies, the 
anemia, hyperesthesia, faulty metabolism and assimilation, and the loiv- 
ered vitality—which are the usual causes—the pain ceases. Enlarged 
and heavy breasts at times continue hypersensitive and are only relieved 
by the removal of all pressure. 
Phrenic Neuralgia 
Peters called attention to phrenic neuralgia. The pains are described 
as radiating along the phrenic nerve, to the diaphragm. I have had no 
experience with this condition. The reported cases were associated with 
painful respiration and mastication, and were symptomatic of pericardial 
or cardiovascular diseases. 
Kidd has reviewed the subject and Raynaud reported tuberculosis as 
a cause. Oppenheim says that in the absence of the lesions above men- 
tioned the prognosis is favorable. He reports one case following fracture 
of the clavicle. 
Brachial Neuralgia 
Neuralgia of the brachial plexus may be due to one of many causes. 
My cases were often associated with neuralgic and myalgic pains in other 
parts of the body, especially in gouty and diabetic patients. 
With diabetes, brachial neuralgia becomes fixed and rebellious to treat- 
ment even after the removal of all traces of sugar. Arteriosclerotics 
often have persistent brachial neuralgia. 
Causes.—Syphilis, hypertrophic cervical pachymeningitis, tumors of 
the cord and the plexus, caries of the cervical spine, multiple metastases, 
neuroma, dislocation and fracture of the humerus and anchylosis, and 
angina pectoris are among the causes. In another group of cases anemia 844 
DISEASES OF THE NERVOUS SYSTEM 
and the neuropathic habit alone explain the existing neuralgia. Unques- 
tionably a number of cases are due to simple neuritis, lead poisoning, 
toxemia associated with the acute infections, malaria, distant visceral dis- 
ease including gall-stones, and in one of my cases I found aneurism of 
the right subclavian during its incipient stage, the cause of persistent 
brachial neuralgia. 
Oppenheim considers idiopathic brachial neuralgia a comparatively 
rare disease. 
The prognosis depends on the ability to cure or remove the exciting 
cause. 
Lumbar Neuralgia 
Lumbar neuralgia involving the lumbar plexus may depend on rheu- 
matic or gouty conditionsj it is often a symptom of disease of the cord 
or its membranes. It may be due to tumors or metastases, including 
carcinoma, glioma, neuroma, sarcoma or osteosarcoma. Lumbar neuralgia 
may be an early symptom of breast cancer with limited metastasis spring- 
ing from the spinal bones, and in some cases it was present before the 
breast growth was discovered. 
Lumbar pains may precede the positive symptoms of caries of tuber- 
culous origin. 
The causes of persisting lumbar pains are often explained by the x-ray 
examination. 
Rectal examination in unexplained cases may disclose conditions which 
by pressure (fibroid uterus, malignant growths, etc.) cause the pain. 
Persistent double lumbar neuralgia should be considered to he of 
organic origin until it is positively proved to be idiopathic—a very rare 
condition. Crural neuralgia is usually (as already suggested in the gen- 
eral consideration of neuralgia) of organic origin dependent upon lum- 
bar pressure. 
Sciatic Neuritis 
{Sciatic Neuralgia, Sciatica, Ischias) 
Neuralgic pains within the domain of the sciatic nerve are almost 
always symptomatic of either neuritis or pressure, or are idiopathic, fol- 
lowing exposure. This latter variety of sciatic pain may be considered 
to be very rare, for in most of the so-called idiopathic sciatic neuralgias, 
mild neuritis or perineuritis may he assumed to he present. 
The neuropathic tendency is less in evidence than with neuralgia of 
the smaller nerves; the fact that the majority of sciatic neuritides are 
found in men, would explain the absence of a neurosis. 
Gowers and Hyde believe that most cases rest on a gouty basis, and 
Ziemssen reports diabetic cases. I Have not found it complicating diabetes 
as often as neuritis of the arms and legs. DISEASES OF THE PERIPHERAL NERVES 
845 
Double sciatic neuralgia is mentioned by Oppenheim as a complica- 
tion of diabetes. I have never met a case; neither has syphilis been a 
frequent cause. 
Causes.—Alcoholism, lead poisoning, acute infections, gonorrhea, sacro- 
iliac synchondrosis tenderness and inflammation, lumbar myositis, ex- 
posure to cold and traumatism, chronic constipation and continuous 
pressure due to sitting on hard chairs are among the removable causes. 
Every sciatic neuralgia which persists—particularly when double— 
should at once excite the suspicion of grave organic pressure, either tumor 
of the cord, metastases to the vertebrae (lumbar), extra-spinal pressure, 
growths within the abdomen, or spinal caries of tuberculous origin. I 
have never seen a case of double idiopathic sciatic neuritis. These cases 
are always of organic origin. 
The results of long continued sciatic neuritis are atrophy of the muscles 
within the domain of the diseased nerve, spinal curvature, with the con- 
cavity toward the unaffected side, due to nature’s effort to allow these 
patients to walk and relieve themselves of the pain at the same time. 
Oppenheim calls attention to a condition, which I have frequently 
met, of reflex neurosis in which the general condition of the patient is 
lowered, there being marked asthenia, hysterical hemianesthesia, trem- 
bling, and other sensory disturbances. 
The acute and rare idiopathic sciatic neuralgias run a satisfactory 
course, as a rule, with rest, though in some cases the duration is discour- 
agingly long. 
The subacute cases dependent on removable causes finally yield to 
treatment; but a sciatic nerve which has once been the seat of pressure or 
neuritis is ready in the future to revolt on slight cause—hence relapses 
are to be expected. 
The chronic but purely neuritic cases may continue more or less 
troublesome during years; periods of improvement are followed by re- 
lapse, though cure is often possible. 
Old patients recover slowly; they often suffer during long periods 
and die of intercurrent disease. 
The prognosis of symptomatic sciatic neuritis depends on its cause. 
Most pitiful is the existence of those cases depending on primary growth 
with pressure or metastases, an easy euthanasia is all that our art offers. 
II. Peripheral Neuritis 
General Considerations.—Peripheral neuritis may be either (1) sim 
gle or (2) multiple, and both of these varieties may he either acute or 
chronic. Neuritis may be primary or secondary, interstitial, or parenchy- 
matous. * 
The secondary neuritides are either syphilitic, tuberculous, cancerous, 846 
DISEASES OF THE NERVOUS SYSTEM 
or leprous. To all of these forms I refer in the separate chapters on 
these diseases, to which the reader is referred. 
With both forms of neuritis there are degenerative changes. It must 
be remembered in offering a prognosis that reparative processes in the 
nerve are active, and that regeneration is possible. The wallerian changes 
are present with both forms of neuritis. 
Most forms of neuritis, particularly the interstitial, are associated 
with inflammation of the perineurium, i. e., perineuritis. With the 
parenchymatous disease degenerative changes predominate over the in- 
flammatory. 
The preaxial neuritis of Gombaults offers a good prognosis. It is a 
mild type in which the axis cylinder remains undisturbed while there is 
a limited degeneration of the myelin substance of the nerve. 
In the chronic and progressive forms of both simple and multiple 
neuritis the prognosis is influenced unfavorably by the disorganization 
of the axis cylinder, the replacing of the normal nerve structure by fatty 
and fibroid tissue, and the increasing changes in the perineurium. 
Most neuritides are of the mixed type in their involvement of both 
the motor and sensory fibers of the nerve. 
Single neuritis when it leads to paralysis, involves only the muscles 
within the domain of the inflamed nerve; multiple neuritis is character- 
ized by paralysis of all four extremities in most cases (quadriplegia). 
Mononeuritis 
The leading features of single neuritis include pain and tenderness 
along the course of the nerve, anesthetic areas, trophic changes along the 
distribution of the nerve, muscular paralysis and atrophy, in accordance 
with the changes in the motor fibers. 
Anesthesia and paresthesia are the most prominent features. 
Traumatic Peripheral Single Neuritis 
The course and prognosis depend on the extent of the injury and the 
amount of destruction of nerve fibers. Single neuritis following limited 
disturbance, contusion and compression, without break of continuity, may 
promptly yield in a few weeks—even sooner in exceptional cases. The 
more severe injuries with partial break of continuity and associated 'paral- 
ysis may require years for regeneration, or may never improve. If there 
is complete separation, restitution of function can only follow surgical in- 
tervention. 
Sensory nerves improve faster after partial separation than do motor 
nerves. This is especially true of the fifth nerve. 
Alcoholics who develop single neuritis after traumatism or exposure 
recover slower than do the temperate. DISEASES OF THE PERIPHERAL NERVES 
847 
The prognosis of traumatic neuritis following injury with paralysis 
depends very largely upon the ability to overcome pressure if present, to 
unite the severed fibers or place them in position to regenerate, and upon 
the condition of the paralyzed muscles as demonstrated by electric reaction. 
The reaction of degeneration with severed nerves clouds the prognosis, 
but restitution of function may still follow after months of gradual prog- 
ress. Experience with traumatic paralysis in children has been less 
favorable than in adults. Children, after the injury of nerves has led 
to paralysis, continue to neglect the function and form what Ehret called 
“habit paralysis.” This “habit paralysis” has, according to some, been a 
powerful factor in the paralysis developed by infants during labor, but 
it may also account for paralysis due to other causes during the early 
years of life, particularly within the domain of the radial and ulnar 
nerves in which the child loses the “memory picture for the performance 
of movements, and with restoration of nerve conduction the function does 
not return” (Oppenheim). 
Exposure to cold leading to single neuritis (facial paralysis—Bell’s 
palsy) offers a good prognosis. The recovery may be slow, but unless 
there are associated conditions it may be expected with but slight remnant 
of the paralysis. 
Single neuritis of secondary origin is frequent from extension of bone 
caries, joint disease, pressure of tumors, and syphilis, exostoses, disloca- 
tions of joints, and consecutive pressure. 
Pressure of crutches is also a cause of neuritis. 
The occupational palsies lead to limited neuritis. With all of these 
neuritides the duration of the disease, the extent of anatomic change, the 
electric reaction, and the ability to remove the cause, are the leading fea- 
tures which influence the prognosis. 
With the reaction of degeneration the prognosis remains clouded and 
uncertain. If with this there is marked wasting of muscle, the chances 
for complete restoration are unfavorably influenced. Early return to nor- 
mal electric reaction is always favorable. Persistence of reaction of de- 
generation does not, as a rule, favor final complete return of function: the 
paralysis may be permanent. In other cases the late improvement, under 
persistent treatment with the underlying cause removed, is occasionally 
surprising. 
In occasional cases even with partial reaction of degeneration and lim- 
ited atrophy the resulting paralysis remains permanent. The rule should 
hold that with complete loss of electric response the prognosis for restora- 
tion of function is bad. 
Single neuritis, during or following the infections, usually yields after 
the effects of the original disease have been dissipated. With persisting 
treatment, the resulting damage in most cases is minimum. 
Oppenheim and Siemerling call attention to the hypersensitive state of 848 
DISEASES OF THE NERVOUS SYSTEM 
the peripheral nerves, caused by the acute infections and intoxications 
which invite neuritis in such subjects. These cases recover slowly with 
the improvement of the general condition of the patient. 
Acute neuritis involving the facial, motor oculi, the radial and the 
ulnar nerves, usually runs a short course when not dependent on a perma- 
nent lesion. Rheumatic facial paralysis offers a good prognosis for prompt 
cure—from four to ten weeks (Lewandowsky). 
Most single neuritides require a longer time for full recovery than do 
the uncomplicated or idiopathic neuralgias. 
The mononeuritides caused by pressure during surgical operations offer 
favorable prognoses. Persistent treatment is finally rewarded by success. 
Paralysis following operations due to cerebral lesions are often serious. 
Apoplexy, thrombosis, or embolism, are the underlying pathogenic factors. 
Postoperative Neuritis 
2. Multiple Neuritis 
(P oly neuritis) 
Single neuritides depend upon external causes, multiple neuritis as a 
rule upon internal or constitutional disturbance. Multiple neuritis is 
either of infectious or toxic origin. Occasional cases have been considered 
idiopathic, no cause being discovered. These will probably prove to be 
infectious or toxic with improved methods of diagnosis. 
For a safe prognosis the etiologic factors deserve close consideration. 
Woodwork classifies the causes as follows: 
“1. Acute specific fevers: diphtheria, influenza, leprosy, typhoid 
fever, scarlet fever and beriberi. 
2. Poisons: alcohol, ether, carbon bisulphid, lead, mercury, 
arsenic. 
3. Wasting conditions: diabetes mellitus, anemia, cancer and 
tuberculosis. 
4. Exposure to cold or overexertion (probably due to some un- 
known infection, as febrile neuritis).” 
To these may be added puerperal infection, abortion and associated 
sepsis, creosote, sulplional, ergot poisoning, and arteriosclerosis. 
The forms of multiple neuritis which interest us most and deserve 
separate consideration are: 
(a) Alcoholic multiple neuritis 
(b) Postdiphtheritic multiple neuritis 
(c) Lead multiple neuritis DISEASES OF THE PERIPHERAL HERVES 
849 
(d) Arsenical multiple neuritis 
(e) Multiple neuritis with leprosy 
(f) Idiopathic multiple neuritis 
(g) Landry’s ascending paralysis 
(h) Puerperal multiple neuritis. 
(a) Alcoholic Multiple Neuritis 
The prognosis of multiple neuritis caused by alcohol depends upon 
many factors. There are cases in which acute alcoholic poisoning leads 
at once to alarming and grave constitutional symptoms, which may pre- 
cede quadriplegic paralysis by a few days, with marked cerebral manifesta- 
tions early, alcoholic meningitis, degenerative changes in the myocardium 
and liver, and death within from seven to fourteen days. 
In occasional cases traumatism in a chronic alcoholic suddenly leads 
to polyneuritis, with or without invasion of the sensorium. Without the 
evidences of “wet brain” such cases otfer a better prognosis. 
Another class of cases includes the suddenly arising symptoms of quad- 
riplegic paralysis in those who after years of overindulgence discontinue 
the use of alcohol. In these subjects, without other constitutional faults 
and good resistance, the disease runs a favorable but slow course to recov- 
ery. Most of these cases are found in women who are steady drinkers. 
Multiple neuritis developing in the course of delirium tremens has in 
my experience proved to run a chronic course—often rebellious. The ma- 
jority of these patients recover. 
Alcoholic meningitis and delirium tremens following shortly after the 
development of positive symptoms of peripheral multiple neuritis are 
among the most serious cases, and in the neglected who come to the hos- 
pitals from unfavorable quarters, who have been exposed to cold, pneu- 
monia is a frequent complication, which usually with “wet brain,” leads to 
death. With stiff neck and retraction the prognosis is unfavorable (Dana). 
Meningeal symptoms are evidences of deep invasion of the sensorium, 
and add an element of danger. 
The development of Korsakoff’s psychosis, in which the patient is with- 
out memory for the events of the present but is able to recall the past, 
does not influence prognosis favorably; recovery is the rule but with the 
added psychosis the condition usually runs a chronic course, in many 
cases leading to full recovery. 
In some cases which are neglected and bedridden during a long time, 
bedsores may lead to sepsis and cause death. 
My experience in an active service has proved that the duration of the 
ataxic cases is longer than that of other types of the disease. 
Pseudotabetic neuritis, in which there are marked sensory symptoms 
resembling tabes, are occasionally malignant. 850 
DISEASES OF THE NERVOUS SYSTEM 
In many cases there are remnants of paralysis, though in most the func- 
tional ability of the extremities is sufficient to allow resumption of the 
original occupation. 
The return of normal tendon reflexes, both patella and Achilles, is 
often long postponed: months and years may pass before these become 
normal. 
Occasional cases of acute alcoholic neuritis of an ascending type, re- 
sembling Landry’s paralysis develop rapidly, and promptly lead to death 
when they involve the respiratory centers. It is difficult to differentiate 
these cases from true Landry’s disease, for they are acute and febrile, and 
at times foudroyant. 
Alcoholic neuritis in the subjects of myocarditis, other serious heart 
lesions, nephritis or tuberculosis, offers an unfavorable forecast. 
With grave constitutional symptoms, the resistance of the patient, his 
cardiovascular tone, and the extent of the brain lesions, are potent factors 
in the outlook. 
The extent of the paralysis is not always an expression of the gravity of 
the disease. Limited polyneuritis and paralysis may he associated with 
grave constitutional and brain symptoms, while fully established complete 
quadriplegia. may run its course with but few added disturbances. 
All polyneuritides associated with tachycardia and dyspnea are serious, 
for vagus and phrenic involvement must be suspected, which is among the 
gravest of all complications. 
The occasional association of optic neuritis or other ocular paralysis 
depends on some complication. The latter, according to Moritz, depends 
on polioencephalitis hemorrhagica. 
The extensive and marked tremor does not influence the outcome unfa- 
vorably. 
Relapsing cases are not uncommon, they are rebellious and may lead 
to permanent damage or cerebral complications. 
(b) Postdiphtheritic Multiple Neuritis 
(See Diphtheritic Paralysis in Chapter on Diphtheria, Section I) 
(c) Lead Multiple Neuritis 
Workmen in lead and those who have been poisoned through food or 
drink, or through one of the many other possible avenues from which en- 
trance is possible, are differently affected. Unrecognized lead poisoning 
due to impregnated drinking water is a cause of indefinite symptoms as 
well as the prolonged ill-health, anemia, headaches, and lethargy of many 
within the precinct thus supplied. DISEASES OF THE PERIPHERAL NERVES 
851 
Children tolerate lead longer and better than do adults, but mental tor- 
por and increasing lassitude with marked anemia characterize the chronic 
ill-health which finally develops. When fully developed serious organic 
disturbances with quadriplegia may follow. 
Children develop paralysis of the lower extremities oftener than adults. 
Children of parents poisoned with lead may develop epilepsy and other 
neuroses as a direct result. The paralysis usually develops in the muscles 
most used, where it is more severe than in other parts of the body. 
“Drop wrist” or extensor paralysis in the domain of the radial nerves 
is characteristic of lead poisoning. There may, however, as in all poly- 
neuritides, be comeplete quadriplegia; it is not as frequent as with other 
toxic paraplegias. The sensory disturbances are less in evidence than with 
other forms of multiple neuritis. 
The severity of the poisoning depends upon the extent of the changes 
produced. With marked blood changes, grave saturnine anemia, marked 
hypertension and arterial change, nephritis and lead encephalopathy the 
prognosis is grave. I have seen no case of lead poisoning in which 
chronic cardiovascular and kidney changes were overcome after once de- 
veloped, though the paralysis in such cases may yield to treatment and 
removal of the cause. 
The occurrence of lead colic and “blue line” do not argue against the 
possibility of recovery. 
The sudden development of encephalopathy with either partial or fully 
developed paralysis is serious: it may lead to delirium followed by coma, 
symptoms of meningitis, and death. 
The more favorable cases are those which develop soon after exposure 
to the poison and in which the early symptoms are recognized by the 
patient, and correctly interpreted by the attendant. 
Chronic lead poisoning with paralysis, atrophy and the reaction of de- 
generation and beginning contracture offers an unfavorable prognosis for 
restitution of function. 
The presence of the reaction of degeneration does not justify an unfa- 
vorable prognosis; most cases recover, if the source of poisoning is re- 
moved. 
Repeated relapses materially influence the outlook unfavorably; these 
cases are aggravated by fresh poisoning, intemperance and overwork. 
Months and years may be required before there is complete restora- 
tion of motor and sensory function in occasional cases. 
Partial recovery with persistence of limited paralysis is not unusual. 
The peroneal muscles often continue weak and partially paralyzed. 
Contractures in chronic cases are often permanent. 
The arthralgias, blood conditions, cardiovascular and renal changes, 
encephalopathies, and colic, are separately considered (Intoxications). 852 
DISEASES OF THE NERVOUS SYSTEM 
(d) Arsenical Multiple Neuritis 
Arsenical muliple neuritis may be either acute or chronic. The acute 
cases are in the majority, though there are many chronic poisonings of 
which a number are never recognized, or even suspected. 
Causes.—The poisoning results from the taking of arsenic by the 
mouth in some form—a single poisonous dose or large or badly tolerated 
dosage during comparatively long periods—through food, water, by inha- 
lation from papered or painted walls or colored carpets, etc. 
There are authorities who are active in their opposition to salvarsan be- 
cause of the occasional occurrence of polyneuritis after its use. My own 
experience with the remedy which has been comparatively large, remains 
negative. It cannot be denied, however, that polyneuritis does occasionally 
develop after the injection of the remedy but should not be charged to 
it directly; it is one of the manifestations of syphilis possibly lighted into 
activity by a reaction following the administration of the drug, a neuro- 
recidive. This verdict is entertained by Ehrlich who considers the phe- 
nomenon as a Herxheimer reaction, while others believe that the remedy 
first shows its poisonous effects in the nervous system. The faulty adminis- 
tration of the drug either in too large or in insufficient dosage may be the 
cause of direct poisoning or the Herxheimer reaction. In the latter event 
the intensive treatment with salvarsan and mercury cures the polyneu- 
ritis. 
This entire question is still sub judice; it will require a larger ex- 
perience and further observation before positive conclusions can be 
reached. 
The prognosis of the neurorecidive is not unfavorable. 
When the improper use of salvarsan leads to symptoms of acute arsen- 
ical poisoning with degenerative changes in vital organs (liver atrophy 
and kidney lesions), the prognosis is grave with or without polyneuritis. 
Associated Symptoms.—Fully developed arsenical multiple neuritis 
is associated with pains and paresthesia in the hands and feet, at times 
arms and legs. Paralysis with atrophy is not long postponed. The early 
gastrointestinal symptoms are often troublesome—varying with the acute 
and chronic cases—in the former, with the amount of the poison taken. 
Fully established paralysis is associated with the reaction of degenera- 
tion, hyperesthesia and anesthesia. The smaller muscles of the hands are 
oftener involved than with the other polyneuritides, and the contractures, 
when they occur, are characteristic (paralysis chiropodale). There is 
greater tendency to flexor paralysis than with alcohol or lead poisoning. 
Pseudotabetic symptoms (ataxia) are frequent with motor paralysis. 
The patella tendon reflex is absent, and the resemblance of some chronic 
forms to locomotor ataxia may be striking (Dana). Oppenheim calls 
attention to choreic symptoms with ataxia. DISEASES OF THE PERIPHERAL NERVES 
853 
The trophic symptoms which accompany the motor and sensory symp- 
toms are herpes (frequent), dermatitis, pemphigus, and pigmentation. 
Bulbar symptoms, are not frequent, though occasional, and with tachy- 
cardia present a serious condition. 
The prognosis of most cases of arsenical polyneuritis is good. Recov- 
ery may at times be slow, occupying long periods, and complications may 
be added; but recovery is the rule. The muscles last paralyzed are the 
first to resume their function. 
Fully established secondary contractures are likely to be permanent. 
Serious complications include the infections, pneumonia especially, 
and myocardial degeneration. 
(e) Multiple Neuritis with Leprosy 
(See Leprosy—the anesthetic and mixed type.) 
(f) Idiopathic Multiple Neuritis 
(Infectious Multiple Neuritis) 
Most forms of so-called idiopathic multiple neuritis are of infectious 
nature, now considered to be “rheumatic” by many. Osier characterizes 
it as acute febrile polyneuritis. 
Temperature.—The temperature is at once high, reaching to 103° to 
105° F. There are marked cerebral symptoms, enlarged spleen, and albu- 
minuria. In most cases the gastrointestinal symptoms are alarming; diar- 
rhea and jaundice are not uncommon. 
Types.—The paralysis may be of the ascending type, or modified forms 
of paralysis; either paraplegia or quadriplegia predominate. 
Associated Symptoms.—In most cases paralysis is preceded by sensory 
disturbances, anesthesias and paresthesias in hands and feet, and finally 
wrist and foot drop are in evidence besides involvement of the sensorium. 
The graver cases include brain symptoms, phrenic and pneumogastric 
paralysis, dyspnea with respiratory paralysis, and tachycardia. The pupil- 
lary reflexes may be changed with Argyll-Robertson pupil. 
In rare cases the cranial nerves, one or more, usually the motor oculi, 
facial or trigeminus, may be involved. In grave cases the resemblances to 
the Landry’s form of poliomyelitis acuta (See Poliomyelitis) are close, 
and require differentiation. 
The prognosis of the idiopathic infectious form of polyneuritis is grave. 
Death may occur during the first week or shortly after, particularly in 
cases with brain symptoms, respiratory paralysis, and heart involvement. 
There are mild cases which recover slowly. In some the paralysis 
seems to remain unchanged during long periods, and then gradually im- 
proves; in others permanent paralyses remain. As a rule if the patients 854 
DISEASES OF THE NERVOUS SYSTEM 
live beyond the acute period they make satisfactory recoveries, though often 
distressingly slow. 
Jacobsohn calls attention to the prognostic significance of complete 
reaction of degeneration, in which he claims recovery of function is not 
to be expected in less than from four to six months. Motor paralysis yields 
long before the return of the reflexes. 
Acute and threatening symptoms may arise suddenly, and seriously 
influence the outcome. 
Aspiration pneumonia has been the cause of death in some cases. 
Classification.—In considering poliomyelitis I included in the clas- 
sification two forms of Landry’s disease; the first presenting sufficient 
features which justified the conclusion that it is identical with poliomye- 
litis. The second form includes those cases which are easily recognized 
during the first twenty-four hours by the increasing paralysis with less 
involvement of the respiratory muscles than in the first form, but in which 
there are all of the symptoms of fully developed ascending multiple neu- 
ritis before the end of the fourth day; in these cases the patients may live, 
but usually continue paralyzed. 
It is impossible in the present state of our knowledge to subscribe to 
any positive conclusion concerning the pathology of these ascending types 
of paralysis. 
All agree that the prognosis is exceedingly grave, that death is the 
usual outcome when there are bulbar symptoms, and that the few who 
live remain with large remnants of the original paralysis. At present I 
prefer to consider Landry’s ascending paralysis as a form of acute polio- 
myelitis, to which chapter the reader is referred for further details. 
Complications.—The multiple neuritides which are occasional compli- 
cations of infections, acute and chronic, not considered in this chapter, 
receive attention in connection with the separate diseases to which the 
reader is referred. 
Beriberi is also separately considered. 
The prognostic data offered in connection with the consideration of 
alcoholic, lead, arsenic and the other forms of polyneuritis will serve to 
make clear the course of the paralyses with mercury, antimony, carbon 
bisulphid, morphin and coal gas poisonings. 
Multiple neuritides of arteriosclerotic or cachectic origin (cancer and 
other tumors, leukemia, pernicious anemia, tuberculosis, etc.) offer an 
unfavorable prognosis. 
({*) Landry’s Paralysis 
(h) Puerperal Multiple Neuritis 
Multiple neuritis following confinement is unquestionably an expres 
sion of infection. There are cases in which hut one or two nerves are in DISEASES OF THE PERIPHERAL NERVES 
855 
volved, the median and ulnar by predilection, but in most fully developed 
puerperal neuritides there is quadriplegic paralysis, with occasional Lan- 
dry’s complex and invasion of one or more of the cranial nerves, von 
Hosslin has reviewed the literature of this subject. 
Seige reports the possibility of multiple neuritis during pregnancy, 
especially in cases of pernicious hyperemesis. 
von Hosslin believes that the poisoning is often due to the dead fetus 
or retained placental remnants. The condition is always grave because 
of its dependence upon virulent infection. 
(i) Gonorrheal Multiple Neuritis 
Gonorrheal multiple neuritis selects the lower extremities by prefer- 
ence; it is at times associated with arthritis; vasomotor and trophic 
changes are often present, and persistent (Oppenheim). These cases are 
not frequent but are exceedingly rebellious to treatment. 
(j) Neuritis of Tuberculous Origin 
The neuritides of tuberculous origin have been separately considered 
(See Complications, Nervous Diseases, in Chapter on Tuberculosis). 
(k) Diabetic Neuritis 
Multiple neuritis due to diabetes mellitus is also separately considered 
among the complications of the disease (See Diabetes Mellitus). The 
prognosis is usually good in cases which are amenable to diet and other 
treatment. 
References 
Bernard. Quoted by Oppenheim [Z. c.]. 
Conard. Inaugural thesis. Bonn, 1889. 
Dana. J. Nervous Dis., xvi; also Diseases of the nervous system, 1915. 
Dana. Brain, ix. 
Gowers & Hyde. Lancet, London, 1896. 
Herter. Diagnosis of organic nervous diseases. New York, 1907. 
Horsley, Rose & Saenger. Neurol. Centralbl., 1895. 
von Hosslin. Arch. f. Psychiat. in Nerv., Bd. 40. 
Jacobsohn. Klinik der Nervenkrank. Berlin, 1913. 
Kidd. Rev. Neurol., 1911. 
Krause, Keen, Spiller & Schwabe. J. Nervous & Mental Dis., 1903. 
Lewandowsky. Prakt. Neurologie. 1913. 
Moritz. Von Mehring & Krehl’s Lehrb. d. inner. Med., 1913. 
Oppenheim. Lehrb. d. Nervenkrankheiten. 1913. 
Oppenheim & Siemerling. Arch. f. Psychiatrie u. Nervenkr., xvii. 856 
DISEASES OF THE NERVOUS SYSTEM 
Osier (Sir William). Practice of medicine. 1913. 
Peters. Arch. General de Medi., 1871. 
Putnam. Boston Med. J1891. 
Reilly. New York Med. Rec., 1899. 
Reynaud. Revue neurol., 1902. 
Seige. Berl. klin. Wchnschr., 1911. 
Woodwork. Manual of medicine. Oxford, 1912. 
Ziemssen. Munch, med. Wchnschr., 1885. 
III. Peripheral Paralysis 
The peripheral paralyses include:— 
1. Paralysis of the cranial nerves 
2. Paralysis of the nerves of the brachial plexus 
3. Combined paralysis of the shoulder-arm nerves 
4. Paralysis of the nerves of the lower extremities 
5. Paralysis of the sacral plexus. 
The causes and pathologic conditions which are mentioned in connec- 
tion with all forms of neuritis and the neuralgias in the preceding chap- 
ters are included in the many factors which produce peripheral paralysis. 
In all, the prognosis is equally influenced. Hence repetition is unneces- 
sary. 
Neuritis is the leading cause of peripheral paralysis. 
A break in a peripheral nerve may be due to a lesion located anywhere 
between the point of exit of its motor root from the brain or cord, to its 
terminal ending in the muscle. 
Paralysis which is associated with a lesion of the motor ganglionic cells 
in the anterior horns of the cord should not be included in the peripheral 
diseases. 
Peripheral paralysis in occasional cases is finally associated with cere- 
bral and spinal lesions. 
Paralysis of the Cranial Nerves 
(a) Paralysis of the Olfactory Nerve 
When loss of smell (anosmia) is due to removable causes, such as 
polypi, rhinitis, or acute inflammation, the prognosis is good. 
When organic lesions cause disorganizing changes in the olfactory, these 
may be due to tumor, or other permanent lesions along its course and 
anosmia persists. 
Syphilitic gummata may cause anosmia; the prognosis is favorable un- 
der treatment. DISEASES OF THE PERIPHERAL NERVES 
857 
Hysterical paralysis of the olfactory, causing anosmia, is associated 
with hyperesthesia of the nasal mucosa and usually yields to treatment. 
Perverted smell {parosmia), is at times an aura of epilepsy, or it may 
be due to a lesion in the cerebral cortex. 
Lesions of the olfactory bulbs with paralysis (anosmia) are usually 
permanent. 
Atrophic changes with locomotor ataxia cause olfactory paralysis, which 
does not yield after it has persisted even a short time. 
Hyperosmia is usually of hysterical origin and is likely to yield with 
the other symptoms. 
(b) Paralysis of Optic Nerve 
Amblyopia is a partial loss or blurring of the siglit. 
Amaurosis is synonymous with complete blindness. 
Blindness of one eye may be due either to change in the nerve between 
the eye and the chiasm, either in the eye itself in the orbit at the optic 
foramen, or in the skull between the foramen and the chiasm. The prog- 
nosis depends on the nature of the lesion. As a rule, the underlying cause 
is either a new growth or some serious lesion. Embolism of the central 
retinal artery is among these. 
The blindness of one eye due to cortical lesions in the opposite hemi- 
sphere, i. e., angular and supramarginal convolutions, unless dependent on 
syphilis or other removable cause, remains unchanged. For prognosis it 
must be remembered that there is in some cases of cortical lesion only 
partial blindness, but there is concentric limitation of the visual field, and 
the pupillary reaction is normal with cortical disease, but diminished with 
optic neuritis. 
Hysterical blindness of one or both eyes offers a good prognosis. When 
the motor nerves of the eyeball are involved with optic neuritis, the disease 
is not due to a parietal cortical lesion. 
Before offering a prognosis in a case of bilateral loss of vision, either 
partial or complete, it should be remembered that it does not often follow 
organic disease of the nervous system as the result of primary or post- 
neuritic optic neuritis or optic atrophy (Herter). 
Errors of refraction without neuritis may cause amblyopia; the prog- 
nosis is good. Improvement almost immediately follows proper treatment. 
Herter mentions “functional amblyopia of one eye from irritation of 
the fifth nerve.” These cases depend upon carious teeth or other remov- 
able causes. 
The lesions of the retina causing blindness are considered with the 
constitutional diseases upon which they depend. (Chronic and acute neph- 
ritis, syphilis, leukemia, the grave anemias, including malarial anemia 
and cachexia, diabetes, purpura, and the poisonings—lead, tobacco, alco- 
hol, etc.). 858 
DISEASES OF THE NERVOUS SYSTEM 
Optic Neuritis 
It is difficult to offer a forecast from the presence of optic neuritis 
alone, as it is a symptom of many conditions. Foremost are those which 
increase intracranial pressure, including tumor and abscess of the brain, 
all forms of meningitis, encephalitis, syphilitic gummata and diseases of 
the cord. 
Russell and Ilerter mention the rare occurrence of optic neuritis with 
myelitis and other spinal lesions without indications of cerebral mischief. 
Ilerter believes that it is to be regarded as “an associated and not a con- 
secutive process.” 
The toxic and constitutional diseases mentioned in this chapter asso- 
ciated with retinal lesions, are also potent in causing optic neuritis. 
Disseminated sclerosis of the optic nerve (retrobulbar disease) is a 
cause of neuritis often overlooked (because of the possibility of a nega- 
tive ophthalmoscopic picture). In 6 per cent of all cases of multiple 
sclerosis optic neuritis is present, often slight and of short duration (Iler- 
ter). Russell calls attention to the possibility of advanced disease of the 
optic nerve without positive ophthalmoscopic evidence. The ophthalmo- 
scopic picture of optic atrophy or neuritis is positive proof of organic dis- 
ease of the nervous system, and in diagnosis and prognosis must always 
remain a powerful factor. 
Optic neuritis may exist without causing symptoms; with central lesions 
it is usually bilateral. When the neuritis is most advanced at the optic 
papilla, the ophthalmoscopic signs of papillitis are positive. 
Optic Atrophy 
Optic atrophy is usually evidence of degenerative disease of the brain 
or cord; including brain tumor, locomotor ataxia, is also found with dia- 
betes and other constitutional diseases. 
There are cases of hereditary family optic atrophy in which several 
male members of a family develop the disease after puberty. 
It is impossible to separate the consideration of peripheral from the 
central cerebral and spinal lesions which are associated with lesions of 
the optic nerve and tract. 
The Prognostic Significance of Hemianopia 
(A loss of vision in one lateral or vertical half of the visual field) 
Hemianopia is usually double; disease of one optic nerve may cause 
one-sided hemianopia. 
Bilateral vertical hemianopia should always be interpreted as of organic 
origin, it may be either temporal, nasal or lateral, i. e., homonymous. 
Temporal Hemianopia (or Bitemporal).—In this variety of hemi- 
anopia the temporal half of each eye is blurred. Such a lesion must of DISEASES OF THE PERIPHERAL NERVES 
859 
necessity include the decussating fibers of each retina, and is therefore 
located in the central portion of the optic chiasm. If there is extension 
laterally and the non-decussating fibers of one side of the chiasm are 
invaded, blindness may result in the corresponding eye, and if there is 
sufficient extension as the disease (tumor usually) advances, to involve 
the opposite fibers, complete blindness results. Locomotor ataxia, syphi- 
lis, abscess, brain tumor, osteosarcoma and chronic meningitis are among 
the causes of bitemporal hemianopia. 
Hemianopia may occasionally prove to be functional, with migraine 
or hysteria. The characteristic attacks of the former, and the preponder- 
ance of the emotional element and variability of the symptoms in the 
latter, clear the diagnosis and justify a favorable prognosis. 
Binasal Hemianopia.—This form is rare. The nasal half of each 
field being obscured, must of necessity involve each side of the chiasm in 
symmetrical lesions without impinging on the central fibers. Such con- 
dition has been found occasionally with vascular disease (small aneurisms) 
causing equal pressure, and with tabes dorsalis. 
Lateral or Homonymous Hemianopia.—With lateral hemianopia, 
corresponding visual fields are affected: with right lateral hemianopia, 
both right lateral fields are blind; with left lateral hemianopia both left 
lateral fields are blind. The lesion must therefore be located back or 
behind the optic chiasm. This may be in one optic tract, in one of the 
lateral geniculate bodies, in the pulvinar of the optic thalamus, in the 
sensory tract of the internal capsule, in the angular gyrus with inclusion 
of the underlying radiating fibers, when there may be “crossed ambly- 
opia” and mind blindness (Osier). Freund's optic aphasia may be asso- 
ciated with mind blindness. 
Lesions of the cuneus, the occipital lobe or in the optic radiation may 
also cause lateral hemianopia. 
To recapitulate: Lateral hemianopia is due to a lesion which is 
located somewhere between the chiasm anteriorly and the occipital lobe 
and cuneus posteriorly (inclusive). This includes the optic tract, the lat- 
eral or external geniculate body, the optic thalamus (pulvinar), the optic 
radiation, cuneus, the angular gyrus—occipital cortex. The lesion is 
located on the side opposite the obscured half fields. 
The further exact localization must depend upon the associated symp- 
toms. Hemiplegia is a frequent attendant. 
Blindness in both eyes may be due to double lateral hemianopia—- 
two lesions—one in each hemisphere—or to disease sufficiently destructive 
to involve the entire chiasm (Tumor, syphilis, etc.). 
Lateral hemianopia may remain unchanged during many years in 
occasional cases. When it has existed for any length of time it does not 
again disappear. It may also develop in the course of migraine—rarely 
with hysteria. 860 
DISEASES OF TIIE NERVOUS SYSTEM 
Further references to ocular symptoms and their prognostic significance 
are included in our consideration of the diseases of the spine and brain, 
the constitutional diseases, and those associated with faulty metabolism. 
Paralysis of the Ocular Nerves 
Causes.—The most frequent causes of paralysis of the ocular muscles 
are syphilitic gummata, locomotor ataxia, progressive paresis, compres- 
sion due to neoplasms, acute infections including diphtheria, influenza and 
meningitis. 
The nerves which supply the muscles of the eyeball are the third, the 
fourth and the sixth. 
The results of paralysis of the ocular muscles, depending on the nerve, 
are diplopia (double vision) and strabismus. The latter is not always 
developed. 
Congenital weakness is an occasional cause of partial paralysis: either 
the levator palpebrae superioris or the superior rectus is involved. 
Congenital ptosis with the levator paralysis is materially improved by 
surgical interference. 
The ophthalmic migraine of Charcot is probably epileptiform. It in- 
cludes paroxysmal headache which spends its force in the eye and frontal 
region of the side affected, associated transitory paralysis of the motor 
oculi which disappears entirely between the attacks. The cause is un- 
known; treatment is without decided influence. 
(c) Paralysis of the Third Nerve (Motor oculi) 
Symptoms.—Ptosis, divergent squint and dilated pupil, with loss of 
accommodation, are the leading features. The symptoms depend upon the 
location of the lesion, its extent, and the branch of the nerve most in- 
volved. 
In children the prognosis is not favorable, for most cases depend on 
tuberculous meningitis, gliomatosis or cerebrospinal meningitis. The diph- 
theritic paralyses of the motor oculi in children offer an excellent prog- 
nosis. 
In the adult, the idiopathic, considered by many rheumatic, and the 
postinfedious paralyses lead to recovery in most cases. The specific (syph- 
ilitic) paralyses, yield to treatment, and are cured unless there are asso- 
ciated grave complications. 
In motor oculi paralyses associated with neoplasms and other diseases, 
the forecast depends on the cause. Cases of locomotor ataxia with ocular 
paralysis are associated with the most chronic forms of the disease; they 
remain stationary during long periods (many years), and the patient 
learns to accommodate himself to the disturbed function. The Argyll- 
Robertson pupil is considered with tabes dorsalis. DISEASES OF THE PERIPHERAL NERVES 
861 
(d) Paralysis of the Fourth Nerve 
The superior oblique being paralyzed, the eyeball is not readily moved 
downward and inward. Convergent strabismus is evident when the patient 
looks downward; there is also diplopia. Accidents from falling when the 
patient wralks down stairs at times lead to the recognition of the paralysis. 
The conclusions reached in connection with motor oculi paralysis are 
applicable for the prognosis of paralysis of the fourth. 
(e) Paralysis of the Sixth Nerve 
I consider the sixth nerve before the fifth, for the reason that with 
the third and fourth, it includes the trio of nerves, one of which is always 
included in paralysis of the muscles controlling the eyeball. The external 
rectus is supplied hy the sixth nerve; hence there is convergent squint. 
Diplopia results when the patient looks to the side on which the muscle is 
paralyzed. When the lesion is located in the nucleus and not in the fully 
formed nerve, the opposite internal rectus controlled from the same source 
is paralyzed so far as it controls the lateral conjugate movement of the 
eyes; the patient is then without power to move either eye toward the side 
of the lesion. The internal rectus can, however, converge in conjunction 
with its fellow of the opposite side. 
The prognosis of paralysis of the sixth nerve is the same as in that of 
the third and fourth nerves. 
The clinician must remember that most paralyses of the ocular muscles 
depend upon lesions of the nerves (in which the nerve alone is involved) 
at the base of the brain. Occasionally a lesion at the base involves both 
motor oculi, usually tumor—malignant, tuberculous or gummatous; occa- 
sionally aneurism. 
“Rheumatic” (?) neuritides are always one-sided, and offer a good 
prognosis. 
The ocular paralysis of tabes considered above is usually nuclear, 
rather than peripheral. 
Ophthalmoplegia is a condition in which all of the ocular muscles are 
paralyzed; ptosis is usually partial or may he complete. The eyeball is 
immobile. The lesion is usually nuclear and chronic. 
Associated Symptoms.—It is associated either with tabes, paresis, 
multiple insular sclerosis, alcoholism, virulent influenza, carbonic mon- 
oxid poisoning, midbrain disease, tumors, hemorrhagic conditions, polio- 
encephalitis—superior and inferior. 
With some cases, multiple sclerosis especially, nystagmus is present. 
These cases are slowly progressive and are not relieved hy treatment. 
(f) Ophthalmoplegia 862 
DISEASES OF THE NERVOUS SYSTEM 
There are cases of acute, and also recurrent or periodical, ophthal- 
moplegia. The acute cases may be hemorrhagic, occasionally diphtheritic. 
The latter offer a better prognosis than do the former. The recurrent type 
of ophthalmoplegia usually involves the muscles within the domain of the 
third nerve of one side. These cases are periodic and usually begin with 
pain; the headache and vomiting are severe; ptosis is frequent; the dura- 
tion of the attack varies—the longer the interval between attacks, the 
longer will be the duration of ophthalmoplegia (average 3 to 6 weeks). 
These recurrent ophthalmoplegias are due to ophthalmic migraine; 
they are controlled with the greatest difficulty. Occasionally life may be 
regulated or some factor is found which seems to control the symptoms, 
but as a rule, the recurrences continue during the active years of life, 
though may grow less frequent with advancing years or may remain unin- 
fluenced throughout life. 
(g) Paralysis of the Fifth Nerve (Trigeminus) 
Primary disease of the trigeminus is not frequent; primary neuritis 
is rare. 
Causes.—The leading causes are inflammatory diseases of the meninges, 
pressure due to neoplasms, fractures at the base of the brain and bone 
disease, aneurismal tumors pressing on the cavernous sinus, growths of 
the sphenomaxillary fossa and syphilitic gumma. 
The trigeminus is composed almost entirely of sensory fibers except 
the third branch, in which motor fibers are included. The nerve supplies 
the skin of the nose and face to the median line, the mucous membrane of 
the nose, tongue and mouth very largely. 
When both halves of the face and the mucous membranes are anes- 
thetic, the lesion is located in the region of the gasserian ganglion upon 
which growths or metastases may press. 
The loss of sensibility varies in accordance with the branch involved. 
Pain is an early symptom which disappears, as a rule, with the in- 
crease of anesthesia. 
Loss of taste and trophic changes are frequent. The former is limited 
to the anterior two-thirds of the tongue, when the lingual branch of the 
trigeminus is diseased between the peripheral distribution and its junc- 
tion with the cauda tympani. 
The trophic changes involve the cornea and conjunctiva; the cornea 
becomes dry and ulcerates; with cases dependent upon permanent lesions 
destructive processes are produced. Herpes zoster is also present, and is 
evidence of disease of the gasserian ganglion or the nerve in front of it. 
The motor paralysis or weakness is due to disease which affects the 
third branch. The muscles included are the masseter, temporal and ex- 
ternal pterygoid. DISEASES OF THE PERIPHERAL HERVES 
863 
Facial Hemiatrophy 
Hemiatrophy of the face is a rare disease; there is atrophy of the 
muscles of one lateral half of the face with trophic changes in the skin 
and often in the bone tissue. The disease is found in the young, rarely 
after the twenty-eighth to the thirtieth year. 
Cause.—The cause is unknown; in occasional cases the disease follows 
trigeminal neuralgia. Jacobsolin mentions the association of symptoms 
referable to the sympathetic and associated papillary changes; he also 
mentions the association with trigeminal neuralgia of epilepsy, chorea and 
chronic spinal disease. 
Disease of the descending root of the fifth nerve has been considered 
by some to be the cause of this rare condition which remains entirely unin- 
fluenced by treatment without threatening life. 
Crossed paralysis of the fifth nerve (the fifth on one side, and the arm 
and leg on the other) is due to a lesion in the pons, and is usually due to 
vascular disease, neoplasm or a patch of sclerosis. 
Carotid aneurism (internal), septic thrombosis, tumors of the orbit 
or cellulitis, and pituitary growths may cause paralysis of the superior 
maxillary .branch. 
Disease of the antrum and of the parotid may cause paralysis within 
the distribution of the second and third branches of the nerve. 
The prognosis of paralysis within the distribution of the trigeminus 
is easily cleared in connection with a study of the previous paragraphs in 
which symptoms and causes are included. For satisfactory prognosis the 
individual case demands first of all the study of the primary cause; finally 
its location and extent, the amount of destructive change produced, and 
the ability to remove it. 
Modern methods and early diagnosis lead to recovery in occasional 
cases but basal lesions, malignant growths, and chronic meningitides, are 
invariably hopeless. 
(h) Facial Paralysis 
(Paralysis of the Seventh Cranial Nerve) 
Facial paralysis is the most frequent of all single nerve paralyses. In 
considering the outcome of facial paralysis it is first necessary to have a 
clear understanding of the underlying pathologic lesion, and second to 
determine whether the disease is located in the upper or lower segment of 
the facial path. In other words, whether the paralysis is supra- or infra- 
nuclear. 
Character and Causes.—The character of the lesion and the causes are 
as a rule different with facial paralysis, in which all of the muscles of the 
face are involved, and in those cases in which the muscles in the lower ha]f 864 
DISEASES OF THE NERVOUS SYSTEM 
of the face are alone involved, which include mainly those above the angle 
of the j aw. 
Bell's Palsy 
(Peripheral Facial Paralysis) 
Causes.—The most frequent causes of Bell’s palsy are exposure to 
cold, disease of the middle ear, and caries of the petrous portion of the 
temporal bone. 
When the facial nerve is affected, after its exit from the stylomastoid 
foramen, peripheral paralysis results, commonly known as Bell's palsy. 
The paralysis is often preceded by a period of neuralgia, due to neuritis 
or pressure. The characteristic facial appearance and changes are 
promptly recognized. There is an absence of normal wrinkling in the 
affected side, the eye does not fully close; the lower lid drops away from the 
eyeball; the tears fall down the cheek; when the cornea remains uncovered 
during long periods, ulcerative changes may follow. The nasolabial groove 
is effaced; the tip of the nose yields to the normal side; the angle of the 
mouth droops; the mouth is also drawn to the sound side. W histling and 
distending the cheek on the paralyzed side are impossible. Sensation is 
unaffected; the tongue is not deviated. If the nerve is involved within the 
fallopian canal, besides the leading symptoms detailed in the preceding 
paragraphs, taste is lost in the anterior two-thirds of the tongue because of 
chorda tympani pressure or disease. In these cases there is usually sup- 
purative middle ear disease with impairment of hearing and chronicity. 
If the facial nerve is the only cranial nerve paralyzed, with normal1 
sense of taste on the paralyzed side, then the disease is peripheral, out- 
side the stylomastoid foramen, or possibly just within the fallopian canal. 
With a lesion of the facial nerve between its exit and the geniculate gan- 
glion, there is paralysis with the usual symptoms, but no loss of taste. In 
these cases hearing is usually disturbed because the auditory nerve is 
likely to be involved by the same lesion. Without this complication hear- 
ing may be hyperacute. 
Facial Paralysis Due to Pontine Disease 
Associations and Causes.—This may be associated with paralysis of 
the sixth or other cranial nerves; usually hemorrhage, degenerative lesions 
with included bulbar paralysis, tumor or chronic meningitis, are among 
the causes. The pontine type of poliomyelitis may also cause this form of 
facial paralysis (See Poliomyelitis). The association of hemiplegia— 
simple or a crossed facial paralysis with hemiplegia—aids in localizing the 
lesion and determining the cause. 
For prognosis after it has been decided that the paralysis is either 
peripheral or central, the pathogenic factor becomes paramount. DISEASES OE THE PERIPHERAL NERVES 
865 
The 'peripheral facial paralyses have been considered by many to be 
“rheumatic they often arise after exposure of the face to cold and in 
the majority of cases lead to complete recovery after a period of varying 
length. 
The electrical response offers most valuable information in most cases 
of Bell’s palsy. The prognosis is best for prompt recovery in the cases 
in which the reaction of degeneration is absent or but slight. Jacobsohn 
reports that in the absence of the reaction of degeneration the duration of 
the paralysis is from one to four weeks; with partial degeneration from 
one to three months, with complete reaction of degeneration, from three 
to six months. I have seen with the latter condition over one year 
lapse before recovery. Erb’s and Oppenheim’s experiences are practically 
the same. I have seen many exceptions to these experiences and agree 
that the electrical reaction is not always a guide to the prognosis of the 
paralysis, and that the severity of the lesion cannot always -be determined 
by the electrical response in the individual cases. It remains, however, 
our most reliable guide for the prognosis of peripheral facial paralysis. 
In many cases peripheral paralysis is without prodromata; it develops 
suddenly in such cases. Uncomplicated Bell’s paralysis rarely remains 
permanent. 
Recurrence is not frequent, but it does occasionally happen that re- 
peated recurrences follow short intervals of normal function; finally 
permanent cure follows. 
With bone and middle ear diseases which cause facial paralysis a 
guarded prognosis should be given. Unless the cause can be removed, 
return of lost function is impossible. Syphilitic lesions causing facial 
paralysis treated early, are favorably influenced. 
Diphtheritic paralysis offers an encouraging forecast; almost all cases 
fully recover. 
Fractures at the base, which recover, are likely, if the facial is in- 
volved, to leave permanent paralysis. 
Mastoiditis, not too destructive, leads to final recovery of associated 
paralysis. 
Growths in the mastoid, or of the face or ear, causing paralysis by 
pressure, lead to permanent paralysis unless they can be removed surgi- 
cally, without inclusion of nerve fibers. The prognosis of injuries and 
division of the nerve depend on the extent and nature of the lesion, and 
the effect of surgical treatment. 
Hemorrhage into the fallopian aqueduct, when absorbed, is followed 
by return to normal function. 
Bulbar paralysis with facial involvement is incurable. 
Hemorrrhage and softening of the pons is often followed by some 
improvement of the paralysis of the facial; naturally the extent of destruc- 
tion varies in different cases, so also the prognosis. 866 
DISEASES OF THE NEKVOUS SYSTEM 
Tumors offer their own discouraging outlook, as do aneurismal dilata- 
tions causing facial paralysis. 
The other infections associated with facial paralysis, also alcoholic 
palsy, offer an encouraging prognosis. 
The differential points which are to be considered in the diagnosis of 
peripheral and central facial paralysis must also be considered in the 
forecast. 
With central lesions, the upper neurons are involved, and the paraly- 
sis must therefore be of the opposite side of the face. 'The voluntary 
movements of the face are lost while the emotional and reflex movement 
are but little, if at all affected. The upper part of the face escapes almost 
entirely. 
The electrical reaction remains normal or but slightly changed, and 
there is no reaction of degeneration. The tongue deviates to the side of 
the facial paralysis. 
Aphasia with paralysis of the right side of the face may be present 
with hemiplegia. The hemiplegia with a lesion of the upper neurons and 
facial paralysis is on the same side as the facial paralysis; the lesion is 
supranuclear (above the facial neucleus). 
With crossed facial paralysis and hemiplegia, the lesion is in the lower 
neurons or segment, the lesion is on the same side as the facial paralysis; 
the hemiplegia opposite. The lesion is pontine. 
Double facial paralysis offers an unfavorable prognosis, for it is due, 
as a rule, to extensive pontine disease, chronic meningitis, tumor, hemor- 
rhage, double otitis media—rarely with diphtheria or alcoholic neuritis. 
Cases have been reported with bulbar paralysis and erysipelas. 
Facial paralyses with family neuropathic tendencies have been re- 
ported by Neumann, Charcot, Frey and Oppenheim, in several members 
of a family (brothers and sisters). These paralyses are likely to recur 
and are influenced by emotion (fright, worry, etc.). 
Facial paralysis is a disease of mature life as a rule, most frequent 
between twenty and forty. When found in children it is due either to 
diphtheritic paralyses, brain tumor, injury, syphilis, meningitis, or some 
other serious lesion. Barring an occasional case of facial paralysis due to 
diphtheria in children, the causes almost always include grave primary 
lesions, making recovery infrequent. 
Neurasthenic and hysterical children often develop facial spasm, which 
is usually rebellious to treatment and a tic habit may develop which is 
overcome with great difficulty and may never yield. 
The tic which is associated with trigeminal neuralgia, particularly in 
old subjects, persists so long as does the neuralgia; sometimes in the aged 
(i) Facial or Mimic Spasm DISEASES OT THE PERIPHERAL NERVES 
867 
and in young subjects it may persist after the relief of pain, or may 
develop as a sequel. Under these conditions it is likely to continue. 
Tic may be purely reflex in character, at times from carious teeth, 
intestinal lesions, worms, polypi, diseased tonsils and lymphatics. If the 
cause is removable the tic yields. In children and young subjects the 
shoulder and head muscles are often involved. Ocular errors should be 
suspected; their relief cures some cases. 
In women facial spasm, without other symptoms of chorea develops 
occasionally during pregnancy which bears no relation to a known patho- 
logic lesion and disappears after labor. 
Tic Convulsive 
True tic convulsive is usually a chronic spasm of the muscles of one- 
lialf of the face, involving the orbicularis palpebrarum. Blepharospasm 
is present in most cases and as a rule, its pathologic fundament remains 
unrecognized. I do not include those cases which are due to cortical 
lesions in which there are spasmodic contractions of the facial muscles. 
Most cases of genuine tic convulsive are found in neurotic, overwrought 
individuals ; in my experience the sexes have been equally affected. 
Clonic spasms which predominate, may alternate with the tonic variety 
and are aggravated by excitement or emotion; they are often influenced 
by suggestion and may cease during short periods, particularly during 
rest. 
The combination of tic convulsive with other neuroses is not infre- 
quent. The French neurologists have reported the association of 
hysteria, neurasthenia, migraine, epilepsy and mental disturbances. The 
majority of my cases when complicated were found with migraine. 
I have never been able to influence facial convulsive tic when fully 
established. The cases which have yielded were blepharospasm, due to 
ocular or other removable causes, some of the mimic spasms of children 
after long treatment in which environment proved a powerful factor. 
Occasionally I have seen facial paralysis develop in the muscles which 
seemed to tire out after years of spasm (Ballett). 
Cases of mimic spasm following trigeminal neuralgia may cease after 
long periods without treatment. 
The majority of cases of convulsive tic have not been associated with 
the explosive noises or psychic symptoms described by the French neurolo- 
gists. 
Convulsive tic does not affect longevity. The last three cases seen in 
private practice were seventy-two, fifty-six and about fifty years of age, 
respectively. The first of these had the spasm over twenty-five years be- 
fore her death from cerebral apoplexy; the second is living and considers 
himself well after twelve years of tic, and the third is an active, healthy 868 
DISEASES OE THE NERVOUS SYSTEM 
man in public life who has never been without facial tic since his earliest 
childhood. 
I have not been able to confirm the conclusion of those who consider 
tic convulsive to be an evidence of degeneration. 
(j) Auditory Nerve 
(Acusticus) 
Primary diseases of the auditory nerv.e are infrequent; rarely do we 
meet idiopathic neuritis of the nerve. 
Causes.—The leading causes of auditory paralysis are tumor, hemor- 
rhage, caries and meningitis. Cerebral syphilis, locomotor ataxia and 
neurorecidives (after salvarsan treatment) are also causes of acusticus 
paralysis. 
Associated Symptoms.—Labyrinthine invasion may follow or be asso- 
ciated with the infections, including scarlet fever, diphtheria, typhoid 
fever, measles, otitis, parotitis, and other less frequent diseases. 
Leukemia and pernicious anemia are occasionally associated with 
labyrinthine vertigo or deafness. 
The anatomic structure of the auditory nerve must be considered, be- 
cause there are in reality two distinct nerves, the cochlear and the vestibu- 
lar, each offers its own symptoms when diseased. 
Cochlear Kerve.—The cochlear nerve is associated more intimately 
with the sense of hearing, whereas the vestibular is connected with the 
vestibule and semicircular canals; its function is associated with the 
maintenance of equilibrium. 
Invasion of both the facial and cochlear nerve is often present with 
many serious central lesions. These include locomotor ataxia, leukemia, 
aneurism, brain tumor, multiple sclerosis, caries, periostitis, syphilis and 
fractures at the base of the skull. 
The degree of deafness depends upon the extent of cochlear change; 
when complete, bone conduction is lost as well as the detection of sounds 
through the air. 
The deafness which results from epidemic cerebrospinal meningitis is 
usually of cochlear origin, is permanent as a rule, and in very young chil- 
dren is a cause of deafmutism. 
Tinnitus Aurium 
Tinnitus aurium is a frequent accompaniment of aural paralysis. 
Though a frequent symptom of auditory disease, it may he due to other 
causes—aneurism, cardiovascular and constitutional disturbances (chloro- 
sis, grave or malignant anemias, uremia, acidosis and cinchonism). The 
significance of the symptom can only be decided after accurate diagnosis. DISEASES OF THE PERIPHERAL NERVES 
869 
Involvement oe the Vestibular Nerve 
Vertigo, impaired hearing, faulty equilibration and explosive seizures 
are the leading features of vestibular disease. Nystagmus is an occasional 
symptom. 
Vertigo 
Aural Vertigo 
Labyrinthine Disease—Meniere’s Disease.—Aural vertigo depends on 
some change in the semicircular canals, and is the leading type of true 
vertigo. Nerve deafness, vertigo and tinnitus aurium are the predominant 
symptoms. 
Labyrinthine vertigo, or Meniere’s disease, is associated with slight 
deafness, tinnitus aurium, vertigo, and recurring disturbances of equilib- 
riation, which may be of sufficient severity to “throw” the patient. 
Lesions and Symptoms.—The disease may arise suddenly from an 
acute labyrinthine lesion, or it may progress gradually. The apoplecti- 
form type is due to hemorrhage into the semicircular canals and is asso- 
ciated with deafness of the ear involved. With tumor of the brain, osteo- 
sarcoma, facial and other paralyses are usually present also. 
There are epileptiform seizures which are preceded by an aura 
including all of the symptoms of labyrinthine disease. Galvanization 
of the cervical sympathetic, acute diseases of the middle ear, in- 
spissated cerumen, the sudden flushing of the external auditory canal 
with water, alcohol and tobacco poisoning may all give rise to the 
Meniere complex. 
Neurasthenia and hysteria occasionally include Meniere symptoms 
which recur at short intervals, and are materially influenced by psychic 
factors. 
Angioneurotic edema has in rare cases caused the Meniere complex 
with the acute onset of symptoms and their sudden disappearance (Lachar- 
riere and Gescheit). 
Locomotor ataxia and multiple sclerosis may he associated with true 
vertigo and symptoms which cannot be differentiated from labyrinthine 
vertigo. 
I have mentioned the lesions and symptoms which are most fre- 
quent, for the reason that they give the data needed for safe prognosis. 
My experience with true labyrinthine vertigo has not been favorable for 
restitutio ad integrum. 
Almost all cases run a chronic course in which, if uncomplicated by 
the serious organic changes which may cause the complex, the patient re- 
mains uninfluenced by any Jcnown treatment or the disease is progressive; 
hearing and equilibration are more and more involved, until the patient 
is incapacitated. In occasional cases with complete deafness the tinnitus 
and vertigo yield. 870 
DISEASES OF THE NERVOUS SYSTEM 
The prognosis in those cases dependent on syphilis, ear, nose and 
throat diseases, and toxemias which are removable, is relatively good. 
Hemorrhagic cases often yield to treatment. Occasional epileptiform 
types yield to intensive treatment, as do also the hysterical and neuras- 
thenic varieties. 
My presage is not so favorable as is that of Frankl-Holzwart, who 
holds that the prognosis of Meniere’s disease is favorable and claims forty 
recoveries in seventy-four cases. 
General Considerations of Vertigo.—Vertigo is frequent with organic, 
functional and nervous diseases, and the toxic states. There are cases of 
so-called “essential vertigo” in which no cause can be determined. It is 
never to be regarded as a disease per se, hence its prognosis can only be 
considered in connection with the conclusions which make clear the method 
and cause of its production. 
Ocular verhigo is always associated with diplopia, and yields with the 
correction of the error upon which it depends. 
Acute vertigo of gastrohepatic and intestinal origin yields promptly to 
rest and treatment. 
Stomachal vertigo of Trousseau is often rebellious, but is finally 
favorably influenced by treatment. These cases demand close investiga- 
tion, for often they prove to be true labyrinthine vertigo. 
Epilepsy and vertigo, in which the latter is an aura, as a rule, recurs 
regardless of treatment, though favorably influenced by change of environ- 
ment and methods of living, etc. 
Petit mat with vertigo is exceedingly rebellious. 
Chronic and acute uremia, acidosis, anemia and other constitutional 
faults in which vertigo is a prominent symptom offer their own forecast. 
Each of these conditions requires the close consideration of the underlying 
disease. 
The organic diseases of the brain, of which vertigo is but a symptom, 
are usually multiple sclerosis, tabes, brain tumor and abscess, cerebellar 
ataxia, hemorrhage, embolism, thrombosis—all of these offer a doleful 
forecast. 
In the so-called “essential vertigo,” persistent and repeated search for 
the toxic state, ocular errors, nasal and aural disturbances, and distant 
(uterine, ovarian, arterial, gastric and kidney) disease, often leads to 
happy results. The possibility of migraine is not to be excluded. 
(k) Glossopharyngeal Paralysis 
The leading features are loss of taste (ageusia), or perverted taste 
(parageusia) in the posterior third of the tongue, anesthesia of the back 
of the tongue and the pharynx, and (dysphagia) difficult swallowing. 
Uncomplicated glossopharyngeal paralysis is so rare that its possibility 
is denied by many neurologists. The glossopharyngeal is involved with DISEASES OF THE PERIPHERAL NERVES 
871 
other nerves, with brain tumor, syphilis, chronic meningitis, aneurism and 
thrombosis of the jugular vein. 
(I) Pneumogastric Paralysis 
The paralyses of the vagus as it is associated with the separate infec- 
tions and toxic states, and the prognostic significance of such conditions, 
are separately considered with the individual diseases. 
Primary disease of the pneumogastric is exceedingly rare. 
Compression of the nerve at the base, due to neoplasm (brain tumor), 
chronic meningitis, aneurism or caries, pressure anywhere along its 
course from enlarged glands, growths, inflammatory disease, intrathoracic 
pressure (aortic aneurism) causing paralysis of the recurrent laryngeal 
branch is easily recognized, and the significance becomes promptly 
apparent. 
In considering multiple neuritis and diphtheria and the poisonings 
(tobacco, alcohol, lead, arsenic), I dilated on the effect of these condi- 
tions and called attention to the long periods during which the tachycardia 
due to vagus paralysis was tolerated. Most of these cases led to recovery. 
With alcoholic neuritis, arsenic, lead and phosphorus poisoning, asso- 
ciated conditions clear the horizon for a reliable forecast. 
Wounds which separate the fibers of the vagus usually offer a grave 
prognosis. 
With multiple sclerosis, bulbar paralysis, syringomyelia and locomotor 
ataxia, pneumogastric paralysis once established, is permanent. 
Cases dependent on neurasthenia and hysteria are often persistent, 
associated with many fears, but finally yield to suggestion and rational 
living. 
Pneumogastric paralysis with ascending disease, Landry's paralysis 
(heart and respiratory symptoms'), is uniformly fatal (See Poliomyelitis 
and Landry’s Disease). 
Tumors, injuries or diseases which cause paralysis of both vagi or re- 
current laryngeal nerves are uniformly fatal. 
Pharyngeal spasm is of hysterical origin—never organic. The pres- 
ence of hysterical symptoms, the globus, the evanescence of the spasm 
make diagnosis and prognosis easy. 
Cheyne-Stokes respiration is always a serious symptom and is asso- 
ciated with grave organic lesions separately considered. 
Laryngeal crises of tabes have in a number of cases been favorably 
influenced by the modern treatment of syphilis. 
(m) Paralysis of the Spinal Accessory Nerve 
Growths located in the region of the foramen magnum are often re- 
sponsible for paralysis of the spinal accessory and other cranial nerves. 872 
DISEASES OF THE NERVOUS SYSTEM 
Nuclear change with progressive muscular atrophy and other oi’ganic 
lesions lead to the paralysis. 
The symptoms vary with the location of the lesion. 
Degenerative lesions involving the nucleus are associated with bilateral 
symptoms, and these are not limited to the trapezius and sternocleido mas- 
toid. Bulbar symptoms are superadded. When the fully formed nerve is 
involved, the sternocleidomastoid and the upper portion of the trapezius 
are paralyzed. There is reaction of degeneration and atrophy. 
Paralysis due to a lesion within the skull includes both portions of the 
nerve, the spinal and the accessory. The nearness of the hypoglossal nerve 
and its inclusion in the process leads to paralysis of the palate on the side 
of the lesion. 
Paralysis of the sternocleidomastoid makes it impossible to rotate the 
head toward the normal side; no contraction of the muscle is felt when the 
attempt is made. If both stemomastoids are involved, the head tends to 
fall backward; it is bent forward with great difficulty. 
With trapezius paralysis the shoulder on the affected side drops and 
cannot be normally raised. The arm is elevated with difficulty. The 
second and third cervical nerves send filaments to the trapezius which 
prevent complete paralysis. 
Caries of the first and second vertebrae, cervical pachymeningitis, 
chronic meningitis, besides tumors and progressive muscular atrophy 
(above mentioned) and traumatism, are the leading causes of paralysis of 
the eleventh nerve. 
Oppenheim acknowledges the possibility of primary neuritis of the 
spinal accessory. 
Locomotor ataxia may involve the nerve; whether the lesion is central 
or peripheral is debatable. 
Each of the causes mentioned in the preceding paragraphs makes prog- 
nosis possible. Surgical methods have been reported to relieve a few 
cases. 
(n) Spasm of the Trapezius and Sternocleidomastoid 
(Spinal Accessory Muscles) 
(Torticollis, Wry Neck) 
Torticollis may be either functional or organic. 
The organic cases of torticollis are due to suppurative disease of the 
tissues of the neck, glandular disease, neck tumors, injuries, and cellulitis. 
All of these are amenable to surgical treatment. With non-malignant 
disease the prognosis is good. 
The functional or spasmodic wry neck represents true torticollis, the 
cause of which remains unrecognized in most cases, though in the majority DISEASES OE THE PERIPHERAL NERVES 
873 
there is a decided neuropathic diathesis, readily recognized. Most of my 
cases have been in young neurotic women and in children, though many 
claim that the disease predominates in the male. In the majority a hys- 
terical element has been in the ascendency. 
I have rarely met the congenital torticollis in practice in which the 
sternocleidomastoid is shortened; it is often degenerated, hard and re- 
sistant. Tenotomy improves these cases. Golding Bird contends that 
even after tenotomy “the facial asymmetry persists” and that “the facial 
asymmetry and the torticollis are integral parts of one affection which has 
a central origin, and is the counterpart in the head and neck of infantile 
paralysis with talipes in the foot” (Osier). 
Symptoms.—The symptoms of functional spasmpdic wry neck are 
readily recognized. The spasm may be tonic or clonic; these may alter- 
nate, or one type may predominate. In hysterical subjects there are long 
periods during which wry neck may persist and suddenly disappear to 
return on slight cause. 
Causes.—Unquestionably wry neck may be caused by reflex disturb- 
ances due to uterine and ovarian disease. Among my cases is one, in 
which during many years the spasm recurred at short intervals, and con- 
tinued during long periods in which an ovarian dermoid cyst was finally 
discovered and removed, with permanent relief of the spasm. 
Course of the Disease.—There are cases which persist uninfluenced 
by any known treatment, either medical or surgical. One of my cases 
has subjected herself to innumerable surgical operations by the best sur- 
geons in America without appreciable benefit. The psychic influence of 
persistent torticollis is most depressing and makes many, particularly 
women of refinement with the neurasthenic habit, wretched, leading them 
to live the life of the recluse. Life is not directly shortened by the dis- 
ease save as the victims are led to suicide or develop a drug habit. The 
acute form of the disease offers a good prognosis. 
Occasional cases of muscular rheumatism of the neck muscles (sterno- 
mastoid and trapezius) lead to several weeks of torticollis, which yields to 
treatment. 
(o) Paralysis of the Hypoglossal Nerve 
Most paralyses of the hypoglossal nerve are of central and nuclear 
origin. Lesions of the nerve after its exit from the skull are exceedingly 
rare. Loss of power in the tongue is the leading symptom of hypoglossal 
paralysis. 
Causes.—When the lesion involves the nucleus, the paralysis is bilat- 
eral, as the nuclei of the separate nerves are close to each other. The 
lesion is degenerative in most cases. Bulbar paralysis, progressive mus- 
cular atrophy, syringomyelia, disseminated sclerosis, locomotor ataxia, 874 
DISEASES OF THE NERVOUS SYSTEM 
hemorrhage, tumor, thrombosis, embolism, aneurism, caries, and chronic 
meningitis, are among the causes of hypoglossal paralysis. 
Syphilitic gummata may cause hypoglossal paralysis; if unrelieved, 
the symptoms of tongue atrophy and paralysis persist. Such paralysis is 
likely to be one-sided, and includes the roots of the spinal accessory which 
causes paralysis of the larynx and pharynx on the same side (Herter). 
With the bilateral paralysis of nuclear origin there may be labial 
paralysis also. 
Crossed paralysis—hemiplegia on the side opposite the lesion with the 
hypoglossal paralysis on the side of the lesion—results from involvement 
of the fibers within the medulla. Hemiplegia is present in most, but not 
in all cases. 
Neck growths and wounds occasionally cause hypoglossal paralysis, 
but these are rare, as are also the cases of hypoglossal neuritis. 
Cerebral apoplexy is the most frequent cause of hypoglossal paralysis 
(Internal capsule with hypoglossal fibers involved). 
The study of the underlying lesions which lead to hypoglossal paral- 
ysis detailed in the preceding paragraphs proves the limitations of our 
art in dealing with it. The specific cases are among those favorably influ- 
enced by treatment. Labial paralysis with atrophy once fully established 
is not likely to yield. 
(p) Paralysis of the Phrenic Nerve 
The anatomic relations of the phrenic nerve expose it to injuries and 
compression; arising from the third and fourth cervical roots it must 
naturally he included in fractures and dislocations of the corresponding 
vertebrae. 
Causes.—Fractures, dislocations, spondylitis, tumors of the cord, caries 
of the spine, hemorrhage, cervical and cerebrospinal meningitis, myelitis, 
and other inflammatory conditions, are the leading causes of phrenic 
paralysis. Aneurisms of the thorax and neck also cause phrenic paral- 
ysis, and in occasional cases multiple neuritis (alcoholic, diphtheritic, 
lead poisoning and beriberi). 
With multiple neuritis, if both nerves are included, it is a dangerous 
accompaniment, particularly if there are respiratory complications, such 
as pneumonia, bronchitis or pulmonary congestion. 
Phrenic paralysis with lesion of the spinal cord is bilateral; usually 
other nerves are also involved. 
Compression and crushing injuries are among the leading causes of 
bilateral paralysis. 
When one phrenic is paralyzed, the diaphragm continues sufficient, 
but when both are included it is insufficient and powerfully influences 
respiration. The thoracic muscles attempt hv increased action to com- DISEASES OF THE PERIPHERAL NERVES 
875 
pensate; the diaphragm is immobile. Dyspnea on exertion may Decome 
extreme. 
The prognosis of paralysis of the diaphragm when bilateral is always 
grave, particularly with multiple neuritis and ascending paralysis, though 
recovery with the former condition is not impossible. The prognosis of 
phrenic paralysis due to the other causes above mentioned, is always influ- 
enced by the underlying lesion; it is usually unfavorable. 
(q) Hiccough—Spasm of the Diaphragm 
Hiccough is due to spasmodic contraction of the diaphragm. The 
efferent impressions are distributed through the phrenic nerve to the 
diaphragm, and through the laryngeal branches of the pneumogastric to 
the glottis. 
Hiccough with inflammatory diseases within the abdominal cavity is 
always suggestive of grave disease, and in some cases of intestinal stasis 
indicates complete obstruction. 
With peritonitis and appendicitis it is equally serious, and is usually 
associated with marked distension and sepsis. 
With hernia—irreducible—it suggests strangulation. 
With hemorrhagic pancreatitis it is associated with other symptoms; 
often collapse. 
With typhoid fever it is almost always serious; it may be a symptom 
of intestinal perforation, hemorrhage or deep toxemia. 
When not dependent upon peritonitis or perforation, hiccough indi- 
cates virulent infection and may persist during several days, materially 
weakening the patient, though it is not necessarily fatal. Cessation of long 
continued hiccough is possible, and convalescence from typhoid followed 
in a number of my cases in which the recovery was scarcely expected. 
Hiccough due to rapid eating, hot or cold drinks, acute and transitory 
gastrointestinal catarrh, acute indigestion, and obstinate constipation is 
easily controlled. 
Hysterical hiccough, at times persists during several days, but is finally 
relieved by rest and treatment. 
Toxemia associated with hiccough is usually deep and threatening. 
Hiccough with the deep coma of uremia, acidosis, alcoholism and 
arsenical poisoning and profound meningeal toxemia is always a serious 
complication. 
(r) Paralysis due to Lesions of the Brachial Plexus 
The causes of neuralgia and neuritis of the brachial plexus already 
mentioned (see Brachial Neuralgia) may also lead to paralysis of the 
plexus, or one or more of its nerves. 876 
DISEASES OF THE NERVOUS SYSTEM 
Paralysis of all of the Nerves of the Brachial Plexus 
Paralysis of all of the nerves of the brachial plexus is rarely due to 
neuritis; usually it is due to traumatism, to fractures of the humerus, or 
to dislocation of the shoulder. 
Sensory and motor symptoms are combined. The extent of the paral- 
ysis must depend on the nerves involved. When, after dislocation reduc- 
tion is long postponed, there is little likelihood of complete restoration 
of function; atrophy and some paralyses usually persist. 
Prompt release of the plexus before degenerative changes have fol- 
lowed often leads to the full restoration of function. In all cases 
alcoholism and other toxic influences reduce the chances of full recovery, 
with complete plexus paralysis. 
Surgical intervention has been efficacious in occasional cases. 
(s) Paralysis due to Cervical Rib 
Paralyses may be due to the presence of a cervical rib; there may be 
both sensory and motor disturbances—hyperesthesia, anesthesia and 
atrophy. The symptoms develop gradually. The presence of the cervical 
rib is not usually suspected because of the absence of symptoms before 
puberty. 
The paralysis is more frequent in women than in men; the cervical 
rib causes symptoms in only a small proportion of cases (5 to 10 per cent). 
With a cervical rib on each side, the paralysis may be bilateral. Cervical 
rib may never cause symptoms. 
The Rontgen examination clinches the diagnosis. 
Oppenheim believes that cervical rib is a stigma of degeneration. 
Surgical removal of the rib has been followed by relief of the nervous 
symptoms, including paralysis in a number of reported cases (Thorburn- 
Beck). 
Paralysis of Two or More Brachial Nerves 
Both the median and ulnar nerves may be paralyzed together in frac- 
tures and other injuries of the wrist. The musculospiral and ulnar, occa- 
sionally the musculospiral, ulnar and median, are injured or compressed 
by fractures of the humerus. 
Paralysis of the brachial nerves may be either (1) supraclavicular, 
or (2) infraclavicular. 
With (1) supraclavicular paralysis the shoulder muscles are included, 
with (2) infraclavicular paralysis the muscles supplied by the radial, 
ulnar, and median nerves, are paralyzed. 
Erb’s Paralysis—Supraclavicular Paralysis.—The supraclavicu- 
lar, or Erb’s, paralysis, is due to the involvement of the muscles which 
are supplied by nerves taking their origin in the fifth and sixth cervical DISEASES OF THE PERIPHERAL NERVES 
877 
roots, and include the deltoid, biceps, brachialis anticus, supinator longus, 
the supinator brevis, rarely the infraspinatus and subscapularis. The 
arm cannot be abducted because of the deltoid paralysis; the forearm 
cannot be flexed at the elbow because of the inclusion of the biceps, 
brachialis anticus, and supinator longus. 
When the infraspinatus is paralyzed the arm may be rotated inward 
to some degree, but it cannot be rotated outward. With subscapular 
paralysis the arm cannot readily be rotated inward. 
Anesthesia is frequent, involving the outer side of the arm from the 
deltoid to the hand, and the skin of the thumb, index finger, and the 
adjacent side of the middle finger. 
The motor point where electrical reactions may be studied is located 
by Erb at the outer border of the sternomastoid muscle about two to three 
centimeters above the clavicle. 
The prognosis of Erb’s shoulder paralysis depends on the cause, the 
amount of atrophy, and the reaction of degeneration. The latter may be 
depended upon to give valuable indications, but should not be considered 
to the exclusion of all other factors. Complete cure or restoration of 
function with supraclavicular paralysis is exceptional. 
The Duchenne paralysis due to injury of the child during labor is 
characterized by supraclavicular paralysis, as are also some cases follow- 
ing anesthesia due to pressure during the operation. In the latter cases 
the paralysis may be double. In the birth paralyses the diagnosis is often 
doubtful during long periods; with bone injury and paralysis complete 
restitution of function is unusual. Atrophic changes are likely to persist. 
Plexus paralysis always offers a more serious prognosis than does paralysis 
due to single nerve involvement. 
Infraclavicular—Klumpke’s Paralysis.—Paralysis of the mus- 
cles supplied by neiAes taking their origin in the nerve roots of the eighth 
cervical and first dorsal roots are included in Klumpke's paralysis. 
The hand muscles, the flexors of the wrist and the fingers are para- 
lyzed. Sensory and vasomotor—trophic disturbances—are almost con- 
stant. The atrophy of the muscles with reaction of degeneration is in 
proportion to the severity of the lesion. 
(t) Paralysis of the Posterior Thoracic Nerve 
With paralysis due to a lesion involving the posterior thoracic nerve, 
the serratus magnus is paralyzed. Pressure due to loads carried on the 
shoulder, or injury, the acute infections, and the muscular dystrophies, 
are among the leading causes. 
The symptoms include (1) “rotation of the scapula on its vertical 
axis when the arm is put forward, with recession of the edge of the scapula 
from the thorax—so-called ‘winged’ scapula*, (2) the lower angle of the 878 
DISEASES OF THE NERVOUS SYSTEM 
scapula is rotated inward and upward when the arm is carried forward; 
(3) the power of elevating the arm above the level of the shoulder is 
greatly weakened” (Ilerter). 
The prognosis of serratus paralysis is not unfavorable when there is 
no break in the continuity of the posterior thoracic nerve; recovery is 
often slow. 
(u) Paralysis of the Circumflex Nerve 
Deltoid paralysis results from disease of the circumflex nerve; abduc- 
tion is impossible save as there is some assistance from the teres minor. 
One of the results of circumflex paralysis is the formation of adhesion 
in the shoulder joint. Many of these cases depend on single and multiple 
neuritis, and yield. Injuries, fractures and organic disturbances each 
offer their own prognosis. 
(v) Paralysis of the Median Nerve 
Paralysis of the median nerve alone is rare, and is usually due to 
traumatism. Injury of the stytoid process is a frequent cause (fractures, 
callus formation, dislocation, osteosarcoma). 
When the paralysis is of short duration, atrophy slight, reaction of 
degeneration incomplete, and the cause removable, the prognosis is good. 
Chronic cases after fracture and dislocation, faulty reduction, and 
callus formation, offer an unfavorable prognosis for restoration of function. 
Symptoms.—The paralysis shows itself in inability to pronate the 
forearm fully; the wrist cannot be flexed toward the radial side; the 
thumb remains unopposed by the tips of the fingers. The second pha- 
langes cannot be flexed on the first, and the terminal phalanges of the 
first and second fingers cannot be flexed; the third angl fourth fingers can 
be flexed because of the intact ulnar half of the flexor profundus. 
Long continued vasomotor and trophic changes with paralysis are 
unfavorable. 
The anesthesia resulting from median paralysis includes the skin of 
the palmar side of the thumb, index, middle and adjoining half of the 
ring finger, the corresponding part of the palm of the hand, and the dorsal 
surface of the corresponding hand and fingers. 
The muscles involved are: the pronator teres and quadratus, flexor 
carpi radialis, flexor digitoruin sublimis, flexor digitorum profundus, 
pollicis longus and brevis, and the opponens pollicis. 
(w) Paralysis of the Musculospiral Nerve. Radial Paralysis 
Complete musculospiral paralysis includes the extensors of the elbow 
and wrist, the supinators and the extensors of the thumb and fingers. In 
the common form, the arm can be extended at the elbow, the nerve being DISEASES OF TI1E PERIPHERAL NERVES 
879 
involved lower, i. e.-, after the nerve has been given off which supplies 
the triceps. 
Drop wrist is a frequent symptom of musculospiral paralysis in which 
the flexor muscles clearly show their ascendency by causing contractions 
in chronic cases. 
If the lesion is sufficiently high to involve the internal and external 
cutaneous branches of the musculospiral, the back of the forearm and 
the outside of the upper arm are anesthetic. 
Causes.—The musculospiral paralyses are often due to toxic neuritis, 
alcohol, lead, arsenic and other causes considered in the chapter on Mul- 
tiple Neuritis. 
Pressure paralyses within the domain of the musculospiral, when 
depending on transitory cause, offer a good prognosis. 
(x) Paralysis of the Ulnar Nerve 
Causes.—Fractures of the ulna and radius, injuries of the elbow joint 
external to the olecranon—of tenor injuries of the forearm and wrist— 
are the causes of ulnar paralysis. Fractures of the humerus and dislo- 
cation, crutch pressure, and knife wounds are also among the causes. 
Fractures of the condyle may be followed after considerable periods by 
paralysis due to callus formation. 
Occupation paralyses of the ulnar nerve are found among watch- 
makers, glassblowers, bakers, telephone girls and bicyclists. 
Toxic and infectious disease (including syphilis, typhoid fever, sepsis, 
lead, arsenic, alcohol) are occasionally complicated with ulnar paralysis. 
The sensory paralysis includes loss of sensation of the ulnar side of 
the back and palmar surface of the hand, the little finger, and the ulnar 
half of the ring finger and about one-half of the radial side of the same 
finger on the back of the hand. 
The muscles supplied by the ulnar nerve are the flexor carpi ulnaris, 
flexor digitorum profundus, abductor pollicis, and the lumbricales and 
interossei. 
Abduction and adduction of the fingers are impossible; the fingers 
cannot be flexed at the metacarpophalangeal joints nor can they be ex- 
tended at the interphalangeal joints (Russell). 
When the “claw hand” and interposed paralysis are developed, little 
hope even of improvement can be offered. 
With long neglected bone injuries and dislocations the paralysis, 
atrophy, reaction of degeneration, and sensory changes, are usually 
permanent. 
(y) Lumbar and Sacral Plexus Paralysis 
The causes of neuralgia of the lumbar and sacral plexuses mentioned 
(See Neuritis and Neuralgia) are included among the causes of sacral 
and lumbar paralysis. 880 
DLSEASES OF THE NERVOUS SYSTEM 
Causes.—Compression due to primary growths and metastases involv- 
ing the vertebrae, diseases of the pelvic organs, retroperitoneal masses, 
abscesses (psoas), inflammatory exudates, fractures of the pelvic bones, 
stab and gunshot wounds, dislocation of the hip, aneurism, gout, diabetes 
and poisonings (alcohol, neuritis and parturition), must all be consid- 
ered as provocative of lumbosacral paralysis. 
The nerves included are the: 
Anterior Crural 
Obturator 
Sciatic 
Gluteal 
External Popliteal 
Internal Popliteal. 
Paralysis of the Anterior Crural Nerve 
Symptoms.—With anterior crural paralysis there is atrophy and motor 
paralysis (quadriceps extensor) ; the knee cannot be extended, there is 
loss of patella tendon reflex, and with damage within the pelvis, the hip 
cannot be normally flexed while the knee cannot be extended. 
The anesthetic area is on the front and inner side of the lower two- 
thirds of the thigh, the inside of the leg and the inside of the foot to 
the big toe. 
With paralysis of the obturator nerve (derived from the third and 
fourth lumbar roots) the adductors of the thigh are involved; there is 
inability to cross the knees. 
The nerve is rarely involved alone, usually with other lumbar nerves 
—occasionally after difficult labor in which there was long continued 
pressure. Such cases usually recover. 
The anesthetic area corresponds with the upper third of the inside 
of the thigh. 
(z) Obturator Nerve 
(aa) Paralysis of the Sciatic Nerve 
The symptoms depend on the seat of the lesion. The prognosis is 
always had with paralysis of both sciatic nerves, or evidences of pressure 
in which there may he full paralysis on one side, and gradually increasing 
symptoms on the other. 
Pelvic and lumbar masses with sciatic paralysis are always un- 
favorable. 
I have seen a number of cases in which metastases to the lumbosacral 
spine from carcinoma of the breast, stomach, intestine, prostate, and other 
organs were complicated, either early or late with sciatic pressure, the 
usual unbearable pains, and in the later stages fully developed paralyses. DISEASES OF THE PEKIPHERAL NERVES 
881 
In most cases of sciatic paralysis there is paralysis of the muscles 
below the knee and anesthesia of the plantar surface, outer side of the 
foot and leg. 
With a lesion above the middle third of the thigh, the flexor muscles 
of the knee and extensors of the hip are paralyzed. 
As suggested in the chapter on sciatic neuritis, persisting symptoms 
referable to the sciatic nerve, one or both, must always create a strong 
suspicion of organic primary disease, and the prognosis can only be made 
after a thorough search for the pathogenic factor. 
(bb) Paralysis of the Gluteal Nerves 
The paralysis within the domain of the gluteal nerves includes the 
gluteal muscles, pyriformis and the tensor of the femoral fascia. 
The superior gluteal nerve arises from the lumbosacral cord, and its 
invasion causes inability to abduct or circumduct the thigh because the 
gluteus minimus and medius are included in the supply. 
Paralysis of the gluteus maximus makes it impossible for the patient 
to extend the hip; it is impossible to rise from the sitting position, to 
climb hills or stairs. 
With involvement of the superior gluteal nerve and paralysis of the 
gluteus maximus and the tensor fasciae, walking may be impossible be- 
cause of the included inability to abduct or circumduct the thigh and the 
turning outward of the foot, due to the tensor fasciae femoris paralysis. 
(cc) Paralysis of the External Popliteal Nerve 
The external popliteal nerve supplies the tibialis anticus, extensor 
longus digitorum, extensor brevis digitorum, and peronei. When these 
muscles are paralyzed the ankle cannot be flexed and the first phalanges 
of the toes cannot be extended. There is “drop-foot,” and as the condi- 
tion increases talipes equinus results, with anesthesia on the outer half 
of the front of the leg and the back of the foot. 
With primary neuritis the prognosis is good. Superficial injuries 
without break of continuity offer a favorable outlook. Fractures of the 
fibula and continuous pressure demand a guarded prognosis. 
The ankle cannot be extended with internal popliteal paralysis and 
standing on tip-toe is impossible; the toes cannot be flexed, neither can 
the foot be everted. 
If the lesion leads to anesthesia this is present over the outside and 
posterior surface of the lower part of the leg and the plantar surface of 
the foot. 
(dd) Paralysis of the Internal Popliteal Nerve 882 
DISEASES OE THE NERVOUS SYSTEM 
Most internal popliteal paralyses follow fractures of the tibia and 
fibula. 
Paralysis of all of the nerves of the lumbar plexus offers a doubtful, 
often an unfavorable prognosis because of the underlying causes—tumors 
(abdominal), abscesses (psoas), metastases (carcinoma, osteosarcoma), 
and caries of the spine. 
The suffering of these patients is often a factor in hastening death, 
and includes pains within the course of the genitocrural, ilio-ingual and 
iliohypogastric nerves. 
Anesthesias may be irregularly distributed, and the paralysis includes 
the muscles supplied by the anterior crural and obturator nerves, in many 
cases. 
With involvement of the entire plexus the prognosis is also grave, 
because of the associated pelvic lesion—malignant or inflammatory in 
many cases. Rectal lesions should also be suspected. 
The paralyses following prolonged labor and associated pressure yield 
after variable periods in different cases; they are not frequent. 
Primary neuritis and paralysis of the plexus offers a favorable 
prognosis. 
When symptoms of atrophy, paralysis, anesthesia and degeneration 
follow a stage of pain or irritation, the prognosis is not encouraging. 
(ee) Paralysis of the Sacral Plexus 
(ff) Paralysis Due to Lesions of the Cauda Equina 
Causes.—Most cauda equina paralyses are due to injury—crushing 
wounds, fractures—caries or malignant growths, causing pressure. The 
lesion usually causes bilateral symptoms, with approximation to sym- 
metry, rarely one-sided symptoms. 
Symptoms.—The symptoms are always suggestive of an intraspinous 
lesion, and are closely related with bladder, rectal and the sexual func- 
tion in the male, with the characteristic distribution of the sensory dis- 
turbance and loss of patella tendon reflex. 
The prognosis is easily made, for the history in most cases is clear 
as to the cause of the symptoms. 
The rapid development of symptoms is characteristic of traumatism. 
With gradually increasing symptoms, without external evidences or 
history of injury, tumor formation should he strongly suspected, and the 
forecast accordingly given. In these cases, the pain is severe in the region 
of the sacrum and down the legs. These symptoms are bilateral and sym- 
metrical and include anesthesia about the rectum and genitals, bladder 
paralysis, atrophy of the legs, loss of knee-jerk, and spasm of the leg 
muscles. DISEASES OF THE PERIPHERAL NERVES 
883 
IV. Tumors of the Peripheral Nerves 
Neuroma 
The tumors of the peripheral nerves may be either true neuromata or 
the false neuromata. The latter are more frequent, and are usually 
multiple. 
True neuromata are a part of the nerve structure, therefore intimately 
connected with the nerve, consist of nerve fibers and include ganglion 
cells. The occurrence of true neuromata without ganglion cells is 
doubtful. 
The false neuromata are composed mainly of fibrous, myomatous or 
sarcomatous tissue. 
The circumscribed and solitary growths of the peripheral nerves are 
either benign or malignant. 
The benign solitary growths are the fibroneuromata, the neuromyxo- 
mata and neurolipomata. 
The malignant growths include neurofibrosarcoma, secondary carcino- 
matous nodules (metastases) and neurofibromata, which finally degen- 
erate and become malignant. 
The neuromata which follow amputation are as a rule benign, but 
after removal they often recur. 
Disseminated Neurofibromata—von Recklinghausen’s Disease 
Symptoms.—Disseminated neurofibromatosis is characterized by the 
development of multiple fibromatous masses of the nerve trunks or ter- 
minals, with multiple pigment deposits (naevi). 
The size of the growth varies from an almond, or smaller, to an 
orange. In occasional cases there are similar deposits in the central 
organs, also Brain and Cord. My only case was not at all affected by 
the presence of the multiple masses and pigmentation. He presented no 
subjective symptoms. Wittman reports mononuclear increase in his cases, 
and Pierre Marie has seen cases of von Recklinghausen’s disease develop 
cachexia and death, with symptoms of malignancy. 
Multiple neurofibromatosis may be associated with sensory symptoms, 
including neuralgia and paresthesia. In some cases there are psychic 
disturbances, malassimilation, extreme wasting, and other trophic changes. 
With central deposits the prognosis is always unfavorable. 
There are chronic cases in which the disease persists without causing 
symptoms or shortening life; it may become stationary. Involution and 
cure is possible, though rare. 
In some cases the disease is congenital, and several members of a 884 
DISEASES OF THE NERVOUS SYSTEM 
family are affected. In these cases other congenital defects are frequent 
—muscle and bone anomalies. 
Tubercula Dolorosa.—Neurofibromata which involve the subcuta- 
neous branches of sensory nerves lead to painful swellings (small and 
numerous) usually around the joints and breasts, easily palpable, and 
exquisitely tender. The condition is known as tubercula dolorosa. 
Plexiform Neuromata.—The plexiform neuromata are congenital 
and hereditary, as a rule. Separate nerve trunks are the seat of multiple 
growths; they may cause no symptoms and are rarely painful. In some 
cases all of the nerves of the body are included in the proliferative disease. 
Elephantiasis neuromatosa shows the characteristic picture of the 
elephantine leg with multiple neuromata of large size. There is enor- 
mous increase of fibrous tissue between the epidermis and the muscle 
fibers, and enlargement of the bones. There is a strong tendency to 
malignant degeneration. The disease begins in early childhood and pro- 
gresses in cycles. There is no relief for the condition. 
Naturally the histologic build and distribution of multiple peripheral 
growths influences prognosis. 
Symptoms of central disease, severe and persistent neuralgias and 
the advent of cachexia are among the factors which presage an unfavor- 
able termination. 
Elephantiasis Neuromatosa 
References 
Adrian. Centralbl. f. d. Grenzgebiete d. Med. u. Chir., 1903. 
Ballett. Gazett des hdpit., 1901. 
Beck. J. Am. Med. Ass., 1904-5. 
Bird (Golding). Quoted by Osier. 
Bruns. Geschw. d. Nervensystem, 1909. 
Frankl-Holzwart. Jahrb. f. Psychiatrie. 1905. 
Herter. Diagnosis of organic nervous diseases. New York, 1907. 
Jacobsohn. Klinik der Nervenk., Berlin, 1914. 
Lacliarriere & Gescheit. Arch. f. Ohrenheilk., xxvii. 
Berl. klin. Wchnschr., 1902. 
Neumann, Charcot, Frey & Oppenheim. Oppenheim,'s Lehrb. d. Nervenkrank. 1913. 
Oppenheim. Lehrb. d. Nervenkrank. 1913. 
Osier (Sir William). Practice of medicine. New York, 1913. 
Russell. Bain textbook of medical practice. London, 1904. 
Thomson. Neuroma & Neurofibromatosis. Edinburg, 1900. 
Thorburn. Brit. Med. J., 1904. 
Wittman. Mohr & Staehelin, 1912, v, 642. DISEASES OF THE SPINAL CORD 
885 
B. Diseases of the Spinal Cord 
{System Diseases) 
I. Diseases of the Afferent or Sensory System 
1. Tabes Dorsalis or Locomotor Ataxia 
2. General Paralysis of the Insane 
3. Taboparesis 
4. Herpes Zoster 
5. Hereditary Ataxia (Friedreich's Disease) 
6. Marie’s Hereditary Ataxia. 
1. Tabes Dorsalis {Locomotor Ataxia)—2, General Paralysis of the 
Insane {Paresis)—3. Taboparesis 
The foregoing (1, 2 and 3) formerly classified as metasyphilitic dis- 
eases are known to he late manifestations of tertiary syphilis and are 
considered among the syphilitic diseases (See Syphilis of the Nervous 
System; Late Manifestations of Tertiary Syphilis), 
4. Herpes Zoster 
{Shingles, Acute Posterior Ganglionitis, Zona,, Zoster) 
Herpes zoster is an acute disease,, probably hemorrhagic and inflam- 
matory, involving the ganglia of the posterior nerve roots and associated 
with neuralgic pains in the corresponding nerves, which usually precede 
a vesicular eruption of the skin along the distribution of the nerve, the 
latter occasionally hemorrhagic. 
The clinical significance of herpes labialis and vesicular eruptions with 
other infections have been separately considered (See Pneumonia). 
Classification.—Herpes zoster is unilateral in almost all cases. The 
lay opinion that when the disease is bilateral (“meets in the middle”) it 
is ominous and usually fatal, is unwarranted. 
Occasionally there have been epidemics of herpes in which the prog- 
nosis was not different than in the sporadic cases, The uiost frequent 
forms of herpes zoster are intercostal, trigeminal (usually the ophthalmic 
branch), and cervicobrachial. Besides these, there are occipital, abdom- 
inal, lumboinguinal, sacrosciatic, and other localizations, 
The neuralgic pains which precede the eruption of vesicles, as a rule 
diminish in intensity with their appearance. 
The vesicles and inflamed base are often tender, and also cause incon- 
venience because of itching. The vesicles dry, usually cause no destructive 886 
DISEASES OF THE NERVOUS SYSTEM 
changes save in exceptional cases, and after their disappearance leave 
brown spots which disappear after several months. 
Confluence does not alter the favorable outcome. 
The hemorrhagic form of zoster leads to limited destructive skin 
changes and permanent cicatrices. 
With malignant cases, herpes may be gangrenous, and cause deep skin 
destruction with corresponding scars. 
Duration.—The duration of the eruption and the healing process in 
the average case is three weeks; there are subacute cases in which there 
are repeated crops of vesicles which continue during several months. In 
anemic individuals, in those reduced by previous disease or diathesis, and 
in the aged, the neuralgic pains may persist during months after the dis- 
appearance of the shin eruption and may recur on slight cause, such as 
change of weather, excitement, and depressing factors. Local hyperes- 
thesia or anesthesia may persist in occasional cases during varying periods. 
Accompanying Symptoms.—Trophic changes may accompany herpes; 
these usually yield. Herpes zoster involving the first (ophthalmic or supra 
orbital) branch of the fifth nerve may cause ulcerative and inflammatory 
changes in the cornea and conjunctiva, rarely suppuration. With com- 
plicating disease in other parts of the nervous system there may be optic 
neuritis and Oppenheim reports paralysis of the motor oculi and the facial 
nerve. 
Davidson reports sacral herpes associated with paralysis of the bladder 
and rectum. 
Course of the Disease.—Herpes zoster which begins with elevation of 
temperature is usually endemic, occasionally idiopathic. These cases run 
a favorable course. The majority of cases remain limited to a single nerve 
or plexus, and there is no tendency to multiple invasion (many nerves). 
There is scarcely another disease in which the appearances and symptoms 
are so characteristic and uniform. The prognosis is uniformly favorable. 
The greatest dangers are from rare destructive eye lesions which may 
prove serious. These already mentioned, include ulcerative keratitis, iritis 
and suppurative ophthalmia. When herpes accompanies the infections, its 
influence is not to be interpreted as unfavorable. The chronic neuralgias 
in elderly patients are rebellious and recur on slight cause. Associated 
trophic disturbances usually yield after varying periods. 
For a full consideration of the pathology of herpes zoster the reader 
is referred to the contributions of Head, Head and Campbell, Sherring- 
ton, and Howard (See references). 
References 
Davidson. Deutsch. med. Wchnschr., 1911. 
Head. Brain, xvi-xvii. 
Head & Campbell. Brain, xxiii. DISEASES OF THE SPINAL COliD 
887 
Howard. Osier’s Practice of medicine. 1913. 
Oppenheim. Lehrb. d. Nervenk. 2d «d. Bd. ii, 15J+. 
Sherrington. Tr. Royal Soc., London, clxxxiv-xcc. 
5. Hereditary Ataxia 
(Friedreich’s Disease) 
Hereditary ataxia does not long remain a system disease; combined 
or disseminated lesions are soon developed. 
Friedreich’s ataxia is a family affection in which several are affected 
—rarely one alone—in which there is a combination of ataxia with motor 
weakness and characteristic deformities. 
The disease is not hereditary in the sense that it is handed down from 
generation to generation, but children of a father and mother in the same 
generation are afflicted. 
There are a number of cases in which epilepsy and mental diseases 
have existed in near relatives, while Bouche considers alcoholism a cause, 
and Starr has seen cases follow acute infections. 
The clinical history and pathology of the disease prove its progressive 
tendencies. The changes are more far-reaching than in locomotor ataxia, 
not only in the posterior columns, but also in the cerebellar tracts, the lat- 
eral columns, and the pyramidal tracts. The greater changes are always 
in the posterior (sensory afferent) columns. Sclerosis may extend to the 
peripheral nerves, and disseminated degenerative changes are extensive. 
Symptoms.—The leading symptoms are motor weakness, nystagmus, 
speech defects, and absence of patella tendon reflex; Babinski is frequent, 
more or less curvature of the spine and cerebellar ataxia. The ataxia first 
affects the lower extremities and extends upwards. 
Course of the Disease.—The disease as already mentioned is pro- 
gressive until the patient is unable to maintain his equilibrium; he falls 
in a heap. Choreiform movements are frequent, ocular paralyses occa- 
sional. 
With the advance of the disease there are memory defects; mental 
weakness is increased without sphincter involvement. Idiocy and laby- 
rinthine vertigo are occasional. 
Contractures of the lower extremities develop and resemble club-foot. 
With Friedreich’s ataxia there is no Argyll-Bobertson pupil, nor are 
there laryngeal or visceral crises. 
The progression of the disease is slow but certain; many unfortunates 
live incapacitated for years. The average age reached is between twenty 
and twenty-five years; Oppenheim reports cases which reached the thirtieth 
and even the fortieth year. Some die early in life of acute infection, par- 
ticularly of pneumonia. 888 
DISEASES OE TILE NERVOUS SYSTEM 
Hereditary ataxia invites malignant infections. Diabetes is an occa- 
sional complication which promptly causes death. 
There is no treatment which prevents the onward march of the degen- 
erations. There are no cases of cure recorded. 
Marie’s Hereditary Ataxia 
Marie described a form of cerebellar hereditary ataxia under the name 
of "Heredoataxia Cerebelleuse” in which the disease begins after the twen- 
tieth year with characteristic cerebellar staggering. The reflexes (patella 
tendon) are exaggerated, and the symptoms confine themselves entirely 
to the cerebellum without spinal invasion. In Marie’s ataxia curvature of 
the spine and club-foot never develop. The disease remains unaffected by 
treatment, and is progressive. 
II. Anterior Diseases—Diseases of the Efferent or 
Motor Tract 
7. Poliomyelitis Anterior (Acute and Chronic)—Infantile Paralysis 
Poliomyelitis is fully considered in the chapter on infectious diseases 
(See Poliomyelitis). 
2. Landry’s Ascending Paralysis 
Landry’s paralysis is considered in connection with poliomyelitis (See 
Poliomyelitis) among the infectious diseases and in the Chapter on Periph- 
eral Paralysis (See Peripheral Paralysis). 
3. Progressive Central Muscular Atrophy 
Progressive central muscular atrophy is characterized by gradually in- 
creasing muscular atrophy which is dependent upon lesions in the cord, of 
a degenerative character, more particularly in the efferent motor tract, 
involving the gray horns (anterior multipolar cells) and the ventral horns 
as the disease advances, with change in the neuroglia. In these cases, 
though contractures and other symptoms of involvement of the lateral col- 
umns are absent, these nevertheless show atrophy and productive lesions. 
There is disappearance of the medullated fibers. This type is known as 
progressive spinal muscular atrophy or Aran-Duchenne muscular atrophy. 
The greater changes in the lateral columns and anterior gray horns in 
some cases give rise to the amyotrophic lateral sclerosis, originally de 
scribed by Charcot. 
With involvement of the medulla oblongata its motor nuclei are in- 
volved, and bulbar paralysis results. I consider therefore: D1SEASES OF THE SPINAL CORD 
889 
(a) Progressive (central) spinal muscular atrophy (Aran-Du- 
chenne muscular atrophy) 
(b) Amyotrophic lateral sclerosis 
(c) Bulbar paralysis (Glosso-labio-laryngeal paralysis). 
(a) Progressive (Central) Spinal Muscular Atrophy 
(.Aran-Duchenne Muscular Atrophy) 
There are two forms of the disease: The adult and the hereditary- 
family or infantile type. In the latter type the leading anatomic changes 
are degenerative and are limited to the anterior horns and the peripheral 
nerves. The lateral columns are not as a rule involved. 
Adult Type.—The adult type of progressive atrophy is found oftener 
in men and after the twentieth year, usually between twenty-five and 
thirty-five; muscular atrophies which develop before twenty or shortly 
after usually belong to the muscular dystrophies. 
None of my cases have proved of specific origin, and heredity was not 
frequent. Osier reported a series of cases in which thirteen members of 
a family were affected in two generations; with the exception of two. 
The cases occurred or proved fatal above the age of forty and the late 
onset speaks rather for a central affection. 
There are cases of Aran-Duchenne atrophy which during several 
years progress gradually, with all of the symptoms of the spinal form of 
the disease—in which there is advance of degeneration to the motor nuclei 
of the medulla oblongata with glosso-labio-laryngeal paralysis—the patient 
rapidly fails. One of my cases of this type remained purely spinal during 
almost two years hut died within two months after the onset of bulbar 
symptoms. 
The progression of atrophy is at first most marked in the interossei of 
the hands, and is symmetrical. The “claw hand” develops wuthout paral- 
vsis but with increasing motor weakness and fibrillary tremor, and never 
with hypertrophy of muscle tissue. 
The atrophy may remain limited to the hands during long periods. 
The disease finally gradually extends to the flexor arm muscles, later to 
the extensors. The reflexes of the arm are weakened or abolished entirely. 
A reverse atrophy is not unusual; then the muscles of the shoulder 
or arm may be first involved. The disease may not progress to the lower 
extremities, or such invasion may be late. 
The unfavorable cases so far as life is concerned, are those in which 
the respiratory center and the other motor nuclei in the medulla oblongata 
degenerate. 
In another class of cases the vagus center may be suddenly involved 
and cause acute symptoms, i. e., tachycardia besides respiratory embarrass- 
ment; death is prompt. 890 
DISEASES OF THE NERVOUS SYSTEM 
With progressiori the atrophy becomes extreme and the patient’s ap- 
pearance is characteristic. The skeleton is covered by skin and a small 
remnant of muscle. 
Most chronic cases develop marked spinal curvature and contractures. 
There is no true paralysis; there is a motor weakness only. In the 
later stages of the disease the weakness may simulate paralysis. There 
are but few exceptions to this rule. 
Reaction of degeneration is incomplete; the reduction of electric excit- 
ability is in direct proportion to the extent of the destruction of muscle 
tissue. 
Remissions have occurred in my cases during which the disease re- 
mained stationary for several years but progression followed; in some 
cases this was rapid and ascending. With the progression of symptoms 
there is increasing neurasthenia, often an hysterical element which adds 
enormously to the unhappiness of the patient. 
Duration.—The average duration of the disease is between ten and 
twenty-five years. Fibrillary twitching is often evidence of advancing 
atrophy. 
Many patients die of intercurrent disease. Aspiration pneumonia is a 
frequent cause of death. 
Cure is unknown. 
Juvenile or Family Type.—The juvenile or family (infantile) type 
of progressive muscular atrophy shows gradual progression of symptoms 
referable to the anterior horns and the peripheral nerves after the sixth 
month of life, at first limited to the thigh, pelvic and spinal muscles, from 
which the extension to the extremities follows in the course of several 
years. As the disease progresses the reflexes are abolished and the reaction 
of degeneration is a guide to the extent of muscle atrophy. There are no 
sensory symptoms. 
Spinal curvature and deformity (kyphoscoliosis) develop as the disease 
advances. 
Bulbar symptoms are not so frequent as in the adult type hut are not 
impossible. A few cases are recorded in which bulbar symptoms preceded 
general muscular atrophy. The disease leads to death in from eight 
months to as many years. 
(b) Amyotrophic Lateral Sclerosis 
Charcot first called attention to the association of disease of the anterior 
horns and lateral columns of adults which usually attacks the cervical 
enlargement, and first includes loss of power, atrophy and rigidity of the 
upper extremities. 
Course of the Disease.—The first stage continues from four to twelve DISEASES OF THE SPINAL COLD 
891 
months; formication with contractures and exalted reflexes characterize 
this stage. 
*4$ the disease advances and the cellular elements degenerate, the re- 
flexes are blunted, the lower extremities are more and more invaded, rigid- 
ity, atrophy and contractures result with fibrillary twitching. The Babin- 
ski and Oppenheim symptoms are usually present. 
In the third stage all symptoms are enormously increased, the reflexes 
are lost, and there are bulbar and cerebral disturbances; the general con- 
dition grows worse, intercurrent disease, sepsis, pneumonia or myocardial 
degeneration lead to death. Atrophy, rigidity and motor weakness are 
the leading features of the disease. The jaw clonus is easily obtained. 
The disease is uniformly fatal, runs its course in from one to three 
years—rarely four—only occasionally longer; there are cases which lived 
ten years. Its cause is unknown; women suffer oftener than men, rarely 
before the twentieth or after the fiftieth year. 
(c) Bulbar Paralysis 
(Glosso-labio-laryngeal Paralysis) 
The disease may limit itself to the motor nuclei in the medulla and 
pons or bulbar paralysis may he an early or late complication of any of 
the other types of progressive muscular atrophy in the adult It may 
complicate multiple sclerosis and other grave organic central disease. 
The degenerative type of bulbar disease is either subacute or chronic. 
The acute form is separately considered and it depends on a variety of 
causes. The chronic or usual form of bulbar paralysis is almost always 
associated with the lesions of the cord already mentioned. 
There is a class of chronic bulbar paralysis in which the nuclear changes 
develop gradually and are due to arteriosclerosis, aneurism, or to the pres- 
sure of tumor or abscess. 
Symptoms.—The separate symptoms due to the paralysis of the in- 
cluded nerves include defective speech (dentals and linguals) difficult 
swallowing with almost continuous salivation in advanced cases, labial 
symptoms, the large mouth and prominent lips, the return of food through 
the nostrils, feeble voice with laryngeal paralysis {aphonia). 
The lip, tongue, pharyngeal and laryngeal paralyses offer the leading 
symptoms in the fully developed case. 
Gradual progress is the rule; once developed the disease always leads 
to death in from one to three or four years. 
Bronchopneumonia (aspiration pneumonia) was the most frequent 
cause of death in my cases. 
Suddenly arising tachycardia with other symptoms of pneumogastric 
paralysis may end life suddenly. 892 
DISEASES OF THE NEKVOUS SYSTEM 
Acute Bulbar Paralysis 
Acute bulbar paralysis is usually of vascular origin, apoplectic, embolic 
or thrombotic, with destruction of the motor nuclei (softening). It may 
be of infectious origin, as is pointed out in the consideration of the bulbar 
and pontine types of poliomyelitis (See Poliomyelitis) ; it may also be a 
sequel of diphtheria. A number of cases are recorded in which high volt- 
age (electric shocks) have caused it. 
Most acute cases are associated with hemiplegia or crossed paralysis. 
The prognosis of acute bulbar paralysis is always grave. Occasionally 
a diphtheritic or typhoid case or poliomyelitis recovers. 
Ilemiplegics with bulbar paralysis, when the pneumogastric is not in- 
volved, may live during varying periods: complete restitutio ad integrum 
is not often to be expected. The same complication which ends the lives 
of those who suffer from the chronic form of bulbar paralysis—pneu- 
monia—causes the death of most acute cases. 
While death often follows hemorrhagic cases in a few hours or days, 
usually from aspiration pneumonia, respiratory or heart paralysis, the 
symptoms may improve and in rare cases there may be apparent return to 
health. This history is not often repeated. 
Oppenheim has seen cases of acute bulbar paralysis recede in diabetic 
subjects. 
Syphilitic cases not fully developed may also improve under rigorous 
treatment. 
The cases of acute bulbar neuritis arising as a part of multiple neuritis 
are not frequent; they are of serious import, the prognosis depending upon 
the extent of the process; with vagus paralysis the outcome may remain 
doubtful during a number of days. Complications including pneumonia 
promptly lead to death. Comte has considered the clinical history of 
the neuritic form of bulbar paralysis (to which the reader is referred). 
Bulbar paralysis with leukemia has been occasionally noted. The 
course of the disease is acute, ending in from two to six weeks. 
Infantile Form of Progressive Bulbar Paralysis 
The infantile form of bulbar paralysis was described by Fazio, Char- 
cot, Fonde and Brissaud. There are hereditary and family characteristics 
(Oppenheim). The disease, according to Oppenheim, develops in the chil- 
dren of consanguineous marriages and the paralysis shows early invasion 
of the upper fibers of the facial nerve with ptosis and ophthalmoplegia. 
The paralysis is associated with atrophy, lowered electric excitability, and 
the reaction of degeneration. The cases are exceedingly chronic unless 
acute infection causes early death. The juvenile form of bulbar paralysis 
offers nothing encouraging. In occasional cases there may be congenital 
absence or defect of motor nuclei in the medulla. DISEASES OF THE SPINAL CORD 
893 
Pseudobulbar Paralysis 
Symptoms.—As a rule pseudobulbar paralysis is not associated with 
atrophy of the lips and tongue as is the bulbar paralysis. With pseudobul- 
bar paralysis there are symmetrical lesions in the motor paths of both hemi- 
spheres localized in the cortex of the lower part of the ascending frontal 
convolution, or in the knee of the internal capsule. The lesions are there- 
fore not in the medulla but are purely supranuclear. 
Causes.—The underlying cause is usually arteriosclerosis of the cere- 
bral arteries leading to multiple softening, hemorrhage, encephalitis and 
other local degenerative processes. 
Course of the Disease.—Hemiplegia accompanies the bulbar symp- 
toms which are apoplectiform. Spastic conditions usually develop. It 
must be remembered that there is no atrophy; there are often psychic dis- 
turbances, and these may be explosive with the development of the emo- 
tional element (laughing and crying); the muscles are not completely 
paralyzed and during emotion, automatically and by reflex action, these 
contract and are often overactive (Oppenheim). 
The prognosis is bad; symptoms may persist during several years and 
may show some improvement, but do not disappear entirely. 
Complications are frequent and are not well borne. 
Infantile Pseudobulbar Paralysis 
Probably these cases depend upon congenital anomalies or encephalitis. 
The prognosis is always unfavorable. 
Myasthenia gravis 
(Asthenic Bulbar Paralysis, Myasthenia gravis pseudoparalytica) 
Erb in 1878 first called attention to a complex of symptoms purely 
bulbar—to which Oppenheim, Eisenlohr, Goldflam and Jacobsohn added 
marked muscular weakness—in which no pathologic lesion has been dis- 
covered to explain the symptoms; neither is the cause of the disease known. 
The disease is found with almost equal frequency in the male and 
female, possibly slightly preponderant in the latter. 
The enormous muscular asthenia increases with use and there may he 
final complete insufficiency. 
The muscles within the domain of the motor oculi, ahducens, facial, 
glossopharyngeal, pneumogastric and hypoglossal are usually included. 
The asthenia may involve the laryngeal muscles. 
The paralysis or extreme exhaustion after use may be transitory to 
recur on further effort, or it may persist. The latter frequently causes 
ocular and laryngeal paralyses. 894 
DISEASES OF THE NERVOUS SYSTEM 
The extreme fatigue of the voluntary muscles is increased by electric 
stimulation. 
Atrophy of muscles is only rarely present. 
Most cases of myasthenia gravis begin with bulbar symptoms and grad- 
ually progress. 
Ptosis and double ocular paralyses are frequent; the former is one of 
the usual symptoms of the disease, with weakness of the muscles of the 
neck and jaw. 
The association of Basedow’s disease (liyperthyroidea) is occasional. 
The neuropathic diathesis has been prominent in all of my cases, while 
persistent thymus is frequent, and Weigert reported a thymus tumor with 
“thymus metastases” in the voluntary muscles involved. Congenital de- 
fects are numerous. II un, Blumer and Streeter report “an infiltration 
of the muscles and of the thymus gland with lymphoid cells and a prolifer- 
ation of the glandular elements of the thymus” (Osier). 
The influence of the internal secretions on myasthenia gravis is not 
definitely settled (Biedl). 
Remissions are frequent. These may continue from four to ten years; 
as a rule they are short. Most cases progress after remissions of varying 
length. 
Recovery is not impossible though it is the exception. Oppenheim re- 
ports 26 deaths in 38 cases. Osier 180 cases, with 72 deaths. 
(Charcot-Marie-Tooth Type of Muscular Atrophy, Peroneal Type of 
Neural Muscular Atrophy) 
4. Progressive (Neural) Muscular Atrophy 
Charcot and Marie, and Tooth called attention to a type of progressive 
muscular atrophy met as a rule during childhood—rarely after the twen- 
tieth year—which is of hereditary and family origin and stands on the 
borderline of central atrophy and muscular dystrophy. 
Course of the Disease.—The disease begins during childhood in the 
peroneal muscles, and club-foot develops, either pes equinus or equino- 
varus. 
The disease may not recur in the descendants of a family more than 
two or three times in from three to five generations. Jacobsolm believes 
that the disease may arise sporadically. 
Extension to the upper extremities is not usual until the atrophy and 
contractures of the lower extremities have existed during many years. 
Rarely is the progress of the disease reverse, beginning in the upper ex- 
tremities. 
Sensory symptoms are frequent. 
Fibrillary twitching is always present. DISEASES OF THE SPINAL CORD 
895 
Reaction of degeneration and reduced electric excitability are constant. 
The disease is usually progressive; occasionally stationary. These 
periods vary in length but are followed by progression. The duration of 
the disease is from twenty to thirty years and longer. 
The disease is of neural origin with involvement of the columns of 
Goll (Virchow, Friedreich, Oppenheim, Dercum). 
References 
Biedt. Inner. Secretion. 1913. 
Brissaud-Marie. Bull. Med., 1893. 
Charcot. Arch, de Physiol., 1870. Also Lecom. Nerv. System. 
Medic. Modem. 1893. 
Charcot & Marie. Revue de Med., 1886. 
Comte. Revue Neurol., 1906. 
Eisenlohr. Jacobsohn’s Klinik der Nervenkr., 1913. 
Fazio. Rifer. Medic., 1882. 
Goldflam. Jacobsohn [L c.]. 
Hun, Blumer & Streeter. Albany Med. Ann., xxv. 
Jacobson. Klinik der Nervenkrank., 1913. 
Londe. Revue de Med., 1893-94. 
Oppenheim. Lehrb. d. Nervenkrankh., 1913, ii, 1381. 
Osier (Sir William). Practice of medicine. New York, 1913. 
Tooth. Brain, 1898. 
Virchow, Friedreich, Oppenheim & Dercum. See Oppenheim, Jacobsohn, etc. 
5. The Muscular Dystrophies 
(Progressive Muscular Dystrophy—Erb) 
The muscular dystrophies are in the majority of cases of hereditary 
origin, depending on primary lesions of the muscles, always progressive, 
though at times hut slowly, characterized by wasting of muscular tissue, 
with or without hypertrophy, with final fat deposit in the connective tissue 
sufficient to cause fatty degeneration, lymphatosis or pseudohypertrophy. 
There may he true hypertrophy and pseudohypertrophy in the same mus- 
cle. As the disease advances, however, the hypertrophied muscle atrophies 
and the hypertrophic muscle undergoes fatty degeneration also. 
The hereditary factor is paramount. With two sets of cases seen while 
writing this chapter, there was in one, a father and three children, in 
another a mother and two children, respectively—in all there were the 
characteristic appearances of the atrophic form of the disease. In the 
children there was primary involvement of the face (Duchenne infantile 
form). 
Symptoms.—The earmarks of muscular dystrophy are, according to 896 
DISEASES OF THE NERVOUS SYSTEM 
Oppenheim and Ilerter, the gradual development of the disease during 
childhood, the hereditary factor, the involvement of the muscles of the 
trunk, pelvis and lumbar region, the femur, the shoulder and the arm, 
the combination of atrophy, hypertrophy and pseudohypertrophy (fatty 
degeneration), the absence of fibrillary twitching, the absence of reac- 
tion of degeneration, and the quantitative reduction of electric excita- 
bility, and the characteristic movements of the patients when lying down 
as they seek to lift themselves. The patients stand with their legs spread 
apart and show a marked spinal curvature. 
This classification of the dystrophies is accepted by Osier and repro- 
duced in his Practice of Medicine (1913). 
Course of the Disease.—As the disease progresses its characteristics 
are clearly manifested. The lordosis (curvature of the spine) is promi- 
nent. One case recently seen, the father of one group of the above men- 
tioned cases, was about forty-five years of age and had the disease over 
thirty years. With marked lordosis, shoulder atrophy and involvement 
of the femoral and pelvic muscles, he is able to support his family as a 
postal official. 
I. The Muscular Dystrophies of Childhood 
1. Hypertrophic Muscular Atrophy 
(a) The Pseudohypertroptiic Form.—The pseudohypertrophic 
form is more frequent in hoys about two to eight years of age. Pseudo- 
hypertrophic muscular atrophy is usually inherited from the mother, 
though she may not herself be afflicted. 
Symptoms.—The “kettle calves” are characteristic. The gastrocnemii, 
glutei, quadriceps extensor, deltoid, triceps, supra- and infraspinati are 
all prominent and enlarged. The pectoralis major and the latissimus 
dorsi, at times atrophy. Lordosis is a late symptom. Reflexes are either 
abolished or weakened in accordance with the atrophy. With progres- 
sion, while these patients walk fairly well on the level, they find great 
difficulty in going upstairs. One of my cases, a bright lad, was greatly 
disturbed because of his trouble in getting into the study room of his 
school on the second floor. All of these children arise when lying down 
by rolling over onto their hands and knees; the hands are moved to the 
knees and they manage to “climb up their legs.” The waddling gait is 
characteristic and increases with progression of atrophy. In none of these 
cases aye there sensory symptoms. 
Classification.—It is a question whether it is wise to attempt to make 
an absolute differentiation of the various forms of the muscular dys- 
trophies ; the combinations are so frequent that at times this seems im- 
possible. 
Erb considers all the different types as dystrophia muscularis progres- DISEASES OF THE SPINAL COED 
897 
siva and divides his cases into (I) those which occur in childhood, and 
(II) those which occur in youth and early adult life. 
The Muscular Dystrophies of Childhood 
I. Hypertrophic muscular atrophy 
(a) Pseudohypertrophic form 
(b) True hypertrophic form. 
II. Atrophic form 
(a) Duchenne Infantile muscular atrophy (face primarily in- 
volved) 
(b) Without involvement of the face. 
Juvenile and Adult Progressive Muscular Atrophy 
(Dystrophia muscularis progressiva juvenum vel adultorum) 
(Erb’s juvenile form). 
These children rarely live beyond the twenty-third or twenty-fifth 
year. They usually die earlier of pneumonia or other infection. 
(b) True Hypertrophic Form.—Most cases show the combination 
of the pseudohypertrophic with the hypertrophic form, and as the disease 
advances the true hypertrophy yields to atrophy or to fatty changes. 
This type, if its separate consideration is justified, will be found to be 
progressive, and shows the usual family characteristics of all dystrophies. 
2. Atrophic Form 
(a) With Primary Involvement of the Pace (Infantile Form 
of Duchenne)—(b) Without Involvement of the Face. 
These cases are all progressive, entirely uninfluenced by treatment, 
and show the leading features above mentioned, with, in almost all cases, 
the involvement of the shoulder muscles early. 
II. Dystrophia muscularis progressiva juvenum vel adultorum 
(Erb: Juvenile Type) 
This type of muscular atrophy is rare. Its leading characteristics are 
its occurrence early during childhood, involving many groups of muscles 
in weakness and atrophy—the shoulder muscles particularly—the upper 
part of the arm, the pelvic girdle, the thigh and the back. The atrophy 
begins in the arm. The forearm and the leg muscles may escape. In 
these cases there may be pseudohypertrophy, or it may be absent. There 
is no fibrillary twitching. The reaction of degeneration is never found. 
The Erb-Landouzy-Dejerine Type.—The Erb-Landouzy-Dejerine 898 
DISEASES OF THE NERVOUS SYSTEM 
type of progressive muscular atrophy resembles the Erb juvenile atrophy; 
it has so many of the same characteristics that a separate division is hardly 
justified. The chief difference is in the muscles atrophied. This type, 
which is also hereditary, may be juvenile or arise in early adult life; the 
muscles of the face, shoulder and arms are mainly involved. The “myo- 
pathic facies” follows the involvement of the orbicularis oris and other 
facial muscles. The lips are separated, the lower lip abnormally promi- 
nent and the patient seems to “pout.” 
The atrophy begins in the face. Pseudohypertrophy is rare; some 
claim that it does not occur. The underlying cause of both the Erb and 
the Erb-Landouzy-Dejerine type is the same; for in the same family both 
forms may be present. 
Complications of Muscular Dystrophies 
Hysteria, neurasthenia and epilepsy may develop during the progress 
of the disease or may antedate it. 
Idiocy and psychic weakness is occasional. 
Medical literature includes other unusual complications, none of which 
I have met; they are tabes, poliomyelitis, spastic paralysis, scleroderma, 
paroxysmal hemoglobinuria, Little’s disease, and Friedreich’s hereditary 
ataxia. 
The prognosis, so far as life is concerned, depends upon the complica- 
tions and the time of the development of the disease. Respiratory compli- 
cations (pneumonia) are unfavorable, as are also atrophic changes in res- 
piratory muscles. 
Early development is likely to lead to early death. 
The infantile offers a less favorable prognosis for life than does the 
juvenile form of muscular dystrophy. 
Cases which have lived to fifty years and beyond are recorded, as are 
also abortive cases. In some cases the disease may remain limited to the 
facial and shoulder muscles (Erb-Landouzy-Dejerine type), without caus- 
ing serious inconvenience or affecting life. 
The disease may cover periods of four or five decades. 
The development of contractures may limit the usefulness of the indi- 
vidual. 
Extreme lordosis with wide-spread atrophy or pseudohypertrophy are 
among the complications which lead to complete incapacity. 
6. Myatonia congenita 
(Oppenheim’s Disease (1900)—Amyotonia congenita) 
Oppenheim’s disease is a congenital degenerative process in which 
there is atony of the musculature with the flaccidity characteristic of ad- DISEASES OF THE SPINAL CORD 
899 
vanced tabes, making extreme flexion of the limbs possible. The voluntary 
movements are limited, making walking and sitting impossible in the 
fully developed cases. The face is not involved. 
The patella tendon reflexes are abolished. Reaction of degeneration 
is never found. The faradic excitability in the muscles is reduced, the 
strong interrupted current is easily borne. 
Contractures of the lower extremities are developed in some cases. 
Oppenheim has seen twelve cases. 
The disease is unquestionably a myopathy which is rarely influenced 
by treatment though the prognosis is not absolutely bad, for a few cases 
have improved without complete cure. 
Collier and Wilson who have analyzed the recorded cases, report that 
“there is always a slow and progressive amelioration.” 
References 
Collier & Wilson. Brain, 1908. 
Herter. Organic nervous diseases, 1907. 
Jacobsohn. Klinik d. Nervenk. Berlin, 1913, 432. 
Oppenheim. Lehrb. d. Nervenk., 1913, ii, 1678. 
Osier (Sir William). Practice of medicine. Appleton, 1913. 
Unverricht. Quoted by Oppenheim [7. c.\. 
III. Lateral Diseases of the Cord 
1. Primary Lateral Sclerosis 
(Spastic Paraplegia, Spastic Paralysis) 
Primary lateral sclerosis of the cord is an infrequent disease due to a 
symmetrical sclerosis of the pyramidal tracts, which is progressive, taking 
its origin in the connective tissue of these tracts; it is associated with 
more or less degeneration of the included tissue; the nerve tubes degenerate 
completely and often the anterior horns are involved. It is a disease of 
adult life; the age is usually between thirty and fifty; women are affected 
oftener than men. The cause is unknown. 
The disease may attack perfectly healthy individuals, in some a con- 
genital anomaly has been suspected to co-exist. In children spastic para- 
plegia has followed injury to the brain from the use of forceps. 
Course of the Disease.—The progression of the disease is characteristic; 
it is uninfluenced by treatment. In typical cases there are three stages: 
First Stage.—This stage is one of incomplete spastic paralysis in which 
the disease advances, while the patient is able to walk with the aid of 
canes. The reflexes are exaggerated. 900 
DISEASES OF THE NERVOUS SYSTEM 
During the second stage—that of complete spastic paraplegia—there 
is increasing rigidity and the patient becomes bedridden. 
The terminal, or third stage, is one of extension of the morbid proc- 
esses with muscular atrophy, bed sores and cystitis. Intercurrent disease 
is usual. 
The weakness of the legs which involves the flexors of the hips, knees 
and ankles may increase gradually, almost unnoticed during many years. 
At times in its progress it is greater in one leg, but with the advance of 
the disease it affects both extremities. The arms are only rarely affected. 
The other characteristics of primary spastic paraplegia develop as the 
disease progresses and include exaggeration of the knee reflex and ankle 
clonus; the extremities become stiff and unyielding, the gait characteris- 
tic; two canes are required; the tottering from side to side of the ataxic 
is absent; watching the ground is unnecessary; there is no run or trot as 
in paralysis agitans. 
Paresis increases with rigidity. 
Symptoms of Advanced Spastic Paraplegia.—The trio of symptoms 
to which the disease advances are: 
(a) Stiffness or rigidity 
(b) Paresis 
(c) Exalted Reflexes. 
The Babinski symptom is present, also tremor or spasmodic twitching, 
and exaggerated abdominal reflexes. The atrophy of the muscles is due 
to advance to the anterior horns. The Oppenheim symptom is also present. 
Uncomplicated cases show no sensory symptoms nor sphincter weak- 
ness save in exceptional cases; neither is there reaction of degeneration. 
The disease may show stationary periods during any one of its three 
stages. It does not of itself destroy life which may continue from ten 
to forty years, the patient remaining bedridden during most of this time. 
Like all system diseases there is always great tendency to involve other 
systems of the cord, with extension to the brain and peripheral nervous 
system. Anterior and posterior sclerosis are among the most numerous 
of such extensions. 
2. Congenital Lateral Sclerosis 
(Little s Disease) 
Cause of the Disease.—In the majority of cases the disease is due to 
a combination of lateral sclerosis with a cerebral lesion, usually encephali- 
tis (non-suppurative). 
Symptoms.—In almost all cases the symptoms of rigidity are apparent 
shortly after birth, though there are exceptions to this rule. The diagnosis 
may not he made until the child attempts to walk when spasticity of gait 
is characteristic. There is with rigidity some motor weakness. DISEASES OF THE SPINAL CORD 
901 
Patella tendon reflex is exaggerated, ankle clonus may he absent. As 
the symptoms develop fully, the patella is prominently pushed forward 
and the ligament of the patella is elongated. Babinski is present. Sensory 
and sphincter symptoms are absent. In most cases the spastic condition is 
limited to the lower extremities, though the arms are occasionally included. 
Forecast.—The hereditary foundation of almost all cases clearly estab- 
lished, makes the forecast for complete cure unfavorable. 
The diplegic character with the other symptoms of the disease accents 
the cerebral involvement, and also darkens the prognosis in pronounced 
cases. There are cases which are attributed to injuries during labor 
(forceps, pelvic pressure, etc.), and which present, no more favorable 
prognosis so far as restitution of function is concerned than do the others. 
Athetosis, epilepsy, dementia, chorea, speech and ocular defects are 
among the associated conditions, none of which are amenable to treatment. 
The cases are most favorable which at birth or shortly after show but 
limited rigidity without marked paraplegia. Slight paraplegia may not 
advance, and with education and mechanotherapy, improvement may re- 
sult; such children become useful, able to help themselves and learn to 
walk. 
The disease may remain stationary. 
Surgical interference in individual cases has improved function, and 
usefulness of the extremities has followed. 
While the condition may improve materially, there is in the most 
favorable cases a remnant of rigidity which is never entirely overcome. 
3. Combined Lateral and Posterior Disease 
(Ataxic paraplegia) 
Ataxic paraplegia depends upon sclerosis of both the lateral and pos- 
terior columns. In these cases the dorsal columns are mainly involved, 
the lesions in the lateral columns show marked diffusion. Vascular 
changes in the cord are frequent. 
It is questionable whether ataxic paraplegia is ever primary; the cases 
which I have seen disprove that possibility almost completely. There 
are those who believe that some cases rest upon a marked neuropathic 
disposition. 
Associated Diseases.—In the order of frequency 1 have found, from 
experience and literature, the following diseases associated with combined 
posterolateral disease: 
1. Arteriosclerosis 
2. Pernicious anemia 
3. Toxemia 
4. Lead poisoning 902 
DISEASES OF THE NERVOUS SYSTEM 
5. Malarial cachexia 
6. General paresis 
7. Leukemia 
8. Pellagra (My own experience with pellagra is too limited to 
j ustify conclusions ). 
Course of the Disease.—The symptoms of fatigue are soon followed 
by more or less unsteadiness and marked incoordination and the Romberg 
symptom. The patient walks with canes and watches the ground; there is 
less rigidity than in uncomplicated lateral sclerosis—no pain as a rule— 
but with the anemias there are often paresthesias and anesthesias. 
The disease as it advances leads to sphincter paralysis. 
When there are mental symptoms the process is advanced. 
I have recently seen one case of pellagra in which, under treatment, 
the symptoms including marked mental disturbance yielded to treatment. 
The reflexes depend entirely upon the extent and location of the dis- 
seminated lesions. 
With advance of the tabetic element and lesions, there are pupillary 
and optic disturbances which usually persist uninfluenced. 
Forecast.—The symptoms of either spastic spinal paralysis or of ataxia 
may predominate, and the reflexes as above suggested are accordingly 
influenced. 
The primary disease must of necessity influence the prognosis, hence 
in considering the diseases with which ataxic paraplegia is associated, I 
have no encouraging forecast to offer. Grave anemias (bothriocephalus, 
etc.) amenable to treatment, are followed by improvement. These cases 
are rare. 
Duration.—The duration varies. The average case rarely lives be- 
yond two years. The underlying cause will make it possible for the 
clinician to give an approximate opinion of the possible duration in the 
individual case. 
4. Amyotrophic Lateral Sclerosis 
(Charcot's Disease) 
See Anterior Disease' of the Cord. 
5. Erb's Syphilitic Spinal Paralysis 
See Syphilis of the Cord (Chapter on Syphilis). 
6. Secondary Spastic Paraplegia 
Course of the Disease.—With transverse lesions of the cord above the 
lumbar enlargement, motor paralysis is finally complicated with the char- 
acteristic symptoms of spastic paraplegia below the level of the lesion. DISEASES OF THE SPINAL CORD 
903 
Spastic paraplegia in these cases shows increased myotatic irritability, 
exaggerated patella tendon reflex and the presence of ankle clonus. The 
paralyzed legs become rigid and contractures are frequent. In these cases 
there is always secondary degeneration in the pyramidal tract which can- 
not be prevented by any known treatment. 
Causes.—These secondary paraplegias may follow long continued pres- 
sure from injury, tumor, metastases, caries, myelitis, meningitis, hemi- 
plegia, meningeal hemorrhage, or other bilateral cerebral and spinal 
diseases. 
Once established secondary spastic paraplegia remains uninfluenced 
by treatment; the length of the patient’s life depends upon the nature and 
extent of the cause. 
7. Amaurotic Family Idiocy 
(Sachs' Disease) 
Symptoms.—B. Sachs, in 1903, called attention to a form of spastic 
paralysis of distinct family type associated with idiocy, which appears 
usually in the first or second year of life, is limited to Jewish children and 
is progressive. 
The paresis leads to paralysis of the extremities and may finally be- 
come flaccid though rigidity may continue. 
The reflexes are usually exaggerated though they may be decreased or 
abolished. 
The amaurosis is characteristic. At first the blindness is not complete, 
but as the disease advances sight is entirely lost. The change in the mac- 
ula lutea is also characteristic—a red spot is seen with a white patch of 
surrounding atrophy. 
The children show their mental weakness early; the progression to 
complete idiocy is surprisingly rapid. Nystagmus, strabismus and aural 
defects are also found in some cases. 
Death is preceded by marked marasmus. 
The duration of the disease is about two years. The course of the 
disease remains uninfluenced by treatment. 
Cause and Pathology.—The true cause and positive pathology of the 
disease are unknown. Sachs believes that the pathologic changes include 
the primitive type of the cerebral convolutions, macrogyria, degeneration 
of the large pyramidal cells, decrease of the fibers of the white matter, 
and absence of tangential fibers (Osier). On the other hand, Schaffer 
contends that the disease is of postpartum origin, advances because of 
insufficiency and inferiority of the nervous system, that the ganglionic 
cells undergo degenerative changes and exhaustion while there are atrophic 
changes in the cerebrum, in the subcortical ganglia and in the medulla 
oblongata. Sachs collected 27 cases with 17 in six families, all in Jews. 904 
DISEASES OF THE NERVOUS SYSTEM 
References 
Sachs (B.). J. Nerv. Dis. 1903. 
Deutsch. med. Wchnschr., 1903. 
Schaffer. Neurol. Zentralbl., 1904 1905. 
J. f. Psych, u. Neurol., Bd. VI. 
IV. Indiscriminate Lesions of the Spinal Cord 
1. Myelitis 
Myelitis is an inflammation of the cord characterized by either focal 
or disseminated lesions leading to softening, with associated secondary 
changes usually including destruction of the substance of the cord after a 
stage of hyperemia in which the elements are replaced by oil globules. 
The ganglionic cells are usually vacuolated, and show evidences of far- 
reaching degeneration. 
The course of the disease is materially influenced by its cause, the 
mode of onset and its distribution. 
Classification.—When the lesions are limited to the gray matter it 
may be characterized as central myelitis or poliomyelitis. This may be 
either acute or chronic and is separately considered among the infectious 
diseases (See Poliomyelitis). 
When the gray and white matter are involved, it is a diffuse or general 
myelitis; a number of foci are found in different parts of the cord. This 
diffuse disease is often of syphilitic origin, or it may accompany other 
acute infections. 
Transverse myelitis is synonymous with compression myelitis and de- 
pends upon compression (accident usually) following fracture of the 
spinal column, caries of the spine (tuberculosis), tumor—either primary 
or secondary—usually metastases to the membranes and vertebrae. These 
cases are not in reality true myelitis, but by common consent have con- 
tinued to be considered in the same chapter. 
Unilateral myelitis gives rise to the Brown-Sequard symptom com- 
plex; it may follow accident, tumor compression or disease of the sub- 
stance of the cord. 
In Bulbar myelitis the disease, either early or late, invades the me- 
dulla, causes the usual “bulbar symptoms” and leads to death in almost 
all cases. 
When the process is limited to a single small area in the cord it is 
known as “focal myelitis.” 
All of these forms of so-called myelitis are either (a) acute or (b) 
chronic and for purposes of prognosis as well as diagnosis I will so 
consider them. DISEASES OF THE SPINAL CORD 
905 
(a) Acute Myelitis 
The majority of cases of acute myelitis are of secondary origin and are 
associated with the infections. Among these are typhoid fever, influenza, 
erysipelas, gonorrhea, smallpox, pneumonia, tonsillitis, measles, cholera, 
diphtheria, dysentery, whooping cough and syphilis. 
Traumatism including fractures and dislocations, alcoholism and com- 
pression with meningitis may also cause the disease. 
Primary Causes.—Primary causes of acute myelitis include exposure 
to cold. It is questionable whether exposure to cold without added infec- 
tion is ever a cause of myelitis. Sexual excesses do not cause myelitis 
when uncomplicated. 
Prognosis.—The prognosis of all forms of acute myelitis depends upon 
the extent and cause of the disease. All cases of acute myelitis present a 
grave prognosis. 
Traumatism (fractures and dislocations) causing transverse myelitis 
by compression, leading to paraplegia (sensory and motor paralysis), blad- 
der and rectal symptoms, as well as trophic changes, including bed sores 
(decubitus), offer an unfavorable forecast. The higher the lesion, the 
more acute the course, the greater are the dangers to life. 
Early symptoms of sepsis are always unfavorable, the condition leads 
to overwhelming toxemia from which the patient rarely rallies; if he does, 
it is to fall into a subacute or chronic stage in which cystitis, bed sores, 
and overwhelming systemic infection lead to exhaustion, increasing stupor 
and death. 
The more extensive the paralyses, the graver the prognosis. The acute 
and suddenly arising paraplegias when not due to continuous compression 
but true myelitis, often offer a fair prognosis. 
Patients with bladder and rectal paralysis rarely recover unless the 
cause is promptly removed. 
Compression or disorganization sufficient to cause sphincter symptoms 
with or without decubitus, which persist during several days or weeks, 
lead to changes which are not likely to disappear completely under any 
treatment, however radical. 
With the removal of the cause, after irreparable degenerative change 
in the cord substance which makes return of function impossible, patients 
may fall into a chronic stage, in which with care, life may be prolonged 
during long periods; the symptoms depend on the location and extent of 
the primary lesion. 
Decubitus (bed sore) is always an evidence of either neglect or of 
serious and destructive myelitis. The accompanying sepsis drains the 
vitality of the patient; if under these conditions life is prolonged, he 
grows more and more anemic, shows the evidences of chronic sepsis or 
pyemia. In the terminal stage the sensorium is involved and the patient 906 
DISEASES OF THE HEKVOUS SYSTEM 
dies with all of the symptoms of profound toxemia. The earlier the bed 
sore appears, the less favorable is the prognosis. 
When the lumbar cord is involved the patella tendon reflex is 
abolished; also the skin reflex; the anesthesia corresponds with the extent 
and location of the pressure. Bladder and rectal symptoms are also per- 
sistent. 
With cervical myelitis dependent upon infection or persisting pressure 
from whatever cause, if the patient lives, atrophy with paralysis of the 
arms develops, also spastic paralysis of the legs with anesthesia of the 
body below the lesion, and in some cases pupillary changes. In these 
cases the development of symptoms is often sudden and with respiratory 
and heart paralysis (vagus) including tachycardia and dyspnea, death 
promptly follows. 
With cervical myelitis, pneumonia, bronchitis, cystitis and bed sores 
are the most frequent causes of death. 
There are occasional cases of acute myelitis in which the symptom com- 
plex is not complete but sufficient to justify the diagnosis, the cause re- 
mains unrecognized; these cases may recover under treatment and rest. 
It may be that in some of these there is a syphilitic fundament. 
With acute infection, or in cases in which the cause remains unrecog- 
nized, the onset of the disease may occasionally be sudden, the symptoms 
develop rapidly and death may follow before the end of the fifth, at times 
the seventh, day. 
These cases are often of the diffuse type. Motor paralysis is prompt 
and ascending, resembling Landry’s disease; this type of the disease is 
associated with high fever. 
In all forms of myelitis irregular and intermittent fever is likely to 
depend upon complications, usually decubitus, cystitis, pyelitis or pyelo- 
nephritis. 
Transverse myelitis from whatever cause offers an unfavorable prog- 
nosis; the majority of these patients die of sepsis with bed sores, cystitis 
and anemia after varying periods of fever and other constitutional symp- 
toms. The more favorable cases of acute myelitis are those due to the 
infectious diseases. 
Oppenheim claims that of these, cases secondary to gonorrhea offer the 
more favorable prognosis. When the gonorrheal cases are complicated by 
endocarditis the prognosis is bad. 
Foudroyant cases (acute hemorrhagic myelitis) with acute infections 
(typhoid fever, erysipelas and smallpox) lead to death within a few 
days. 
Acute syphilitic myelitis recognized early and promptly treated offers 
a fair prognosis (See Syphilis, Spinal Complications). 
When the symptoms of myelitis develop gradually and there is no 
recession of these, the prognosis is less favorable than in those cases in 907 
DISEASES OF THE SPINAL CORD 
which there is sudden development of incomplete symptoms after a short 
prodromal period. 
Neither blood examination nor the withdrawn cerebrospinal fluid offer 
any data of value for prognosis. 
(b) Chronic Myelitis 
Causes.—Most forms of chronic myelitis are of syphilitic origin, and 
are separately considered (See Syphilis of the Cord). There are chronic 
cases which develop from the acute, to which reference has been made in 
the preceding paragraphs. 
Chronic myelitis which develops independently of other disease is so 
rare as to justify a strong doubt of the possibility of its existence. Most 
cases which are diagnosticated as chronic myelitis are due either to com- 
pression myelitis, i. e., tumor, multiple sclerosis or spinal syphilis. 
Associated Diseases.—There are cases of chronic lead ‘poisoning asso- 
ciated with symptoms of myelitis in which conditions remain unchanged 
during long periods. 
Naturally the prognosis is unfavorable in those cases of chronic spinal 
meningitis with chronic myelitis, caries of the spine, new growths and 
aneurism. 
Compression myelitis due to metastases to the spine secondary to 
cancer of the breast, stomach, intestines, uterus or other organs, runs a 
chronic course; it is among the most painful of all affections and leads to 
death with characteristic cachexia and exhaustion. These cases are not 
infrequent and at times are an early complication of breast or stomach 
cancer. 
Myelitis which develops during pregnancy may yield to treatment. 
Some of these cases relapse and create the strong suspicion of multiple 
sclerosis. With the history of chronicity the chances of the recovery of 
such cases are small. 
In some cases of subacute myelitis developing from the acute form 
of the disease, several weeks or months may lapse before the symptom com- 
plex is complete. 
Death is the fate of most myelitics with symptoms of sepsis or pyemia, 
bed sores and cystitis, though there are a good number of cases recorded 
in which disseminated myelitis led to recovery. 
Long periods of latency in chronic cases are not infrequent. 
Cases of multiple neuritis which are associated with symptoms of mye- 
litis occasionally recover. 
In both acute and chronic myelitis the general condition of the patient 
and possible complications are powerful factors in prognosis. 
The aged and enfeebled offer a uniformly bad prognosis. 908 
DISEASES OF THE HERVOUS SYSTEM 
Reference 
Oppenheim,. Lehrb. d. Nervenk., Berlin, 1913. 
2. Multiple Sclerosis of the Brain and Spinal Cord 
(.Disseminated Nodular Sclerosis, Sclerosis en Placques) 
Characterization.—Multiple sclerosis of the brain and spinal cord is 
as a rule a chronic progressive disseminated disease of uncertain origin, 
characterized by the development of numerous indiscriminately located 
sclerotic nodules, easily recognized by the unaided eye. The process is 
degenerative and productive. 
The disease presents the anatomic characteristics of chronic interstitial 
myelitis. 
The nodules or placques are of a gray color, translucent, resistant and 
hard. 
Course of the Disease.—When the disease is fully developed the 
“islands” are scattered throughout the cord and brain, and the peripheral 
nerves may also show “sclerosis.” The placques or nodules are distinctly 
outlined and microscopically the neuroglia is found reticulated and 
fibrillated. 
In the brain, the seats of predilection are the pons, the centrum ovale, 
the walls of the lateral ventricles, the corpus callosum, the gray matter of 
the central ganglia and the cortex. The cord is involved at various levels. 
The medulla oblongata often escapes. In the cord, the pyramidal tract 
is the favorite seat of sclerosis (white fibers) but as Charcot pointed out 
years ago, large numbers of axis cylinders escape, thus preventing com- 
plete paralysis. 
Secondary degeneration is rarely present—never extensive. 
With the advance of the disease, the vessel walls are thickened but the 
placques show no tendency to contract. There is, according to Striimpell, 
a marked similarity to central gliosis and he considers the process one of 
“gliomatous degeneration.” The possibility of regeneration of the axis 
cylinder accounts for the improvement in some cases after varying periods. 
Age.—The majority of my cases were found between the ages of 
20 and 30 (rarely after 45). The sexes are equally affected. I have 
seen no case occurring during early childhood. Oppenheim demonstrated 
the presence of congenital stigmata in the few cases in early life which he 
has seen, and Eichhorst reports a child 8 months of age with marked 
sclerosis en placques in which the mother was also suffering from the 
disease. 
It may be safely assumed that when the disease is found fully 
developed between the tenth and fifteenth year of life that it has already 
existed during a number of years. In such cases the advance is always so DISEASES OF THE SPINAL CORD 
909 
slow as to remain almost unnoticed until the leading features of the fully 
developed disseminated deposits are characteristic. 
Cause.—The cause of multiple sclerosis is uncertain. The majority 
of my cases have followed acute and grave infections; of these typhoid 
fever was the most frequent. Among the remaining infections which 
have preceded multiple sclerosis are diphtheria, influenza, smallpox, scar- 
let fever, measles and malaria. Syphilis is not considered to he a frequent 
cause of multiple sclerosis. 
Spiller and Woods (quoted by Oppenheim) have reported a number of 
cases which they believe rest upon a syphilitic fundament. Most authori- 
ties deny the association of syphilis as a causative factor. 
There are a number of cases in medical literature which followed 
childbirth. 
Striimpell believes that traumatism is a comparatively frequent cause 
of the disease and calls attention to the importance of this fact in “acci- 
dent practice.” I have never in my experience seen a single case of 
multiple sclerosis after injury of any hind. 
In the large majority of insular scleroses the cause remains unrecog- 
nized. 
Whatever the cause in the individual case, it may be safely concluded 
that it does not materially influence the forecast of the fully developed 
disease. 
The disease is more frequent in England than on the Continent of 
Europe, where it is oftener found than in the United States. Unques- 
tionably many of the atypical types (“formes frustes”) have been incor- 
rectly diagnosticated in our country. The more thorough knowledge of 
the clinical history of these cases and the better knowledge of its pathology 
are already leading to more frequent and correct diagnosis. 
Symptoms.—The leading features of the disease—intentions tremor, 
muscular rigidity, nystagmus, exaggerated tendon reflexes (Babinski phe- 
nomenon), scanning speech, vertigo, often optic neuritis, spastic and 
paretic gait, final muscular weakness—once established, usually remain, 
and while there may be periods of latency and at times apparent recessions, 
the lesions which cause the symptoms are not often overcome. 
I have never seen disappearance of symptoms in typical cases in which 
with loss of abdominal and cremaster reflexes there was nystagmus, scan- 
ning speech, and exalted knee reflex. 
The typical symptoms above mentioned may follow a complex referable 
to the optic nerve with nystagmus and but slight change in speech after 
months or years. After these periods of latency the onward march is 
usually continuous but slow. 
Optic neuritis is only partial as a rule and rarely leads to complete 
optic atrophy. In most of my cases optic change was among the early 
lesions ; it may precede by a number of years most of the other usual 910 
DISEASES OF THE NERVOUS SYSTEM 
symptoms, as Frank and Windmuller have also demonstrated. There is 
in occasional cases marked improvement of the ocular symptoms or periods 
of latency or remission. 
Uhthoff and many observers have called attention to the frequency of 
extreme pallor of the temporal half of the optic disk in fully developed 
multiple sclerosis. The prognosis so far as sight is concerned in these 
cases is not bad, for complete blindness as a complication is exceedingly 
rare and the anemia may persist without causing subjective symptoms. 
In some cases there is contraction of the visual field, and in occasional 
cases blindness of one eye has continued during varying periods, after 
which it disappeared. The pupillary changes rarely lead to loss of the 
light reflex. 
Multiple sclerosis in which the early symptoms are referable to the 
eye progress slowly, are likely to have long periods of latency, and are 
among the most chronic of all cases—at times the history includes several 
decades of symptoms. 
Papillitis is often evanescent in the midst of other symptoms of insular 
sclerosis. 
There are cases which begin with marked ataxia, are associated with 
ocular symptoms and are also exceedingly chronic. 
The bulbar or bulbopontine complex may characterize some cases early 
and lead to erroneous diagnosis and prognosis, or after years of typical 
symptoms bulbar lesions develop and lead to death. 
Scanning speech may persist during years in the presence of other 
evidences of sclerosis without influencing the course of the disease. Scan- 
ning speech, which is slow and decided with marked spastic paraplegia, 
nystagmus, intentions tremor and optic neuritis, is evidence of advanced 
and far-reaching dissemination and in most cases there is no decided 
improvement of any of the symptoms, though the diseases may remain 
stationary during long periods without threatening life. 
There are cases in which apoplectiform seizures occur, and after a few 
hours or days the associated hemiplegia gradually disappears. These 
apoplectiform attacks are often associated with hyperpyrexia, rapid pulse, 
and respiratory symptoms. Rapid progression of the disease often follows 
the attack. 
Once developed, epileptiform attacks are likely to recur; these are not 
often true epilepsy, though the latter may in rare cases complicate mul- 
tiple sclerosis. No treatment influences the explosive seizures. 
Staggering, headache and vertigo are persistent and often prove a 
serious handicap (cerebellar type). 
When the disease advances to the stage in which there are evidences of 
mental deterioration, improvement is not to he expected. 
Impulsive laughing and crying have in my experience been associated 
with the more advanced cases in which the mental state is more or less DISEASES OF THE SPINAL CORD 
911 
disturbed, or in those with hysterical tendencies—cases which are pro- 
gressive as a rule. 
Paralysis of ocular muscles occasionally disappears; as a rule it is 
persistent. 
There are a number of cases recorded in which ophthalmoplegia which 
is not a frequent complication, disappeared (Oppenheim). 
Diagnosis and Prognosis.—The behavior of the cutaneous reflexes in 
contradistinction to the tendon reflexes is of great importance for diagnosis 
and prognosis. 
The cutaneous reflexes are usually markedly reduced, and the absence 
of the abdominal and cremaster reflexes is one of the early and most impor- 
tant features of the disease to which Striimpell and E. Muller have called 
attention (Striimpell and Oppenheim). 
When with suspicious symptoms of incipient insular sclerosis the ab- 
dominal reflex is abolished, the diagnosis may be made with great certainty 
and the prognosis accordingly given. 
Persisting incontinence of urine and rectal disturbances are evidences 
of advanced sclerosis. Transitory sphincter symptoms are not unusual 
during the early stage of the disease and are not of serious importance. 
Lumbar puncture offers no data for prognosis. In a few cases globulin 
(Eonne reaction, Phase 1) will be found, and lymphocytosis is not unusual. 
In framing the diagnosis and prognosis of multiple sclerosis, cautious 
inquiry into the history of cases with fully developed symptoms which 
may appear to have been developed within a limited period, will prove 
that the disease has in reality existed during several years; that it is insidi- 
ous and as a rule, there are periods of latency, often of remission. 
The partial motor insufficiencies of the early stage of multiple sclerosis, 
marked weakness in some cases, disappear as a rule, and do not influence 
the prognosis materially. 
It should be remembered that temporary improvement, remission, re- 
peated relapse and chronicity are characteristic of the disease. 
The increase of symptoms in cycles, in a measure, accounts for the 
duration. 
Only rarely does the disease progress to a fatal termination rapidly; 
such progression as already mentioned, is most likely to follow apoplecti- 
form attacks. 
Death may occur early in the exceptional cases in which the medulla 
oblongata is invaded or it may promptly follow in chronic cases when such 
complication is added. 
; Bramwell reports four cases of multiple sclerosis which recovered; 
Maas also believes that recovery is among the possibilities; Oppenheim 
reports a cure after facial erysipelas, while Charcot and Marie many years 
ago insisted that the prognosis was not absolutely unfavorable in all cases. 
Atypical Types of Multiple Sclerosis.—Atypical types of mul- 912 
DISEASES OF THE NERVOUS SYSTEM 
tiple sclerosis are numerous; each offers features which materially in- 
fluence prognosis. 
There are cases which are latent during long periods in which the 
clinical features are so incomplete as to remain unrecognized in which 
apoplectiform seizures arise suddenly, are followed by remission, later by 
epileptiform attacks and early death. In these cases the lesions of the 
fully developed disease are found post mortem. 
Cases ivith symptoms of spastic spinal paralysis are as a rule chronic 
and are likely to be complicated by optic atrophy, but do not often lead to 
blindness. 
Spinal hemiparesis (Oppenheim) and cerebral hemiplegia of sclerotic 
origin may develop slowly; tremor persists in one-half of the body. These 
cases run a protracted course. 
I have already mentioned in preceding paragraphs of this chapter 
the course of the disease with bulbar involvement. The rare cases of 
acute and promptly fatal insular sclerosis are likely to be of this type when 
not apoplectiform. 
There are cases of multiple sclerosis which closely resemble transverse 
myelitis. In these cases there are cerebral lesions so limited as to cause 
but few symptoms. These cases also run a chronic course, usually show 
ocular changes but are not completely incapacitated until the late stage of 
the disease. 
Cases with ataxic symptoms in the ascendency in which there are loss 
of patella tendon reflex, sensory disturbances, including crises and the 
Argyll-llobertson pupil, include besides the usual lesions of multiple scle- 
rosis, degeneration of the posterior columns. These case progress slowly 
and finally lead to a paralytic stage in which bed sores, cystitis and sepsis 
precede death. In the sacral type, bladder incontinence is present early; 
there is flaccid paralysis of the lower extremities and loss of patella tendon 
reflex. These cases progress slowly. 
The majority of atypical cases are progressive though stationary pe- 
riods and remissions with improvement of individual symptoms are 
frequent. 
Whatever the type of multiple sclerosis, the disease justifies only the 
gravest prognosis in spite of the few cases mentioned in which recovery is 
supposed to have been complete. The fate of the sclerotic if he does not 
yield to intercurrent disease is chronic invalidism which includes months 
and years during which he is bedridden with many complications, includ- 
ing urinary incontinence, cystitis, bed sores, and often mental lethargy. 
Great caution in prognosis is necessary because of the long periods of 
latency and remissions which characterize the disease, and which may lead 
the enthusiastic and inexperienced to favorable but wrong conclusions. 
The favorable forecast concerning sight mentioned in this chapter is 
justified, for in a long experience, blindness has never complicated my 
cases. DISEASES OF THE SPINAL CORD 
913 
It is not uncommon to find cases which have lived over twenty years, 
and I number among my material one man who lived forty years with 
well marked symptoms of the disease, incapacitated during thirty years— 
over twenty years of which he was practically helpless in bed or in a roller 
chair. He died of pneumonia. 
Complications.—Most cases of insular sclerosis yield to complica- 
tions. 
Pneumonia is a frequent cause of death, particularly during the last 
stage of the disease. 
Septic and pyemic conditions are provoked by bed sores, cystitis, pyelo- 
nephritis and other complications; there may be weeks of symptoms be- 
fore death; rarely does septicemia end acutely. 
Locomotor ataxia, paralysis agitans, epilepsy and syringomyelia have 
occasionally developed. 
Tuberculosis kills a small proportion of multiple sclerotics. 
3. Pseudomultiple Sclerosis 
(W estphal-Strumpell) 
Westphal and Striimpell have reported cases which lead to death, 
with many of the symptoms of multiple sclerosis but without character- 
istic discoverable lesions, in which the diagnosis is exceedingly difficult 
and which are known as pseudomultiple sclerosis. 
Symptoms.—The leading features are the early development of psy- 
chic disturbances, violent emotions, outbursts of anger and maniacal 
attacks with the persistence of oscillatory tremor, rigidity of facial ex- 
pression without ataxia, but with persistence of the deep reflexes and 
spasticity. The optic nerve is not involved. 
For prognosis and diagnosis the early appearance of dementia with 
other symptoms of multiple sclerosis and the slow oscillatory tremor will 
prove valuable, besides the fact that the tremor, in contradistinction ta 
the intentions tremor of multiple sclerosis persists during repose. ISTystag 
mus does not develop. 
For the thorough study of the clinical features of pseudosclerosis, the 
reader is referred to the papers of Westphal and Striimpell, to which 
reference is here made and to the literature which is included in Oppen- 
heim’s treatment of the subject. 
References 
Bramwell. Rev. of Neurol. & Psych., 1905. 
Frank. Ztschr. f. Neurol., 1899, xiv. 
Maas. Berl. klin. Wchnschr., 1907. 
Oppenheim. Berl. klin. Wchnschr., 1887. 
Lehrb. d. Nervenk., Bd. i, 447. 914 
DISEASES OF THE YEKVOUS SYSTEM 
Striimpell. Ztschr. f. Neurol., Ed. xii. 
Textbook of medicine. Appleton, 1911, ii. 
Spiller & Woods. Quoted by Oppenheim. 
Uhthoff. Quoted by Striimpell. 
We8tphal. Arch. f. Psych., Bd. xiv. 
Windmuller. Ztschr. f. Neurol., Bd. xxxix. 
4. Abscess of the Spinal Cord 
Abscess of the spinal cord occasionally develops; it is always secon- 
dary to coexisting lesions which are usually due to traumatism or infec- 
tion. It is therefore metastatic as a rule. 
Associated Symptoms.—The cases recorded have followed distant pus 
deposits in the prostate, purulent cystitis and bronchitis, gonorrhea, and 
purulent meningitis, and have led to a fatal termination with all of the 
symptoms of meningitis, which usually preceded paralyses, motor and 
sensory, and trophic disturbances (bed sores). 
Course of the Disease.—The rapid advance of the disease after the 
initial symptoms of spinal meningitis is characteristic; the paraplegia 
is promptly developed with the other features of indiscriminate disease 
of the cord including in some cases ascending symptoms, anesthesias and 
sphincter involvement. 
The blood picture of the associated infection and cultural methods 
aid in diagnosis and prognosis. 
The disease, as a rule, runs an acute course, terminating in death 
within the first seven days. Only rarely is the course of the disease 
protracted after the metastases to the cord, though such a history is not 
impossible. 
5. Syringomyelia 
(Gliosis of the Spinal Cord) 
Symptoms.—Syringomyelia is characterized by the formation of ab- 
normal cavities in the spinal cord, often of congenital origin, either a 
dilatation of the central canal of the cord (hydromyelus) or central gliosis 
and the secondary formation of cavities—true syringomyelia. 
Schlesinger, whose article should be consulted for full clinical data, 
found that the majority of cases are exceedingly chronic, usually begin 
before the thirtieth year, and after that men suffer three times as often 
as women. 
While the majority of cases rest upon a congenital basis, there are 
evidences which justify the conclusion that traumatism in the predisposed 
may prove an exciting factor. 
Slight congenital (hydromyelus) dilatations of the central canal are 
often found post mortem without having caused symptoms during life. DISEASES OF THE SPINAL CORD 
915 
Congenital hydromyelus may follow the faulty closure of one of the 
divisions of the central canal of the cord (,Herter). 
In true syringomyelia there is a “disintegration of gliomatous forma- 
tion which usualy originates in embryonal tissue about the central canal.” 
Pressure from tumors may cause hydromyelus and offers data for 
diagnosis and prognosis. 
Classification.—True syringomyelia may cause dilatations in any part 
of the cord besides the central canal, in one or both anterior or posterior 
gray horns, by predilection in the cervical spine. It should be considered 
of congenital and neoplastic origin with subsequent disorganization of the 
new tissue, more particularly in the gray matter of the cord and the con- 
secutive formation of cavities. 
The disease does not lead to lesions of the peripheral nerves except 
in rare instances. Oppenheim reports such involvement but says that it 
is of no importance for symptomatology, hence of no prognostic value. 
The course of syringomyelia is slowly progressive and characteristic. 
There is a trio of typical symptoms which deserves consideration: 
1. Muscular atrophy 
2. Sensory disturbances 
3. Trophic symptoms. 
1. Musculae Atrophy.—When there are symptoms of muscular 
atrophy showing involvement of the cervical spine of the Aran-Duchenne 
type of progressive muscular atrophy with fibrillary contraction and 
reaction of degeneration, there are usually sensory symptoms as -well. 
The triceps reflex is soon lost, the progression to the muscles of the face 
and lower extremities is not usual. The atrophy may remain unchanged 
during long periods and the reaction of degeneration may be limited to 
single muscles or parts of the larger muscles during indefinite periods. 
The reaction of degeneration is not always present. 
With the advance of the process and involvement of the ciliospinal 
center, myosis, ptosis and enophthalmus may develop, while one-sided 
atrophy of the tongue, facial paresis and partial pneumogastric paralysis 
may also complicate some cases—all depending upon the location and 
extent of the gliosis. 
Unilateral paralysis of the vocal cords, demonstrated by laryngoscopic 
examination will often prove of great diagnostic avid prognostic value. 
2. Sensory Disturbances.—Sensory symptoms of syringomyelia 
are characteristic; once present they persist and remain uninfluenced by 
treatment. 
Among the earliest symptoms are often complete or partial loss of 
sensation of heat, cold, and analgesia (loss of the pain sense) without 
interference with the tactile sense. The last case included in my mate- 
rial covered a history of over three decades, during which these sensory 916 
DISEASES OF THE NERVOUS SYSTEM 
symptoms persisted and in which acromegaly with other complications 
developed without marked muscular atrophy but with the Morvan syn- 
drome (Eisner). 
In these cases it is often possible for patients to continue at occupa- 
tions in which they are protected from injuries due to burns and other 
wounds. 
The dissociated sensory disturbance depends upon the seat of the 
atrophy. With sensory symptoms of the face there is usually atrophy. 
As a rule atrophy and the characteristic sensory disturbances are co- 
existent. 
Tactile anesthesia, disturbance of the muscle and the pressure senses 
are evidences of advanced disease. These sensory disturbances are never 
early manifestations of syringomyelia; they are usually absent through- 
out the disease, and when present denote advance to the white posterior 
columns. 
3. Teopiiic Symptoms.—Morvan s disease, to which I have referred 
in connection with the sensory disturbances, is a variety of syringomyelia 
in which trophic changes are in the ascendency, including recurring whit- 
lows, often multiple, with muscular atrophy, analgesia and paresis. Both 
upper and lower extremities may be involved. The prognosis of these 
cases is unfavorable, the course chronic. 
There are cases of syringomyelia in which trophic symptoms are 
prominent from the beginning, and continue so throughout the entire 
course of the disease. 
Necrobiotic processes and vesicles are often recurrent. Ulcerative 
destruction does not, as a rule, repair easily. Repeated injury, burns 
and other wounds of tissues without normal resistance or vitality, open 
avenues for infection; in some cases there are almost continuous 
surface lesions. Perforating ulcers may lead to deep destruction of 
tissue. 
Trophic disturbances of the nails, overgrowths of the shin, edematous 
swellings and bone lesions remain uninfluenced; they are likely to in- 
crease or become multiple. 
I have seen several cases with Raynaud's symmetrical gangrene en- 
tirely uninfluenced by treatment. 
The anomalies of perspiration, anidrosis, hyperidrosis, hemidrosis 
may develop early or late. 
The cardinal symptoms and course of the disease are easily under- 
stood if we associate the analgesia and thermanesthesia with changes in 
the posterior horns, the muscular atrophy with the anterior horns, the 
trophic vasomotor disturbance with the gray matter and the spastic paral- 
ysis with the lateral columns. Tabetic ataxic symptoms with tactile dis- 
turbance show involvement of the posterior column. 
Spontaneous fracture and dislocations, also arthropathies, are trophic DISEASES OF THE SPIRAL CORD 
917 
changes of the advance stages of the disease. The latter complicate from 
8 to 12 per cent of all cases. 
Spmal curvature frequently develops; it is also found in the younger 
subjects; it develops gradually in adults and in the advanced stage leads 
to marked deformity. 
The atrophy and paresis of the spinal muscles, often one-sided, is a 
cause of scoliosis, but as Striimpell says, does not explain all cases; the 
unexplained, he says, are “an expression of the abnormal conditions of 
development and growth in the vicinity of the spinal cord.” 
Cases which develop bulbar symptoms are usually associated with 
hemiatrophy of the tongue and are often complicated by pneumonia or 
other acute infections, which shorten the duration materially, or the pro- 
gression may be rapid after the beginning of the central invasion. Bulbar 
symptoms may develop suddenly after years of chronicity. 
Diabetes mellitus developing in young subjects with syringomyelia 
leads to prompt emaciation and death, with symptoms of acidosis. Such 
cases are but little influenced by diet or other treatment. 
Syringomyelia occasionally complicates cervical hyper,trophic pachy- 
meningitis (Oppenheim, Holmes-Kennedy, Phillipe-Oberthiir). The 
course of these cases is exceedingly chronic. In the later stages the lower 
extremities are involved; the patient becomes bedridden, with in the end, 
most of the complications of the typical cases including cystitis, bedsores 
and sepsis. 
Tabes dorsalis and paresis may be complicated by syringomyelia with 
optic atrophy and the Argyll-Robertson pupil. 
Pseudotabetic gliosis described by Oppenheim is progressive and de- 
notes posterior invasion resembling, in its symptomatology, true locomotor 
ataxia. As the disease advances there are evidences in symptoms of 
dissemination of the process in various parts of the cord. 
Psychic disturbances are not among the early symptoms; when pres- 
ent they complicate the terminal stage. 
Caries of the spine when complicating syringomyelia leads to a febrile 
state in some cases with rapid pulse and evidences of toxemia, besides 
the usual trio of symptoms due to indiscriminate disease of the cord. 
The development of keloid tissue, ankylosis of small joints, Dupytren 
contractures and necrosis of bone—usually of the terminal phalanges of 
the fingers—do not as a rule influence the prognosis materially so far as 
life is concerned. 
The addition of symptoms referable to the lower extremities, spastic 
paraplegia with cystitis or rectal disturbances denotes far reaching 
gliosis and is unfavorable. In some cases associated with spastic condi- 
tions early (amyotrophic disease), sensation may remain normal during 
many years. 
While syringomyelia is a disease which may continue with but slight 918 
DISEASES OP THE NERVOUS SYSTEM 
progression during long years, it remains uninfluenced by treatment. It 
is a disease which, as already suggested, is dependent upon congenital 
anomalies which lead to early and often unrecognized symptoms, making 
the duration of the disease one of the longest of all diseases of the central 
nervous system. In one of my cases the history covers almost fifty years 
and the patient is still alive. 
The average duration is between fifteen and twenty years. With 
bulbar invasion it is considerably shorter. 
As a rule death is not directly due to the disease but to some 
complication. 
Cystitis, bed sores, pyelonephritis, sepsis following burns and injuries, 
pneumonia and occasionally tuberculosis, are among the more direct 
causes of death. 
The clinician is not to be deluded by apparent remissions and periods 
of latency, for it will be found that once established the disease remains 
and ultimately leads to death, either directly or indirectly. 
It is often surprising to note how long many of these patients are 
able to continue their occupations with clear minds. 
The association of syringomyelia with acromegaly is usually accom- 
panied with great mental depression. In one of my cases there was 
strong suicidal tendency. 
References 
Eisner (Henry L.). Am. J. Med. Sc., May, 1914. 
Herter, etc. Diagnosis of the organic diseases of the cord. New York, 1907. 
Oppenheim. Lehrb. d. Nervenk., 1913, i. 
Charite Ann., 1886. Also Arch. f. Psych., xxv. 
Phillipe-Oberthiir. Rev. Neurol., 1900. 
Schlesinger. Die Syringomyelia. Wien, 1902. 2 Aufl. 
Striimpell. Textbook of medicine. New York, 1913. 
6. Tumors of the Spinal Cord 
Tumors of the spinal cord, with the exception of gumma, are unin- 
fluenced by medical treatment. Unless treated surgically the prognosis 
is absolutely had. 
Primary growths of the cord are comparatively speaking, exceedingly 
rare. Pathologic evidence argues against the occurrence of intravertebral 
growths of primary origin, and in favor of the preponderance of sec- 
ondary deposits which are either extramedullary or intramedullary. 
Classification.—The classification of Bruns divides the growths of the 
cord into: (I) extramedullary tumors: growths which originate in tissues 
around the cord and invade its substance secondarily by growth with 
extension; and (II) intramedullary growths: growths which originate in DISEASES OF THE SPFNAL COED 
919 
the substance of the cord; these are oftener primary than are the extra- 
medullary tumors. 
I. Extramedullary Tumors 
(a) Vertebral tumors. These originate in the vertebrae or in the 
surrounding soft tissues. 
(b) Intravertebral tumors. These growths originate in the spinal 
membrane, and they may be either (1) Extradural or (2) intradural. 
Extradural tumors originate in the periosteum of the vertebral canal, 
the external surface of the dura, or in the extradural tissue (fat, etc.). 
Intradural tumors originate from the inner surface of the dura, the 
arachnoid, the ligamentum denticulatum, the nerve roots or the pia mater. 
II. Intramedullary Tumors 
Growths which originate in the substance of the cord—in the medul- 
lary substance—are intramedullary. 
7. Extramedullary Tumors 
The majority of spinal growths are intravertebral—either extra- or 
intradural, oftener extradural. Jacobsohn reports the proportion of 
extra- to intramedullary spinal growths as 3:1. Further he reports 6 
cases of spinal tumors in 9,626 cases of diseases of the nervous system 
treated at the Moabit Hospital in ten years. 
Schlesinger reports 147 tumors of the cord in 35,000 autopsies. In 
151 tumors of the brain and cord of 6,540 tumors, Starr found brain 
tumors thirteen times more frequent than those of the cord. 
In 5,115 cases of internal diseases I found 9 spinal tumors. 
“Metastasis in the central nervous system secondary to carcinoma 
elsewhere in the body may assume many forms. It may occur as a mul- 
tiple carcinomatosis which may or may not be a part of a general car- 
cinomatous process elsewhere.” 
“There may be only a few cancer nodules within the central nervous 
system, or the process may involve the brain or cord and the meninges 
extensively, or the meninges alone. The meningeal infiltration may be 
either diffuse, as a carcinomatous meningitis, like the sarcomatous 
meningitis, or may be in the form of multiple tumors. Metastasis to 
the substance of the cord is exceedingly rare and is nearly always from 
the periphery of the cord. Metastasis to the vertebrae is most common” 
(Spiller and Weisenberg). 
The metastases of the cord and spine which interest the internist 
most are due to cancer of the breast, stomach, and intestines. 
The study of the relative frequency of metastasis to the spine from 920 
DISEASES OF THE NERVOUS SYSTEM 
breast and stomach cancer proves the former to be twice as frequent as 
the latter. 
Schlesinger’s statistics are conclusive on this point. Thus, hi 54 cases 
with metastases to the'vertebrae and spinal membranes there were can- 
cers of the breast, in 10 cases; esophagus, in 9 cases; thyroid in 9 cases; 
uterus in 6 cases; bronchus, in 5 cases; stomach, in 4 cases; prostate, in 
3 cases; gall-bladder, in 2 cases; ovary, in 1 case; sigmoid flexure, in 1 
case; rectum, in 1 case; kidney, in 1 case; adrenal, in 1 case; pancreas, 
in 1 case; not specified, in 1 case. 
The metastases to the nervous system, particularly, the extra- and 
intradural growths, are oftener due to breast cancer than to other pri- 
mary growths. It is not uncommon to find advanced symptoms of 
pressure due to metastases to the dura or vertebrae giving rise to symp- 
toms before the diagnosis of breast cancer has been made. Thus, in a 
case of transverse myelitis clearly due to compression, the patient had 
never mentioned the presence of scirrhus of both breasts. The masses 
were accidentally discovered during the physical examination of the ad- 
vanced case in which myelitis alone had been suspected. 
Long periods of latency of breast, stomach, intestinal, prostatic and 
other cancer do not preclude the possibility of extensive and increasing 
metastases to distant organs—spine, brain and peripheral nerves. 
There may be palpable tumors of the stomach, breast, intestines or 
distant organs without marked symptoms in which the prognosis of the 
primary growth is not threatening, but in which early metastasis to the 
cord or spine, occasionally to the peripheral nerves or brain, may lead 
to death or may during considerable periods overshadow entirely the 
symptoms of the primary growth, because of the intense suffering and 
paralysis due to compression and infiltration. 
The possibility of long periods of improvement in the visceral car- 
cinomata due to periods of latency which positively exist, have not 
been generally recognized by the profession, and it is during these periods 
that metastases to distant parts may follow. A small cancer nodule in 
the stomach or intestines may exist without local symptoms, and may 
remain unrecognized; painful metastasis to the spine or to the membranes 
of the cord may offer the first evidence of malignant disease. Cases of 
stomach cancer without symptoms in which metastases to the nervous 
system are present may exist, in which, as in dogs, after gastrectomy the 
intestinal tract soon learns to compensate for the loss of the stomach 
function. It is not uncommon, because of a sufficient remnant of gastric 
follicles and functionating mucosa, to find the characteristic features of 
cancer of the stomach absent during comparatively long periods. This 
condition does not preclude the possibility of metastasis to distant organs. 
The majority of tumors originating in the meningeal coverings of the 
cord are benign and of slow growth. Hence symptoms of compression DISEASES OF THE SPINAL CORD 
921 
of the substance of the cord are long postponed, and the recognition of 
the nature of the process during the early period when neuralgic pains 
are among the leading manifestations with prompt localization and opera- 
tion, will lead to the most satisfactory results. 
Correct interpretation of neuralgia, persisting, and rebellions to treat- 
ment, will often lead to the accurate diagnosis; rational and radical 
treatment will be rewarded with increasing success as experience grows. 
Sciatic pain, one-sided, uninfluenced during a reasonable period, 
which finally becomes double and continuously rebellious, is often an 
expression of compression due to tumor; the prognosis depends on the 
nature of the growth, its extent and location. It will be found that a 
few (comparatively speaking) of these growths will prove to be operable. 
In prognosis it is always wise to consider sensory symptoms, long 
localized and persistently uninfluenced by treatment, referable to the 
cord, to be due to compression, either to inflammatory, tuberculous, malig- 
nant or non-malignant disease. This is particularly true of sciatic pains. 
Symptoms of irritation, spasms, convulsive seizures, associated with 
other focal symptoms and persistent pain which are suggestive of com- 
pression, often continue during many months without rapid advance of 
the disease. 
There are both rapidly and slowly growing tumors of the cord and 
spine in which the absence of sensory symptoms (pain), spasm and focal 
symptoms, are frequent, but progression is nevertheless positive. 
Many tumors of the cord are benign; some are only semimalignant. 
Cachexia even with the malignant metastases may be absent during 
long periods; the absence of cachexia ivith positive symptoms of metas- 
tasis, following the removal of distant malignant growths, does not argue 
against the same histologic build of the secondary growth. 
The prognosis of these metastatic growths without cachexia is uni- 
formly unfavorable; the course may be chronic. 
The behavior of the tendon reflexes with spinal growths as they begin 
to compres the cord, is quite characteristic and its thorough understand- 
ing in operable cases may lead to the necessary early diagnosis. 
Often exaggerated reflexes are among the earliest symptoms—patella 
tendon reflex, ankle clonus and Babinski phenomena are prominent— 
particularly in the limbs in which paralysis is most advanced. 
The abdominal reflexes are absent or weakened. 
Brown-Sequard paralysis makes localization easy. 
The cautious outlining of the level of sensory symptoms (anesthesia, 
hyperesthesia, etc.) in most cases makes it possible to localize the growth, 
often after a long period during which extension has been gradual. 
Bladder and rectal paralyses are evidences, as a rule, of compression; 
they are usually found in advanced cases and are unfavorable symptoms. 
The presence of bed sores in such cases leads to overpowering sepsis. 922 
DISEASES OE THE NERVOUS SYSTEM 
The usual seat of tumors springing from the meninges is in the dorsal 
region. 
Cervical invasion very often leads to spastic paralysis. Finkelnburg 
calls attention to development of flaccid degenerative paralysis of the 
arm muscles after a period of neuralgic pains; the invasion of the dorsal 
cord causes changes in the adjacent sympathetic and the development of 
pupillary symptoms. 
The prognosis of extramedullary growths of the dorsal region for 
surgical interference is more favorable than is that of cervical lumbar 
or caudal invasion. This is equally true of extra- and intramedullary 
growths. 
Gowers, Horsley and Oppenheim contend that intradural growths are 
almost always operable; they grow slowly, are likely to be benign and their 
attachment to the cord itself is easily overcome. 
“Out of twenty-four laminectomies performed in the Neurological 
Institute during the year ended Nov. 30, 1913, there was only one death, 
and this patient died after a second-stage laminectomy for a suspected 
tumor of the cervical cord, a highly precarious region. Considering this 
slight mortality, I feel little hesitation in recommending exploratory 
laminectomies by skillful operators in cases in which spinal cord tumor 
may exist, especially in view of the fact, now established, that painless- 
ness does not deny such existence” (Bailey). 
II. Intramedullary Growths 
The increasing success following the surgical removal of the intra- 
medullary tumors is encouraging and has, since the radical statements 
made by Gowers and Horsley, encouraged the clinician to the belief that 
these growths are often operable and that a successful issue may be 
expected in a large proportion of cases if the growth is removed early, 
before destruction of the cord substance. 
In many, the growth cannot be diagnosticated until compression 
symptoms and disorganization are in evidence. 
Another fact which influences the early diagnosis of intramedullary 
growths is the absence of neuralgic pains during the early stages in a 
large proportion of cases. 
Schlesinger’s statistics prove the great prognostic significance of the 
preceding statement for they show that almost one-third of all tumors 
of the cord are within the medullary substance (of 302 tumors of the 
cord, 125 were intramedullary). These include sarcoma, tubercle 
nodules, gumma, lipoma, cysticercus, neuroma, cholesteatoma, myxoma, 
teratoma, adenoma and endothelioma. 
Elsberg says ‘‘many of these intramedullary growths infiltrate the 
cord substance and increase in size by extending upward and downward, DISEASES OF THE SPINAL CORD 
923 
but some enlarge. in their transverse diameter, are encapsulated and of 
small size.” The more favorable growths for operation are those which 
are encapsulated and of small size. 
Gowers, whose experience cannot be ignored in our consideration of 
the forecast of intramedullary growths, calls attention to the tendency 
of “these tumors, in some cases to blend with the substance of the cord.” 
Infiltrating disease is less favorable for successful surgical relief than 
are those cases in which the “tumor is sharply limited 
Intramedullary tumors may, as Schlesinger has demonstrated, expand 
in such a way as to make these appear to be of extramedullary origin. 
The encouraging experiences of Elsberg and others including Bruns, 
Allen Starr, Cushing, Bailey and Beer as well as Oppenheim, justify 
the unqualified statement of Elsberg that localized growths of the cord 
substance must not be considered as inoperable. “They should be 
attacked by the neurological surgeon as readily as subcortical tumors of 
the brain. The results should be at least as good as those obtained in 
subcortical intracranial growths.” 
It will often be impossible to differentiate the extra- and intra- 
medullary growths, so closely may the symptoms parallel each other, but 
it may be assumed that a long period of neuralgic pains favors the extra- 
medullary origin of the growth and in these cases, as already suggested, 
the secondary nature of the disease must be considered in prognosis in 
spite of great chronicity. Years of symptoms are not uncommon par- 
ticularly with breast cancer. 
The usual posterior and lateral location of tumors of the cord adds 
to the success of early surgical interference. 
Starr reports in a series of 58- cases of tumor of the cord operated, 
that it was possible in all but 3 to remove the growths. These included 
16 completely successful and 10 partially successful. In all of these cases 
the prognosis depends upon the amount of compression and destruction 
of the cord. Degenerative changes cannot be overcome. “The impor- 
tance of an early diagnosis of these tumors is emphasized by the fact 
that most of them can be successfully removed if taken in time, and the 
fatality, which otherwise attends them, arrested” (Church and Peterson). 
Putnam and Warren found that 70 per cent of recorded cases were 
operable, and of 33 operated cases one-half resulted successfully. Sturs- 
berg in his tabulated cases reports 32.2 per cent of cures. 
In some cases life is saved but a remnant of spastic paraplegia per- 
sists. Naturally multiple are less favorable than are the single growths. 
Schlesinger’s statistics of 400 tumors included 273 single and 127 multi- 
ple growths. 
Sarcoma of the cord is of rapid growth, is likely to involve the mem- 
brane and the posterior surface of the cord, and does not lead to rapid 
destruction of the cord substance; it is therefore favorable for early 924 
DISEASES OF THE NERVOUS SYSTEM 
operation. The ease with which sarcoma can be stripped from its resting 
place is a favorable fact. The growth is not likely to be encapsulated. 
Infiltration is characteristic of some spinal sarcomata, the effect of 
which is rapidly destructive to the substance of the cord. Such behavior 
is the exception rather than the rule. 
Multiple sarcoma of the spine offers scant, practically no chance of 
recovery; it is not common in such cases to find multiple growths spring- 
ing from the cerebral dura and the brain at the same time. 
Carcinoma of the cord offers an unfavorable prognosis; it is always 
secondary, more frequently found in woman (70 to 80 per cent of all 
cases) and is usually metastatic. 
Tubercle of the cord and brain is separately considered (tuberculosis, 
etc.). Starr reports a case in which a single tubercle nodule was easily 
removed from the cord by McBurney. The patient developed general 
tuberculosis and spinal meningitis two months after the operation. 
I have had no experience with echinococcus and cysticercus cysts. 
Those described in monographs and textbooks have shown rapid growth 
and evidences of compression myelitis. There is no reason why opera- 
tion for growths of echinococcus origin should not be followed by the 
same results as have been mentioned in connection with the operation for 
other spinal tumors—lion-malignant. 
The fibromata, psammoma, fatty growths, myxoma, and osteoma offer 
a good prognosis for surgical treatment. 
Glioma always offers an unfavorable prognosis, for it grows rapidly 
and its dissemination with infiltration is far-reaching. 
Multiple neuromata of the cord, brain and peripheral nerves may 
exist together; the prognosis so far as removal of the growths is con- 
cerned, is bad. These patients may live during long periods and may 
die of intercurrent disease. 
To determine whether a tumor of the cord is primary or secondary 
may in exceptional cases require a varying period of observation and, 
in puzzling cases, always demands thorough search of all possible sources 
for the primary disease. 
The rectum, uterus and prostate as well as the intestines, stomach 
and breast supply metastases in some of these puzzling cases and should 
be suspected. The possibility of bronchial or pulmonary growths should 
not be ignored. 
The growth of the spinal tumor in its bony, non-yielding canal must 
of necessity cause compression in most cases; hence to save these patients 
and change the prognosis, the early pains require correct interpretation. 
In cases of single, non-infiltrating primary tumors, cautious observation 
should lead to early diagnosis and surgical treatment in an increasing 
number of cases; as the surgeon improves his technic and his experience 
grows, the prognosis will improve. Metastases however, wherever found, DISEASES OF THE * SPIHAL CORD 
925 
in the membranes or substances of the cord, offer only the gravest prog- 
nosis. 
Secondary growths in the cord and spine are as a rule chronic, and 
the history covers a period of from eight months to several years in most 
cases. Cases have been reported in which patients lived so long as six, 
eight and even ten years. It is often surprising to note how long patients 
may live with metastases to the vertebrae, spinal meninges and cord. 
I include cases which lived from three to five years after the diagnosis 
was made. 
Cases in which there are early manifestations of complete transverse 
myelitis from extradural growths may run a course shorter than the 
average. 
Cases of metastasis to the spine and cord following the surgical 
removal of breast cancer have in my experience averaged between eighteen 
months and three years after the beginning of continuous symptoms. 
Spinal gliomatosis usually runs a rapid course. In these cases the 
infiltration is not limited to the cord, and before death there are evidences 
of cerebral invasion. 
Glioma, it must be remembered, is rarely single; it is usually diffuse 
and its infiltration is far-reaching. 
In almost all cases of tumor which involve the cord when death re- 
sults, it follows a period of septic symptoms in which there are evidences 
of ascending genito-urinary invasion, often with bed sores and extreme 
emaciation. 
Compression myelitis fully established with disorganization resulting 
from tumor, the growths of large size, infiltrating disease, multiple 
growths, carcinoma, metastases, glioma, all inoperable cases, offer only 
the gloomiest prognoses and are among the most painful of all diseases. 
The early removal of growths of limited size—non-malignant—offers 
the most favorable prognosis of all operable growths. 
It is unwise, in spite of the encouraging reports of surgeons and 
brilliant results in individual cases to give an unguarded prognosis in 
any case of tumor of the cord or vertebrae, wherever located. 
The relation of trauma to tumors of the cord is of considerable im- 
portance, and we quote from the splendid article of Bailey as follows: 
“There are a great many instances in which injury to the back, in a 
previously healthy person, has been followed in the course of a few 
months by characteristic appearances of spinal cord tumor, and in many 
of these cases operation has been done. The occurrence of pain in such 
cases is interesting, for at the time of the injury to the back there is 
immediate pain at the point of injury, and this pain does not entirely 
disappear, but remains until finally it develops into the pain of a spinal 
cord tumor.” 
X-Ray Examination.—The Rontgen rays may prove of great assist- 926 
DISEASES OF THE NERVOUS SYSTEM 
ance in vertebral and extramedullary growths in localizing bony metas- 
tasis, and may thus prove of early prognostic as well as diagnostic value. 
X-ray examination fails to give satisfactory results in tumors of the 
cord itself. 
Lumbar Puncture.—Marked increase of intraspinal pressure with 
tumor is evidence of compression, and with corresponding increase of 
albumin in the fluid and globulin (Phase 1, Reaction of Nonne), and a 
low lymphocytic content or entire absence of lymphocytes, the prognosis is 
unfavorable. 
Plant reports that hemorrhages have at times been found in the tissue 
about the tumor after lumbar puncture, due to the sudden lowering of 
pressure by the withdrawal of fluid. 
Klieneberger, Ivindborg, and others including Quincke, report a yel- 
low color of the spinal fluid in cases of tumor of the cord due to the 
presence of blood coloring matter. These cases are ominous and are 
usually far advanced. In exceptional cases the results of lumbar punc- 
ture added to the thoroughly digested clinical history will prove of con- 
siderable prognostic value; the data derived from the examination of the 
fluid alone, ought not to be relied upon. 
Tumors of the conus and cauda equina 
Tumors of the conus when fully developed cause anesthesia of the 
external genital organs, the perineum, anus, the inferior gluteal region 
and the posterosuperior area of the thighs. The anesthesia may reach 
the genito-urinary mucosa. Paralysis of the bladder and rectum with 
incontinence or retention and “involvement of the sexual function and of 
the sensation of ejaculation,” pain, motor power of the legs unchanged 
while the reflexes are normal, are the usual symptoms (Gordon). 
With tumors of the cauda equina the prominent symptoms, if the 
growth does not involve the conus, are pain in the lumbosacral region 
and in the legs. In advanced cases movement aggravates the symptoms. 
Paresthesia and anesthesia within the region of the perineum, anus, 
and genitals, is the rule. 
Paralysis is usually present from the beginning of the tumor pressure, 
is flaccid, is soon associated with atrophy of the muscles and the reaction 
of degeneration. 
Sphincter symptoms are usual, either early or develop as the disease 
progresses, and with the advancing infiltration, bed sores, cystitis and 
sepsis are not uncommon. 
The prognosis when the above symptoms are included in the clinical 
history is unfavorable. Sphincter paralysis, bladder and septic symptoms 
are permanent; no treatment will relieve them. 
After a period of varying length with symptoms of compression DISEASES OF THE SPINAL CORD 
927 
myelitis and sepsis, death follows. The more frequent growths are sar- 
coma or fibrosarcoma. The size of the vertebral canal permits of consid- 
erable growth before pressure symptoms follow. 
Tumors may involve the conus and cauda equina at the same time. 
Bailey. Painless spinal tumors. J. Am. Med. Ass., July 4, 1914. 
Bailey & Beer. See Elsberg [l. c.]. 
Bruns. Die Geschwulste des Nervensystems. Berlin, 1897. 
Church & Peterson. Nervous and mental diseases. Philadelphia, 1914. 
Cushing. Johns Hopkins Hosp. Bull., Nov., 1910. 
Elsberg. Am. J. Med. Sci., 1912. 
Eisner (Henry L.). Metastasis to the nervous system from cancer of the stomach and in- 
testines. New York Med. J., Jan. 21, 1911. 
Finkelnberg. Curschmann’s Lehrb. der Nervenk. Berlin, 1909. 
Gordon. Diseases of the nervous system. Philadelphia, 1908. 
Gowers. Diseases of the nervous system. London, 1888. 
Gowers & Horsly. Diseases of the nervous system. 1899. 
Jacobsohn. Klinik d. Nervenk., Berlin, 1913. 
Kindborg. Inner. Med., Berlin, 1914, Hi. 
Oppenheim. Lehrb. d. Nervenk. 1913. 
Plaut, Rehm & Schottmuller. Zebrospinalfliissigkeit. Jena, 1913. 
Putnam & Warren. Am. J. Med. Sci., Philadelphia, Oct., 1899. 
Quincke. Quoted by Plaut [Z. c.]. 
Schlesinger. Beitr. z. Klinik des Riickenmarks u. Wirbeltumoren. Jena, 1898. 
Spiller & Weisenberg. Carcinoma of the nervous system. J. Nerv. & Mental Dis., 1906, 
xxxiii. 
Starr. Organic nervous diseases. New York, 1909. 
Stursberg. Centralbl. f. Grenzgebiete der Med. u. Chir., 1908. 
References 
7. Caisson Disease 
See Diseases Due to Physical Agents (Section XII). 
8. Affections of the Blood Vessels of the Spinal Cord 
(a) Anemia of the Spinal Cord 
Anemia of the cord may follow arterial obstruction; local anemia may 
lead to necrosis and consecutive inflammation. 
Spinal anemia is a secondary process, a part of a general anemic 
condition which leads to symptoms which have been characterized by 
some as “spinal irritationThere are forms of spinal anemia which 
are in fact mild types of myelitis and are known as “funicular myelitis.” 
The syndrome of persisting symptoms associated with pernicious 928 
DISEASES OF THE NERVOUS SYSTEM 
anemia which were originally fully described by Lichtheim, and to which 
I have given the name of “Lichtheim symptoms” are fully considered in 
the chapter on pernicious anemia. 
The prognosis of all forms of anemia of the spinal cord necessarily 
depends upon the underlying cause. 
Symptoms of anemia accompanying the grave constitutional disturb- 
ances persist, and yield only to the successful treatment of the primary 
disease when that is possible. 
Embolic and thrombotic obstruction of the abdominal aorta and its com- 
pression cause paraplegia; these are rare, and offer an unfavorable fore- 
cast. 
Complete anemia of the spinal cord from whatever source at once 
leads to loss of function and death, if not promptly relieved. 
Anemic conditions of the spinal cord materially influence symptoms 
and prognosis in the terminal stages of leukemia, in cases of ulcerative 
endocarditis, malignant malaria, carcinoma with metastases, some cases 
of tuberculosis, suprarenal disease and the chronic intoxications, includ- 
ing lead poisoning and alcoholism. With many of these there are changes 
of an organic nature in the lateral and posterior columns of the cord. 
Symptoms referable to the spine dependent upon simple anemia, 
chlorosis, anemia due to sudden depletion (hemorrhage, accident, etc.) 
all offer an encouraging prognosis. 
(b) Hyperemia of the Spinal Cord 
Active hyperemia of the cord, independent of other disease, is so rare 
as to require no consideration; it is a question whether it ever occurs 
save as the distended vessels mark the initial stage of myelitis or meningo- 
myelitis. 
Passive spinal congestion is also exceedingly rare; I have no data, 
either clinical or pathological, which justify its separate consideration., 
Hematorrhachis and hematomyelia are separately considered. 
Reference 
Lichtheim. Zur Kenntniss d. perniziosen Anemie. V. Kongress f. inner. Med., 1887. 
(c) Spinal Endarteritis—Arteriosclerosis 
(d) Spinal Embolism and Thrombosis 
Changes in the arteries which supply the cord are more frequent than 
is generally supposed, and, disregarding specific arteritis which is sepa- 
rately considered, lead to either transitory or permanent symptoms in 
accordance with the extent of the underlying lesions and their location. DISEASES OF THE SPINAL CORD 
929 
Change in the spinal blood vessels, particularly endarteritis, is an impor- 
tant factor in many forms of spinal disease. Gradually increasing symp- 
toms in patients beyond forty-five or fifty years of age, with or without 
evidences of general arteriosclerosis in which there are no positive etio- 
logic factors, are in the majority of cases due to sclerosis of the vessels 
which on post mortem examination prove to be peri- or endarteritic, often 
resting on a specific basis, with or without involvement of the meninges 
(gummata), to the obliterating type of endarteritis, or changes in the 
larger arteries (vertebral, anterior or posterior spinal), often including 
miliary aneurisms. 
The prognosis is only favorable in syphilitic cases in which the true 
character of the disease has been appreciated early and the patient ration- 
ally treated. The prognosis of arteriosclerosis of the spinal vessels, large 
or small, is not encouraging. In many cases the process remains latent 
during long periods, in others the advance is surprisingly rapid, while 
in a third class there may be advanced thickening of the spinal vessels 
without subjective or objective symptoms. In patients who have general 
arteriosclerosis including cerebral invasion with spinal endarteritis, there 
may be a long period of helplessness, mental weakness, urinary incon- 
tinence with other uncontrollable symptoms and death follows either after 
coma, due to a septic condition resulting from the cystitis, which finally 
develops in such cases, intercurrent infections (pneumonia, etc.), or cere- 
bral miliary aneurism may lead to apoplexy. 
Advanced change in the spinal vessels, non-specific, cannot he over- 
come by medical treatment. Emboli may occasionally block the spinal 
arteries leading to immediate symptoms, the latter depending upon the 
artery involved. The vertebral artery may be the seat of embolic block 
which is promptly washed onward without lasting symptoms. Cerebellar 
symptoms in such cases are prominent. In one of my cases there was 
repeated blocking of the vertebral artery, with chronic cardiopathy and 
arteriosclerosis, in which the patient finally developed cerebral symptoms 
without recurrence of embolism. The prognosis of a large number of the 
acute and chronic diseases of the cord is often influenced by thrombosis 
of one or more of the medium sized or smaller arteries of the spinal cord 
with advanced endarteritis. 
Sudden paraplegia is not infrequent in the subjects of organic heart 
disease in which embolism of the cord is the cause of the symptoms. In 
most of these cases there are at the same time infarcts with other organs 
—spleen, kidney or the brain. In these cases the prognosis is unfavor- 
able. With malignant septic endocarditis there are occasionally symptoms 
of spinal embolism with other infarcts; the prognosis is uniformly bad. 
Senile paraplegia offers an unfavorable prognosis. The paralysis as 
the disease advances, becomes more and more spastic, and if the patient 
lives long enough, contractures with exaggerated reflexes may develop. 930 
DISEASES OF THE NERVOUS SYSTEM 
In these cases there are often associated degenerative changes in the brain 
(senile dementia, etc.). The prognosis is absolutely bad. 
Reference. 
Collins-Zabriskie. New York Med. Rec., 1904. 
Demange. Revue de Med., 1884. 
Herter & Clark. Diagnosis of organic nervous diseases. New York, 1907. 
Hirsch. J. Nerv. Dis., 1903. 
Sachs, Dupre & Lemaire. Revue Neurologique, 1905. Also quoted by Oppenheim. 
Spielmeyer. Deutsch. med. Wchnschr., 1911. 
V. Diseases of the Spinal Membranes 
1. Hemorrhage into the Spinal Membranes and Cord 
{Spinal Hemorrhage, Hematomyelia {Hemorrhage into the Cord), 
Ilematorrhachis {Hemorrhage into the Membranes of the Cord), 
Meningeal Apoplexy, Pachymeningitis spinalis hemorrhagica 
interna) 
Causes.—The cord is so well protected from injury that hemorrhage 
into its substance or membranes due to traumatism, except from crushing 
accidents, stab or gunshot wounds, is seldom. Ordinary accidents are not 
to be considered as a frequent cause of spinal hemorrhage. 
Hemorrhage due to disease is also rare. 
Occasionally arteriosclerosis and fatty degeneration cause limited 
hemorrhage. 
Spontaneous hematomyelia occasionally arises in young subjects with- 
out known cause or with purpura. One such case of suddenly arising 
paraplegia with other positive evidences of purpura I saw in a girl aged 
fifteen years who made a perfect recovery. 
Symptoms following Hemorrhage.—Hematomyelia may lead to the 
formation of cysts with persisting paralysis and focal symptoms. Such 
cases are favorable if recognized early and are promptly operated. 
Syringomyelic symptoms may develop after hemorrhage into the mem- 
branes and cord. 
All of our cases developed suddenly without loss of consciousness, but 
there was almost always complete paralysis. The extent of the paralysis, 
shock and subsequent course depend upon the location and extent (amount 
of destruction) of the hemorrhage. 
Sphincter symptoms may develop after a few days and in those cases 
which live or are subacute, there are bed sores and symptoms of trans- 
verse myelitis. DISEASES OE THE SPINAL CORD 
931 
The prognosis of traumatic cases is as a rule bad as the injuries are 
severe, extensive and destructive; they usually show external evidences of 
the accident. 
The development of some paralysis and symptoms of pressure is im- 
mediate; the increase is rapid, depending on the amount of blood and 
the compression. The higher the hemorrhage the worse the prognosis. 
Injuries with hemorrhage into the cervical cord often involve the 
medulla and pons, when they cause prompt death. 
Purpuric cases when not malignant, if not extensive or unfavorably 
located as in the case above mentioned, offer a good prognosis. 
The cases in which malignant disease, disease of the vertebrae, caries 
and suppurative processes lead to hemorrhage, usually die with the symp- 
toms of compression myelitis. 
There are small meningeal hemorrhages associated with the acute 
infections which are not of great prognostic significance. 
Aortic aneurism has occasionally ruptured into the vertebral canal 
and caused sudden death. 
2. Spinal Hematoma 
Pachymeningitis hemorrhagica interna 
Occasionally there are evidences of spinal pachymeningitis hemor- 
rhagica interna in which there are coincident hematomata in the brain 
and spinal cord. These are found in paretic subjects and other forms of 
insanity, with the grave and the pernicious forms of anemia and in 
cachectic children. The condition is rarely diagnosticated intra vitam. 
When associated with brain hematoma, the spinal fluid is clear or 
yellowish in color; there is slight leukocytosis or lymphocytosis, some 
blood coloring matter; pressure is usually increased; albumin is also 
increased; globulin is present; and with infectious cases the staining and 
cultural methods assist in diagnosis and prognosis. 
The patients die of intercurrent diseases—not often from the hema- 
toma directly. 
3, Spinal Meningitis 
There are but few cases of spinal meningitis of primary origin. The 
most frequent forms of meningitis are cerebrospinal fever or meningo- 
coccus meningitis, tuberculous meningitis, and chronic syphilitic spinal 
meningitis. These are all separately considered (See Cerebrospinal 
Meningitis, Chapter on Tuberculosis and Syphilis of the Nervous Sys- 
tem). Pneumococcus meningitis (usually cerebral) is also separately 
considered (See Pneumococcemia). • 
Cases of meningismus are associated with the acute infections and are 
of cerebral origin, rgrely spinal. 932 
DISEASES OF THE NERVOUS SYSTEM 
Sfriimpell reports cases of cerebrospinal meningitis following empy- 
ema and pulmonary gangrene; these cases are always grave. 
(a) Spinal Pachymeningitis 
Spinal pachymeningitis or inflammation of the dura mater may be 
either internal or external. When it begins in the dura and spreads 
from that membrane, it is internal, when the dura is involved from con- 
ditions outside, it is external. 
External Spinal .Pachymeningitis.—External spinal pachymeningitis 
is therefore almost always secondary to diseases of the spinal vertebrae, 
caries, tuberculosis, carcinoma, bed sores, suppurative processes, throm- 
bosis, retropharyngeal abscess, syphilis and erysipelas. 
External pachymeningitis may follow surgical operations near the 
spine with consecutive infection. 
The prognosis of external pachymeningitis is always grave because 
the cause is not often amenable to treatment, and the invasion of the 
membranes adds enormously to the danger. 
The lumbar fluid with pachymeningitis externa, due to caries and 
cancer, shows albumin increase without marked increase of lymphocytes. 
The fluid is yellowish and coagulates spontaneously. 
Internal Spinal Pachymeningitis.—Internal spinal pachymeningitis is 
exceedingly rare. Inflammation does not limit itself to the dura ; there 
is usually a predominating leptomeningitis. The prognosis is always 
grave but in occasional cases the patient is brought safely into port after 
weeks of close attention and care, with but little damage. 
(b) Hypertrophic Cervical Pachymeningitis 
Charcot in 1871 first described hypertrophic cervical pachymeningitis 
which is a chronic inflammation of the cervical dura mater associated 
with enormous fibrous thickening of the membrane. 
The periosteum is also involved in most cases; the dura is adherent 
to it and cannot be easily separated. The symptoms of compression are 
in the ascendency. 
Degenerative processes follow in the motor nerves and muscles of the 
upper extremities, with degeneration of the pyramidal tract 
in the cord. 
The symptoms of involvement of the motor fibers are in evidence and 
from the beginning progressive; the pain is at first severe (periode 
douloureuse of Charcot) and continues several months, after which there 
is an advance to motor paralysis and muscular atrophy. 
Spastic paralysis of the lower extremities develops as the case becomes 
more and more chronic without marked atrophy of the leg muscles and DISEASES OF TIIE SPINAL CORD 
933 
without change in electric excitability, while the arms show decided 
atrophy and the reaction of degeneration. 
In the late stage, bladder symptoms are not infrequent. One of my 
cases, a man, recovered completely after two years with but little damage, 
some contractures, but not sufficient to prevent return to his grocery. 
As a rule the disease is chronic and the paralysis persists unchanged 
during many years. The disease may become stationary in any one of its 
stages. The prognosis is always grave, and acute complications or pro- 
gression may lead to death. 
There is a class of cases usually syphilitic, in which there is great 
sensitiveness along the cervical spine, persisting pain in the neck and 
along the arms, without paralysis but with motor weakness, with pares- 
thesia and hyperesthesia, at times anesthesia of the hands. These cases 
are probably due to cervical periostitis with more or less pachymeningitis; 
they tend to recur, are favorably influenced by specific treatment and 
counter irritation. 
Acute inflammation of the arachnoid rarely limits itself to the spine 
hut involves the cerebral membranes as well. (The epidemic form of 
cerebrospinal meningitis (meningococcus meningitis) is separately con- 
sidered. ) 
In occasional cases the spinal symptoms in acute non-epidemic lepto- 
meningitis predominate. The disease in my experience is so rarely 
idiopathic as to require no further mention than it has received in its 
consideration as a complication of many infections to which the reader 
is referred (particularly the Chapters on Tuberculosis, Syphilis, Ery- 
sipelas, Pneumonia, Typhoid Eever, Septicemia, Scarlet Fever; also 
Diseases of the ISTasal Fossae and Skull and Chronic Nephritis, Arterio- 
sclerosis and Gout). 
Whenever the diagnostician finds the symptoms of acute leptomenin- 
gitis, his first duty is to establish the primary cause—which is easily 
accomplished in almost all cases—after which prognosis is comparatively 
easy. Lumbar puncture and blood-cultural methods are of enormous 
assistance. 
In all cases which originate in the spine, extension to the cerebral 
meninges is to he expected. 
(c) Acute Spinal Leptomeningitis 
(d) Chronic Spinal Leptomeningitis 
Chronic spinal leptomeningitis as a primary disease is infrequent. 
I agree with Striiinpell that in the cases so diagnosticated originally, 
in the end some other condition is found. 
Syphilis of the spine with chronic meningeal changes is separately 
considered. 934 
DISEASES OE THE NERVOUS SYSTEM 
Whenever the diagnosis of chronic spinal leptomeningitis is justified, 
the disease is secondary and the primary cause must be unfolded before 
prognosis is possible. It is a part of tabes dorsalis, myelitis, multiple 
sclerosis and progressive muscular atrophy. In most of these there are 
adhesions to the dura. 
Syphilis and tuberculosis, metastases and multiple sclerosis will be 
found, to be among the most frequent causes„ 
(e) Postbasic Meningitis 
{Sporadic Spinal Fever) 
I also mention this form of cerebrospinal meningitis in connection 
with the epidemic form of the disease. Lees and Barlow call attention 
to these cases in which there are tonic spasms which are limited. In 
over one-half of these cases (50 post mortems were made) of postbasic 
meningitis, the spinal membranes were involved. These cases are con- 
sidered sporadic and always serious. The mortality is high; rarely in 
my experience below 50 per cent. Striimpell believes that the so-called 
idiopathic cases are identical in their etiology with the epidemic form. 
I believe that all cases of postbasic meningitis should he considered 
infectious cerebrospinal meningitis. 
References 
Charcot. Hypertrophic cervical pachymeningitis. 1871. 
Lees & Barlow. Allbutt’s System of medicine. 1st & 2d eds. 
Striimpell. Textbook of medicine. 1911, ii. 
C. Diseases of the Brain and its Membranes 
I. Diseases of the Membranes of the Brain 
1. Pachymeningitis—Inflammation of the dura mater 
(a) Pachymeningitis interna 
(b) Pachymeningitis externa. 
(a) Pachymeningitis interna 
(Pachymeningitis hemorrhagica interna) 
General Considerations.—Unquestionably there are many cases of 
hemorrhage of the dura mater resulting from traumatism which give 
rise to hut few or no symptoms, often recover without leaving permanent 
damage, or are accidentally discovered post mortem. 
The majority of cases of internal pachymeningitis due to traumatism DISEASES OF THE BRAIN AND ITS MEMBRANES 
935 
are associated with fractures of the cranial vault or its base. These cases 
are almost always associated with profound cerebral disturbances, are 
serious and are likely to lead to death after a train of meningeal symp- 
toms, including loss of consciousness, the Kernig symptom, and changes 
in the spinal fluid as shown by lumbar puncture. The fluid may escape 
(Plaut, Rehm and Schottmiiller) under normal or increased pressure. 
The cases in which the fluid is markedly hemorrhagic with high pressure 
offer an unfavorable outlook. The fluid in occasional cases of pachy- 
meningitis may continue clear or yellowish when blood coloring matter 
has been present during varying periods. The appearance of the fluid 
depends very largely on the primary cause of the internal pachymenin- 
gitis and the chronicity of the individual case. The fluid may show no 
red blood corpuscles, in spite of the presence of blood coloring matter and 
a yellow tinge. This is also true of chronic cases. Albumin is present 
with a positive globulin reaction. 
Failure to demonstrate microscopically or culturally the presence of 
microorganisms with positive infection, has no bearing on the prognosis 
of the individual case (Schottmiiller). In noil-traumatic cases the cellu- 
lar count may continue normal or slightly increased without influencing 
the forecast. 
In occasional cases, cysts with multiple partitions filled with serum 
may follow hemorrhage and lead to focal symptoms (hygroma durae 
matris). These cases, when recognized and localized early, treated sur- 
gically offer some encouragement for restoration of function when this 
is disturbed. The prognosis of these cases is good in proportion to the 
time of operation (early is best), the resistance of the patient, the exact 
localization of the cyst, and the escape from injury of the surrounding 
brain tissue. 
Causes and Development.—Chronic alcoholism is often the cause of 
pachymeningitis. Many of these cases are finally complicated with 
ependymitis and bronchopneumonia—these are almost uniformly fatal. 
Paresis with acute hemorrhagic pachymeningitis interna leads to 
death with pressure symptoms in from three to four days. In the chronic 
cases the course is prolonged—may cover months—and death often follows 
acute exacerbations. 
Senile dementia is not infrequently associated with dural hemorrhage 
in its terminal stage. Purpuric conditions, non-malignant, may develop 
internal hemorrhage (pachymeningitis) and yet, if this is not too exten- 
sive, recovery may follow. If the hemorrhage is extensive and there are 
complications, if the infection is malignant, then the prognosis is bad. 
Cases dependent on nephritis and chronic cardiopathies are always seri- 
ous. In all of these cases the amount of cerebral compression becomes an 
element of the greatest importance in prognosis. 
Persistent and unchanging symptoms of compression or increasing 936 
DISEASES OE THE NERVOUS SYSTEM 
evidences of pressure are among the unfavorable features of all cases of 
pachymeningitis. 
Streptococcus, pneumococcus and syphilitic infections when the cause 
of pachymeningitis always justify a guarded prognosis. Of these, the 
syphilitic cases are the most favorable. Erysipelatous infection with 
acute pachymeningitis, particularly in alcoholics, is among the gravest 
of all forms of the disease. While recovery is rare, it is not impossible. 
The clinician is not to be deceived by periods of remission of symptoms 
in chronic cases; such improvement (usually of the sensorium) is only 
transitory, and deep coma is likely to follow at any time. Some acute 
cases remain unconscious during several weeks (usually syphilitic) and 
gradually mend and recover. In these cases the pulse may be persistently 
small and feeble, breathing irregular, temperature not elevated. The 
complicating paralyses depend upon the location of the hemorrhage. The 
cranial nerves are rarely involved. 
Convulsions of the jacksonian type are occasionally present; when 
dependent upon cyst formation or when uncomplicated, surgical inter- 
ference may save the life of the patient. 
Coma long continued is always unfavorable. Pernicious anemia in 
its terminal stage may cause dural hemorrhage. This is also true of 
the leukemias, hemophilia, and malignant endocarditis. 
. Puerperal sepsis and scarlet fever with pachymeningitis are almost 
always fatal. 
The chronic form of internal pachymeningitis may cover a period of 
years, with acute exacerbations and repeated remissions. Unquestionably 
a small proportion of these cases in which the process is limited, may 
recover, but in no case should the prognosis be given unguardedly. This 
conclusion is justified by the post mortem evidence of chronic pachy- 
meningitis in subjects who presented no symptoms of the lesion during life. 
The prognosis of hemorrhagic pachymeningitis dependent upon 
meningeal hemorrhage has in a number of reported cases been favorably 
influenced bv lumbar puncture and surgical intervention (Michaux, 
Jaboulay, Ueisser-Cushing, Seitz, Curschmann and Devreigne). 
(b) Pachymeningitis externa 
General Considerations.—Pachymeningitis externa is, according to 
Ernst, a 'periostitis involving the skull and external surface of the dura 
which is in close contact with the bone. The process is likely to he lim- 
ited—localized—and may lead to pus accumulation (abscess), i. e., extra- 
dural abscess, or may lead to localized osteomyelitis of the skull. 
Most external pachymeningitides are secondary and follow middle 
ear inflammation, mastoid disease, tonsillar • infection, or fractures of 
the skull. DISEASES OF THE BRAHST AND ITS MEMBRANES 
937 
Development.—The disease may complicate influenza, scarlet fever, 
measles, diphtheria, typhoid fever and smallpox. Ernst has found among 
the leading microorganisms, strepto-, staphylo-, diplo-, and pneumococci, 
and the pyocyaneus. 
I have seen a number of cases in which destructive specific disease 
of the skull has led to pachymeningitis externa with fatal result. 
Cases of erysipelas with this disease have shown a very high mortality. 
While the majority of cases are secondary and offer an unfavorable 
prognosis, when the disease is not extensive and is promptly treated sur- 
gically there are some cases which recover. Gowers has called atten- 
tion to cases which are primary, which are acute in their course, leading 
to prompt suppuration between the dura and the bone. These cases, how- 
ever, are more likely to he spinal—rarely cerebral. 
The prognosis of external pachymeningitis depends on the malignancy 
and location of the primary infection, the extent and location of the 
injury in 'traumatic cases, as well as the extent of the meningeal com- 
plication, the amount of compression and location of the brain lesion, if 
any, in all cases. External pachymeningitis offers the best prognosis of 
all the meningitides. There will always be a large number of cases of 
external pachymeningitis which will remain unrecognized during life 
because of the proximity of the primary disease, the symptoms of which 
remain in the ascendency, obscuring those of the complication. 
References 
Curschmann. Deutsch. med. Wchnschr., 1910. 
Cushing. Am. J. Med. Sd., 1905. 
Devreigne. Presse med., 1905. 
Ernst (P.). Aschoff’s Pathologische Anatomie. Jena, 1913, 2.Bd. 
Gowers. A manual of diseases of the nervous system. Philadelphia, 1886. 
Huguenin. Ziemssen’s Handb. Bd. xi. 
Jacobsohn. Klinik d. Nervenkrankh. Berlin, 1813. 
Michaux, Jaboulay & Neisser. Quoted by Oppenheim. Lehrb.d. Nervenk. 6th ed. 1913. 
Mohr & Staehelin. Handb. d. inner. Med. 1912. Bd. v. 
Phelps. Traumatic inquiries of the brain. 1897. 
Plaut, Rehm & Schottmiiller. Zeribrospinalflussigkeit. Jena, 1913. 
Seitz. Centralbl. f. Gynak., 1907. 
Schottmiiller (FI.). Munch, med. Wchnschr., 1910, No. 38. 
2. Leptomeningitis 
(Inflammation of the pia mater and arachnoid) 
(a) Purulent leptomeningitis 
(b) Serous leptomeningitis 
(c) Chronic leptomeningitis. 938 
DISEASES OF THE NERVOUS SYSTEM 
(a) Purulent Leptomeningitis 
Causes.—Pus-producing organisms from the surrounding tissues or 
from neighboring organs infecting the cerebral membranes are the cause 
of this type of meningitis. 
Metastatic leptomeningitis is less frequent than direct infection from 
the nose, middle or internal ear, the mastoid, caries of the temporal bone, 
direct injury of the skull with associated infection, abscess of the brain 
and meningitis by contiguity (per continuitatem) (Jacobsolm), or the dis- 
ease may follow nasal operations (removal of polypi or bone tissue with 
subsequent purulent infection), influenza, and not infrequently latent pus 
deposits in the brain or the surrounding tissues. 
It is not unusual to find that middle ear suppurations, supposed to 
have been fully controlled, i. e., healed, lead to the development of 
meningeal symptoms without a long prodromal period, and meningitis 
may promptly follow. 
The microorganisms most frequently responsible for purulent lepto- 
meningitis are the pneumococcus, meningococcus (cerebrospinal menin- 
gitis separately considered), streptococcus, typhoid bacillus, staphylo- 
coccus, and the bacillus coli communis. 
Metastatic leptomeningitides are usually dependent upon pneumonia, 
ulcerative endocarditis, typhoid fever, polyarthritis (rheumatism), scar- 
let fever, measles or smallpox. Other acute infections may be compli- 
cated by this serious condition. 
Meningitis occurring with the acute infections may not always be 
due to the same cause as the primary disease but mixed infections are 
to be considered in offering a forecast (See Pneumonia). 
Its Occurrence as a Complication.—Quoting from Edwin Bramwell: 
“The relative frequency of leptomeningitis as a complication and cause of 
death is considered.” 
“Osier found meningitis in 8 of 100 autopsies, while among 253 
cases of pneumonia examined after death, Aufrecht met with 7 in which 
meningitis was present. Musser and Norris found a post mortem record 
of meningitis in 180 of 4,833 cases of pneumonia. . . . Anders in his 
analysis of 1,674 cases of erysipelas does not refer further to it than to 
remark that it is an occasional complication.” 
“Typhoid fever is very rarely complicated by true meningitis. Cole 
has collected 21 cases of meningism, serous and purulent meningitis, 
from the literature, and 6 instances were present in the Johns Hopkins 
Hospital series of 1,500 cases of typhoid fever analyzed by McCrae.” 
“Dubois, in 1903, collected 11 cases in which purulent meningitis was 
due to Pfeiffer’s bacillus.” 
In the German army of 55,263 cases of influenza there were but 4 
cases of meningitis. DISEASES OF TIIE BRAIN AND ITS MEMBRANES 
939 
It may be assumed for diagnosis and prognosis that when meningitis 
of the convexity is bilateral it is due to pyogenic organisms; when uni- 
lateral it is likely to be secondary to middle ear disease. 
Basilar meningitis is usually but not always of tuberculous origin; 
traumatism, nasal disease (nasal operations), may open the avenue for 
infection which may spread to and from the base to the meninges. 
Postbasic purulent meningitis is likely to be of epidemic meningo- 
coccus origin. 
Councilman reports 60 consecutive leptomeningitides in which he 
found the pneumococcus in 18 cases, streptococcus in 18, meningococcus 
in 21 and staphylococcus in 2. 
The pneumococcus and meningococcus are responsible for the majority 
of the primary meningitides (Marchal), (50.5 per cent are due to the 
meningococcus, 42 per cent to the pneumococcus). 
I have frequently referred to leptomeningitis as a complication of 
the acute infections in other chapters. 
Meningitis following erysipelas is of the suppurative type, and offers 
an unfavorable prognosis. 
Leptomeningitis with metastatic parotitis in my experience has been 
almost uniformly fatal. Oppenheim has had a more favorable experi- 
ence with his cases. It is held by Dopter, who has considered this sub- 
ject, that most of these cases are due to the serous type of the dis- 
ease. 
Infectious sinus thrombosis with meningitis is promptly associated 
with fully developed symptoms, and death usually results. 
General Conclusions.—No case of leptomeningitis, however mild the 
symptoms may appear during the early stage of the disease, should be con- 
sidered otherwise than serious. 
Cases in which the process is limited and within a safe area for 
operation offer a much better prognosis than do the other forms of the 
disease in which the process is diffuse. 
Cases of otitis with symptoms of meningismus which are treated rad- 
ically and early, often lead to recovery without the full development of 
meningitis. 
Cases in which the Kernig symptom is present with involvement of 
the sensorium, with moderate coma, gradually increasing or deep coma, 
rarely recover. 
Muttering or wild delirium with the Kernig symptom, with or with- 
out paralysis of one or more of the cranial nerves, usually leads to stupor 
which in the course of twenty-four to forty-eight hours is followed by 
deep coma and death. 
In most cases active delirium is followed by stupor and coma. 
Active delirium (delirium ferox) with great unrest early, the Kernig 
symptom and increasing elevation of temperature is always ominous— 940 
DISEASES OF THE XERVOUS SYSTEM 
usually fatal. Early and persistent vomiting robs the patient of resist- 
ance and adds an element of danger. 
The addition of paralysis of the cranial nerves, one or more, proves 
the presence of basilar meningitis. 
Optic neuritis is not to be interpreted favorably. 
Inequality of pupils with other symptoms of paralysis (faulty reac- 
tion), and acute symptoms are unfavorable. 
Early convulsions in children are less significant than in adults, but 
in both, in all stages of the disease, they are of serious import. 
Involuntary discharge of urine and feces is always unfavorable— 
showing deep involvement of the sensorium. 
An abnormally slow pulse early, soon (in two or three days) followed 
by a rapid, small and erratic pulse, argues in favor of a rapidly increas- 
ing and fatal process. 
Primary pneumococcus meningitis may be considered as almost uni- 
formly fatal. The exceptions are so rare that the diagnosis may be 
questioned when a patient recovers. 
Paralysis of the extremities, one or more, is as a rule evidence of an 
advanced process. 
The loss of the tendon reflexes after their persistence during several 
days should be unfavorably interpreted. 
Occasionally otitic meningitis recovers after rupture into the middle 
ear. In such cases we must always consider the greater likelihood of 
cerebral abscess and not a simple uncomplicated purulent leptomeningitis. 
Gowers has reported two cases of recovery from puerperal meningitis. 
Mulhit and Tanon have seen recovery from gonococcus meningitis. 
The prognosis of parotid meningitis is comparatively favorable 
(Oppenheim). 
Purulent meningitis following orbital disease or the surgical treat- 
ment of the orbit or eye have in my experience finally been diffuse and 
uniformly fatal. 
The warning of Hippocrates, that no injury to the head is to be lightly 
regarded in spite of the absence of immediate symptoms proves that he 
appreciated the possibility of infection of the meninges long after 
traumatism. 
It is possible for purulent meningitis to develop after injuries to the 
head in which there is no break of the skin or evident external infection, 
when pathogenic organisms are already present in the blood (Huisman, 
IT. Curschmann [Raecke]. 
Cheyne-Stokes breathing is always ominous and usually fatal; it is 
indicative of reduced excitability of the respiratory center. 
Rigidity of the neck, painful movement of the head with retraction— 
opisthotonos—shows involvement of the meninges of the cervical cord. 
The Kernig symptom to which we have already referred was present DISEASES OF THE BRAIN AND ITS MEMBRANES 
941 
in over 94 per cent of our cases and should always be interpreted in the 
presence of other symptoms of meningeal irritation as indicative of menin- 
gitis. An occasional error may be made by such reasoning but this will 
be exceedingly rare in the practice of the cautious clinician, and the 
acceptance of the rule will often lead to early diagnosis and prognosis. 
Lumbar Puncture.—The knowledge gained from lumbar puncture 
in acute leptomeningitis is most valuable for diagnosis and it is of con- 
siderable prognostic value as well. Repeated lumbar puncture has also, 
in a fair number of cases, led to improvement of symptoms, and if the 
conclusions of Kummell, Curschmann, Voss, Bokay and others are con- 
firmed by added experience, we will save at least a small proportion of 
cases by the timely and repeated withdrawal of lumbar fluid, which with- 
out such treatment, present a more serious forecast. 
The prognosis depends in a measure upon the virulence of the infect- 
ing agent. Purulent meningitis offers a more favorable outlook than 
does the tuberculous form of the disease. Lewandowski says he never 
saw recovery when the lumbar fluid gave evidence of streptococcus in- 
fection, while he has seen, as all have, recoveries from staphylococcus, 
and influenza infection. In all of these cases lumbar puncture gives 
valuable prognostic data. In some cases of fully developed meningitis, 
there may be no bacterial contamination; with a cloudy fluid, evidence 
of a limited and localized process, the condition is more favorable than 
when there is dissemination and positive bacterial contamination of the 
spinal fluid. 
Evidences in the spinal fluid of the proliferation of the infecting 
agent in the free meningeal exudate is always unfavorable. 
Plant (etc.) insists that the presence of bacteria in the spinal fluid 
with meningitis is proof of a widespread meningitis—the disease is then 
no longer limited. 
Once the pneumococcus is found in the spinal fluid (the micro- 
organism which is most frequently responsible for the complication), the 
prognosis is exceedingly grave. When the fluid escapes under high pres- 
sure (250-400 mm. of Hg.) and the quantity of fluid is materially in- 
creased, is cloudy, not purulent as a rule, the prognosis is unfavorable in 
the overwhelming number of cases, for the disease may under such con- 
ditions be assumed to be advanced. 
Polymorphonuclear increase is characteristic of pneumococcus men- 
ingitis. 
The presence of the streptococcus viridans in the lumbar fluid, may 
prove the association of chronic infectious malignant endocarditis with 
meningitis often with infarct, and is grave. 
In cases which recover there are often remnants of lesions which are 
destructive and which may lead to deafness of one or both ears, ocular 
defects, chronic suppurations, hydrocephalus and other serious disturb- 942 
DISEASES OF THE NERVOUS SYSTEM 
ances, including mental enfeeblement, paralysis-—either limited or 
extensive. 
The duration of acute purulent leptomeningitis is variable. So-called 
“lightning cases” may lead to prompt death—from 24 to 48 hours—with 
deep involvement of the sensorium early; such histories are not infrequent. 
Operable cases may present grave and threatening symptoms during 
the first day or two; some of these, when localized and drained maTe 
satisfactory recoveries. 
The average duration of the disease is between 12 and 14 days. Sinus 
thrombosis or abscess, without marked—at times no—symptoms, often 
lead to the sudden development of positive symptoms of leptomeningitis 
and death in a few days, unless localized. 
References 
Bokay. Orvosi Hetil., 1907. 
Bramwell (Edwin). Osier’s Modern medicine. 1910, vii. 
Councilman. Quoted by Edwin Bramwell, Osier’s Modern medicine,. 1910, vii. > 
Curschmann. Deutsch. med. Wchnschr., 1910. 
Dopter. Paris Med., 1910. 
Hippocrates. The prognostics, etc. (Adams). 
Huisman (H. Curschmann). Deutsch. med. Wchnschr., 1904. 
Jacobsohn. Klinik d. Nervenkr., Berlin, 1913. 
Kernig. Berl. klin. Wchnschr., 1884, xxi, 829-882. 
Kummell. Deutsch. med. Wchnschr., 1909, No. 48. 
Lewandowsky. Praktische Neurolgie, etc. Berlin, 1912. 
Macewen. Pyogenic infective diseases of the brain and spinal cord. New York, 1893. 
Marchal. Quoted by Oppenheim. Berlin, 1913. 
Milhit & Tanon. Presse Med., 1908. 
Oppenheim. Lehrb. d. Nervenkr., Berlin, 1913. 
Plaut, Rehm & Schottmiiller. Zerebrospinalflussigkeit. Jena, 1913. 
Quincke. Berl. klin. Wchnschr., 1891-1895, 1902. 
Deutsch. med. Wchnschr., 1905. 
Raecke. Arzl. Sach., 1909. , 
Voss. Charite-Ann., xxix. 
(b) Serous Leptomeningitis 
(I) Serous Meningitis 
(II) Acquired Hydrocephalus 
(III) Congenital Hydrocephalus. 
Idiopathic Internal Hydrocephalus, Angio-neurotic Hydrocephalus 
(Quincke) DISEASES OF THE BRAIN AND ITS MEMBRANES 
943 
(I) Serous Meningitis 
Serous meningitis (Quincke) often offers a favorable prognosis, and 
is in all probability dependent upon the same vasomotor disturbances 
which cause other forms of Quincke’s disease or angioneurotic edema. 
This form of meningitis may be of primary origin. 
Serous meningitis may be a complication of the acute infections, pneu- 
monia, typhoid fever, tuberculosis, whooping-cough and measles, in which 
there is, according to Rothman, lowered virulence of the infecting micro 
organisms. These cases should be separated from the Quincke type of the 
disease. 
Lumbar puncture gives data in cases of idiopathic serous meningitis 
which strengthens the diagnosis; the prognosis is more favorable than 
in other forms of leptomeningitis. The fluid escapes under enormously 
high pressure, is markedly increased, contains but a trace of or no albu- 
min, but few lymphocytes, and may show the presence of a few bacteria. 
Marked improvement of symptoms in these cases after puncture is favor- 
able in spite of the fact that exacerbations may follow. 
Cases in which the diagnosis of serous meningitis seems justified not 
infrequently run a self-limited course and heal spontaneously, or if lum- 
bar puncture proves insufficient to drain, puncture of the ventricles has in 
some cases led to recovery. 
Cases in which the pressure is sufficient to force brain substance into 
the foramen magnum as the result of overpowering edema lead to prompt 
death, unless lumbar or ventricular puncture or decompression relieve. 
(II) Acquired Hydrocephalus 
Acquired hydrocephalus and idiopathic internal hydrocephalus may run 
anomalous courses: acute exacerbations may follow a long period of ill- 
defined or even positive symptoms. 
In cases of acquired hydrocephalus death may occasionally follow 
suddenly after several years of symptoms. There are cases of acquired 
hydrocephalus with but few symptoms—headaches, vertigo; the neuras- 
thenic state (Oppenheim) in which the disease itself is little influenced by 
treatment, does not destroy life directly; the patients often die of inter- 
current disease after years of indefinite symptoms and chronic invalidism. 
Chronic acquired hydrocephalus may heal spontaneously or become 
latent. 
Cases of acquired hydrocephalus simulating brain tumor offer an un- 
favorable prognosis though different patients live during periods of vary- 
ing lengths. 
Acute exacerbations are characteristic of hydrocephalus and may lead 
to death in a few hours in coma with or without preceding optic neuritis, 944 
DISEASES OF THE NERVOUS SYSTEM 
or the end may follow a few days of increasing symptoms of meningitis 
with final coma. 
(Ill) Congenital Hydrocephalus 
(.Hydrocephalus interims) 
General Statements.—The appearance of the hydrocephalic child is 
characteristic, with its enormous head, strikingly prominent forehead, open 
fontanelles, and small face—expressionless. The size of the face is out 
of all proportion to the size and weight of the entire head. There is mod- 
erate exophthalmos. The fluid increase in the dilated ventricles is often 
associated with an enormous accumulation between the brain and the 
dura. The greater accumulation is found in the ventricles as a rule 
(interims). At term, the child with congenital hydrocephalus is often 
threatened with destruction because the head cannot be forced through 
the pelvis. 
There are data which prove that congenital hydrocephalus may be 
of the “family type”—when several children of the same family are 
born with the anomaly—or the hydrocephalus may prove to be hereditary. 
Father and son without syphilitic taint have both been hydrocephalic in 
my experience. 
Occasionally the process is arrested and if originally limited, not far 
advanced, an approach to normal conditions may follow. Such patients, 
if there are no other congenital defects may live to the twentieth or twenty- 
fifth year in comfort, even longer. 1 have seen children with large 
heads (hydrocephalus) without improvement in the physical or mental 
status live during periods varying from four months to eighteen years. 
There are but few with unchanged hydrocephalus who live beyond the 
fifth year. 
The large proportion of hydrocephalic children die shortly after con- 
finement, or within a few months of birth. 
Syphilitic children with small hydrocephalus may improve under treat- 
ment, and in occasional cases are cured. 
Spontaneous rupture of the hydrocephalus through the membranes into 
the sutures is exceedingly rare. Huguenin reports nine (9) such cases 
with five (5) recoveries. Some rupture into the nasal fossa. None of 
my cases have been permanently benefited by any surgical treatment, lum- 
bar or ventral puncture. 
The prognosis of congenital hydrocephalus is not materially influ- 
enced by its cause; in the majority of cases the true pathogenesis is doubt- 
ful and remains so. 
Causes and Development.—Traumatism has been assigned, cachexia, 
drunkenness, constitutional diseases, syphilis particularly, have also been 
considered among the causes of hydrocephalus. In all, the prognosis con- DISEASES OF THE BRAIN AND ITS MEMBRANES 
945 
tinues exceedingly grave unless as occasionally happens, the process proves 
to be limited or the fluid is absorbed. 
Hydrocephalus in syphilitics may occasionally reach its greatest devel- 
opment at puberty. The slight congenital anomaly may previously have 
escaped detection. 
The development of the brain is almost always materially and unfa- 
vorably influenced by hydrocephalus. Intelligence is blunted and remains 
so in the fully developed cases. 
Hydrocephalic children are, as a rule, unfit to be received in either 
public or private schools. About one-eighth of all hydrocephalic children 
attempt to keep up with their school work: failure is the rule with most 
hydrocephalic children. 
Accompanying motor paralyses—hemiplegia or monoplegia—are likely 
to remain; secondary contractures always follow if the children live. 
Moderate, unchanging hydrocephalus may be present without materially 
influencing the mind; in rare cases, hydrocephalics have been unusually 
brilliant, talented far above the average man. Cuvier and Helmholtz 
were the subjects of moderate hydrocephalus (Oppenheim and Hause- 
man). 
Hydrocephalic girls present menstrual anomalies—development is com- 
paratively tardy and incomplete. 
Complications.—Epilepsy with hydrocephalus may be an early com- 
plication; it does not yield to treatment. Active treatment, persistent 
medication, may at times postpone the seizure but does no more. 
Spastic paralysis occasionally develops in cases in which there is com- 
pression of the pyramidal tract. 
Blindness is among the most frequent complications involving the 
special senses, and is never relieved by treatment. Other ocular anom- 
alies, including strabismus, as well as nystagmus, choroiditis, optic atrophy, 
once established remain uninfluenced by treatment. Involvement of other 
cranial nerves is infrequent. 
The spinal fluid offers nothing which, after the diagnosis has been made, 
favorably influences prognosis. 
There is as a rule, increased pressure; the fluid is normal in appearance 
also the cellular elements. Acute inflammatory (cerebral or cerebrospinal) 
complications are promptly recognizable by change in the spinal fluid in 
accordance with the nature of the disease. 
Intercurrent disease is a cause of death in cases which live beyond the 
first few months; these include gastro-intestinal, pulmonary, and occasion- 
ally other infections. 
Among my cases of hydrocephalus only one lived to be 30 years of 
age. Gall reports one case which died in his 54th year. 
Tuszek and Cramer had a hydrocephalic patient with idiocy who died 
in his thirty-second year of infection (phlegmon). There are many with 946 
DISEASES OE THE NERVOUS SYSTEM 
congenital hydrocephalus who live with almost no human attributes dur- 
ing periods of varying length. 
Syringomyelia only occasionally develops in cases of hydrocephalus; 
naturally its progress cannot be halted. 
There is occasional development of suprarenal disease with hydro- 
cephalus (Czerny). 
Children with marked hydrocephalus rarely learn to walk and are 
unable to stand or sit without support because of the enormous weight 
of the head. 
References 
Czerny. Centralbl. f. allg. path. Anat., 1899, No. 7. 
Hauseman. XJeber das Gehirn von Herman v. Helmholtz. 
Ztschr. f. Psychol. 
Iluguenin. Ziemssen’s Handb. d. spez. Path. u. Therap., 1878, lx. 
Oppenheim. Charite-Ann., 1890, xv, 307. 
Prince (Morton). J. Nerv. & Ment. Dis., 1897, 502. 
Quincke. Meningitis serosa, etc. Ztschr. f. Nervenheilkunde, Bd. ix. 
Volkmann’s Sammlung klin. Vortrage, 1893, No. 67. 
Schultze. NothnageVs spec. Path. u. Therap., Wien, 1901. 
Tuszek & Crama. Arch. f. Psychiatrie, Bd. xx, Hft. 2. 
Chronic changes in the membranes of the brain (pia-arachnoid) are 
not unusual complications of alcoholism, chronic toxemias, chronic neph- 
ritis, diabetes mellitus, encephalitis, dementia paralytica, or jacksonian 
epilepsy, and may follow traumatism. 
Chronic adhesive leptomeningitis when circumscribed with adhesions 
may simulate brain tumors. 
In all of these conditions the prognosis depends upon the ability to 
influence or remove the underlying cause. As a rule this is impossible, 
though occasionally surgical interference proves curative, or latency fol- 
lows. 
(c) Chronic Leptomeningitis 
References 
Knoblauch. Krankh. des Zentralnervensystem. Berlin, 1909. 
Lewandowski. Neurologie, etc. Berlin, 1913. 
Oppenheim. Lehrb. d. Nervenkr., 1913. 
Osier (Sir William). Practice of medicine. New York, 1914. 8. ed. 
Quincke. Deutsch. Ztschr. f. Nervenkr., 1909. 
Rothmann. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912. DISEASES OF THE BRAIN AND ITS MEMBRANES 
947 
3. Syphilitic Cerebral Meningitis 
See Syphilis. 
4. Tuberculous meningitis 
See Tuberculosis of the Nervous System—Chapter Tuberculosis. 
5. Cerebrospinal Meningitis (Epidemic) 
See Infectious Diseases. 
II. Circulatory Disturbances of the Brain 
1. Anemia 
General Considerations.—Anemia of the brain is of secondary origin, 
and the prognosis therefore depends upon the underlying cause. 
The prognosis of brain anemia per se which folloivs sudden loss of a 
large quantity of blood is not bad. It very often happens that there are 
symptoms of alarming anemia following the loss of .blood during labor 
(placenta previa, post partum hemorrhage) in which the patient is thor- 
oughly exsanguinated, and with the control of the hemorrhage gradual re- 
turn to health is the rule. 
Associated Symptoms.—The cerebral anemia secondary to other con- 
trollable hemorrhages offers a favorable prognosis. 
The anemia associated with the benign chloroses and anemias is usu- 
ally favorably influenced by treatment, and leads to prompt improvement 
and gradual return to health as the general condition of the patient im- 
proves. Marked evidences of cerebral anemia with pernicious anemia, the 
leukemias, splenic anemia, malignant or pernicious malaria, cachexia, can- 
cer, phthisis, are usually associated with grave constitutional symptoms 
and often precede death by only a few days, particularly when there is 
stupor and coma. 
Anemia due to vascular spasm, the latter resulting from advanced arte- 
rial disease, may yield temporarily; the patient may die of intercurrent 
disease. The prognosis of the underlying fault is bad and in the majority 
of cases the disease advances; vascular spasm with associated anemia 
recurs. Hyperemia may finally displace the anemia, or in some cases 
cerebral apoplexy ends the scene. 
The prognosis of cerebral anemia dependent upon insufficient heart 
strength, unless the latter is due to transitory or removable causes, is 
always grave. 
Localized cerebral anemia which depends upon obstruction to the free 
flow of blood through one or more of the cerebral vessels offers an unfa- 948 
DISEASES OF THE NERVOUS SYSTEM 
vorable prognosis; if it persists for any length of time, sudden death may 
follow or the brain tissue may undergo degenerative changes, i. e., soft- 
ening (See Embolism and Thrombosis). 
Transitory paralyses are often due to anemia of the brain following 
vascular spasm (See Arteriosclerosis). The cerebral anemia due to senile 
degeneration remains almost entirely uninfluenced by treatment. 
The ordinary and frequent anemia of the brain associated with the 
phenomena of the “faint spell” is without serious import unless depend- 
ent on organic cause. Many individuals develop cerebral anemia—faint— 
on slight cause, are materially inconvenienced by this idiosyncrasy, but 
the prognosis, so far as life is concerned, is always good. 
The delirium of inanition is due to anemia of the brain; its prognosis 
depends entirely upon the nature of the primary cause. 
Cerebral anemia with co?ivulsions is always ominous, and is as a rule, 
dependent upon grave primary and organic disease. 
Cerebral anemia with unconsciousness, dilated and immobile pupils 
offers an unfavorable forecast. 
Lively pupillary reaction with cerebral anemia is always encouraging.. 
Marked cerebral anemia with uremic intoxication is always unfavor- 
able. 
Cerebral anemia with lead poisoning, acute delirium, and other evi- 
dences of lead encephalopathy, is exceedingly grave and calls for a guarded, 
usually a serious prognosis. 
Oppenheim reports cases of retrobulbar neuritis following profuse hem- 
orrhage and anemia of the brain. Ziegler found parenchymatous de- 
generation of the optic nerve; and Scagliosi found marked changes in the 
ganglionic cells of the brain, and so did Soukhanoff. Bouveret and others 
have found localized edemas of the brain with anemia, and the former 
reports one case in which after an alarming hematemesis, hemiplegia and 
aphasia developed. Such complications either lead to prompt death, or the 
improvement following is surprisingly rapid. 
Paralyses which owe occasionally associated with the secondary anemia 
of childbirth (due to hemorrhage) are as a rule, due to arterial or venous 
thrombosis. The prognosis depends entirely on the way in which the 
patient reacts from the hemorrhage and the extent and location of the 
thrombus, as well as the gravity of the primary disease. 
References 
Bouveret. Revue de Med., 1899. 
Herter and Clark. Diagnosis of organic nervous diseases. New York, 1907. 
Oppenheim. Lehrb. d. Nervenlcr. Berlin, 1913, Bd. ii. 
Scagliosi. Deutsch. med. Wchnschr., 1898. 
Soukhanoff. Wiener med. Wchnschr., 1907. 
Ziegler. Beitrag. zur path. Anat., ii. DISEASES OF THE REA IN AND ITS MEMBRANES 
949 
2. Hyperemia of the Brain 
(Congestion of the Brain) 
General Considerations.—Hyperemia of the brain is symptomatic, and 
like anemia must be considered to be of secondary origin—never a condi- 
tion per se. 
We have but scant knowledge of the true pathology of cerebral con- 
gestion and should not lightly assume that it is often a chronic con- 
dition. The results of post mortem examinations are almost entirely 
negative: no characteristic lesions have been found which explain the 
symptoms. 
A large number of unexplained cases are unquestionably due to toxemia 
of some kind. 
Experimentally no marked increase in the quantity of arterial blood 
can be produced suddenly; an increased flow of blood through the brain 
follows abnormally strong systolic contraction and consecutive rise of arte- 
rial pressure (Leonard Hill). 
Sir William Gowers has said: “Of all regions of cerebral pathology, 
that of congestion of the brain is most obscure. We have very little precise 
knowledge regarding it; and as is often the case, theory has flourished in 
proportion to the deficiency of fact.” 
“It is highly probable that many symptoms have been erroneously 
ascribed to cerebral hyperemia which should be placed at the door of cere- 
bral venous congestion, or of anemia of the brain” (Leonard Hill). 
Hill further concludes: 
“I. Arterial hyperemia of the brain does not exist as a pathological 
state. 
II. Sphygmometer readings of arterial pressure in man show that the 
tension of the cerebral arteries is constantly varied by change of external 
temperature, exercise, sleep, bath, food, etc. Such variations are purely 
physiological. 
III. There is every indication that the quality of the blood which 
flows through the brain is of greater importance than the quantity. 
IV. Mental exhaustion probably does not arise during the stage of 
hyperemia produced by continued over-effort, but supervenes at that period 
when the circulatory mechanism begins to fail, and venous congestion 
accompanied by a deficient supply of oxygen is the fate of the exhausted 
cerebral centers.” 
Nevertheless, there are clinical conditions which arise which remain 
unexplained, requiring consideration, and which suggest the presence of 
a brain which may be abnormal, filled with blood, presenting characteris- 
tic symptoms. To these I refer in the following pages. 
Classification.—Primary conditions in which there is associated acute 
cerebral hyperemia are either (a) active, or (b) passive. 950 
DISEASES OF THE KERVOl'S SYSTEM 
Ill framing prognosis we must suspect that in both forms of cerebral 
hyperemia the blood vessels are over-distended; that the failure to empty 
the capillaries is responsible for the symptoms; that, as Herter has dem- 
onstrated, the abrain suffers from a deficiency of oxygen in consequence 
of the stasis, but in passive congestion there is also an excessive accumula- 
tion of carbonic acid in the capillaries.” 
With active hyperemia the arteries are overfilled with blood, with pas- 
sive hyperemia the veins are overfull. 
Five-sixths of all cases of acute cerebral hyperemia were formerly 
supposed to be active. In the light of our present knowledge we assume 
that the majority of these are toxic or due to vascular fault. There are 
many causes which may be responsible for both varieties of cerebral 
hyperemia, and these demonstrate the enormous difficulties encountered 
in offering a dependable prognosis. 
Among the leading causes which should be considered are, hyperpy- 
rexia, infection—acute and chronic—sunstroke, faulty ventilation, over- 
eating, violent exercise, excitement, long continued constipation, pressure 
(particularly neck constriction) any circulatory fault which obstructs the 
return cerebral circulation, alcohol, highly seasoned foods, opium, bella- 
donna, quinin, the salicylates, amyl nitrite, nitrites generally, tumors of 
the neck, erysipelas, localized brain disease, including tumor, hypertrophy 
of the left ventricle, myocardial insufficiency, long continued worry, mental 
over-activity, anxiety, arteriosclerosis of the cerebral vessels, emotional 
acts, and all diseases associated with faulty metabolism including gout 
and perverted tissue change. 
During the first stage of acute and active cerebral hyperemia, there are 
as a rule, no threatening symptoms. With the slow pulse and hypertension 
which are frequently present, the annoying dreams, increasing mental 
lethargy, restlessness in bed, sluggish mental processes, failure of sleep 
to give the expected rest, halting speech, in many cases, heavy head, fail- 
ing memory from week to week, occasional illusions and delusions, irrita- 
bility, headache, tinnitus aurium, ocular disturbances, numbness or weak- 
ness of one-half of the body at times, cerebral congestion of the arterial 
variety may at least be suspected and the chances are strongly in favor 
of progression to the second stage in which the symptoms, according to their 
severity, may be either apoplectiform, paralytic, convulsive, soporific, ma- 
niacal or aphasic. 
In the apoplectiform variety of cerebral congestion, sudden loss of con- 
sciousness with possible paralysis develops and may continue for several 
hours or days. The face is rarely paralyzed, respiration in the favorable 
cases, though changed, does not become irregular or Cheyne-Stokes. In 
favorable cases there is no involvement of the sphincters, The patient 
in favorable cases, in a limited time (few hours to one or two days) 
gradually returns to a dazed condition, somewhat damaged; at times to DISEASES OE THE BRAIN AND ITS MEMBRANES 
951 
a fairly good condition, with more or less mental depression. When the 
sleep is deep, prolonged, and the breathing irregular, the prognosis is cor- 
respondingly bad. 
Gradual increase of soporific hyperemia with apoplectiform symptoms, 
i. e., increasing from a stupid condition to coma, is always unfavorable. 
It is characteristic of all forms of cerebral hyperemia to recur, and one 
form may merge into another. 
The aphasic and apoplectiform varieties may be allied, and recovery 
may follow. With such a combination, increase of stupor and coma usu- 
ally leads to death with respiratory irregularity and all the evidences of 
compression. At least one-half of the cases of so-called cerebral hyperemia 
are apoplectiform. 
In the paralytic form there are as a rule no prodromal symptoms but 
there is a sudden paralysis or paresis, usually one-sided, and from such 
a condition there may be deepening of all symptoms. In these cases with 
advanced arterial degeneration, hemorrhage may follow and the paralysis 
becomes permanent; on the other hand, the paresis may promptly disap- 
pear with the relief of the congestion. 
The convulsive forms of cerebral hyperemia are rarely found before 
the fortieth year. They may develop with or without prodromal symp- 
toms ; may recur at short intervals; may be followed by a period of stupor 
from which the patient may rally, or following the convulsion and stupor 
coma becomes deep, and death follows. The convulsions do not occur 
during sleep. In the severe cases the pupils are at first contracted; there 
is insensibility to light; vomiting may persist, and the pulse from normal 
frequency in unfavorable cases becomes rapid, irregular and erratic. 
The soporific variety is usually due to passive hyperemia; the gradual 
onset of symptoms without paralysis, more or less headache with dilated 
pupils slowly lead to coma after days of “heavy-headedness” and a final 
period of somnolence. Such patients may for years, without advance of 
symptoms, fall asleep at their work or when in society and particularly 
when trying to read. In many of these cases careful search reveals a toxic 
cause for the soporific stale and it is a question whether in these chronic 
cases the symptoms are not, as a rule, due to renal invasion—rather than 
secondary congestion—in spite of the fact that albumin is almost con- 
stantly absent from the urine. 
Hyperemia with mania—symptoms of marked mental derangement, 
active delirium—may lead to violence. The symptoms may develop sud- 
denly; paralysis may be an accompaniment; death may follow early, or 
there may be secondary involvement which finally leads to death. 
The aphasic form develops suddenly; there is marked aphasia and 
confusion of thought. If there is improvement, the speech returns slowly, 
while the patient remains mentally heavy during a number of days. 
These attacks in some cases recur at short intervals until finally there is 952 
DISEASES OF THE NERVOUS SYSTEM 
overwhelming engorgement; pressure symptoms precede a period of coma 
and death. With advanced arterial disease in this form of hyperemia, 
secondary changes in the brain are prominent, and the patient does not 
often recover from a condition in which symptoms are more or less con- 
tinuous during varying periods. 
The overfull condition of the veins of the brain is usually an accom- 
paniment of old age. There is greater tendency to stupor than in the 
so-called active types of congestion; sleep is disturbed and is likely to 
remain so; dreams and hallucinations are frequent in the intial or pro- 
dromal period. 
Passive hyperemia is more serious than are the active types. 
The prodromal stage of passive hyperemia may he followed by condi- 
tions in which apoplectiform, paralytic, convulsive, soporific, maniacal 
or aphasic conditions prevail; or as with the more acute clinical types, 
there may be a mixed symptom complex. Difficulties of differentiating 
the so-called active from passive hyperemia hardly influence prognosis 
materially. 
The depth of cerebral invasion, the general condition of the patient, 
the character of the p?dmary and underlying lesion with the extent of 
cardiovascular and renal disease in all cases, offer the leading data upon 
which prognosis is founded. 
Passive hyperemia of the brain due to compression of the veins by 
tumors, goiter, mediastinal growths, broken compensation, pulmonary em- 
physema, “fixed thorax,” remain uninfluenced by treatment as a rule, 
save as growths are removed by surgical menas. 
The “apoplectic habit” when accompanied with polycythemia, certainly 
predisposes to cerebral engorgement and cerebral apoplexy. 
Occasional cases which suggest hyperemia because of persistent head 
symptoms suffer from chronic constipation. Many of these cases are 
chronic, have acute exacerbations, and yield to rational treatment. 
It may be safely assumed that the acute or active variety of hyperemia 
offers a better prognosis than does the passive, that much depends on the 
ability of the patient to regulate his habits, particularly during the pro- 
dromal stage, as to work, diet and all other factors which directly influ- 
ence his life. 
The apoplectiform and soporific forms of the symptom complex are 
most grave for they are likely, because of pressure, to fall into coma. 
I recognize the fact that the clinical types to which I have referred 
rest upon an uncertain pathology, but I realize that the clinician fre- 
quently meets them in practice and the study of their prognosis therefore, 
deserves consideration; for the present at least, we can offer no more appro- 
priate chapter for their consideration. DISEASES OF THE BRAIN AND ITS MEMBRANES 
953 
References 
Dana. Textbook of nervous diseases. New York, 1913, also 1915. 
Gowers (Sir William). Quoted by Leonard Hill [£. c.]. 
Herter and Clark. Diagnosis of organic nervous disease. New York, 1907. 
Hill {Leonard). Allbutt & Rolleston’s System of medicine. London, 1910, viii. 
Lewandowsky. Praktische Neurolgie fur Aerzte. Berlin, 1912. 
Mohr & Staehelin. Handb. d. inner. Med. Berlin, 1912, Bd. v. 
Oppenheim. Lehrb. d. Nervenkrank. Berlin, 1913. 
Starr. Organic nervous diseases. New York, 1913. 
3. Occlusion of the Cerebral Vessels 
{Cerebral Softening) 
(a) Cerebral Embolism 
(b) Cerebral Thrombosis. 
The plugging of a cerebral vessel either by an embolus, a thrombus, or 
by pressure, is at once followed by change in the tissues originally supplied. 
Nutrition is cut off, and function is either destroyed entirely or mate- 
rially reduced. 
Collateral circulation may come to the rescue, but as a rule there are 
persistent symptoms so long as the occlusion continues, depending natu- 
rally on the artery or vein involved and the brain area included within the 
distribution of the vessel. 
(a) Cerebral Embolism 
When a plug is lodged in a cerebral vessel brought to the brain from 
a distance, it is as a rule, detached from one of the valves of the heart or 
from the free endocardium. This accident is more frequent in chronic 
valvular disease, than with acute and non-malignant endocarditis. 
Mitral stenosis is the most frequent cause of cerebral embolism. Aortic 
valvular lesions are less frequently the cause of cerebral infarct than are 
the mitral anomalies. 
The prognosis of all infections in which there is thrombosis in the left 
ventricle of the heart with final cerebral embolism is exceedingly grave— 
only rarely does recovery follow. 
The embolic infarcts of acute septic or malignant endocarditis are not 
infrequent with that variety of serious, and usually fatal, infection. 
The prognosis of embolism must naturally depend upon the amount of 
secondary softening of the brain tissue. The size of the area involved is 954 
DISEASES OF THE NERVOUS SYSTEM 
variable. The prognosis is worse when several arteries are plugged or 
when an embolus leads to extensive associated thrombosis and a corre- 
spondingly large region of the brain is robbed of its blood supply. 
Septic emboli very promptly lead to gangrenous patches, multiple 
brain abscesses (metastatic brain abscesses) and death. Such cases often 
follow embolism dependent upon gangrene of the lung or septic endocar- 
ditis (Rothmann). 
Embolic infarcts of the brain dependent upon thrombosis of the pul- 
monary vein with pneumonia offer a very grave prognosis. 
The left middle cerebral artery is the most frequent seat of embolism. 
The area of softening includes the lenticular nucleus, part of the optic 
thalamus, the internal capsule—the great basal ganglia—with the cortex 
very often, because of the closure of the cortical branch of the middle or 
anterior cerebral arteries. 
With embolism, the onset is sudden and the mental condition is clearer 
than with thrombosis or cerebral apoplexy. 
Recovery is more complete with cerebral embolism than with throm- 
bosis or with most apoplexies. 
If the case becomes chronic, the symptoms of brain degeneration per- 
sist; the prognosis of all forms of occlusion or rupture (embolism, throm- 
bosis and apoplexy) is practically the same. 
Embolic infarcts of the brain are much less frequent than is cerebral 
apoplexy. 
Lewandowsky reports 4 cases of embolism to 100 of hemorrhage. 
Eull and persistent loss of consciousness, coming on suddenly, attribut- 
able to embolic infarct, always offers an unfavorable forecast. 
Cerebral fat embolism following fractures, often comminuted, opera- 
tive interference, or other trauma, is always serious and usually leads to 
death in from 1 to 5 days after the beginning of cerebral symptoms. 
Cerebral emboli breaking away from aneurismal coagulum often lead 
to prompt softening with consecutive disturbance of function and always 
offer a gloomy forecast. 
Cerebral plugging with puerperal infection is always a grave accident 
and rarely mends. 
Embolism causes more deaths among women than men. 
Osier says that this is due to the greater frequency of mitral stenosis 
in women. Pitt, on the other hand, found that of 70 cases at Guy’s Hos- 
pital 44 were males and 35 females. Saveliew reports 54 per cent in 
women. 
Diphtheria and Hemiplegia.—With diphtheria, hemiplegia is 
usually of embolic and of endocardial origin; it is serious; rarely do the 
patients recover full use of the half of the body affected. Rolleston found 
in 0,075 cases of diphtheria (6) of hemiplegia; of these (4) died. In one 
of these there was an embolus in one of the cerebral vessels. DISEASES OF THE BRAIN AND ITS MEMBRANES 
955 
References 
Lewandowsky. Prakt. Neurol. Berlin, 1912. 
Osier (Sir William). Practice of medicine. New York, 1914. 
Pitt (Newton). Guy’s Hosp. Rep. 
Rothmann. Mohr & Staehelin’s Handh. d. inner. Med. Bd. v. 
Saveliew. Osier [Z. c.]. 
(b) Cerebral Thrombosis 
Thrombosis is more frequent than has been generally supposed; many 
cases formerly considered due to cerebral apoplexy are now known to be 
of thrombotic origin. 
Pathologic conditions which predispose to cerebral thrombosis are all 
grave and include arterial degeneration—arteriosclerosis—infectious 
diseases, myocardial insufficiency, lowered systolic blood pressure, brain 
tumor, abscess, all diseases associated with cerebral pressure and obstruc- 
tion of the sinuses of the brain—malnutrition and inanition. 
The left cerebral vessels, as in embolism, are more frequently involved 
than are those of the right side. The deeper branches are oftener plugged 
than the more superficial, hence foci of softening result very often in the 
pons and in the medulla oblongata, a complication at once threatening and 
serious. 
In many cases death follows before softening of the brain tissue has 
had time to develop. There are occasional cases in which both sylvian 
arteries are obstructed at the same time and a large part of the brain 
softens in consequence—always hopeless. 
When the thrombus forms slowly and is small, the symptoms increase 
gradually, and the prognosis is more favorable, always depending, however, 
on the vessel involved. 
In some cases of malnutrition, multiple “marantic” thrombi form, a 
large number of foci of softening resulting; the cortex is mainly involved 
and the prognosis of this condition (athrepsia—Parrot’s disease) is always 
grave. 
Primary thrombosis of the longitudinal sinuses is a condition found in 
young subjects, children oftenest, who are suffering from extreme weak- 
ness, or prostration—the result of malnutrition. Both the underlying con- 
ditions as well as the complication are dangerous, and death usually 
results. 
Grave anemias and leukemias occasionally end with sinus thrombosis, 
also cancer and pulmonary tuberculosis. 
Sinus phlebitis or thrombosis following otitis, usually suppuration, is 
as a rule, a serious complication, but prognosis has been materially im- 
proved by early detection and radical surgical treatment (See Surgical 
Treatises and the more recent Monographs by aural surgeons). 956 
DISEASES OE THE NERVOUS SYSTEM 
When a thrombus forms about an embolus, symptoms are likely to in- 
crease, degeneration is progressive, and in most cases the prognosis is bad. 
Thrombosis of any of the cerebral vessels due to blood changes and 
weakened heart usually leads to deep involvement of the sensorium, coma, 
and death. 
Thrombosis associated with specific endarteritis (See Syphilis) often 
with hemiplegia, not infrequently shovrs very satisfactory results from 
rigorous treatment. In many cases there is a remnant of hemiplegia which 
remains uninfluenced by any treatment; often the mental condition of the 
patient is normal, though these subjects are without normal resistance; 
fatigue follows slight physical and mental effort while some remain per- 
manently emotional, forgetful and below par in all respects. 
In senile subjects with arteriosclerosis, gradually increasing thrombo- 
sis leads to death within a limited time. 
Thrombosis of one or more of the cerebral vessels with chronic alco- 
holism is an occasional complication; uwet brain” is usually developed 
in these cases, and death is the result. 
Cerebral thrombosis during the puerperal period with or without sepsis 
is always serious; usually fatal with sepsis. 
Thrombosis of the vertebral or basilar artery may give rise to symp- 
toms of pseudobulbar paralysis. 
Thrombosis of small arteries may exist without giving rise to symp- 
toms of any kind. Cases have been reported in which there were multiple 
but small thrombi with unchanged intelligence. 
The prognosis so far as life is concerned, following the initial coagu- 
lum, is not as bad as with either cerebral hemorrhage or embolism. 
Jones reports that death follows within the first 24 hours in 30 per 
cent of apoplexies, 15 per cent of thromboses, and 7.5 per cent of 
embolisms. 
Coma is better and longer borne by patients with thrombosis and 
embolism than by the subjects of cerebral hemorrhage. If the coma 
deepens or is deep from the beginning, the prognosis is correspondingly 
bad. 
The condition of the cardiovascular organs is of the utmost importance 
in the prognosis of cerebral thrombosis. Marked myocardial weakness is 
almost always followed by death. 
Thrombosis with paralysis, hemiplegia bulbar paralysis, pneumogas- 
tric or phrenic involvement always offers a grave forecast. Unless the 
paralyses disappear within a few they are likely to remain unin- 
fluenced. In all cases the location of the thrombus and the size of the 
focus of softening are of enormous prognostic significance. 
The mental condition is better in embolism than in thrombosis as a 
rule. 
Softening of brain tissue is as a rule more favorable for the continu- DISEASES OF THE BRAIN" AND ITS MEMBRANES 
957 
ance of life than is cerebral hemorrhage. The foudroyant cases are less 
frequent in which death follows within a few hours with embolism or 
thrombosis than with cerebral hemorrhage. 
If patients live, the final damage to brain tissue is greater with soften- 
ing (embolism or thrombosis) than from cerebral hemorrhage. 
The paralysis due to brain degeneration (softening) is likely to be 
more persistent because of the complete destruction of tissue and the 
extension of the destructive process, than with hemorrhage. 
References 
Dana. Nervous diseases. New York, 1913; also 1915. 
Gordon. Diseases of the nervous system. Philadelphia, 1908. 
Hochhaus. Deutsch. med. Wchnschr., 1908. 
Jones. Brain, 1905. 
Nonne. Neurol. Centralbl., 1900. 
Oppenheim. Lehrb. d. Nervenkrank. Berlin, 1913. 
Osier (Sir William). Practice of medicine. New York, 1914. 
Starr. Organic nervous diseases. New York, 1913. 
Tyson & Fussell. Practice of medicine. Philadelphia, 1914. 
Von Mehring & Krehl. Lehrb. d. inner. Med. Jena, 1913. 
4. Cerebral Hemorrhage 
Apoplexy (Cerebral) 
General Considerations.—An escape of blood within the intracranial 
centers is bnt a symptom as a rule, of degenerative, and possibly complex 
conditions. 
The diagnosis of cerebral apoplexy once established, the forecast, be- 
cause of the pathologic conditions underlying, must always be guardedly 
given and the lesion should be considered of grave import. 
Cerebral hemorrhage is evidence of diseased vessels and usually raised 
blood pressure, often associated hypertrophy of the heart, and in many 
cases vascular change in the kidney and other organs. 
There are cases in which hemorrhage occurs without increase of blood 
pressure; it may be assumed, however, that when disease of the cerebral 
blood vessels exists, increased blood pressure is the most active factor in 
causing cerebral hemorrhage. 
Associated Symptoms.—High blood pressure, with symptoms of either 
incipient or advanced change in the cerebral vessels may be expected on 
slight cause to lead to rupture, with all of the attending dangers. This is 
to be specially feared with the chronic changes mentioned above and asso- 
ciated chronic nephritis with the usual hypertrophy of the left ventricle. 
Increased blood pressure may be associated with a number of condi- DISEASES OF THE NERVOUS SYSTEM 
958 
tions, but when present with hypertrophy of the left ventricle, particularly 
when there is broken compensation, the cerebral vessels are in great 
danger. 
Cerebral hemorrhage is often associated with chronic interstitial 
nephritis. In these cases the lesions of both conditions resemble each 
other, for in both the arteries are sclerosed. Chronic granular kidney in- 
cludes hypertension, and in most cases deep involvement of the cerebral 
vessels. Chronic interstitial nephritis cannot be divorced from arterio- 
scleroses, particularly of the cerebral vessels. 
Many hemiplegias supposed to be due to cerebral hemorrhage are 
found on post mortem dependent on thrombotic softening; this is also true 
of the cases mentioned in the preceding paragraph, in which there is 
marked hypertension with positive clinical manifestations of granular 
kidney (Janeway). 
Hypertension alone, without vascular lesions, is not sufficient to cause 
rupture of the vessels. The presence of miliary aneurisms with abnor- 
mally high systolic blood pressure and often an extra and sudden strain, 
are the factors which are paramount in causing the majority of cerebral 
hemorrhages (Charcot). 
Arteriosclerotic processes may be largely limited to the cerebral 
arteries while changes in distant vessels may be so slight as to remain 
unnoticed, or the opposite condition may exist in which the cerebral vessels 
are spared and arteries of the extremities or other internal organs, as the 
heart, intestines, kidneys, and spleen, may alone show advanced degenera- 
tion. As a rule it may be assumed that with true cerebral apoplexy there 
are likely to be marked and advanced lesions in the heart muscle, its ves- 
sels, and the arterial tree. 
The influence of sudden increase of arterial blood pressure, in the sub- 
jects of cerebral miliary aneurism following excitement, over-eating, sex- 
ual indulgence, muscular strain, hurry—under stress—worry, and often 
acute infection, alcoholism, and tobacco poisoning upon existing cerebral 
vascular degeneration is enormous, and is often responsible for hemor- 
rhage. 
The influence of the sudden contraction of the cutaneous vessels 
(after or during a cold hath or exposure) in the subjects of cerebral 
arterial degeneration, demands the closest consideration in framing the 
prognosis. 
Patients with arteriosclerosis and fair-sized miliary cerebral aneurisms 
may, as the result of increased venous pressure (straining at stools, cough- 
ing, sneezing, laughing, during epileptic convulsions, women during labor, 
or whooping cough), rupture a small or large vessel in the brain. In these 
cases the veins are likely to be primarily diseased. 
When cerebral hemorrhage is a complication of grave constitutional 
disease (typhoid, puerperal fever, endocarditis, nephritis, purpura, per- DISEASES OF THE BRAIN AND ITS MEMBRANES 
959 
nicious anemia, leukemia, scorbutus, etc.) the prognosis is clouded, and is 
the more unfavorable because of the malnutrition of the vessels. In some 
of these complications the hemorrhage may be multiple. 
Age.—Deaths from cerebral apoplexy are increasing, as is all arterio- 
sclerotic disease, with the onward march of civilization and the stress of 
modern life. This is shown by the increase of cerebral apoplexy in young 
subjects. Until within the past three decades, death from cerebral hemor- 
rhage was comparatively rare before the fortieth year of life, now while 
as before the arterial changes which underly the hemorrhage are largely 
dependent upon the habits of the individual, there is an increase in fre- 
quency with each succeeding decade. 
I exclude from consideration the traumatic cerebral hemorrhages, 
which are numerous during the first years of life. Thomas offers the 
tables, condensed from the Census Report. “The estimated population 
Table I. Condensed prom the Census Report of 1907. 
DEATHS FROM APOPLEXY AND PARALYSIS 
Decade 
Cases 
Proportion per 1,000 of Deaths 
First 
670 
20.1 
Second 
121 
3.6 
Third 
370 
11.1 
Fourth 
998 
30. 
Fifth 
2,250 
67.7 
Sixth 
4,836 
145.4 
Seventh 
8,491 
255.3 
Eighth 
9,877 
297. 
Ninth 
5,100 
153.4 
Tenth 
544 
16.4 
Total 
33,257 
100.0 
Table II. Condensed prom the Census Report of 1906. 
Population of Registered States 
in 1907, Distributed 
According to Ratios Found in 1900 
Deaths from 
Apoplexy and 
Paralysis 
in 1907 
Liability per 
100,000 
Population 
Relative 
Liability 
First decade 
6,984,883 
670 
9.6 
5 
Second decade 
6,204,278 
121 
2. 
1 
Third decade 
6,260,922 
370 
5.9 
3 
Fourth decade 
5,171,628 
998 
19.3 
10 
Fifth decade 
3,760,575 
2,250 
59.8 
30 
Sixth decade 
2,550,957 
4,836 
189.6 
95 
Seventh decade 
1,579,307 
8,491 
537.6 
269 
Eighth decade 
734,016 
9,877 
1,345.6 
673 
Ninth decade 
180,990 
5,100 
2,817.8 
1,409 
Tenth decade 
13,406 
544 
4,057.9 
2,029 960 
DISEASES OF THE NERVOUS SYSTEM 
in. the Registration States in 1907 was distributed among the decades ac- 
cording to the ratios found in the census of 1900, and compared with the 
number of deaths in each decade which were reported during 1907. The 
error introduced cannot be great. The relative liability in the different 
decades is expressed in proportion, taking the liability in the second decade 
as 1. The increase in liability with each succeeding decade is certainly 
striking.” 
Frequency is not to be confounded with liability to hemorrhage. 
The prognosis in each decade is materially influenced by the etiology 
of the individual cases. During early life traumatism is an important 
etiologic factor. 
The United States Census Report for 1906 shows that of 961 deaths 
due to apoplexy and paralysis, 882, approximately 92 per cent, occurred 
in the first 5 years of life. A large number of these were congenital. 
The influence of acute infections during the first decade of life is para- 
mount. Spontaneous rupture of a cerebral vessel is unlikely in the child. 
In the infections of early life, rupture is only possible when there are 
degenerative changes in the walls of the blood vessels. A fair proportion 
of these cases recover, leaving more or less damage. 
During the first decade of life infantile convulsions are only occa- 
sionally followed by hemiplegia dependent upon hemorrhage. In these 
cases, particularly if epileptic, the paralysis when present is not likely 
to be due to hemorrhages but to other organic disease. Rupture of an 
artery during an epileptic convulsion is a rarity. 
Hemiplegia following convulsions in young subjects is due in the 
majority of cases to acute encephalitis (Striimpell), to the cerebral type 
of infantile palsy, to thrombosis and embolism associated with the infec- 
tions, to whooping-cough in which intracranial hemorrhages may occur, 
following great increase in venous pressure during paroxysms of coughing. 
All of these cases offer prognoses in accordance with the malignancy of 
the primary infection, the extent and character of the cerebral lesion. 
Inflammatory changes in the brain, hemorrhage, thrombosis, and em- 
bolism during the first decade, rarely leave the brain undamaged—more 
or less permanent paralysis persists during life. A large number of these 
children die during the initial stage of the complication. 
It is safe to conclude that in children with symptoms of hemorrhage, 
including paralysis, except in the cases of encephalitis and with positive 
evidences of infection, there is invasion of the vascular system and the 
prognosis is grave in consequence. 
The infections include whooping-cough, typhoid fever, diphtheria and 
measles. Scarlet fever is rarely associated with hemiplegia (Rolleston). 
Malignant endocarditis in early as well as in adult life, with embolic 
infarct leading to hemiplegia, is always fatal. 
Hemiplegia due to hereditary syphilis in early life under proper treat- DISEASES OE THE BRAIN AND ITS MEMBRANES 
961 
ment may recover with but slight damage; if neglected, secondary descend- 
ing contractures and paralysis remain. 
Hemorrhage with glioma early in life may hasten the end. 
Infantile cerebral paralysis, whether hemiplegic or paraplegic, may be 
complicated by posthemiplegic chorea, athetosis, or epilepsy. Develop- 
mental anomalies are frequent and are never entirely overcome; on the 
other hand cerebral paralysis in the child may be severe, and yet recovery 
may follow without damage. The liability to apoplexy in the second de- 
cade of life is decidedly less than in the third. Statistics prove that there 
are fewer cerebral apoplexies between the tenth and twentieth year than 
at any other period during life. The factor of accident, including the 
birth palsies is largely removed. 
As we advance to the third decade of life syphilis becomes an important 
pathogenic factor in cerebral hemorrhage and hemiplegia (See also Cere- 
bral Syphilis). Specific endarteritis with ultimate apoplexy in cases recog- 
nized early and not too extensive, admits of successful treatment. In many 
of these cases, particularly in young subjects, I have had excellent results. 
Cerebral hemorrhage, aphasia, and hemiplegia, complicating the puer- 
peral period is always a serious complex. I have recently treated such a 
case, in which after several weeks, symptoms of renal calculosis 
developed; the stone was located by x-ray and successfully removed. The 
hemiplegic has made a fairly satisfactory recovery with but small damage. 
If in these cases (puerperal), coma is deep at once and the patient fails to 
react in from 36 to 48 hours, the prognosis is bad, and death follows after 
a number of hours of irregular breathing. 
Patients with endocarditis between the twentieth and fortieth year not 
infrequently suddenly develop symptoms of cerebral apoplexy which are 
due to embolic infarct and in the majority of cases, if the latter is of con- 
siderable size or the pons or medulla are included, the prognosis is bad. 
Non-malignant endocarditis may be associated with infarct; paralysis* 
may exist and yet restoration of fair functional ability may follow; death 
may result from intercurrent disease early or years after the paralysis. 
So-called “spontaneous cerebral hemorrhage” in subjects before the 
fiftieth year is exceedingly rare, and when it is suspected demands close 
examination. In the majority of cases a lesion will be discovered which, 
as a rule, makes the forecast gloomy. 
The larger number of cases of cerebral apoplexy demanding our atten- 
tion are found in subjects between the fiftieth and seventieth years. It is 
during this span that arteriosclerosis plays a most important role. 
Syphilitic hemiplegia due to specific endarteritis is less frequent after 
the fiftieth year than between the twentieth and forty-fifth years. 
Monakow found that 0.9 per cent of the population of Canton Zurich 
died annually of apoplexy. Only 15 of 269 of these cases died before the 
fortieth year; 3.7 per cent of all deaths were due to cerebral apoplexy. 962 
DISEASES OF THE NERVOUS SYSTEM 
Heredity.—Family history gives important prognostic data in many 
cases of cerebral hemorrhage. It is not unusual to find several members 
of a family yield to apoplexy at about the same age, with almost parallel 
symptoms; as a rule such cases are not likely to become chronic, but early 
death after a short period of hemiplegia and coma is the rule. When, 
after coma and hemiplegia these patients live, they rarely make recoveries 
which are satisfactory. Such patients may with hemorrhages into the 
internal capsule or other centers, live during periods of varying length— 
paretic and with but little of their original spirit. 
In connection with the subject of heredity Monakow contends that 
“these children inherit a lowered resistance of their cerebral arteries,” 
possibly a weakness of the intima, a tendency to aneurismal dilatations, a 
predisposition to diseases of other organs (kidney, heart, etc.) which in- 
vite arterial change. 
Sex.—The census reports fail to show that sex is a factor of impor- 
tance in causing cerebral hemorrhage. In hospital practice there is 
usually a preponderance of male deaths over the female. 
Thomas in America, and Monakow in Switzerland have both reached 
the same conclusion, i. e., that sex does not appear to have a marked 
influence. Thomas reports that “among 1,000 of the aggregate popula- 
tion within the Registration States the proportion in 1900 was: 505.8 
men and 494.2 women, while among 1,000 deaths from apoplexy and 
paralysis in 1906 there were 504.5 men and 495.5 women.” 
In my hospital service I find again as many men as women. Mona- 
kow found no noteworthy difference in his home (Zurich) in Switzerland. 
Climatic Influence.—Hot weather, sudden changes—either excessive 
heat or extreme cold, the former more particularly—prove to be unfavor- 
able to the subject predisposed to apoplexy. The prognosis of cerebral 
apoplexy in a plethoric subject, when stricken during extremely hot 
weather, is usually unfavorable. 
Habitus apoplecticus.—The influence of the apoplectic habit on my 
material justifies the conclusion that the plethoric and obese subject, if 
he becomes intemperate in any of his habits, is more likely to develop 
degeneration of the arterial wall than are normal individuals. This sub- 
ject, in spite of its age, is still sub judice. 
Overeating, alcoholic excess and dissipation are all factors in reducing 
vitality and resistance, as well as changes in many organs with final 
degenerative changes in cerebral arteries and heart. 
Given an apoplectic, obese and plethoric subject with the habitus 
apoplecticus, it is safe to conclude that in such a subject the chances of 
recovery or partial restitution are materially reduced. 
Gout and rheumatism produce changes which invite arterial degen- 
eration—hence cerebral atheroma and hemorrhage. 
Cerebral apoplexy in subjects surcharged with lead is associated as a DISEASES OF THE BKAIJST AND ITS MEMBRANES 
963 
rule with marked cardiovascular and renal changes, which make the 
prognosis grave. The combination of hemorrhage, uremia and plumbism 
not infrequently leads to prompt death. 
Occupation.—All occupations which include stress and hurry, which 
are sedentary and which require great physical force invite arterio- 
sclerosis and consecutive apoplexy (See Arteriosclerosis and Occupation). 
The Influence of Special Symptoms on Prognosis 
Prodromata.—In all cases, whatever the symptoms, the localization 
of the lesion in the brain and size of the hemorrhage remain the most 
important prognostic factors. 
Hemorrhages into the brain substance following a period of prodro- 
mata oiler no different prognosis than do those cases in which the positive 
evidences of apoplexy are fully developed without a moment’s warning. 
The prodromal symptoms of approaching hemorrhage which often include, 
besides vertigo, somnolence, nosebleed, high blood pressure with hyper- 
trophy of the heart and positive evidences of chronic nephritis, may 
prove of advantage when correctly interpreted, for the warning leads to 
rational treatment and living which may postpone rupture of a cerebral 
vessel. 
The early appearance of retinal hemorrhage with positive evidences 
of cerebral sclerosis, high blood pressure, heart and renal changes, made 
positive by physical signs, vertigo at times, occasional vascular spasm 
(cerebral), includes a symptom complex which argues unfavorably for 
the future. Only a small proportion of such cases live to have apoplexy; 
most of them die of cardiac or renal insufficiencies. When intracranial 
pressure is added, the prognosis in the majority of cases is bad and life 
is not easily prolonged. There are exceptions to this conclusion, but they 
are few. 
The influence of symptoms on the prognosis of the average cerebral 
hemorrhage demands the consideration of— 
(a) The apoplectic attack 
(b) The period of reaction 
(c) The period of paralysis. 
1. The Apoplectic Attack 
Coma.—In the majority of cases coma follows hemorrhage into the 
brain substance. The deeper the coma, the graver is the prognosis in 
most cases. While coma is the pronounced and the earliest symptom 
recognized as being most significant, there are but few cases in which 
other positive evidences of the presence of hemorrhage are wanting before 
there is loss of consciousness (Trousseau). 
In some of these cases the cerebral hemorrhage may be so slight or 964 
DISEASES OF THE NEKVOUS SYSTEM 
so localized as to remain unnoticed by the patient, or by those about and 
with the patient. There are many small cerebral hemorrhages which 
give rise to but few or no symptoms, which are finally encapsulated or 
absorbed. Such cases may precede larger and fatal hemorrhage. Post 
mortem examination of large and promptly fatal hemorrhages often 
shows the presence of the remnant of previous small hemorrhages which 
caused no symptoms. 
When during the early stage there are convulsive movements, the 
prognosis is bad. 
Irregular breathing with coma early, is ominous. 
Cheyne-Stokes breathing is the most notable example of pathologic 
abnormality in respiratory rhythm. It is always significant of deep in- 
vasion of the central nervous system except in early childhood, when it is 
often physiological. There are respiratory abnormalities which approach 
the Cheyne-Stokes breathing, in which there is gasping respiration, with 
nodding of the head, “the chin being thrown quickly upward at each 
respiration and falling slowly with expiration.” Such breathing indi- 
cates approaching death. It is also found in the terminal stage of uremia, 
as well as in brain compression from hemorrhage or other causes. 
Yon Monakow in his exhaustive treatise on cerebral hemorrhage 
reports, after an analysis of a large number of cases, that coma is an 
accompaniment of hemorrhage which is near to the central gray matter 
of the third ventricle, the nuclei of the optic thalamus, and that it is less 
likely to be present when the white matter of the cerebrum is involved. 
Jones (quoted by Thomas) found consciousness lost when the hemorrhage 
ruptured into the ventricle. He found that there was coma in 85.5 per 
cent of such ruptures, “while in the non-ventricular hemorrhages the 
percentage of loss was only 69.4 per cent. These cases offer an unfavor- 
able prognosis.” 
The duration and the depth of coma influence prognosis powerfully. 
The average duration in favorable cases is short—from one-half to 
three hours. Monakow’s experience is the same. Coma which persists 
beyond 24 hours is always serious, and the majority of such cases die 
within 48 to 72 hours. It often happens that patients recover from deep 
coma with gradual return to consciousness, though the sensorium may 
remain dull during a number of days or weeks. When patients fail to 
awaken from the coma, .death may be postponed several days during 
which they remain completely unconscious, and with rapid and irregular, 
often Cheyne-Stokes breathing, the rattling (mucus) in the throat in- 
creases, the pulse grows more and more rapid and irregular, the face 
loses its color, the facies change entirely (at times are Hippocratic) and 
with increasing rise of temperature, at times hyperpyrexia, death results. 
Evanescent paralysis of one extremity, or hemiplegia—paresis,t with 
evidences of vascular spasm usually recurring with advanced arterio- DISEASES OF THE BRAIN AND ITS MEMBRANES 
965 
sclerosis and as a rule, high blood 'pressure, is likely to lead to final 
hemorrhage with deep coma from which the patient rarely rallies. In 
some cases there may he short periods during which the sensorium is 
blunted, and there are occasionally epileptiform seizures before the final 
deep coma leads to death. 
I have seen cases in which the vascular spasm or epileptiform 
attacks recurred during long periods (6 to 18 months) before the final 
deep coma due to hemorrhage developed. Many of these cases were found 
in nephritis (chronic interstitial nephritis). 
Pupils.—Extreme contraction of the pupils is characteristic of hem- 
orrhage into the pons; the forecast is not encouraging. 
The size and reactions of the pupils vary, and offer but little assistance 
in the majority of cases for prognosis. The pupils in serious cases may 
be of normal size, or they may be contracted, unequal or dilated. As a 
rule it is safe to hold that in the most serious cases the light reflex is 
abolished while in the milder cases the reactions continue, though they 
may be abnormally sluggish. 
The sensorium during the attack is differently affected; its long dis- 
turbance is serious. Hemiplegia dependent on hemorrhage without loss 
of consciousness during the “attack” offers a very favorable outlook so 
far as life is concerned, in the majority of cases. 
Temperature.—Temperature study is of great prognostic value. 
Long continued subnormal temperature following outspoken symptoms 
is unfavorable. In most cases there is a fall of temperature (l°-2.5°) 
early, but for the favorable forecast this subnormal temperature should 
yield to a gradual rise of a few degrees within from 1 to 3 hours. 
A long period of subnormal temperature with rapid, irregular, and 
small pulse is unfavorable. 
Marked rise of temperature during the first 24 hours—hyperpyrexia 
—is found in the gravest cases and with deep coma, evidences of menin- 
gitis, these patients die within a limited period (12 hours to 2 or 3 days). 
The highest temperatures following cerebral apoplexy are suggestive of 
invasions of the pons or medulla oblongata. 
The most favorable cases for continuation of life are those in which 
the fall of temperature has not been extreme, the reaction prompt, and 
the sensorium but slightly disturbed. Such cases often show complete 
hemiplegia just as do the more serious cases, and the return to approxi- 
mate health may be as slow as in the cases in which the symptoms of the 
attack—early—were more threatening. 
Pulse.—The pulse early in the attack is slow; it may fall to 45. 
The average case offers a full bounding pulse of about 60 per minute. 
With persistent collapse and finally rapid heart action the prognosis is 
unfavorable. With accompanying nephritis, the persistence of an abnor- 
mally slow and tense pulse after the first 24 hours is always ominous, 966 
DISEASES OK THE NERVOUS SYSTEM 
for in the majority of cases, the blood pressure may continue high to the 
end, but the pulse will soon show the evidences of heart weakness; it 
becomes erratic, rapid and intermittent as well as arhythmic, and refuses 
absolutely to respond. The slow, tense, and bounding pulse is likely to 
show evidences of insufficiency if it persists as suggested above—beyond 
the average period. 
Before death, in most cases, there are indications which include sur- 
render of the heart before respiration is paralyzed, for the breathing con- 
tinues during a limited time after the pulse ceases to beat. When the 
attack is rapidly fatal the respiratory and cardiac centers in the medulla 
are comparatively often involved. Such occurrence is not frequent. 
Even with previous hemorrhages and recurrence, sudden death is not 
the rule. 
Acute Bed-sores.—The acute bed-sore which appears on the buttock 
of the paralyzed side is always a menace. It extends with surprising 
rapidity, is large and destructive, is associated with the septic state, and 
almost always leads to death. This acute bed-sore, fully described by 
Charcot, usually develops about seven to ten days after the development 
of hemiplegia. 
An extensive erythematous blush over the buttocks early, particularly 
if there are vesicles present, is suggestive of acute bed-sore, and local 
gangrene may be expected. 
Ophthalmoscopic Examination.—Ophthalmoscopic examination 
does not offer evidence which proves of material assistance in the prog- 
nosis of apoplexy; there are so many symptoms upon which a forecast 
can be based without the ophthalmoscope. Further there is the fact that 
it is not often at hand when desired during the attack, and that usually 
the average clinician fails to use it early in these cases. Knowledge of 
the condition of the blood vessels, however, may be gained by using the 
ophthalmoscope. By its use the interpretation of intracranial tension 
may be aided, retinal hemorrhage recognized and its influence on prog- 
nosis, which is not usually favorable, determined. 
Duration.—Jones’ table which was compiled from cases verified by 
autopsy is most instructive, for it gives evidence of the duration of the 
attack concerning which only an indefinite forecast can be given in the 
larger number of individual cases: 
Lesion 
Number of 
Collected 
Cases 
Percentage 
Dying within 
24 Hours 
Within 
One Week 
Within 
One Month 
Hemorrhage 
828 
30.4 
63.8 
79.4 
Thrombosis 
158 
15.8 
38.0 
74.7 
Embolism 
273 
8. 
35. 
56. DISEASES OF THE BRAIN AND ITS MEMBRANES 
967 
The average duration of early fatal cases may be placed between 
7 and 10 days. 
2. The Period of Reaction 
The sooner the patient reacts the more favorable is the prognosis, 
provided the heart shows fair strength and the respiratory center is not 
profoundly involved. Reaction within 4 to 6 hours is favorable. The 
average period is between 24 and 48 hours. 
There are unfavorable cases in which the sensorium is only slightly 
involved in which there is prompt reaction, possibly only slight delirium, 
and paralysis may be complete (hemiplegia) but the heart continues 
feeble, erratic and irregular. In from 18 to 36 hours the pulse becomes 
exceedingly rapid, the breathing irregular, and death follows within the 
following 24 to 36 hours. 
Hemorrhage into the cerebellum and into the pons may not be asso- 
ciated with loss of consciousness, in the reactionary period; vomiting and 
collapse may, with feeble systolic force, threaten the life of the patient. 
Before and during the reaction the head and eyes may be turned in the 
same direction (Prevost conjugate deviation)—evidence of a severe con- 
dition. The deviation should always be interpreted as signifying grave 
danger; it is temporary as a rule, and is connected with a lesion of the 
lower parietal lobe. 
Failure to react with increasing accumulation of mucus in the trachea 
and bronchi does not often yield, hut with increasing stupor leads to death. 
Return to consciousness, partial or complete, during the early days 
or hours, early during the period of reaction, and lapse into partial coma 
with respiratory involvement is always unfavorable and such patients 
usually show increasing evidences of compression from which they do 
not, as a rule, rally. In such cases the pulse may remain full and tense, 
and the systolic pressure comparatively high during several days, after 
which the break includes irregular breathing (Cheyne-Stokes) and final 
heart insufficiency, small, erratic and irregular pulse. 
Rise of temperature with hurried or irregular breathing after reac- 
tion is always unfavorable. With hyperpyrexia during the period of 
reaction there is occasionally glycosuria. When this persists and the 
mind becomes clouded, as it often does with such complications, the out- 
look is not encouraging. 
With tonic contraction of the non-paralyzed side, the suspicion of 
rupture into the lateral ventricle is justified, and as elsewhere suggested, 
such rupture is serious. 
Convulsive seizures—either general or local, usually general—when- 
ever present early or during the period of reaction, are evidence of irri- 
tation of the cortical region (motor area) and demand close consideration 
before their influence is finally decided. 968 
DISEASES OE THE NERVOUS SYSTEM 
Retention of urine during the period of reaction or before, ought not 
to be considered unfavorable in most cases. 
The involuntary loss of urine and feces in the first and second stage 
is more serious than retention, though many patients in whom there is 
loss of control finally improve. With a favorable mental condition the 
bladder and rectal functions return. 
3. The Period of Paralysis 
The hemiplegic who lives beyond the second stage of cerebral apo- 
plexy is as a rule damaged, however favorable the course of the disease 
has been; he is often subject to subsequent attacks. This is the generally 
accepted dictum, but a strikingly large proportion of patients escapes 
second and repeated hemorrhages. Most hemiplegics are able to walk 
after a varying period. The arm always improves slower than the leg, 
and the secondary contraction due to descending degenerative changes (?) 
is, as a rule, more damaging and persistent in the arm than in the leg. 
The exalted lenee reflex is present in 92 per cent of all hemiplegias 
due to hemorrhage and is persistent (Ganault) ; rarely does the reflex 
become normal. When the knee reflex is not exaggerated during the 
period of paralysis, some complication should be suspected. In such 
cases Oppenheim found the presence of tabes in one, and cerebral tumor 
in another. 
The prognosis is not unfavorably influenced by the presence or absence 
of the Babinski phenomenon. When late, it shows degenerative change 
in the lateral column. The absence of the cremaster reflex on the affected 
side is of no great prognostic significance. 
Atrophy of muscles, the cause of which remains problematic, does 
not materially influence the outcome in the individual case. There are 
occasional cases in which the limb remains cyanosed, cold and edematous 
with contractures, in which a return of function is hardly to be expected. 
In occasional cases in which for some reason—either central (focal) 
or peripheral (neuritis)—the extremities (usually the hand and arm) 
are painful, the suffering continues during long periods and in some cases 
never entirely disappears. The flexor muscles of the arm show greater 
tendency to resume their function than do the extensors. 
Secondary contractures once fully established are likely to be perma- 
nent; improvement of muscle strength may follow so that the extremity 
often becomes useful. Contractures of the tendo achillis, resulting 
equinovarus particularly, leads to deformity which remains a persistent 
handicap 
The motor fibers are often separated from each other by the effused 
blood following the hemorrhage without being broken or destroyed; hence 
fair or even full function may often be expected after absorption of the DISEASES OF THE BRAIN AND ITS MEMBRANES 
969 
blood under such conditions. It is possible, on the other hand, for resti- 
tution of function to follow the destruction of fibers in the direct motor 
tract following apoplectic insult. This is true of destructive hemorrhage 
into the internal capsule, or very often the radiating fibers. 
In most cases the motor paralysis is associated with an increase of 
the reflexes in the paralyzed limbs. This is not unfavorable. The extent 
and duration of the paralysis must always depend upon the location and 
size of the hemorrhage and the condition of the brain tissue. 
In the mildest attacks, in those cases which promise most there may 
be only a transitory vertigo, no loss of consciousness, no paralysis, severe 
headache at times, numbness of one extremity or one-half the body. In 
these “transitory cases” the return to a favorable condition is the rule. 
Such attacks may be repeated at short intervals, or after a period of 
prodromal symptoms there are in some of these attacks the fully devel- 
oped symptoms of the more serious attack with ultimate hemiplegia. 
While the majority of hemiplegias are preceded by symptoms—more 
or less profound—of cerebral disturbance, paralysis may develop sud- 
denly without the clouding of the intellect. 
Hemianesthesia depends on the invasion or destruction of the poste- 
rior third of the internal capsule and the optic thalamus when it accom- 
panies hemiplegia, and does not per se influence the outcome materially. 
Exceptional cases show the sensory without the motor paralysis; in these 
cases the sensory fibers alone are involved. 
There are cases in which aphasia, hemiplegia, and hemianesthesia 
are associated. As a rule, hemianesthesia does not persist long unless 
there is complete destruction of the posterior part of the internal capsule. 
Improvement may be long postponed, but in the end in most cases there 
is at least partial return of sensation with motor improvement, and 
later almost complete restoration, though some sensory disturbance may 
continue. 
Hemiplegia which remains unchanged during three or four months 
following the initial hemorrhage is likely to persist until the end of the 
patient’s life. 
Improvement of motor function which begins within from three to 
six weeks after the insult, is likely to lead to almost full restoration of 
function. 
There are cases in which years may lapse between attacks without 
material improvement, or there may never be a recurrence of hemorrhage 
in such cases. 
Rupture into the ventricle is rare before the sixtieth year, but as 
already suggested, it is a grave condition. 
Aphasia with hemiplegia due to cerebral apoplexy offers a relatively 
favorable prognosis so far as life is concerned. Speech in most cases 
returns, though the improvement is often discouragingly slow and the 970 
DISEASES OF THE NERVOUS SYSTEM 
failure of the patient to express himself satisfactorily leads to marked 
depression; in those who are emotional this element becomes ascendent. 
In occasional cases complete aphasia may persist during the life of the 
patient. This is less likely to be the case with apoplexy than with 
obliterating endarteritis of the cerebral arteries and associated thrombosis. 
A remnant of aphasia must be expected in a proportion of cases. 
The patient should in favorable cases, where there is even slow improve- 
ment, be encouraged to look for greater improvement ultimately—barring 
recurrence of hemorrhage. 
The prognosis of aphasia with hemiplegia in young subjects is much 
better than in adults, and the child is often easily educated to speak by 
the development of the corresponding portions of the brain. In young 
subjects the compensatory power of the opposite hemisphere is often sur- 
prising, though at times the improvement may be slow. In the adult 
hemiplegia with aphasia offers a less favorable prognosis for restoration 
of function. As already suggested in some cases speech may never fully 
return, and if it does there is likely to be an apparent defect, the mis- 
placing of words. The great irritability of the patient with the emotional 
element in the ascendency makes the patient exceedingly unhappy. 
Re-education is possible in a proportion of cases. Many are taught 
successfully to write with the left hand. 
Hemianopsia is likely to persist unless there is marked improvement 
within the first four weeks. Hemianopsia often disappears entirely 
within the first fourteen days. If the visual path at the sensory crossway 
is destroyed or injured, hemianopsia persists. 
During the period of paralysis the contractures already mentioned 
develop (1 to 4 months). It occasionally happens that the contractures 
do not follow, and in rare cases, contractures which may have persisted 
during a number of years disappear with the appearance of extreme 
atrophy of the muscles. This condition follows secondary lesions in the 
trophic centers of the cord. 
Contractures once fully established are not likely to disappear. 
Any evidence at any time of inclusion of the medulla oblongata at, 
once demands an unfavorable prognosis. This includes glycosuria with 
respiratory and circulatory symptoms. 
Transitory albuminuria with symptoms of disease of the medulla 
is ominous. 
Swellings of the joints (arthritis), edema of the arm and hand with, 
at times, excessive sweating and increasing contractures of the fingers 
and hand are symptoms which usually persist; they are exceedingly an- 
noying and are not influenced materially by treatment. 
Among the posthemiplegic motor complications are rhythmic contrac- 
tions, irregular, at times sudden, contractions of the paralyzed extremity 
and, athetosis. DISEASES OE THE BRA 1N AND ITS MEMBRANES 
971 
With these symptoms the motor paralysis is not complete, and as 
Church and Peterson contend “their presence implies a condition of irri- 
tation somewhere in the path of the upper motor neuron. This is usually 
furnished by lesions in the region of the basal ganglia, especially those 
affecting the optic thalamus and impinging upon the capsular fibers.” 
Posthemiplegic chorea does not often complicate hemiplegia in the 
adult dependent on hemorrhage. The movements may be continuous or 
accompany movements in connection with voluntary motions of the para- 
lyzed, occasionally of the unaffected, side. 
Hemorrhage into the anterior lobe and into the centrum ovale of 
considerable size without lasting symptoms is not impossible. Hemor- 
rhage into the posterior lobes of the brain is likely to leave disturbances 
of vision and remnants of aphasia. 
Mental Condition Following Cerebral Hemorrhage 
In the majority of cases in which there has been deep coma during 
a limited period, return to full consciousness may require several days, 
often longer, during which time the patient does not fully appreciate 
his condition nor is he entirely conscious of his surroundings. lie may, 
if aroused, be able to answer questions of minor importance intelligently, 
but any mental effort requiring thought will as a rule prove to be im- 
possible. This conclusion holds for the majority of cases, but there are 
exceptions depending naturally on the extent and location of the lesion 
and the rapidity of the absorption of the effused blood. 
In those cases in which the mental condition does not improve with 
the motor paralysis, careful inquiry into the previous mental condition 
of the patient should be made. In a large number of such cases the 
advanced arteriosclerotic condition of the cerebral vessels had, before the 
hemorrhage, produced positive evidences of mental deterioration. 
Hemiplegia may never be associated with mental anomalies in occa- 
sional cases. In mild attacks there are no apparent mental after effects. 
A large number of hemiplegics continue emotional during long periods, 
though some of these, in spite of a persistence of partial paralysis, must 
be credited with testamentary capacity; they assume responsibility and 
display good judgment. 
Dementia fully developed following cerebral apoplexy is dependent 
upon cerebral softening (encephalomalacia). Oppenheim believes that 
this complex rests upon “general atheroma and more particularly follows 
apoplectic insult which is of syphilitic origin.” 
“The power of intelligent attention suffers most in damage from any 
cause to the prefrontal lobes” (Robertson). 
Change of disposition is not infrequent; idiosyncrasies may develop 
and yet judgment may not be impaired. The larger number of deep 972 
DISEASES OF THE NERVOUS SYSTEM 
apoplexies which improve or in which there is a return to approximate 
health will show some enfeeblement of mental power. 
Repeated hemorrhages weaken the intellect; there is increasing 
feebleness of mind and body in most of these cases. Finally with in- 
ability to move about, bladder and rectal control is lost in the terminal 
stage, and the end is not long postponed. 
In young subjects during the early days of apoplexy the mental symp- 
toms may be prominent; these are likely to yield with the general 
improvement of the patient. In many, during long periods, the memory 
for remote events is fairly well retained while recent occurrences are 
promptly forgotten. 
Maniacal disturbances sufficient to justify commitment may occa- 
sionally develop after cerebral hemorrhage. The duration of such a con- 
dition is not long as a rule—varying from two to four weeks, rarely 
longer. Relapse is possible usually after from two to four weeks. 
Cerebral apoplexy in the insane may be followed by a striking change 
in the patient; it has been noted that the noisy and troublesome are often 
more quiet and more easily controlled than before the hemorrhage. The 
mental status of the insane patient is lower, as a rule, after the hemor- 
rhage. With general paresis, the hemorrhage is usually of sufficient size 
to cause deep coma and death in from twenty-four to seventy-two hours. 
Large hemorrhage into the internal capsule may exist without symp- 
toms referable to the mind. 
Special Considerations 
In planning the life of the subject of cerebral hemorrhage who has 
gone beyond the acute period, the clinician should remember the great 
likelihod of recurrence. The underlying and serious degenerative arterial 
disease cannot be overcome when once established; the slightest initial 
hemorrhage may be followed by a more serious and promptly destructive 
insult. 
During the attack and during the period of reaction pneumonia may 
develop and lead to death within from thirty-six to seventy-two hours; 
rarely is the end long postponed. 
Pneumonia is of all complications the most serious after cerebral 
hemorrhage. Once the patient finds himself beyond the acute attack and 
in the stage of reaction, even after he may be said to be convalescent, 
inflammation of the lung is a menace which threatens the patient; it 
claims a large number of victims. 
The average duration of life of the hemiplegics has been in my expe- 
rience between five and six years. I have never yet found a case 
which proved to my satisfaction that cerebral apoplexy was in any way 
a conservative measure, or that the enforced rest which followed the DISEASES OF THE BRAIN AND ITS MEMBRANES 
973 
"‘shock” was of material value in preventing “arterial strain,” or that 
life was thereby prolonged. 
References 
Allen. J. Am. Med. .Ass., 1908. 
Charcot & Bouchard. Arch, de Physiol., 1868. 
Church & Peterson. Nervous and mental diseases. Philadelphia, 1914. 
Dana. Med. Rec., New York, 1903. 
Frank. Berl. klin. Wchnschr., 1911. 
Ganault. These de Paris. 1898. 
Janeway {Theodore). Arch, of Med., Chicago, 1907. 
Jones. Brain, 1905, 546. 
Monakow. NothnageVs Spec. Path. u. Therap. Gehirnpath. 1897, Bd. ix. 
Oppenheim. Lehrb. d. Nervenkrankh. Berlin, 1913. 
Robertson {Alex.). Tuke’s dictionary of psychological medicine. Philadelphia, 1892, ii. 
Rolleston. Rev. Neurol. Psychich., 1908. 
Romberg. Berl. klin. Wchnschr., 1909, No. 43. 
Rothmann. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912, Bd. v. 
Strumpell. Textbook of medicine. New York, 1911. 
Thomas. Osier’s Modern medicine, vii. 
Trousseau. Clinical medicine. Paris & Philadelphia, 1873. 
5. Encephalitis 
( non-suppur ati ve ) 
{Acute and Chronic Encephalitis, Acute Hemorrhagic Encephalitis) 
Encephalitis may be considered a symptom complex due to infection, 
usually secondary, in which there are foci of inflammation throughout 
the brain, in the majority of cases accompanying hemorrhagic deposits, 
often due to infarcts. 
Pyogenic cocci may cause either the suppurative or the non-suppura- 
tive variety of the disease. 
Ernst has demonstrated the occurrence of encephalitis following 
traumatism, cases due to metastases and a class of infections which spread 
from neighboring inflammatory foci; most of these are conveyed through 
the lymph stream. The cases of encephalitis of hematogenous origin or 
those which spread by contiguity, show the primary changes in the con- 
nective tissue and blood vessels. 
Encephalitis secondary to the acute infections (acute polyarthritis, 
cerebrospinal meningitis, typhoid fever, scarlet fever, erysipelas, measles, 
diphtheria, influenza, rabies, pyemia, splenic fever and endocarditis) is 
usually of the hemorrhagic type; it is often associated with large embolic 
infarcts, is of grave import and always materially increases the dangers 974 
DISEASES OF THE NERVOUS SYSTEM 
of the primary infections. The strength of the patient has already been 
wasted and the resistance is low; the prognosis is correspondingly bad. 
The larger number of encephalitides associated with hydrophobia, 
pyemia, malignant endocarditis and splenic fever are hemorrhagic. In 
all of such cases the prognosis is bad. 
The prognosis naturally depends upon the size of the hemorrhage 
(infarct) and the malignancy of the primary infection. All sizes of 
hemorrhages occur. 
In the chapter on typhoid fever, attention is called to the bad effect 
of hemorrhagic complications. There are epidemics of typhoid fever in 
which the hemorrhagic tendency is overpowering, and in which non-sup- 
purative encephalitis is frequent and often fatal. 
Cure is not impossible in these hemorrhagic cases, for the infarcts 
may be—usually are—circumscribed, may be absorbed or may lead to 
more or less sclerotic change in the process of repair. Healing of hemor- 
rhagic encephalitis with the formation of a cyst and focal symptoms may 
follow within a reasonable time (6-10 Aveeks) in occasional cases. With 
such conditions cerebral localization is often possible and surgical inter- 
ference, Avhen the cyst is superficial, is successful in a small proportion of 
cases. The surgical treatment of the more chronic cases is less likely to 
be successful because of the permanent disorganization of brain elements, 
leukocytic infiltration and productive changes, cellular deposit and vas- 
cular growth (Ernst). 
Acute encephalitis, a frequent complication of influenza, adds an 
element of great danger. In some of these cases the influenza bacillus 
has been found in the brain substance (see below). 
Traumatic encephalitis (non-suppurative) may follow Avithout break 
of the overlying tissues; disseminated encephalitis, Avithout abscess for- 
mation, may also develop with middle ear and nasal infection (after 
nasal operations) ; AAuth both of these conditions the prognosis is bad in 
proportion to the extent of the process—it is never to be lightly regarded. 
There is a larger number of cases than is generally supposed in which 
the meninges are also involved (meningo-encephalitis). In these cases 
the clinical picture and thoroughly considered history lead to the suspicion 
of the complex character of the secondary infection; the Ivernig symptom 
is present in over ninety-five per cent of the cases and the deep involve- 
ment of the sensorium after a period of indefinite symptoms depending 
upon the localization of the encephalitic foci must be regarded as being 
exceedingly serious. 
Rothmann mentions the possibility of the association of encephalitis 
(non-suppuratRe) with small brain abscesses; the surrounding tissue is 
usually involved. If the abscess is not deep-seated, old or large, and is 
Avithin reach of the surgeon’s knife, the encephalitis yields Avith free 
drainage of the abscess. DISEASES OF THE BRA 1X AND ITS MEMBRANES 
975 
Suddenly arising cases with grave constitutional infection, hyperemia, 
early and mental torpor increasing to coma, are conditions which justify 
only the gloomiest prognosis. 
Evidences of multiple encephalitic foci with increasing evidence of 
meningeal involvement or with high fever, rapid and irregular pulse— 
Cheyne-Stokes breathing—are found in the more serious cases. 
Occasional cases show marked improvement during periods of remis- 
sion and in spite of several exacerbations, recovery may finally be com- 
plete and permanent. Rothmann calls attention to this frequent favor- 
able behavior of influenza hemorrhagic encephalitides. 
Tn cases which live, in which during the acute or subacute period 
paralyses were prominent, there is rarely complete restoration of motor 
function. This is particularly true of the encephalitis of early life, which 
it may be safely concluded is responsible for many permanent paralyses 
(hemiplegia) and other serious complications including epilepsy (See 
Cerebral Palsies of Childhood). 
The cerebral type of poliomyelitis (infantile paralysis) should be 
considered to be polioencephalitic. The majority of children stricken 
succumb to the disease. The prognosis is worse in those cases in which 
there is prompt loss of consciousness. In the severe, usually fatal cases, 
the loss of consciousness is sudden and complete. Tt is exceedingly diffi- 
cult to differentiate from postbasic or other forms of meningitis save by 
lumbar puncture. Paralysis of the respiratory and glossopharyngeal 
muscles develops in the more serious cases, often hemi- or monoplegia 
before death. 
Lumbar puncture offers no data which influences prognosis, though 
it assists in the diagnosis. These cases are fully considered in the chapter 
on infectious diseases (poliomyelitis). 
Polioencephalitis (acute) Superior.—Wernicke called attention 
to the acute encephalitis of alcoholic origin in which there are well 
defined cerebral symptoms, much like those of influenzal origin to which 
I have above referred. 
The delirium, cephalalgia, and somnolence are often associated with 
paralysis of one or more of the cranial nerves, usually the motor oculi. 
Striimpell mentions the occurrence of nystagmus and complete bilateral 
ophthalmoplegia. The association of alcoholic multiple neuritis in hos- 
pital practice is comparatively frequent. These cases rarely recover. 
Respiratory paralysis with increasing heart weakness (rapid uncon- 
trollable heart) with deep coma leads to death in from one to three weeks 
in the majority of cases, though an occasional case may recover after 
weeks of symptoms. 
Psychic disturbances may persist during many weeks in cases which 
finally clear entirely; on the other hand, recovery with permanent mental 
defect and remnant of paralysis is also possible—and not unusual. 976 
DISEASES OF THE NERVOUS SYSTEM 
Cases in which with either polioencephalitis superior or inferior, 
bulbar symptoms develop, may follow the Landry symptom complex. 
These cases should be considered polioencephalomyelitic. Their patho- 
genesis is similar to that of poliomyelitis; occasionally they have been 
traced to the influenza bacillus. The prognosis is bad. 
Acute Encephalitis following Arsenical Poisoning.—Ment- 
berger calls attention to acute hemorrhagic encephalitis following the 
injection of salvarsan. He insists that the fatal complication is due to 
arsenical poison which suddenly overwhelms the brain, promptly causes 
characteristic symptoms of encephalitis hemorrhagica without warning 
(cyanosis and edema of the face, clouding of the sensorium, vomiting, 
diarrhea, dyspnea, hiccough, pupillary paralysis, tonic and clonic 
spasms, final collapse and coma). Age nor sex seem to influence 
this complication though there is a decided predilection for young 
subjects, those without previous lesions of the brain or cord. It is 
further held that the complication may follow in any stage of 
syphilis, regardless of the dose of salvarsan injected. The complica- 
tion may folow either the first or any subsequent injection. The en- 
cephalitis may develop within a few hours or several days after the 
injection. 
The minority of those who have suffered from this form of encepha- 
litis recover. The length of time during which symptoms persist is 
variable. Mentberger insists that the majority die, and that the deaths 
are most frequent among those who have appeared strongest. 
In a large experience with salvarsan and the study of the material of 
many large hospitals I have failed to find experiences which parallel 
those of Mentberger. (For a full consideration of the subject of 
encephalitis due to salvarsan the reader is referred to the literature in- 
cluded in the work of Mentberger, also Fisher, Almquist and Oppenlieim. 
See references.) 
Polioencephalitis (inferior) is limited to the floor of the fourth ven- 
tricle and is fully considered in the chapter on bulbar paralysis. 
Primary acute hemorrhagic encephalitis occasionally develops. Thor- 
ough search, as a rule, proves the process in the majority of cases to be 
secondary, but that there are unexplained cases which Striimpell believes 
justify their consideration as primary cannot be denied. In some of 
these cases the onset is acute; there is high fever and cerebral symptoms, 
delirium, stupor, severe headache, at times focal symptoms, aphasia, 
hemianopsia and evidences of cortical involvement. These symptoms may 
persist during several weeks or only a few days, after which there is 
improvement. But few symptoms persist during a varying period with- 
out progression, finally to disappear in most cases. Striimpell has called 
attention to the presence of “a marked optic neuritis with more or less 
marked venous congestion.” There are some cases which lapse after a DISEASES OF THE BRAIN AND ITS MEMBRANES 
977 
period of improvement. In occasional cases sudden and unexpected 
death occurs. 
Lumbar puncture offers no data which influence the prognosis of any 
form of encephalitis. 
6. Cerebral Paralysis of Childhood 
(Spastic Infantile Hemiplegia (Benedikt), Cerebral Paralysis of Chil- 
dren, The Acute Encephalitis of Children, Spastic Diplegia— 
Paraplegia) 
The Cerebral Paralyses of Childhood include: 
(a) Paralysis due to intra-uterine anomalies 
(b) Birth palsies 
(c) Acute encephalitis of children—Spastic infantile hemiplegia 
(Benedikt). 
(a) Paralysis Due to Intra-uterine Anomalies 
Whatever the variety of paralysis due to congenital defects of the 
brain, the prognosis must be considered to be unfavorable. Faulty and 
arrested development is the most frequent cause, though intra-uterine 
hemorrhage or thrombotic softening are also factors. 
The development of cysts during fetal life and resulting paralysis 
offers no hope for the relief of the resulting paralysis. 
Arrest of development of the cortex cerebri is as a rule a disseminated 
process involving both hemispheres with resulting paralysis, which can- 
not be influenced by any known means. 
The majority of children who are born with cerebral defects die early 
or are helpless with crippling contractures and mental weakness (idiocy). 
But few of these children live beyond the third year. 
A large number of children who live beyond the third year also 
develop epilepsy. Cases in which there are convulsions early in life are 
not likely to live long. A long continued period of mental lethargy 
presages idiocy if the child lives. When with the cessation of convulsions 
the child brightens, the prognosis is correspondingly better. 
Forty-five per cent of all infantile cerebral palsies develop epilepsy. 
“This occurs furthermore in about 50 per cent of the cases of hemiplegia, 
about 30 per cent of all forms of diplegia, and 36 per cent of paraplegias.” 
The Influence of Heredity on the Production of Epilepsy after Infantile 
Cerebral Palsies 
Pierce and Sharp have offered some very interesting data bearing on 
this subject. 
Cerebral palsies are oftener followed by epilepsy than is generally 978 
DISEASES OF THE NERVOUS SYSTEM 
supposed. The question arises in the study of the cerebral palsies whether 
the individual case is likely to be followed by epilepsy. The severity of 
the paralysis does not seem to be a factor in causing epilepsy, for the 
investigation of the material at the Craig Colony proved that the mildest 
cases are often followed by the most severe epilepsy. The influence of 
heredity in epilepsy following infantile cerebral palsy is, as in so-called 
“idiopathic epilepsy,7’ the leading factor. In 443 cases of cerebral (in- 
fantile) palsies with epilepsy complicating, compared with an equal 
number of cases of ordinary epilepsy the influence of heredity was the 
same in both forms. 
In both, heredity proved to be a factor in approximately 70 per cent 
of cases, and in both alcoholism, mental disturbances and the neurotic 
constitution are of equal pathogenic significance in the offspring. 
In the prognosis of cerebral (infantile) palsies therefore, heredity must 
be considered the most important factor. Cases with a family history of 
epilepsy are more likely than are others to develop the complication. 
(b) Birth Palsies 
Intra partum insult is the most frequent cause of birth palsies. 
Premature birth, compression of the head in a narrow pelvis, twin 
births, asphyxia, hemorrhages due to constriction, cord constriction and 
forceps pressure are all factors which lead to meningeal hemorrhage 
invading the motor area of the cortex (Sarah McNutt and Cushing). 
It is not always possible to differentiate the acquired and congenital 
paralyses at birth or later, for the symptoms of both may be the same 
and conclusive data may be lacking. The congenital or birth palsies 
during the first years of life are progressive. Unless there are associated 
disturbances which cause early death, the child as a rule learns how to 
walk much later than the normal time while speech development is also 
tardy. 
In the cases of the “Oppenheim-Vogt type” the non-paralyzed side 
becomes rigid, and motor weakness is developed while athetosis is also 
prominent. The cases are known as a “spastic diplegia(Diplegia 
spastica infantilis). 
The intelligence of these children is not disturbed as a rule, and they 
may grow to manhood with characteristic contractures and facial expres- 
sion, with persistent athetosis and unchanged spasticity. The associated 
symptoms are interesting; they include dislocation of the jaw, which is 
recurrent, bulbar symptoms, with, in occasional cases, inability to hold 
the head upright. Such children as they grow older are easily frightened 
by the slightest noise. 
Freud classifies the cases of diplegia among the birth palsies to which 
Oppenheim agrees. Such diplegics live without increase of symptoms DISEASES OF THE BRAIN AND ITS MEMBRANES 
979 
after they mature, are handicapped by their contractures, athetosis and 
motor weakness, and usually die of intercurrent disease. 
(c) Acute Encephalitis of Children 
Spastic Infantile Hemiplegia (Benedikt) 
There is a definite form of hemiplegia which is found in children 
between one and four years of age which is dependent upon encephalitis 
which is hemorrhagic and acute. In the midst of apparent health the 
child develops high fever, lassitude and malaise. There may be a short 
period of nausea and vomiting; in the severe cases repeated convulsions 
are followed by prompt coma. The convulsions may be followed by 
paralysis without the development of coma, or the hemiplegia may not 
be recognized until the child brightens. 
Improvement of the constitutional symptoms is prompt, but the paral- 
ysis, while it improves materially, does not entirely disappear. The arm, 
as the child recovers, is worse than the leg. Permanent trophic changes 
follow; there is arrested development, and in the most favorable cases 
there is among the remnants of symptoms some loss of motion. 
Contractures are more or less developed in all cases with exaggera- 
tion of the patella tendon reflexes. There is rarely paralysis of any of 
the cranial nerves, neither do sensory symptoms develop save in occa- 
sional cases; there is some blunting of the touch sensation, and with closed 
eyes the ability to differentiate objects is lost. 
In a number of cases of hemiplegia, epilepsy finally develops; the 
attacks may be either of the large or small variety and do not yield per- 
manently to any form of medical or surgical treatment. 
Athetosis is frequently present and remains a permanent symptom. 
Chorea is another refractory complication. 
Speech defect is frequent; mental development is often retarded, but 
in many hemiplegic children the mind is bright and normal, though a 
limited number of these finally develop epilepsy. Idiocy is to be feared 
as is a perverted moral sense. 
Sachs and Osier both contend that hemorrhage and embolic infarct 
are responsible for the majority of hemiplegias of early life. 
Aphasia with hemiplegia in the hemorrhagic form of encephalitis 
early in life disappears as a rule. 
Patients with remnant of paralysis after hemorrhage during early 
life may reach old age. 
Hereditary syphilis may prove to be the cause of hemiplegia in the 
child. 
The infectious diseases of early life are occasionally associated with 
hemiplegia (measles, scarlet fever with nephritis, endocarditis, whooping- 
cough and smallpox). These cases are either embolic or hemorrhagic. 980 
DISEASES OF THE NERVOUS SYSTEM 
The prognosis depends upon the nature of the underlying infection and 
the amount of injury to the brain, as well as the location of the lesion. 
Choreic Paresis 
There are cases of infantile cerebral paralysis in which the paralysis 
is not prominent but the symptoms develop gradually with chorea and 
athetosis in the ascendency. Freud has characterized these cases as 
“choreic paresis.v These cases do not often develop before the third 
year of life, and rarely after the sixth. 
There is no danger of the development of aphasia, epilepsy or de- 
mentia—contractures are not prominent. Chorea and athetosis are the 
leading symptoms. Londe reports the case of a woman who was fifty 
years of age and who had this type of the disease since early childhood 
(spastic-athetotic). 
References 
Almquist. Munch, med. Wchnschr., 1911. 
Church. J. Nerv. & Ment. Dis., 1901. 
Collier. Brain, 1905. 
Dana. Med. Rec., New York, 1900. 
Ernst. Aschoff’s Patholoqische Anatomie. Jena, 1913. 3. Aufl. 
Fisher. Munch, med. Wchnschr., 1911. 
Freud. Die Infant. Zerebralldhmung. In: Nothnagel’s Pathol, u. Therapie. Bd. ix. 
Lcnde. Rev. Neurol., 1901. 
Oppenheim. Ztschr. f. Nervenkrankh. Bd. xliii. 
McNutt (Sarah) & Cushing. See Oppenheim [l. c.]. 
Oppenheim. Lehrb. d. Nervenkh. Berlin, 1913. 
Oppenheim & Cassirer. Die Encephalitis. In: Nothnagel’s Handb. 2. Aufl. Wien, 
1907. 
Osier (Sir William). Practice of medicine. 8th ed. New York, 1914. 
Pierce & Sharp. J. Nerv. & Ment. Dis., New York, 1914. 
Rothmann. Mohr & Staehelin’s Handb. d. inner. Med. 1912, Bd. v. 
Sachs (B.). Am. J. Am. Sci., 1889. 
Nervous diseases of children. New York, 1895. 
Striimpell. Textbook of medicine. New York, 1912. 
Wernicke. Rothmann & Striimpell. Quoted by Oppenheim [£. c.]. 
Ziehen. Handb. d. Nervenkrankh. des Kindesalters. 
7. Abscess of the Brain—Suppurative Encephalitis 
Abscess of the brain or purulent encephalitis is always of infections 
origin, either secondary to aural disease, traumatism, or pus deposit in 
distant organs—one or more—and is rarely due to direct infection of 
the brain through the blood stream. It is safe to conclude that the so- DISEASES OF THE BRAIN AND ITS MEMBRANES 
981 
called idiopathic abscess of the brain does not exist, and when it is 
strongly suspected thorough search will ultimately reveal a focus which 
may have given rise to neither subjective nor objective symptoms, may 
have been hidden during the lifetime of the patient, and may have been 
either acute or chronic. 
The brain often tolerates the accumulation of pus during surprisingly 
long periods, either single or multiple; death in such cases may follow 
acute symptoms in a comparatively short time. A few hours or a single 
day have sufficed. Pus accumulation in the substance of the brain, unless 
it is given free exit, is always a menace and will in the end destroy life. 
The bacterial infections which are responsible for the majority of 
infections which finally lead to brain abscess are either the streptococcus, 
staphylococcus, the influenza bacillus, bacillus typhosus, pneumococcus, 
the meningococcus, and the tubercle bacillus. The staphylococcus viridans 
is also included. Actinomycotic abscesses are occasionally found in the 
brain. 
ISTaturally the prognosis is materially influenced by the location and 
the primary cause of the abscess. Ernst insists that TO per cent of all 
brain abscesses are of local origin, and of these 24 per cent follow trau- 
matism, and 42 per cent aural infections. Distant factors causing 
hematogenous metastases are prominent in 15 per cent, and in about 10 
per cent of all cases the causes remain unrecognized. Seventy-five per 
cent of all cases are found in men while abscess due to traumatism is five 
times more frequent in the male than in the female. Abscess due to 
aural infection is again as frequent in man than in woman. 
Jacobsohn’s classification of brain abscess seems fully justified for 
our purposes with but one addition, for it is based upon the data offered 
in the preceding paragraphs and includes all clinical pictures of the 
disease. 
Jacobsohn considers: 
(a) The Traumatic Abscess of the Brain 
(b) The Otitic Abscess of the Brain 
(c) The Metastatic Abscess of the Brain 
to which I add 
(d) Rhinologic Abscess of the Brain. 
Tuberculous abscess of the brain is considered in the chapter on 
tuberculous meningitis; its prognosis is always bad. 
(a) Traumatic Abscess of the Brain 
The traumatic abscess of the brain may develop without a break in 
the overlying soft or hard tissues. Contusion may be sufficient. An open 
wound of the soft tissues, without fracture, may suffice to give rise to 982 
DISEASES OF THE NERVOUS SYSTEM 
fatal suppuration of the brain substance, to either single or multiple 
abscess, with or without purulent leptomeningitis (see Purulent Lepto- 
meningitis). In occasional cases traumatism may not cause symptoms 
of abscess of the brain until weeks or months after the injury. In some 
of these cases there are suddenly arising symptoms; the entire course of 
the disease becomes fulminating, and unless there are focal symptoms 
or other features which lead to localization of the pus deposit and early 
surgical relief, death promptly follows. In another class of cases the 
development of the abscess is gradual, the symptoms positive, and with 
their increase the diagnosis becomes comparatively easy though exact 
localization may not always be possible. Exact localization either before 
or during operation which justifies drainage will succeed in saving over 
fifty per cent of these patients. 
Cases which develop immediately after injury (fracture, contusion, 
etc.) are often complicated at once with purulent leptomeningitis; they 
involve the sensorium, develop the Kernig symptom, show characteristic 
changes in the fluid removed by lumbar puncture, and are less favorable 
than are the uncomplicated cerebral abscesses due to traumatism. 
Bergmann contended in his classic treatise that “simple contusion of 
the scalp or soft tissues never leads to brain abscess.” The majority of 
clinicians, medical and surgical, do not subscribe to this conclusion. In 
the consideration of this subject for purposes of prognosis I grant, as 
already suggested, the possibility of infection leading to brain abscess 
without discoverable break of the tissues but recognize that in the large 
majority of cases there is an open and demonstrable wound primarily. 
Stab and gunshot wounds are among the leading causes of traumatic 
brain abscesses (Bergmann, Bruns, Oppenheim, Macewen) ; both may 
lead to multiple deposits with leptomeningitis. In these cases the prog- 
nosis is bad. 
In many cases of traumatic abscess of the brain the abscess is super- 
ficially located and easily reached (often cortical). 
The cases in which there is a long interval between the injury and 
the development of symptoms of abscess are less favorable than are those 
cases with frank and fully developed local symptoms immediately or 
soon after the injury. In the former cases the pus deposit is often deep 
seated and beyond the reach of the surgeon. In these cases the symptoms 
may not permit of localization; suddenly arising meningitis is occasion- 
ally the first suggestion of the presence of a lesion. 
(b) The Otitic Abscess of the Brain 
Suppurative disease of the ear furnishes the focus for over 42 per 
cent of all brain abscesses. The majority of these otitides are chronic 
and the infection extends as a rule through the tegman tympani to the DISEASES OF THE BRAIN AND ITS MEMBRANES 
983 
temporal lobe, or from the mastoid cells to the cerebellum. In most of 
these cases there is also perforation of the tympanic membrane. 
The abscess almost always develops on the side of the primary 
infection. 
With double otitis media suppurativa I have found mastoiditis and 
abscess of the brain on both sides at the same time. In one of these cases 
the symptoms of pus accumulation were limited to one side and yielded 
to surgical intervention. The deposit on the opposite side gave no evi- 
dence of its presence during twelve months, when without previous symp- 
toms or warning fulminating purulent leptomeningitis developed, ending 
the life of the patient in three days. 
Jacobsohn’s statistics prove that the abscess is located in the temporal 
lobe or its neighborhood four times as often as in the cerebellum. 
Jansen offers the encouraging data which show but 7 abscesses of the 
brain in 5,000 cases of otitis. 
Heiman found that of 570 otitic abscesses of the brain, 457 were 
due to chronic and 113 to acute aural suppuration. He further reports 
456 abscesses in the cerebrum and 188 in the cerebellum. 
Ilegner found in 5,000 cases of chronic otitis in the Heidelberg Clinic, 
17 abscesses of the cerebrum and 6 of the cerebellum. 
Dench found that among 100 cases of cerebral abscesses 20 followed 
acute otitis. 
Caries of the temporal bone following otitis media and the final de- 
velopment of brain abscess with leptomeningitis are among the graver 
complications, and offer a gloomy outlook. 
In considering the effect of otitis during early life the clinician 
should remember that neglected cases may remain without symptoms for 
years, and that they may lead to brain abscess after puberty, though the 
discharge from the ear may have ceased, and that persistent and neglected 
otitis with discharge may infect the brain years after its first appearance. 
Chronic and encapsuled pus deposit between the dura mater and the 
bone may remain without symptoms during unlimited periods, but finally 
such accumulation is (in most cases) followed by brain abscess—either 
single or multiple—and unless promptly relieved ends in death. 
The possibility of the occasional abscess formation on the side oppo- 
site to the primary otitis should be borne in mind. The prognosis is 
good in such cases if the abscess is recognized early and radical treatment 
is instituted. 
With diabetes mellitus and otitis media with caries of any part of 
the temporal bone and brain abscess—an occasional association of lesions 
-—the prognosis is absolutely bad. 
With sinus phlebitis which is extensive, brain abscess may develop at 
a considerable distance from the primary lesion. 
Otitic brain abscess is usually single, rarely multiple; this fact with 984 
DISEASES OF THE NERVOUS SYSTEM 
its early recognition makes a favorable forecast possible in many cases. 
Between ten and fifteen per cent of abscesses of the brain following ear 
disease are multiple. 
Perforation of otitic abscesses of the brain through the nose, ear, or 
through the temporal bone, is not frequent. Occasional rupture into the 
ventricle may cause sudden death, or rupture, which involves the 
meninges, may cause rapidly fatal meningitis. 
Pyemia from aural and brain abscess occasionally develops; in these 
cases the prognosis is often doubtful during a limited period. The 
tendency to multiple pus deposits and the effect of general infection always 
make the prognosis grave. 
Ophthalmoscopic examination often shows optic neuritis and choked 
disk. In the majority of cases the background of the eye remains un- 
changed. Ocular changes with abscess may occasionally lead to blind- 
ness. Compared with tumor of the brain changes in the background of 
the eye in abscess are much less frequent. 
With otitic as with all other abscesses of the brain slow pulse early 
with increasing rapidity, arhythmia, and erratic behavior of the heart 
with or without respiratory irregularities are always of serious signifi- 
cance. The addition of Cheyne-Stohes breathing is not frequent but is 
always serious. 
Focal symptoms even with large otitic abscesses of the brain may be 
absent, or there may be but few. In the majority of otitic abscesses the 
left temporal lobe is involved, and sensory disturbances of speech are 
often present persisting until the abscess is drained. 
With sensory aphasia, word blindness may occasionally develop. 
The focal symptoms naturally develop in accordance with the location 
and size of the lesion. Abscess in the occipital lobe and angular gyrus, 
as a rule, leads to hemianopsia, though abscess of this region (Rothmann) 
may develop without visual disturbance. 
With cerebellar abscess, ataxia is a prominent symptom. 
With marked pressure on the direct pyramidal tract in the pons and 
medulla there is hemiplegia with a spastic condition, exaggerated reflexes, 
and Babinski. 
The presence of paralysis of one or more of the cranial nerves aids 
in localization; the prognosis is exceedingly grave in most cases in which, 
with basilar pressure, such paralysis exists. 
Bulbar symptoms with brain abscess are evidence of disease of the 
pons and medulla and are always serious. 
(c) The Metastatic Abscess of the Brain 
The prognosis of the metastatic abscess of the brain is invariably 
grave; a large number of these are multiple and the primary disease is 
always threatening. DISEASES OF THE BRAIN AND ITS MEMBRANES 
985 
The majority of the metastases to the brain from distant infection 
are embolic and develop on the left side, within the domain of the middle 
cerebral artery. 
Among the infections which lead to metastases are purulent diseases 
of the lung, bronchitis, empyema, abscess, and gangrene. 
Nather found 8 cases of brain abscess in 100 cases of pulmonary 
gangrene. 
Pyemic and septic infection, ulcerative endocarditis may develop 
brain abscess, with or without focal symptoms; the deposit may be unsus- 
pected. In all death follows within a limited time. 
Brain abscess with pneumonia or a sequel of the disease is usually 
fatal. 
Clay tor gives the report of 58 cases of brain abscess following lung 
infections, of which 20 were associated with bronchiectasia, 10 with 
empyema, 9 with purulent bronchitis, 7 with gangrene of the lung, 6 with 
tuberculosis, 3 with pulmonary abscess, and 2 with pneumonia. 
Brain abscess with any of the many distant infections other than 
those above mentioned, including malignant carbuncle, appendicitis, liver 
abscess, suppurative arthritis, osteomyelitis, uterine phlebitis and septic 
endometritis, dysentery, and ascending genito-urinary infection unless 
limited, with focal symptoms sufficient to make early diagnosis possible 
and with a good general condition and unusual resistance, offers no hope 
of relief by any known method of treatment. 
(d) Rhinologic Abscess of the Brain 
Brain abscess following nasal operations or spreading from nasal in- 
fection may develop without focal symptoms, or may be associated early 
with basilar purulent leptomeningitis. My experience with brain abscess 
following nasal infection has been exceedingly discouraging; the majority 
have died with symptoms of meningitis within from seven to ten days. 
Caries of the ethmoid or other nasal bones, erysipelas, infection after 
removal of polypi and orbital phlegmon are among the primary causes 
from which the brain abscess may develop. 
Brain abscess may occasionally follow tonsillar infection or operations 
for adenoids or other nasopharyngeal operations. 
Parry reports such occurrence after the operations mentioned, and 
after septic disease of the eustachian tubes. The prognosis of these cases 
is based upon the same data as are paramount in reaching conclusions in 
the other forms of brain abscess. 
There are cases of brain abscess without hnown primary cause. 
These are almost uniformly fatal. They are occasionally met during 
epidemics of cerebrospinal meningitis, and are probably due to the 
meningococcus of Weichselbaum. 986 
DISEASES OF THE NERVOUS SYSTEM 
Conclusions.—Clinicians are agreed upon the following conclusions: 
Brain abscess is almost always fatal unless relieved by surgical means. 
Over 50 per cent of traumatic and other abscesses of the brain are 
saved by prompt localization and drainage. Metastatic and rhinologic, as 
well as abscesses of unknown origin, offer an unfavorable prognosis in the 
majority of cases. 
Multiple brain abscesses are uniformly fatal. Surgery offers no en- 
couragement in these cases. 
Metastases to the brain due to septic processes may be present (as a 
rule the lesions are multiple) without symptoms, either general or focal; 
but such deposits hasten the end. 
Pressure, edema, hydrocephalus and meningitis are the leading factors 
besides the constitutional infection which cause death. 
Statistics.—Improved technic and rational diagnosis are improving 
the statistics of the operative treatment of brain abscess. 
Oppenheim reports 60 cases of traumatic brain abscess operated, with 
38 recoveries; 138 otitic abscesses, with 62 recoveries. 
Oppenheim and Cassirer report 206 cases of otitic temporal abscess 
and 76 of otitic cerebellar abscess, of which 148 (70 per cent) and 35 (45 
per cent) respectively were saved. 
Macewen’s statistics are most encouraging for he has had 18 recoveries 
in 19 cases of brain abscess. 
Dench reports a successful issue in over 50 per cent of cases (100— 
with 52 recoveries). In his own practice he operated 18 cases with 6 
recoveries. 
Additional Considerations.—Extradural pus deposit offers an encour- 
aging prognosis if operated early. 
Otitic leptomeningitis (diffuse) is a fatal complication in most cases. 
Otitic sinus thrombosis (purulent) if unoperated is always fatal. Re- 
coveries may be expected in over 65 per cent of cases radically treated. 
Lumbar puncture offers no data which influence prognosis. Diagnosis 
is strengthened in doubtful cases by the withdrawal and examination of 
the fluid. 
Jacobsohn’s concluding sentence in his consideration of the prognosis 
is worth quoting: “The prognosis of untreated abscess of the brain is very 
discouraging; spontaneous recovery is within the domain of the possibili- 
ties but in practice it cannot be considered. Without timely surgical inter- 
ference the patient dies either in coma, at times in convulsions, or in 
other cases with sudden exacerbation of brain symptoms. In some cases 
death follows rupture with symptoms of fulminating meningitis.” 
The duration of brain abscess has been considered with the separate 
etiologic factors and the complications. As a rule the duration varies and 
in the more chronic cases, from whatever primary source developed, there 
may be a history which covers months or even several years of indefinite DISEASES OF THE BRAIN AND ITS MEMBRANES 
987 
symptoms, at times only slight headache or recurring severe headaches. 
There are cases which finally terminate fatally after months during which 
there have been exacerbations of symptoms, at times severe, with improve- 
ment during several weeks or even longer periods. In some of these 
exacerbations there are rigors followed by severe headache and sweats. 
Rupture into a lateral ventricle may lead to sudden death while men- 
ingitis, which frequently develops as the end sequel of abscess, may cause 
death in from three to seventeen days. 
In chronic cases there may be after long latency a considerable period 
of pressure symptoms, edema of the brain, hydrocephalus with final rup- 
ture in the ventricle, or death after a few days of meningitis. 
Cases of self cure, encapsulation or calcifications, are of such rare 
occurrence as to merit no consideration in offering a forecast. 
Hature makes a supreme effort to control brain abscess or limit its 
spread by the formation of a connective tissue enclosure in chronic—at 
times acute—cases; this usually fails, for the abscess may extend in spite 
of its improvised wall. This protective process, however, is responsible 
for the latency of many cases which finally, as the result of fresh infec- 
tion, trauma or other causes, either rupture, extend, or lead to leptomen- 
ingitis. 
References 
Bergmann. Die ckir. Behandlung d. Hirnkrankh. Berlin, 1899. 
Bruns. Die Gesckwiilste des Nervensystems. Berlin, 1897. 
Clayton. Brit. Med. J., 1891. 
Dench. Am. J. Med. Sci., 1907. 
Ernst. Aschoff’s Pathol. Anatomie. 3. Aufl. Jena, 1913. 
Hegner. Quoted by Oppenheim [l. c.]. 
Heiman. Arch. f. Ohrenheilkunde, Bd. Ixvi. 
Jansen. Quoted by Jacobsohn [L c.]. 
Jacobsohn. Klinik d. Nervenkrankh. Berlin, 1913. 
Koerner. Die otitischen Erkrankh. des Hirns. 3. Aufl. 1902-1908. 
Macewen. The pyogenic infective diseases of the brain, etc. Glasgow, 1893. 
Nather. Arch. f. klin. Med., Bd. xxxiv. 
Oppenheim. Der Hirnabscess. In: Nothnagel’s Spec. Path. u. Therap. Berlin, 1909, 
Bd. ix. 
Oppenheim & Cassirer. Der Hirnabscess. In: Nothnagel’s Handb. 2. Aufl. 1909, 
Bd. ix. 
Parry. Lancet, London, 1909. 
Rothmann. Mohr & Staehelin’s Handb. d. inner. Med. Bd. v. 
8. Aneurism 
See Tumors of the Brain and Aneurism 988 
DISEASES OE THE NERVOUS SYSTEM 
III. Tumor of the Brain 
General Considerations.—The insidious growth of brain tumors, the 
unfortunate localization of the majority, the frequent long periods of focal 
symptoms including Jacksonian convulsions, without marked advance, the 
erratic clinical behavior and the innumerable anomalies of a neoplasm in 
an organ which is not particularly tolerant to attack, all tend, with in- 
numerable other factors to be presented in this chapter, to make the prog- 
nosis bad. 
The leading varieties of brain tumor are: 
(1) Tubercle 
(2) Sarcoma 
(3) Glioma 
(4) Carcinoma 
(5) Entozoa (Cysticercus hydatid) 
(6) Syphiloma (Gummata) 
(7) Abscess (Suppurative encephalitis) 
(8 s) Aneurism. • 
Besides the tumors mentioned I have elsewhere in this work called 
attention to the occasional involvement of the brain with actinomycosis, 
and would call attention to the occasional development of 'psammoma, 
cholesteatoma, angioma, adenoma, dermoid cyst and other cysts following 
hemorrhage and traumatism. 
In 6,150 cases of internal disease I diagnosticated brain tumor 13 
times (excluding gummata), or .002 per cent of all internal diseases. In 
9,626 cases of nervous diseases there were 165 brain tumors (Jacobsohn). 
Bruns reports that of 4,300 patients who consulted him with disease of 
the nervous system, he found 80 in whom the diagnosis of brain tumor 
was justified (about 2 per cent). 
Tumors of the cord are not so frequent as are brain tumors. Metas- 
tases to the cord are more frequent than to the brain. The percentage of 
men with brain tumor is 62.5 against 37.5 among women. Bruns’ statis- 
tics of autopsied cases show the proportion to have been 23 males and 8 
females in 31 cases. 
Gowers’ statistics run almost parallel with Bruns’. He found in 650 
cases of brain tumor 440 men and 210 women. Starr based his conclu- 
sions on an analysis of 600 brain tumors and presents the following tables: 
Age.—Most brain tumors develop in persons between the ages of 15 
and 30 years. The second decade in frequency is between 30 and 40. 
More than one-half of Bruns’ cases were between 20 and 40 years of age. 
Brain tumor in old age is exceedingly rare. Experienced clinicians and 
specialists in this field report the rarity of brain tumor after the sixtieth 
year. Bruns says he has seen but one case. Brain tumor in early life is DISEASES OF THE BRAIN AND ITS MEMBRANES 
989 
Situation 
Tuber- 
culous 
Sarco- 
matous 
Glio- 
matous 
Glio-sar- 
comatous 
Cystic 
Carci- 
nomatous 
Gumma- 
tous 
Other 
Varieties 
Total 
I. Cortex Cerebri 
13 
9 
1 
46 
6 
19 
8 
1 
19 
13 
12 
21-127 
II. Centrum Ovale 
III. Cerebral Axis: 
1. Basal Ganglia and Lateral 
6 
2 
5 
7 
1 
11 
i 
4 
15 
1 
3 
1 
1 
5 
4 
35—51 
Ventricles 
2. Corpora quadrigemina 
14 
3 
5 
8 
3 
9 
1 
1 
1 
2 
3 
5 
27-34 
and crura cerebri 
16 
1 
3 
2 
1 
2 
5 
1 
1 
7 
21-14 
3. Pons 
19 
11 
5 
1 
10 
2 
1 
i 
2 
3 
1 
38-17 
4- Medulla 
2 
i 
1 
2 
1 
6- 2 
5. Base 
3 
1 
3 
2 
i 
1 
1 
1 
4 
1 
9 
6. Fourth Ventricle 
1 
1 
1 
1 
1 
2 
1 
1 
5- 4 
IV. Cerebellum 
47 
8 
10 
13 
15 
8 
i 
6 
9 
3 
11 
10 
96-41 
V. Multiple Tumors 
34 
4 
3 
5 
2 
2 
1 
2 
1 
3 
3 
1 
43-57 
152 
41 
34 
86 
37 
54 
5 
25 
30 
2 
10 
31 
2 
20 
30 
41 
300-356 
The study of 1,277 cases reported by the authors included in Starr’s Table II demonstrates the fact that 9 per cent of all brain tumors 
are operable. 
Author 
No. of Cases 
Operable 
Reference 
100 
10 
Pepper’s System, 1886, Vol. V. 
Hale White. / 
100 
10 
Guy’s Hospital Reports, 1888. 
300 
16 
Med. News, Jan. 12, 1889 (children). 
40 
2 
Intracranial Growths, 1891. 
Gray 
53 
4 
Sajous’ Annual, 1891. 
49 
6 
“ “ 1891. 
100 
3 
Verhand, Deut. Gesell. f. Chir., 1892. 
T)ana 
29 
5 
Trans. N. Y. Acad. Med., Jan., 1893. 
300 
21 
Brain Surgery, 1893 (adults). 
50 
3 
Edinburgh Med. Jour., June, 1894. 
23 
1 
Die Geschwulste des Gehirns, 1896. 
Bruns 
33 
3 
Encyclo. Jahresbericht, 1896. 
Starr 
100 
20 
Personal cases to 1903. 
1,277 
104 
TABLE I (The First Column are Children’s Tumors; the Second Adults’ Tumors) 
TABLE II. Percentage of Brain Tumors Removable 990 
DISEASES OF THE NERVOUS SYSTEM 
relatively frequent. Gowers claims relative immunity during the first 
five months of life. Tubercle may develop early (after the sixth month). 
About one-third of all cases of brain tumor are found in children. Gowers’ 
statistics included 18.5 per cent of his brain tumors in the first decade of 
life, 14 per cent in the second—figures which tally very closely with those 
of Bruns and most other English, German, and American neurologists. 
Social status does not seem to influence the development of brain 
tumor, except the tubercle which is more frequent among the poorer 
classes. 
Metastases to the brain are less frequent than to tloe spinal cord. Car- 
cinoma is oftener of metastatic origin than is sarcoma. 
Traumatism plays only a small part in the etiology of brain tumor. 
While this factor is relatively infrequent, there are cases in which there is 
strong evidence in favor of the possibility of tumor development following 
injury. In such cases the tumor may follow closely upon the trauma, or 
a considerable period may lapse before symptoms develop. It must be 
remembered in considering the relations of traumatism to brain tumor 
that not infrequently it is found on careful inquiry that some suspicious 
and suggestive symptoms antedated the injury and that the symptoms of 
tumor, glioma particularly, follow traumatism because of the rupture of 
vessels in the growth, the structure of which is enormously vascular. This 
accident in an existing growth at once leads to unmistakable symptoms 
and prompt diagnosis. 
I have seen cases in which the growth was so far advanced as to 
suggest it, as the cause of the fall which produced the injury. The medico- 
legal aspect of this subject is exceedingly important and demands close 
consideration. 
Another important fact to be considered with the effect of injury is the 
enormous tolerance of the brain. In many cases of sarcoma, at times 
carcinoma of the brain, varying periods in different cases may lapse with- 
out symptoms in the presence of growths which are however promptly 
developed after shock, hemorrhage, or laceration of brain tissue. 
Bruns denies the possibility of degenerative change into true malig- 
nancy in a hemorrhagic focus or in contused brain tissue, as advocated by 
Starr and Oppenheim. 
There are cases in which following trauma, the tumor has developed 
directly in or close to the injured tissue. Oppenheim reports cases in 
which following a period of epilepsy, tumor developed (See also Hitzig, 
Thomas, Bartlett, Keen, and Annandale). 
Aneurismal dilatation following injury is not likely to develop in a 
normal artery, but in vessels which are previously degenerated. 
Heredity is not a factor of importance in brain tumor. Tooth contends 
that it is practically a negligible factor. 
The location of the tumor materially influences the symptoms produced, DISEASES OF THE BRAIN AND ITS MEMBRANES 
991 
as do the rapidity of its growth and the extent of infiltration. Tumors 
which originate in the meninges may, during a long period, produce com- 
pression without giving rise to symptoms; on the other hand, meningeal 
tumors (sarcoma) may cause symptoms early, severe headache, and one 
or more of the leading symptoms of brain tumor with early ocular and 
cardio-respiratory symptoms, depending entirely upon the part of the 
brain compressed. Tumors with multiple symptoms usually grow rapidly, 
and promptly undermine resistance. 
Tumors which cause motor, sensory, and mental symptoms at the same 
time are as a rule, rapidly growing, often associated with meningitis; 
they are often unfavorable for surgical operation, and run a comparatively 
rapid course. 
The leading symptoms of brain tumor are either focal or general. 
Focal Symptoms 
The focal symptoms depend, as do focal symptoms in all brain lesions, 
upon the location of the growth. 
Increase of focal symptoms is proof of increasing infiltration, or in- 
crease in the size of the growth, or both. 
Compression may give rise to but few or no symptoms; it may during 
a varying period cause symptoms due to increased cortical irritation, or as 
the compression persists it may lead to destructive changes and final 
paralysis. 
The focal symptoms are unilateral as a rule; they include spasm, mono- 
plegia, hemiplegia, paresthesias, hemianopsia, aphasia and apraxia, often 
paralyses of one or more cranial nerves (Church and Peterson, Starr, 
Bruns, Dana). 
Hemiplegia which increases gradually, in which thrombosis and 
arteriosclerosis (endarteritis obliterans) can be excluded, is likely to be 
due to brain tumor and when present long before the radical operation in 
operable cases, is not encouraging. 
Paralysis of two or more cranial nerves with or without hemiplegia, 
particularly wdien the nuclei or fully formed nerves are distant from each 
other, in most cases influences prognosis unfavorably. 
The more complex the focal symptoms the greater is the danger in the 
individual case and the less likely is surgery to save the patient. 
Focal symptoms dependent upon compression of the motor area, the 
radiating fibers, the superficial structures or other accessible parts of the 
brain in which the tumor is not infiltrating, offer a far better outlook than 
do those cases in which disseminated deposits are early recognized. 
Mental disturbance, including hallucinations, with brain tumor and 
focal symptoms, with optic neuritis and paralysis, either limited or ex- 
tensive, offers only the gloomiest prognosis wherever the growth is located. 992 
DISEASES OF THE NERVOUS SYSTEM 
General Symptoms 
The leading general symptoms are 
(a) Headache 
(b) Vertigo 
(c) Vomiting 
(d) Psychic disturbances 
(e) Slow and irregular pulse 
(f) Fever 
(g) Spasms and convulsions 
(h) Optic neuritis or optic atrophy 
(i) Emaciation 
(j) Weakness 
(k) Constipation 
(l) Venous obstruction. 
(a) Headache.—Headache is the leading symptom of brain tumor 
wherever localized or whatever its build. The symptom is persistent, and 
is not easily controlled except in the specific deposits. 
Nocturnal exacerbation of headache with symptoms suggestive of 
luetic disease offers a favorable prognosis. The symptom is promptly con- 
trolled in most specific cases. 
The effect of lumbar puncture on this symptom varies; some headaches 
are favorably influenced. In occasional cases lumbar puncture aggravates 
the headache, in spite of the lowering of intracranial pressure which 
usually results. 
The persistence of headache in one location, with local tenderness, may 
in occasional cases serve to assist in the localization of the lesion. Urder 
such conditions the growth is likely to be superficial and often favorably 
located. Occasional cases have been reported in which the headache has 
been so intense and severe as to lead to suicide. 
Starr believes that the distensibilitv of the skull in children is the 
reason for the milder character of the headaches in early life than in 
adults. 
Subcortical tumors without headache, not too deeply located, with 
sufficient symptoms to localize the growth offer a favorable prognosis if 
operated early. 
(b) Vertigo.—Bruns found vertigo particularly prominent as a symp- 
tom of cerebellar and frontal growths. The clinical and prognostic signifi- 
cance of vertigo is important for it assists in localizing the lesion and it is, 
in some cases, an epileptic equivalent (Church and Peterson). 
(c) Vomiting.—Vomiting often assists in early diagnosis. Persistent 
vomiting has in a number of my cases caused extreme weakness and death. 
In non-tuberculous brain tumor, vomiting is less likely to be an early 
symptom than with either tuberculosis or syphilitic deposits. DISEASES OF THE BRAIN AND ITS MEMBRANES 
993 
Vomiting which persists with the characteristic features of "cerebral 
vomiting” is an early symptom of tuberculous meningitis (tubercle) and 
(specific) gummata. In the tuberculous cases of early, or even late life 
it may yield in exceptional cases but it is likely to recur before the stage 
of paralysis which ends the life of these children. 
In the syphilitic cases vomiting yields as the patient is brought under 
the influence of specific treatment. 
Vertigo and vomiting are often present together, the latter following 
acute exacerbation of the former symptom. These cases are often of cere- 
bellar origin. 
Vomiting and headache may cease during limited periods at times. 
When vomiting recurs after temporary cessation, the headache is likely 
to recur with increased intensity. At times both symptoms are promptly 
associated with stupor or other evidences of profound cerebral involvement 
—such behavior may be the precursor of an early fatal termination. 
(d) Psychic Disturbances.—Fully developed mental symptoms are 
usually evidence of advanced infiltration; they are associated with other 
symptoms indicative of early death. In some cases of sarcoma, carcinoma, 
and gummata, there may be early psychic disturbance which persists with- 
out marked advance of deterioration. When convulsions are associated 
with mental weakness, the growth as a rule may be expected to lead to 
early death. In some cases mental symptoms and severe headache may be 
materially relieved during periods of varying length, to return with marked 
increase of pain and mental hebetude. Persistent apathy is unfavorable. 
Tumors of the frontal lobes are likely to be associated with mental symp- 
toms, and these appear early with such lesions. 
(e) Slow and Irregular Pulse.—Marked compression is usually asso- 
ciated with characteristic slow pulse during the early days of the disease. 
When the pulse, formerly slow and full, suddenly becomes rapid and 
erratic, intermittent or arhythmic, it may be assumed that death is im- 
minent. 
Tumors of the medulla or its immediate neighborhood without marked 
general features may cause the slow pulse and respiratory symptoms 
(Cheyne-Stokes) which together are always ominous. 
(f) Fever.—In some cases slight elevation of temperature early is 
suggestive of tuberculous meningitis. Sudden hyperpyrexia with brain 
tumor is always serious, and may be due to invasion of the medulla. As a 
rule it is an expression of deep involvement; it may be associated with 
suddenly arising glycosuria, polyuria and great exhaustion. Death in such 
cases is not long postponed. Slight rise of temperature during the evening 
hours is frequent during the terminal stage of brain tumor, and is asso- 
ciated with wasting and erratic heart action. With persistent fever, de- 
lirium, rapid erratic and intermittent heart action, brain tumor ends life 
in a large proportion of cases. 994 
DISEASES OF THE NERVOUS SYSTEM 
Meningitis may develop in the course of brain tumor causing fever, at 
times sudden hyperpyrexia,. The added evidences of meningeal involve- 
ment are easily interpreted, and with increasing coma death follows in 
from three to seventeen days. If hyperpyrexia is an early symptom, the 
duration of the meningitis is short. 
(g) Spasms and Convulsions.—Spasms and convulsions may be due 
either to limited (focal) pressure or to disseminated disease of the brain. 
With the latter the convulsions are epileptiform in character, and 
generally with the former the spasms are an expression of a lesion in the 
motor area. 
General epileptic seizures in advanced life, occasionally early in life, 
may prove ultimately to be symptomatic of brain tumor—a diagnosis 
which may be confirmed in a large proportion of cases by ophthalmoscopic 
examination. Sixty per cent of all brain tumor subjects have con- 
vulsions. 
Unless the focal lesion which causes jacksonian convulsions is removed, 
general convulsive movements will finally follow, showing advance of infil- 
tration—extension of the growth. Early convulsive movements are 
limited, and with focal lesions aid in localization. With lesions in the 
motor area these early spasms may persist during a variable period, yield- 
ing finally to paralysis of the part originally convulsed. 
Epileptic seizures dependent upon the pressure of brain tumor rarely 
yield unless the growth is removed. The prognosis even with operative 
interference is not encouraging, though an occasional case recovers. With- 
out surgical relief the prognosis of all epilepsies due to tumors, save the 
gummata, is absolutely bad (See Epilepsy). 
Convulsive movements are of great value in the diagnosis of brain 
tumor and often allow the early localization of the growth. Persistence 
of convulsions or spasm after surgical operations is unfavorable, such cases 
are progressive and fatal. 
Convulsions may recur at short intervals, or they may be truly epilep- 
tic with long periods of freedom. In some cases these recur many times 
during a single day or during a limited period, to recur after several 
months of freedom. 
In most cases persistence of convulsions or recurrence at short intervals 
should be interpreted as indicating rapid growth of the neoplasm. Death 
in convulsions is comparatively frequent with brain tumor. The associa- 
tion of hydrocephalus secondary to tumor or hemorrhage may provoke 
convulsions, and prompt death. 
(h) Optic Neuritis and Optic Atrophy.—Choked Disk.—Changes 
which are easily recognized by ophthalmoscopic examination in the optic 
disk are, according to Bruns, the most important of all the general symp- 
toms of brain tumor. There are but few cases in which optic neuritis is 
not present at some time during the growth of the tumor. Oppenheim DISEASES OF THE BRAIN AND ITS MEMBRANES 
995 
reports optic neuritis in most of his cases and holds that the presence of 
choked disk (“Stauungspapille”) is proof of organic disease of the brain 
and, “last but not least,” is almost certain evidence of brain tumor (90 
per cent). 
Optic neuritis is present in the early stages of brain tumor; optic neu- 
ritis is usually present and easily recognized by the aid of the ophthalmo- 
scope within three to four months of the beginning of the growth. When 
the papilla or disk is prominent and dips into the fundus, it is spoken of 
as “choked disk Optic atrophy is a condition which may develop early, 
or may be postponed until the late stage of brain tumor. With the appear- 
ance of atrophy, the swelling of the disk, edema of the optic nerve or 
“choked disk” begins to disappear, while the whiteness of the papilla 
(atrophy) becomes striking. Such progression is characteristic of ad- 
vancing infiltration and growth. 
These ocular changes are most likely to occur with tumors of the cere- 
bellum and with growths which involve the visual paths at the base of the 
brain. Marked prominence of the papilla (choked disk) is always sug- 
gestive of cerebellar invasion. Tumors of the chiasm are also associated 
with changes in the optic disk. 
Optic neuritis occurs with nine-tenths of all brain tumors. Optic 
neuritis is a frequent attendant of meningitis. Meningitis is not unusual 
in the membranes of the brain surrounding the tumor. 
Choked disk is not an. early symptom of brain tumor save in growths 
in which the cerebellum and visual paths are involved, therefore without 
evidence of cerebellar invasion the appearance of choked disk or optic 
atrophy with other evidences of brain tumor must suggest advanced infil- 
tration and an early unfavorable termination. The larger the growth, the 
greater the compression, the more prominent is the papilla. There are 
exceptions to this rule. Usually the more intense neuritis is on the side 
of the tumor. Starr, as the result of his large experience, says of optic 
neuritis: “It is present in 80 per cent of the cases and should be looked 
for in every case which presents cerebral symptoms.” 
Stewart holds that in time optic neuritis in most cases progresses to 
optic atrophy with its accompanying blindness. 
Optic neuritis may persist during considerable time without blindness. 
Optic neuritis and headache may improve after decompression without 
the removal of the growth. In cerebellar and frontal tumors the progres- 
sion and greater intensity of optic change tends to be on the same side as 
the tumor. 
(i) Emaciation.—Extreme emaciation may promptly develop after 
only a short period of symptoms; this often follows in cases with uncon- 
trollable vomiting, in metastatic carcinomata (multiple) with primary 
visceral growths. In some cases the rapid loss of flesh with increasing 
heart weakness is striking. 996 
DISEASES OF TIIE NERVOUS SYSTEM 
Glycosuria with rapid emaciation has been noted in a number of cases, 
particularly with tumors of the medulla. 
Multiple growths (usually carcinomata, gliomata, or sarcomata) are 
likely to cause rapid loss of flesh. 
(j) Weakness.—Extreme muscular weakness with rapidly increasing 
focal and general symptoms, often persistent headache which can only be 
controlled by enormous doses of morphia, presents a complex which may 
persist during several weeks or months. These are among the most pitiful 
pictures met in the practice of medicine. 
(k) Constipation.—Obstinate constipation is present, and an annoy- 
ing symptom, in a large proportion of cases. Directly obstipation does not 
influence prognosis unfavorably. 
(l) Venous Obstruction.—The pressure of a large tumor, or one so 
located as to impede the venous circulation, may cause a certain degree of 
hyperemia (local). Cases in which the venous stasis is sufficient to be 
prominent have also general and focal symptoms associated, which makes 
it easy to prognosticate. The outlook is bad. 
Some general symptoms usually precede the focal and in most cases 
the course of the disease is insidious, though there are many exceptions to 
this rule. Remission and exacerbation of general symptoms are frequent, 
and often lead one to doubt the original diagnosis, but finally continuous 
symptoms with optic atrophy or neuritis, progressive emaciation, and 
mental hebetude cause death. 
Prognostic Influence of the Nature of the Growth 
(1) Tubercle.—Tubercle is the most frequent neoplasm which in- 
vades the brain. Its presence may be tolerated without subjective symp- 
toms during long periods. I have considered brain tubercle fully in the 
chapter on tuberculosis (Tuberculous Meningitis) to which the reader is 
referred. 
(2) Sarcoma.-—Sarcoma of the brain is second in frequency of occur- 
rence. The growth may originate in the membranes of the brain or in the 
brain tissue or cord. There is a difference of opinion as to the consistence 
of the majority of sarcomata; Starr believes they are hard, while others 
consider them soft. In considering the clinical course and complications 
of cerebral sarcomata because of the histologic build of these growths, the 
absence of blood vessels in most, sudden apoplectic conditions need not be 
feared. The sarcomata do not infiltrate, are often encapsulated, and when 
operable are easily enucleated. 
Sarcomata grow rapidly, are usually single though they may be mul- 
tiple. When metastatic, the prognosis is absolutely bad. We have seen 
multiple and symmetrical sarcomata invading both halves of the brain. 
When springing from the bony structures at the base of the brain and DISEASES OF THE BRAIN AND ITS MEMBRANES 
997 
causing pressure, also involving the brain tissue (osteosarcoma,), the course 
of the disease is short. 
(3) , Glioma.—In the majority of cases glioma of the brain is a 
single growth. It may be multiple. It is the characteristic growth of 
the brain and nervous system and is not as a rule a circumscribed 
growth—which fact argues against a favorable outlook—unless removed 
early. Its favorite seat is the cerebrum; its rich vascularity invites 
rupture, consecutive paralyses, and at times sudden death from hemor- 
rhage. Glioma of the brain is usually primary. Gliosarcoma of the brain 
is rare. 
Spiller and others believe that their clinical material justifies the con- 
clusion that glioma may exist many years “without causing symptoms and 
may be of comparatively slow growth.” My experience in several autop- 
sied cases corroborates this conclusion. 
Depending on its location, tumors other than glioma may during long 
periods cause no symptoms; they may grow so slowly as to remain unsus- 
pected and suddenly present with a fully developed train of symptoms 
which promptly lead to death. 
(4) Carcinomatous Deposits.—Carcinomatous deposits in the 
brain are almost always secondary, are usually of rapid growth inclined to 
show multiple deposit, and as all cancers wherever found, are infiltrating. 
Brain cancer rarely develops early in life—usually after middle life. 
Brain symptoms following breast or distant carcinomata should at once 
make the diagnostician suspicious of cancer. 
(5) Entozoa.—Cysts due to parasites may remain without marked 
symptoms during indefinite periods; they may on the other hand cause 
all of the symptoms of brain tumor, and with increasing symptoms lead to 
death. In some cases echinococcus may cause symptoms during a limited 
period, then become encysted, and remain latent during many years (See 
also Parasitic Diseases of the Brain). 
(6) Syphilomata or Gummata.—Syphilomata or gummata of the 
brain offer a good prognosis if treated early and rigorously. 
I have fully considered the prognosis of syphiloma (gummata) in 
the chapter on brain syphilis. Of all brain tumors the gumma or syphilo- 
ma offers the most favorable prognosis. 
In my experience the iodids have only benefited or influenced cases in 
which the tumor was of syphilitic origin. It may be positively assumed 
that malignant growths—non-syphilitic—are in no way influenced by 
iodin, mercury, or by any medical treatment. Starr believes that in some 
cases he has seen good results, more particularly symptomatic relief from 
the use of the iodids. 
(7) Abscess.—Abscess of the brain (suppurative encephalitis) is 
separately considered (See Suppurative Encephalitis). 
(8) Aneurism.—Aneurismal dilatation of the cerebral arteries is 998 
DISEASES OF THE NERVOUS SYSTEM 
also separately considered (See Miliary Aneurism in connection with cere- 
bral apoplexy and the full consideration of arteriosclerosis). 
My cases have all been found after the forty-fifth year, in which there 
were fair-sized tumors (aneurism) ; in all there were symptoms which 
strongly suggested the nature of the growth; in all there were pressure 
symptoms which persisted, usually involving the cranial nerves—one or 
more. 
In the majority of cases the localization of the growth is made possible 
by the focal symptoms. In considering the separate symptoms and their 
pathologic significance I have frequently referred to the influence of 
location on prognosis. It should always be the aim of the clinician to 
localize as nearly as possible the seat of the growth. Unfortunately only a 
small percentage of exact localizations will lead to successful radical treat- 
ment. 
The literature which has accumulated during the past two decades on 
the results of the surgical treatment of brain tumors, proves that only 
from three to five per cent of brain tumors make satisfactory recoveries, 
and less than seven per cent are operable. 
The so-called “pseudo tumors” of the brain in which recovery follows 
are not veritable neoplasms, but present symptoms which resemble those of 
brain tumor. These are cases of meningo-encephalitis according to Oppen- 
heim, and are often tuberculous. Recovery is often slow. Remnants of 
symptoms may remain (Nonne). 
There are occasional (exceedingly rare) cases in which the diagnosis 
of brain tumor has been made, in which there is improvement of symptoms 
and apparent recovery due in all probability to degeneration of the tumor. 
In most of these cases after a limited period, particularly in the malignant 
cases, the symptoms recur and there are evidences of multiple or spreading 
disease and increasing compression. With rupture, escape of cerebro- 
spinal fluid through the nose in tumors with hydrocephalus, the symptoms 
may, during a short period, improve or be partially relieved; but soon pro- 
gression must be expected and death follows. 
Focal symptoms with spasmodic contractions (jacksonian) due to cor- 
tical irritation (tumor) may yield in the presence of such tumor, to be 
followed by fully developed motor paralysis. In such cases there is no 
further improvement, but with increasing evidences of brain compression 
and motor insufficiency, the general and ocular weakness as well as other 
focal symptoms increase until death follows. 
Symptomatic improvement may occasionally follow lumbar puncture, 
but never cure. 
Lumbar puncture is not without danger to life in cases of brain tumor. 
Additional Considerations DISEASES OF THE BRAIN AND ITS MEMBRANES 
999 
Decompression may also relieve the symptoms in an occasional case, 
but the growth unless removed is in no way modified. 
Enormous assistance for localization, treatment and prognosis may 
follow stereoscopic x-ray pictures. 
Periods of latency with the persistence of but few symptoms, have 
occasionally led to erroneous prognosis. Such cases may remain quiescent 
during limited periods to suddenly advance with increase of exhaustion, 
optic neuritis and other symptoms, depending on the location of the tumor. 
In some of these cases with the development of blindness or psychic dis- 
turbance, the patient may continue to live during several weeks or months. 
Such cases are likely to die suddenly, or with increasing coma and evi- 
dences of added basilar meningitis death follows. There are recorded 
cases in which tubercle nodules and sarcomata degenerated, calcified, and 
their growth was inhibited. The echinococcus may die, and with an en- 
closing membrane and calcification may never give rise to symptoms (See 
Parasitic Diseases of the Brain). 
Positive symptoms of tumor may disappear during considerable 
periods in which repeated epileptic convulsions have been the leading 
symptom. Epilepsy may be the only symptom of brain tumor during 
unlimited periods before the continuous or positive symptoms of the 
growth. With tumor and epileptic seizures, the former may remain unsus- 
pected and the diagnosis is made post mortem. 
The duration of brain tumor varies in accordance with its histologic 
build, its location, and the rapidity of its growth. 
Tooth’s analysis of 500 positive cases without operation in which 
glioma was the most frequent growth (49.2 per cent), showed that in these 
growths the survival was from six weeks to nine years, “but only one case 
had so long a period.” The average period was ten and one-tenth months. 
Tumors in the frontal region survive longest, the temporosphenoidal 
region next, and “the corona radiata” last. Tooth found the shortest sur- 
vival period in tumor of the midbrain—“pons-cerebellum, and base of the 
brain—in which it was twenty-four days—this was a glioma of the pons; 
and the longest two years, also a tumor of the pons.” “The average 
survival period was nine and one-tenth months; not much less than that 
for the forebrain.” 
Endothelioma, according to Tooth, offers a better prognosis than the 
growths above mentioned; when operable it is not likely to recur. The 
average survival period in Tooth’s cases was four years and it is held by 
his reviewer (Spiller) that “this figure errs on the side of underestima- 
tion.” 
Tooth’s cases of pituitary tumor averaged seven and one-half years. 
Most authors and clinicians give three years as the average duration of 
brain tumor. 
Tooth’s resume of 500 cases of brain tumor operated at the National 1000 
DISEASES OF THE HERVOUS SYSTEM 
Hospital during a period of ten years proves that a high mortality follows 
all operations on the brain “even in the hands of the most experienced sur- 
geons.” Simple craniectomy has shown a high mortality. All are agreed 
that the success of all operations is largely influenced by the location 
attacked. The danger is generally regarded by surgeons as greater in the 
cerebellar region, least in the region of the midbrain. Cushing finds cere- 
bellar tumors favorable for attack. 
In considering the factors which influence the results in operable brain 
tumor, we face the danger of shock, sudden collapse, respiratory and cir- 
culatory failure, including hemorrhage. The sudden respiratory or circu- 
latory embarrassment may follow within a few hours, or late paralysis 
may promptly end life without a moment’s warning several weeks after 
operation. 
Hyperpyrexia following operation is not unusual, and with the Kernig 
symptom and other evidences of meningitis may end life within a few 
hours. Hyperpyrexia and circulatory embarrassment may, without evi- 
dences of meningitis, promptly cause death. There have been cases in 
which the removal of a growth of doubtful, but supposedly innocent build 
has been promptly followed by the rapid growth of near and distant 
metastases of a malignant nature, with increase of general and focal symp- 
toms and death. This occurrence is purely accidental and does not argue 
against the radical treatment of all growths which are operable. 
Tumors of the hypophysis cerebri have been successfully attacked of 
late, and with a growing experience the results are increasingly successful. 
The brilliant work of Schloffer, v. Eiselberg, Krause, ITirsch, and Cush- 
ing lead to the hope of greater accomplishment in this field in the future. 
The palliative operations (trepanning the skull, decompression) are 
justified in properly selected cases, for they occasionally bring the relief 
which, if it does no more, gives the unfortunate victim an easy euthanasia. 
Cushing justifies operative interference because among other benefits 
he includes “a Sellar decompression”—“the partial removal of a tumor or 
struma for the relief of neighborhood symptoms.” 
The hope of attacking the forebrain as well as the midbrain for the 
removal of growths is strengthened by the results of Horsley, Krause, 
Cushing, and a score of other operators. 
Lumbar Puncture.—Lumbar puncture in brain tumor is not without 
danger and should be undertaken with great caution. Increased pressure 
(300-600 mm. Hg.) is not unusual. The higher the pressure the more 
serious the condition of the patient. In some cases the fluid is yellow- 
tinged, and in advanced tumor fibrin coagulum is found. There is but 
little albumin while Phase I (JSTonne), i. e., globulin, is absent. 
Cellular increase is not great and in the majority of cases does not 
exist. With specific deposit (gummata) there is usually lymphocytic and 
albumin increase. Meningeal hemorrhage with tumor shows blood in the DISEASES OF THE BRAIN AND ITS MEMBRANES 
1001 
fluid; such cases are grave. Cholesteatoma (basilar) shows cholesterin 
crystals and “fat needles/’ without albumin and cellular increase (Plaut, 
Rehm, Schottmiiller). 
Brain puncture in the hands of the expert will finally lead to localiza- 
tion of growths, will make clear their histologic structure and will thus 
assist in the diagnosis and prognosis (See Rothmann). 
References 
Bergmann. Die chir. Behandlung d. Hirnkrankheiten. Berlin, 1899. 
Bramwell. Intracranial tumors. London, 1888. 
Bruns. Die Geschwiilste d. Nervensystems. 1908. 
Wien. klin. Rundschau, 1897, No. 46. 
Church & Peterson. Nervous and mental diseases. Philadelphia, 1914. 
Cushing. The pituitary body and its disorders. Philadelphia, 1912. 
Dana. New York Med. Rec., 1904; also Diseases of nervous system, 1915. 
von Eiselberg. See Oppenheim [l. c.]. 
Hirsch. Berl. klin. Wchnschr., 1911, xlviii. 
Hitzig, Thomas, Bartlett & Amandale. Quoted by Oppenheim. 
Lehrb. d. Nervenkranlch. Berlin, 1913. 
Horsley (Victor). Lancet, London, 1886, i, 5. 
Brit. Med. J., 1906, if, 411-423. 
Jacohsohn. Klinik der Nervenkrank. Berlin, 1913. 
Krause. Chir. d. Gehirns u. Riickenmarks. 1908-1911. 
Krause (F.). Hirnchirurgie. Deutsch. Klin., 1905, viii, 1004- 
Mills. Cerebellar tumors. 1905. [/See above.] 
Mills, Frazier & de Schweinitz. Tumors of the cerebellum. New York, 1905. 
Mills, Frazier & Spiller. Tumors of the cerebrum. Philadelphia, 1906. 
Nonne. Deutsch. Ztschr. f. Nervenh., Bd. xxvii, 33. 
Oppenheim. Die Geschwiilste des Gehirns. 
Nothnagel’s Path. u. Therap. Bd. ix. 
Oppenheim & Krause. Berl. klin. Wchnschr., 1906. 
Plaut, Rehm & Schottmiiller. Leitfaden z. Untersuchung der Zerebrospinalfliissigkeit. 
Jena, 1913. 
Rothmann. Mohr & Staehelin’s Handb. d. inner. Med. 1912, Bd. v. 
Schloffer. Wien. klin. Wchnschr., 1907. 
Spiller. Progressive medicine. Philadelphia, Sept., 1913. 
Starr. Brain surgery. New York, 1894. 
J. Nerv. & Ment. Dis., 1903. 
Am. J. Med. Sci., 1910. 
Organic nervous diseases. New York, 1903. 
Stewart. Brain, 1904. 
Diagnosis of nervous diseases. New York, 1912. 
Tooth. Proceedings of the Roy. Soc. Med., Neurol. Sect., Oct. 31, 1912» 
Int. Congress of Med., Sect, of Neurology, 1913. 1002 
DISEASES OF THE NERVOUS SYSTEM 
IV. Parasites of the Brain 
Echinococcus is fully considered in the preceding chapter on tumor of 
the brain. 
The cysticercus cellulosae is rarely found in the brain in the United 
States; on the Continent it is relatively frequent. The prophylactic treat- 
ment of infected meat (Tenia solium) is reducing the number of these 
cases. Solitary cysts are the rule (Stern). 
With the death of the cysticercus the contents of the cyst may calcify, 
and if fortunately located, symptoms may end and the patient may live 
without material handicap. The life of the cysticercus may continue from 
three to twenty years. 
Echinococcus of the brain is a rare disease; hut 22 of 327 echinococcus 
subjects were found with brain deposit. Cysticercus and echinococcus may 
be accidentally discovered post mortem without a suspicion of their previ- 
ous existence. It is surprising to note how, with deposit near vital brain 
centers, both may continue latent and life not be disturbed. In the 
majority of cases cerebral parasites do cause symptoms which include 
many of those considered in the chapter on brain tumor. Most promi- 
nent are headache, vertigo, and mental disturbance. In some cases neu- 
rasthenia, hysteria, epilepsy and well-defibed psychoses have been promi- 
nent. 
Griesinger has called attention to the frequency of convulsions with 
brain parasites. 
With growth and pressure, the cranial nerves, one or more, may be- 
come involved. Optic neuritis, choked disk and atrophy are less frequent 
than with the ordinary forms of brain tumor. Mild neuritis occasionally 
develops. 
Cases in which glycosuria, circulatory and respiratory symptoms de- 
velop prove a dangerous localization of the tumor, and death is not long 
postponed. 
Paralysis is not an early symptom and is not likely to develop in the 
average case. Cysticercus of the brain is always serious. It is often 
latent, as already suggested, and may be cured by nature’s process at any 
stage of its existence. Oppenheim reports the case of a male patient who 
was treated during many years for cortical epilepsy of cysticercus origin 
(he also had cutaneous cysts) in whom the convulsions finally ceased, and 
he remained cured. 
Lumbar puncture is of great value in the diagnosis of cysticercus and 
echinococcus of the brain, and in some cases prognostic data may also be 
obtained (Plaut, Relim, and Schottmiiller). DISEASES OF THE BRAIN AND ITS MEMBRANES 
1003 
References 
Griesinger. Gesammte Abhandlungen. 1872, i. 
Herschberg. Berl. klin. Wchnschr., 1904. 
Oppenheim. Die Geschnnilste d. Gehirns. 2. Aufl. Wien, 1902. 
Plaut, Rehm & Sc hot tm idler. Leitfaden z. Untersuchung d. Zerebrospinalfliissigkeit. 
Jena, 1913. 
Stern. Ztschr. f. klin. Med., Bd. Ixi. 
V. Cerebellar Disease 
In connection with tumor of the brain the prognosis of cerebellar 
growths is considered, a favorite and probably the most frequent seat of 
neoplasms. 
With the exception of cerebellar ataxia, cerebellar tumor and abscess, 
cerebellar paralysis of children, and the arteriosclerotic and other vascular 
changes which lead to cerebellar symptoms, the other lesions of the cere- 
bellum are unimportant, rare, and usually associated with disseminated 
disease. 
Ataxia once fully developed -with cerebellar disease, remains a perma- 
nent symptom—it is the leading symptom of such a lesion. The faulty 
equilibriation, tendency to fall or sway to one side, is also permanent and 
characteristic. The ataxia is always on the same side as the focal change 
or deposit, and the swaying is also toward the same side. In man, as in 
other animals, compensation may occur so as to “permit of but little 
evidence of incoordination.” 
Naturally congenital defects of the cerebellum—heredo-ataxie cere- 
belleuse (Marie) remain uninfluenced by treatment. 
With senile cerebellar atrophy there are symmetrical changes, partic- 
ularly in both hemispheres and in the cerebello-olivary fibers. The proc- 
ess is progressive and a part of an apparent general decay. 
Cerebellar staggering due to arteriosclerotic changes in the vertebral 
artery—its branches, the basilar or cerebral arterioles—is usually associ- 
ated with far-reaching change in the arterial tree, and persists. Cerebral 
apoplexy, uremia or cardiac insufficiency are the usual causes of death 
in these cases. 
Besides arterial degeneration with sclerosis of the cerebellum, hemor- 
rhage and thrombosis are among the vascular lesions. 
Hemorrhage, as Nothnagel suggested, may be suspected if, without 
motor pai'alysis at the beginning of an attack, vomiting is a persistent 
symptom. There may be a considerable focus in the center of one hemi- 
sphere without paralysis, but there are other persisting symptoms of cere- 
bellar disease. 
Hemorrhage into the middle portion of the vermiform process may 1004 
DISEASES OF THE NERVOUS SYSTEM 
lead to dyspnea, deviation of eyes to the left, tremor of the left half of 
the face, great unrest, and respiratory paralysis. The nearness of the 
pons is the cause of hemorrhage into it and the cerebellum at the same 
time, with an unfavorable ending as a rule. Thrombotic lesions of the 
cerebellum are small, and may cause no symptoms. 
The fact that the reflexes—patellar tendon—may in the same case 
at different times be either exaggerated, diminished, or abolished, does not 
influence prognosis. 
Cerebellar lesions, tumors particularly, are “especially liable to optic 
neuritis early and in severe degree, leading rapidly to loss of sight and 
consecutive atrophy” (Russell). 
Nystagmus is one of the most constant symptoms of cerebellar disease, 
though it is not always present. 
Hemiataxia and hemihypotonia are characteristic of cerebellar ataxia 
and simulate hemiplegia at times. These symptoms persist. Hypotonia 
is also persistent and uninfluenced in almost all cases; it is characteritic 
of cerebellar disease. Bastian first called attention to the fact that mus- 
cular tonus is derived from the cerebellum. 
With Wernicke’s polioencephalitis hemorrhagica superior (alcoholic) 
(see Encephalitis), cerebellar ataxia and other focal symptoms with de- 
lirium and ocular paralysis form a threatening symptom complex. 
Lesions which begin in the middle cerebellar peduncle usually invade 
the pons as they extend. Disease of the middle peduncle may remain sta- 
tionary and “lesions which simply exert pressure on it may cause no char- 
acteristic symptoms” (Herter). 
The prognostic significance of cerebellar symptoms, functional and or- 
ganic, have been separately considered in connection with the systemic 
and indiscriminate lesions—hence repetition in this chapter is unnecessary. 
There are many functional and organic diseases (multiple sclerosis, 
hysteria, neurasthenia, etc.) in which cerebellar symptoms are prominent; 
the prognosis is always influenced by the nature of the primary condition 
as well as that of the complication. 
References 
Arndt. Arch. f. Psychol., Bd. xxvi. 
Bastian. Med. Chir. Tr., 1890, 207-217. 
Paralysis—cerebral, bulbar & spinal. 1886. 222-228. 
Ferrier. Functions of the brain. 1886. 
Fickler. Deutsch. Ztschr. f. Nervenh., 1911, Bd. xli. 
Herter & Clark. Diagnosis of organic nervous diseases. New York, 1907. 
Marie. La Semaine Med., 1893, 
Nothnagel. Topische Diagnose. 187. 
Russell. Brit. Med. J., 1910, 626. 
Sanger (Brown). Brain, 1892, xv, 250. GENERAL DISEASES OE THE NERVOUS SYSTEM 
1005 
D. Functional and General Diseases of the 
Nervous System 
“Everything which vividly affects the mind, everything which power- 
fully stimulates the imagination, favors the development of hysteria in 
persons predisposed thereto” (Charcot). 
1. Hysteria 
General Consideration 
To gain an approximate idea of the true nature of the complex proc- 
ess included under the head of hysteria, we must recognize that the under- 
lying conditions are psychical; that clinically, hysteria must be considered 
a psychoneurosis; that it is not due to an organic disease of the nervous 
system; that it is a disease in which the “normal course of the psychical 
processes” (Striimpell) is disturbed and that their “association with the 
purely corporal processes of innervation” are also deranged. There can he 
no doubt that the initial anomaly is always to he found within the “psychic 
domain.” 
Hysteria is a condition which in its various manifestations may 
simulate true organic disease. Indeed, it may mimic disease of any 
organ of the body, and so closely very often that it frequently be- 
comes an exceedingly difficult problem to decide between this psycho- 
sis, with its close resemblance to pathological conditions but without 
organic change, and organic disease with the hysterical accompaniment 
in the ascendency. The mimicry of true organic disease by a psychoneu- 
rosis (hysteria) is by no means easily overcome but should be considered 
to be a grave disorder—in spite of the fact that it does not destroy life— 
for the reason that it is rarely completely cured and that there are but 
few hysterical subjects who fail, when conditions favor it, to develop an 
ungeared condition in which the normal relations of the mind to the 
body are disturbed. In other words, such subjects promptly become 
“hysterical.” While long periods of immunity may be enjoyed by these 
subjects, it may be accepted as true in the overwhelming majority of cases 
that a confirmed hysteric, one who has “the stigmata of Charcot” will 
always remain subject to the disease. The symptoms, one or many, will 
appear even after years of immunity under stress, or will follow one or 
more of the many inviting factors in the subject. The latter, because 
of an innate weakness, an inability to will, in spite of the fact that to will 
is his strongest desire, again falls into a condition in which constantly 
recurring autosuggestion gains the mastery. I assume that the “hys- 
terical symptoms” in all cases, when (as not infrequently happens) such 
symptoms accompany organic disease in one or more organs are without 1006 
DISEASES OF THE NERVOUS SYSTEM 
pathologic fundament; that hysteria per se does not destroy life; and fur- 
ther that the psychic element in the causation of symptoms or their disap- 
pearance is always predominant. 
The hysterical subject is a psychopath; there is the persistence of a 
vivid and ever ready imagination. Such a mental state justifies the defi- 
nition of Mobius, who holds that “hysteria is any disease which is pro- 
duced by the imagination.” 
At the very outset of the study of the prognosis of hysteria, before 
considering its separate manifestations, it must he forcibly insisted that 
under stress, particularly under emotion or excitement, under conditions 
(psychic) which would pass without influencing the mental processes of 
the normal subject, the psychoneurotic is likely to be ungeared, and falls 
into a condition in which one or more symptoms gain the ascendency and 
dominate his being. A further factor of exceeding importance is found in 
the fact that at the bottom of almost all true hysteria is the congenital, the 
inherited anomalous, predispositon of the nervous system. It is this psy- 
chopathic and neuropathic condition which leads me to the conclusions to 
which I have referred in the preceding paragraphs that when hysteria 
is fully developed, the patient is likely to become hysterical on slight cause 
even after long periods of apparent health. This does not mean continu- 
ous symptoms of hysteria, but the prompt awakening of a mental condition 
with full imagination and a train of symptoms characterized by their 
evanescence and mutability. 
Considering the influence of etiology upon the control of symptoms, it 
is clearly evident, inasmuch as psychic causes—emotion, excitement, 
shock, physical injury, terror, fear, anger or agitation—provoke attacks, 
that the regulation of the life of the patient proves enormously advan- 
tageous in controlling symptoms and improving his mental condition. 
Whenever the attention of the neurotic patient is centered upon one part 
of the body, he becomes hysterical; he is, because of his own continuous 
suggestion, unable to divorce himself from the organ which has taken 
possession of his brain, and he continues in this mental attitude until by 
a stronger suggestion or a transfer of attention to another or several other 
organs, he is partially released. Mutability of symptoms, their evanescence 
and rapid displacement are characteristic. 
When the psychoneurotic subject after long periods of worry or sor- 
row is finally disappointed, and suffers a single blow, which appears 
irreparable and which to him is of paramount importance, he may promptly 
become hysterical, and his condition is associated with many symptoms or 
one which is exceedingly distressing—to him always of transcendent im- 
portance. Such patients are controlled with great difficulty and yield only 
,after long periods of suggestion and treatment. The average human 
being is provided with a nervous system which can easily withstand re- 
peated insult and disappointment. The hypersensitive, with neuropathic GENERAL DISEASES OF THE NERVOUS SYSTEM 
1007 
tendencies are less fortunate, and held by faulty mental processes, their 
imagination gains control to the exclusion of normal activity. 
The diagnostician in offering his prognosis is not to he misled by the 
sudden cessation of symptoms which have been long persistent, for the 
period of immunity may only be short-lived. The leading symptoms of 
one attack may never return, but a multitude of complaints which hold 
the patient with equal firmness are likely to he substituted during unlim- 
ited periods in the less tractable subjects, or the period of freedom from 
symptoms may cover years during which the unhealthy and disturbed 
imagination continues dormant. 
So far as offering a forecast of the behavior of individual symptoms 
in well-established hysteria is concerned, it may be said in the average 
case that single symptoms will in almost all cases yield during varying 
periods to suggestion or other rational treatment, that in spite of condi- 
tions which mimic the gravest organic diseases, release may be predicted. 
Psychic disturbances or events will always be found closely related to 
hysterical exacerbations or the awakening of a dormant, previously unsus- 
pected, psychoneurosis into activity. The localization and persistence of 
symptoms are also enormously influenced by psychic factors; thus a hys- 
terical paralysis may limit itself to the part of the body which was but 
slightly bruised or injured in an accident, and the same is equally true of 
the hysterical joint. Such symptoms are often continued by an auto-sug- 
gestion which in turn is nurtured and sustained by litigation or other fac- 
tors which bear forcibly on the future material welfare and happiness of 
the patient. That the element of suggestion is decidedly in the fore- 
ground even in honest cases there can be no doubt, as is demonstrated in the 
consideration of the traumatic neuroses (See separate chapter—Traumatic 
Neurosis). 
Tn the general consideration of the prognosis of hysteria, all agree that 
cases which are without strong predisposition to. diseases of the nervous 
system, without enslaving heredity, which are so balanced that they have 
a sufficient remnant of healthy autosuggestion, are less likely to become 
permanently phychoneurotic than are those with a less favorable history; 
and in these subjects the prognosis for complete cure is relatively good. 
The acquisition of the neuropathic predisposition is possible, and is 
among the unfortunate incidents of life; it may lead to years of wretched- 
ness with a train of symptoms similar to those present with the inherited 
disposition. In the cases in which neuropathic-hysterical tendencies have 
been fostered and sustained, really developed by faulty processes and en- 
vironment in subjects without hereditary taint, the imagination may be so 
encouraged as to influence prognosis unfavorably. The persistence of 
innumerable symptoms literally “disjointed,” unreasonable from the path- 
ologic point of view, during long periods, is characteristic of such cases. 
The old theory which traced all hysteria to the sexual organs in both 1008 
DISEASES OF TIIE NERVOUS SYSTEM 
the male and female, has long since been discarded by the erudite clini- 
cian. It is exceedingly dangerous to become one-sided in our reasoning in 
connection with the etiologic factors which lead to this psychoneurosis; if 
we do, our treatment must of necessity suffer and prognosis is robbed of 
its rational fundament. There is a safe middle course for the diagnos- 
tician to follow; this divorces us in our prognosis from false premises and 
gives us the breadth of vision so much needed. I fully appreciate the 
influence of psychic-sexual factors in many cases, but forcibly deny their 
paramount influence in all cases of hysteria. The consideration of the 
possibility of the sexual causes in the individual case should be thoroughly 
weighed but the greatest discrimination and keenest judgment are needed 
lest we awaken in the subject a train of thoughts by psychanalysis which 
in the end may prove of serious consequences. 
Unquestionably in a proportion of well selected cases the hysterical 
manifestations have been overcome by the so-called “cathartic method” of 
Freud in which, by psychanalysis, there are laid bare to the observer and 
to the patient the unconsciously repressed group of ideas against which 
the patient has been struggling and against which the hysterical manifes- 
tation represents a defensive mechanism. Once these repulsive ideas are 
brought to light, discussed and reacted to with the natural and appropriate 
emotions instead of being repressed as too repellant for thought, the need 
for defensive reactions vanishes and the hysterical manifestations disap- 
pear, while at the same time the disturbed emotional content becomes 
normal. 
In offering a prognosis from the study of the separate symptoms of hys- 
teria, clinical experience establishes the fact that symptoms which arise 
acutely in one case and which may be of short duration in others are 
often exceedingly rebellious and chronic. This absence of any rule so 
far as the behavior of symptoms is concerned is characteristic. 
The disappearance of symptoms (paralysis, spasm, anesthesia, pares- 
thesia, vomiting, ocular symptoms') suddenly, after mental emotion, sud- 
den shock or other deep psychic disturbance, is to be expected, and with 
added suggestion and healthy occupation of the mind the clinical picture 
may be favorably influenced—in some cases permanently changed for the 
better. 
The possibility of the latency of symptoms should be considered before 
offering a positively favorable forecast in cases which have simulated the 
organic diseases. 
The tendency to long periods of latency in hysteria not dependent upon 
exogenous causes, needs to be repeatedly impressed upon the clinician in 
the study of the individual case. The forecast will always demand the 
full appreciation of the possibility of relapse in cases which are burdened 
by an unfortunate heredity or in which the environment during early life 
was unfortunate and often stifling. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1009 
Heilbronner has emphasized the fact that the prognosis is most favor- 
able in hysteria which originates from exogenous causes, rather than those 
in which “the habitual departure from the normal psychic type” has been 
in the ascendency. 
There is no organic disease which hysteria, may not simulate, but 
there is no organic disease in which symptoms are so evanescent and con- 
tradictory as in hysteria. In the prognosis of all types of hysteria the 
emotional element becomes an important diagnostic and prognostic factor 
to which we must cling. In prognosis, the great danger of suggestion 
by the physician should be studiously avoided for in the examination 
hysterical symptoms are often unearthed which when recognized by the 
patient, at once lead to the stimulation of the imagination and the con- 
sequent increase of subjective symptoms. Striimpell is correct in his 
statement “that numerous hysterical stigmata develop only through the 
medical examination, inasmuch as the ideas of the patients are influenced 
by the examination.” 
The ascendency of the emotional element in the hysterical subject is 
likely to persist. 
Fully developed hysterical psychoses may last only during a short 
period (few hours) or they may persist during discouragingly long periods 
(months). In the end, the psychoses are favorably influenced by treat- 
ment, but whenever stigmata of hysteria remain in such subjects, their 
mental instability is likely to lead to psychoses. 
Loss of memory—amnesia—is not a cause for worry. These subjects 
recover and by properly directed hypnosis, the void may be filled. 
Hypnosis (suggestion) has proved a valuable method of relieving 
many of the unusual psychic abnormalities of hysteria “dual personality” 
(“second etat”)—hysterical melancholia, postfebrile hysteria including 
delirium, puerperal hysteria and other postinfectious neuroses. 
Anesthesia and Sensory Disturbances 
When insignificant causes lead to supposedly grave symptoms as wide- 
spread and complete anesthesia, the hysterical fundament of such symp- 
toms is easily established, and the prognosis becomes correspondingly good. 
Total analgesia with sensory anesthesia, amblyopia, contraction of the 
visual field, anosmia, and other symptoms, readily recognized as of func- 
tional, psychic origin, offer a good prognosis. They are often promptly 
influenced by rational treatment and a strong personality (suggestion). 
Complete hemianesthesia should always be interpreted as hysterical, 
for as Moebius has said, “there is no organic lesion of the nervous system 
of ivhich complete hemianesthesia is a symptom.” The symptom is often 
evanescent and yields, but in chronic cases is displaced by other sensory o- 
visceral disturbances. 1010 
DISEASES OF THE NERVOUS SYSTEM 
Hemianesthesia after sudden shock, injury, fright or other factors, 
all acting promptly, with prominence of the emotional element, offers a 
favorable prognosis, but the “predisposition” insures only uncertain peri- 
ods of freedom, a ready return to a condition in which the suggestibility 
of the patient makes substitution of a variety of symptoms possible and 
control often difficult. 
Anesthesia which is characteristic of hysteria in a large proportion of 
cases is rarely recognized by the patient. The areas are indiscriminately 
distributed; they bear no relation to the sensory nerve distribution. The 
influence of psychic factors is paramount. Anesthesia may yield sud- 
denly to either suggestion or deep mental emotion, or shock may prove a 
factor of paramount importance in causing prompt relief. 
The sharp line of demarcation of anesthesia or analgesia which is 
characteristic of hysteria is at once of diagnostic and prognostic value. 
Hysterical hemianesthesia reaches to the middle line—no further; organic 
hemianesthesia is associated with motor paralysis, the cause of which is 
easily localized. It does not yield to suggestion, is not evanescent, there is 
complete absence of mutability of symptoms—all of which make the prog- 
nosis of the monosymptoms of hysteria favorable. 
Absolute or complete sensory disturbances of hysteria within the area 
involved are always more favorable because complete anesthesias are not 
characteristic of organic disease. 
Pain 
The 'pains of hysteria may simulate the sensory symptoms of severe or- 
ganic disease. Pains are not always easily controlled. Once tlie hys- 
terical subject has pains with symptoms which are interpreted during fright 
as of grave organic origin, the element of suggestion assists to continue the 
symptom. This is particularly true of such cases as simulate angina pec- 
toris; in women with palpitation; a heart which is overactive and strikes 
the chest wall with undue force; in certain cases of pleurodynia with car- 
diac neurosis; and with the globus or clavus in which the sense of constric- 
tion, weight, pressure or fulness “chokes” the patient. Such patients live 
during varying periods in constant fear of approaching death, and it is 
only by repeated assurance and suggestion that they are finally relieved. 
Patients who have recurring pains in the precordium, with hysterical 
tendencies, particularly women who have Glenard’s disease (gastroptosis, 
gastrectasia, mobile kidney with or without cardiac neuroses) are among 
the most difficult of all hysterical patients to treat successfully, unless they 
are removed from depressing and unfavorable surroundings. 
The lumbar and sacral pains besides intercostal neuralgias frequently, 
when of functional hysterical origin, yield to treatment only after long 
trial. Many of these cases are associated with visceral disease—functional GENERAL DISEASES OF THE NERVOUS SYSTEM 
1011 
and organic—or there is some constitutional disturbance, often anemia. 
Oases in which pains are a leading symptom, wherever located, require the 
closest possible investigation as too many are diagnosticated as of hys- 
terical or functional origin which finally prove to be due to grave cardio- 
vascular lesions or disease of the nervous system. 
The presence of few or many hysterogenous points have no bearing on 
prognosis; they are present in severe as well as in mild cases. 
Symptoms referable to the organs of special sense are not always ap- 
preciated by the patient; when they are, fear takes possession and there 
is profound depression. 
Taste and Smell.—Perversions of taste and smell are not, as a rule, 
persistent symptoms. Abnormal taste is limited to portions of the tongue 
and mouth. 
Hearing.—When hearing is involved it is exceptional to find com- 
plete hysterical deafness. 
Chavanne has demonstrated that with hysterical deafness there is more 
or less anesthesia of the auditory canal, of the head and the face, on the 
same side as the deafness. Anesthesia of the tympanic membrane is not 
frequent. Hone of these conditions are permanent. 
Ocular Anomalies.—The leading ocular anomalies are fully des- 
scribed by Parmaud, Gilles de la Tourette and de Schweinitz in “The 
Eye and Nervous System” (Posey and Spiller), and to these the reader 
is referred (See References). The leading features are: 
(a) Contraction of the visual field 
(b) Faulty color perception 
(c) Errors of accommodation 
(d) Hysterical blindness (amaurosis) 
(e) Hysterical amblyopia (incomplete anesthesia of the visual 
sense) 
(f) Hysterical asthenopia 
(g) Hysterical pupillary phenomena 
(h) Hysterical paralyses of the eyelid 
(i) Paralysis of the ocular muscles 
(j) Hysterical contractures 
(k) Palpebral and bulbar anomalies. 
(a) Contraction of the Visual Field.—The concentric contraction of 
the visual field is the most prominent ocular symptom of hysteria. It 
represents, according to Parmaud, “an insensibility of a portion of the 
field to white light, and this insensibility develops from the circumference 
to the center in such a way that a graphic drawing of the contraction 
Special Senses 1012 
DISEASES OE THE NERVOUS SYSTEM 
would be represented by an almost circular line.” The contraction of the 
visual field in hysteria may persist during long periods. Different cases 
differ, but in most, it does not yield so long as the psychic element is 
prominent. There are cases in which the contraction may continue during 
years; in other cases a few weeks or months prove to be the limit. The 
variations in the size of the field are insignificant until full recovery 
takes place. With recovery from hysteria the field returns to its normal 
size. 
(b) Faulty Color Perception.—In hysteria, besides contractions of 
the visual field for form and light perception there is concentric contrac- 
tion of the color fields (dyschromatopsia, achromatopsia and hyperchroma- 
topsia). 
In hysteria the normal order is changed. The color fields in the 
normal subject may be tested with “saturated colors in good illumination” 
and “occur from the periphery to the center in the following order: blue, 
yellow, red, green, violet.” In hysteria the red field frequently exceeds 
the blue and “the color lines coincide or cross one another, or it may 
exceed it and become the most peripheral of the color circles” (De Schwei- 
nitz). 
The disappearance of the color fields is in the following order, violet, 
green, blue, yellow and finally red. With lifting of the hysterical condi- 
tion the faulty color perception is likely to yield, though it not infre- 
quently happens that both contraction of the visual field and faulty color 
perception may persist long after the emotional element has been con- 
trolled. 
(c) Errors of Accommodation.—The hysterical subject may occasion- 
ally present errors of accommodation which, as a rule, make near vision 
faulty. 
(d) Hysterical Blindness 
(e) Hysterical Amblyopia 
(f) Hysterical Asthenopia. 
Naturally hysterical blindness is most alarming, but the assurance may 
be given that vision will return no matter what the form or accompanying 
hysterical complex, without a remnant of the former defect. The dura- 
tion of some rare cases of amaurotic blindness cannot be determined; how- 
ever, cases in which blindness continues during unlimited periods are in 
all probability of organic origin and not hysterical (Sachs, Mauthner, 
Sclimidt-Rimpler ). 
Hysterical blindness may appear suddenly, and is often lifted with 
equal suddenness. Patients with unilateral blindness see with both eyes, 
as may be readily proved by means of the stereoscope when the picture 
appears just as it should when viewed with both, and not with one eye. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1013 
In hysterical subjects partial blindness is more frequent than the total 
blindness (amaurosis). 
(g) Hysterical pupillary phenomena 
(h) Hysterical paralyses of the eyelids 
(i) Paralysis of the ocular muscles 
(j) Contractures of ocular muscles 
(k) Palpebral and bulbar anomalies. 
The foregoing anomalies (g to k inclusive) are occasionally met with 
other ocular symptoms (contraction of the visual field and faulty color 
perception). They may simulate organic disease, but the emotional ele- 
ment with the associated symptoms irregularly distributed and their muta- 
bility, as well as the absence of all data which admit of exact localiza- 
tion with other stigmata of hysteria, prove their functional-psychic-charac- 
ter and justify a good prognosis. The possibility of the existence of 
paralysis of the eye muscles of hysterical origin has been warmly denied 
by many good ophthalmologists and neurologists. Binswanger has never 
seen, in a large experience, “any isolated paralysis of an eye muscle, and 
believes with Parmaud and other writers that the so-called hysterical pal- 
sies should be explained by what is sometimes described as an associated 
ocular paralysis.” “There is a paralysis of movement and not of the 
muscles supplied by a given nerve.” 
Hysterical paralyses may mimic oganic paralyses; but in this, suc- 
cess is never complete. The cautious diagnostician will easily, in the 
majority of cases be able to differentiate, though in occasional cases he may 
hesitate during a limited period. 
Monoplegia, paraplegia, hemiplegia, or indiscriminately distributed 
paralysis may be expressions of hysteria. 
The tendency, through psychic influence to keep one—a single—symp- 
tom prominently in the foreground, is often exemplified by the behavior 
of the hysterical mono paralysis. The hand, a foot, an arm or leg may 
alone remain motionless and analgesic or anesthetic during unlimited peri- 
ods awaiting a profound impression, shock, mental emotion, successful 
suggestion of transfer of symptoms, or a sudden awakening which cannot 
be satisfactorily explained before the return of emotion and sensation. 
The return of power is complete in paralyzed extremities without any 
of the atrophy or the reaction of degeneration which characterize organic 
paralysis. In exceptional cases atrophy (limited) may result from long 
continued disuse, but this is never extreme and promptly disappears after 
a short period of activity. 
Paralysis 1014 
DISEASES OF THE NERVOUS SYSTEM 
Hysterical paralysis of the vocal cords (aphonia) is probably the most 
frequent form of the functional hysterical paralysis. It yields to sugges- 
tion as a rule, promptly, though in some cases only after long periods; 
it is likely to recur on slight cause. 
Hysterical paralysis disappears so soon as the paralysis of the will is 
relieved. Sir James Paget in his essays eloquently gave the following 
example, which may stand for all forms of hysterical paralyses: 
“A girl who has will enough in other things to rule the house has yet 
not will enough in regard to her limbs to walk a step with them, though 
they are as muscular as ever in her life. She says, as all such patients do, 
“I cannot”; it looks like “I will not”; but it is “I will not will.” 
Spasm 
Hysterical spasms may simulate grave forms of explosive nervous dis- 
ease—epilepsy, catalepsy, uremic convulsions, etc. 
So-called “hystero-epilepsy” is not to he considered as true epilepsy. 
The features are so different as to make diagnosis easy in most cases, and 
prognosis relatively good. 
Hysterical esophagismus (spasm) may be either acute or chronic. 
When acute, it is likely to be the single prominent symptom during an 
exacerbation and yields to treatment; when chronic, the spasm recurs at 
varying intervals. Months may lapse between seizures in cases which 
at times offer almost continuous symptoms during prolonged periods. Oc- 
casional cases may follow hearty laughter, may be associated with hic- 
cough, and are often suddenly produced by trivial causes—usually emo- 
tional. One of my patients, a neurotic man with large responsibilities sud- 
denly develops esophagismus while eating a hearty meal or while laugh- 
ing during a play; sudden disagreeable news may have the same effect. 
The spasm may not last more than a few minutes, or may recur during 
several hours if he attempts to swallow. Ho treatment has prevented re- 
currence. 
Contractures of hysterical origin “attain their maximum at once”—a 
factor which is of the greatest importance in differential diagnosis and 
prognosis. Organic contractures are gradually developed. Hysterical con- 
tractures are not found without other stigmata of hysteria. 
Contractures with anesthesia (hemianesthesia often) in which the 
sensory symptoms are evanescent and in which with fresh recurrence 
of the latter symptoms, usually opposite areas are selected, will under 
proper control and after varying periods, recover—usually without a rem- 
nant of change. 
Contractures GENERAL DISEASES OF THE NERVOUS SYSTEM 
1015 
The exaggeration of reflex excitability in the hysterical subject is often 
of great value in strengthening the favorable prognosis in contractures, 
paralyses, and anesthesias, which at times seem intractable. It may hap- 
pen that in the hysterical subject, particularly after injury, the con- 
tracture may precede paralysis or the latter may never develop. Such 
cases usually yield to treatment or to the settlement of the claim in cases 
which are litigated. In all of these cases sudden and complete recovery 
may be expected. 
Charcot repeatedly demonstrated that “the constitutional revolution” 
ended the contracture of individual cases. He also used the magnet to 
“provoke a transfer of the contracture to the opposite side,” and further 
successfully predicted that in a large number of these transfers “the con- 
tracture will exhaust itself.” 
Reflex Excitability 
Hysterical Joints 
Both Sir Benjamin Brodie and Sir James Paget called attention to 
the joint manifestations of hysteria which at times are refractory during 
long periods. The great hyperesthesia of the joint is striking and out of 
all proportion to the objective signs. These joints yield to proper treat- 
ment though it has been held by many that long continued joint symptoms 
of hysterical origin may ultimately, if unrelieved, lead to grave organic 
changes which persist. 
The hysterical joint recovers as a rule, without deformity. Paget 
cites Flowers’ case of a man “whose skeleton is at Marburg, who was 
encased by his relatives for twenty years in a space in which he could only 
sit with his limbs doubled Up and in which he could have had only very 
narrowly restrained movements of his joints; yet his limbs did not become 
deformed and his joints retained their normal textures.” 
“Innumerable cases of hysterical joints after years of contraction re- 
cover fully and without deformity 
Hysterical outbreaks, convulsions, hystero-epilepsy, cataleptic states, 
ecstasy and innumerable anomalous mental states may during varying 
periods remain in the foreground with or without a multitude of other 
symptoms; at times during these periods in which the psychic disturb- 
ances are prominent, there may be a disappearance of most of the preced- 
ing leading features, or a single symptom may remain unchanged. The 
prognosis of the single symptom is absolutely unfavorable, the outbreaks 
are usually controlled under proper guidance but no assurance can be 
given that relapse may not occur. In patients with the “.hysterical tem- 
perament” and hysterical outbreaks, the prognosis for permanent recov- 
ery is less favorable than in those who have become psychoneurotic as the 
result of injury or depressing factors. The improvement of the social 1016 
DISEASES OF THE NERVOUS SYSTEM 
status of such patients, better homes, cheerful surroundings, and healthy 
suggestion, repeatedly change the character, of symptoms and assist mate- 
rially in the restoration of the normal balance. However troublesome the 
psychoneurosis and however discouraging the mental status of the patient 
to the layman, permanent mental alienation need not be feared. 
Cases in which grave mental disease exists with the hysterical tem- 
perament and stigmata are occasionally met, but the latter complication is 
accidental and is not responsible for the former. It not infrequently 
happens that with the late nervous manifestations of tertiary syphilis the 
symptoms have a tinge of hysteria. The latter complication does not in- 
fluence the course of organic and usually fatal disease. 
The spontaneously arising hypnotic hysterical conditions include cata- 
lepsy, periods of lethargy, somnolence and somnambulism. These states 
may arise suddenly after excitement, disappointment or long continued 
worry. The period during which the symptoms continue varies in differ- 
ent cases. In my last case a young, sensitive, and confiding girl was dis- 
appointed in love; without warning she became cataleptic and remained so 
during six weeks. Her rally was as sudden as the fall. 
Cataleptic conditions are dissimilar. One or more extremities may 
escape. The recovery is, as a rule, full and perfect. There are no rem- 
nants of rigidity, and the tendency to relapse is finally fully overcome 
in most cases. There are cases in which the cataleptic state has persisted 
during many years. Lancercaux reports one case which continued twenty 
years. The majority of cataleptic periods are short—a few hours; rarely 
more than a day or two. 
There is as a rule, complete amnesia,; the events of the lost interval can 
be recalled by hypnotic suggestion. 
The “grande hysterie” of Charcot is not often repeated in this coun- 
try or in Germany. In France, at the Salpetriere, these larger attacks 
were unquestionably nurtured by repeated suggestion. The full attack 
includes severe epileptiform convulsions with loss of consciousness fol- 
lowed by contortions and the “grand movements,” and finally the “atti- 
tudes passionelles” which are strikingly suggestive. In the production of 
the “grand attack” the element of suggestion which leads to the stimulation 
of the ideas is fully accented by the attack. ' 
Loss of muscular sense (perte do la conscience musculaire of Duchenne) 
may complicate hysterical hemianesthesia which yields with other hys- 
terical stigmata under favorable conditions, though relapse is frequent. 
Astasia-abasia—unsteadiness in walking, with or without eyes open 
(astasia) or unsteadiness in walking without true or full incoordination 
may be present in hysteria, and demand differentiation and interpretation. 
The withdrawal of ocular guidance causes greater disturbance in hyster- 
ical unsteadiness than in organic disease, true ataxia. Astasia-abasia may 
exist without other symptoms of hysteria. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1017 
Burr reports a case of hysterical astasia-abasia occurring in acute mul- 
tiple neuritis in which the history justifies the conclusion that both the 
functional and organic diseases were of alcoholic origin. Astasia-abasia 
is unquestionably dependent upon an amnesia, and in the majority of cases 
yields after a longer or shorter period. 
Akinesia Algera (Moebius).—I have elsewhere called attention to 
akinesia algera of Moebius in which, because of pain on the movement 
of a limb, or on swallowing, or after any other muscular effort, the patient 
ceases to help herself and sooner or later becomes bedridden with char- 
acteristic symptoms; these seem to deserve separate consideration because, 
contrary to uncomplicated hysteria, these patients may die (See Akinesia 
Algera). All of my cases have been women. 
The mimicry of cancer by hysteria, particularly of the breast and 
tongue often requires repeated reassurance before the mental pang is 
allayed. Neuralgic pains in any part of the body known to the patient 
to be liable to cancer, may start the mimicry of the disease. 
“It is strange to observe the tenacity with which some of the patients 
cling to the most dismal view of their cases. Though nothing wrong can 
be felt or seen, and though months or even (as I have known) years may 
pass without any disease appearing, yet will they believe themselves on 
the brink of misery with cancer of the tongue” (Paget). 
Perverted Appetite.—Perverted appetite, at times complete anorexia, 
during long periods characterizes some cases with or without other vis- 
ceral symptoms. In occasional cases women who fear an increase of 
weight or because of a psychosis refuse to take food, are only released after 
repeated suggestion. 
Hysterical Vomiting.—Hysterical vomiting may continue during con- 
siderable periods. There need he no fear of starvation, for the majority 
either hold their weight or the loss is insignificant. It always strengthens 
the diagnosis of hysteria, when with vomiting, often apparently uncon- 
trollable, there is a strong emotional element; these patients as a rule, sud- 
denly return to normal conditions. 
Constipation.—Constipation is one of the most frequent attendants of 
hysteria and at times true obstipation appears threatening. When this is 
associated with tympanitis, the patients, usually women beyond twenty- 
five, are filled with fears; they often have “delirious hearts.” Such cases 
even with extreme meteorism are relieved, hut recurrence of symptoms is 
the rule. 
Diarrhea.—Diarrhea of hysterical origin does not debilitate as do the 
ordinary enteritides, but when membranous colitis is almost continuously 
present, the psychic depression resulting is unfavorable and in rare cases 
Internal Organs 1018 
DISEASES OF THE NERVOUS SYSTEM 
these patients are bedridden—often during long periods—and are only 
raised by the overpowering influence of the attendants, change of scene, 
and oft-repeated reassurance. 
Membranous Colitis.—Membranous colitis is often one of the most 
persistent of all hysterical conditions. When the patient has been brought 
to understand that the passage of intestinal casts or large mucous masses 
is never serious, that it may be present and continue during years without 
influencing the general health, that it yields in the end, the horizon is 
cleared and there is almost at once a decided change in the attitude of the 
patient. 
Fecal Vomiting.—Fecal vomiting and long periods of intestinal inertia 
are among the rarer stimulations of organic disease. I number among 
my cases, one which recovered after thirty days of obstipation. The diag- 
nosis in this case was made easy by the previous history of a train of 
symptoms, including hysterical paralysis with the prominence of the emo- 
tional element. 
Menstrual Anomalies.—Menstrual anomalies in young hysterical sub- 
jects may materially influence the symptoms in individual cases; most of 
these irrgularities yield after a limited period, often with improvement or 
disappearance of the hysterical accompaniment. 
Hysterical Cough.—Hysterical cough is a frequent symptom in young 
children, girls usually; it may recur during adult life on slight cause; it 
is almost always of the same character—paroxysmal and barking—and is 
in most cases promptly influenced by change of climate or scene, if not by 
suggestion. 
Vasomotor and Secretory Disturbances.—Vasomotor disturbances as 
well as secretory disturbances are separately considered (Nervous Dyspep- 
sia, also Diseases of the Sympathetic System). It often requires the 
clearest judgment after the full consideration of the history of the indi- 
vidual case to decide whether there is simulation, imaginary disease, or an 
organic lesion. 
Hysterical Fever.—Hysterical fever offers a good prognosis. That 
psychoneurotics of the severer types develop fever—hyperpyrexia—on 
slight cause is positively established. Here too, the diagnostician must 
remain alert. Hysterical fever cannot be diagnosticated until all possible 
sources of the hyperpyrexia have been eliminated. Hysterical fever does 
not usually lead to great loss of weight; the period of convalescence is short. 
Trophoneuroses.—All of the trophoneuroses of hysterical origin are 
without significance. They are easily recognized as a part of rapidly fol- 
lowing evanescent symptom complexes without a single feature to justify 
the suspicion of organic change. 
Sexual Anomalies.—Among the most intractable conditions are the 
sexual anomalies originating in the imagination of the patient. These 
are more frequent in the male than in the female. In the male the psy- GENERAL DISEASES OF THE NERVOUS SYSTEM 
1019 
chic element which leads to sexual weakness, impotence and the perver- 
sions of the sexual function is often in the foreground and is relieved only 
by the greatest tact and most powerful suggestion of the attendant, with 
the cooperation of those who have a moral right to be interested. The 
prognosis of this condition is often improved by reading to the obsessed 
patient extracts from the classic lecture of Sir James Paget on Sexual 
Hypochondriasis (see Reference end of chapter). In women there are 
sexual perversions of hysterical origin which make these patients exceed- 
ingly wretched at times. These too are relieved by proper treatment and 
honest suggestion unless there is associated organic disease of the brain. 
Hysterical Tachycardias and Bradycardias.—The hysterical tachycar- 
dias and bradycardias are among the symptoms which promptly ungear 
the hysterical subject. Most of these patients, especially those who are 
normally neurasthenic, often become panic stricken with either of these 
anomalies; often the globus is added. The accompanying faintness adds 
an element of alarm, and the fear of death takes possession of the patient. 
Recovery with recurrence on slight cause, until the general and the mental 
conditions have been returned to their normal balance, is the rule. 
Hysterical Torticollis.—I have seen a number of cases of hysterical 
torticollis in girls at or near puberty. Some of these were associated with 
convulsive attacks of the large type; others seemed to bear a close relation 
to genito-urinary anomalies. Hone of these were permanent. One con- 
tinued to recur during a number of years, to disappear after the removal 
of a large dermoid-ovarian cyst. 
Additional Considerations 
This chapter might he extended to include the mimicry by hysteria 
of almost all organic disease. Such treatment of the subject is unneces- 
sary, and would prove to be a work of supererogation. In the consideration 
of hysteria as well as in the differentiation of organic diseases such pos- 
sibilities cannot be ignored, neither can the fact be overlooked which I 
have previously accented that organic disease may be materially influenced 
by that psychoneurotic element (hysteria) which is present in both men 
and women—oftener in the latter. It will often prove exceedingly dif- 
ficult in such cases to separate the symptoms of the organic process 
from those of functional origin, and to give to each its prognostic value. 
With the more serious diseases of the nervous system (multiple sclerosis, 
multiple neuritis, tabes dorsalis, myelitis, arteriosclerotic processes involv- 
ing the brain and cord, cerebrospinal lues), the addition of a troublesome 
psychoneurosis may not shorten the life of the victim but it has a power- 
ful influence in making him exceedingly wretched. 
In private and dispensary pmctice whether hysteria is associated with 
organic disease or not, it is evident that among certain people (Jewish par- 1020 
DISEASES OF THE NERVOUS SYSTEM 
ticularly) the element of psychoneurosis is so powerful as frequently to 
thwart the efforts of the therapeutist. 
To lift these unfortunates above the level which makes them wretched 
through the exercise of an imagination which is encouraged by heredity 
and environment requires changed social conditions, hygienic homes, right 
living and release from economic slavery in which the toiler is without the 
means necessary to provide adequately for himself or those dependent 
upon him. 
In a large experience I have but rarely found organic disease follow- 
ing hysteria; it is so rare as to justify the conclusion that when it does 
occur it is purely accidental. I fail to recall a single death positively 
traceable to uncomplicated hysteria. When in a hysterical subject death 
is charged to the psychoneurosis, thorough search will reveal the presence 
of some organic disease. 
Resistance may be reduced by the so-called hysterical vomiting. In 
the overwhelming number of these cases organic disease of the stomach, 
toxemia or other pathologic fundament is found responsible if death occurs. 
The favorable influence of change from the location in which the symp- 
toms originated or from the surroundings in which the accident occurred 
which awakened the dormant hysteria to activity, is often of inestimable 
value, for it not infrequently—particularly in young subjects—dissipates 
all symptoms and materially changes the prognosis for the better. 
It cannot be too often nor too forcibly impressed upon the clinician that 
hysteria is a disease winch is not easily overcome. Thorough investigation 
of those who have shown symptoms during a prolonged period will rarely 
fail to disclose one or more of the stigmata, always present during the 
remission. Children offer a better prognosis than do adults; after thirty- 
eight or forty the prognosis for full restoration is not encouraging. 
References 
Binswanger. Die Hysterie. Wien, 1904. 
Burr. Hysterical astasia-abasia. New York Med. J., Dec. 26, 1914. 
Charcot. Clinical lectures, etc. Paris, 1888. 
Chavaune. Oreille et hysterie. 1901. 
Church & Peterson. Nervous and mental diseases. Philadelphia, 1911 & 1914. 
Freud. Monatschr. f. Psych, u. Neurol., No. 18. 
Friedlander. Psycho-neurol. Wchnschr., 1910. 
Gilles (de la Tourette). Traite Clinique et Therapeutique de V Hysterie. Paris, 1891• 
Heilhronner. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912, Bd. v. 
Lancereaux. Acad, de Med., 1904, Rev. Neurol 
Moebius. Ztschr. f. Nervenheilk., i & ii. 
Nervenkrankheiten. Leipzig, 1894. 
Oppenheim. Lehrb. d. Nervenkrankh. Berlin, 1913. 
Paget (Sir James). Selected essays, etc. London, 1902. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1021 
Parmaud. The ocular manifestations of hysteria. System of diseases of the eye. Norris 
& Oliver, 1900, vi. 
Pitres. Cliniques sur I’hysterie. Paris, 1891. 
Sachs. J. Nerv. & Ment. Dis., 1899, xxvi. 
de Schweinitz, Posey & Spiller. The eye and nervous system. Philadelphia, 1906. 
Striimpell. Textbook of medicine. New York, 1911. 
Ziehen. Ueber Hysterie. Deutsch. Klinik, vi. 
2. Traumatic Neurosis 
(Traumatic Hysteria, Railroad Spine, Concussion of the Spine—Erichsen) 
The diagnosis of traumatic neurosis or traumatic hysteria is occasion- 
ally justified, but it must be remembered that following trauma there are 
so many factors which encourage autosuggestion, and in the designing sim- 
ulation, it requires the greatest circumspection to separate the spurious 
from the honest cases. There are in most cases no symptoms which sug- 
gest the presence of an organic lesion; indeed the psychoneurotic element is 
constantly present. Suggestibility is a leading feature and the differen- 
tiation of hysteria and traumatic neurosis is in many cases impossible. 
The complex of symptoms does not as a rule, develop immediately 
after the injury, but days, weeks, or months may lapse before a train of 
continuous symptoms follow which may, to the inexperienced, simulate 
grave disease of the nervous system or disease of other organs of the body. 
It is surprising to note how quickly after symptoms develop, the mimi- 
cry of organic disease is complete; how within a few hours there is often 
paralysis of the hysterical type; how within an unreasonably short period 
these patients become self-centered; how the ego is at once placed promi- 
nently in the foreground; and how in cases which lead to litigation, the 
worry associated with the approaching trial makes thought of almost all 
else appeal insignificant to the litigant. 
In honest cases of traumatic neurosis it will be found that there is an 
inherent weakness of the will, a neuropathic predisposition which is often 
inherited. 
Evidences of this ungeared condition of the will with symptoms of 
hysteria—traumatic neurosis—following injury, may at times in the sub- 
jects of true organic disease be present, and may add an element of con- 
tradictory symptoms which in the end offer the same prognosis as do those 
exactly parallel, without the presence of preceding organic disease. 
Litigation begets “litigation symptoms'” (Page) as will be demonstrated 
in this chapter, and the fate of these symptoms depends very largely, in 
the majority of cases, upon the termination of the litigation. 
Repeated autosuggestion during periods of uncertainty exerts an enor- 
mous influence in continuing the symptoms. The verdict in a large pro- 
portion of cases is expected to bring the means for restoration and the DISEASES OF THE NEBVOUS SYSTEM 
1022 
healthy suggestion is only commenced, when because of the successful 
issue the goal has been reached, or with continued inactivity and paral- 
ysis of the will in unsuccessful cases, poverty and ruin must be faced. 
Thus the end of litigation, favorable or unfavorable to the plaintiff, be- 
comes at once the most important factor in the prognosis of litigated cases 
of traumatic neurosis. 
It is unsafe for the clinician to follow Erichsen whose description of 
“Spinal Concussion” includes all kinds of lesions following railroad in- 
juries without external evidences of the accident at any time. For years 
this work proved to be the fountain from which innumerable lawsuits 
sprung; it was, so far as the doleful prognosis which it gave, the ready 
support of the plaintiff against the railroads and other corporate .bodies. 
Page came on the scene in 1881 and his work on “Injuries of the Spine 
and Spinal Cord” has done more to overthrow the authority of Erichsen 
than any other work. The essay of Page was based upon thorough clin- 
ical study and scientific observation. 
In considering the prognosis of traumatic neurosis following accident, 
it must be assumed by the unbiased observer and diagnostician that the 
spinal cord is the best protected of all. of the organs of the body; that in 
cases of traumatic hysteria (neurosis) there is no evidence or positive 
objective sign of a true organic lesion of the cord or its encasement; that 
injuries which are of sufficient force or extent to give rise to symptoms of 
organic change are severe, immediate, and are likely to prove continuous 
or fatal. 
Fracture of the spine, crushing injuries, stab wounds of the cord, and 
dislocations at once lead to the symptoms which permit of a correct inter- 
pretation of the extent of injury to the nervous structures (cord, meninges 
and peripheral nerves). 
The symptoms following what Jonathan Hutchinson called a “shake 
of the cranial contents without structural lesions of importance” are purely 
neurotic-psychic symptoms; as such they should be considered and dis- 
cussed, and on such a foundation prognosis should be based. Whether we 
accept the classification of Oppenheim (1889) and considey the term 
“traumatic neurosis” justified or whether we accept the dictum of Char- 
cot of the purely functional nature of all symptoms in cases without evi- 
dent organic change, and further agree that it is impossible to differen- 
tiate these cases from true neurasthenia and hysteria, is of little moment 
in framing the prognosis, for with a settled mind, the element of fear, 
suggestion, and all other depressing factors eliminated, the prognosis is 
correspondingly better and full recovery is the rule. I exclude from 
consideration of this subject all injuries of a surgical character in which 
there are evident lesions and in which there has been organic change, the 
result of such injury, in which cases such changes take place as to make 
exact localization easy and positive. In the majority of such cases the GENERAL DISEASES OF TIIE NERVOUS SYSTEM 
1023 
symptoms are immediate, and the prognosis depends upon the extent of 
the injury—always graver than in uncomplicated traumatic neurosis. 
With organic injury, as the result of fright, sudden shock, or from 
other causes in neurotic patients, true psychoneurosis (traumatic neuro- 
sis) may develop and prove stubborn and persistent. 
The surgical conditions must always be separately considered; each 
offers its own prognosis. 
There are cases of traumatic neurosis—usually with hysteria in the 
ascendency—in which there is no thought of litigation, in which serious 
and paralyzing conditions may continue during surprisingly long periods. 
The depression and changed mental attitude of the patient who suffers 
from traumatic neurosis may lead to a train of symptoms already referred 
to as “litigation symptoms,’’ which in many cases are honest and in all 
cases offer a good prognosis for restoration of function. 
The persistent melancholia which characterizes some cases of traumatic 
neurosis, as Oppenheim has demonstrated, does in a few instances, differ- 
entiate these forms of the disease from true hysteria. The prognosis of 
this condition is good, though improvement may he slow and full recov- 
ery is often long postponed. ' 
Traumatic neurosis may at times include “psychic attacks” resembling 
epilepsy (Westphal) or as ISfonne has demonstrated, attacks of hystero- 
epilepsy, with or without direct injury to the head. 
Localized muscular spasm and convulsive tic, without loss of conscious- 
ness, are not infrequently present in fully developed cases. These condi- 
tions usually yield with the other symptoms. 
Arhythmia, “nervous and irritable heart action,” is not unusual. The 
heart may behave just as it does with non-traumatic hysteria, and the 
prognosis is almost always good. I have seen no case in which traumatic 
neurosis per se lead to organic disease of the heart or arteries. 
Goldscheider, Oppenheim, and Leers believe that dilatation and hyper- 
trophy of the heart and arteriosclerosis may proceed from traumatic neu- 
rosis. 
When Graves disease or other organic nervous or cardiovascular changes 
follow traumatic neurosis, it is likely that these diseases would have de- 
veloped without the trauma. It cannot be denied however, that accident 
and shock are factors in lighting Graves disease to activity. 
Vasomotor symptoms, including cyanosis, abnormal blushing, dermo- 
graphia are usually evanescent and if they recur, as they often do, are 
finally fully controlled. 
The manifestations of traumatic neurosis may be as numerous as are 
those of non-traumatic hysteria, and the prognosis of the individual symp- 
toms must be considered in connection with the individual case. 
It is positive that the neuroses with monosymptoms offer a less favorable 
prognosis for prompt cure than do those with multiple symptoms. 1024 
DISEASES OF THE NERVOUS SYSTEM 
Psychic disturbances which are not promptly relieved are likely to 
persist during unlimited periods. Cases in which organic changes have 
followed after electric shock, in which later the element of traumatic hys- 
teria is developed, offer an unfavorable prognosis because the changes in 
nerve tissue are not, as a rule, overcome, and the wretchedness of the patient 
is sufficient to continue suggestion which does not permit of escape from 
the added traumatic neurosis (Jellinek). 
The severity of the trauma does not stand in direct relation to the 
severity of the nervous manifestations. Insignificant injury may lead to 
obstinate neurosis. 
Occasionally traumatic neurosis leads to suicide. 
The most chronic and previously intractable case may recover after 
years of symptoms; often the improvement is sudden and unexpected. 
Heredity and alcoholism always influence prognosis unfavorably. 
What is the influence of traumatism on the development of general 
paralysis ? Certainly traumatism does not make the syphilitic subject 
immune, hut as Meyer has said “it is apt to add to the chances of pre- 
cipitating the cerebral reaction;—traumatism will hardly he able to bring 
about the paralytic brain changes without previous syphilis.” I believe 
the association to he purely accidental. 
I have never known death to follow uncomplicated traumatic neuro- 
sis. Previous arterial and renal disease affects the prognosis unfavorably. 
It is impossible to give any opinion of value which will determine the 
duration of any case of traumatic neurosis. The factors of greatest im- 
portance, besides those already mentioned are: age, the nature of the psy- 
chosis, the previous history and the time of the existence of symptoms, the 
nature of the treatment received, as well as the environment of the patient 
and his circumstances. 
References 
Bailey. Diseases of the nervous system resulting from accident injury. London, 1906. 
Bruns. NothnageVs Handb., etc. 1901. 
Charcot. Progrbs Med., 1885, 1886, 1887. 
Erichsen. On concussion of the spine. London, 1876. 
Goldscheider. Berl. klin. Wchnschr., 1906. 
Jellinek. Virchow’s Archiv. Bd. clxx. 
Leers. Neurol. Centralbl., 1906. 
Meyer {Adolph). Observations, Worcester Insane Asylum, 1896-1902. 
Nonne. Mittheil d. Hamburger Staats Krankheiten, viii. 
Oppenheim. Berl. klin. Wchnschr., 1884. 
Lehrb. d. Nervenkh. Berlin, 1913. 
Die traumat. Neurosen. Berlin, 1888-1892. 
Riegler. Ueber d. Folgen d. Verletz. auf Eisenbahn., etc. Berlin, 1879. 
Strumpell. Berl. Klinik, 1888. 
Westphal. Berl. klin. Wchnschr., 1879. 
Charite-Ann., 1880. GENERAL DISEASES OF TIIE NERVOUS SYSTEM 
1025 
3. Neurasthenia 
(Nervous Prostration, Nervous Exhaustion, Beard's Disease, The 
American Disease, Nervenschwdche) 
General Statements.—Neurasthenia is rarely a primary disease; it 
is almost always secondary and furnishes a complex of symptoms which is 
encouraged by lowered dynamic energy, lack of normal recuperative poiver, 
inherent weakness, an unstable mental state, and persistent autosugges- 
tion. 
I would define neurasthenia therefore as an anomalous condition 
without substantial disease discoverable in nerve structures, in which there 
are abundant evidences of weakened nerve force, tendency to exhaustion, 
lack of reserve, increased irritability with, in the majority of cases, mim- 
icry of organic disease, with a radiation of symptoms to parts distant from 
the supposed disorder, depending largely upon the self-suggestibility of the 
patient. 
The unusual mental character of the neurasthenic and the predominant 
emotional element are characteristic, and powerfully influence prognosis. 
Such mental characteristics “good or bad, higher or lower than the aver- 
age, something outstanding or sunken” brand the neurasthenic; they are 
often inherited, and because of this fact the prognosis for complete release 
is relatively bad. The “ego” is always in the ascendency; self-effacement 
is impossible; the mind is set upon some supposed grave organic disease; 
and continuous autosuggestion is practiced. 
Neurasthenia has been spoken of as an “American disease.” It is not 
a modern disorder, nor can it be considered a purely American disease. 
The symptoms of this complex were known to the ancients, and Hippocrates 
described diseased conditions resembling it hundreds of years ago. Beard 
and Bouchut made no revelations in medicine when they described this 
condition, for mention was made of kindred conditions by Sydenham, 
Robert Whytt, Raulin, and Pomme, while Hasse published cases of neu- 
rasthenia in 1855 taken from a German clientele exactly similar to those 
described by Beard. 
Neurasthenics in whom there is no attending or provocative disease— 
primary neurasthenia—early in life show the “irritable weakness” which 
characterizes all neurasthenic states. Such individuals are born with low- 
ered resistance, their cerebrospinal system and cellular elements lack the 
ability to rebound after even ordinary strain; throughout their entire lives, 
the neurasthenic complex is ready to come to the foreground on slight 
cause. The prognosis in such cases for full recovery is bad. Long peri- 
ods of freedom from a multitude of symptoms may lead to the belief that 
the condition has been overcome; on slight cause, very often there is a 
return of neurasthenia, and the persistent suggestion continues to influ- 1026 
DISEASES OF THE NEKVOUS SYSTEM 
ence the lives of these patients. The brain is often abnormally active but 
is easily fatigued and the patient soon learns his limitations. 
Stewart makes the unmodified statement that “neurasthenia is not a 
primary disease,” that it is always “exogenous” and the “result of some- 
thing else.” In those predisposed, usually between twenty and fifty years 
of age, the most frequent causes are mental or physical strain. Neuras- 
thenia is more likely to develop in the active and productive than in the 
laggard, and in such subjects it proves to be a serious handicap because 
z>f its persistence, often during many months, and the tendency to recur on 
slight cause. 
Cleghorn found in 6,000 cases that the complex was more frequent in 
men than in women and that two-thirds of his cases were between the 
twentieth and fortieth years of their lives. Sedentary habits in all cases 
aggravate the symptoms, and idleness invites the suggestion which leads 
to the neurasthenic state. 
Causes.—Idleness in those predisposed to any neurosis is one of the 
leading causes of the neurasthenic state, and makes it impossible for the 
patient to regain the equilibrium necessary to make him normal. The un- 
occupied man has only himself to consider; he may suffer from a minor 
ailment or acute indisposition when his mind dwells upon it to the exclu- 
sion of all else; he sees in his symptoms only the gravest significance and 
this imaginary gravity takes possession of him. Luxury, idleness, and the 
faults of modern civilization are at work to rob the predisposed of their 
resistance; judicious occupation brings with the dissipation of the symptom 
complex, happiness, a sound mind, organs ready to fight disease, and ban- 
ishes the emotional element which is often predominant. The neuras- 
thenic without associated organic disease, who continues self-centered, who 
has one or more symptoms continuously before his mental vision, cannot 
recover without sufficient mental pabulum included in an honest sugges- 
tion and a healthful occupation. 
Unquestionably the leading features to be considered in prognosis are 
the influence of race and heredity. This fact is forcibly impressed on the 
clinician in connection with his Jewish clientele, for the Jews are enor- 
mously neurasthenic; dispensary practice in all large cities burnishes 
the majority of cases. The predisposed are likely to become neurasthenic in 
high altitudes. Any condition which lowers vitality or adds any other in- 
viting factor in subjects with “neuropathic inheritance” provokes anew the 
train of symptoms included in the complex, and unfavorably influences the 
prognosis; such patients do not die, but they are exceedingly wretched 
with one or more symptoms prominent and the associated and character- 
istic fear of impending death. 
Insufficient early discipline, absence of self-control and failure to live 
the normal and average life, influence the resistance and recuperative 
power unfavorably. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1027 
Faulty hygiene with improper education are potent factors which rob 
these patients of the power to lift themselves above the condition into 
which they usually fall on slight cause. 
The influence of the occupations on neurasthenia is paramount. Occu- 
pations in which worry and excitement are almost continuous, in which the 
neurasthenic is unable to prevent the formation of toxins which result 
from fatigue, are injurious to the neuropathic subject, and unless changed, 
the prognosis for complete restoration remains bad. Occupation often im- 
proves the condition of these patients if it is agreeable and there are no 
associated worries or undue excitement. It is surprising to note how the 
confirmed neurasthenic often responds to suggestion and an occupation 
which keeps his brain active without fatigue, and how the heart under such 
conditions is kept light. Work in favorable surroundings which the pa- 
tient enjoys, which is permissible unless the underlying pathogenic fac- 
tors make it impossible, often leads to the dissipation of all or most symp- 
toms. 
Associated Conditions.—Neurasthenia may follow or be associated 
writh the infections, particularly influenza, typhoid, syphilis, tuberculosis, 
pneumonia, and other acute and chronic bacterial disease. The prognosis 
in these cases depends largely on the patient’s antecedents, the life which 
he leads and his ability to get the needed treatment, change from his unfa- 
vorable surroundings if indicated, and a variety of factors which for prog- 
nosis need to be faced in the individual case. 
A surprisingly large number of influenzas are followed by neuras- 
thenia. This is particularly true of such patients as return to their 
occupations before they have fully regained their strength and are of neuro- 
pathic habit. The brain worker, who has been reduced by grippal infec- 
tion, of sedentary habits, whose occupation is associated with large respon- 
sibilities and many risks, recovers slowly unless he is given complete rest 
and the necessary relaxation. Most neurasthenias following grippal in- 
fection recover fully after long periods, though the graver psychoses not 
infrequently develop. Remissions and exacerbations are not unusual. 
Gouty patients, the diabetic and the alcoholic, transmit to their off- 
spring a lowered resistance, limited endurance, and the predisposition 
which lead to a self-centered state in which neurasthenia becomes predomi- 
nant and is eliminated with the greatest difficulty. 
In practice we find the most rebellious cases in the subjects of cardiac 
neuroses and gastro-intestinal disturbances,—Glenard’s process particu- 
larly. 
Traumatism and the resulting neurasthenic state has been separately 
considered (See Traumatic Neurosis). 
In connection with the consideration of the prognosis of neurasthenia 
the fact may be once more accented that patients with inherent tendencies, 
or those who for some other reason are without normal resistance, are likely 1028 
DISEASES OF THE NERVOUS SYSTEM 
to develop the full train of neurasthenic symptoms after either slight or 
severe injuries. The perfectly normal subject without neuropathic tend- 
encies occasionally develops neurasthenia after strain or injury. In such 
cases the prognosis is relatively better than in those who by habit are neu- 
rasthenic. 
The most unfavorable cases are those in which the neuropathic tend- 
ency, with weakened resistance and abnormal nervous development, is im- 
parted to the offspring of those whose habits and modes of life are in 
direct antagonism to all that is healthful and uplifting. It will he noted 
further that the prognosis is less favorable in those in whom baneful influ- 
ences (heredity and environment) make it impossible to shake off minor 
ailments. The prognosis is far better in the “willful” than in the “will- 
less.” 
Clinical Varieties.—The clinical varieties of neurasthenia derive their 
names from the organ or set of organs to which the leading symptom in 
the individual case is referred. With the neurasthenic condition pointing 
to any one of the organs most frequently the seat of symptoms (the brain, 
the spine, the stomach, the prostatic urethra,- the genitalia, the eyes, the 
liver, the intestines, the heart, the uterus, the ovaries, etc.) modern meth- 
ods of diagnosis in a large proportion unearth underlying anomalies which 
may be relieved by treatment, with relief often of the neurasthenic symp- 
toms. 
Cerebral neurasthenia, or as Beard characterized it, “cerebral exhaus- 
tion,” may be a symptom of disturbed circulation—cardiac asthenia— 
faulty blood states, faulty assimilation or metabolism including the effects 
of toxins, ptomains, acidemia, oxaluria, phosphaturia, and a variety of 
other abnormal conditions which time and patient study of the individual 
case will detect and often relieve with consecutive relief of the cerebral 
asthenia. 
Patients frequently present with symptoms referable to the spine 
(spinal neurasthenia) in whom -the underlying cause proves to be venereal 
excesses, changes in the generative organs which are of themselves often 
insignificant; at times there are constitutional disturbances. 'The sexual 
neurasthenic is a difficult patient to influence. lie has, as a rule, been mis- 
led by designing quacks or debasing literature which has magnified his 
symptoms, and has started an almost continuous self-suggestion which is 
depressing. At times these patients fall into a melancholy or hypochon- 
driacal condition after a period of uncomplicated neurasthenia, from which 
they are raised hut slowly. A strong personality with convincing sugges- 
tion often leads these patients from darkness to light. 
Among the most intractable neurasthenics are those who, as the result 
of repeated suggestion have become “sexual hypochondriacs.” Repeated 
nocturnal emissions, the slightest cloudiness of the urine, imaginary impo- 
tence, a slight discharge of mucus, remorse after a period of masturbation, GENEKAL DISEASES OF THE HEKVOUS SYSTEM 
1029 
premature emission during coitus, all impress the neurasthenic and inter- 
fere with recovery, until by thorough diagnosis and honest suggestion the 
patient is enlightened and released. 
In cases of sexual neurasthenia without suspicion of congenital inferi- 
ority, especially the “anxiety neurosis” of Freud, a careful examination 
of the urogenital tract should be made for sources of reflex irritation. 
Often when the neurosis has been attributed to the psychic effect of im- 
proper sexual habits, to the sudden cessation of normal sexual life, to 
chronic masturbation, coitus interruptus, or premature ejaculation, it will 
be found that while these conditions are present, they are concerned only 
indirectly and that the nervous and psychic symptoms are directly condi- 
tioned by an actual irritation of some part of the genital tract; often this 
is to be found in a congested veruinontanum and posterior urethra, in 
which region the genital reflex is believed to originate. If we assume that 
the constant stimulation of the sexual centers to which such a condition 
would give rise is equivalent to constant sexual excitement without ade- 
quate and normal discharge, it is easily understood why such widespread 
nervous and psychic symptoms should result. With the source of irrita- 
tion discovered and proper local treatment applied, the prognosis for the 
neurasthenic symptoms is entirely good. 
Sexual anomalies in women are often'as rebellious as in men. The 
recurrence of sexual neurasthenia is often discouraging; most cases finally 
recover. 
Factors Which Influence the Course of the Disease.—The urinary 
anomalies which have been charged with provoking and continuing neuras- 
thenia, in a preceding paragraph, including phosptiaturia, oxaluria, hyper- 
acidity, quantitative increase or reduction of secretion demand close study 
in individual cases. In most cases, usually men, the control of the appe- 
tite, temperance in the use of wines and liquors, the discontinuance of 
the use of tobacco (often badly borne), the return to rational living, the 
leading of a normal sexual life with local treatment as needed, will prove 
sufficient to overcome most neurasthenias dependent upon the so-called 
diatheses. 
In occasional cases it has been found that the effect of operation for 
varicocele has had a beneficial effect. Such patients often make perma- 
nent recoveries if the operation is followed by right living and a healthy 
suggestion, while before the operation they were self-centered and the 
gravity of their trouble was continually before their mental vision. 
I have already mentioned the frequent occurrence of neurasthenic 
symptoms with cardiac neuroses. Grave organic heart disease in the face 
of approaching death is rarely associated with marked neurasthenia. It 
is with the cardiac neuroses that fear takes possession of the patient. The 
most chronic types of neurasthenia (marked tendency to recurrence) 
in practice have been associated with cardiac neuroses. Periods of latency 1030 
DISEASES OF THE NERVOUS SYSTEM 
are followed by long periods of persisting symptoms just so soon as the 
arhythmia or other evidences of faulty heart action appear. Complete 
cure is not infrequent. 
The muscular weakness promptly following any well directed effort, 
true myasthenia often, in which sustained effort is impossible, may lead 
to chronic invalidism in which the patient finally becomes bedridden and' 
cannot be induced to make the necessary effort to arise. Some of these 
patients spend years in bed and never recover. The “personal equation” 
of the attendant becomes an enormous factor in the prognosis of these 
cases; it is this class of neurasthenics which is often favorably influenced 
by some one of the many unscientific cults. Recovery in these cases may 
be sudden, unexpected, and complete. 
The increased tendon reflexes in neurasthenia are without prognostic 
significance; as in hysteria the reflexes are usually increased. 
Fear and imagination are among the most frequent accompaniments 
of the neurasthenic state; it not infrequently happens that the neurasthenic 
manifestations may suddenly disappear when psychic disturbances (psy- 
cliasthenia) continue during unlimited periods. Under such conditions 
fear or phobias may take possession of the patient. These symptoms may 
disappear after a limited (short) period; at times the cases remain un- 
changed during a number of months, or symptoms recur on slight cause. 
The phobias of true neurasthenia are as a rule easily controlled, and 
are often entirely dissipated by reassurance and the correct interpretation 
of symptoms for the patient by one in whom he has full confidence. 
Arteriosclerosis, according to Watson and others, is not an important 
factor, per se, in the causation of psychoses, more particularly involution, 
and when present in the neurasthenic does not per se exert a marked in- 
fluence on the prognosis of the symptom complex. 
Psychasthenic states invite insanity. Neurasthenics who have fallen 
into the habit of sleeping badly, in whom the primary or predisposing 
cause has been removed, will after a few nights of induced sleep learn to 
sleep and promptly improve. 
“Neurastlienic habits” can be overcome and many symptoms may in 
consequence be relieved, but to succeed requires the reassurance which 
accompanies repeated healthy suggestion and enormous attention to detail, 
as well as tact. 
Paralysis and abolished patella tendon reflex are not present in neu- 
rasthenia without organic disease—neither are there anesthetic areas. 
In considering the prognostic significance of ocular and aural symp- 
toms it should be remembered that they are preeminently those of fatigue 
rather than of the mimicry of organic disease. With the removal of the 
cause, the blurring of the eyes and the sensitive eyeballs and aural dis- 
turbances are relieved. 
The sensory symptoms of neurasthenia are numerous and exceedingly general diseases of the NERVOUS SYSTEM 
1031 
troublesome. They include besides headache, which is one of the most con- 
stant attendants, a variety of sensations referred to the head, “splitting,” 
occipital pain and tenderness, “throbbing,” “beating,” “hammering.” All 
of these sensations are not truly painful, but as Church and Peterson say 
“rather some variety of discomfort difficult to describe.” Other sensory 
symptoms include peculiarly located and persisting backache, tender spine 
(superficial), sensations of heat and cold, numbness of the extremities, 
prickling, stinging sensations, paresthesias, persistent “tired feeling,” and 
a variety of abnormal sensations which may be referred to the abdominal, 
the genito-urinary, the pelvic or the thoracic organs without the earmarks 
of organic disease. 
Gastro-intestinal anomalies are unquestionably present with neuras- 
thenia in a large proportion of cases. The association of Glenard’s dis- 
ease with neurasthenia is surprisingly frequent and obstinately chronic. 
Such patients are often handicapped and made more neurasthenic by 
faulty elimination, toxic conditions and the association of heart neu- 
rosis. 
Constipation is a frequent attendant. The relief of the constipation 
and support to the abdominal viscera which should also include the sup- 
port of the mobile or prolapsed kidney and the general treatment of the 
neurasthenic habit (change of scene, wholesome suggestion, and repeated 
reassurance) lead to long periods of freedom from symptoms, and in some 
cases complete cure. 
The “brain fag” or “mental fatigue” which is associated with muscu- 
lar fatigue, yields with the removal of the underlying cause. In some 
patients who find that return to their original work causes headache and 
prompt fatigue, change to out-of-door occupation which includes exercise 
short of fatigue causes prompt improvement, often relief of symptoms 
during indefinite periods. 
There is a class of neurasthenics in whom the ocular symptoms are in 
the ascendency, fatigue of accommodation promptly follows the use of 
the eyes while there is also more or less retinal hypersensitiveness. These 
patients are materially improved—often cured—by change of scene, rest 
during a limited period, and the correction of existing errors by the oph- 
thalmologist. 
The ability of the therapeutist to control the general condition of the 
neurasthenic depends very largely upon the associated disturbance, the 
organs from which the reflexes radiate. 
Emaciation with Glenard’s process, the nervous dyspepsia of Leube, 
with sexual neurasthenia, is by no means serious nor threatening and may 
promptly yield under favorable conditions—often more promptly than do 
cases in which the general nutrition has remained unchanged. 
Faulty nutrition of the body—malassimilation of food—is one of the 
chief factors in the production of the neurasthenic state; this fact fully 1032 
DISEASES OF THE NERVOUS SYSTEM 
appreciated by the clinician in bis treatment, will lead to marked improve- 
ment, often full recovery. 
To discuss fully the prognosis of neurasthenia and all of its manifes- 
tations would take us into almost every field of medicine. Each of the 
many specialists to whom these cases find their way has a chapter to add 
which demonstrates to him the paramount importance in prognosis of his 
own limited field. All, however, if evenly balanced appreciate the impor- 
tance of recognizing the underlying inherent weakness with which we must 
reckon in the prognosis of the complex. 
Success means cooperation of physician and patient. The latter must 
be willing to strive “after self-effacement”; he must have ideals which lift 
him from the depths to which he has fallen; he must return to an occupa- 
tion which will bring strength; he must learn to bear his suffering 
with equanimity. If the clinician has the hearty cooperation of the pa- 
tient and his full confidence, the prognosis of neurasthenia is not bad; it is 
often cured, though as I have frequently held in this chapter, recurrence 
must be expected. Much depends upon the ability of the patient to take 
advantage of change of surroundings and he must have freedom from care 
and the many anxieties of life. A single but persistent mental pang, may 
be sufficient to continue the complex indefinitely in the predisposed subject. 
The course of neurasthenia is chronic. The asthenia, growing muscu- 
lar enfeeblement, and tendency to do less and less from day to day, im- 
press the patient until the “irritable weakness” is fully established. 
The prognosis is best in those cases in which the attendant gains the 
cooperation of the patient; in those who are able to take advantage of 
complete change of scene; in those who are not burdened with an unfavor- 
able heredity; who have been piloted without the formation of an enslav- 
ing drug habit. 
The younger patients, those who develop the disease before the twenty- 
fifth year, may improve after short periods of symptoms, but relapse is to 
be expected. In older patients, those beyond middle life, the prognosis 
naturally depends upon the underlying cause of the complex. With per- 
sistent functional or organic disease in such subjects, the neurasthenic ac- 
companiment is not easily overcome, though it often happens that with 
increasing evidences of organic disease (bodily infirmities) the symptoms 
of neurasthenia may give way to those of the graver disease. 
The recognition of neurasthenia as a symptom complex—secondary as 
a rule—will prompt the clinician to search for and remove the cause, thus 
improving the prognosis in the individual case. The regulation of the 
lives of those who lack normal recuperative power and the education of 
those with inherent weakness and an unstable mental state ever ready tq 
practice autosuggestion, will go far toward reducing the number of neuro- 
paths. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1033 
References 
Abrams. The blues (splanchnic neurasthenia), etc. New York, 1904, and subsequent 
editions. 
Allbutt. System of medicine. 1899, and subsequent editions, viii. 
Beard (G. M.). American nervousness, etc. New York, 1881. 
Nervous exhaustion. New York, 1886, 1889, 1905. 
Church & Peterson. Nervous and mental diseases. 8th ed. Philadelphia, 1914. 
Cleghorn. New York Med. Rec., April 27, 1907. 
Eisner (Henry L.). New York Med. J., 1897, i, 491. 
Gilles (de la Tourette). Semaine Med., Paris, 1898. 
Heilbronner. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912. Bd. v. 
Kraepelin. Munch, med. Wchnschr., 1902, xlix, 1641-1644- 
Rockwell (G. W.). New York Med. Rec., 1897, ii, 297-299. 
Savill. London, 1900. 
Stewart (Purvis). The diagnosis of nervous diseases. New York, 1912. 
Strumpell. Nervositat u. Erziehung. 
Watson. Boston Med. & Surg. J., Jan. 12, 1912. 
4. Paralysis agitans 
{Shaking Palsy, Parkinson's Disease (1817) 
General Statements.—Paralysis agitans is a disease of unknown 
pathology characterized by trembling of the extremities, one or more in the 
early stages, later of the trunk and entire body, with marked tendency to 
muscular rigidity and ultimate slowing of all movements, increasing weak- 
ness, and premature ageing of the patient. The trembling may, in occa- 
sional cases he limited to one-half of the body during long periods, extend- 
ing finally to the unaffected side; or the disease may remain limited and 
follow a chronic course without progression (See Parathyroid Therapy 
below). 
While paralysis agitans is a disease of advanced life, when it attacks 
patients during middle life there are evidences in the early turning of the 
hair, the facies, the movements, and in the cardiovascular tree, of prema- 
ture decay. 
Arteriosclerosis is not a cause of paralysis agitans, but its presence with 
other evidences of premature changes have been strikingly characteristic 
in our material and demand attention for diagnosis; prognosis is mate- 
rially and unfavorably influenced by the presence of rapidly advancing 
arterial change. 
Juvenile forms of paralysis agitans (Stier) are occasionally found 
with characteristic symptoms including tremor, muscular rigidity and 
unsteadiness on standing. In the advanced stages locomotion is almost 
impossible. Such symptoms may begin early and persist during mature 
life. In all of these cases the clinician, before he offers a final prognosis, 1034 
DISEASES OF THE NERVOUS SYSTEM 
must fully satisfy himself that the symptoms are not of hysterical origin. 
Mendel asserts with positiveness that all paralysis agitans which begins 
before the fortieth year should always arouse a strong suspicion of hys- 
teria. For prognosis and differentiation of the juvenile type the absence 
of sensory symptoms and the persistence of muscular tension during sleep, 
argue against hysteria and modify prognosis unfavorably. The gradual 
increase of symptoms without the history of traumatism or litigation, 
also argues in favor of paralysis agitans and against hysteria. 
Willige found in studying 47 cases of so-called “juvenile paralysis 
agitans”—all of which commenced before the thirtieth year—only 12 in 
which the diagnosis was positively justified. 
Frequency.—The frequency of paralysis agitans in practice is demon- 
strated by the statistics of Curschmann who found 5 cases among 300 in- 
mates of an institution which corresponds with our “poor houses” or 
“county hospitals.” Berger’s report of Parkinson’s material included 37 
cases among 6,000 diseases of the nervous system; Mendel’s material offers 
50 cases in 25,000 cases of diseases of the nervous system (.2 per cent) ; 
my material included 28 cases among 6,300 internal diseases carefully 
cross-indexed (.04 per cent). It may be concluded that relatively the 
disease is rare. The disease is more frequent in England, Germany, and 
France, than in Southern Europe; strikingly frequent among the Irish. 
McCarthy makes the statement that “it does not seem at all rare in 
America.” 
Factors Which Influence Prognosis.—Erb found men more subject to 
the disease than women (5:2). Hart’s material corroborates Erb’s con- 
clusions; his proportion of males and females in 219 cases was 7:4. Pov- 
erty, exposure, mental strain and traumatism are inviting factors. In 
one-fifth of the cases at the Berlin Clinic there was a history of trauma- 
tism. 
In Gowers’ material the average age was 52 years for the onset of 
symptoms. My material includes cases which commenced after the sev- 
entieth year and progressed slowly; the majority of these “senile cases” 
died of intercurrent disease; their general health sfeemed unaffected by 
the neurosis. When they lived over ten years after the onset of symptoms, 
the progression was slow, as a rule. 
The influence of heredity on the prognosis of paralysis agitans is in- 
significant. In the material at my command I have only rarely found 
the disease among other members of the family. The positive statistics 
given by Lundborg of familial types of the disease, also its association with 
the familial types of myoclonus are not generally accepted by those, includ- 
ing Erb and Wollenberg, who have had ample opportunity to study a large 
material; and the latter warn against the consideration of heredity for 
diagnosis or prognosis. 
From a cautious study of the pathogenesis and pathology of paralysis GENERAL DISEASES OF THE NERVOUS SYSTEM 
1035 
agitans, we are unable to offer reliable data from the included material. 
In our own country, the painstaking reports which Dana, Gordinier, and 
others have presented to the profession, including atrophy, pigmentation, 
vacuolation, and other degenerative changes in the cells of the anterior 
horns, etc. (Dana), and the perivascular sclerosis (Gordinier and Redlicli), 
have not been confirmed. 
The myogenic hypothesis including changes in the muscles offers 
nothing positive, though it has been strongly supported by Camp in an 
able article (See References). 
Parathyroid Therapy.—The theory which has recently interested the 
profession and which seemed to some, because of improvement after the 
administration of the parathyroid substance (Alquier, Lundborg, Mobius, 
Berkeley) to favorably influence prognosis, is based upon the hypothesis 
that paralysis agitans is a symptom complex due to disturbance of internal 
secretion. Alquier’s report of the histologic changes found post mortem 
of a sclerotic hypo or hypoplastic nature have not been confirmed, neither 
have others paralleled the favorable results of Berkeley following the 
administration of the parathyroid. The hypoparathyroidism of these re- 
porters and the favorable prognosis based upon their conclusions have been 
strongly controverted by the claims of Roussy and Clunet who found 
epithelial hyperplasia of the parathyroids causing hyperparathyroidism. 
The encouragement for prognosis which would seem to follow if we 
accepted without question the enthusiastic reports of those who claim suc- 
cess or improvement from parathyroid treatment is not justified by the 
observations of Greenwald, who at the chemical laboratory of the Monte- 
fiore Home in Hew York has conducted a series of experiments which 
prove that the acid-soluble phosphates in the blood serum of patients with 
paralysis agitans is not greater than in normal individuals, which would 
be the case if there was true parathyroid insufficiency. Tests with his 
material “do not support the view that parathyroid insufficiency plays a 
role in the etiology of paralysis agitans.” We must, therefore, reluctantly 
refuse to base a favorable prognosis on parathyroid therapy. 
Course of the Disease.—Tremor once established, is not likely to dis- 
appear. There may be periods of remission, or under excitement, exacerba- 
tion, but in true Parkinson’s disease, while years may pass without marked 
increase of the tremor, it continues a prominent symptom with the varia- 
tions characteristic of individual cases and increasing rigidity as the dis- 
ease progresses. Paralysis of the trembling arm and leg (hemiplegia) as 
a rule causes cessation of the involuntary movement. 
Muscular rigidity is unrelieved by any known treatment; it is more 
important for diagnosis than is the tremor, and is the most prominent and 
diagnostic symptom of the disease. 
Paralysis agitans may exist and progress without tremor (“sine agita- 
tione”), entirely uninfluenced by treatment. The rigidity is persistent; 1036 
DISEASES OF THE UERVOUS SYSTEM 
slowness of movement fully established is also continuously present with 
marked resistance to passive movement. 
The characteristic stooping posture, the hold of the hand and arm, 
the facial expression (lack of expression) and “trotting gait” continue so 
long as the patient is about. The tendon reflexes offer no data of impor- 
tance for prognosis. As the disease progresses muscular contraction is 
tardy and there is, according to Borgherieni, reduced irritability of the 
muscles and nerves to the electric current. 
During the many years of persisting symptoms the sphincters are not 
involved; when they are, late in the disease, due to complications, the end 
is not usually long postponed. 
In my material the mental condition of the patient has not been influ- 
enced by the disease; when it has been, the change was due either to arterio- 
sclerotic complication, senile dementia, or acute and added infection. 
The urine offers no data in the average case. 
It may be safely concluded that while the disease, per se, does not cause 
death, it is incurable by any known methods of treatment. There is a 
strong tendency in some cases to latency, indeed in some, the develop- 
ment is so slow as to remain almost entirely unnoticed. There are cases 
in which there is perceptible progression during periods varying in length 
in different cases, with stationary periods of short or long duration, often 
following, of considerable length. I have recently seen the chronic case 
of a woman about sixty-five years of age who, despite the presence of 
lively tremor of both upper extremities and a characteristic “trot,” was 
able to dance the modern dances without unusual fatigue, and this in a 
public ballroom. The tremor in both arms persisted while dancing, the 
head was well controlled and the legs seemed to give no trouble. 
Complications.—Fractures and other trauma in advanced cases as a 
rule aggravate existing symptoms. 
Unless patients die within the first twenty to twenty-five years with 
progressive symptoms and acute or chronic complications in the majority 
of cases the rigidity advances to such an extent as finally to make loco- 
motion impossible, and they become bedridden. This however has been 
an exceptional experience in my material. The chronic cases when bed- 
ridden, are likely to develop bedsores, cystitis, ascending genito-urinary 
infection with evidences of general sepsis; often pneumonia, marasmus, 
or other intercurrent disease. 
Complications referable to the nervous system, which affect prognosis 
unfavorably are hemiplegia, the association of chorea and epilepsy in cases 
with hereditary taint, perforating ulcer of the hand or leg, locomotor 
ataxia, hysteria, and joint changes resembling arthritis deformans (Spil- 
ler)—in one of my cases meningitis. 
Patients with paralysis agitans are not immune to the infectious, con- 
stitutional, or local disease, and they often develop these. As a rule, it GENERAL diseases of the NERVOUS SYSTEM 
1037 
has been my experience that the resistance to added disease is materially 
reduced in the presence of shaking palsy. 
References 
Alquier. These de Paris, 1903. 
Revue Neurol., 1904. 
Apert & Rouillard. Perfor. ulcer, etc. Revue Neurol., Paris, 1912. 
Berger. Eulenberg’s Real Encycl. 1st ed. 
Berkeley (W. N.). Internat. Clin., series 22, iv. 
Borgherieni. Wien. med. Wchnschr., 1890. 
Camp. J. Am. Med. Jlss., xlvii. 
Curschmann. Mohr & Staehelin’s Handb. d. inner. Krankh. Berlin, 1913. Bd. 
Dana (C. L.). New York Med. J., Nov., 1899. 
Duschek. Mitth. d. Gesellsch. f. inner. Med. u. Kinderheilk. Wien, 1914, xvii. 
Ebstein (E.). Neurol. Centralbl., Leipzig, 1912. 
Erb. Paralysis agitans. Deutsch. Klin., Berlin, 1901, Bd. v, Abt. 6. 
Gordenier. Mohr & Staehelin, v. [1. c.]. 
Greenwald. Am. J. Med. Sd., 1914, cxl. 
Hart. J. Nerv. & Ment. Dis., xxxi, 177. 
Lundborg. Hygiea, Bd. Ixii. 
Deutsch. Ztschr. f. Nervenkh., Bd. xxvii. 
Neurol. Zentralbl., 1912, No. 4- 
Mendel. Berl. klin. Wchnschr., 1914, No. 31. 
Paralysis agitans. Berlin, 1911. 
Moebius. Quoted by Mohr & Staehelin. Bd. v [l. c.]. 
Oppenheim. Berl. klin. Wchnschr., 1913, i, 793. 
Parkinson (James). Essay on shaking palsy. 1817. 
Redlich. Jahrb. f. Psych., xii. 
Roussy & Clunet. Compt. rend. Soc. de biol., Paris, 1910. 
Stier. Berl. klin. Wchnschr., 1914, No. 31. 
Willige. Ztschr. f. d. ges. Neurol, u. Psychol., iv, No. J+- 
Wollenberg. Mohr & Staehelin [Z. c.]. vol. v. 
5. Chorea 
{Sydenham’s Chorea, Chorea Minor, St. Vitus’ Dance, Infectious Chorea) 
“Everything connected with this disease is extraordinary; its name is 
ridiculous, its symptoms singular, its course unusual, its cause unknown, 
and its treatment problematic.” 
While some of the problems associated with chorea are being cleared, 
the statement quoted from Bonteille (Preface of his “Traite de la Choree,” 
1810) is in the main true today. We are fast establishing facts however, 
which prove that chorea is a hyperkinetic disease, which in the majority 
of cases is either directly associated with infection or follows it. 
Chorea is a curable disease of the central nervous system, usually of 
childhood, characterized by motor disorders, irregular, involuntary mus- 1038 
DISEASES OF THE NERVOUS SYSTEM 
cular contractions—all purposeless—which may continue during rest but 
are likely to cease during sleep, and are increased by excitement and 
emotion. Children and adults with chorea in most cases show psychic dis- 
turbances, more or less, in accordance with the natural tendencies (neuro- 
pathic) of the individual or the severity of the disease. The disease should 
be considered a neurosis, and the presence of endocarditis and arthritis at 
some time suspected. 
History.—Chorea minor as a disease per se dates from Sydenham who 
in 1686 and 1693 fully described it and divorced it from the conglomerate 
mass of conditions with which it was associated during the middle ages 
(hysteria, mania, epilepsy, etc.). 
Haturally the prognosis of chorea depends upon its cause and the asso- 
ciated pathologic lesions. 
Conditions Which Influence Chorea.—Sex.—The disease is found to 
be more frequent in the female than in the male. Osier in his classic mon- 
ograph reports 554 cases of which 161 were males and 390 (70 per cent) 
females. Gowers’ ratio of females to males is 3 to 1. Wollenberg’s sta- 
tistics in 3,595 cases showT 30 per cent men, 70 per cent women. 
Age.—Heubner holds that chorea minor is not a disease of the suckling 
babe; but 3.6 per cent cases are found between the first and fifth year; 
from 6 to 15 years, 75 per cent (the larger number between 9 and 11 
years) ; between 16 and 20 years, 13.5 per cent, while chorea after the 
twenty-fifth or thirtieth year, particularly among men, must lead to the 
suspicion of organic disease—Huntington’s hereditary chorea, tic, or other 
central lesions (Wollenberg). The senile form of chorea is usually one- 
sided. 
Moisture and exposure exert an unfavorable influence on those predis- 
posed, and bear the same relation to chorea as they do to mono or polyarth- 
ritis. The influence of cold is further established by the greater frequency 
(50.5 per cent) of all cases during the four winter months (Czerno- 
Schwarz u. Lunz). 
Unfavorable hygienic conditions, faulty homes, and overcrowding are 
factors which unfavorably influence the course of all forms of infectious 
chorea. Heredity does not materially influence the prognosis of acute 
chorea, depending as the disease does on infection. Wollenberg in 539 
cases found but 2 per cent in whom there was a direct hereditary influence. 
It should be assumed however that in children who show the hereditary 
neuropathic tendency or habit, chorea is more easily developed than in 
those with normal resistance. 
The Negro and American Indian seem to show a decided immunity to 
the disease. Of 175 cases at the Johns Hopkins Hospital 5 were in the 
negro race (Osier). 
Psychic disturbances aggravate symptoms when present, and are un- 
questionably inviting factors in the presence of infection. Thus fright GENERAL DISEASES OF THE NERVOUS SYSTEM 
1039 
and worry in children often during examinations or tests in school, over- 
study, masturbation, and unusual and prolonged application to one line of 
work may be included. In almost all of these cases, careful inquiry will 
establish a source of primary infection which may have been latent or 
active. The majority of “imitation choreas” are of hysterical origin and 
yield to rest and removal from school or from the unfavorable atmosphere 
of infectious chorea. 
Associated Diseases.—Tonsillar Disease and Chorea.—Nasal in- 
fection associated with or without preceding nasal abnormalities, as well 
as tonsillar infection, may not only lead to chorea but may be the underly- 
ing factors in continuing the symptoms during long periods. The removal 
of the primary focus exerts a favorable influence on the course of the 
disease. In my experience I have found on careful investigation that 
the majority of tonsillitides which have been associated with chorea 
developed joint symptoms, and in most of these there was, as shown by 
physical signs (in the presence of murmurs), positive evidence of endo- 
carditis. 
Arthritis and Chorea.—The association of infectious arthritis with 
chorea is undeniable; the former is distinctly a cause of the latter, and 
unquestionably the disease is continued and sustained by the same micro- 
organic life and its toxins which may be considered to have been the patho- 
genic factors of the primary disease. 
Pathologists are fast subscribing to the dictum of Poynton and Pain 
which has received confirmation from the researches of Rosenow, which 
declares acute polyarthritis (rheumatic fever, inflammatory rheumatism) 
to be due to the streptococcus rlieuinaticus or some modification of the 
ordinary streptococcus (Rosenow), and upon this conclusion we are entitled 
to base the prognosis of a large number of choreas. There is association 
with arthritis or rheumatism in between 25 or 30 per cent of choreas, 
according to reported cases. This percentage is too low, for the thorough 
investigation of my material proves the presence of some symptoms of 
rheumatism, often only mild and suggestive in the majority of cases— 
over 80 per cent. This is corroborated by the data given by Cursclimann 
and others. I have rarely found malignant endocardial infection asso- 
ciated with rheumatism and chorea. I lost one case—a girl of 8 years 
of age with malignant endocarditis, unquestionably of the streptococcus 
viridans type, after a period of subacute polyarthritis followed by the 
chronic type of malignant endocarditis and chorea which persisted several 
months before death. 
Additional Diseases.—Richards also reports two cases of chorea with 
streptococcus viridans infection. The prognosis of such cases is almost 
uniformly bad; most patients live during several months and finally die 
with evidences of multiple hemorrhagic infarcts. 
The prognosis of chorea associated with purpura rheumatica is good, 1040 
DISEASES OF THE NERVOUS SYSTEM 
though recovery is often, slow. Chorea with polyarthritis and gonorrhea 
when associated with endocarditis offers an unfavorable prognosis. Chorea 
following or associated with grippal infection runs an average course to 
recovery in almost all cases, psychic symptoms which are prominent in 
some yield but slowly; these cases may relapse at short intervals during 
varying periods. 
While chorea may be associated with most infections of childhood— 
scarlet fever particularly—the acute infections as a rule, when developed 
at the height of the disease, are likely to check the movements or dissipate 
them entirely. 
Chorea gravidarum 
Pregnancy is a provoking cause of chorea; it is in all probability due 
to toxemia; is most frequently present during the first half of pregnancy 
and in subjects who during childhood or later, had the same disease. 
Chorea during pregnancy is as a rule severe, not easily controlled, and is 
likely to be associated with active psychic disturbances. Mild forms are 
the exception. The prognosis is grave for both the mother and child. 
Frank reports 182 cases with a mortality of 23.6 per cent, for the former, 
and 4.7 for the latter. Oui reports 10-12 per cent mortality among the 
children. The prognosis for the mother is materially improved with 
termination of pregnancy by artificial means. 
Factors Which Influence Prognosis 
Ocular Errors.—It not infrequently happens that persisting chorea is 
favorably influenced by the correction of existing ocular errors. The safe 
conclusion to reach after a full study of the literature of this subject, in- 
cluding the original articles of Stevens, C. S. Bull, and De Schweinitz 
seem to me tff he included in the statement of the latter quoted by Osier, 
“that ordinary chorea and many of the forms of facial spasm, habit spasm, 
etc., are materially benefited by correcting refractive errors and anomalies 
of the ocular muscles, just as they are helped by a variety of other treat- 
ments, hut I do not believe that there is any proof to show that eye strain 
of itself is responsible for their origin, with perhaps the single exception 
of the so-called habit spasm affecting the orbicularis and immediate facial 
area. Certainly many of these will disappear promptly after the refractive 
error is corrected without any treatment whatsoever, and they will not 
disappear if you do not relieve the eye-strain. In a constitution predis- 
posed to chorea I presume eye-strain is a very important factor in fostering 
and perhaps provoking attacks, hut that is all.” 
Mental Symptoms.—The psychic disturbances are prominent in most 
cases of chorea; only occasionally are they entirely absent. The irrita- 
bility of the child is characteristic; violent outbursts of temper are also 
frequent; memory is faulty, and concentration almost impossible. In the GENERAL DISEASES OF THE NERVOUS SYSTEM 
1041 
severe cases there may be hallucinations, delusions and mania (Chorea 
insaniens). Collins and Abrahamson show that 54 per cent of cases had 
psychic disturbances. Dementia does not develop or follow simple (non- 
huntingtonian) chorea. 
The prognosis of the psychic disturbances of chorea is, as a rule, 
favorable, though their duration may be variable and a positive forecast 
giving a time limit is absolutely impossible. 
Sensory Disturbances.—The disturbances of sensation are only rarely 
prominent. There are occasional cases in which there are persistingly 
painful points, numbness, tingling or burning sensation. In some there 
may be an element of added hysterical hemianesthesia. In all of these 
conditions the symptoms yield as the choreic movements cease—or shortly 
after. 
Motor Disturbances.—Cases in which there is the greatest motor ac- 
tivity and agitation, those which appear most severe, often terminate very 
suddenly; while others with little choreic movement and less agitation 
often drag a weary course. 
Latent chorea is slow to recover, and may persist during months with 
repeated exacerbations in some cases. Langmead is correct in concluding 
that “the two most important questions to ask in such cases are with regard 
to sleep and feeding. As long as the child is sleeping well, and can be fed 
naturally, no untoward result need be feared.” 
Muscular Weakness.—Muscular weakness associated with or follow- 
ing chorea yields to treatment—rest particularly—and disappears entirely 
without leaving a remnant. 
The weakness may simulate motor paralysis—either hemiplegia, para- 
plegia, or monoplegia; it requires accurate differentiation in occasional 
borderline cases. In all of these a favorable prognosis may be given. 
Additional Factors.—Marked loss of flesh does not influence progno- 
sis unfavorably. Choreic children are often much reduced by the active 
movements and sleeplessness but their convalescence is usually prompt, 
and satisfactory return of weight is the rule. The involvement of the 
sphincters is only present in the terminal stages of the most malignant 
choreas in which the forecast is exceedingly grave. The urine offers no 
prognostic data. 
Eosinophilia in Chorea.—While the examination of the blood of 
choreic patients offers no data for prognosis, the experience of Macalister, 
Brown, Cabot, and Leopold tends to prove that eosinophilia is present in 
most cases of true chorea. The persistence of eosinophilia or its recur- 
rence forecasts a relapse (Leopold) ; its presence in abnormally high per- 
centage (children normally show slight eosinophilia) is proof of incomplete 
cure. Absence of eosinophilia according to Leopold “may prove of some 
diagnostic significance in borderline and doubtful cases and has, therefore, 
a relative prognostic value.” 1042 
DISEASES OF THE NERVOUS SYSTEM 
Heart.—Cautious observation and physical examination reveal heart 
anomalies in most cases of chorea. These may be either functional or 
organic. The irritable, erratic, and tumultuous heart with overactive sys- 
tolic force is characteristic of chorea. Systolic murmurs are common, as 
are changes in the size of the heart. It is often difficult to decide whether 
there is endocarditis or only functional anomaly. Unquestionably endo- 
carditis, occasionally pericarditis, are responsible for the physical signs 
in a large proportion of cases, and materially influence prognosis. 
Endocarditis is almost constantly present in fatal cases of chorea. 
Osier says “There is no known disease in which endocarditis is so con- 
stantly found, post mortem, as chorea; it is exceptional to find the heart 
healthy.” 
In those who have had chorea, Osier’s contention is correct that “the 
primary heart trouble in chorea is in a majority of cases, at least, an endo- 
carditis.” In most of these cases the cardiopathy continues during life 
without causing secondary disturbances, often but faint physical signs. 
51 3/7 per cent of 140 cases examined from 16 to 2 years after the cure 
of chorea, showed evidences of a damaged heart. 
The majority of endo car ditides associated with chorea in young girls, 
however loud the murmurs or persistent the physical signs during the prog- 
ress of the disease, yield to treatment with the disappearance of all sub- 
jective symptoms; about the time of puberty there is but faint remnant of 
the previous endocarditis in physical signs, though thorough examination 
shows a slight cardiopathy. The complication of pericarditis influences 
prognosis unfavorably. 
Gibson has shown the frequent presence of pericarditis with and with- 
out endocarditis in fatal cases of chorea and polyarthritis, while Osier 
in his oft-quoted monograph reports “in 19 of the recent autopsies in 
chorea which I have collected, pericarditis occurred as a complication, and 
in 17 it was associated with endocarditis.” Myocarditis with endo- or 
pericarditis, the presence of which is made positive by physical signs of 
cardiac insufficiency, offers an exceedingly grave outlook. Poynton has 
called attention to the persistence of tachycardia associated with chorea 
and the progression of mitral stenosis. , 
In most of my cases of chorea fatal endocarditis with pericarditis was 
of rheumatic origin. Typical mild chorea minor without serious compli- 
cations, with the “choreic heart” and usual motor and psychic symptoms 
runs a favorable course when cautiously watched and treated in from seven 
to ten weeks. The severe cases may persist with or without remission 
during from four to seven or eight months. 
Special Considerations 
Improvement of the psychic disturbances is usually promptly followed 
by the gradual cessation of the involuntary movements. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1043 
The mortality of chorea is between 2.5 and 3.5 per cent. Wollenherg 
places it at 3 per cent. Endo- and pericarditis are the leading causes of 
death in most cases. The prognosis of chorea at puberty or shortly before 
is less favorable than between the sixth and tenth year. 
Chorea in the aged is a formidable disease. I have rarely found it 
primary. One of my cases was associated with diabetes mellitus in a man 
seventy years of age. As a rule it will be found, as already suggested else- 
where in this article, that cautious diagnosis will prove the great rarity of 
adult, particularly senile chorea. 
There are occasional foudroyant cases associated with deep involvement 
of the sensorium, febrile movement, uncontrollable insomnia, heart lesions 
(endocarditis) which run a rapid course to death in from five to twelve or 
fifteen days. 
A similar rapid and unfavorable termination may occasionally follow 
or be associated with scarlet fever, diphtheria, or typhoid fever. 
Relapse is frequent and must be expected in about fifty per cent of all 
cases. With our appreciation of the infectious nature of the disease, the 
search for the infecting focus, and its removal, relapses will be less fre- 
quent in the future. Females are more subject to relapse than are males. 
Relapses in males rarely follow the third, while females may have as many 
as twelve to fifteen. 
The severity of succeeding relapses is progressively reduced, as is also 
the duration (See Reports; 139, 80, and 55 days as the duration of the 
first three attacks respectively—Church and Peterson). The interval be- 
tween remissions is variable; the average in my cases was between ten and 
thirteen months. The condition of the heart may remain unchanged with 
succeeding attacks. In some cases there may be no positive evidences of 
heart involvement during the first attack but subsequent attacks usually 
show positive “choreic heart,” evidences of endocarditis, or chronic car- 
diopathy. 
There are subacute and chronic cases of chorea; the majority of these 
finally recover, though it should be remembered that occasional chronic 
cases with remissions and exacerbations may continue during several 
years. There are but few cases in which uncomplicated choreic disease 
persists indefinitely. 
Recurring chorea and the endocarditis, or functional disturbances of 
the heart which accompany it, interfere very materially with the education 
and development of the child. Such children are handicapped in spite of 
the fact that many choreic children, girls particularly, are unusually 
bright. Cases of tic are often mistaken for chorea in adults, and this fact 
should be remembered in diagnosis and prognosis (See Tic Convulsive). 
Complications other than those mentioned are exceedingly rare, and 
prognosis is easily made in connection with the study of the heart 
anomalies. 1044 
DISEASES OF THE HERVOUS SYSTEM 
References 
Bouteille. Traits de la Choree. Paris, 1910. 
Brown (Thos. R.). Maryland Med. J., ISO2. 
Cabot (R. C.). Clin. exam, of blood. 1904. 
Collins & Abrahamson. Philadelphia Med. J., v. 
Curschmann. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912. Bd. v. 
Czerno, Schwarz & Lunz. Jahrb.f. Kinderheilk. {N. F.), Bd. lx, lift. 6. 
Frank. Chorea gravidarum. Inaug. Diss., Kiel, 1904. 
Gibson. Reynold's System of medicine. 
Habner (O.). Charite-Ann., 1911, Bd. xxxv. 
Lang mead (F.). Lancet, London, 1913, ii, 1753-1755. 
Leopold (S. S.). New York Med. J., Aug. 1, 1914. 
Macalister. Brit. Med. J., 1909, ii. 
Osier (Sir William). On chorea. Philadelphia, 1894. 
Poynton & Pain. Researches on rheumatism. London, 1913. 
Ranney. New York Med. Rec., May 5 & 12, 1894. 
Richards (J. H.). J. Am. Med. Ass., 1914, Ixii, 110. 
de Schweinitz. New York Med. J., 1887, 1. 
Osier’s Chorea [l. c.]. 
Stevens. New York Med. Rec., Aug., 1876. 
Stevens & Bull. See Osier [l. c.]. 
Sydenham. Latham's Translation. Sydenham Soc., ii. 
Wollenberg. Chorea {full literature). In: Nothnagel’s Handb. Bd. xii, 2. Theil, 3. Abt. 
{Huntington’s Chorea, Chorea of the Aged, Family Chorea, Chronic Pro- 
gressive Chorea, Acute Hereditary Chorea) 
Huntington’s Disease (18Z2) 
Huntington of Long Island has received the credit for calling the atten- 
tion of the profession to a variety of chorea which he found among a num- 
ber of families in south-eastern Hew York, in whom for years his father 
and grandfather had observed the patients who were known as “shakers,” 
Waters in 1842, and Lyon in 1863, both reported authentic cases of heredi- 
tary or chronic progressive chorea before Huntington’s article appeared 
(1872). The disease proved to be hereditary and was easily traced 
through several generations, attacking more victims than any other familial 
disease in the individual families stricken—at times one-half the entire 
family. The disease does not reappear after the “hereditary chain” is 
broken (Church and Peterson) ; hence it does not skip a generation. 
Males are more frequently attacked than females. 
Chronic chorea presents positive histopathologic changes and ought not 
to he classified pathologically with true Sydenham chorea. The most 
marked changes are found in the basal ganglia, and the lenticular and 
caudate nuclei. “The lesions consist principally in large accumulations of GENERAL DISEASES OE THE NERVOUS SYSTEM 
1045 
neuroglia cells, fiber degenerations, and considerable cell destruction. 
The quantity of products of disintegration in the basal ganglia is aug- 
mented as a result of the parenchymatous changes” (Dynan). Dynan 
gives a full report of eight cases of chronic progressive chorea; of five 
cases tested, the Wassermann reaction with the blood serum “was negative, 
and examination of the cerebrospinal fluid in one case for Wassermann 
reaction was also negative, its appearance clear, protein content not in- 
creased, and there were only four cells per cmm.” 
It is not a disease of early life and appears after the thirtieth year, 
usually between the thirtieth and the forty-fifth year, though it may 
develop later in life. The prognosis is absolutely bad as can be readily 
concluded from the “three marked peculiarities in this disease: 
1. Its hereditary nature 
2. A tendency to insanity and suicide 
3. Its manifesting itself as a grave disease only in adult life.” 
Huntington in his graphic rehearsal of the course of the disease ac- 
cented the fact above mentioned that “if by any chance these children go 
through life without it (the disease), the thread is broken, and the grand- 
children and great grandchildren of the original shakers may rest assured 
that they are free from the disease.” 
There are no recoveries from true Huntington chorea recorded ; neither 
are the symptoms relieved, but they gradually increase after beginning as 
does ordinary chorea. Before death, every voluntary muscle of the body 
is affected. If members of a “shaker family” live beyond the fortieth 
year without chronic symptoms, the chances are that they will escape the 
disease. 
The duration of the disease may be twenty or more years—some of the 
patients have reached the age of seventy. Death may follow extreme 
marasmus with dementia, acute intercurrent infection, or suicide. 
References 
Bing. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912. Bd. v. 
Dynan (N. J.). Am. J. of Insanity, Jan., 1914, 589-636. 
Ewald. Ztschr. f. klin. Med., Bd. vii, Sup. Hft. 1884. 
Hoffmann. Virchow’s Arch. Bd. Hi. 
Huber. Virchow’s Arch. Bd. cviii. 
Huntington. Med. & Surg. Rep., Philadelphia, April 13, 1872. 
Lyon (Irving IT.). Am. Med. Times, Dec. 19, 1863. 
Oppenheim & Hoppe. Arch. f. Psychiatric, Bd. xxv. 
Osier (Sir William). On chorea. Philadelphia, 1894. 
Sachs (B.). Mohr & Staehelin [l. c ], 725. 
Waters (C. O.). Letter in Dunglison’s Practice of medicine, 312-184-2. 
Westphal. Mohr & Staehelin [l. c.], 725. 1046 
DISEASES OE THE NERVOUS SYSTEM 
Dubini’s Disease 
(.Electrical Chorea) 
Dubini in 1845 described a disease which he found in the malarial dis- 
tricts of Italy which does not resemble true chorea; it has some earmarks 
of myoclonus and hysteria as well. It is without known pathology. In- 
fection of some kind—malaria, tuberculosis, meningitis—may precede or 
accompany the disease. The disease derives its name “electrical chorea” 
from the fact that the extremities suddenly show contractions (spasms) as 
if responding to an electrical stimulus, though the electrical reactions are 
normal. There is no loss of consciousness during the spasm which often 
recurs with considerable regularity, and may simulate epileptic convul- 
sions (without loss of consciousness). There are as a rule so sensory 
disturbances, though the skin in occasional cases may remain hypersensi- 
tive during a short time. There is in almost all cases progression during 
from three to five months; the convulsions recur at shorter periods as the 
disease advances until finally the status epilepticus persists. Death fol- 
lows in coma. In a few cases there have been remissions, but these are 
usually followed by exacerbations and continuous symptoms. 
(Tetanie, Tetanilla, Intermittent Tetanus) 
6. Tetany 
See Disease of the Parathyroid Gland, Section X, V, I 
7. Epilepsy 
(.Falling Sickness, Morbus divinus, Morbus sacer) 
General Considerations.—Epilepsy is a paroxysmal disease character- 
ized by the irregular recurrence of general convulsions, which usually in- 
volve the entire body, associated with loss of consciousness in its typical 
and most frequent form (grand mat). There are cases in, which there is 
only an evanescent—fleeting—loss of consciousness without general con- 
vulsions, or the convulsive movements are so slight as to remain unnoticed. 
These are the “smaller attacks” (petit mat). Both of these types are 
known as “true” or “genuine” epilepsy, also “essential” or “idiopathic” 
epilepsy, and are of primary origin so far as we know at the present time; 
they are without known pathologic fundament. 
The “epileptic equivalents” consist of “apparently volitional or coor- 
dinated motor or mental actions during a state of modified consciousness” 
(Herter-Clark) (“psychical epilepsy,” “psychical epileptic equivalent”). 
These lapses with motor, sensory, visceral and psychic manifestations, may 
and usually do substitute minor attacks (grand and petit mal). In con- GENERAL DISEASES OF TIIE NERVOUS SYSTEM 
1047 
sidering the prognosis and diagnosis of epilepsy it should be remembered 
that one form of “essential epilepsy” may merge into another, or different 
forms may be combined in the same subject; or in occasional cases after a 
period of grand mal, years of petit mal may follow without more than an 
occasional grand mal or none at all, or after varying periods of alternation 
of the grand and petit mal, psychical epilepsy may follow. There are no 
possible data by which the clinician can forecast, with any degree of cer- 
tainty, the vagaries of the disease. It may be assumed with considerable 
positiveness that minor attacks are interspersed, which are so fleeting as to 
escape recognition in many chronic cases, and that the recurrence of noc- 
turnal and modified attacks of grand mal, in which the tongue is not 
bitten, frequently remain unnoticed. 
In the acceptance of “the anitopathological study in the epileptics,” 
according to Pierce-Clark, “we now recognize more and more that true 
epilepsy is a real cortical disorder of which the fits are but one of the 
psychic incidents, and that the seizures should no longer usurp the whole 
field of attention with their special and specific therapy of sedation.” 
Focal or jacksonian epilepsy is secondary and dependent upon focal 
and organic lesions; the convulsive movements are limited, and localiza- 
tion of the lesion in the motor (cortical) area is, as a rule, possible. 
Epilepsy, therefore, may be considered to be of (a) primary or (b) 
secondary origin. 
The epileptic convulsion may be an expression of a disease per se of 
which the explosive seizures are the leading symptoms, or the seizures in 
the “epileptic” individual may prove to be symptomatic of one of many 
conditions. When epileptic seizures recur on slight cause in the subject 
of chronic epilepsy, it must be assumed for our purposes that the cortical 
cells are ready for an explosion and that the underlying and important 
factor remains the instability of the cortex or the subcortical tissue, and 
this we are unable to eliminate, though we may in some cases partially 
control the exciting factors. 
The Primary Epilepsies are: 
(I) Major Epilepsy (Grand Mal) 
(II) Minor Epilepsy (Petit Mal) 
(III) Psychic Epilepsy or Epileptic Equivalents. 
Secondary or focal epilepsy, jacksonian epilepsy. 
(a) The Primary Epilepsies 
The epileptiform seizures which are toxic, of traumatic or reflex origin, 
due to cerebral lesions (outside cortical area), heart lesions (Adams- 
Stokes), or uremic lesions, are not included among the true epilepsies, 
neither does so-called “hystero-epilepsy” deserve consideration in this con- 1048 
DISEASES OF THE NERVOUS SYSTEM 
nection. I naturally exclude from consideration epileptiform conditions 
associated with the meningitides, encephalitis, fractures, tuberculous 
sclerosis of Vogt, hydrocephalus, brain tumor, and disseminated or local- 
ized cerebral or cerebrospinal syphilis. 
Convulsions in children due to reflex disturbances, teething ( ?), worms 
( ?), and other questionable causes, are not epileptic and are considered 
separately. 
In establishing the pathogenesis of epilepsy the consensus of opinion 
favors the cortex as the starting point of all essential epilepsies. For 
prognostic purposes the result of experimentation may at the present time 
be accepted which proves that cortical irritation may cause all of the phe- 
nomena of the genuine epileptic seizure. Cortical irritation being, in the 
large proportion of cases aggravated or produced by toxic agents, the prog- 
nosis of the individual case of chronic epilepsy, must be favorably 
influenced by the control of such factors as act directly or indirectly as 
cortical irritants (alcohol, syphilis, lead, mercury, morphin, chloroform, 
ether, circulatory anomalies resulting from excess, overwork, and a vari- 
ety of other controllable factors). 
Factors Which Influence Frognosx 
Age.—No age is exempt from epilepsy, though most cases are found 
during early life. Oppenheim’s material proves three-fourths of his cases 
to be below the age of 20. Osier reports 460 cases of epilepsy in children, 
of which he recorded the ages of the initial paroxysm in 437: 
First Year 74 
Second Year 62 
Third Year 51 
Fourth Year 24 
Fifth Year 17 
Sixth Year 18 
Seventh Year ; 19 
Eighth Year 23 
Ninth Year 17 
Tenth Year 27 
Eleventh Year 17 
Twelfth Year 18 
Thirteenth Year 15 
Fourteenth Year 21 
Fifteenth Year 34 
The prognosis is most unfavorable for control in those cases which 
begin before the age of ten years. “Infancy and puberty are the most 
dangerous periods for the appearance of the disease” (Munson). Turner GENERAL DISEASES OF THE NERVOUS SYSTEM 
1049 
holds that cases which begin at puberty offer a more favorable prognosis 
than do those younger. From 20 to 35 years of age the prognosis is bad. 
The average age at death at Sonyea (Craig Colony) was 30.08 years. The 
largest number of deaths at any one age was at 19; 50 per cent of the 
deaths were between 15 and 25 inclusive. 
With the increase of arteriosclerosis, “senile epilepsy” is more fre- 
quently met than formerly. Epilepsy which shows its first symptoms after 
the fortieth year with evidences of vascular or cardiovascular changes 
offers an unfavorable outlook. Most of my senile epilepsies in which the 
symptoms were characteristic died in coma after shortening of the inter- 
vals between the attacks, often preceding evidences of dementia and the 
gradual development of the status epilepticus. Some of these patients 
have died of apoplexy, angina pectoris, myocardial insufficiency 
denly)—rarely rupture of the heart (only one). 
TIekedity.—Heredity, in spite of the contentions of many able au- 
thorities remains an important factor in epilepsy. Statistics upon this 
point are contradictory, but the weight of authority is in favor of the over- 
powering influence of heredity in the causation, eithen directly or in- 
directly of the symptom complex. The experience of Gowers proves direct 
heredity in 35 per cent of his cases. Osier’s statistics include 435 cases; 5 
only in which the epileptics were children of epileptic parents, and in these 
the disease was traceable to the mother in every instance. He says “in 
my list there were only 31 cases in which there was a history of marked 
neurotic taint, and only 3 in which the mother has been epileptic.” 
My experience establishes hereditary factors as exceedingly important 
in epilepsy, and the prognosis has been unfavorably influenced in the 
children of epileptics, the insane, neurotics, alcoholics or those otherwise 
handicapped by vicious habits or blood taint. 
It is not unusual to find several children in the same family afflicted; 
in these, the control of the paroxysms is often difficult or impossible. The 
most unfavorable cases in my experience have been found in the offspring 
of neurotics, epileptics, or those with other chronic disease of the nervous 
system with the history of alcoholism. 
Clark in a recent article presents views which deserve space in this 
work. He holds that if we conclude that epilepsy “would seem to be de- 
pendent upon certain unknown complex hereditary factors producing a 
form of cortical or subcortical instability upon which a variety of endo- 
genous toxins may act, causing the disease,” we may hope that a therapy 
may ultimately be established as the result of further experimentation and 
the thorough study of metabolic processes in cases of this disease, which 
will lead to better results than we have obtained in the past. Clark empha- 
sizes the fact that “hereditariness is no bar to recovery from epilepsy. 
Indeed it would seem to be for a good prognosis rather than against it, as 
shown by numerous studies, and especially my own data, where two-thirds 1050 
DISEASES OF THE HERVOUS SYSTEM 
of the recoveries were recruited from the hereditary cases.” Clark further 
quotes Southard’s contention. He adds “Hot a little light is thrown on 
the reason why the hereditary epilepsy recovers, if one accepts Southard’s 
contention that the hereditary factor is permissive and not mandatory for 
the occurrence and continuance of epilepsy in the descendants of neurotic 
family stock.” 
It is possible that in the individual “hereditary” case which can he 
thoroughly and continuously safeguarded, much can he done to overcome 
exciting factors by the study of the metabolic processes and habits of the 
patient and their scientific regulation; hence the warning given by the 
hereditary tendency may influence prognosis favorably. The history of 
heredity in uncomplicated cases of epilepsy “does not necessarily mili- 
tate against the prospects of arrest or improvement in any given case.” 
Sex.—Sex exerts no influence on epilepsy or its prognosis. At the 
Craig Colony “the proportion of males and females dying is practically 
the proportion admitted, though the males are very slightly in excess” 
(Munson). Spratling in G8,040 cases in this country and Europe found 
36,865 males and 31,175 females. 
Alcoholism.—Alcoholics not infrequently develop epilepsy, and the 
prognosis is unfavorably influenced by the chronic secondary changes due 
to the long continued poisoning. As already mentioned, alcoholism in the 
parent unfavorably influences epilepsy in the offspring. 
Syphilis.—Syphilis may cause epileptiform convulsions. The ma- 
jority of these cases are probably dependent upon positive pathologic 
change, which with radical treatment, leads to recovery. 
Syphilitics who are also of neurotic habit, who are burdened with an 
unfavorable heredity or whose habits are vicious, may without definitely 
demonstrable lesions develop epilepsy during the secondary period. The 
prognosis of such cases is not altogether bad. Under treatment and control 
from 10 to 20 per cent of such patients are relieved. It should be remem- 
bered that the majority of syphilitics who develop epileptiform symptoms 
suffer from syphilitic disease of the brain, and are not true epileptics. 
Traumatism.—When traumatism causes epilepsy there is usually a 
focal lesion which may be localized, in which event the treatment is likely 
to be surgical; the epilepsy is secondary, and the prognosis depends en- 
tirely upon the ability of the operator to remove the cause. Such cases 
are likely to be of the jacksonian type and are separately considered. 
Epilepsy (true—grand or petit mal) may follow trauma without 
demonstrable lesion in focal symptoms. In these cases the usual symptom 
complex of essential epilepsy is present. The trauma simply proved to be 
the exciting factor. The prognosis of most of these cases is the same as 
all others without known anatomic lesion. 
I have elsewhere (encephalitis, cerebral hemorrhage, etc.) consid- 
ered cases of posthemiplegic epilepsy—in all of these, in spite of the GENERAL DISEASES OF THE NERVOUS SYSTEM 
1051 
return (usually partial) of motor power, the epileptic complex continues 
but little influenced by treatment, as a rule uninfluenced entirely; but 
rarely do the convulsions cease after years of recurrence. 
Sunstroke.—Epilepsy occasionally follows sunstroke. Such cases 
are unquestionably due to organic change—meningo-encepbalitis, etc.— 
and remain practically uninfluenced by treatment in my experience (See 
Sunstroke). 
Fright—Acute Infections, etc.—Epilepsy may remain dormant 
or unrecognized during long periods—even years. In such cases an insig- 
nificant factor may prove sufficient to light the case to activity, fright, sud- 
den emotion, long continued worry, prolonged masturbation or other 
venereal excesses, and acute infections (typhoid) are included. It is not 
likely that in the normal subjects—those with average resistance—these 
alleged causes, usually without effect, produce the disease; when they do, 
it will be found that there is the “predisposition,” evidences of degeneracy 
often with an abnormal heredity. These cases offer the average prognosis 
of the disease. 
Diet.—Diet will always remain one of the most important factors in 
the prognosis of epilepsy, for the majority of cases show faulty metabolism. 
“The theory by wThich cures or arrests are brought about is rather unsatis- 
factory speculation. TTevertheless the whole successful plan of hygienic 
treatment speaks very favorably for the preconceived idea that the disor- 
der in most cases is a metabolic one, and a setting right of the personal 
habits and plan of living restores the patient to a stationary state equal, 
if not superior, to his health before epilepsy began” (L. Pierce Clark). 
Pregnancy.—The Germans and some English authorities hold that 
pregnancy exerts a favorable influence on epilepsy. This is not proved by 
the examination and thorough consideration of a large material. It is safe 
to conclude that gestation has but little influence upon the disease. Turner 
says “At the best there may he only a temporary respite, but pregnancy is 
the forerunner of the puerperium, a period which is especially prone to 
epileptic attacks.” “There are three periods when epileptic fits were 
prone to develop: at quickening, during the first few days of puerperium, 
and during lactation.” 
Ocular Anomalies.—It is questionable whether cases which yield to 
the correction of ocular anomalies (strain usually)—and some do—are 
essential epilepsies. The fact remains that these cases cannot be differ- 
entiated from genuine epilepsy. The number which yields to the correc- 
tion of ocular defects is small—in the large majority of cases of true epi- 
lepsy such treatment has, in our experience, proved futile. 
Amblyopia, etc.—In considering amblyopia and other ocular symp- 
toms it should he remembered that temporary amblyopia, involving both 
eyes, occurs in certain functional diseases of the brain, particularly in 
epilepsy and migraine. In both of these conditions the loss of sight ia 1052 
DISEASES OF THE NERVOUS SYSTEM 
always transitory and paroxysmal. In epilepsy the loss of sight usually 
precedes the convulsion. No permanent blindness need be feared. 
Babinski Phenomenon.—In the prognosis of epilepsy and epileptoid 
disease, for which accurate differentiation is imperative, the persistence of 
the Babinski phenomenon after the seizure, during several hours, is proof 
of symptomatic epilepsy—usually hysteria and not true epilepsy; the 
prognosis is usually correspondingly good. The phenomenon disappears 
shortly after the attack. 
Disordered Nutrition.—Disordered nutrition is responsible for the 
recurrence of paroxysms in many cases of grand mal—a fact which is cor- 
roborated by urinary examination. It has been found that intestinal 
putrefaction is closely related to the explosive seizures of epilepsy. Under 
these conditions there is evidence in the urine of a disturbance of the 
normal relation between the “preformed and the combined or ethereal sul- 
phates in the urine 10-1)” (Herter and Clark). The persistent presence 
of indican (indoxyl sulphate) in the urine of epileptics is striking in a 
large number of cases. There is a decided increase of these substances 
just before and during the epileptic fit to be decreased immediately after. 
The ability of the therapeutist to influence intestinal fermentation by 
treatment, with the removal of the ethereal sulphates from the urine, 
exerts a wholesome influence in decreasing the number of paroxysms in 
some cases. The release of a troublesome phimosis has occasionally re- 
lieved epileptoid conditions which could not be differentiated from epi- 
lepsy. The surgical treatment of a peripheral local irritation has in rare 
cases produced the same favorable result (cicatrices in peripheral nerves, 
etc.). Such cases naturally cast a suspicion upon the diagnosis. 
(Course of the Disease) 
Epilepsy which originates during scarlet fever (most frequent), 
typhoid, measles, smallpox, influenza, pertussis, malaria, which follows 
meningitis, prolonged labor or forceps delivery, is not easily controlled— 
rarely entirely overcome. It may be concluded that the acute infections 
often exert an inhibitory influence on the convulsions. After convalescence 
but few cases continue to show any wholesome effect from the added 
infection (Turnowski). 
The aura bears no relation to the severity of the attack in most cases. 
The absence of an aura has been noted in both mild and severe epilepsies. 
I have found a number of cases in which the absence of the aura proved 
alarming because of the sudden severe convulsion without warning 
serious bodily injury resulted. In one of my cases a molder was burned 
by the melted iron which he was pouring. In a number of cases the warn- 
ing, i. e., the aura, may protect against injury. One of my cases, a street 
car conductor, is always able to foretell the approach of an attack two GENERAL DISEASES OF THE NERVOUS SYSTEM 
1053 
hours before its outbreak by a peculiar “bandlike” sensation about the 
bead which makes it possible for him to call bis substitute and reach bis 
home where be protects himself against injury by getting into bed. 
The ability to abort the epileptic seizure by pressure of an extremity 
when the aura begins in a band or foot is possible. Such efforts are 
not always successful in the individual case. Convulsions which recur at 
short intervals, are severe, and continue beyond the average duration which 
are associated with long periods of stupor and final amnesia (forgetful- 
ness), are evidence of progressive degeneration. Such cases are likely to 
develop dementia. Loss of self control, confusion of intellect shortly after 
the convulsion, a desire “to get away” may recur for years without ma- 
terial advance toward complete mental alienation. One such case, a 
woman, now under treatment, age thirty-four, has continued since early 
childhood to have periods of delirium and passionate outbreaks in which 
she is belligerent, without the slightest evidence of mental unbalance dur- 
ing the interval between attacks; in fact she continues unusually bright 
and cautious in the handling of her affairs. 
The development of active mania with homicidal tendencies may fol- 
low the attack and continue in some during periods varying from a few 
hours to several days. Such symptoms recur and are often uninfluenced 
by treatment. Cautious surveillance alone prevents the destruction of life 
under such conditions. Epileptic delirium may recur at short intervals, 
and offers an unfavorable prognosis for control. Cases in which convul- 
sions of the grand or petit mal type recur at short intervals are likely to 
continue lethargic mentally; they remain uninterested in current events 
and often become confused during long periods. Such cases may show long 
periods of improvement under treatment and rest, but the chances are 
that eventually, unless there is some acute complication which terminates 
life, the mental deterioration will progress to the full development of 
epileptic insanity. Cases in which delirium or mental disturbance follow 
the epileptic fit usually clear in the course of a few hours; the same is 
true of motor weakness and sensory disturbances, as a rule. Paretic con- 
ditions of one or more extremities in individual cases (non-jacksoni'an) 
yield to rest and time—often in a few hours or days. 
I. Grand Mal 
Dislocation of the humerus is an occasional complication of grand mal. 
One of my cases lived to be sixty-five years of age; during fifty years of 
his life he had epilepsy, and for twenty years had grand and petit mal. 
In all attacks of grand mal he dislocated one or both humeri always requir- 
ing ether anesthesia for reduction; the quantity of ether used was enor- 
mous. Mental lethargy finally followed, and he died in the status epilep- 
ticus. 1054 
DISEASES OF TIIE NEKVOUS SYSTEM 
The postepileptic period is not as a rule associated with danger to life. 
I have never seen a death following closely upon epileptic seizure in which 
there was not some added complication. The majority of epileptics are 
more or less affected by the seizure. They appear lethargic, somnolent, 
without their normal energy. This condition does not in average cases 
continue beyond three or four hours. In some cases the patient falls into 
a deep sleep from which he is aroused with difficulty, and immediately falls 
asleep again. The majority of patients are fatigued after their experience 
in spite of the period of sleep. 
A small proportion of cases seems unaffected mentally and physically 
by the attack. Once over, they are again bright and ready to go on with 
their work; the majority of these belong to the “petit mal” class. The 
thread of conversation or line of work may not be interrupted; without 
the break of a sentence I have seen these patients resume as if nothing 
had happened. 
Nocturnal epilepsy, as already suggested, may persist during many 
years, often so mild as to escape detection. This variety of epilepsy may 
not materially influence the general condition of the patient or interfere 
with his activities, until as usually happens, there are diurnal attacks and 
the patient often falls into a somnolent condition during unusually long 
periods following the convulsion. At times without added symptoms I 
have seen these patients in semi-coma for days; pulse but slightly accel- 
erated, and entirely without fever. Such cases are not easily influenced by 
treatment, and the majority of chronic nocturnal epileptics have finally 
died in the “status epilepticus” or from pulmonary tuberculosis. 
The “status epilepticus” is a condition in which epileptic seizures follow 
in such rapid succession as to continue unconsciousness almost without 
interruption. This condition continued beyond thirty-six to forty-eight 
hours is of serious import. Such patients gradually fall into a deep and 
uninterrupted coma in which they usually die. With the persistence of 
high temperature the prognosis is bad and the duration short. There are 
no criteria which make it possible to foretell the length of the interval be- 
tween attacks. In the same subject, convulsions may follow each other in 
rapid succession; may sometimes recur many times during a single day; 
and may not recur for months or even years thereafter. It is not uncom- 
mon to find epileptics free from all symptoms without the slightest sugges- 
tion of the disease during such long periods as to lead both the patient and 
physician to the conclusion that the disease is under control, when without 
warning or known cause there is a fresh outbreak. If there is any reg- 
ularity in the time of the recurrence of convulsions, as during menstrua- 
tion in women, rest and treatment may postpone the explosion. 
Grand mal in chronic cases may be expected to recur in the average 
uncontrolled case once or twice each month. GENERAL DISEASES OF THE NERVOUS SYSTEM 
1055 
All authorities are agreed that the prognosis of the smaller attacks— 
petit mal—is less favorable for control than is that of grand mal. There 
is great danger of bodily injury in those cases in which sudden vertigo 
throws the victim without warning. The minor attacks are not so easily 
influenced by drugs as are the larger. The ability to arrest or influence 
the frequency of the attacks was studied by Turner, who found that 49 
per cent of grand mal, 35 per cent of combined grand mal and petit mal, 
and only 26 per cent of petit mal were influenced by treatment. 
(II) Petit Mal 
(Ill) Epileptic Equivalents 
Psychic epilepsy is exceedingly rare. Of-1,325 cases of epilepsy col- 
lected by Spratling at Sonyea, only 4 were of this type. The prognosis is 
best in those cases without early or evident intellectual weakness or with- 
out “striking intellectual aura.” 
My experience has been that the psychic equivalent in essential epi- 
lepsy appears only at long intervals in most cases. One of my cases be- 
came an epileptic automaton during which he traveled far from home after 
suddenly disappearing, and was found wandering uninjured in a large 
city where he had taken a room in a leading hotel without exciting the 
slightest suspicion. This man lived many years after this occurrence; he 
had repeated grand and petit mal and finally died of intercurrent disease. 
All cases of suspected psychic equivalents demand close study that a 
forecast may be given of the existing mental status, and it should be re- 
membered that such patients may, if unguarded, execute major crimes of 
which they have no knowledge and for which they are not responsible. 
(b) Secondary or Focal Epilepsy—Jacksonian Epilepsy 
(Hughlings Jackson, 1869) 
General Considerations.—Jacksonian epilepsy belongs within the do- 
main of the surgeon. It is due to a positive and localizable lesion and if 
within the reach of the knife, unless of long standing, offers at least the 
possibility of cure. Jacksonian epilepsy may, in advanced cases, alternate 
or be complicated with either grand or petit mal, usually the former. 
Long continued grand mal with primary jacksonian convulsions offers an 
unfavorable prognosis for any treatment—medical or surgical. 
Frequent and full references to the epileptic syndrome and to jack- 
sonian epilepsy are made in the chapters on brain tumor and other organic 
diseases of the nervous system, to which the reader is referred (See 
Index). 
Epilepsy, when a complication of meningitis or meningo-encephalitis 1056 
DISEASES OF THE HEBYOUS SYSTEM 
or dependent on these causes, offers an unfavorable prognosis for relief of 
the convulsions. The convulsions are frequent in the paralyzed limbs, be- 
sides being general. 
With added organic disease of the nervous system I have seen epi- 
lepsy disappear entirely, change its form from the grand to the petit mal 
type, or continue uninfluenced. I have recently in dispensary practice 
seen two cases of tabes dorsalis in which with the advance of the latter 
disease, ejnlepsy which had existed since early childhood of the grand mal 
form, was found to have been relieved and only an occasional “wave” of 
petit mal was noticeable. 
The examination of the cerebrospinal fluid withdrawn by lumbar 
puncture offers no prognostic data. 
The Blood.—Fackenheim at the recent Congress fur Innere Medi- 
zin (1914) concluded that before the attack there was a marked reduction 
of hemoglobin, the destruction of both red and white corpuscles, and these 
conditions with increased coagulability of the blood he believes are of 
diagnostic and prognostic value. His observations have not yet been con- 
firmed. The large mononuclear lymphocytes are increased before the 
attack. There is poikilocytosis and microcytosis during the attack. 
Course of the Disease.—A small proportion of epileptics die from in- 
jury during the attack, a few are drowned, and an occasional victim com- 
mits suicide. It is surprising that there are so few serious accidents when 
the large number of epileptic fits from which many suffer are considered. 
The tongue biting does not as a rule inconvenience the epileptic long, as 
the organ heals promptly. 
Epilepsy itself—directly—rarely causes death, but those who have had 
the largest experience with the disease recognize its menace, and are agreed 
with Munson of the Craig Colony when he says “Our experience at the 
Colony is that the disease carries with it. very grave dangers; the span of 
life is shortened and there is a special liability to certain diseases and to 
traumas.” 
Complications.—Pulmonary tuberculosis is the most frequent cause of 
death. Munson in his conclusions holds that “the causes of deaths in epi- 
leptics are quite largely associated with the disease itself and may be 
divided into two main groups: pulmonary conditions, and conditions of a 
purely epileptic character.” 
Pulmonary edema may develop during the attack; Shanahan has re- 
ported such cases. The prognosis of these is exceedingly grave. 
Pneumonia following the attack in which the patient was neglected 
has been a cause of death in a number of my hospital cases. In Munson’s 
material there were 142 cases of pneumonia; these cases were not 
neglected during the attacks, but were under surveillance. 
No epileptic during the attack is free from danger, for death may sud- 
denly follow from causes already mentioned (particularly trauma, GENERAL DISEASES OF TIIE EERVOUS SYSTEM 
1057 
asphyxia, edema) and a number of deaths will occur without apparent 
cause. These facts justify a better prognosis in those cases which are 
cautiously guarded and nursed. 
General Conclusions.—The general condition of the epileptic varies 
with different types of the disease, and is influenced by a variety of causes. 
A\ bile many epileptics appear to be in good general condition, the disease 
is likely to undermine resistance. There is gradual loss of strength until 
the average epileptic is below par almost continually, and life is materially 
shortened indirectly by the disease. 
If a patient has remained without attacks 9 years (Turner) it may be 
concluded that he is cured. Sinkler observed only 4 cases of relapse out of 
a total of 24 after 9 years’ remission. In one case there was a remission 
of 27 years with final recurrence. Spratling believes that the time limit 
of Turner is too long, that “a person may be cured of epilepsy and then 
have it again.” I would recommend the longer period for prognostic 
conclusions, and would argue against the assumption that an epileptic 
who showed recurrence had been completely cured. 
Spratling after an experience of 14 years in the daily care and treat- 
ment of 1,800 cases of epilepsy in persons of all ages, reported 34 cures, 
and concluded “that epilepsy is curable in from 5 to 10 per cent of all 
cases.” Spratling holds that “the failure to secure better results generally 
in the treatment of this disease must frequently be laid to the failure to 
treat the individual and his disease as a unit and to treat them both along 
the very broad, comprehensive, and unyielding lines they both require.” 
The prognosis before the introduction of the bromid, now unquestion- 
ably used at some time in the treatment of almost all cases, does not differ 
materially from that of today. Turner mentions in the pre-bromid days 
Hufeland’s cures of 5 per cent; Russell Reynold’s 10 per cent; Trousseau 
20 cures in 150 cases, or 13 per cent; Herpin 19 cures in 38 cases, 50 
per cent (questionable). Post-bromid days: Hothnagel 5 per cent of 
cures; Laehr gives 6 per cent; Ackerman 7.6 per cent; Dana 5 to 10 per 
cent; Wildermuth 8.5 per cent; Habermas 10.3 per cent and Alt gives 
12.5 per cent. Volland reports 4,215 cases observed, of which 245 were 
discharged cured. R. Stern reports an unusually large percentage of 
cures. 
Cases which are influenced favorably by the bromids should show no 
mental torpor, marked improvement from doses which remain without dis- 
agreeable constitutional effects, and should not fall into the status epilep- 
ticus when the remedy is withdrawn. 
Boekelman has reported cases in which the withdrawal of the bromids 
has precipitated the epileptic state. I quote from Clark: “To my mind, 
the introduction of special medicaments of sedation in the epilepsies has 
been fraught with more harm than good. The sedatives have clouded the 
issues of causation and prognosis to a remarkable extent. They have dis- 1058 
DISEASES OF THE NERVOUS SYSTEM 
located and cloaked the errors of metabolism in the epilepsy problem with- 
out giving commensurate aid. I decidedly take issue with Fere’s and 
Turner’s views that the introduction of the bromids has aided the prog- 
nosis, especially as regards permanent cures. The bromids mask the 
progress of the disease and make a full understanding of the forces at 
work in the individual case almost unbelievably complex. I have seen 
many patients treated by sedatives steadily advance in physical, mental 
and moral deterioration in the face of a steady cessation of fits—suppres- 
sion of fits is squared by an outburst of status epilepticus or a furious 
maniacal outbreak.” 
Cases which are favorably influenced by treatment, as a rule, show 
marked decrease in the number of convulsions during the first year of 
continuous treatment (50 per cent). 
The least favorable cases are those of acquired or congenital mental 
anomalies with any of the forms of epilepsy. 
Surgery has been unable to materially influence the prognosis of es- 
sential or idiopathic epilepsy. Cases which are amenable to surgical 
treatment must be of focal origin, usually jacksonian. Epilepsy depend- 
ent on a discoverable lesion offers a better prognosis than does the true 
epilepsy, and should not be considered in the same class. 
The clear statement of Hippocrates in his Prognostics shows that scant 
progress has been made in the treatment or cure of the disease since his 
day—twenty-five hundred years ago. He wrote: “If the Sacred Disease 
attacks little children the greater number die. If youths and young 
adults, recovery may take place but there is danger of its becoming habit- 
ual and even increasing, if not treated by suitable remedies. Such also is 
the case when it attacks children. When it attacks people of advanced 
years it often proves fatal. When a person has passed the twentieth year 
of his life the disease is not apt to seize him, unless it has become habitual 
from childhood. When the disease has prevailed for a length of time it is 
no longer curable.” 
Alzheimer. ZurFrage des Spdtepilepsie. Breslauer psych. Neurol. Verein, v, 17, ii, 1913. 
Binswanger. Epilepsy. In: NothnageVsSpec. path. Therap., xii. 
Binswanger (Otto). Die Epilepsie. 2d ed. Wien, 1913. 
Bokelmann. Therap. Monatsh., 1906. 
Clark (L. Pierce). Am. J. Insanity, Ixx, No. 2, 885-410. 
Arch. Int. Med., ix, 1-21. 
Boston Med. & Surg. J., July 18, 1912, clxvii, 78. 
Clark & Sharp. J. Nerv. & Ment. Dis., xl, No. 10. 
Curschmann. Mohr & Staehelin’s Handb. d. inner. Krankh. Berlin, 1912, Bd. v. 
Dana. Textbook. New York, 1898. 
Fackenheim. Congress f. inner. Med., Wiesbaden, 1914. 
Gowers (Sir William). Epilepsy. 2d ed. 1901. 
References GENERAL DISEASES OF THE NERVOUS SYSTEM 
1059 
Hahn. Syphil. Epilepsie. 
Ztschr. f. d. ges. Neurol, u. Psych., Orig., Bd. xvii, H. S. 519-612. 
Herter & Clark. New York, 1907. 
Hippocrates. Sydenham Soc. (translation), ii, 850, etc. 
Numson. New York Med. Rec., Jan. 8, 1910. 
Oddo & Corsy. La myoclonie epiliptique. Rev. de psych., xvii, x, 307-J+01. 
Oppenheim. Lehrb. d. Nervenkrankh. Berlin, 1913. 
Osier (Sir William). Practice of medicine. New York, 1914. 
Shanahan. New York Med. Rec., Jan. 11, 1908. 
Spratling {W. P.). New York Med. J., April 9, 1904. 
Stern (R.). Jahrb.f. Psychiat., Bd. xxx. 
Turner (W. 4.). Lancet, London, June 13, 1903. 
Turnowski. Wien. med. Wchnschr., 1901. 
Vogt. Tuberose Himsclerose. Bibliographic d. gesam. inner. Med., etc. Berlin, 1913, 
Ztschr. f. Psych., Bd. Ixiv. 
Epilepsie Kindesalter. Berlin, 1910. 
Volland. Ztschr. f. Psychiat., Bd. Iviii. 
8. Migraine 
(Hemicrania, Sick Headache, Blind Headache, Bilious Headache) 
Migraine is a painful, paroxysmal affection, characterized by headache 
—usually confined to one side of the head—associated with all kinds of 
nervous and dyspeptic symptoms; often aura early during the attack 
with anorexia, nausea, vomiting, ocular symptoms; at times motor weak- 
ness and sensory anomalies; often suggestive manifestations of faulty 
metabolism, vascular spasm and irritation or paralysis of the cervical 
sympathetic. 
Migraine does not lead to death; pathologic investigation has there- 
fore been impossible. There are no evidences that the complex is depend- 
ent upon organic change, but a strong and justified suspicion that the 
disease is a neurosis dependent in over 60 per cent of cases upon heredity; 
that in most cases the exciting factor of the individual paroxysm is either 
fatigue in the non-resistant, error of diet, ocular strain, sexual excess, sud- 
den psychic disturbance, or some toxic condition dependent upon gastro- 
intestinal upset or faulty metabolism. 
Influencing Factors.—Heredity.—Ulrich’s statistics relating to hered- 
ity are exceedingly interesting. He finds: positive hereditary influence in 
64 per cent, probable hereditary' influence in 25 per cent, absence of 
hereditary influence in 11 per cent. 
In his hereditary cases he traced the complex to the mother in 74 per 
cent of 147 cases (106 women and 41 men) ; to the father in 17 cases—9 
per cent (9 females and 8 males) ; to both parents in hut two of his cases 
(one male and one female). In 24 cases—12 per cent—several brothers 
and sisters had migraine, and it was not uncommon to find the disease 1060 
DISEASES OF THE NERVOUS SYSTEM 
transmitted through three generations. In some cases one or more genera- 
tions may be skipped. 
Traumatism.—When migraine follows traumatism it may be assumed 
that it is a part of a traumatic neurosis or hysteria, or if it persists, it is 
due to organic disease, therefore symptomatic. 
Infection and Other Toxic States.—Cases of migraine wdiich have fol- 
lowed infection or other toxic states are not uncommon. In some of these, 
the lowered vitality in the predisposed was the exciting factor. In some, 
the disease continues during many years uninfluenced; in a small propor- 
tion of cases with the general improvement of the patient the paroxysms re- 
curred at longer intervals, and finally ceased entirely. 
Tuberculosis.—The association of migraine and tuberculosis (Moe- 
bius, Ulrich and others) has been noticed. Prognostic data are hardly 
justified by such association. The prognosis of the infection is, however, 
scarcely influenced by the occurrence of an occasional migraine. 
Additional Influences.—Alcohol, tobacco, lead and morphin unques- 
tionably increase the paroxysms, and release from the poisons acts favor- 
ably. Metabolic faults, as aggravating causes, have long been recognized. 
Trousseau said: “Migraine and gout are sisters.” The general improve- 
ment of a gouty or diabetic subject often banishes migraine during indefi- 
nite periods. Patients with goiter—Basedoio’s disease—have in my expe- 
rience been relieved by treatment or operation. It not infrequently hap- 
pens that chronic constipation, gastro-intestinal dyspepsia and tape worm 
have proved causative factors. In such cases the relief of the underlying 
condition cures the migraine. The correction of menstrual anomalies and 
the relief of diseases of the genito-urinary organs improve prognosis, and 
infrequently lead to cure. 
Prognosis during Climacteric Period.—The climacteric period is fa- 
vorable for the disappearance of the complex; indeed, if the paroxysms 
are not entirely dissipated, it may be safely concluded that they recur at 
longer intervals, and when persistent are less severe. Migraine when it 
appears during the climacteric period is not likely to persist long there- 
after. 
Classification.—Gordon considers the following forms of migraine: 
(a) Ophthalmic migraine 
(b) Hemicrania sympatheticotonica (white migraine) 
(c) Hemicrania sympatheticoparalytica (red migraine) 
(d) Migraine associated with the epileptic equivalent 
(e) Abortive migraine. 
(a) Ophthalmic Migraine 
In more than 60 per cent of all cases there are during, or just preced- 
ing the paroxysm, disturbances of vision of a sensory character, which are GENERAL DISEASES OE THE NEEVOUS SYSTEM 
1061 
as a rule unilateral. They include amblyopia, in some cases hemianopsia, 
in other cases a bright and moving spot limited to one side of the visual 
field, scintillating (scotoma) or other annoying features (zig-zagging lines, 
continually moving concentric circles, repeated flashes of light, etc.). 
With the blurring of sight the vision is partially defective, and there may 
he—often is—vertigo, nausea and other motor, sensory and psychic phe- 
nomena. Complete loss of vision is not present as a rule, but there is a 
distinctly paroxysmal amblyopia ivhich is partial, unilateral and transi- 
tory. 
With the ophthalmic, as with all forms of migraine in which there 
are ocular symptoms, unless the latter are dependent on organic disease 
they are transitory, leave no permanent effect, and are likely to recur with 
subsequent attacks of migraine. 
In some cases motor weakness or even paretic conditions are prominent 
during limited periods (few minutes or hours) ; they disappear without 
leaving a remnant. Such symptoms may not he present during all parox- 
ysms, hut they are prone to recur. Oppenheim has mentioned the transi- 
tory occurrence of cerebellar ataxia during seizures of ophthalmic mi- 
graine. These are without prognostic significance. Aphasia may be a 
prominent symptom (amnesic)- in individual cases following or associated 
with the paroxysm, yielding promptly as the other phenomena disappear; 
hut it is likely to recur with most subsequent attacks. Marked depression, 
apathy, and visual hallucinations have in some cases remained annoying, 
at times preceding the attack, in other cases accompanying or following it. 
Gordon has reported cases with marked psychic disturbances (confu- 
sion, stupor and delirium). T have found a number of such migraines. 
Tn all, the symptoms have been transitory and in spite of occasional per- 
sistence during several days in severe cases, their disappearance may be 
positively promised. 
The long continued paralysis of the motor oculi (at times as long as 
two or three weeks) finally disappears, and may or may not return with 
subsequent paroxysms. It will require thorough study of borderline cases 
that no mistake in diagnosis and prognosis is made in giving to acute oph- 
thalmoplegia its significance. It should be remembered that with migraine 
the paralysis is coincident with the paroxysm, which is always character- 
istic, with relief from pain as the ophthalmoplegia appears. The ophthal- 
moplegia of syphilis does not show sudden paralysis; if there is headache, 
it is present before and continues with the ocular manifestations. These 
points are of great value for diagnosis and prognosis. 
Therje are a number of ophthalmic migraines which precede progres- 
sive paralysis of the insane. Ilerter and Clark call attention to their 
history, in all of which cautious investigation clears the horizon. It 
should be remembered however, that there are cases of pure and uncompli- 
cated migraine in ivhich during limited periods visual anomalies, slow 1062 
DISEASES OF THE NERVOUS SYSTEM 
and hesitating speech, and lapses of memory, may he present. Such symp- 
toms are transitory, and during the intervals there is absolutely no evi- 
dence of organic disturbance or subjective manifestations of mental defect. 
There is never with migraine, progression of any symptoms which resem- 
ble those of progressive paresis. 
(b) Hemicrania sympatheticotonica (White Migraine) 
and 
(c) Hemicrania sympatheticoparalytica (Red Migraine) 
Hemicrania sympatheticotonica and hemicrania sympatheticopara- 
lytica are probably due to irritation and paralysis of the cervical sympa- 
thetic, respectively (See Diseases of the Sympathetic System). 
(d) Migraine Associated with the Epileptic Equivalent 
The association of migraine with epilepsy in the same individual is by 
no means uncommon. Charcot and Fere in France insisted upon the in- 
timate relation of migraine to epilepsy, while Oppenheim and Strohmever 
were equally enthusiastic in Germany in controverting the dictum of the 
French School. 
The more unfavorable cases are those which bear a close resemblance 
to epilepsy in the presence of aurae with motor, sensory, and psychic symp- 
toms, and attacks which closely resemble petit mal (fleeting). Flrich’s 
material shows that 99 of 500 cases (20 per cent) were either directly or 
indirectly related to epileptic conditions. His conclusions must influence 
prognosis powerfully: 
(I) “Migraine may he symptomatic of epilepsy—it may he an epilep- 
tic equivalent.” 
(II) “Both may he present in the same subject independent of each 
other.” 
(III) “Eclamptic conditions with characteristic migraine may be 
caused by acute infections (reflex eclampsia). In these there is not likely 
to be recurrence.” 
(IV) “Persistent migraine may finally merge into true epilepsy 
(Moebius) just as Gowers has demonstrated that repeated syncope may 
finally prove an inviting factor of epilepsy.” 
(V) “Migraine may in the presence of epilepsy disappear, just as both 
conditions have vanished with the development of grave organic diseases 
of the nervous system (tabes, dementia, etc.)” (See Epilepsy). 
(e) Abortive Migraine 
Abortive attacks may be interspersed between any of the other vari- 
eties, or there may never be severe headache; simply ocular disturbances GENERAL DISEASES OF THE NERVOUS SYSTEM 
1063 
of short duration which do not as a rule interfere materially with the 
activities of the patient. Some cases may persist during years with slight 
“blurs” or “balls of fire” or “zig-zagging of lines” with but little or no 
headache; many of these are relieved permanently by proper attention to 
ocular or metabolic faults. It happens in some cases that abortive alter- 
nate with fully developed paroxysms. 
Conclusions 
Symptomatic migraine may depend upon syphilitic infection, malaria, 
uremia with nephritis, progressive paralysis, brain lesions (tumor) and 
arteriosclerosis with vascular spasm, with or without hypertension. In all 
of these, the prognosis depends upon the gravity of the causative factor. 
The safest prognosis of migraine is based on the assumption that while 
heredity is an important factor and supplies the basis for the development, 
of the symptom complex, there is as a rule an exciting cause which with 
careful search can be unearthed, and while the majority of cases cannot 
be cured, they may be materially relieved and may continue to live in 
comparative comfort to old age. With increasing years there is tendency 
to recurrence at longer intervals, until in many cases there is final com- 
plete relief. The possibility of distant causes should not he overlooked. 
While the eye will claim attention in all cases, there are rare cases (Mar- 
gulies) in which labyrinthine disease proves provocative, and its relief has 
a wholesome effect on the accompanying migraine. 
The contention of Spitzner that “migraine is due to a constitutional 
anatomical defect, namely, an absolute or relative stenosis of the foramen 
of Munro” (Jelliffe), remains without confirmation. 
The clinician will do well to consider many causes responsible for what 
seems predominant in migraine, i. e., vasomotor disturbances, and will 
prognosticate accordingly. 
References 
Charcot. Poliklin. Vortrdge, Bd. i. 
Legon de Mardi. Paris. 
Church & Peterson. Nervous and mental diseases. Philadelphia, 1914. 
Fere. Epilepsie. Paris, 1896. 
Rev. de Med., 1897, No. 12. 
Gordon. Diseases of the nervous system. Philadelphia, 1913. 
J. Am. Med. Ass., Jan. 5, 1907. 
Gowers. Diseases of the nervous system. London, 1892. 
Herter & Clark. Diagnosis of organic nervous diseases. New York, 1907. 
Jelliffe (Smith Ely). In: Osier’s Modern medicine. Philadelphia, 1910, vii. 
Margulies. Migraine otique. Prager Med. Wchnschr., 1913, No. 27. 
Mobius. Die Migraine. 
Nothnagel’s Handb. der spec. Path. u. Therap., xii. 1064 
DISEASES OF THE NERVOUS SYSTEM 
Oppenheim. Lehrb. d. Nervenkr. Berlin, 1913, ii. 
J. f. Psychiat. u. Neurol., 1906, Bd. vi. 
Spitzner. Ueber Migraine. 1907. 
Ulrich. Monatschr. f. Psych, u. Neurol., Bd. xxxi. 
Ergnzngshft., 1912, 13//.-203. 
9. Occupation Paralyses and Neuroses 
The long continued or improper and overworked muscles and nerves of 
certain combinations used for the performance of special movements may 
lead to fatigue or paralysis. 
Writers’ Cramp and Other Occupational Paralyses 
The most frequent occupation neuroses is found in writers (writers 
cramp). 
Among the other professional paralyses are those of the violinists, 
piano players, telegraph operators, typewriters, milkers, machinists, drum- 
mers, seamstresses, crocheters, cigar makers, hammer and file makers, 
miners and other occupations including oarsmen and diamond polishers. 
The milder cases, which promptly yield with the discontinuing of the 
occupation present with some pain, paresthesias and anesthesias. There 
is no marked paralysis, but evidences of a mild neuritis in tenderness along 
the nerve involved. The muscles are also tender, and in the more advanced 
cases are more or less atrophied. 
Myositis and neuritis are probably the pathologic basis of most profes- 
sional paralysis. 
When once established, if the special ivork which caused the motor 
weakness is continued, in spite of improvement during periods of rest, the 
symptoms recur and become chronic. There are but few exceptions to this 
rule. 
In rare cases mechanical appliances bring relief—but this is only 
partial. 
The symptoms of writers' cramp (Scriveners’ palsy) are either spas- 
modic or paralytic. Most cases are spasmodic. By the spasm of the ex- 
tensor muscles the fingers separate and extend, and the pen is dropped. 
The spasm of the flexor muscles makes writing impossible; the pen sticks 
into the paper, and the pain with spasm may affect the entire arm. For 
a time writers manage by posture and other devices to overcome the spasm, 
but in the end, if much writing is done, the spasm recurs with increased 
symptoms and pain. 
With the paralytic form of writers' cramp and other occupations, the 
muscles weaken suddenly while in use, they are relaxed, and the special 
work becomes impossible. 
In most cases the disease does not lead to noticeable atrophy of the GENERAL DISEASES OF THE NERVOUS SYSTEM 
1065 
muscles nor to electrical changes. In severe cases there may be increased 
excitability to both faradism and galvanism. 
Writers’ cramp usually develops in both arms, when one is used after 
the other has become troublesome. 
References 
Bittorf. Munch, med. Wchnschr., 1905. 
Oppenheim. Lehrb. d. Nervenkrank., 1913. 
10. Infantile Convulsions 
(.Eclampsia inf an turn) 
Predisposition.—There are children who upon insignificant cause de- 
velop fever, and are at once thrown into active convulsions from which 
they promptly recover—as a rule without damage. Recurrence with 
every added insult or fresh infection is the rule, until the susceptible and 
hyperesthetic child lives beyond babyhood. In occasional cases the tend- 
ency to convulsions in such subjects persists until puberty. The spasm 
of the glottis (larvngo-spasm—laryngismus stridulus) is without danger 
in almost all cases. It is likely to recur, particularly in rachitic and under- 
fed children on slight cause. 
Causes.—For the purpose of the clinician it may be assumed that 
infantile convulsions are symptomatic, as a rule an accompaniment of 
acute infection; at times they are due to nutritional faults; in other cases 
there is a fundament in organic disease of the nervous system (poliomye- 
litis, meningitis, meningismus, brain tumor, etc.). Toxic states with 
gastro-intestinal disturbance, worms, uremic poisoning, reflex causes, alco- 
holism in the parent, rachitis, congenital defects of the heart and thymus 
enlargement are also responsible. The significance of convulsions in chil- 
dren with these conditions is fully considered separately. The reader is 
referred to the included sections. 
Influence on Acute Infections.—It may be assumed that the acute in- 
fections are unfavorably influenced by added convulsions; the explosive 
seizure is an expression of the depth of the infection. With malignant 
scarlet fever and diphtheria children may die in the convulsion, or with 
hyperpyrexia and cardiac asthenia they may succumb in coma after the 
convulsion. The same behavior often characterizes other deep infections. 
In all cases the rapidity of the pulse (heart weakness) the behavior of 
the respiratory organs, the duration of the convulsion, the resistance of the 
child, the presence or absence of respiratory obstruction (cyanosis), and the 
depth of the stupor, become important prognostic features, while the na- 
ture and extent of the primary disease m,ust always remain the paramount 
factor in offering a reliable forecast. Most diseases are not unfavorably 1066 
DISEASES OF THE NERVOUS SYSTEM 
influenced by the occurrence of the initial convulsion, but usually it may 
be concluded that the disease itself proves to be of grave import, as a rule, 
when the infection or the toxemia leads to convulsions. 
Conclusions.—Convulsions in children, while they last, are never to 
he lightly regarded. The prompt relief of irritating or inviting condi- 
tions favorably influences the outcome. In some cases of infection and in 
organic disease, it is of enormous importance to prevent recurrence be- 
cause of possible hemorrhage and subsequent cyst or organic change in 
brain tissue which occasionally follow convulsions (See separate diseases 
of the nervous system). 
Accurate diagnosis will lead to trustworthy and timely prognosis in 
most cases. 
E. Diseases of the Sympathetic System 
Vasomotor and Trophic Disturbances 
1. Erythromelalgia 
{Red Neuralgia) 
Characteristic Symptoms.—in 1872 a paper was written by Weir 
Mitchell describing a peculiar condition to which he gave the following defi- 
nition: “A chronic disease in which a part or parts—usually one or more 
extremities—suffer with pain, flushing, and local fever, made worse if the 
parts hang down.” 
Mitchell called attention to the change in the color of the dependent 
member which became red, at the same time painful, without attending 
phlegmon or inflammatory changes. The profession gave but little notice 
to Mitchell’s original communication, but his second article published in 
1878, in which fifteen cases of the disease were reported in Mitchell’s 
graphic style, with the title “On a Rare Vasomotor Neurosis of the 
Extremities and on the Maladies with Which It May Be Confounded” 
aroused interest and since that time “Red Neuralgia” has been fre- 
quently (comparatively) diagnosticated and the complex of symptoms, be- 
cause of the erythema and pain has been known as erythromelalgia. 
Pathological Findings—Associated Symptoms.—The pathological 
findings have materially changed our original conception of this painful 
and obstinate affection, for it has been demonstrated by many trustworthy 
clinicians and pathologists that the contentions of Mitchell which sepa- 
rated erythromelalgia from Raynaud’s disease and other organic lesions 
of the arteries and nervous system—which claimed that gangrenous and 
other necrobiotic process could never complicate the disease—have been DISEASES OF THE SYMPATHETIC SYSTEM 
1067 
upset. In considering the prognosis of erythromelalgia, its true patho- 
logic fundament must be considered. 
There are unquestionably cases of erythromelalgia in which there are 
no discoverable associated lesions, which correspond very closely with the 
original description of Mitchell. The majority of cases, however, when 
thoroughly investigated prove that the so-called neuroses which affect the 
extremities are likely to complicate each other; that one may merge into 
the other; that seasonal influence materially affects the clinical history of 
each; that there may he evidences of acroparesthesia and erythromelalgia 
in the same subject at the same time; that these symptoms may he accom- 
panied by evidences of the first stage of Raynaud’s disease; that the symp- 
toms of one of these tropho-neuroses (?) may disappear during a limited 
period to recur later, or they may never return. 
Eisner, Dehio, Sachs and Wiener, Rolleston, Sternberg, Mills, and 
many others have reported authentic cases of the disease in which the 
changes were purely vascular, of arteriosclerotic, endarteritic or endophle- 
bitic character. Sachs holds “surely erythromelalgia is as much an arterial 
as a nerve disease.” 
My case (Eisner) was certainly a remarkable instance in which ery- 
thromelalgia and Raynaud’s disease were combined. The patient at first 
had in 1893 numb feelings in the hands and intolerable headaches. The 
following winter there were the acute sufferings of erythromelalgia, burn- 
ing in the palms and backs of both hands, and with the pains, the charac- 
teristic erythema. In 1896 the pains increased in the hands to an intol- 
erable degree with hyperesthesia and profuse sweating. The redness dis- 
appeared suddenly from the thumb in September, 1896, and at the same 
time a red spot appeared on the right tragus, which became asphyxiated 
and gangrenous. A second gangrenous patch appeared over the middle of 
the left sternocleidomastoid muscle. Soon there was gangrene of the 
thumb with gradual separation of the phalanx, and final recovery. 
Some cases of erythromelalgia which have persisted during long peri- 
ods—twenty years and longer—have failed to show microscopic changes 
in the nerve structures of the painful parts; all of my cases, which I 
have elsewhere reported, which were examined microscopically gave evi- 
dence of “thickening of the intima of both the large and small arteries. 
About the small arteries were occasional foci of infiltration with lymphoid 
cells.” 
I have considered the association of vascular changes with erythro- 
melalgia to impress upon the clinician the possibility of destructive proc- 
esses with chronic cases of red neuralgia, the possibility of Raynaud’s 
process or localized gangrene. My material justifies the conclusion that 
in occasional cases red neuralgia may be limited to an extremity—one or 
more toes or fingers—in which gangrene, deep or superficial, may develop 
with final relief of the pain. In all of these cases the symptomatology of 1068 
DISEASES OF THE XERVOUS SYSTEM 
red neuralgia is so characteristic as to make differentiation impossible if 
that is not the correct diagnosis. The prognosis of these conditions in 
which destructive processes are finally associated with erythromelalgia is 
further strengthened by the facts which Thoma has established in his 
epoch-producing work which proves that compensatory changes take place 
in the arteries which have remained distended for a considerable time, aud 
which in truth are too large for the blood which courses through them. 
It is a question whether erythromelalgia deserves to be dignified as a 
disease per se. In framing prognosis let the reader consider the fact that 
besides the conditions to which I have already referred, it may be associ- 
ated with ascending degeneration of the posterior columns of the cord 
(Schenck), with myelitis (Woodnut), indiscriminate lesions of the cord 
(Collier), degenerative changes in the posterior nerve roots of the lumbar 
and sacral nerves without degeneration of the cord substance (Auerbach). 
(The only post mortem of a case of erythromelalgia on record). In my 
cases the material was obtained from amputated or sloughing fingers or 
toes and the nerves and arteries of tissue left behind. 
Erythromelalgia is always a chronic process. As a rule it is progres- 
sive; in occasional cases there are periods of improvement, but rarely 
complete relief. Usually the pain, redness, and localized sweating are 
uninfluenced by treatment reaching a climax finally, and in uncompli- 
cated cases remain unchanged during months and years (Senator, Ger- 
hardt, Ileiman, Eieden). Eulenberg reports a case which continued 28 
years; the patient was 54 years of age. When 22 years of age formica- 
tion and pain commenced, persisting 10 years, to be followed by the con- 
tinuous symptoms of the fully developed complex. 
Auerbach’s case continued 20 years—finally developed tabes dorsalis 
with limitations of the lesion in the lumbar and sacral roots. In all cases 
death is due to some complication and not to erythromelalgia. Cassirer 
reports 5 deaths: hemiplegia in 2 (Henoch and Graves), in one dementia 
paralytica (Machol), one case reported by Weir Mitchell in which there 
was no autopsy, and one by Auerbach, above cited, in which there was 
tabes dorsalis with the limitation of the lesions in the lumbar and sacral 
roots. 
Course of the Disease.—The disease may halt and remain stationary 
at the point reached; in rare cases there may be retrogression. I have 
seen one such case with final complete relief. Improvement may take 
place after years of suffering from this most obstinate disease, which 
includes a persistence of acute suffering almost unequalled by any other 
peripheral pain to which man is subjected. 
In the average case complete dissipation of all pain and the associated 
manifestations—trophic and sensory—rarely follow. A dubious prognosis 
is safest; to offer some encouragement is justified because of improvement 
during considerable periods following rest of the painful part; in occa- DISEASES OF THE SYMPATHETIC SYSTEM 
1069 
sional cases the complex cures itself or yields to radical surgical treatment 
when gangrene follows (Eisner). 
Life is not endangered though resistance is unquestionably lowered. 
Morphinism is likely to be the fate of many. When the complex is an 
expression of organic—cerebral, spinal, or vascular lesions—prognosis 
must be framed in accordance with the more prominent disease. 
References 
Auerbach. Deutsch. Ztschr. f. Nervenh., 1897, Bel. xi, 1-2. 
Cassirer. Vasomotor u.troph. Neurosen. 1901. 
Collier. Lancet, London, 1898, ii, 401-404- 
Dehio. Bed. klin. Wchnschr., 1896, N'o. 37. 
Eisner {Henry L.). New York Med. News, 1897, Ixx, 817-821. 
Idem., March 16, 1901. 
Eulenberg. Deutsch. mcd. Wchnschr., 1893, No. 50. 
Gerhardt. Bed. klin. Wchnschr., 1892, 1125. 
Graves. Clin. Led., 1864, 826. 
Henoch. Gesellsch. d. Charite Aerzle, 1892. 
Machol. Berl. klin. Wchnschr., 1892, No. 51, 1319. 
Mills. Berl. klin. Wchnschr., 1894, 146. 
Mitchell {S. Weir). Philadelphia Med. Times, 1872. 
Am. J. Mcd. Sci., July, 1878. 
Aled. Arews, New York, 1893, Ixiii. 
Clin, lessons on nervous diseases. Philadelphia, 1897. 
Mitchell {Weir) & Spiller. Am. J. Med. Sci., Jan., 1899. 
Nieden. Arch. f. Augenh., xxvii, 81. 
Rolleston. Lancet, London, 1898, 781-783. 
Sachs & Wiener. J. Nerv. & Ment. Dis., 1899, xxvi, 372-374- 
Schenck. Wien. med. Presse, 1896, No. 45, 1401. 
Senator. Berl. klin. Wchnschr., 1892, 1127. 
Sternberg. Eisner [l. c.]. 
Tlioma. Deutsch. Arch. f. klin. Med., 1888, xlii, 409. 
Virchow's Arch. f. path. Anal., Bd. xciii, 113-116. 
For further "literature, see Index Catalogue of the Library of the Surgeon- General's 
Office, Eisner's articles above cited, also Cassirer. 
2. Raynaud's Disease 
(Symmetrical Gangrene, Angiospastic Gangrene') 
Characteristic Symptoms.—In 1862 Raynaud described a variety of 
symmetrical dry gangrene “affecting the extremities, which cannot he ac- 
counted for by vascular obstruction; a variety characterized by a remark- 
able tendency to symmetry, affecting always similar parts of the upper 
or lower limbs, all four at once, in certain cases the nose and ears, and T 
shall try to show that this form of gangrene has its origin in a disturbance 
of the innervation of the capillary vessels.” 1070 
DISEASES OF THE NERVOUS SYSTEM 
In 6,300 cases of internal disease I number 6 of Kaynaud’s process. 
Of 23,000 medical cases at Johns Hopkins Hospital in 20 years, Osier 
reports 19 cases, Cassirer in his classic monograph reports 168 cases col- 
lected from medical literature, and Monro reports 180 cases and esti- 
mates “that about one case occurs in 3,000 patients.” 
Influencing Factors.—Sex Influence.—Monro reports 62.5 per cent 
women and 37.5 per cent among men. 
Age.—The disease in my experience is rarely met early in life, though 
Cassirer reports 22 cases under 5 years of age. 
5-10 years of age 8 cases 
11-20 “ “ “ 25 “ 
21-30 “ “ “ 40 “ 
31-40 “ “ “ 27 “ 
41-50 “ “ “ 28 “ 
Above 00 “ “ “ 18 “ 
Family Predisposition.—It occasionally happens that family predis- 
position is present as lias been noted in the cases of Colman and Taylor, 
Makins and Braman. The latter found three brothers afflicted. 
Seasonal Influences.—In chronic and mild forms, during the state of 
cyanosis, seasonal influences materially affect the symptoms—one case 
now under observation is entirely without symptoms during the summer 
months but with the approach of winter, she has a combination of acropares- 
thesia with “marble fingers” and hand, alternating with “beefsteak” 
hand. Medicines are without influence in this case; now in its fourth 
year, heat and protection against cold seem to control the symptoms best. 
Thus far there has been no necrotic loss. 
Syphilis, etc., Not Factors.—We exclude symmetrical gangrene due to 
syphilitic arteritis—it is not true Baynaud’s disease. It offers a good 
prognosis, however. Monro in his monograph includes syphilis as a factor 
in a small proportion of cases—2.8 per cent. 
Symmetrical and asymmetrical gangrene secondary to arteriosclerosis, 
diabetic endarteritis', nephritis and perforating ulcer of tabes are never to 
be included in the list of Raynaud’s disease. 
The stages of the progressive type of the disease may be divided into; 
First stage—Local syncope 
Second stage—Local asphyxia or cyanosis 
Third stage—Symmetrical gangrene (dry gangrene). 
First Sta^e—Local Syncope 
For several years in mild cases (formes frustes) the extremities in- 
volved may give symptoms only on exposure during cold weather, occa- 
sionally during extreme hot weather in other cases, during which there is 
characteristic change of color, throbbing, aching, formication and symp- DISEASES OE THE SYMPATHETIC SYSTEM 
1071 
toms resembling acroparesthesia very closely. Such cases improve very 
often, hut return should be prophesied in the majority. 
Girls at puberty and after occasionally present with the “beefsteak” 
hand. Progression may never follow, but persistence of discomfort and 
vasomotor symptoms are likely to persist. In occasional cases there is, 
during the first stage, some evidence of the disease in the cheeks or in one 
or both ears. In one of my cases there was a limited necrobiosis (super- 
ficial) of one tragus with subsequent improvement of the hands, so far as 
subjective symptoms were concerned, but the fingers were more or less stiff 
as the result of a sclerodermic thickening which followed. 
In most of the mild cases there is no marked cyanosis; when present 
it is of short duration, insufficient to cause destructive change. In some 
cases with freedom from care, emotion, or exposure, the fresh attacks of 
syncope may be prevented or postponed. 
Cases in which the mild form or early stage is limited to one toe or 
finger may never progress beyond this stage or extend to other parts. I 
have noted a few cases in which, after there has been local syncope during 
a number of years, there have been characteristic pinhead or split-pea 
sized, cup-shaped losses of epithelium from the toes or fingers with subse- 
quent scleroderma and some change in the shape of the digits beyond 
which the disease has not extended, and siich patients were but little in- 
convenienced, lived many years, and died of intercurrent disease. 
Patients may go on with “dead fingers”—numb and analgesic—during 
varying periods (hours, days, or months) with final relief, or the condition 
may remain, or there may be progression to gangrene. 
Second Stage—Local Asphyxia or Cyanosis 
During this stage in accordance with the severity of the disease the 
extremities involved are cold and cyanotic. Severe and rapidly advancing 
cases may escape the first stage entirely and at once present marked evi- 
dences of cyanosis. Deep blue and black discoloration of the nails with 
corresponding changes in the skin argue in favor of a severe process, and 
such cases usually advance with considerable rapidity to the third stage, 
•or gangrene. There may be periods of improvement after the second 
stage is fully established even in cases which at times appear threatening 
to the parts involved. In some of these the advance to but limited loss of 
tissue (epithelial or superficial) may end the gangrenous feature of the 
disease. Kot all members will he equally involved in average cases, for 
one finger may show marked asphyxia while its neighbor may remain in 
syncope. In some of these cases active hyperemia may persist during long 
periods; in other cases the sequence of syncope and asphyxia of a member 
may he exceedingly and surprising short. 
As a rule, in an acute exacerbation, there is first the “marble hand” 1072 
DISEASES OF THE NERVOUS SYSTEM 
or finger, in which the part is anemic (white), then follows active hyper- 
emia in which the color is deep—usually blue—and finally a longer period 
of red. Repeated or long continued active hyperemia with final asphyxia 
may lead to necrosis or gangrene. In the severe cases involvement of the 
nose and ear, one or both at times, may be present and losses of tissue, 
either deep or superficial follow. 
When asphyxia persists and the livid part is pricked and only dark 
blood escapes, gangrene may soon be expected to follow. Monro says: 
“The duration of the attack varies from a few minutes to hours or even 
days. Several attacks may occur in one day, or one in several days or 
weeks, or the intervals may be much longer.” Some cases show “a high 
degree of paroxysm, while others which persist with but little change for 
prolonged periods can justly be ascribed as chronic.” 
The general condition of these patients remains uninfluenced in most 
cases during this and the first stage, save as the sensory disturbances de- 
press, rob them of sleep and appetite. Recurrence of local asphyxia may 
continue during many years without marked advance of trophic change. 
Young children have been reported as permanently relieved after a pro- 
longed series of repeated exacerbations of local asphyxia. In one of these 
cases (Johnston) the “local asphyxia came to an end suddenly and perma- 
nently after two months.” Monro feels justified in holding “an attack 
of Raynaud’s disease may be constituted simply by one attack of local 
asphyxia prolonged over months without interruption. 
Third Stage. Symmetrical Gangrene 
Monro, whom we frequently quote because he is unquestionably the 
ablest authority on the subject, says: “While local syncope is met with 
in 50 per cent, and local asphyxia in 94 per cent, necrosis of tissue, either 
slight or serious, occurs in 68 per cent of Raynaud’s disease.” 
Years may lapse before the first or second stages are followed by gan- 
grene. Occasional cases may develop gangrene without preceding circu- 
latory symptoms or trophic changes of any preceding stage. The loss of 
tissue or a member (usually toe or finger tip) is in most cases followed 
by prompt repair, but with more or less trophic changes. The deep gan- 
grenous changes may leave surfaces which require several months to heal ;■ 
often the reparative process is exceedingly slow. Church and Peterson re- 
port deaths in infants a few days after the beginning of symptoms, and 
occasionally from uremia in aged patients. Such termination I have not 
experienced in uncomplicated cases. 
The acute infections (typhus, typhoid, smallpox, scarlet fever, diph- 
theria, measles, pertussis, erysipelas, influenza, syphilis, tuberculosis, ma- 
Complications DISEASES OF THE SYMPATHETIC SYSTEM 
1073 
laria, rheumatism, rheumatoid arthritis, quinsy, splenic enlargement, hem- 
orrhagic and suppurative processes) have in rare instances been followed 
by Raynaud’s disease (Monro). 
I have seen two deaths from tuberculosis follow Raynaud’s disease. 
The relatively high mortality from tuberculosis of Raynaud patients has 
been noted by many clinicians, but there are no positive evidences, because 
of the general prevalence and frequency of tuberculosis, that Raynaud’s 
disease bears more than an accidental relation to the former. 
Rheumatism unquestionably bears a close relation to the disease for it 
is found to have preceded it in a large number of cases. 
Psychic disturbances were present in 4} per cent of Monro’s cases. 
Scleroderma already mentioned is frequent. This is usually associated 
with the multiple cup-shaped and limited losses of tissue mentioned in the 
preceding pages or follows more extensive gangrene. 
Basedow’s disease with mitral lesions has been found in occasional 
cases (Tompson, Bret and Chalier). 
Osborne makes the positive statement that “Raynaud’s disease is not 
a distinct entity . . . the disturbance of one or more internal secreting 
glands . . . there is always apparently some disturbance of the thyroid 
gland, perhaps a diminution of the vasodilator stuff of this gland.” 
Osborne further claims that the prognosis of the syndrome is improved 
in the majority of cases, perhaps all, by the thyroid treatment and that it 
“cures some cases.” 
The association of erythromelalgia with asphyxia and gangrene has 
been separately considered (See Erythromelalgia). In these cases the 
terminal stage of Raynaud’s process may be followed by the relief of all 
sensory symptoms, and barring the deformity and stiffness resulting, there 
is no further suffering. 
Kidney, cerebral, and ocular symptoms may influence prognosis un- 
favorably; such complications are infrequent. 
Albuminuria may be transitory without influence on the process, 
though it is probably due to vascular anomalies of a fleeting character. 
Repeated paroxysmal hemoglobinuria may finally cease entirely, or in 
occasional cases nephritis may finally develop. 
The eye symptoms—temporary amblyopia—probably due to vascular 
spasm, are not lasting. 
In occasional cases moderate paresis of one extremity or hemiplegia 
may come and go without leaving permanent damage. The same is true 
of aphasia which may in the occasional cases of transitory hemiplegia 
alarm the patient who may ultimately recover. 
Osier and Thomas report a most interesting and unique case in which 
“the wide symptomatology of the disease” was illustrated. The patient 
was 23 years of age, “had typical Raynaud’s disease—fingers, toes, ears, 
nose—and cyanosis often preceded superficial necrosis. The attacks oo 1074 
DISEASES OF THE NERVOUS SYSTEM 
curred in tho winter; in warm weather he was perfectly well. Epileptic 
attacks accompanied the outbreaks of local cyanosis, but only in the win- 
ter, when he also had hemoglobinuria.” The case was followed for over 
three years, the cyanosis persisted but necrosis was “never widespread.” 
After three years “the epilepsy ceased but the winter attacks came on as 
usual and were associated with crises of abdominal pain, just like those 
of angioneurotic edema, and he had swelling of the spleen.” I quote 
this case fully because it shows the protean character of the disease and 
complicating conditions, and the prognostic problems associated are fully 
accented by it. 
I have never in practice had a death directly traceable to the dis- 
ease, neither has it seemed to shorten life when uncomplicated. Great 
caution is necessary in the prognosis of individual cases for it is impossi- 
ble to foretell the course of even advanced cases, much less the incipient. 
The majority of my cases, in which complications did not interfere, lived 
to fall into long periods of comparative relief after the separation of the 
gangrenous tissue; in some there were exacerbations during the winter 
months, in a small proportion change of work and scene or removal to an 
equable and warm climate had a wholesome effect. 
Bramann. Osier [Z. c.], 628. 
Bret. Quoted by Curschmann [l. c.]y 983. 
Cassirer. Die Vasomotor troph. Neurosen. Berlin, 1901. 
Chalier. Quoted by Curschmann [Z. c.\, 983. 
Colman & Taylor. Osier [l. c.]. 
Curschmann. Mohr & Staehelin’s Handb. d. inner. Krankh. Berlin, 1912, Bd. v 
Johnston. Cited by Monro [Z. c.]. 
Makins. Osier [l. c.\, 628. 
Monro (T. K.). Glasgow, 1899. 
Osborne. Am. J. Med. Sci., Aug., 1915. 
Osier (Sir William). Modern medicine. 1909, vi. 
Osier & Thomas. Johns Hopkins Hosp. Rep., 1891, ii, 114. 
Raynaud. Thesis, 1862. 
Arch. gen. de Med., 1874. 
New Sydenham Soc., 1888. 
Tompson. Quoted by Curschmann [Z. c.], 983. 
References 
3. Acroparesthesia 
In 1890 Fr. Schultz described a condition in which it may be assumed 
that there is more or less vasoconstriction of the hands associated with 
'paresthesia—tingling, numbness, clumsiness, “velvety feeling,” creeping 
crawling sensations—at times burning, with pain in some eases. It is 
usually found in women (washerwomen)—those whose hands are in water 
while at work. In the United States it is relatively frequent, as are most DISEASES OF THE SYMPATHETIC SYSTEM 
1075 
trophoneuroses of the extremities among Jewish patients in dispensary 
practice. 
There are unquestionably cases in which with positive evidences of 
acroparesthesia there are suggestive appearances of syncope and asphyxia; 
in fact the relations of the various trophoneuroses which affect the extrem- 
ities are so close as to lead to the conclusion that, as I have suggested 
in the study of erytliromelalgia and Raynaud’s disease, these various com- 
plexes may exist together or one may follow the other. 
Acroparesthesia is most likely to develop upon a fundament of hered- 
ity, upon a psychoneurotic basis, often in the presence of hysteria, or neu- 
rasthenia. When the disease develops in men, these stigmata are particu- 
larly prominent and it is not at all unusual to find complications which 
may include organic disease of the nervous system or of the ductless 
glands. One of my cases which persisted during many years—most of 
which time the man traveled carrying heavy satchels (to which fact he 
attributed his sensory disturbances) suddenly developed an atypical type 
of hyperthyroidea. The development of the disease is usually symmetri- 
cal, hut there are exceptions to this behavior. 
Acute and frequently repeated exacerbations may be prophesied with 
considerable certainty. In some cases symptoms (paresthesia) may be 
continuous, and these may merge into the milder forms of Raynaud’s 
disease. Excessive sweating may he the end of a period of acute symp- 
toms. Migraine and gastric disturbances may persist during acute ex- 
acerbations. Acroparesthesia per se does not lead to asphyxia or gan- 
grene—neither will the muscles of the affected parts atrophy, though 
there may he transitory weakness as shown by the dynamometer. 
In women who are obliged to support themselves, usually by washing, 
it has seemed that removal from damp homes, the proper ventilation of 
bed and workrooms, the relief of uterine anomalies, the menopause, change 
of scene with rest and psychic influences, have had a wholesome effect— 
with the correction of gastro-intestinal disturbances which are present in 
most cases. 
The complex per se is not of serious import; is likely to prove chronic, 
and, while a slight remnant of paresthesia usually remains, it is not suffi- 
cient to prove a serious or annoying handicap. 
4. Angioneurotic Edema 
(Giant Urticaria, Acute Circumscribed Edema, Quincke s Disease (1882), 
Periodic Swelling) 
Milton in 1876 described a condition of “giant urticaria” which was 
finally fully considered in Quincke’s description of edema circumscriptum 
cutis in 1882, to which the name of Quincke’s disease has been given. 
The symptoms develop suddenly and consist of edema of the face, as a 1076 
DISEASES OF THE NERVOUS SYSTEM 
rule, with corresponding deforming enlargement of the parts involved, 
which continues during several hours—rarely a day or two—usually asso- 
ciated with more or less gastro-intestinal disturbance, foul breath, at times 
threatening edema of the larynx, with or without swelling of the tongue. 
The edema may be associated with itching and in most cases abnormal 
“fullness.” In most cases recurrences may be prognosticated. 
It is exceedingly difficult in the individual case to determine the under- 
lying cause of these oft-repeated edemas. The interval between the at- 
tacks is variable; in some cases several years may elapse, in others there 
seems to be a cycle of evanescent edemas usually swelling parts of tbe 
face at a time, or the genitalia, or there may be alternation with gastro- 
intestinal crises. Roger Morris believes that he has demonstrated from 
the bits of mucosa in the wash water taken from the stomach, positive evi- 
dences of edema. Single attacks average from six to eight hours. They 
are not painful or threatening save as they cause respiratory obstruction 
due to edema of the glottis. This may in occasional cases involve but 
one-half of the glottis—a condition which I found alarming and de- 
manded immediate free incision to prevent increasing air hunger. 
Pulmonary edema and edema of the glottis are the leading life-threat- 
ening features of Quincke’s disease; without these the disease is not seri- 
ous, but exceedingly annoying. Most of my cases have cured themselves 
after several years (2 to 10) of recurring symptoms. The individual case 
offers encouragement for prognosis in proportion to the ability of the 
clinician to unearth the cause; usually this is impossible. The cases bur- 
dened with a striking heredity (Quincke, Osier), purpuric conditions, 
recurring erythema with visceral complications and nephritis or cyclic 
albuminuria may prove serious—more because of the associated lesions 
than from the giant urticaria. With the disappearance of the annoying 
edema, the patient usually returns to perfect health and in some cases life 
is “of exceptional duration.” Young subjects offer a favorable prognosis. 
There are unquestionably cases of gastro-intestinal edema which give rise 
to visceral symptoms resembling acute infections (appendicitis, enteritis, 
intestinal obstruction) which require accurate differentiation, that incor- 
rect diagnosis and prognosis may not lead to radical (surgical) measures 
(See also Serous Meningitis). 
References 
Cassirer. Die vasomol. troph. Neuroses. Berlin, 1901. 
Milton. Edinburgh Med. J., 1876. 
Morris (Roger S.). Am. J. Am. Sci., Nov., 1904. 
Osier (Sir William). Am. J. Med. Sci., 1905, cxxx. 
Jacobi's Festschrift. New York, 1900. 
Am. J. Am. Sci., 1895, cx. 
Idem., 1888, xcv. 
Quincke. Monatschr. f. prak. Dermatologic, 1882. DISEASES OF THE SYMPATHETIC SYSTEM 
1077 
5. Scleroderma 
Thirial in 1845 described a peculiar nutritional skin lesion, either 
circumscribed (morphea) or diffuse, in which there is a leathery thick- 
ening or induration of the skin 'which is tightly stretched over and adher- 
ent to the underlying subcutaneous tissue. The disease is progressive, 
atrophic, and may involve the subcutaneous connective tissue, the muscles, 
and the bone tissue under the changed skin. 
Heredity plays only an unimportant role in the pathogenesis of this 
unique condition. The true cause is unknown though cases have been 
traced to a variety of causes, including the acute infections (typhoid, 
erysipelas, influenza, syphilis, tuberculosis and smallpox), exposure to 
heat and cold, to wet, pregnancy, trauma, psychic factors—as sudden 
shock, emotion and long continued worry. I have found in most of my 
cases which developed late in life, organic disease of the heart and vascular 
system. I also refer to localized scleroderma as it follows or is associated 
with acroparesthesia, erythromelalgia and Raynaud’s disease (See separate 
chapters). 
Typical cases progress slowly, and as a rule symmetrically. There 
are acute cases, but these are exceedingly rare. 
Pigment deposit and, bronzing are late developments, when the skin is 
so tightly drawn over the underlying tissue as to prevent folding. When 
the face is involved and the disease progresses, the skin is tightly drawn 
and in the end the expression is characteristic, 
Recession of lesions is not to be expected though the changes may halt 
in any stage of the disease. Atrophy is the fate of the involved skin and 
tissues. 
f‘Sclerodactylia” is the term used by the Germans to characterize the 
changes of a sclerodermic character associated with Raynaud’s disease and 
tissue loss (gangrene) (See Raynaud’s Disease). 
Circumscribed scleroderma (morphea) involves only limited stripes or 
areas of skin, without far reaching damage. 
Joint changes may be expected in some cases with some contraction, as 
a rule; these do not materially interfere with the activity of the patient, 
When scleroderma is a complication of Graves' disease or Addison s com- 
plex, the prognosis of the more serious disease decides the fate of the 
patient, 
General Observations.—To recapitulate from the foregoing state- 
ments: Scleroderma is a chronic progressive disease which remains unin- 
fluenced by treatment, which may remain circumscribed to a limited area 
or may be diffuse. It does not destroy life and it may remain stationary 
after months or years of progression. Acute cases (Ileynacher) have 
been observed in which cure followed. It is not uncommon to find cases 
which have persisted as long as thirty and forty years. Involvement of 1078 
DISEASES OF THE NERVOUS SYSTEM 
the face and fixation of the jaw may cause nutritional disturbances— 
marasmus—and consecutive asthenia. Children (Tomaczewski) offer a 
favorable prognosis in individual cases. Once advanced to the stage of 
atrophy there is no hope of restitution. In infants acute diffuse sclero- 
derma may be associated with general infection -which may lead to death, 
as was proved by Barker’s case in which the sclerodermic child, aged two 
and a half months, died of pleuropneumonia aud general streptococcus in- 
fection. 
The majority of sclerodermics die of intermirrent disease. The influ- 
ence of thyroid feeding has encouraged some dermatologists and neurolo- 
gists to offer a better prognosis than has been previously given. My 
experience with a limited material and thyroid therapy does not justify any 
conclusions of value at the present time. 
Barker (Le welly s F.). Arch. Pediat., New York, 1893, x, 890. 
Cassirer. Monograph. Tropho-neuros, etc. Berlin, 1901. 
Curschmann. Mohr & Staehelin’s Handb. d. inner. Med. Berlin, 1912, Bd. v. 
Heynacher. Deutsch. med. Wchnschr., 1903, No. 15. 
Thirial. J. de Med., Paris, 1845, Hi, 137-161. 
Tomaczewski. Quoted by Curschmann [l. c.]. 
References 
6. Adiposis dolorosa 
(Dercums Disease) 
Dercum, in 1888, called attention to a condition found in male adults 
oftener than in women, with fat deposits which are painful or sensitive, 
in which there may be marked weakness, some genito-urinary disturbance, 
and mental anomalies. The fat deposits may be either nodular, circum- 
scribed, or diffuse. The disease, in the light of our increased knowledge 
of the functions of the pituitary body, should be considered to be due to 
hypopituitarism. Indeed tumor of the pituitary (Dercum and McCarthy) 
has been found to present the characteristic clinical picture of adiposis 
dolorosa with “hypoplasia of the genital organs, extensive infiltration of 
the fat and hemolympli glands.” 
Price’s observations in eight autopsies confirm the conclusions con- 
cerning these painful fat deposits to which pathologists are fast subscrib- 
ing, which attribute the symptoms to organic change in the pituitary gland. 
Pain is the leading feature and is persistent, and with the general weak- 
ness remains uninfluenced by treatment. 
The psychic symptoms may remain unchanged or may advance to full 
mental alienation. The disease does not lead to death, but unless based on 
the theory of hypopituitarism, and unless surgical intervention or pituitary 
therapy brings relief (at present sub judice), we shall be forced to give 
a doleful prognosis so far as the relief of symptoms is concerned, DISEASES OF THE SYMPATHETIC SYSTEM 
1079 
References 
Dercum. Univ. Med. Mag.,-1888. 
Am. J. Med. Sci., Nov., 1892. 
J. Nerv. & Merit. Dis., Aug., 1900. 
Ewald. Berl. klin. Wchnschr., 1895, No. 2, 3. 
McCarthy. Adiposis dolorosa. 
Osier’s Modern medicine. Philadelphia, 1909, vi 
Price. Am. J. Med. Sci., May, 1909. 
7. Intermittent Dropsy of the Joints 
(.Angioneural Arthrosis—Solis-Cohen) 
Perrin in 1845, Moore in 1852 and 1868, Friedenberg in 1888, and 
Schlesinger in 1900, called attention to a class of cases in which there is 
paroxysmal return (intermittent) of dropsy of one or more joints. Cohen 
includes the intermittent dropsy of joints (not dependent upon infection) 
among the “angioneural arthroses.” He says “the term ‘hydrops articu- 
lorum periodica’ or ‘hydrops articulorum intermittens’ has been applied 
to the one variety of vasomotor joint disorder that has thus far been defi- 
nitely recognized; but it is applicable to that variety alone.” It is a 
question whether these suddenly recurring effusions into the joint are not 
atypical types of angioneurotic edema (Quincke’s disease). The knee 
joint is usually dropsical, though in some, both knee joints are suddenly 
involved; other joints may swell, and occasionally there is invasion of the 
jaw and separate parts of the spinal column. 
Schlesinger has reported intermittent dropsies of the tendon sheaths 
and Cassirer painful edemas of the muscles. Cohen’s characterization of 
these cases as fvasomotor ataxia’ is a happy and suggestive one. Once the 
disease is established, recurrence should be expected at intervals which 
average between seven to fourteen days. Three months have elapsed with- 
out return in reported cases. In a few cases there is great regularity in 
the time of recurrence. Periods of four weeks may be considered long. 
Oppenheim reports recurrence and disappearance during intervals of a 
few minutes. There are patients in whom there is such marked periodicity 
as to make it possible to foretell the day of return of the joint dropsy. 
One of my cases during many years developed dropsy of the right hip with 
each menstrual period, entirely uninfluenced by rest or treatment. I 
have seen but three cases in private and hospital practice, in all of which 
there were no marked pains; in none was there fever nor constitutional 
disturbances. The duration of the swelling is not always the same. It 
may continue but a few hours, a single day, or in the average case, from 
two to seven or eight days. 
My cases were not dependent upon discoverable causes. His reports 
gouty conditions complicating the complex, while Oppenheim has found it 1080 
DISEASES OF THE NERVOUS SYSTEM 
with Basedow's disease, and angina pectoris. Schlesinger and others prove 
that the association with functional and organic disease is not uncommon. 
Differentiation of polyarthritic conditions, gout, and other afebrile 
arthritic lesions is not difficult. Cohen believes that the process may be 
influenced and attacks postponed by treatment. It is questionable whether 
the cases reported as cured (Wiesinger) by surgical interference (aspira- 
tion and iodin injection) were true ‘angioneural arthrosis.’ The progno- 
sis so far as control of the symptoms is concerned is not good; the process 
is exceedingly rebellious and chronic. Psychic influences (suggestion) 
have seemed to exert some control over the disease in subjects with a 
marked hysterical or neurasthenic habit. 
References 
Cassirer. Tropho-newrosen, etc. Berlin, 1901. 
Friedenberg. New York Med. Rec., June 16, 1888. 
His. Charite-Ann., Bd. xii. 
Moore. Med. Chir. Tr., 1852 and 1865, l, 21. 
Oppenheim. Lehrb. d. Nervenkr. Berlin, 1913. 
Perrin. J. de Med. de Trousseau, 1845, 82. 
Schlesinger. Mitth. aus d. Grenzgeb. d. Med., etc. Bd. v. 
Solis-Cohen (S.). Angioneural arthroses. Am. J. Med. Sci., 1914, cxlvii, 228. 
Wiesinger. Deutsch. med. Wchnschr., 1903. 
8. Persistent Hereditary Edema of the Legs 
(Milroy’s Disease, Hereditary Tropho-edema) 
T Lave had no experience with hereditary edema in my practice. 
Milrov, in 1893, was the first to describe persistent and hereditary edema 
of the legs which gave the disease its name—Milroy’s disease. 
Henry Meigs (1899) reported a family in which eight members were 
atfected, both men and women, through four generations. All of these 
cases were without known cause and without general disturbance. Osier 
says: “It is a fairly common complaint affecting males and females 
equally.” 
In six generations among 97 in Milroy’s series, 22 presented with 
characteristic symptoms. Hope and French found in their series 13 to 42 
persons in five generations. All of these cases presented the same features: 
painless edema of the legs which persisted, usually appearing about 
puberty. In some cases there were febrile disturbances following chills 
and acute exacerbations in swellings. The condition does not influence 
the general health of those chosen, causes but little discomfort; it has not 
been known to shorten life, but refuses to yield to any known treatment. DISEASES OF THE SYMPATHETIC SYSTEM 
1081 
References 
Hope & French. Osier [l. c.]. 
Meigs. Nouv. Icon, de la Salpet, Dec., 1899. 
Milroy. New York Med. Rec., 1893. 
Osier (Sir William). Practice of medicine. New York, 1913, 1124 
Diseases of the Sympathetic Nervous System 
Much light has been thrown on the anatomic structure of the sympa- 
thetic system during the past few years by Eulenberg and Guttman, Gaskel, 
Langley, Anderson, and many others. Our knowledge of the influence of 
the sympathetic on constitutional and visceral disease, while materially 
enlarged thereby is still exceedingly limited. 
The sympathetic system innervates the nonstriated muscles of the 
body, the blood vessels, the intestines, the heart and glands, and delivers 
impulses to the central nervous system from the viscera. 
From the anatomic structure and the distribution of the sympathetic 
nerve, we recognize its influence in many diseases of the vital organs. 
It cannot be considered alone in the prognosis of these innumerable con- 
ditions. 
9. Paralysis of the Cervical Sympathetic 
Causes.—Paralysis of the cervical sympathetic may follow a lesion 
anywhere in its course. The leading causes are myelitis, traumatism, 
leading to injury of the upper dorsal segments of the cord, vertebral caries, 
of tuberculous origin, metastases or tumors (aneurism) causing pres- 
sure. 
Birth palsies have occasionally included the cervical sympathetic. 
Congenital and hereditary paralyses of the cervical sympathetic have 
also been reported. 
Symptoms.—The symptoms of cervical sympathetic paralysis are con- 
tracted pupil (myosis) on the side of the lesion, narrowed palpebral fis- 
sure, sunken eye, anomalies of sweat secretion on the same side of the 
face, and often paralysis of the Klumpke type (lower brachial). 
Facial hemiatrophy and the premature change of the hair to gray on 
the side of the lesion has also been noted. 
There is a superior sympathetic center in the medulla oblorigata which 
accounts for symptoms of sympathetic paralysis in some cases of disease 
of the medulla. Besides the symptoms of sympathetic paralysis above 
noted, there is weakness of the limbs of the opposite side, tendency to fall 
toward the side of the lesion, vertigo, nystagmus and involvement of the 
muscles of phovation, articulation and deglutition. 
Prognosis.—In none of the conditions in which an organic lesion has 1082 
DISEASES OF THE NERVOUS SYSTEM 
caused cervical sympathetic paralysis does treatment exert the slightest 
influence. 
The symptoms referable to disturbance of the visceral sympathetic sys- 
tem are vague and uncertain. 
Various symptoms have been charged to sympathetic disturbance but 
the entire symptomatology is still in the realm of speculation and positive 
conclusions are not justified. Whether the sympathetic is the cause of 
gastric crises and other visceral and distant symptoms of tabes, is also 
problematic. 
The influence of the sympathetic in exophthalmic goiter and supra- 
renal disease has been differently interpreted and is also unsettled (See 
separate consideration of both diseases). 
10. Irritation of the Cervical Sympathetic 
Irritation of the cervical sympathetic causes the following symptoms 
which are the opposite of paralysis, and include mydriasis (dilated pupil), 
widened palpebral fissure, prominent eyeball, and delay in the lowering of 
the eyeball (Graeffe symptom). 
(For a full consideration of the influence of the sympathetic system on 
symptomatology without positive conclusions but with abundant references 
to recent work, the reader is referred to Holmes’ article in Volume VII, 
Allbutt and Bolleston’s System of Medicine, second edition, pages 
492-500.) 
11. Vagotonia 
Included in the functional disturbances attributed to altered function 
or a changed reciprocal relation of the sympathetic system and the pneumo- 
gastric nerve, Eppinger and Hess have called attention to the fact that 
there are individuals who react abnormally to drugs which influence the 
vagus or the sympathetic, and they speak of these as vagotropic and sym- 
pathicotropic, respectively. 
Normally pilocarpin (0.01 gm., 1/6 grain) produces hyperidrosis, sali- 
vation, hyperacidity, eosinophilia, slows the pulse, and causes spastic con- 
stipation. 
Atropin paralyzes the pneumogastric, hence has the opposite effect of 
pilocarpin, causing rapid pulse and pupillary changes with dryness, etc. 
There is a reciprocal relation which continues the normal balance or tone. 
With the vagotropic disposition there is a powerful idiosyncrasy, over- 
sensitiveness to pilocarpin,. and the symptom complex of vagotonia, 
which is a true neurosis and is associated with a marked neurasthenic pre- 
disposition results. The symptoms of vagotonia are contracted pupil, 
bradycardia, asthma, laryngeal spasm, gastrosuccorrhea, pyloric spasm, 
vagotonic conditions of the stomach shown by x-ray examination, mucous DISEASES OF THE SYMPATHETIC SYSTEM 
1083 
colitis, and obstinate constipation; all of these symptoms are favorably 
influenced by atropin, and these patients show a high tolerance for adrena- 
lin and the carbohydrates. 
In all of these cases before giving a favorable prognosis, so far as life 
is concerned a cautious differentiation is necessary, as paroxysmal brady- 
cardia and some of the associated symptoms may be caused by organic 
lesions—among these, Stokes-Adams disease and myocardial degeneration, 
arteriosclerosis, and cerebral lesions. 
Life may not be materially shortened by uncomplicated vagotonia, but 
it is a condition which is likely to be chronic and recurrent. Most of my 
cases in which I originally made the diagnosis were finally found to be 
of organic origin, due to one of the above mentioned conditions. 
Sympathicotonia is associated with the opposite symptoms, i. e., tachy- 
cardia, adrenalin glycosuria, and adrenalin mydriasis. In these cases 
pilocarpin is without effect and fails to produce the physiologic symptoms 
above mentioned. 
The entire subject of vagotonia and the opposite condition, sympathico- 
tonia are under consideration by the profession, and while there is much 
which tends to prove the contentions of Eppinger and Hess that there 
are vagotropic and sympathicotropic individuals, positive anatomic lesions 
must always, as already suggested, lead to the thorough consideration of 
the suggestive symptoms and great caution must he used in determining 
the tolerance of the patient to the drugs—particularly adrenalin—which 
may, in large doses, lead to pulmonary edema and emboli in the liver and 
mesentery. 
Bergman and Curschmann have also called attention to the dangers 
associated with the use of adrenalin in large doses. 
The prognostic significance of the many other conditions referable to 
the sympathetic nervous system are considered in connection with neuras- 
thenia, hysteria and the trophoneuroses to which the reader is referred. 
12. Sympathicotonia 
References 
Anderson (H. K.). J. of Physiol., 1902, xxviii, 510. 
Bergman & Curschmann. Ztschr. f. Neurol., Bd. xlv. 
Eppinger & Hess, von Noorden’s Sammlung klin. Abhand. Berlin, 1910. 
Eulenberg & Guttman. Die Path. d. Sympatheticus. Berlin, 1873. 
Gaskil. Allbutt & Rolleston’s System of medicine, vii, 492. 
Holmes. Article in: Allbutt & Rolleston’s System of medicine, vii. 
Langley. Schaefer’s Textbook of physiology. 1900. 
Ergeb. d. Physiol. 1903. 
RoUeston. System of medicine, 2d ed, 492-500, Section VIII 
Diseases of the Locomotor System 
A. Diseases of the Muscles 
1. Myalgia—Myositis 
{Muscular Rheumatism) 
Causes.—Myalgia, or muscular pain, is probably due to a mild form 
of myositis in most cases. There are individuals who are predisposed to 
myalgia on slight cause, in whom it may be safely assumed that there is 
some metabolic fault or toxemia. Trauma, exposure to cold, syphilis, and 
acute infections are among the causes of myalgia. 
The Myalgias.—The occupational myalgias are also of myositic ori- 
gin (piano and violin players, shovelers, molders, and a score of other 
occupations). 
Lumbar myalgia or lumbago is frequent in those predisposed, as is 
also the cervical variety. In some lumbar and pectoral myalgias, anemia 
is a pathogenic factor, and in women, there are reflex pains in the muscles 
of the body which are due to menstrual anomalies or diseases of the gen- 
erative organs. 
Prognosis of the Myalgias.—The prognosis of the myalgias is good. 
The disease yields to rest and local treatment in from two to four days in 
most cases. Recurrence is the rule. The cause naturally influences the 
prognosis. 
In gouty, diabetic, and so-called rheumatic patients, also with arterio- 
sclerosis, there are those in whom some muscles are almost always tender 
and in whom the movement of these is exceedingly painful. There are 
also patients in whom parts of a muscle are found tender on deep pressure 
(uMuskelschwiele”) which massage relieves temporarily. These cases are 
only cured or relieved when the underlying fault is unearthed and removed. 
Myositis.—True myositis is not a frequent disease; it may be local- 
ized or general. With the infections there are often symptoms of poly- 
1084 DISEASES OF THE MUSCLES 
1085 
myositis. Among the diseases in which muscle pains are severe are 
trichinosis, smallpox, Asiatic cholera, also influenza. 
Dermatomyositis and neuromyositis are rare. In the former the myo- 
sitis is multiple and there is more or less dermatitis and edema, fever 
and constitutional disturbances and absence of reflexes; in the latter there 
is a mixture of neuritis and myositis. When there are complicated serious 
diseases—such as tuberculosis—the prognosis is grave. In the idiopathic 
dermatomyositis the prognosis may be ominous, though most cases recover. 
The mortality is 20 per cent. 
When the heart muscle (myocarditis hemorrhagica) is involved the 
prognosis is correspondingly bad. 
When the disease is without known cause, trichinosis should always be 
suspected. Neuromyositis may at times prove to be a forerunner of pro- 
gressive muscular atrophy. 
Gummata of the muscles yield to treatment (See Syphilis). 
Abscess of the muscle offers a good prognosis unless multiple and de- 
pendent on malignant infection. 
2. Progressive Myositis ossificans 
Myositis ossificans is a rare disease in which there are periods of more 
or less fever and evidences of local muscular inflammation followed by the 
deposit of bone tissue in the muscle. There are repeated exacerbations 
—almost always febrile, always associated with evidences of fresh myosi- 
tis, which in turn are followed by fresh deposit of bone. The disease usu- 
ally begins in the back and neck muscles. When progressive—the usual 
tendency—uninfluenced by treatment, it may involve most of the volun- 
tary muscles of the body, causing malformations and limiting the useful- 
ness of the patient. 
The symptoms of the acute exacerbations may persist several days or 
weeks. 
3. Thomsen’s Disease 
{Myotonia) 
Thomsen’s disease is a 'primary myopathy in which voluntary move- 
ment is checked by a spasm of the muscles. 
The disease was first described by Thomsen, in whose family it has 
continued during four generations, and includes over twenty cases. 
There are occasional cases not hereditary; in some of these the symp- 
toms disappear without being reproduced in the offspring. Male children 
are oftener afflicted than female; the symptoms begin during the first years 
of life. 
The muscular development is good; at times there is overdevelopment 
but there is almost always muscular weakness. 1086 
DISEASES OF THE LOCOMOTOK SYSTEM 
The spasm—rigidity of the muscle on voluntary movement—always 
remains the characteristic of the disease and this continues during several 
seconds. 
The reflexes are not changed, neither are there sensory symptoms. 
The myotonic reaction of Erb is present in which the muscular con- 
tractions caused by either the faradic or galvanic current are abnormally 
slow and relax gradually, while the wavelike contractions pass from the 
negative to the positive pole. Weak faradic current causes tonic con- 
traction which continues abnormally long. There is no reaction of degen- 
eration. The spasm is increased by excitement or hurry. 
The disease does not shorten life; it remains uninfluenced by treatment 
and shows no tendency to progress. As the children grow, they learn to 
accommodate themselves to the spasm; occasionally there are periods of 
remission. 
In some cases there are psychic disturbances, epilepsy, migraine, and 
congenital anomalies, which are persistent. No treatment influences these 
complications materially. 
4. Paramyoclonus multiplex 
(.Myoclonia) 
Friedreich, in 1881, first called attention to this disease in which 
there may he continuous or 'paroxysmal contractions of the muscles of the 
extremities—usually in males. The contractions are usually short and 
clonic with fibrillary tremor following in some cases. They are symmetri- 
cal without changed electric reaction, and are increased by emotion, fright 
and exhaustion, Exercise tends to decrease the spasm. 
The reflexes are slightly exalted. There are no associated symptoms 
referable to the nervous system. 
Only rarely arc the contractions tonic or severe; when they are, the 
differentiation of the disease from epilepsy will be necessary and easy, as 
the spasm may be sufficiently severe to throw the patient. 
Myoclonus seems to he a family disease, particularly those forms which 
are epileptoid in character, which Unverricht described, also Jacobsohn. 
The spasms cease during sleep and are uninfluenced bv treatment. 
The disease is without effect on the general health of the patient. 
5. Akinesia algera 
Moebius described a complex which is characterized by such extreme 
pain as to lead to unwillingness of the patient to move the muscles of the 
body; it leads to chronic invalidism during which the patients are bed- 
ridden much of the time. DiSEASES OF THE MUSCLES 
1087 
There is no known pathologic cause. 
The patients are usually neurasthenic, hysterical individuals, often 
depressed and hypochondriacal. In a case recently seen there were no 
movements of any muscles, including deglutition, which the patient did 
not fear to make because of the pain. The pains continue for several min- 
utes after the muscles are used. These patients hesitate long before at- 
tempting to move or act. There is no paralysis. 
Moebius and Erb relegate the pains to the psychalgias. 
Whatever the cause or pathology, the complex is associated with great 
suffering, including mental pang; the patients are practically helpless 
when in the advanced stage—because no attempt is made to move any 
part of the body and only the necessary acts are performed to maintain 
life, and for these repeated suggestion and encouragement are required. 
The eve muscles are involved in the psychalgia which leads the patient 
to lie with the eyes closed most of the time. One of my cases developed 
photophobia with intense pain and emaciation because of the dysphagia 
and her fear of taking food. 
My material includes two cases: one has been bedridden over twenty 
years, without the slightest improvement, extremely emaciated, taking 
only sufficient food to sustain her; the second case has advanced in six 
years so that there is fear of all movement, tachycardia, and psychasthenia. 
With increase of symptoms and advance of the hypersensitive condition 
of the muscles, the fear of impending death has in the second case been 
among the most annoying of the symptoms. In this case repeated lumbar 
puncture and Wassermann reactions have given no clue to a pathologic 
change. 
Occasional cases recover under the influence of suggestion, painstaking 
and long continued supervision, even after advanced akinesis, but only 
when the patients are removed from their usual surroundings. In a num- 
ber of cases death is caused either by complicating infection, other com- 
plications, or with marasmus and extreiffe asthenia; the end follows years 
of suffering. Akinesia algeria is comparatively rare, in over 6,700 in- 
dexed cases of internal disease, I found but two well pronounced exam- 
ples of the complex. It is always to be considered of grave import. 
Friedreich. Virchow’s Archiv, 1881, Bd. Ixxxvi. 
Jacobsohn. Klinik d. Nervenkr., Berlin, 1913. 
Moebius. Ztschr. f. Neurol., Bd. i-ii. 
Oppenheim. Lehrb. d. Nervenkrank., 1913, ii. 
References 1088 
DISEASES OF THE LOCOMOTOR SYSTEM 
B. Diseases of the Joints 
Destructive Chronic Polyarthritis 
(a) Arthritis deformans 
{Rheumatoid Arthritis) 
(b) Chronic Articular Rheumatism 
(a) Arthritis deformans, or chronic rheumatoid arthritis, and (b) 
chronic articular rheumatism are so closely allied pathologically and clin- 
ically that many consider their differentiation impossible. “Chronic rheu- 
matism” is a term which should he discarded, and I have therefore 
considered it wise to classify these kindred conditions under the head of 
Destructive Chronic Polyarthritis. 
The type usually known as arthritis deformans is a chronic progres- 
sive joint affection, in all probability at first a chronic inflammation in- 
volving the articular cartilages, periarticular tissue, ultimately changing 
the bone structure and the joint as a result of progressive hypertrophy 
with changes in the synovial membranes, all of which are associated with 
loss of function and deformity leading to misshapen joints and associated 
muscular atrophy. 
Herberden, in 1804, recognized arthritis deformans as different from 
gout and rheumatism. ISTo benefit can come from an attempt in the pres- 
ent state of our knowledge to differentiate cases of arthritis deformans in 
practice from those cases of so called “chronic rheumatism” because the 
latter is a misnomer; the conditions, as in the former, are due to infec- 
tion, and while in some the lesions are limited to the fibrous structures of 
the joint, as the process advances slowly, arthritic changes follow which 
parallel true arthritis deformans. I therefore exclude “chronic rheu- 
matism” from consideration betieving that the deforming arthritides 
should include all such cases as are not classified under the acute or sub- 
acute infectious polyarthritides (See Infectious Diseases) and prefer their 
characterization as “destructive polyarthritis.” 
Etiology and Pathology.—The profession is passing through a transi- 
tion period so far as the etiology and pathology of arthritis deformans 
are concerned. The results of recent investigations justify the conclusion 
that the overwhelming number of joint conditions which have in the past 
been considered of “doubtful origin,” known as arthritis deformans, are 
secondary and dependent upon a focus somewhere in the body, which in 
many cases can be discovered and attacked. On the other hand there are, 
comparatively considered, a large number of cases in which the joint 
symptoms are the same as in those cases in which a primary focus of infec- 
tion is discoverable, in which careful search fails to give the slightest clue DISEASES OF THE JOINTS 
1089 
of the cause and the disease remains uninfluenced, stationary, or the multi- 
ple invasion of joints progresses. 
Causes and Sources of Infection.—For purposes of prognosis it is 
safest to assume that all forms of the disease are infectious, that the the- 
ories advanced in the past which included a close relation of the far-reach- 
ing changes with rheumatism and gout or an inherent tendency to joint 
changes (diathesis), faulty nutrition, tendency to characteristic degen- 
erations, changes in the nervous system (cord), and a variety of other 
causes including traumatism must he surrendered (See McCrae). Natu- 
rally the prognosis of any form of arthritis is materially improved by the 
detection of the pathogenic focus; without such knowledge the process can- 
not be influenced. The work of Rosenow, Billings, and others in this 
field proves the great importance of correlating the bacteriologic with the 
clinical study of individual cases. 
Let it he remembered that the focus may hold the streptococcus with- 
out giving rise to active local symptoms of disease. The tonsils harbor 
the germ in much the larger number of cases; often it is possible only by 
thorough enucleation to trace the infection to these, because of the sur- 
prising and almost immediate improvement which follows. 
Advancing arthritis with or without febrile movement may be traced 
by means of x-ray pictures to the dental alveoli, in which cases there are 
often no other clinical evidences of anomalies. Acting upon the infor- 
mation gained, the prognosis in these cases becomes encouraging. In over 
50 per cent there is pyorrhea alveolaris and carious teeth (Cambridge Re- 
port, etc.). Some of the results after the treatment of the local process 
have been surprisingly prompt and favorable. In one case seen while 
writing this chapter, a woman aged about forty-two, in which the disease 
was making rapid advance, the refinements of diagnosis proved alveolar 
and tonsillar infection which when radically removed, lead to almost 
immediate remission of all constitutional and joint symptoms after more 
than a year of progression. 
Infection to the joints which becomes chronic may proceed from any 
of the mucous surfaces of the body, including the gall-bladder, the intes- 
tinal mucosa, the appendix, the bladder, and the prostate gland. In the 
aged, “morbus coxarius senilis” and occasional types of “stiff spine” 
unquestionably originate in preceding infection, in which the joint changes 
were insidious, finally reaching their full development as the resistance 
of the patient is reduced. This experience I have repeatedly confirmed 
in practice when, with advancing cardiovascular or nephritic changes, 
the joints have grown progressively worse. Chronic myositis often com- 
plicates arthritis and in severe cases may be general. 
The prognosis is improved by the ability of some (by keeping in mo- 
tion) to help themselves and to influence faulty metabolism. 
&ex.—The collective investigation of the Cambridge Committee proved 1090 
DISEASES OF THE LOCOMOTOR SYSTEM 
the predominance of females over male chronic arthritis (76.5 to 23.5 per 
cent). 
Age.—Age is no bar to the disease, though children are rarely afflicted. 
In the Cambridge collection one case was found in a child 18 months old. 
The Cambridge cases gave the following ages when they first came 
under observation: 
Years. 
Number. 
Percentage. 
1-10 
4 
1.1 
11-20 
18 
5.1 
21-30 
68 
19.4 
31-40 
90 
25.7 
41-50 
64 
18.2 
51-60 
57 
16.2 
61-70 
37 
10.5 
71-80 
10 
2.8 
81-90 
2 
0.6 
Experience proves the greater frequency of the involvement of one 
large joint (hip usually) in the older subjects, while the periarticular and 
atrophic forms are more frequent in early life than is the osteitic and 
hypertrophic disease. 
Race.—McCrae has called attention to the relative immunity of the 
colored race, for which he has no explanation to offer. 
Occupation.—The larger number of my cases show slight influence of 
occupation but little of social status. Of four cases now under treatment 
which represent the average, none are living under unfavorable surround- 
ings and all have always had comfortable and sanitary homes. Unques- 
tionably many rheumatoid arthritics have been unfavorbly influenced by 
indoor occupations; in men, alcoholism has seemed to prove inviting. 
Marie’s Disease.—With spondylitis (Marie’s disease) “spondylose 
rizomyelique” traumatism is often (25 per cent) supposed to be the 
exciting factor (Wehrsig), but close study of these cases will prove that 
the condition simply required the match to kindle the fire. The frequent 
complication of tuberculosis with Marie’s stiff spine is due to the low- 
ered resistance of these patients and their inability to take advantage of, 
favorable conditions. 
Marie’s disease advances to complete stiffness of the spine; it is not 
infrequent, considering the entire number of typical forms of arthritis de- 
formans. My material includes 7 cases of stiff spine in 6,300 of internal 
diseases and 49 of the typical forms of rheumatoid arthritis. The radio- 
graph in the advanced cases shows positive and characteristic changes. 
Chronic cases will not be relieved by treatment. This is particularly true 
of the disease after middle life. Associated with multiple joint changes 
and not far advanced in young subjects in whom a focus of infection is 
discovered and removed, the prognosis is relatively good. In a number DISEASES OF THE JOINTS 
1091 
of cases the changes limited to the spine alone progress to stiffness, limit 
motion, but do not advance. Such patients learn to accommodate them 
selves to the handicap. The early detection of the disease in young 
and active subjects, in whom the cooperation of the patient can be thor- 
oughly enlisted, adds to the chances of controlling the process. Those 
with a strong will, who persist in the use of the affected parts in spite 
of acute pain, who are in a position to nourish themselves well and attend 
to metabolic faults, often control the disease satisfactorily. Naturally, as 
has been repeatedly stated, the prognosis in these cases is improved by 
the radical removal of the cause. 
Facts Which Influence Prognosis.—The neurasthenic and hysterical, 
the non-resistant, those who are burdened with an unfortunate heredity, 
are likely to fall into a condition in which they are of no assistance to 
themselves in checking the advance of the disease. There are cases in 
which, in spite of energetic and radical treatment, the disease after an 
almost acute onset remains uninfluenced and progresses to the involve- 
ment and deep changes of many joints at once. With an acute onset as 
a rule the prognosis, however, is more favorable than in the chronic 
forms. In such cases, following the subsidence of the acute symptoms, the 
progression is likely to be slow. As a rule authorities have given an un- 
favorable forecast in cases which begin at the menopause. My experience 
has been that most of these cases advance to a condition in which the joint 
structure is moderately changed and then remain stationary. 
It is exceedingly difficult to give a forecast though all data are at 
hand in the individual case, because of the vagaries of the disease and the 
variety of changes which may be included. 
In all cases the general condition of the patient remains paramount. 
This is influenced by the amount of pain suffered, the ability to use the 
extremities and jaw—making proper feeding easy—and the localization 
of the joint changes, besides the factors already mentioned. 
In the atrophic type of the disease the prognosis for restoration of 
function is bad. The joints are stiffened and malformed; hence their 
function is limited. Pain is a leading feature and makes the patient 
wretched and unable to enjoy life. He becomes depressed in consequence 
and presents a pitiful picture in contrast with the victim of the hyper- 
trophic type of the disease. - 
The hypertrophic arthritides offer a relatively good prognosis: so 
far as life is concerned it is good; so far as restoration of function, it is 
bad. These patients are not bedridden; they are often able to help them- 
selves and continue at their work, if it is not too strenuous. They often 
travel and are not discontented. The hypertrophy is likely to limit itself 
to one joint. There is no tendency to the disorganization and destruction 
of joint tissue which characterizes atrophic arthritis. 
Herberdens nodes may be present for years unchanged, and with 1092 
DISEASES OF THE LOCOMOTOR SYSTEM 
slight associated enlargement of a few smaller joints there seems to he 
no marked tendency to advance; neither do they cause noticeable incon- 
venience. 
The hypertrophic changes of the hip (morbus coxarius senilis) in 
elderly patients already mentioned remain uninfluenced when once ad- 
vanced. 
Still’s Disease.—Still’s disease is in all probability a form of arthri- 
tis deformans occurring in children, the leading features of which are 
chronic arthritis, enlarged lymphatic glands, and enlarged spleen. The 
disease is slow to progress and is periarticular—the glands and spleen are 
palpable. The prognosis of Still’s disease is not absolutely bad. I have 
seen marked retrogression of all the lymphatic glands and spleen and but 
slight final residual thickening. 
The periarticular form of the disease is the most frequent and offers 
the best prognosis for ultimate usefulness and general health, though mixed 
types are not infrequent in the same subject. 
Causes of Death.—In considering my material I have found inter- 
current infection the most frequent cause of death, in those cases which 
have progressed and become practically helpless. Pneumonia, tubercu- 
losis, cystitis with bed-sores in neglected cases, have been the leading 
causes of death. I do not in my series count a single death directly 
traceable to the disease. I have at present a patient in my wards who 
has been an inmate of the hospital and bedridden because of ankylosis over 
25 years. Ilis general condition continues good and he is the least trouble- 
some patient in my service. 
Blood and Urine.—Blood and urine analysis offer no data for prog- 
nosis in uncomplicated cases. 
Climate.—Climatic conditions unquestionably influence the comfort of 
most arthritics. A dry warm climate seems most favorable; occasionally 
the disease has been stayed by a timely change. 
Conclusion.—In offering a prognosis the attendant is never to be too 
sanguine of success in overcoming joint changes, in spite of the fact that 
he may have unearthed and removed the possible source of infection, for 
there may be multiple sources some of which remain undetected, or the 
destructive lesions in the joints are so far advanced as to offer no chance 
for improvement. 
References 
Billings (Frank). Illinois Med. J., Jan., 1914. 
Archiv. Int. Med., Chicago, April, 1912. 
J. Am. M. Ass., Sept. 13, 1913. 
Cambridge Committee. Bull., Committee for the Study of Special Dis., Cambridge. 
Jacobsohn (Eugen.). Mittheil. Grenzgeb. der Med. u. Chir. Bd. xxviii, 611, 
McCrea. Arthritis deformans. 
Osier’s Modern medicine, Philadelphia, 1909, vi, DISEASES OF THE POKES 
1093 
liosenow (E. C.). Illinois Med. J., Jan., 1914. 
J. Am. M. Ass., 1914, ii. 
Still. Med.-Chir. Tr., London, 1897. 
Allbutt’s System of medicine, 1897, Hi. 
Wehrsig. Virchow’s Archiv. Bd. ccii, 305. 
C. Diseases of the Bones 
1. Osteitis deformans 
(Paget’s Disease) 
General Statements.—Our present knowledge of the pathology of ex- 
cessive and purposeless deposits of hone is purely theoretical. We may 
finally find that these anomalies with family resemblances will he found 
with a single underlying cause, modified by varying conditions respon- 
sible for existing differences, including changes in bone of a rarefying 
nature and at the same time marked evidences of overgrowth—a combi- 
nation which is now considered characteristic of osteitis deformans. 
Virchow, in his “Krankhaften Geschwiilste,” gives a clear account 
of the many conditions in which there are bony changes now known as 
hyperostosis, leontiasis, giantism, osteitis deformans, and Marie’s hyper- 
trophic pulmonary osteo-arthropathy. Malpighi, as early as 1697, called 
attention to hyperostoses and overgrowths of the bones of the skull. 
Sir James Paget, in 1876, first furnished a systematic rehearsal of the 
symptoms and pathology of osteitis deformans. The disease has since 
been known as “Paget’s disease.” 
Paget characterized the disease in his original paper as follows: “The 
disease affects most frequently the long bones of the lower extremities 
and the skull, and is usually symmetrical; the bones enlarge and soften; 
those bearing weight yield and become unnaturally curved and misshapen. 
The spine, whether by yielding to the weight of the overgrown skull or by 
change in its structure, may sink and seem to shorten, with gradual in- 
creased dorsal and lumbar curves; the pelvis may become wide; the 
necks of the femora may become nearly horizontal; but the limbs how- 
ever misshapen, remain strong and fit to support the trunk.” 
The disease usually begins in middle life or later; its progress is ex- 
ceedingly slow—requiring many years for its full development—and does 
not usually affect the general health. The inconveniences to which the 
disease gives rise are due to the changes of shape, weight, size, and direc- 
tion of the diseased bone—as was shown in my cases (Eisner) in one of 
which the disease was not symmetrical but involved one-half the cranial 
vault (right side), including the right zygoma, the frontal, parietal, tem- 
poral, and occipital bones, directly to the median line. The left clavicle 
was three times its normal thickness; the right ilium was enormously 1094 
DISEASES OF THE LOCOMOTOR SYSTEM 
enlarged while the right femur was curved like one-half of a yoke and 
thickened. The only history which bore on the etiology of this case 
was a fall on the head early in childhood. Not all cases progress to such 
full development, and as already suggested, symmetry characterizes the 
enlargement of the hones in most cases. I have reported two cases— 
my entire experience with the disease. 
Paget gathered 23 cases before his death. Two cases were found at 
Johns Hopkins Hospital in 20,000 medical cases. X-ray pictures are char- 
acteristic. Packard and Steel have reported 99 cases of supposed osteitis 
deformans. They concluded that 66 of the 99 cases were authentic, and 
they added one of their own—41 were males, 24 females, and in two cases 
the sex was not stated. Both of my cases were females. My second case 
is the youngest reported, and was 12 when the enlargement of the rami 
of the jaws was first detected. 
The frequency of involvement of the bones of the body are in the 
order following: the skull, tibia, femur, spine, pelvis, ribs, radius, and 
ulna. 
In all cases when the skull is involved the spinal column yields and 
deformity results. The disease progresses gradually, but the deformity is 
so characteristic as to be striking. All of these patients with skull in- 
volvement look alike, just as myxedematous patients grow to resemble 
each other. 
There is a striking frequency of malignant growths with hyperostoses. 
In Packard and Steel’s cases (67) there were 5 with sarcoma, 3 carcino■* 
mata and 2 had non-malignant growths complicating. Therefore 4.5 per 
cent with cancer, and 7.5 per cent with sarcoma. 
Mentally these patients with deformities of the head become depressed; 
they withdraw from society because they are hypersensitive. Headaches 
may become unbearable; ocular and aural disturbances are not uncom- 
mon. Four of Paget’s 23 cases after many years became blind, one from 
choroiditis and three from retinal hemorrhage. 
There are as a rule in most cases no evidences of cerebral compression. 
I have found no history of a case dependent upon syphilis—none has 
been reported to yield to mercury or to the iodid. 
Diffuse hyperostoses which cause narrowing or closure of the foramina 
of the skull and associated pressure symptoms, such as blindness, exoph- 
thalmos or paralysis, are not to be diagnosticated as osteitis deformans. 
There will always be a certain number of “purposeless enlargements of 
bone” in which, because of close family resemblances, accurate differentia- 
tion cannot be made early; a limited number of these will progress. 
Atrophy and absorption is the ultimate fate of the bone in most cases of 
Paget’s disease with consequent weakening of the bony structure involved, 
and compensatory strengthening by the growth of what may be looked 
upon as a variety of callus, the occasional formation of definite tumors DISEASES OF THE BONES 
1095 
and in some, fatal cachexia (Lunn). These views of Lunn are contro- 
verted by Sillock, Paget, and Butlin who lean to the theory that “the 
essential features of the osseous lesions of the disease are indistinguishable 
from, if not highly characteristic of, inflammation.” 
Duration.—Eltinge claims that “it requires from five to fifteen years 
to reach its maximum.” My cases would extend that period. ISTo treat- 
ment has the slightest influence in controlling the disease. If we adopt 
Adami’s and Aschoff’s views of the pathology that “there are two oppos- 
ing pathologic processes at work, resorption and osseous hyperplasia,” we 
must depend on nature’s compensatory provision, by which the denser 
bone is finally deposited, not entirely decalcified, to stay the disease. 
References 
Adami. Pathology. 
Aschoff. Path. Anat. Jena, 1913. 
Butlin. Eisner [l. c.]. 
Eltinge. Johns Hopkins Bull., 1901, 843. 
Eisner (II. L.). New York J. of Med., June, 1910. 
Lunn. Tr. Path. Soc., London, 1887-8, xxxix, p. 265; also 1901-1902, xxxv, 197. 
Malphigi. Opera posthuma. 1697. 
Packard, Steel & Kirkbride, Jr. Am. J. Med. Sci., 1901, 559. 
Paget (Sir J.). Tr. Med. & Chir. Soc. of London, 1876. 
Prince (M.). Am. J. Med. Sci., 1902, ii, 797. 
Sillock. Illust. Med. News, London, 1889, ii, 182-186. 
Tr. Path. Soc. of London, 1884-1885, xxxvi. 
Virchow. Krankhafte Geschwiilsten. Berlin, 1863-1867. 
2. Leontiasis ossea 
(Lion Face) 
Leontiasis ossea (Virchow) is a rare condition in which there is a 
diffuse hypertrophy of the bones of the skull, usually involving the bones 
of the face so as to give the appearance of the lion face. In the only case 
which [ have seen in practice, the young man, age twenty, was otherwise 
perfectly well. Atrophic changes commenced in the teeth (upper jaw) ; 
gradually the alveolar processes receded and the maxillae thickened evenly. 
There were no further enlargements of the bones of the skull or body. 
1 n my case there was gradual progression until the recognition of the con- 
dition was easy even by laymen, and the young man become so embar- 
rassed that he left his home town to escape his old comrades. 
There is no way of influencing the gradual progress of the hyperos- 
tosis; it does not interfere with the general health of the patient. The 
process is held by some to be one of osteitis deformans. In reported cases 
it has continued from twenty to thirty years, and longer. 
General hyperostosis of the skull (Prince) is also held to be a form of 1096 
DISEASES OF THE LOCOMOTOll SYSTEM 
osteitis deformans from which it cannot be differentiated. Prince found 
in the cases which he collected from literature (21 in all) symptoms of 
compression as the skull increased in size—particularly of the foramina— 
leading to neuralgia, blindness, deafness, bilateral facial paralysis and 
more or less trouble in chewing and swallowing; in some cases there was 
paralysis which caused marked respiratory embarrassment. Exophthalmos 
has also developed in rare cases. These cases of enlargement of the skull 
are ultimately likely to develop mental symptoms, marked depression, 
convulsions, and paralysis of the extremities. 
Prince. Tr. Ass. Am. Phys., 1902, xvii, p. 882. 
Virchow (R.). Die KrankhafteGeschwiilsten. Berlin, 1863-1867. 
For full bibliography see catalogue, Surgeon-General’s Library (Leontiasis Ossea). 
References 
3. Hypertrophic Pulmonary Arthropathy 
{Hypertrophic Pulmonary Osteopathies, Clubbed Fingers, 
Hypertrophiante pneumique) 
Hypertrophic osteopathies (arthropathies) are always secondary to 
other diseases, as was demonstrated by Marie in his study of his cases. 
The lesions within the lung were almost uniformly present; hence the con- 
dition is known as a “pulmonary osteoarthropathy.” There is a sym- 
metrical enlargement of the terminal phalanges of the fingers and toes 
with, in some cases, enlargement also of the distal ends of some of the long 
bones. 
“’Clubbed fingers” are recognized as frequent attendants of chronic 
pulmonary disease—tuberculosis particularly. Marie’s description of 8 
cases included thickening of the long bones near the joints with the char- 
acteristic deformity of the fingers and toes above mentioned. Four of 
his cases had pulmonary disease, in three the history was vague, and in 
one there was no evident relation to lung disease. Wynn found pulmo- 
nary disease in 68 per cent of his 100 cases, and Emerson quotes Alexan- 
der as having 77 of a total of 103 cases. Emerson reports 4 cases from 
the Johns Hopkins Hospital material in one of which there was empyema, 
one bronchiectasis, one chronic bronchitis and pleurisy, one with both 
bronchiectasis and pulmonary tuberculosis. 
There are cases in which congenital heart lesions and acquired valvu- 
lar defects are present without pulmonary lesions. Wynn reports 11 cases 
with hypertrophic cirrhosis of the liver. Ho tuberculous lesions need be 
expected in these cases in the changed bones. The real provoking cause 
remains problematic. 
For a full clinical history of individual cases the reader is referred 
to Thayer’s report of 1 cases from his clinic. DISEASES OF THE BONES 
1097 
As the enlargement of the bones progresses the surrounding tissues 
atrophy, and in some cases arthritis may be expected. 
Hypertrophic arthropathy is not a disease per se; its prognosis must 
depend upon the nature and extent of the primary lesion. The “club- 
bing,” which is the most constant clinical feature, does not interfere with 
the progress of the initial disease. In some cases there have been acute 
exacerbations with remissions and final long periods of chronicity, in ac- 
cordance with the history of the benign pulmonary disease. 
References 
Alexander. Emerson [L c.]. 
Emerson. The hypertrophic osteopathies. In: Osier's Modern medicine. Philadelphia, 
1909. 
Marie. Rev. de Med., 1890, x. 
Thayer (W. T.). New York Med. J., 1896, Ixiii. 
Wynn. Birmingham Med. Rev., 1904, Iv. 
4. Fragilitas ossium 
Fragilitas ossium is also considered in connection with osteomalacia. 
With fragilitas ossium there is, because of a distinct nutritional fault, a 
tendency to fracture of one or more of the long hones. The hones are 
abnormally brittle. The change which loads to fracture may be due to 
secondary changes in the bone as the result of disease, local tumor, disuse, 
senility, locomotor ataxia, rachitis, chronic joint disease, the terminal stage 
of malignancy, phosphorus poisoning, scorbutus; or the condition may be 
primary without preceding disease or local lesion. 
Deformities may result from the provisional callus following repeated 
fractures. In some cases of primary fragilitas ossium the bones, because 
of their chemically anomalous build, fracture on the slightest cause. Cases 
are reported in which as high as thirty fractures have followed each other 
in the same subject. There are no means of controlling the idiopathic 
cases. In cases of locomotor ataxia with fragilitas, I have imagined that 
the use of the lime salts (usually deficient) has been of some value. 
Cases with hereditary tendencies may lead to fractures early in life; 
the prognosis so far as preventing recurrence of fractures in such cases, is 
not good. 
Osteogenesis imperfecta.—In osteogenesis imperfecta, i. e., fra- 
gilitas ossium of the fetus, there are brittle bones which may fracture in 
utero, or there may be deformities due to the bending of bones. In such 
embryos the cranium is deformed. Death is the fate of most of these in- 
fants, though occasionally one escapes in whom with proper treatment, 
the nutritional fault is overcome and the bone growth becomes normal. 
The process of repair leads to good results in those who survive. Section IX 
Metabolic Faults 
1. Gout 
(.Arthritis urica vel uratica, Goutte (French), 
Gicht (German), Podagra) 
Theories.—To consider the theories of gout, or the chemobiology of 
the disease in all of its protean manifestations fully, is not within the 
province of this work. I can only give an abstract of the leading theories 
which deal with uric acid formation, retention, and elimination, as related 
to the disease: 
1. Garrod contends that an acute attack of gout is invariably pro- 
duced by an excess of uric acid in the blood, due to increased formation 
and greatly decreased elimination; also that inflammation is caused by 
the deposition in the joints of sodium biurate. 
2. Haig holds that there is a diminished alkalinity of the blood, and 
that the latter cannot therefore hold the uric acid in solution so that it is 
deposited in the form of urates. 
3. Ebstein thinks it probable that there is primarily a cartilaginous 
necrosis, that the deposition of uric acid from the surcharged blood is 
secondary—with associated local inflammatory changes. 
4. Sir William Roberts believed that acute attacks of gout are depend- 
ent upon the precipitation of the crystalline biurate of sodium; that the 
urate is transformed into the less soluble biurate in the blood; that normal 
blood or the blood of gout does not contain uric acid, as such, in solution. 
5. Von Noorden concludes that the essential process is a tissue necro- 
sis attributable to the presence of a hypothetic ferment, and that the uric 
acid, which is without etiologic effect, is deposited at the necrotic focus. 
6. Klemperer has shown, as the result of observations made in cases 
of gout, that so long as the function of the kidneys is not materially inter- 
fered with, the presence of considerable amounts of uric acid in the blood 
must be attributed to increased formation. The presence of an equivalent 
of uric acid in the blood in other affections, however, than gout (e. g. 
leukemia) shows that this factor is not the sole cause of gout. 
7. Mordhorst, in dealing with the pathogenesis of gout, states that in 
1098 METABOLIC FAULTS 
1099 
any alkaline liquid the basic substances combine with the uric acid, if this 
is present, to form a urate. These uratic precipitations are met in non- 
vascular tissues only, the alkalinity of which is less than that of the blood, 
and that they are the essential cause of the symptoms. 
8. Kolisch maintains that the more serious features in gout, only 
exist in the presence of impairment of the renal function. When the kid- 
neys are healthy, the alloxuric bodies are in great part increased at the 
expense of the uric acid. Chittenden and others hold, however, that the 
xanthin bases are practically free from toxic effects. 
9. Luff thinks that uric acid is formed in the kidneys from a combina- 
tion of urea and glycogen, an increased amount of the latter substance 
being formed in the liver. 
10. Brugsch and Schittenheim contend that gout is due to metabolic 
faults which interfere with the conversion of the purin bases. 
Conclusions.—The safest conclusion for the clinician to reach are that 
uric acid and the xanthin bases are derivatives from a parent substance, 
i. e., purin which possesses both basic and acid properties; further, that the 
purin bodies are characteristic products of decomposition of nucleoproteids 
and that within the body they arise from the nuclein taken with the food 
(“exogenous origin”), or they result from the katabolism of the body tis- 
sues containing nuclein (endogenous origin). Bains’ conclusions are 
founded on these chemical facts, and for treatment and prognosis deserve 
to be kept before our mental vision. He regards the “uric acid phe- 
nomenon as an important incident” in gout though the “real or essential 
factor has so far eluded detection.” The origin of the disease is probably 
in the alimentary tract. 
Definition.—I base my treatment of the p'ognosis of gout upon a 
broad definition ivhich must include its acute and chronic anomalies ivhich 
may be associated with both local and general symptoms at the same time. 
For all diagnostic and prognostic purposes gout may be defined as a 
constitutional disease characterized by the deposit of the biurate of sodium 
in crystalline form in the cartilages and textures of the joints, including 
fibrous tissues associated with attacks of acute articular inflammation, sys- 
temic disturbances due in all probability to faulty conversion of foods and 
improper elimination, often associated with grave changes in the various 
organs of the body—preferably the heart, kidneys, and blood vessels. 
Gout is therefore a chronic constitutional disease in which uric acid 
formation and elimination are disturbed because of faulty metabolism. It 
is subject to acute exacerbations with intervals of apparent health, or its 
manifestations may be continually in evidence to make the victim a 
chronic invalid. 
History.—The history of gout and its accumulated literature should 
prove of great interest to the student of medicine. Hippocrates described 
the disease 500 years B. C. Celsus during the first century of the Chris- 1100 
METABOLIC FAULTS 
tiap era Kad a clinical knowledge of the disease, and Lucian in a satirical 
comedy proved the overpowering influence of the Goddess Podagra over 
mankind. The first accurate and systematic rehearsal of the clinical his- 
tory of gout must be credited to Sydenham (1624-1689) which will always 
live as a classic in medical literature, than which there is no better guide 
to the differentiation of all forms of arthritis, nor is there a clearer presen- 
tation of the symptomatology of the disease (See Brugsch). 
Causative Factors.—Heredity.—Heredity is the most important 
causative factor of gout. My cases show a positive hereditary tendency 
in 60 per cent. Gout appearing before the age of 30 in subjects burdened 
with heredity is not thrown off. Such subjects continue gouty throughout 
life. The disease is transmitted from generation to generation, though 
occasionally a generation may be skipped. There is a strong tendency 
toward transmission through the female line of the family to subsequent 
generations. Heredity will always prove an obstacle to a favorable prog- 
nosis though years may lapse without recurrence of symptoms after the 
initial attack. 
Age.—In those who are strongly predisposed, gout may develop before 
puberty in rare instances. Sydenham and Ileberden never saw true gout 
during childhood. Ebstein has reported juvenile gout. The larger num- 
ber of cases are found during middle life (30 to 45 is the preferable 
period). It is not likely to develop after the fifty-fifth year. Of 180 men 
afflicted, Brugsch shows the percentage of first positive symptoms of gout 
as follows: 
In 3 per cent the patients were between 25 and 30 years 
In 8 “ “ “ “ “ “ 30 “ 35 ' “ 
In 21 “ “ “ “ “ “ 35 “ 40 “ 
In 40 “ “ “ “ “ « 40 “ 45 “ 
In 18 “ “ “ “ “ “ 45 “ 50 “ 
In 4 " “ “ “ “ “ 50 “ 55 “ 
In 3 “ “ “ “ “ “ 55 “ 60 “ 
In 2 “ “ “ “ “ “ 60 “ 65 “ 
In 1 “ “ “ “ “ « 65 “ 70 “ 
Sex.—Men are oftener afflicted than women; the latter when victims 
of the disease are likely to develop it after the menopaufce, when symptoms 
are often more or less continuous. 
Habits.—Habits of life are important prognostic factors. Sedentary 
habits invite the disease, particularly in those with hereditary taint. 
When such individuals add to their inactivity errors of diet, live on rich 
foods and drink immoderately, all factors are combined to invite and con- 
tinue the disease. Alcohol, particularly sherry, port wine, champagne, 
and the heavy ales, provoke the disease and acute exacerbations, particu- 
larly in the predisposed. The distilled spirits are better borne than are 
the heavy wines, METABOLIC FAULTS 
1101 
Idiosyncrasies to certain foods are frequent in the gouty. Tlie study 
and rational treatment of such cases will often prevent the persistence of 
atypical symptoms and the recurrence of regular attacks of acute gout. 
A diet composed largely of carbohydrates and proteids (including purin 
bases) with improper exercise and faulty ventilation may include the un- 
derlying exciting cause of symptoms. Overeating will certainly prove an 
important factor which, when discontinued, often changes the picture 
satisfactorily. The English, probably because of their excessive beef 
eating and ale drinking, are more subject to gout than are the Americans. 
It is less prevalent in Germany than in England. 
Lead Poisoning.—Garrod reports that 33 per cent of his cases had 
lead poisoning. Oliver noted that “lead workers in the southern part of 
England developed gout in the northern part of England, whereas the 
natives under the same conditions seldom became gouty even though the 
kidneys were affected.” Bain noted: “In districts where gout is un- 
known, the disease does not appear to be provoked by lead poisoning, but 
gouty persons are particularly susceptible to the influence of lead even in 
medicinal doses.” 
Loivered Standard of Health.—Gout is, in the gouty, hastened by the 
lowering of the standard of health, by depression, grief, sorroiv, continued 
worry; fatigue has been a frequent cause of recurring symptoms. Faulty 
homes, continued living in damp houses and exposure to wet arid cold, 
and in some, minor factors without effect on those with normal resistance, 
prove sufficient to aggravate existing latent gout to activity or to cause 
acute attacks. 
Gout may be: 
(a) Acute gout 
(b) Chronic gout 
(c) Irregular (abarticular gout—metastatic gout). 
(a) Acute Gout 
Initial Symptoms.—The initial symptoms of acute gout are fiery and 
painful; there is usually considerable febrile disturbance; the “sthenic 
condition” is predominant, while the local manifestations are characteris- 
tic. These symptoms, while associated with some acceleration of the pulse 
and often increased tension, with temperatures between 101° to 103° F. or 
higher, are without serious import and yield in the course of a few days. 
The urine is concentrated and reduced in quantity, may even contain 
albumin with an occasional cast (hyaline or epithelial), in a subject who 
before had no urinary anomaly. The prognosis under these conditions 
without added complication is good. 
In my experience added, infection or serious complication during the 
persistence of acute exacerbations of gout has been exceedingly rare. METABOLIC FAULTS 
1102 
Evidences of Approaching1 Remission.—The evidences of approaching 
remission include free perspiration, increased urinary secretion, fall of 
temperature, relief from the severe pain and local joint swelling. 
Course of the Disease.—The prognosis is best for prompt subsidence 
of symptoms in monarthritic cases (big toe usually) which commenced 
with free outspoken symptoms, usually high temperature. When, as 
occasionally happens, one large and severalosmaller joints are acutely at- 
tacked, the symptoms yield slowly. The limitation of acute gouty inflam- 
mation to the smaller joints of the hands and feet is not frequent; when it 
appears, convalescence is slow. In over 70 per cent of my cases the joint 
changes during the initial acute attack were limited to the first metatarso- 
phalangeal articulation of the big toe. Following the acute attack, the 
patient may appear to be in perfect health; will be able to return to his 
work somewhat reduced in flesh but without permanent damage to the 
joint, though it may continue tender during several days or weeks. 
Duration.—The average duration of the acute attack is between three 
and six days. Acute exacerbations in chronic cases are likely to recur; 
it is impossible to foretell when these acute exacerbations will recur. 
There are patients who always have “twinges,” who have insignificant or 
persistently annoying evidences of chronic and irregular gout, who may 
live during many years without acute joint symptoms. On the other hand, 
patients with evidences of persisting atypical gout may at short intervals 
develop acute gouty arthritis—limited to one or more joints.. In some, 
there are no “interval symptoms” of gout, but recurrence after short res- 
pite cannot be prevented. 
In cases of recurring arthritis the joint structure shows organic change 
and chronic gouty arthritis develops to continue during life. When such 
changes have followed, tophi, the characteristic sodium urate deposit of 
gout, will be found studding the ear (helix) and other parts of the body. 
The shorter the- interval between the attacks, the longer the acute ex- 
acerbations, the more likely are organic changes in the joints to follow. 
With associated irregular gout in the intervals, with cardiovascular and 
renal complications, the worse is the prognosis for full restoration to 
health. 
Determining Symptoms.—Persistent albuminuria with high blood 
pressure, or the latter alone with slight hypertrophy of the left ventricle, 
must lead to the suspicion of associated nephritis—probably interstitial— 
and the prognosis given accordingly. The urine analysis is of great value 
in the prognosis of the acute attack. With diminution of uric acid and the 
alloxuric bodies in the urine of the gouty individual which has been cau- 
tiously watched, an acute attack may be anticipated; with the reappear- 
ance of the normal balance or the increase of uric acid output the attack 
may be expected to yield. Naturally during the attack the uric acid of 
the blood shows increase (Garrod thread test) (Maase-Zondek Test). METABOLIC FAULTS 
1103 
The acute attack may occasionally lead to recognizable anemia, which 
is not likely to continue long. This is more likely to follow after repeated 
attacks at short intervals and should always arouse a suspicion of possible 
nephritis. 
During the acute exacerbation there is usually some leukocytosis with 
moderate eosinophilia. Polycythemia in obese and plethoric subjects has 
been noted; these are often without satisfactory resistance. DaCosta re- 
ports one case in which the red blood corpuscles numbered 7,125,000 in 
the e.mm., the whites 14,000, hemoglobin 100 per cent, and myelocytes 4 
per cent. 
(b) Chronic Gout 
As already suggested, acute gout may lead to a chronic gouty state in 
which repeated acute exacerbations are to be expected. Chronic articular 
gout is a persistent arthritis in which the joint structure is changed, and 
never returns to a normal condition. In most cases of chronic gout there 
are extra-articular lesions which are included in the complex of irregular 
gout, and the length of life in such cases depends more upon the associated 
lesions than upon arthritic changes. 
With limitation of gout to the joints and hut slight cardiovascular or 
renal disturbances, these patients may live for years in comparative com- 
fort. Indeed, IIeberden’s nodes with limited change in joints may argue 
in favor of the long life of such gouty subjects. 
Ulcerative articular processes in chronic cases, unless leading to sepsis, 
may heal or remain without bad results. Such processes are usually 
limited. 
The disorganizing and destructive changes within the joint are perma- 
nent. The extent of the joint changes naturally influences the life of these 
subjects and with marked pain, tenderness, swelling, distortion, destruc- 
tion, and added irregular gouty symptoms, they may become bedridden or 
so handicapped as to make locomotion impossible. 
The assistance which x-ray examination gives for prognosis may be 
valuable in such cases as are associated with cardiovascular changes and 
other symptoms suggesting renal calculus, in which positive diagnosis for 
relief of the accompanying and threatening complications becomes neces- 
sary. 
Anchylosis and muscular atrophy remain practically uninfluenced by 
treatment. 
(c) Irregular Gout 
(Abarticular Gout) 
Gout may affect almost any organ of the body without showing change 
in a single joint. This is not the rule but it is oftener true than is 
generally believed by the average clinician. 1104 
METABOLIC FAULTS 
Complications.—Gouty disturbances of the nervous system (neuras- 
thenia, neuritis) recognized early and radically treated offer an excellent 
prognosis (See Neurasthenia). Migraine of gouty origin is controlled 
with great difficulty—often entirely uninfluenced. Arterial degeneration 
resting upon a long-continued gouty fundament is a frequent complica- 
tion and in uncontrolled cases is associated finally with ventricular hyper- 
trophy and kidney involvement (chronic gouty kidney—chronic inter- 
stitial nephritis). The prognosis of these conditions is separately consid- 
ered. When lesions are advanced it is unfavorable. Patients with “gouty 
hearts and kidneys” may live many years in comfort, even to old age, with 
proper care. They demand watching and always stand on the edge of a 
precipice. 
The small trace of albumin with an occasional hyaline cast in the 
patient after fifty, who may or may not be of gouty habit (usually he is) 
may prove beneficial, for it often leads to right living with consecutive 
prolongation of life. 
Irregular gout including any of the preceding complications, with 
myocardial degeneration, with coronary or mesenteric sclerosis, with dia- 
betes mellitus (a frequent complication of gout in such subjects) offers an 
unfavorable forecast. Diabetes mellitus in obese, gouty subjects without 
other serious complications does not lead to early death when recognized 
and rationally treated. Some of these subjects reach old age. That the 
presence of the diabetic condition is a handicap, camiot be denied. I 
have seen patients with gouty kidneys, low specific gravity urine, live to 
old age. Complications (uremia, pneumonia, and other infections) are to 
be feared. Amyloid disease develops in some—it is always fatal and 
general. 
Gout, as it influences digestion—gouty dyspepsia—is usually second- 
ary to some other condition—hyperacidity or faulty renal elimination. It 
may be functional and associated with marked neurasthenia. Tb*3 prog- 
nosis depends upon the ability to regulate tlm patient’s life and mental 
processes. 
Pyrosis, flatulence, constipation and other gastrointestinal symptoms 
are in most cases easily and favorably influenced. It is surprising to 
note how the relief of constipation or an occasional free catharsis improves 
the gouty subject during a considerable period. The functional symptoms 
referable to the heart in irregular gout are usually relieved by the treat- 
ment of the gastro-intestinal tract and attention to the urinary secre- 
tion. 
The skin lesions of gout are often rebellious, but in the end are likely 
to yield to rational living and proper diet. Recurrences are frequent, 
often during long periods. They include eczema, erythema, urticaria, 
pruritus universalis et genitalia. 
Stone in the bladder and kidney of gouty origin offers a favorable fore- METABOLIC FAULTS 
1105 
cast when recognized early, in the presence of a good resistance and the 
absence of cardiovascular and renal changes. 
Gouty subjects with enlarged, prostates and cardiovascular changes, 
also nephritis (interstitial), do not bear prostatectomy well and often die 
within the fir§t twenty-four or forty-eight hours following operation, with 
evidences of deep uremia. 
Gouty bronchitis, asthma, and emphysema are best influenced by cli- 
matic change. Often they continue rebellious to any other treatment. 
Pericarditis may prove an occasional serious complication. The changes 
in the endocardium are less likely to be of inflammatory than degenerative 
origin and are a part of the arteriosclerotic process. 
Tuberculosis may be invited in the gouty subject, particularly the 
younger with bad heredity, who early develop deep joint changes and who 
live under unfavorable conditions. Tuberculosis in gouty subjects is likely 
to have early hemoptysis which may not recur; in gouty subjects it is, as a 
rule, exceedingly chronic (See Stockvis, Pollock, Pye-Smith and Moore). 
Moore reports, in 80 gouty patients, 3 gall-stones and 6 with pul- 
monary tuberculosis. 
Gall-stones and cirrhosis of the liver have been noted in a compara- 
tively large proportion of cases (Murchison). 
Gouty invasion of the eye is often slow to yield; is subject to recur- 
rence; may lead to adhesions (iritis), and with arterial involvement, to 
retinal hemorrhage. The inflammatory conditions as a rule are fully 
healed. 
References 
Bain. Textbook of Medical Practice. London, 1904. 
Brit. Med. 1900, i. 
Brugsch (Theo.). Gicht, Spec. Pathol, u. Therap., etc,, 1913, Lieferung I-IV. Wien it. 
Berlin. 
Brugsch & Schittenheim. Gicht, etc. Jena, 1910. 
Celsus. De re Medica libr. 8°. 2d ed. 1665. 
Da Costa (John C., Jr.). Clinical hematology. Philadelphia, 1905. 
Duckworth (Dyce). Treatise on gout. London, 1889. 
Epstein. Gicht, etc. Wiesbaden, 1906. 
Fothergill. The relations of gout to diseases of the heart. Birmingham Med. Review, 1877, 
vi, 40-49. 
Garrod {A. B.). Treatise on gout and rheumatic gout. London, 1876. 
Haig. Brit. Med. J., 1888, ii. 
New York Med. Rec., 1901, lix. 
Uric acid, etc. London, 1898. 4th ed. 
Heberden. Brugsch [l. c.]; also Gigon. In: Mohr u. Staehelin’s Handbuch der inneren 
Krankheit. Bd. iv. 
Hippocrates. Prognostics, etc. 
{Adams Ed., Transl. London-Sydenham Soc., 1849.) 
Hoffman. Lehrbuch der Konstitutions Krankheiten. Stuttgart, 1893. 
Klemperer. Ztschr. f. klin. Med., Berlin, 1895, Bd. xxvii. 1106 
METABOLIC FAULTS 
Kolisch. Allgem. Wien. med. Ztg., 1895, xl. 
Lucian. Brugsch [Z. c.]. 
Luff. Gout, etc. London, 1898. 
Lancet, London, 1897, i. 
Murchison. Clinical lectures on the diseases of the liver. New York, 1877. 
Moore. Pathol. Soc. Tr., London, xxxiii. 
Mordhorst. Pathogenesis of gout. Lancet, London, 1897, ii. 
Maase & Zondek. Munch, med. Wchnschr., 1915, Ixii, 1110. 
von Noorden. Samml. klin. Abhandl. uber Path. u. Therap. der Stoffwechselk., 1909, II 
7 & 8. 
Pollock. Elements of prognosis in consumption. London, 1865. 
Pye-Smith. Guy’s Hosp. Rep., London, 1874. 
Roberts (Sir William). Croonian Lectures. London, 1892. 
Urinary and renal diseases. Philadelphia, 1885. 
Stockvis. Centralbl. f. med. Wissen., 1875, 801. 
Sydenham. London, 1763. 
Sydenham Soc., etc. Tractus Podagra, 1681, in Opera Universa. 
2. Diabetes mellitus 
General Considerations.—Whenever there is faulty metabolism de- 
pendent upon organic changes in one or more organs, discoverable or not, 
with more than 0.2 per cent of glucose in the blood and more than 0.1 per 
cent—0.2 per cent in the urine, both persistently present, it may be safely 
concluded that the patient is suffering from diabetes mellitus. 
In considering the prognosis of diabetes mellitus there are a number 
of underlying facts which deserve accentuation: 
Our exact knowledge of the most important facts bearing upon the 
chemo-biologic processes and pathologic anomalies which perpetuate glu- 
cosuria and which finally lead in most cases, to innumerable symptoms, is 
limited. 
We do know that the liver stores carbohydrates to convert them into 
glycogen to be ultimately delivered to the blood as glucose (grape sugar), 
thence to the tissues for final oxidation (Claud Bernard). This theory 
has never been successfully controverted. 
An excess of intake of sugar may produce glucosuria (See Alimentary 
Glucosuria). Claud Bernard established the fact that lesions of the floor 
of the fourth ventricle in the medulla produced hyperglycemia and glu- 
cosuria. We know that nervous influences increase symptoms in diabetics; 
we do not know whether without added alimentary conditions a true 
chronic neurogenous diabetes can persist. 
Factors in Producing Glucosuric Condition 
Pancreatic Disease.—Pancreatic disease or injury is the most con- 
stant pathologic attendant of diabetes mellitus; the usual change is a far- METABOLIC FAULTS 
1107 
reaching fibrosis, though other pathologic processes both acute and chronic 
may lead to the symptom complex. 
Opie, von Mehring, and Minkowski have established the fact that 
glucosuria may be produced experimentally by the removal of the pan- 
creas ; particularly the “islands of Langerhans” which furnish an internal 
secretion needed for the normal conversion of carbohydrates. There are 
but few, ‘probably no cases of diabetes mellitus without pancreatic insuffi- 
ciency. For prognosis it is important to recognize the fact that in children 
there is (as von Noorden holds) progressive atrophy of the islands of 
Langerhans. Hence the prognosis is bad during early life. In adults, 
pancreatic function may during limited periods be restored, the process of 
fibrosis or degeneration may remain stationary, or there may be compensa- 
tory changes which lead to material improvement; under stress or inju- 
dicious diet glucosuria may return, but it may be absent during encourag- 
ingly long periods. 
Adrenalin.—Herter established the relations of the suprarenal sub- 
stance (adrenalin) to glucosuria. He found that if the pancreas is painted 
with a solution of adrenalin chlorid a transient glucosuria results with 
corresponding glycemia, while no glycemia or glucosuria follows a similar 
application to the spleen or liver. Once the chlorid undergoes oxidation 
the power to produce glucosuria or to raise blood pressure is lost. Adrena- 
lin poisoning causes granular degeneration of the islands of Langerhans. 
Glucosuria is not uncommon with suprarenal disease. 
Diabetes Bronze.—Diabetes bronze, a condition which is fatal, in 
which glucosuria is present with pigmentation of the skin and cirrhosis 
of the liver or other productive changes, is uniformly associated with pan- 
creatic anomalies (See Aschoff) and hemochromatosis. Suprarenal 
secretion is intimately concerned in the control of liver function. “It is 
the second of the guards placed over the liver which regulate the excita- 
bility of the sugar factory” (von Hoorden). 
Disease of the Hypophysis.—Disease of the hypophysis (Cushing) 
particularly tumors, acromegaly and trauma may cause glucosuria. Cush- 
ing has demonstrated experimentally the influence of the posterior lobe 
of the pituitary in carbohydrate metabolism. 35 to 40 per cent of 
acromegalics show sugar (Borchardt). 
Administration of Thyroid Extract.—The association of glucosuria or 
true diabetes mellitus with exophthalmic goiter and the production of 
glucosuria following the administration of thyroid extract are frequent 
occurrences, von Noorden says “probably the parathyroids also stand in 
metabolic relationship to the pancreas.” 
Diseases of the Liver.—Most diseases of the liver in which glucosuria 
persists are associated with pancreatic disease (organic usually). Naunyn 
has observed cases without pancreatic lesions. I have seen cases in which 
recurring glucosuria was present with gall-stones which disappeared after 1108 
METABOLIC FAULTS 
operation or passage. Acidosis is not a frequent accompaniment of dia- 
betes, which seems to depend upon liver degeneration. 
Traumatism.—When traumatism has seemed to be a factor in the pro- 
duction of glucosuric conditions brain injury has, in my experience, been 
the cause. Grave symptoms of fracture or concussion have been prompt, 
sugar Avas demonstrable early, and the course of the disease rapid. With- 
out evidences of grave injury the presence of sugar may be attributed to 
preceding disease:. 
Skeletal Muscles—Proteid and Fat.—Sugar does not provide the only 
source of glucose in the blood for it may be formed from, the proteid and 
fat elements ingested ; in diabetes, particularly in the malignant types, also 
during starvation, the skeletal muscles and the remnant of fat furnish it 
under the “changed metabolic relations.” “The liver uses fats for the 
purpose of forming sugar only when the poverty of other materials makes 
it necessary” (von Xoorden). These facts have an important bearing on 
prognosis, particularly as it is related to the rational dietetic treatment of 
the individual case. 
Negative Factors 
Kidney.—Probably the kidney itself is not an important factor in the 
production of glucosuria. With pliloridzin poisoning or its injection into 
animals (pliloridzin glucosuria), when renal lesions are present as the 
only accompaniment of organic change, there is never hyperglycemia as 
in ordinary diabetes mellitus. The kidney has simply lost its ability to 
prevent glucose elimination. The presence of nephritis in gouty subjects 
with diabetes mellitus does not argue in favor of the former (nephritis) 
as the provocative factor in causing the latter; both are dependent and 
secondary to the same constitutional fault, though one may aggravate the 
other and influence the prognosis. 
Contagion.—In spite of Senator’s suspicions, diabetes mellitus can 
never he considered to be contagious. The reports showing the relative 
frequency of the disease in husband and wife may for our purpose be 
considered coincidence only—possibly dependent at times, upon the same 
improper diet or other unknown factors. 
Alimentary Glucosuria 
There are transitory forms in which the urine, during limited periods, 
and the blood as well, contain more than the normal sugar content known 
as glucosuria—of which alimentary glucosuria is the most prominent 
example. 
Tolerance.—The tolerance to assimilate sugar is not the same in all 
subjects. Persistently loto tolerance is abnormal—occasional intolerance 
may not be. When there are repeated evidences of intolerance (re- METABOLIC FAULTS 
1109 
peated alimentary glucosuria), particularly in those predisposed (heredity, 
etc.) cautious watch should he instituted, for finally in the majority of 
these cases diabetes mellitus develops. Prognosis of repeated alimentary 
glucosuria must be guardedly given and only after a sufficient period of 
observation which leads to the determination of the tolerance of the sub- 
ject, which is not always the same even under normal, and unchanging 
conditions. Hofmeister, however, holds that for the same individual and 
the same carbohydrate, the tolerance varies so little as for practical pur- 
poses to be considered unchanging. 
Large quantities of sugar given on an empty stomach to normal indi- 
viduals will produce glucosuria promptly, and this is of no prognostic 
significance per se. Naunyn has established the fact that the normal 
tolerance of man makes it possible to take larger quantities of sugar into 
the full than into the empty stomach without causing glucosuria, due to 
the more gradual absorption of sugar under such circumstances and the 
consequent slower flooding of the blood. 
The tolerance varies between 50 and 200 grams under different condi- 
tions. The normal subject can tolerate 100 grams of sugar without recog- 
nizable glucosuria two hours after a breakfast of coffee with milk and 100 
grams of bread (ISTaunyn). 
Origin.—True alimentary glucosuria is often of functional origin 
when, as not infrequently happens, in the predisposed and neurasthenic 
with traumatic neurosis, at times glucosuria develops, also with brain 
anomalies (meningitis, debility, mania and paralysis) (von ISToorden) ; 
or there are pancreatic disturbances of a transitory nature in which, for 
some unexplainable reason, function is disturbed in which there is be- 
cause of faulty stimulation, marked inability of the liver to store glycogen. 
In all of these conditions we may assume theoretically that the liver proves 
itself inadequate when excess of sugar is suddenly brought to it from the 
portal vein. It is by no means easy to cause alimentary glucosuria in the 
presence of organic disease of the liver through levulose, as Strauss has 
demonstrated, easily passes into the urine in all diseases of the liver, and 
alimentary levulosuria is conceded to be evidence of liver insufficiency— 
“insufficience hepatique.” 
Relation to Diabetes.—The development of glucosuria from the inges- 
tion of starch should be interpreted as being pathologic. 
When glucosuria recurs persistently, in spite of intervals of freedom, 
suspicion of the presence of diabetes mellitus in its incipiency is justified 
and prognosis should be given accordingly. With a bad family history 
this forecast is strengthened. It often happens that with hereditary pre- 
disposition there are repeated periods during which there is supposed ali- 
mentary glucosuria. 
Relation of Lactosuria to Diabetes.—Lactosuria found during preg- 
nancy, after childbirth, during a limited period following weaning from 1110 
METABOLIC FAULTS 
the breast, is not of serious import; it continues but a short time, and 
bears no relation to true diabetes. 
Glucosuria Following Drinking of Beer, Etc.—For insurance exam- 
iners it is important to emphasize the insignificance of transitory ali- 
mentary glucosuria after the drinking of beer, champagne, and other 
sweet drinks excessively, in some even in limited quantities. In all such 
cases a period of observation is needed to clear the diagnostic horizon. 
Glucosuria Following Anesthesia.—The appearance of glucose in the 
urine, after anesthesia (chloroform, ether, etc.) or coal gas poisoning, is 
not per se of serious significance. Deep narcosis in the presence of fully 
developed diabetes often exerts an unfavorable influence on sugar elimina- 
tion. 
Factors Which Influence Prognosis of Diabetes 
Heredity.—Heredity is one of the most prominent features of diabetes 
and when present influences the case unfavorably as a rule, though many 
exceptions to this conclusion, have been filed by competent observers. The 
history of diabetes in the family was found in 20 per cent of my cases. 
I have the records of as many as five diabetics among the children of a 
diabetic parent. The disease in several brothers and sisters is strikingly 
frequent. Most inherited diabetes is associated with the neuropathic dis- 
position. Long continued worry, sudden shock., emotion, and acute infec- 
tion are factors which hasten the disease in those burdened by an unfor- 
tunate heredity. Among young children heredity is particularly striking; 
I have seen three brothers—all less than five years of age—die of the 
disease. 
Sex.—The majority of diabetics are men—possibly the average pro- 
portion from all collected statistics is three to two. My material shows 
118 diabetics among 6,300 internal disease—about .2 per cent—of which 
there were 80 males and 38 females. The prognosis under like condi- 
tions is not affected by sex; men are more exposed to the infections, are 
less able as a rule to care for themselves than women, and are also less 
amenable to treatment (diet, etc.). 
Age.—The influence of age on the prognosis of diabetes mellitus is 
powerful. The general rule may be accepted which holds that before the 
tenth year the disease is uniformly fatal, and death follows within a 
limited period; that from ten to twenty-five the disease is almost always 
fatal, though its duration is longer and it is more amenable to diet than 
during the first decade of life; that from twenty-five to forty the prognosis 
is less favorable for control of both glucosuria and glycemia than later in 
life; that the complications due to infection and hyperglycemia are, with 
acidosis, the most frequent causes of death; that the prognosis for the 
prolongation of life after the forty-fifth year is far better than before, 
provided the disease is recognized early, is rationally treated and the neu- METABOLIC FAULTS 
1111 
ropathic habit is not in the ascendency, the dangers of infection are 
escaped and there are no complications which undermine the resistance of 
the patient. In other words, it is plain that in young subjects tolerance 
for carbohydrates once reduced to cause diabetes cannot be re-established 
unless due to a removable cause. 
Riesman, speaking of the mild diabetes in children, says that mild 
diabetes in children may be successfully treated. He reports four cases in 
detail which responded to diabetic treatment; all recovered. He believes 
that there.may be several cases in the same family without the usual col- 
lateral symptoms of diabetes; they are mild cases and get well. I have 
had no such favorable cases to treat in my practice. 
Control of Hyperglycemia.—True diabetes and its complications de- 
pend very largely upon the control of hyperglycemia (sugar in the blood) 
because it is the leading factor in causing the disorganizing and degenera- 
tive changes in vital organs. Young subjects, because of failure to control 
metabolism, are prone to the early development of acidosis. 
Race and Geographic Location.—Jewish patients outnumber all others 
in their tendency to develop diabetes. They were found by Frerichs to 
include over 25 per cent of all cases. Naunyn, Osier, Tyson, and most 
authorities offer the same conclusion. Negroes develop diabetes but not 
with the same frequency as do whites. The prognosis of the disease per se 
is not influenced by racial factors, though among Jewish patients with 
overpowering neuropathic habit, emaciation is often rapid and polyuria 
prominent—conditions which unfavorably influence the outcome, for they 
shorten life. The mortality statistics of Prussia during 1897 showed 6-7 
times as many deaths among Jews as Gentiles, and 1.1 per cent of all 
deaths among Jews were due to diabetes. 
Dickinson in his monograph holds that the disease is more prevalent 
in the country districts of England than in the cities. In central New 
York the relative frequency of diabetes among farmers has unquestionably 
increased, and this increase holds for the diabetes of early life as well. 
Light complexioned races, Scandinavians, are prone to the disease, though 
the disease is more frequent in Southern Europe, Italy, also in India, than 
in Russia, Holland or in South America—Brazil particularly. Diabetes 
is increasing in frequency in all civilized countries; this fact is demon- 
strated by life insurance statistics and the material which is admitted into 
the general hospitals of our own country and Germany. During two three 
year periods the Germans report: 
During 1877-1879: 
Total number patients admitted 1,330,000—Diabetics 575. 
During 1905-1907: 
Total number patients admitted 4,560,000—Diabetics 10,725. 
The increase in admissions was 3.3 times greater; the number of diabetics 
19 times greater. 1112 
METABOLIC FAULTS 
Diabetes in Infancy and Childhood 
von Hoorden says: “With few exceptions diabetes in childhood knows 
Do cure, no matter how mild it may appear in the beginning nor how 
gradual its development in the first months or even years.” Cases reported 
as cured among children are not true diabetes m,ellitus. There have been 
cases reported as cured in which there was unquestionably transitory glu- 
cosuria, others in which long periods of latency proved misleading. 
Transitory and alimentary glucosuria in children may disappear per- 
manently but cases of “so-called alimentary glucosuria” in children are 
exceedingly rare and should be cautiously watched. In the end, it will be 
found that most are diabetics. Intolerance for carbohydrates may 
show itself early in life, may persist, but in some cases may never lead to 
true pancreatic diabetes. In children the cardinal symptoms—thirst, 
polyuria, emaciation, hunger, with sugar in the urine are prominent early, 
and in most cases make diagnosis positive. My experience with the 
diabetes of early life has been comparatively large and as stated above, not 
a single case has lived; most have died of acidosis within the first six 
months following the detection of the disease, but few have lived an entire 
year; none were alive who were less than six years old at the end of 18 
months. In cases between 15 and 25 I have occasionally met long pe- 
riods of latency. In one such case I was tempted to change my diag- 
nosis. A young man aged 17 was losing between 3 and 5 per cent of 
sugar. Under hospital treatment he was taught to diet; he became 
“sugar-free’ during five years, so far as could be determined. At the end 
of the fifth year he presented with all of his original symptoms, marked 
acidosis, and died in coma enormously emaciated in a few months. Such 
experiences are occasionally repeated and need correct interpretation. 
Diabetes in the Obese 
(See also Obesity) 
When obesity has been extreme and diabetes persistent with albumi- 
nuria, the feature which is finally added and most serious has been myo- 
cardial insufficiency. These patients often live many years uninfluenced 
by the glucosuria but they are bad risks, and with increasing dyspnea 
are ready for one of many further complications which may end life. My 
cases have usually died of degenerative rather than direct toxic processes. 
Obesity with gout and diabetes offers an unfavorable prognosis so far 
as life is concerned, with associated degenerative changes, but moderately 
fat people with limited gouty disease may live many years. 
Obesity with mild diabetes without associated disease or other com- 
plications may persist many years, and these patients may die of intercur- 
rent disease. METABOLIC FAULTS 
1113 
Obesity, arteriosclerosis with or without heart lesions and diabetes, 
may remain stationary during long periods or may progress with surpris- 
ing rapidity. Such patients are always uncertain of their future. 
Acute Diabetes mellitus 
Acute diabetes is more frequent than has been supposed in the past, 
though it is comparatively a rare disease. I have examined the first 
thirty volumes of the Transactions of the London Clinical Society and find 
but one case (Hale White) of acute diabetes reported. The disease may 
present so suddenly without prodromata as to prove puzzling to the 
diagnostician. 
Mv experience includes 8 cases during 30 years. All of these died 
within ten days, most before the end of seven days. Two were in adults, 
both males, 30 and 45 years of age respectively; five were in children less 
than ten years of age, and one was in a girl aet. 15, in whom there was 
sudden acidosis with rigid abdomen over the pancreas and enormous 
sugar loss. In all the polyuria and “melting away” was striking. The 
oldest patient—aet. 45—was perfectly well prior to exposure to cold 
and wet, and died in coma before the end of the seventh day. Besides the 
glucosuria and the fulminating course (there was no doubt of his previous 
good health) the enormous polyuria, specific gravity between 1,015 and 
1.025 (1,000 c.c. every two hours during the last days of his life), and 
complete paralysis of the bladder were the leading features. In the cases 
of acute diabetes in the younger children, exposure to extreme cold was 
unquestionably responsible for two deaths. One case seemed to follow 
worry over approaching school examinations; in the other case the cause 
was not suspected. The urinary evidences in all acute cases are positive; 
all have polyuria and acidosis; all die. 
The Relative Value for Prognosis of Individual Symptoms 
Chronic Diabetes mellitus 
Duration.—There is no time limit to mark the duration of chronic 
diabetes. Deaths during the first or second year are uncommon—thirty 
years and longer are not unusual periods for the continuance of symptoms. 
Hunger.—Persistent hunger, which remains unrelieved by rational 
diet, which is associated with progressive emaciation, offers an unfavor- 
able forecast for control of the disease. 
Normal appetite, with gain in weight after the detection of the disease 
and favorable influence on the sugar loss, offers an encouraging outlook. 
Abnormal appetite with great thirst and polyuria, usually with per- 
sistent diacetic acid in the urine with or without albumin, is unfavorable 1114 
METABOLIC FAULTS 
and death is not long postponed in such cases. This is particularly true 
when with the above complex there is also hurried respiration—a symptom 
of acetone poisoning always threatening when present. 
The safest diabetic is the one whose appetite remains normal, whose 
sugar loss is not markedly increased, easily controlled, and who “holds his 
weight” without the development of cardiovascular or renal complications. 
Thirst.—Persistent thirst after a reasonable period of rational diet, 
with or without marked change in the sugar loss, should always call for a 
guarded prognosis. 
Relief of thirst by diet and the return of the urine to approximately 
normal conditions, the relief of polyuria, if present, are favorable. Persist- 
ent thirst with progressive loss of weight—no matter what the sugar loss, 
is never favorable and these cases, though sugar may for a time disappear 
entirely from the urine, are likely to develop acetone poisoning, and die. 
Emaciation.—The initial loss of weight per se in an undetected and 
untreated case should not materially influence prognosis. If the case is 
not acute, the prognosis should be held sub-judice until the patient has 
received dietetic treatment. Progressive loss of weight with persistence 
of hyperglycemia and other cardinal symptoms is unfavorable. 
Increase of weight or stationary weight which approaches the normal 
of the individual argues in favor of control. With added chronic infec- 
tion, particularly tuberculosis, loss of weight is likely to be rapid and the 
process promptly destructive of lung tissue with high temperature, rapid 
and increasing heart weakness, and early death. 
Polyuria.—In the average case of true diabetes there will always be 
a tendency to increased urine secretion so long as the glucosuria remains 
uncontrolled. Slight increase of urinary secretion with small sugar loss 
in chronic diabetics without complications may continue during many 
years without materially influencing the comfort of the patient or his 
general condition. Polyuria which continues uninfluenced by diet, no 
matter what the specific gravity of the urine or the amount of sugar 
loss, should always lead to the suspicion of serious complication, unin- 
fluenced hyperglycemia, chronic interstitial nephritis, or grave central 
nervous disease. It always demands a cautious prognosis. 
Control of polyuria with improvement of other cardinal symptoms is 
among the favorable features of the disease. 
Pulse and Blood Pressure.—Persistently rapid pulse, arhythmia, 
erratic or delirious hearts, are unfavorable. The tendency of chronic, par- 
ticularly uncontrolled diabetes, is to cause or to be finally associated with 
heart and arterial change. The longer these are postponed, the more 
favorable is the prognosis for life. After middle life arteriosclerosis and 
diabetes mellitus are often associated and may persist unchanged during 
long periods under favorable conditions (proper living and diet). The 
prognostic data associated with the pulse must be considered in connec- METABOLIC FAULTS 
1115 
tion with the vital organs likely to be changed because of long continued 
irritation (hyperglycemia). My clinical material demonstrates that 
diabetes mellitus is not a hypotensive disease—the cases have, as a rule, 
when beyond the early stage, shown normal or approximately normal sys- 
tolic pressure. As the disease has advanced in those beyond middle life 
with the associated arteriosclerosis and cardiac hypertrophy, there has 
been higher systolic pressure—usually between 100 and 180 mm. lTg. 
In these cases the diastolic reading has been relatively low—pulse ampli- 
tude has consequently averaged between 60 and 80 mm. Hg. This is 
probably due to the associated cardiovascular and renal complications of 
the disease when it has existed long in those beyond the meridian of life. 
Persistent gastro-intestinal disturbances with dry tongue, decaying 
teeth, and gingivitis is an unfavorable combination. 
The Mental State.—The fact that diabetes mellitus has persisted dur- 
ing many years, at times with appreciable sugar loss uncontrolled and 
often in the presence of arteriosclerotic changes, should not lead to the con- 
clusion that these subjects are mentally incompetent or that they lack 
testamentary capacity. The majority of diabetics until they develop the 
final, fully developed diabetic coma, are alert, mentally active and normal, 
unless they suffer from chronic toxemia. Pronounced mental hebetude 
due to acetonemia is likely to remain uninfluenced during long periods; if 
relieved it is likely to return. Those who begin with mental symptoms 
usually run a rapid course for they are poisoned early (See Diabetic 
Coma, Acetonemia). 
Acidosis.—Acidosis (Kussmaul) has ended the lives of over 60 per 
cent of my cases; all acute diabetics have died of it. Acidosis results 
from the faulty consumption of the fats. B-oxybutyric acid is the impor- 
tant factor in the production of diabetic coma and the alarming symp- 
toms of poisoning—acute and chronic—which terminate the lives of many 
diabetics. 
When acetone is present, diacetic acid is reasonably certain to show 
in the urine. The latter is easily detected by the ferric chlorid test. The 
most convenient test for the busy physician for acetone is known as 
Garrod’s modification of the Rothera test. (To 5 c.c. saturated solution 
of ammonium sulphate add 5 c.c. of the suspected urine, then 3 drops of 
freshly prepared saturated solution of sodium nitro-prussid, and finally 2 
c.c. of ammonia. Acetone will, if present, gradually develop the per- 
manganate color which is positive and not shown by anything else.) 
In all cases of acidosis the prognosis will depend upon the severity of 
the toxemia, the resistance of the patient, the associated complications, the 
recognition of the condition early and its prompt and thorough treatment 
(Gordon). 
In young subjects acidosis once developed is not likely to yield, if it is 
associated with symptoms of deep involvement of the sensorium. 1116 
METABOLIC FAULTS 
There are cases of chronic acidosis in which the urine always gives 
characteristic reaction—at times in the absence of glucose—which live 
during long periods but they are always in danger. 
Acetone poisoning may develop and, prove serious in the chronic severe 
cases ivhen a too rigorous diet has been insisted upon. Such cases may 
fall into deep coma without prodromata, and promptly die. 
Profound acidosis in chronic cases may yield to alkaline flushing. 1 
have seen several such cases in which life was prolonged during several 
years. In the end these patients are likely to die in coma. Hurried respi- 
ration in the diabetic should always arouse the strong suspicion of acidosis. 
In children this is one of the positive and most frequent symptoms of 
acidosis and persists until death, which usually follows promptly. In 
these cases the sweetish breath, as in all acidosis, and the sunken eye with 
pinched facies and emaciation are characteristic. Insomnia and other 
mental symptoms, some transitory, may be traced to chronic ac< tonemia. 
Muscular Weakness.—The marked and suddenly arising 'weakness of 
the chronic diabetic is often due to acetone poisoning, large sugar loss, or 
some complication. The weakness may prove persistent during consider- 
able periods. The extreme muscular weakness in mild or medium cases is 
usually not persistent. Extreme muscular weakness with persistent aci- 
dosis is always unfavorable. 
The Urine.—I have in the preceding paragraphs referred to poly- 
uria and its prognostic significance. 
The quantity of urine voided, the tissue destruction and faulty oxida- 
tion, of which it proves a reliable index if cautiously studied, are impor- 
tant prognostic factors. Urine which is persistently of high specific 
gravity, particularly when the sugar loss is high, with or without evi- 
dences of acidosis, in the presence of other cardinal and uncontrolled 
symptoms, indicates severe diabetes. The urine is the most reliable index 
of the influence of diet on sugar loss; at the same time its cautious exam- 
ination makes possible the early recognition of associated toxicity—an 
elementary statement—but one which requires repetition because of the 
repeated failure of the clinician to take advantage of the laboratory to 
assist him throughout the treatment of these cases. It is not always pos- 
sible to prognosticate from the amount of sugar present, for there are 
innumerable cases which during long periods lose relatively large quanti- 
ties of sugar and live without complications. In some, the sugar is finally 
reduced and may persist at an unchanging level during years. The sud- 
den disappearance of sugar in the severer forms is ominous and may pre- 
cede acidosis. 
The presence of small quantities of sugar as shown by frequent 
polariscopic examination in the majority of cases without complications, 
which are cautiously treated, may not in any way interfere with the gen- 
eral health. The ridding of the urine of sugar when associated with METABOLIC FAULTS 
1117 
general improvement and the control of leading symptoms is always 
favorable. 
The presence of an occasional trace of albumin without more than a 
hyaline cast after the age of fifty in a diabetic urine requires watching 
but is not to be interpreted as of serious import. Urine which is charac- 
teristic of advanced nephritis (chronic interstitial) with sugar, is usually 
evidence of arteriosclerosis and myocardial change (hypertrophy)—all 
likely to develop in many of these cases. 
The Blood.—The method of Bang for the estimation of sugar in the 
blood is probably the best we have, but it is too complicated for the busy 
clinician. The mischief which hyperglycemia is doing in the individual 
case is best interpreted by its clinical features (thorough physical exam- 
ination) and repeated urine analysis. The blood itself deserves cellular 
examination in all cases. In the severe cases there is marked polycythemia 
(as high as 7,000,000 to 8,000,000 per c. mm.). High red counts are to 
be expected in most chronic diabetes. 
The alkalinity of the blood is materially reduced in the severe cases, 
particularly before the appearance of acidosis. Excess of fat is frequent; 
always an unfavorable condition. Digestion leukocytosis is of no prognos- 
tic significance. It is frequently present. 
Sexual Anomalies.—Periods of sexual weakness, at times impotence, 
may be present during the early stages in men of neurotic habit without 
grave diabetes, or it may be a symptom in the severer forms of the ad- 
vanced disease. As a rule with improvement following diet, the sexual 
appetite returns, though it may not always reach the normal. In the 
uncontrolled cases in men, sexual weakness may persist. Diabetic women 
are likely to abort on slight cause—their general condition is usually 
aggravated by pregnancy, and in the more severe forms there is increase 
of all symptoms and progression following delivery. I have seen preg- 
nant diabetics die of suddenly arising acidosis. In some women the 
emaciation has been extreme and rapid. Diabetic women are not likely 
to become pregnant. Alimentary glucosuria is present at some time 
{during varying periods) in 80 per cent of pregnant women (Mag- 
nus-Levy). 
Infection of the Diabetic.—I have repeatedly in this section* re- 
ferred to the ease with which the diabetic is infected. Among the most 
frequent infections are tuberculosis, pneumonia, skin infections (fur- 
uncles), necrotic foci, pulmonary gangrene and other minor infections 
including laryngitis, bronchitis and otitis. I have separately considered 
these complications in the chapters dealing with the individual diseases. 
Syphilis rarely causes diabetes, the association of the disease with the 
infection is possible and relatively frequent. The general rule may be 
accepted that any acute infection with diabetes is serious. 
Pneumonia offers a decidedly unfavorable prognosis, though I have 1118 
METABOLIC FAULTS 
had successful issues, among these a severe diabetes in a man 50 years of 
age. 
Tuberculosis with diabetes is uniformly fatal. The diabetic who 
develops tuberculosis offers but little resistance to the onward march of 
the infection and seems to “melt away” with prompt breakdown of lung 
tissue, high fever and rapid heart. In the severe types of diabetes tubercu- 
losis is, next to acidosis (coma), the most frequent cause of death. Febrile, 
i. e., infectious diseases may occasionally affect glucosuria favorably. This 
is only true of the milder cases. As a rule following severe infection there 
is progression in the malignant forms of the disease. 
Diabetic gangrene is usually a terminal process dependent upon endar- 
teritis (arteriosclerosis) obliterans, though occasionally it may limit itself 
to a superficial patch of skin tissue following infection. The prognosis of 
diabetic gangrene is unfavorable; it leads to death in coma, in most cases. 
Furuncles are frequent accompaniments of diabetes and may be present at 
any stage. They are often the first complication to lead to the correct 
diagnosis. Diabetic tissue in the advanced stages offers lowered resistance 
to infection and breaks down with surprising rapidity. Every carbuncle 
in a diabetic ought to be considered a serious complication. In the pres- 
ence of acute or chronic pronounced acidosis it is almost uniformly fatal. 
Without acidosis a small carbuncle or multiple boils are often controlled. 
It is often surprising to find how rapid the tissues break dowm and how 
certainly coma develops after a few days of'mental cloudiness. Vulner- 
ability of tissues in diabetes is due to the faulty pabulum received from 
the surcharged blood. The diabetic should be warned against the possi- 
bility of infection from cuts and superficial wounds. The careless cut- 
ting of corns in the diabetic subjects has led to frequent malignant infec- 
tion and death. 
Skin Lesions.—The prognosis of superficial skin lesions (infections) 
must depend upon the associated conditions. In the reduced and in the 
toxic, furuncles may promptly involve the deeper tissues and lead to death 
with all of the symptoms of sepsis and acetonemia. 
Universal pruritus, or of the genitals, may be an early or late compli- 
cation. When early it usually disappears as the urine is cleared or im- 
proves. My experience with severe pruritus has been exceedingly satis- 
factory in most cases. 21 per cent of diabetics develop pruritus (von 
Noorden) at some time during the course of the disease. 
Nervous System.—The prognosis of diabetes or glucosuria associated 
with chronic diseases of the nervous system, regardless of the true patho- 
genesis of the former, is influenced by the extent and nature of the latter. 
In alcoholics with polyneuritis I have met glucosuria which has disap- 
peared with the cure of the neuritis. In my experience the glucosuria with 
most chronic organic lesions of the nervous system has not been continuous, 
but has returned from time to time ; thus with brain tumor sugar may be METABOLIC FAULTS 
1119 
found only occasionally; the same is true of multiple sclerosis and tabes 
dorsalis as well as syphilis of the nervous system. Glucosuria with menin- 
gitis is found in the most serious form of the latter. 
Neuritis-polyneuritis.—The peripheral neuritides are frequent, often 
controlled with great difficulty. In the majority of cases, when an early 
complication, the pains and other symptoms yield to treatment (diet). 
When there are peripheral pains in old diabetics, particularly in the ex- 
tremities, arterial invasion is likely and gangrene should be considered 
among the possibilities. It is safe to promise the majority of diabetics 
that their pains will disappear as the sugar output and combustion are 
improved. 
Disturbances of the Eye.—There are frequent ocular infections in 
chronic cases; the prognosis of these is usually good. Diabetic cataract 
and changes in the fundus (vascular) are frequent and deserve considera- 
tion by the specialist. Schmidt-Rimpler mentions the following ocular 
disturbances in the order of their frequency: cataract, muscular anomalies, 
retinal changes, amblyopia without discoverable lesion, paralysis of the 
external and internal eye muscles, iritis, choroiditis and opacities of the 
lens, von ISToorden found retinitis oftener than cataract. Cataract opera- 
tions in cases of diabetes offer a favorable prognosis. 
Disturbances of the Ear.—Disturbances of the auditory apparatus are 
late complications. Furunculosis of the external auditory canal in mild 
cases may be an early complication; in some cases it was fully relieved by 
diet and prompt local treatment. The otitis of diabetes, when fully devel- 
oped, is profusely suppurative and there is marked tendency to bone (mas- 
toid) involvement with a fair prognosis following operation. 
Gout and Diabetes.—The combination of gout and diabetes mellitus 
is frequent and as a rule the sugar loss is limited; the patients live during 
many years but are naturally subject to the accidents of both diseases. 
Diet exerts a most satisfactory influence in these cases. When gout is 
advanced and there are visceral lesions (kidney, heart, or arteriosclerosis) 
the addition of the severe form of diabetes may promptly lead to marked 
loss of flesh and asthenia. Death due to angina pectoris, cardiac asthenia, 
pulmonary edema, or cerebral apoplexy, has been the fate of some of our 
cases. 
Diabetes and Surgery 
The clinician is frequently forced to decide upon the feasibility of a 
surgical operation in the diabetic subject. It is often exceedingly difficult 
to decide in the presence of a surgical complication whether the glucosuria 
is permanent or simply transitory. 
Surgical lesions may cause glucosuria. Smith and Durham have re- 
ported cases in which glucosuria disappeared after the removal of slough- 
ing malignant growths. Sugar may appear after surgical operations. 1120 
METABOLIC FAULTS 
Phillips showed in his analysis that of 16 cases of malignant disease of the 
mouth and face in diabetics operated, 11 recovered—or 68.75 per cent— 
and 31.25 per cent died. “Of purely mouth and lip cases, 9 out of 12— 
or 75 per cent—recovered” (Risley). Kisley reports operations on the 
breast of 15 cases; 13—or 86.6 per cent—recovered, and 13.4 per cent 
died. The fatalities were generally due to sepsis and erysipelas. Of 24 
operations on the female generative organs, 23 patients gave 5 deaths. 
Operations on the male generative organs gave a mortality of 50 per cent. 
Following fractures, Smith and Durham report numerous cases of 
“perfect union.” Phillips believes that “considerable doubt should be 
expressed that non-union is more common.” von Roorden recommended 
the use of lime carbonate because of its decrease in diabetic blood for all 
fractures. 1 have already considered gangrene, as a complication (See 
Gangrene). Phillips found that all cases with albuminuria died, and 
agrees that with acetonemia and an increase in the amount of ammonia 
excreted the prognosis is bad. 
Preliminary treatment often improves the reparative processes of the 
diabetic. Sugar increases the pus producing ability of infectious agent's 
but diminishes their virulence. Phillips’ percentage of recoveries was 
72.28—a mortality of 27.72 per cent in the entire material he gathered. 
Risley concludes that “glucosuria should not deter the surgeon from per- 
forming any operation of emergency.” “Other cases should not be 
operated in which acetone, diacetic acid, and ammonia cannot be reduced 
by preliminary treatment.” “A mortality of 20 to 30 per cent is to be 
expected in this class of cases.” “This total amount of ammonia must 
always be estimated. Ro operation except of the extremest emergency 
should be performed if there is one gram of ammonia excreted in 24 hours, 
until this has been reduced to the normal amount—.75 gm.” “Operation 
should be postponed when there is acetone or diacetic acid, even if the 
ammonia is normal.” “Much albumin in the urine is a contraindication 
to operation and even in small amounts is of bad prognostic import.” 
The clinician in his treatment of all diabetics should remember that in 
spite of all statistical reports there is in the individual diabetic increased 
vulnerability of tissues and in severe cases the danger of coma after all 
operations needs to be considered. 
The profession is in full accord with Tyson who holds that “diabetes is 
a disease in winch the expectant plan of treatment is disastrous. It is a 
disease which never gets well of itself and always gets worse if not properly 
treated." A patient with diabetes continually stands on the edge of a 
precipice, he is between rocks, and it is exceedingly difficult to tell when 
he is to be wrecked. 
The patient can do much to increase cellular resistance in cases which 
do not show malignant tendencies from the beginning, thus preventing the 
dreaded added infections which kill so many and the intoxications (acido- METABOLIC FAULTS 
1121 
sis, etc.) which end the lives of many more. Underlying all prognostic 
rules must be placed the one which cannot be controverted, i. e., the future 
of the diabetic must largely depend upon his ability to tolerate carbohy- 
drates, as demonstrated by urine analysis and the determination of the 
sugar content of the blood. 
Joslin believes that the fasting method of treating diabetes is a decided 
advance in the treatment of the disease, and that the advance has been 
greater during the past year than ever before. Allen’s recent observations 
are under consideration. 
The secondary manifestations may be largely prevented or postponed 
in the majority of diabetics, for in the final analysis of my material I 
find that the mild cases are in the majority. 
No diabetic can truthfully be told that he is cured; his symptoms only 
are controlled; once truly diabetic there is no assurance from past clinical 
experience that the patient does not always remain diabetic, though he may 
be "sugar-free” during long periods, and finally die of other disease. 
There are so many factors which influence the outcome that the indi- 
vidual case must give the data upon which the safest prognosis is based 
and this can usually be given with considerable certainty when the patient 
is thoroughly guarded and controlled. In no other disease depending upon 
metabolic fault are we able to accomplish so much to compensate for exist- 
ing anomalies as in diabetes mellitus provided the patient is earnest and 
willing to subscribe to the regimen indicated. 
"Eternal vigilance” must be the slogan if the prognosis of diabetes 
mellitus is to be influenced favorably. “Diabetes is not of necessity a fatal 
malady. It is the metabolic derangement which proves fatal to most dia- 
betics, hence the efficacy of restricted diet, which is a symptomatic therapy, 
which has ameliorated the lot and prolonged the lives of many sufferers 
from diabetes” (Garrod). 
References 
Allen. Treatment of diabetes, long fasting, etc. Tr. 13th Annual Meeting vlss. Am. Phys., 1915. 
Aschoff. Pathol. Anat. Jena, 1913. 
Bang. Blut Harnzucker. Wiesbaden, 1913. 
Borchardt. Zeit. f. klin. Med., 1908, Bd. Ixvi. 
Bernard Claud. Vorlesungen iiber Diabetes. Berlin, 1878. 
Cushing. The pituitary body and its disorders. Philadelphia, 1912. 
Eisner (Henry L.). Acute diabetes mellitus. Philadelphia Med. J., Aug. 19,1899. 
Frerichs. Berlin, 1884. 
Gordon. New York Med. J., May 15, 1913. 
Herter. Quoted in Aschoff’s Pathol. Anal., Jena, 1913. 
Hofmeister. Archiv f. klin. exp. Path, u- Pharm., xxv, Beitr. x, Ztschr. f. phys. Chem., I. 
Klemperer. Renaler Diabetes. Berl. klin. Wchnschr., 1892. 
Berl. klin. Wchnschr., May 18,1896. 1122 
METABOLIC FAULTS 
Kussmaul. Deutsch. Arch. f. klin. Med., 1874, xiv. 
Magnus-Levy. Kraus & Brugsch’s Spec. Path., etc. Wien, 1913. 
Naunyn. Didb. Mellitus. In: Nolhnagel’s Handb. 2. Aufl. Wien, 1906. 
Minkowski. Mitth. aus d. med. Klinik zu Konigsberg, 1888. 
Opie. Diseases of the pancreas, causes and nature. Philadelphia & New York, 1903. 
Osier {Sir William). Pract. of med. 8th ed. New York, 1914. 
Phillips. Lancet, London, May, 1902. 
Riesman. Tr. 13th Annual Meeting Ass. Am. Phys., 1915. 
Risley. Boston Med. & Surg. J., Jan. 21, 1915. 
Schmidt-Rimpler. NothnageVs Handb. d. spec. Path. 1898. 
Erkrankungen d. Auges. 
Senator. Berl. klin. Wchnschr., 1908, No. J). 
Smith & Durham. Guy's Hosp. Report, xlix. 
Strauss. Newer aspects of diabetes. Quoted by von Noorden. New York, 1912. 
Tyson. Practice of medicine. 6th ed. Philadelphia, 1914. 
von Mering. Ztschr. f. klin. Med., 1888, xiv; also 1889, xvi. 
von Noorden. Diabetes. New York, 1907. 
New aspects of diabetes. New York, 1912. 
Diabetes Mellitus Handb. d. Path. d. Stoffwechsel. Berlin, 1907. 
White {Hale). Tr. London Clin. Soc. 
Monographs {other than included above). 
Bouchardat. Paris, 1875. 
Cantani. Berlin, 1880. 
Gigon. Neuere Diabetesforschungen. Ergeb. d. inner. Med., 1912, ix, 206. 
Mohr & Staehelin. Berlin, 1912, Bd. iv. 
Schmitz. Prognose u. Therapie der Zuckerkrankh. Bonn, 1892. 
Williamson. Diabetes mellitus. London, 1899. 
3. Diabetes insipidus 
Characteristic Features.—The characteristic features of diabetes in- 
sipidus are marked and persistent polyuria, low specific gravity urine, and 
great thirst. The true nature of the disease is unknown, it is always 
chronic. Possibly we are in error when we dignify the symptom complex 
as a disease per se; there is no proof of its being a clinical entity. 
Dietrich Gerhardt believes that there is an idiopathic diabetes insipidus 
and that it depends upon a functional disturbance of the kidney. E. Meyer 
claims to have demonstrated by functional tests the correctness of Ger- 
hardt’s contentions (See original articles; also Umber). 
Cases in which the functional tests recommended by Gerhardt, Meyer 
and Umber fail to localize the cause we look to the central nervous system 
for the pathologic factor (secondary diabetes insipidus). 
We do know that in some insanities, hypochondriasis, paranoia, and 
after concussion of the brain, polyuria, and inordinate thirst are promi- 
nent symptoms; and further we know that polyuria without sugar can be METABOLIC FAULTS 
1123 
produced experimentally by puncture of the floor of the fourth ventricle 
near the origin of the auditory nerve, in front of the point which when 
punctured (between the auditory and the vagus nuclei) causes glycosuria 
to follow. 
Experimentally and clinically there are data which tend very strongly 
to establish the influence of the hypophysis in the production of polyuria, 
great thirst, and all of the symptoms of the disease (Magnus, Schafer, 
Frank, Oppenheim and Simmonds). Brain tumors of specific origin have 
produced the symptom complex (Nonne). I have seen the complex fol- 
low acute infections, but in my material, syphilis has been the leading 
attendant. Contrary to Umber’s experience I have not been able to con- 
trol the complex in those cases by specific treatment. Umber gives a good 
prognosis in cases which seem to rest on a syphilitic fundament. 
Weil reports families in which the disease persisted during several gen- 
erations. He reports one family through five generations in which among 
220 there wTere 35 with diabetes insipidus. Among some of these the 
disease commenced in nursing babes and continued to old age. The oldest 
of Weil’s cases lived to be 92, 87, and 83 years of age respectively. 
My cases have shown no hereditary influence. In 6,700 patients 
(internal diseases) I have had but 4 of the disease. The complex may 
affect any age. It is three times more frequent in women than in men 
in England; in Germany Umber found it oftener in men, and the larger 
number between 15 and 35 years of age. 
The quantity of urine secreted may reach between 8 and 10 pounds 
in 24 hours. There are cases in which 43 pounds were voided (Trous- 
seau). The specific gravity averages between 1,000 and 1,002. In almost 
all cases the bladder finally becomes tolerant and distended. In some 
cases the thirst may be somewhat relieved by withholding from 1,500 to 
2,500 c.c. of fluid during 24 hours. If the withholding of water is too 
great patients may suffer excessively and fall into a condition which re- 
sembles uremic poisoning; then there is marked unrest, insomnia, delirium, 
and with severe headache there is likely to be alarming tachycardia. This 
picture changes with the drinking of sufficient water to quench the inordi- 
nate thirst. There are exceptions to this rule; the symptoms of irritability 
may at times continue several days and become threatening. The blood 
picture in the average case is not markedly changed except when fluid has 
been withdrawn during sufficient time to aggravate the cardinal symptoms; 
the blood then shows abnormal concentration and high specific gravity 
(polycythemia). 
The heart and blood pressure are not usually disturbed, neither does 
the disease in the average case lead to demonstrable change of normal 
metabolism. The urine remains sugar free unless there is organic central 
disease (in which localization makes such a combination possible), or 
there are, as Haunyn holds, two separate processes independent of each 1124 
METABOLIC FAULTS 
other (See Senator-lSTaunyn, Heiberg and Umber). One of my cases bad 
persistent and uncontrollable backache. 
We are unable to make any favorable impression on these cases by 
treatment. In cases which seem to justify the surmise that the com- 
plex is 'primary and of renal-functional origin, the general health remains 
unaffected as suggested during years, though the thirst and polyuria make 
the patients wretched. 
Symptomatic cases attending organic disease or injury to the nervous 
system offer prognosis in accordance with the nature of the cause. There 
are occasional cases, which because of extreme muscular exhaustion, be- 
come bedridden; they usually die of intercurrent disease. Specific cases 
unless associated with focal symptoms have not in my experience been in- 
fluenced by treatment. 
Conclusion.—Diabetes insipidus is an incurable complex though it 
rarely directly destroys life. 
References 
Frank (E.). Berl. klin. Wchnschr., 1912, ix, 393. 
Gerhardt {Dietrich). Diabetes Insipidus. In: NothnageVs Path. u. Therap. Wien, 
1899. 
Heiberg. Ztschr.f. klin. Med., 1911, Bd. Ixxiii, 319. 
Magnus. Quoted by Umber [l. c.]. 
Meyer (Erich). Arch.f. klin. Med., 1905,Bd. Ixxxiii, 1. 
Naunyn. Diabetes Mellitus. 2. Aufi. Wien, 1906. 
Nonne. Syphilis u. Nervensystem. Berlin, 1909. 
Oppenheim. Die syph. Erk. d. Gehirns. Wien, 1903. 
Schafer. Quoted by Umber [Z. c.]. 
Senator. Deutsch. med. Wchnschr., 1897, No. 2J+, 385. 
Simmonds. Munch, med. Wchnschr., 1913, 127. 
Trousseau. Lectures on Clinical medicines, New Sydenham Society, London, 1868. 
Umber. Lehrb. d. Ernahrung u. Stoffwechselkr. Wien, 1909. 
Kraus u. Brugsch’s Spec. Path. u. Therapie, etc. Berlin, 1913. 
Weil (Sr.). Virchow’s Archiv, etc. 1884, Bd. xcv, 70. 
Weil (Jr.). Archiv f. klin. Med., 1908, Bd. xciii, 180. 
4. Obesity 
(F ettleibigkeit) 
Causes.—Obesity, or the abnormal and excessive deposit of fat in the 
body, is due to faulty metabolism, probably dependent upon perversions 
or the changed reciprocal relations of one or more of the internal secre- 
tions (hypophysis). There is not only an abnormal, usually insufficient 
oxidation of ingested foods, but there may be incomplete combustion with 
the excessive absorption of foods which make fat. The condition may be 
either hereditary or acquired. METABOLIC FAULTS 
1125 
Hereditary Obesity.—There are those who bv heredity are disposed to 
be obese, who in spite of cautious diet and right living are unable to con- 
trol the excessive deposit of fat. In over 36 per cent of all cases heredity 
is the leading factor. Such subjects present a hopeless prognosis so far 
as the marked and continued reduction of weight is concerned, though 
their general condition may not be materially affected during long periods. 
They offer, as do all the obese, lowered resistance to acute disease and 
show tendency very often, as they reach middle life, to degenerative 
changes. 
It has been noted that with the hereditary tendency to metabolic faults, 
different members of the same family are differently affected—thus one 
may develop obesity, another gout and obesity, another gout alone, while 
in the same family gout, obesity and diabetes may exist together or alone 
or there may be several members who are only obese. Unquestionably the 
development and prognosis of these conditions in the presence of a strong 
heredity are enormously influenced by the habits (diet, exercise, etc.) of 
the individual. In some families no method of treatment will in any way 
prevent abnormal fat deposit in its female members at the menopause 
and in some at puberty, and during one or two years after the development 
of menstruation there is an enormous fat deposit which in many cases 
yields; the development of the girl is uninfluenced by the period of obesity. 
I have seen a number of these girls in whom the improvement was 
striking and rather sudden. Those in whom there is an inherent tendency 
to abnormal fat deposit may occasionally find it possible to prevent the 
condition by close attention to diet and exercise. 
Acquired Obesity.—The acquired obesities are dependent upon a vari- 
ety of causes—unquestionably the leading factors are faulty diet, insuf- 
ficient exercise, and disease. The influence of diet in these cases is para- 
mount ; when excessive intake and faulty digestion are coupled with seden- 
tary habits obesity is invited, and it offers a favorable prognosis only when 
the underlying faults are corrected. This means scientific treatment and 
the cooperation of the patient. In the obese sedentary habits, as already 
suggested, invite fat deposit in many subjects while the overexercise 
of some of these obese subjects, particularly those in whom there is at the 
same time fatty degeneration of the myocardium, may lead to serious car- 
diac insufficiency—often sudden death. The obese subject, whether fat 
because of his heredity or with obesity acquired, who continues “his rich 
and unstinted diet,” as well as the inordinate use of alcoholics (beer 
particularly) who with all else fails to take the needed exercise or lives 
in an atmosphere which is unfavorable to the normal process of oxidation, 
cannot hope to be relieved. 
Anemic subjects are prone to develop obesity, or they may hold an ab- 
normal fat deposit without increase. 
Unquestionably the relief of sexual anomalies has a favorable influence 1126 
METABOLIC FAULTS 
on obesity which may be considered symptomatic. Abnormal fat deposit 
which develops at the menopause is likely to continue. 
“Constitutional inclination” is, according to Ebstein, a congenital dis- 
position to corjDulency which can be confirmed by daily experience and 
proves an enormous factor in prognosis. The “constitutionally inclined” 
are influenced with great difficulty, and it is not easy to explain the in- 
crease of fat in spite of rational diet, exercise and exemplary living in all 
respects. In considering the prognosis of the acute infections—particularly 
typhoid fever and pneumococcus—I have called attention to the handicap 
of the obese. The prognosis of all acute infections is more unfavorable in 
the fat. Sir James Paget has also clearly insisted, as have the best 
authorities through all the ages, that “after the age of forty years persons 
either diverge into spareness or become more or less obese; the former, as 
a rule, enjoy the happier and longer lease of life.” 
There are men, who are well developed muscularly, and who after 
the thirty-fifth year—often near forty—become moderately obese, who 
are able to continue at their work and often walk without discomfort. 
This does not apply to men after fifty who become obese, for they do not 
bear the fat accumulation well. After middle life, in those cases without 
hereditary burden, under favorable conditions, the fat is absorbed and 
the associated disturbances are likely to disappear. As a rule it will be 
found that the prognosis is far better in acquried obesity than in the 
hereditary cases. ISTaturally there are exceptions. Laziness and the 
phlegmatic habit increase all of the ills of the obese; unless these in- 
dividuals can be aroused, advancing secondary changes make the out- 
look grave in many cases. Gout in diabetic subjects with abnormal 
corpulence is considered in the chapters on gout and diabetes (See 
Diabetes in the Obese), as are also cases with arterial and myocardial 
changes. 
Dyce Duckworth has wisely said what interests us enormously for 
the prognosis of many cases: “It is not sufficiently recognized that fat 
deposits are constantly undergoing change by decomposition and reforma- 
tion. As with all other tissues, intimate change proceeds even in the 
densest layers of fat; and in no part of the body does any fatty deposit 
lie out of the current of life and unaltered.” 
In considering the prognosis of myocardial disease I call attention 
to the association of the fatty heart with obesity, also the dangers of heart 
weakness due to insufficient exercise (See Myocardial Disease—Section 
III, E, 3 (a) and 7). 
The dangers of corpulence and inconveniences include besides depress- 
ing mental pang in many, continuous tax on the myocardium not only to 
carry the extra weight of the body, but to propel the blood through com- 
pressed infiltrated and degenerated organs. There is also the faulty oxi- 
dation which in many is associated with complicating excretory faults. METABOLIC FAULTS 
1127 
Each case presents features which make the study of its prognosis possible 
and reasonably certain. 
Complications.—The prognosis of obesity also depends largely upon 
the complications. The most serious of all complications is myocardial 
insufficiency. This is, when extensive, associated with threatening symp- 
toms and is fatal in the end. There are cases in which the insufficiency is 
not extreme, in which the muscle is not extensively involved, in which 
there are no attending complications, in which treatment (Oertel, Schott- 
Eauheim, diet, etc.) leads to improvement and comparative comfort. 
The interference with locomotion, often edema of the ankles early, later 
edema of the extremities, makes exercise impossible and hastens, because 
of the enforced inactivity, the cardiac insufficiency. 
Cardiac asthma with myocardial degeneration is often serious, but in 
a fair number of cases, diet with mechanotherapy and resisted movements, 
may prolong life. 
Emphysema with chronic bronchitis and insufficient heart muscle offer 
a bad prognosis in most cases. 
Chronic constipation with hemorrhoids is frequent and the latter often 
bleed and add to the anemia. In the presence of cirrhosis of the liver, a 
frequent combination in the obese due to alcoholism, the prognosis is 
serious. 
Arteriosclerosis with myocardial change and obesity offers a grave 
prognosis. Obesity in beer drinkers with chronic interstitial nephritis, or 
nephritis from any cause with obesity, is always serious. 
The obese often die suddenly; the cause is easily explained when we 
consider the complications referable to the heart, arterial system and 
kidney mentioned. An occasional trace of albumin with or without a 
hyaline cast in an obese subject after fifty without heart involvement de- 
mands watching, but is not of necessity serious. 
Acute hemorrhagic pancreatis with obesity, particularly with fat em- 
boli, is fatal. 
In a surprisingly large number of cases, the control of the deposit and 
the prevention of complications must depend upon the will power of the 
patient. 
In the plethoric with obesity, there is tendency to hypertrophy of the 
ventricles, and with increasing arterial resistance there is a stage of hyper- 
tension with final arteriosclerosis. The latter condition may precede the 
changes mentioned. Such patients promptly have broken compensation 
with edema of the lung—always serious. 
I have seen the obese with angina pectoris and myocardial insuf- 
ficiency. The prognosis for life with angina and obesity is very bad; 
these patients rarely live long after the first attack, particularly if there is 
associated nephritis and aortic change. Once the respiration has become 
irregular (Cheyne-Stokes) the prognosis is exceedingly grave. Cerebral 1128 
METABOLIC FAULTS 
(vascular) complications offer a bad prognosis. It is always unfavorable 
to find hypotension-falling systolic blood pressure in these cases with albu- 
minuria and occasional casts. 
In the asthenic or anemic cases as the disease advances, dyspnea and 
increasing pallor with small pulse and edema of the ankles are warnings 
which call for great caution in prognosis. The degenerative processes are 
usually progressive after these symptoms appear. Such patients add to 
their danger because they are unable to exercise. Duckworth calls atten- 
tion to the frequency of the anemic type of obesity and the symptoms in 
women “before full growth of the body is established, namely before the 
age of twenty-two.” Amenorrhea or scanty menstruation should be ex- 
pected in the obese. Pregnancy is less frequent in the corpulent than in 
normal women. 
Dropsy once developed with obesity makes the outlook dark; sudden 
death is to be feared. 
Obese patients furnish a comparatively large proportion of sudden 
deaths. In the anemic, syncope has been noted; apoplexy, angina pec- 
toi'is, rupture of the heart, uremia, with diabetes acidosis, and of late the 
unscientific use of thyroid extract, often in large and long continued doses, 
have furnished the causes of death. 
All life insurance companies refuse to accept obese subjects, and with 
justice. Statistics prove that the obese, whether the disease is inherited 
or acquired, are in a class which is unfavorable and life is uncertain be- 
cause of the lack of resistance and the tendency to degeneration. Obese 
patients are as a rule unfavorable subjects for serious surgical operations. 
Change of occupation in acquired cases from the sedentary to the active 
often influences prognosis favorably. The introduction of the animal 
extracts for the treatment of obesity in children and young adults has in- 
fluenced some cases favorably, particularly those to whom the pituitary 
substance has been given. I accent once more the danger of unscientifc 
dieting and the use of thyroid extract in large doses and without medical 
supervision. Left to itself, uncontrolled by appropriate treatment early, 
obesity is likely to advance, become chronic and exceedingly rebellious and 
it unquestionably tends to shorten life. 
The cases of dystrophia adiposo-genitalia due to faulty function or 
organic disease of the hypophysis offers a clear clinical picture of the eunuch 
type, with enormous fat deposit, particularly over the hips, the breasts 
and the mons veneris. In these cases the genitals are underdeveloped 
(hypoplasia) and finally symptoms of tumor of the hypophysis may be 
added—including pressure, headache, increased intraspinal pressure, bitem- 
poral hemianopsia, increasing amaurosis and final choked disk (Umber). METABOLIC FAULTS 
1129 
References 
Duckworth (.Dyce). Allbutt & Rolleston. London, 1908, iv. 
Ebstein. Fettleibigkeit. Wiesbaden, 1904. 
von Mehring & Krehl. Lehrb. d. inner. Med. Jena, 1913, i. 
von Noorden. Internat. Med. Mag., 1902, xi, 400-1+04- 
Oertel (M. J.). Twentieth century -practice. New York, 1895, ii, 635-725. 
Osier (Sir William). The principles and practice of medicine. New York, 1914. 
Paget (Sir James). London, 1879. 
Philadelphia, 1860. 
Schott (Theodore). Philadelphia, 1914. 
Stern (Heinrich). New York Med. J., 1902, Ixxx- 529-532. 
Umber. Med. Klin., Berlin, Dec. 7, 1913, 2014• 
5. Rachitis 
(Rickets, Englische Kranklieit) 
Causes.—Rickets is a disease of infancy due to disturbed nutrition of 
the body in which the greater changes are found in the bones, though the 
skin, muscles, respiratory and digestive organs and the blood building 
apparatus are usually involved. The disease is usually limited to children 
between the ages of three months and the fourth year; it is occasionally 
found in children after the fourth year when it has been characterized as 
"rachitis tarda” or late rickets. The disease is easily traced to the poorer 
classes among whom faulty ventilation, dingy homes without sunlight, and 
improper nourishment prove to be the causes which lead to the faulty 
growth of the bone, the insufficient deposit of the lime salts. In all coun- 
tries patent foods, improperly prepared milk—below the standard—and 
the failure to supply the proximate principles are responsible for the 
nutritional faults included in rickets. There are children who are pre- 
disposed to rachitis; thus, in the same family it has been noted that in 
twins equally fed one may develop the disease, the other escapes (His). 
Heredity is an important factor as is also hereditary syphilis. Ad- 
vanced rachitis, often with marked changes in the long hones and consti- 
tutional defects, may heal spontaneously with but small remnant of de- 
formity or ultimate stunting of growth. Rachitic children are predisposed 
to gastro-intestinal diseases and are without resistance to these and to 
the other diseases of early life. They promptly fall after infection and 
are enormously disposed to all forms of tuberculosis. 
Course of the Disease.—The bony changes include, when the disease 
is fully developed, enlarged head, thinning of the bones of the cranium 
(craniotabes), open fontanelles, retarded dentition, poor teeth ready to 
decay, epiphyseal thickening, bowing of the long bones and knock-knee 
(genu valgum). Bending of the long bones and “green-stick fracture” on 1130 
METABOLIC FAULTS 
injury are frequent. Deformities of the pelvis and spinal curvature often 
persist during adult life. 
The “rosary”—prominence at the costochondral articulations of the 
ribs—usually yields with the other bony changes in the majority of 
properly treated children. With persistent improper respiration the abdo- 
men is prominent, the lungs are insufficiently filled with air, oxygenation 
of the blood is faulty, and the general condition of the infant suffers. In 
these cases the “Harrison sulcus” is found (a transverse depression at the 
level of the ensiform cartilage). The lime salts in the bones are reduced 
to less than 50 per cent of their normal content. The excessive sweating 
of the head is an usual symptom but does not brand the case as being 
severe. 
The tardiness of walking of rachitic children does not affect the prog- 
nosis unfavorably, neither does tardy dentition argue against complete 
recovery. 
Ilutchinsonian teeth in rachitic children are frequent because many 
are luetic. Thorough treatment of these leads to very satisfactory results. 
The flabby musculature may be improved to normal by persistence, proper 
diet, exercises and healthy environment. The slight leukocytosis and 
chlorosis of rachitis yields to treatment, with the disappearance of the 
other symptoms. 
The enlarged spleen and liver, often displaced by existing deformities, 
disappear as time is given for general improvement, and metabolism be- 
comes normal. All symptoms and skeletal changes may he increased and 
may become permanent under a long continued starchy and other faulty 
diet. 
Cases may be considered severe in which there are repeated laryn- 
gismus stridulus, tetany, convulsions and motor excitability (facial spasm). 
In rachitic children all infections are more serious than in the normal, 
and ordinary catarrhal conditions of the respiratory organs demand cau- 
tious treatment to prevenet bronchopneumonia and other complications. 
This is particularly true of the bronchitis of whooping-cough, measles, etc. 
In neglected cases the chondrodystrophies may lead to permanent deform- 
ities. 
The natural tendency of rickets is to recovery, and the evident and 
palpable deformities, the constitutional disturbances, the faulty respira- 
tion, the anemia, the dental decay and the many other symptoms referable 
to the internal organs, including changes in the spleen, liver and blood 
may be expected to give way to normal conditions under lational regime. 
Permanent deformity of the pelvis and thorax is not frequent when we 
consider the large number of rachitic children. With increasing intelli- 
gence and the dissemination of knowledge among the masses, rickets is 
decreasing and infant life is made more comfortable, while deformities are 
correspondingly reduced. METABOLIC FAULTS 
1131 
In rare cases there is a rapid progression—an acute course which leads 
to death within a few months. These cases are associated with rapid 
bone changes, respiratory, and profound nervous symptoms. 
References and Literature 
Bramwell. Adult rickets. Clinical Studies. Edinburg, 1908-1909. 
Cheadle. Allbutt & Rolleston’s System of medicine. New York & London, Hi, 108-144- 
Forchheimer. Internal. Clinics. Philadelphia, 1892. 2d series, i, 173-181. 
Hirschfeld (M.). Die Englische Krank. (Gesundheit in Wort u. Bila). Berlin, 1907. 
His. von Mehring u. Krehl’s Krankh. d. Bewegungsorgane. Jena, 1913, ii. 
Jacobi (A.)* Pediatrics. New York & London, 1896, ii, 55-59. 
Monte (A.)* Rachitis. Wien. Klin., 1900, xxvi, 39-108. 
Schlossmann. Beitrage z. Kentniss d. Rachitis. Munich, 1891. 
Still. Osier’s Modem medicine. New York, 1907, i, 864-892. 
Virchow. Verhandl. d. Berl. Med. Gesellsch. (1899), 1900, xxx, pt. i, 88, 102, 110. 
Woodwork. Manual of medicine. Oxford, 1912. 
6. Achondroplasia 
(Fetal Chondrodystrophy, Fetal Cretinism) 
Virchow gave the name of fetal cretinism to a condition in which 
there is a dystrophy of the epiphyseal cartilages secondary to connective 
tissue invasion from the periosteum; there is a premature union of the 
epiphysis and the shaft which results in dwarfing with the normal devel- 
opment of the head and thorax. The condition is possibly due to dys- 
pituitarism, is congenital, and is held by Jansen to follow amniotic pres- 
sure and is considered by him to be closely related to other congenital 
malformations. He opposes the pituitary origin of the disease. Osier 
says: “But it is an argument in favor of some associated disturbances of 
the pituitary gland that achondroplasics often show precocious sexual 
development.” Most of these infants die during the first few weeks of 
life; if they live they are dwarfs with normal intelligence and fair re- 
sistance. 
Apert. Achondroplasia. Bull. Soc. Anat. de Paris, 1895, Ixx, 772-775. 
Jansen (M.). Achondroplasia. (Monograph), 1912. 
Ztschr.f. orthop. Chir. Stuttgart, 1913, xxxii, 1-114. 
Virchow. Cellular pathol. Berlin, 1858-1862. 
Krankhafte Geschw., Berlin, 1863-1867. 
References 
7. Osteomalacia 
(Mollifies ossium) 
The loss of lime salts from the bones of the extremities and trunks 
during adult life associated with softening and bending are characteristic 1132 
METABOLIC FAULTS 
of osteomalacia. The condition is exceedingly rare. In 6,700 cases con- 
secutively examined we have not met a single case. When the disease 
attacks women during pregnancy it is known as (epuerperal osteomalacia” 
and in these cases, each subsequent pregnancy is associated with increas- 
ing bending and yielding of bone. It has been held that there is an 
association of mollities ossium Avith a changed ovarian secretion. As the 
disease progresses there is evident yielding and the patient is shorter; the 
gait is “wobbling” “like walking on eggs” and it is difficult to climb stairs. 
It has been noticed that the menstrual function is undisturbed, concep- 
tion, it is held, is made easier and twin pregnancies are surprisingly fre- 
quent. These cases are usually met in country districts, in women who 
are underfed, who have many children and in whom the respite between 
pregnancies is short. About three-fourths of all cases are met during 
pregnancy. 
Early recognition and rational treatment have led to brilliant results. 
The disease may be controlled. Some have been successful after oophorec- 
tomy, but without hygienic or dietetic treatment improvement is not likely 
to follow. 
Uncontrolled cases finally fall into helpless conditions; they emaciate, 
appear cachectic, develop gastro-intestinal symptoms, respiratory embar- 
rassment, and die after a period of marked asthenia, or they develop infec- 
tions, including pneumonia or bedsores and sepsis. 
8. Scorbutus 
(Scurvy) 
(a) Adult Scurvy, (b) Infantile Scurvy (Barlow’s Disease) 
(a) Adult Scurvy 
Origin and Association.—Adult scurvy is probably of metabolic ori- 
gin, and is associated with spongy gums and repeated hemorrhages from 
the mucous membranes of the body and into the skin, with consecutive 
anemia. 
Causes.—Adult scurvy is caused and increased by faulty hygiene and 
improper and insufficient diet. It is hastened by mental fatigue and 
worry as well as excitement. There are clinical facts which create the 
strong suspicion of infection in some cases. Most scurvies, however, are 
caused by faulty food and may be relieved by change to a favorable envi- 
ronment where proper nursing is included and a dietary including vege- 
tables and fruit acids with sufficient sodium chlorid. The scurvy which 
has followed long cruises at sea on vessels insufficiently provisioned has 
in the past claimed many victims. With our knowledge of dietetics 
scurvy has been prevented, and it is exceedingly rare to meet it on the METABOLIC FAULTS 
1133 
ocean at the present time. Osier holds that it is not a rare disease in the 
United States. In Central Few York we rarely see a case save in tramps, 
who, neglected and filthy, usually vermin-covered, present at our hospital 
for admission with large skin hemorrhages, they are thoroughly depleted. 
When the disease is endemic,* as it occasionally is in camps, there is 
besides filth, faulty feeding. Attention to detail and diet promptly brings 
relief and while convalescence is often slow, if there are no organic lesions 
complicating, recovery is the rule. There are occasional cases which are 
malignant from the beginning, in which there are infarcts, and at times 
the suspicion of infection and malignant endocarditis; these offer a very 
grave prognosis. 
Symptoms and Infections.—Ulcerative gingivitis with bleeding from 
the gums is evidence of severe scurvy. Delirium and other meningeal 
symptoms increasing to coma are found in the severe cases which create 
the suspicion of infection. 
Bleeding from the kidney or bladder is not per se serious—most of 
these cases recover. Profound evidences of toxemia with deep and 
superficial hemorrhages may lead to the appearance of graver disease and 
yet the prognosis is not of necessity bad. The pulse in many cases which 
end in recovery is rapid, small, and thready and hemic murmurs may 
persist until the blood picture of secondary anemia has disappeared. 
Albuminuria, not dependent upon chronic nephritis, does not influence 
prognosis unfavorably unless there are other evidences of malignancy; 
neither does the presence of casts (hyaline) under similar conditions 
signify danger. Ocular hemorrhages usually leave the eye normal. 
Cerebral apoplexy may develop, and if it is extensive and into vital 
centers causes sudden death. Limited hemorrhagic infarcts (non-majig- 
nant) into the membranes or into the brain tissue do not, as a rule, lead 
to death. The greater danger from adult scurvy is from the malignant 
cases and added infection. Death rarely results from simple uncompli- 
cated scurvy. 
(b) Infantile Scorbutus 
(Barlow's Disease) 
Scorbutus during infant life offers an excellent prognosis in the ab- 
sence of complications. Its recognition and rational treatment is at once 
followed (almost as if by magic) by improvement and the complete cessa- 
tion of the usual painful symptoms. 
Causes.—Faulty food is the cause of infantile scurvy. Barlow’s dis- 
ease in the United States is almost always caused by patent baby foods 
which naturally eliminate from consideration the needs of the individual 
child, and as a rule fail to meet the demand. 
Symptoms.—It is the exception to find breast-fed children scorbutic, 
though it does occasionally happen. The leading features of Barlow’s 1134 
METABOLIC FAULTS 
disease include tender epiphyses of the lower extremities, as a rule, par- 
ticularly at the junction with the shaft (the slightest movement makes the 
babe cry), subperiosteal hemorrhages causing slight swelling, petechial 
spots, ecchymoses—conjunctival usually—spongy and bleeding gums, and 
anemia. There may be considerable weakness and some elevation of tem- 
perature. In severe cases intramuscular hemorrhages may continue the 
tenderness during a considerable period. 
The faulty feeding leads to the subperiosteal hemorrhage; the promi- 
nent feature of the disease, which is readily overcome, as already sug- 
gested by prompt recourse to proper diet and hygiene. 
9. Multiple Myeloma 
(Kahler’s Disease (1889), Myelopathic Albumosuria, Bence-Jones 
Albumosuria (1848)) 
Bence-Jones albumose is found in the urine with Kahler’s disease, 
occasionally in grave pneumonia, in purulent processes, and with nephritis 
(rarely) of specific origin. Albumosuria may be detected by boiling the 
urine, which gives a white precipitate on the addition of nitric acid, when 
it disappears to reappear as the urine cools. With multiple myeloma, or 
Kahler’s disease, the prognosis is absolutely bad. The disease is not 
frequent; I have seen two cases in my series—both died—both gave 
the Bence-Jones reaction. Christian has fully decided that the myeloma 
is a veritable neoplasm with cells resembling the plasma “rather than the 
myelocytes of the bone marrow” (Osier). 
. Both of my cases were in males beyond middle life; both died within 
12 months. In both I was positive that the bone deposit was primary 
—in neither were there metastases—both were painful. Kahler’s original 
case lived with positive symptoms of multiple myelomata from 1879 until 
1887. He was a physician, aged 46, when first seen, and during the 
eight years of his illness he developed all of the bone changes and deform- 
ities characteristic of the disease without lymphatic or splenic involvement. 
The case was examined post mortem with confirmation of the diagnosis; 
there were no metastases. 
In the diseases above mentioned in which albumosuria is found 
without multiple myeloma the quantity is infinitesimal. Marked albu- 
mosuria, when associated with fragility of the bones or symptoms of grave 
anemia, almost always signifies multiple mvelomatous deposit in the 
bones though the condition may be present during a considerable period 
before the Bence-Jones bodies show in the urine. Hence, albumosuria 
with bone symptoms may be considered to be due to advanced multiple 
myelomata, and the prognosis is uniformly fatal. The blood picture is 
one of grave anemia without features otherwise characteristic. Weber METABOLIC FAULTS 
1135 
makes this unqualified statement: “The presence of Bence-Jones proteid in 
the urine is practically invariably of fatal significance and nearly always 
indicates that the patient is suffering from “multiple myeloma,” and fur- 
ther, “it is always the result of disease of the bone marrow.” “Meta- 
static tumors in the bone marrow do not give rise to Bence-Jones albu- 
mosuria.” 
References 
Hamburger. Bull., Johns Hopkins Hosp., 1901, xii, 38. 
Hammer. Virchow’s Archiv. 1894, cxxxvii, 280. 
Kahler. Prager med. Wchnschr., 1889, xiv, 35-1+5. 
(Full report of original case and abundant references.) 
MacCallum (W. G.). J. Exp. Med., NewYork, 1901-1902, vi, 53-63. (Excellent references.) 
Morawitz. Mohr u. Staehelin’s Handb. d. inner. Med. Berlin, 1912, Bd. i. 
Osier (Sir William). Practice of medicine. New York, 1914. 
Paltauf. Ergebnisse d. allgem. Path., etc. 
Lubarsch u. Ostertag, 1896, Hi, 1, 676. 
Weber (F. P.). Med. Chir. Tr., 1903, Ixxxvi, 395. 
Am. J. Med. Sci., Philadelphia, 1903. 
New series, cxxvi, 61+1+-665. 
Wieland. Inaug. Dissert. Basel, 1893. 
Winkler. Virchow’s Archiv, clxi, 252. 
Wright. Welch Vol. Contrib. to the Sci. of Med. Baltimore, 1900. 
Editorial, Univ. Med. Mag., Philadelphia, 1898-1899, xi, 1+52. Section X 
Diseases of the Ductless Glands 
A. Thyroid Diseases 
1. Growths 
(a) Tumors—Thyroiditis 
(b) Goiter 
2. Hyperthyroidea 
(a) Exophthalmic Goiter 
(b) Myxedema—Cretinism. 
1. Growths 
(a) Tumors—Thyroiditis 
Both tumors of the thyroid gland and goiter belong in the domain of 
the surgeon. 
Neoplasms.—The leading neoplasms are carcinoma, sarcoma and ade- 
noma. In all new growths of the thyroid there is great tendency to 
metastases. In most thyroid growths there is marked hyperthyroidea or 
perverted thyroid function. It is possible, if the patient lives, for the 
gland “to wear itself out,” when hypothyroidea (myxedema) is substi- 
tuted. The malignant growths give the usual unfavorable prognosis unless 
primary, detected early and radically treated. Adenoma is amenable to 
surgical treatment. 
Inflammatory Conditions.—Thyroiditis.—Inflammatory conditions, 
thyroiditis—suppurative or non-suppurative—may develop in normal or 
enlarged thyroids causing swelling, and these may complicate the infec- 
tions including measles, pyemia, scarlet fever, pneumonia, polyarthritis, 
tonsillitis, influenza, etc. With these conditions, as with new growths, 
symptoms of perverted function, hyperthyroidea (usually), or hypothy- 
roidea may develop and in rare cases death may be caused by overpower- 
ing and acute hyperthyroidea. Naturally the primary infection remains 
1136 THYROID DISEASES 
1137 
the paramount factor in prognosis. Roger and Gamier have called atten- 
tion to the clinical features of the infections and their dangers. 
I have seen a number of cases in which there has been acute swelling 
with the thyroiditis without evident primary infection, hut atypical hyper- 
thyroidea and alarming tachycardia, in which life was in danger during 
several days. A number of such cases have died before the end of the 
seventh day. The productive or sclerotic thyroiditis of Riedel is likely 
to run a rapid course, is associated with symptoms of malignancy and 
compression. In some cases there has been laryngeal paralysis. This is 
always a serious condition. 
(6) Goiter 
(Endemic Goiter, Struma, Bronchocele) 
Association.—The relations of the thyroid to vital organs and to the 
genitals are better understood than ever before, and we are daily accumu- 
lating material which justifies the conclusions that any goiter is a swell- 
ing which demands close attention, which because of changed function 
may lead to threatening symptoms without warning, in spite of the fact 
that simple parenchymatous goiter in the majority of cases remains with- 
out annoying complications. The close examination of a large material 
will demonstrate the fact that many simple and unsuspected goiters are 
associated with cardiovascular or other symptoms, that perverted thyroid 
function is present at some time during the history of most goiters, and 
that no clinician can offer any forecast which will he of value in deciding 
whether goiter, in the individual case, wdll always remain free from the 
symptoms due to faulty function of the gland. It may be assumed that 
the patient will be spared the cardinal symptoms now considered due to 
excessive functional activity hut the presence of a goiter is always signifi- 
cant and its degeneration is possible at any time with all of the accom- 
panying symptoms. 
The reciprocal relations of the ovaries and thyroid have been recog- 
nized by the lay world and the profession during all the ages. 
Frequency.—Simple uncomplicated goiter is increasing in frequency. 
In 5,370 cases of internal diseases I found 186 goiters—3.46 per cent. 
Of this number 89, or 1.66 per cent, were simple uncomplicated goiter 
(Eisner). In France there are supposed to be, according to Baillarger, 
one-half million goitrous persons. I cannot agree with McHarrison who 
believes that goiter is less frequent now than formerly. In India there 
are five million persons with bronchocele. 
Distribution.—Goiter is certainly a “place disease”; there are, as 
may he learned from its close study, endemic areas (Alps, Himalayas). 
In these there may be periods of fluctuation. 
Influencing Factors.—Heredity is a powerful factor in the develop- 1138 
DISEASES OF THE DUCTLESS GLANDS 
ment of simple endemic goiter. Goitrous mothers are likely to beget chil- 
dren with goiter—often myxedematous. 
Persons of lymphatic and nervous temperament in goitrous areas are 
likely to develop the growth and “newcomers to an endemic area are very 
susceptible to it” (McHarrison). 
The infections invite goitrous growth; and gastro-intestinal disease, 
climatic influences, faulty ventilation, sexual overactivity, pregnancy, 
fright, long continued worry and repeated emotion—all, in the neurotic, 
invite thyroid hyperplasia. Contrary to general belief the sexes are about 
equally affected. 
Outlook.—My experience justifies the belief that the majority of sim- 
ple goiters recover spontaneously, and this often when there are symptoms 
suggestive of perverted thyroid function. Return of the growth after dis- 
appearance with or without final hyperthyroidea is relatively frequent. 
Spontaneous recovery is held by some to give immunity against recurrence 
(McHarrison). The prognosis is materially improved when the patient 
moves from the goitrous area. 
Complications.—It is not uncommon to find physical signs of heart 
changes in the presence of goiter without subjective symptoms. These 
are the cases in which there is probable atypical hyperthyroidea which on 
slight cause (worry, overwork, sexual excess and other excitement) 
promptly develop three or more of the cardinal symptoms of exophthalmic 
goiter. Goiter with symptoms is likely to show some anemia, though in 
most cases it is not extreme; unless complications are superadded, no 
serious complication need he feared from the blood. 
Association with Soil and Water.—In goiter areas, there is a possible 
infectious origin, the water and the soil are strongly suspected as being 
the vehicles of transportation. McHarrison, Berard and Gaylord and 
March have, by experiment, demonstrated the association of soil and water 
with goiter. 
References 
Baillarger. Quoted by Me Harrison [Z. c.], 71. 
Berard. Soc. Biol., 1913, Ixxiv, 13. 
Biedl. Innere Sekretion. Wien, 1913. 
Eiselberg. Krankh. d. Schildruse. Stuttgart, 1901. 
Eisner (H. L.). Am. J. Med. Sd., May, 1914. 
Eppinger-Falta-Rudinger. Ztschr. f. klin. Med., 1908, Bd. Ixvi. 
Falta. Mohr & Staehelin’s Handb. d. inner. Med., Bd. iv. 
Gaylord & March. Bull., Bureau of Fisheries, Washington, 1914, xxxii. 
Kocher. Kongr. f. inner. Med. Wiesbaden, 1906. 
McHarrison. Endemic goiter. 
The Practitioner, London, Jan., 1915. 
Roger & Gamier. La glande, thyroid dans les malad. infect. Presse Med. 1899, 181. THYROID DISEASES 
1139 
2. Hyperthyroidea 
(Moebius) 
[Parry’s Disease (1825), Graves Disease (1835), Basedow’s Disease 
(1840), Basedowoid Disease (formes Frustes-Stern) (1908)] 
(a) Exophthalmic Goiter 
Symptoms.—Typical exophthalmic goiter includes a complex with 
four leading symptoms—tachycardia, goiter, prominent eyes and tremor. 
Perverted, deranged or excessive thyroid secretion leads to a complex of 
symptoms of which tachycardia is the most prominent; the others may or 
may not he present; they are enlarged thyroid gland, abnormally promi- 
nent eyes, tremor, increased tissue waste and mononucleosis. Our in- 
creased knowledge of the physiologic effects of thyroid administration and 
anomalous thyroid function have made recognition easy and have thus 
enormously increased the number of recorded cases of atypical exoph- 
thalmic goiter and have also proved its increasing frequency. 
For purposes of prognosis it is important to clearly recognize (1) the 
minimum of symptoms which justify the diagnosis of exophthalmic goiter 
and (2) to establish the separate clinical forms of the disease. 
(1) Minimum Symptoms.—Such knowledge is necessary because we 
know that hyperthyroidea may exist without all of the cardinal symptoms 
mentioned in the definition at the head of the chapter, indeed but one 
symptom (tachycardia) persisting without goiter hut with the neuropathic 
habit, may justify the strong suspicion of perverted thyroid function. 
The cardiovascular symptoms are always the most prominent in the clin- 
ical history, and the diagnosis may be made without any of the other 
cardinal symptoms, hut with added mononucleosis, occasional psychic dis- 
turbances or cephalalgia. 
Associated with tachycardia in the atypical cases which I hold to be 
the most frequent of all hyperthyroideas, are symptoms referable to the 
sympathetic system (paralysis or irritation of the cervical sympathetic— 
Eppinger and Hess), including excessive sweating, moist skin with char- 
acteristic ocular manifestations, either the Graeffe, Stellwag or Moebius 
symptoms—usually the first of these. The diagnosis may be firmly estab- 
lished with tachycardia and one or two ocular symptoms. Such cases 
include the “goiter heart” and the Graeffe symptom alone, or the Stell- 
wag also. 
With tremor and a single ocular symptom, the suspicion of faulty 
function is justified. Periods of improvement in such cases may tend to 
upset the diagnosis hut soon the cardiovascular symptoms are in the fore- 
ground and the true condition is recognized. There are cases in which 
the goiter is not a constant accompaniment of the disease but with an 
acute exacerbation, goiter, either one-sided or double, becomes noticeable 1140 
DISEASES OF THE DUCTLESS GLANDS 
and abnormally tense; all subjective symptoms increase and during vary- 
ing periods the complex includes most of the cardinal features. 
So varied are the clinical features of the anomalous types of faulty 
thyroid function that it is occasionally exceedingly difficult without thor- 
ough investigation into the previous history of the patient to clear the 
horizon. Thorough vigilance will lead to conclusions that prove the pro- 
tean character of the disease. In this connection I would once more 
emphasize the frequent development of positive hyperthyroidea from the 
degeneration of supposedly innocent small or large chronic goiters. Not 
infrequently the small, one-sided goiter may be associated with more 
prominent symptoms than are found with the larger growths—there is 
no rule to guide the clinician. It must be remembered that acute exacer- 
bations in slightly but previously changed thyroids may promptly cause 
symptoms and these may subside within limited periods. 
Typical and atypical types of the disease by their symptomatology 
and course, prove that the fundamental fault in both is the same, that in 
the typical, the toxemia is deeper and the increased metabolism definite 
and striking. The larger number of tachycardias in women which cannot 
be explained, whether associated with thyroid enlargement or not, are due 
to perverted thyroid function. 
My material analyzed at the end of 1913 included 5,370 cases of 
internal disease among which I found 186 of goiter (3.46 per cent). 
Of this number 89 (1.66 per cent) were simple uncomplicated goiter; 
97 (1.8 per cent) were diagnosticated as belonging to the class of exoph- 
thalmic goiter. Of this number 55 (1.2 per cent) of the total number of 
cases proved to be atypical exophthalmic goiter; 42 (.78 per cent) were 
typical in all symptoms. These statistics prove that over 50 per cent of 
all exophthalmic goiters are atypical, i. e., they may be recognized with- 
out the presence of all of the cardinal symptoms of the typical type of 
the disease. 
(2) Clinical Forms.—The second important factor for prognosis is 
the recognition in the individual case of the leading features which jus- 
tify classification. Sattler’s statement receives corroboration from all- 
clinicians; he says, “There are types rich in symptoms and even at the 
height of the disease types poor in symptoms.” 
I would classify my cases as: 
I. Typical exophthalmic goiter 
(a) Acute exophthalmic goiter 
(b) . Chronic exophthalmic goiter 
II. Atypical exophthalmic goiter 
Basedowoid—formes Frustes (Stern). 
The former (I) are those which include in their symptomatology four 
or five cardinal symptoms of the disease; the (II) atypical types include THYROID DISEASES 
1141 
those cases in which one or more cardinal symptoms of the disease are 
absent during varying periods and in which they may never appear. In 
all of these cases the dictum of Charcot must be upheld: “Sans tachv- 
cardie il n’y a pas de maladie de Basedow.” (“Without tachycardia there 
is no Basedow’s disease.”) 
Heredity.—Heredity plays an important role in this disease. It is 
not at all unusual to find two or more members of the same family with 
the disease and to note how emotional causes in the predisposed increase 
a train of previously ill-defined symptoms. The disease selects females 
by preference and during the period of sexual activity. Acute hyper- 
thyroidea in my material has been more frequent in the male. One male 
to nine females has been my experience. Buschan in 980 cases of ex- 
ophthalmic goiter found 175 in men and 805 in women. Leonard 
Williams makes the unqualified statement that “the greater number of 
subjects of Graves’ disease are degenerates.” I cannot entirely subscribe 
to this statement. 
i. Typical Exophthalmic Goiter 
(a) Acute exophthalmic goiter 
While the overwhelming number of cases of the disease develop gradu- 
ally, there are a few in which it suddenly overpowers the patient without 
warning. My material includes live cases of acute hyperthyroidea; all 
ended fatally. These latter included one woman, aet. 43, who developed 
the disease about six weeks after confinement ; two were boys aged respec- 
tively 12 and 21; one was a man whb had an old goiter which had never 
given rise to symptoms, and one was a girl who out of a clear sky had 
acute hyperthyroidea with evidences of compression, cyanosis and the car- 
dinal symptoms, and who promptly died. 
In none of my cases was there improvement after the initial symp- 
toms; in all there was extreme asthenia, marked cardiac insufficiency, 
rapid increase in the size of the thyroid, prominent eyes, but not marked 
exophthalmos; tremor was extreme; there was cyanosis in the terminal 
stage and glucosuria in two. The temperature was only slightly elevated. 
Blood pressure was normal until reduced by the terminal myocardial 
insufficiency. 
When acute hyperthyroidea includes severe gastro-intestinal symptoms 
the loss of flesh and weakness are rapid, the heart becomes insufficient 
within the first four days, the toxemia causes deep involvement of the 
sensorium, and death is the rule. 
In four of my cases there was mental torpor and these were uncon- 
scious during the last hours of life. In the males and the young girl there 
was delirium. The woman, aet. 43, was conscious to the end. I have 
seen none of the cases described by others (Sattler) in which after an 1142 
DISEASES OF THE DUCTLESS GLANDS 
acute period the symptoms subsided completely without recurrence. Of 
the five cases of acute exophthalmic goiter above mentioned only two are 
included in the 186 cases of goiter, the others were met before the begin- 
ning of the series here included. 
Manipulation of a goiter, compression for treatment, may promptly 
produce all of the cardinal symptoms of acute hyperthyroidea and death. 
One such case I recently saw in consultation (the young man, aet. 21, 
above mentioned) who had a small goiter for which manipulation was 
used. ITis acute hyperthyroidea followed the second treatment and he 
died before the end of the seventh day. Similar cases have been reported 
by Briege (vibration treatment). 
Acute exophthalmic goiter has followed the use of x-rays to the gland 
(Cvostek, H. E. Schmidt) and it should not be forgotten that in the 
presence of goiter alarming or fatal acute hyperthyroidea may follow the 
administration of thyroid extract in large doses (Hotthaft) (A. Kocher). 
That acute hyperthyroidea of mild character may recover there can be no 
doubt. Cases of acute iodtliyroidism run a rapid course. 
(b) Chronic Exophthalmic Goiter 
(Chronic Typical Hyperthyroidea) 
1. Parry’s Disease 
2. Graves’ Disease 
3. Basedow’s Disease. 
The cardinal symptoms of the typical disease are easily recognized— 
four always leading—the accompanying clinical features are so many, 
that to consider the significance of all would lead us to dilate on most of 
the organs of the body. 
Besides cardiovascular symptoms, ocular symptoms, including exoph- 
thalmos and muscular insufficiencies, goiter, tremor, symptoms referable 
to the sympathetic system, the leading clinical manifestations which com- 
plicate the disease include: 
Spasms—Tic—clonic spasms, tetany, spastic torticollis and convulsive dis- 
turbances of the speech 
Chorea—(adult and infantile) (A. Jacobi) 
Epilepsy— 
Paralytic Conditions—Paraplegia, hemiplegia 
Myasthenia 
Ophthalmoplegia and Bulbar Paralysis 
Acute Bulbar Paralysis 
Spinal Lesions—Amyotrophic disease; atrophic, anterior disease 
Progressive Muscular Paralysis 
Multiple Neuritis 
Sensory Disturbances THYROID DISEASES 
1143 
Reflex Anomalies 
Migraine 
Insomnia and Somnolence. 
OTHER COMPLICATIONS REFERABLE TO THE NERVOUS SYSTEM INCLUDE: 
Brain Tumor 
Cerebral Hemorrhage 
Syringomyelia 
Paralysis Agitans 
Progressive Paresis 
Multiple Cerebrospinal Sclerosis 
Locomotor Ataxia 
Hysteria 
Neurasthenia 
Meniere’s Complex 
Psychoses 
Vasomotor Disturbances 
Digestive Symptoms 
Respiratory Symptoms 
Diseases of the Genito-urinary Organs 
Skin Changes—Urticaria 
Pigmentation 
Pruritus 
Erythema 
Purpura 
Multiple Fibromata 
Edema—localized or general 
Dercum’s Disease 
Myxedema 
Glycosuria and Diabetes 
Urinary Anomalies—Polyuria 
Polydipsia 
Albuminuria. 
The Prognostic Significance of the Leading Clinical Features.— 
Cardiovascular Symptoms.—Tachycardia and other cardiovascular dis- 
turbances influence prognosis very materially. Long continued rapid and 
uncontrolled hearts with gastro-intestinal symptoms and associated emacia- 
tion, particularly if there he diarrhea, is a bad and unfavorable compli- 
cation. The chances for the patient with the “goiter heart” are not bad 
and it is often surprising to note how erratic and arhythmic the heart 
may remain during long periods and yet there is final improvement, though 
not, as a rule, complete recovery. It is further a noteworthy fact that 
these patients may for years without danger continue at their work, when 
not too strenuous, without aggravating their heart condition. The prog- 
nostic significance of the heart anomalies must be interpreted in connec- 
tion Avith the individual case and must include cautious consideration of 
all the associated conditions. If the myocardium is tired or dilated, with- 
out marked degeneration, in spite of abundant blowing systolic sounds and 1144 
DISEASES OF THE DUCTLESS GLAUDS 
arhythmia, the prognosis is not of necessity (for life) had. Most deaths 
directly due to hyperthyroidea without complications yield to myocardial 
degeneration after long periods of uncontrolled tachycardia and dilatation. 
The persistence of a blowing systolic bruit over the enlarged thyroid is 
characteristic of true hyperthyroidea and may be associated with “shaking 
head” with each cardiac impulse (Musset’s phenomenon). 
These symptoms usually yield with the general improvement of the 
patient. In self-limited cases or in those relieved by surgical operation 
the heart is often sloiv to regain its normal balance; it continues irritable, 
often with relative insufficiencies, dilated, and revolts on slight cause. The 
majority of these hearts after many months improve and remain service- 
able though they may never become absolutely normal. Decompensation 
is rare unless provoked by carelessness, overwork or added disease (neph- 
ritis, arteriosclerosis). 
Blood pressure study of exophthalmic goiter, contrary to what might 
be expected from the small, rapid and often thready and erratic pulse, 
offers but little of value for prognosis. Exophthalmic goiter is not a 
hypotensine disease; systolic pressure is likely to be normal or little 
changed during the active period of the disease; at times it is slightly 
above the normal, rarely hypotensine during the height of symptoms. In 
the terminal stage or with threatening cardiac insufficiency it may fall 
far below normal; the associated symptoms at such times offer the 
indications for safe prognosis. 
The pulse amplitude may remain about normal or in the late stages 
register between 10 to 25 mm. Hg. With hyperthyroidea, glucosuria, 
arteriosclerosis, and kidney involvement high blood pressure is present 
and demands interpretation. Such patients properly nursed and rested 
may live during long periods. 
Tremor.—Mild atypical or typical cases are not materially disturbed 
by tremor. There are but few cases of the complex in which tremor is 
not present at some time during the course of the disease. There are 
cases in which tremor is marked, in which it persists uncontrolled by treat- 
ment, but it does not per se add to the dangers of the disease. Active 
tremor is very likely to be present with the more profound poisoning and 
is, therefore, when considered with the other grave and uncontrolled symp- 
toms, of serious import. 
Tremor or chorea with deep involvement of the sensorium is always 
serious and is rarely an accompaniment of the milder types of the disease. 
Chorea is found occasionally in cases of the disease in early life (Jacobi) 
and adds to the danger in the presence of endocarditis or pericarditis. 
Spasm.—Painful cramps are annoying but not serious. Spasms may 
be tonic or clonic. Tetany has complicated one of my cases and was 
associated with spasm of the glossopharyngeal muscles and threatening 
asphyxia. In this case there was cyanosis, and it became necessary to THYROID DISEASES 
1145 
do an emergency thyroidectomy which saved the life of the patient. In 
one year, however, there was a return of the same threatening symptoms 
—glossopharyngeal spasm, tetany, tic convulsive and tachycardia. In this 
case, as in most which run a parallel course, the parathyroids are probably 
involved. This complication is exceedingly rare. 
Kocher has seen but three cases in his material with tonic spasms. 
The Trousseau and Cvostek phenomena were present in my case and in 
others reported (Kocher, Mattiesen, Steinlechner, Marinesco, Stumme 
and Loewenthal and Wiebrecht). 
Eye Symptoms.—Exophthalmos or protrusion of the eyeball may be 
double or one-sided. The atypical cases may escape with hut slight 
exophthalmos; the typical show more or less. The most serious cases 
have the more prominent eyes, though this is not a rule without many 
exceptions. 
Of all the cardinal symptoms of the disease, prominence of the eyes is 
most frequently absent. In 1,415 cases of Basedow’s disease 330 never 
showed exophthalmos, i. e., 23.2 per cent (Sattler). 
Exophthalmos as a single symptom is of little prognostic value; its 
persistence with other uncontrolled symptoms argues in favor of deep 
toxemia. It is not always constant, may recede during long or short 
periods. It is not likely to return alone, hut always with one or more 
of the cardinal symptoms—usually erratic heart (tachycardia). The 
other vascular symptoms are not indicative of the seriousness of the 
disease. 
Goiter.—Throughout this chapter I have repeatedly referred, in con- 
nection with my consideration of the influence of symptoms, to the en- 
largement of the thyroid gland, and I feel that I have demonstrated the 
fact that the size of the goiter does not bear close relation to the severity 
of the symptoms; indeed small insignificant enlargement is often asso- 
ciated with malignancy of symptoms and large masses may do their great- 
est harm by pressure. Acute increase in the size of the gland is always of 
significance. The small one-sided goiter may, when its activity is in- 
creased, prove a serious menace. My material includes cases in which 
such a condition frequently threatened the life of a patient whose hyper- 
thyroidea finally yielded without operation, with the result that she has 
remained well during eight years. 
Thymus enlargement is a frequent complication of hyperthyroidea; 
it may cause serious pressure symptoms or it may lead to sudden “thymus 
death.” It is my belief that in occasional acute cases with suddenly 
enlarging thyroid and thymus, the latter has been the more important 
factor in causing death. The thymus is involved in most severe hyper- 
thyroideas. 
Repeated attacks of tonsillitis have a decidedly unfavorable influence 
on the disease and tonsillar infection is easily contracted. Tonsillectomy 1146 
DISEASES OE THE DUCTLESS GLANDS 
has in a number of cases prevented repeated infection with associated 
depression. 
Sweating.—Excessive sweating has a depressing effect in some cases; 
as a rule it is not of great prognostic import. It is usually associated 
with disagreeable “flashes of heat” and erythema, and is more uncom- 
fortable than weakening. 
Loss of Weight.—Faulty metabolism and rapid waste are charac- 
teristic of many cases. The loss of weight may he enormous during the 
early period of the disease or with acute exacerbations of chronic hyper- 
thyroidea. Loss of weight alone offers but little which justifies prognosis. 
Without other symptoms of overpowering toxemia it is not of serious 
import; if, however, loss of weight is associated with marked cardiac 
asthenia, dilatation, myasthenia and persistent gastro-intestinal symptoms 
(vomiting, diarrhea and anorexia) the forecast should be guardedly given. 
Most of these cases unless promptly controlled end fatally within a lim- 
ited period. 
Mental State.—Patients with marked mental anomalies may im- 
prove very materially, but complete return to the former normal state in 
chronic cases is hardly to be expected. With the psychoses fully devel- 
oped we have been very unfortunate. Some have been committed to state 
institutions and have not improved; others have remained at home— 
chronic psychopaths never materially improved; while others have devel- 
oped acute manias and have died within a few weeks or months of the 
development of the psychosis. Hysteria, hystero-epilepsy and the emo- 
tional element are not easily controlled in the chronic cases. Periods of 
improvement are often followed by relapse. 
The Complications Referable to the Nervous System.—The 
organic changes of the nervous system mentioned above are not materially 
influenced by the presence of hyperthyroidea; while the latter is unfavor- 
ably influenced by the addition of any one of the graver anomalies of the 
central or peripheral systems. I have elsewhere in this volume con- 
sidered the association of epilepsy with exophthalmic goiter, a combina- 
tion which may not end in death directly from the combination, but it 
offers little or no hope of relief. 
Migraine, insomnia and somnolence with hyperthyroidea are in most 
cases amenable to treatment. 
Paralytic conditions once present are likely to persist; their prognosis 
must be based on the associated primary lesion. The addition of acute 
bulbar paralysis is promptly fatal. 
Digestive Disturbances.—I have frequently referred to the over- 
powering influence of digestive disturbances The most unfavorable cases 
are those in which digestion is impaired beyond repair, in which colliqua- 
tive diarrhea with the typical disease saps the patient’s strength. 
The Respiratory Symptoms.—These may be due to the toxemia, to THYROID DISEASES 
1147 
pressure, to infection or indirectly to heart lesions. Each of these causes 
demands separate consideration in the individual case. 
The Skin Changes.—Urticaria, 'pruritus, erythema, edema (localized 
and general) may yield after medical or surgical treatment. Purpuric 
conditions are always serious; they should lead to cultural tests when 
present with symptoms of infection; they may he due to malignant endo- 
carditis, when they end fatally. The pigmentation, fibrosis and trophic 
disturbances are permanent (see separate chapters—Dercum’s Disease, 
etc.). 
Genito-Urinary Organs.—There are but few cases of exophthalmic 
goiter which in women are not preceded or accompanied by menstrual 
disturbances. I have shown in an article recently published that 15 per 
cent of all cases of goiter are associated with uterine myoma or flbro- 
myoma. In these cases there is a strong hereditary tendency to both 
goiter and uterine myoma. 
A family of seven daughters was found in which a number of aunts 
and cousins on the father’s side had goiter; six of the seven daughters 
had uterine myomata and four had goiter. The mother was free from 
myoma or goiter. 
Operations for the uterine growths offer a good prognosis; the removal 
of the goiter does not influence the myoma; the removal of the myoma 
does not materially influence the goiter, hut it often influences the tachy- 
cardia favorably. The genito-urinary complications are not usually of 
serious import. Transitory albuminuria is not infrequent. Nephritis 
may prove a serious complication but is not usual. 
Typical and severe exophthalmic goiter has been seriously affected by 
profuse hematuria in two of my cases; in both, there was nephritis with 
probable purpura. 
Glucosuria and Diabetes.—I have elsewhere considered the influ- 
ence of the ductless glands on the liver, sugar production, retention and 
associated acidosis (See Diabetes Mellitus). 
There is a close relation between the thyroid and the pancreas; the 
secretion of the former materially modifies the function of the latter. 
The presence of glucose in the urine in hyperthyroidea depends upon a 
changed relation in all probability of these organs to each other—a fact 
which is strengthened by our inability to produce glucosuria after thy* 
roidectomy or in myxedema. 
With profound involvement of the adrenals and associated diabetes or 
glucosuria weakness becomes extreme, tremor excessive, the cardiovascular 
symptoms are aggravated, there is rapid tissue waste, and the outlook 
is bad. 
Myxedema.—Exophthalmic goiter with all of its typical symptoms 
of hyperthyroidea may, w7hen the gland has worn itself out, be displaced 
by fully developed myxedema and in these cases the hyperthyroidea does 1148 
DISEASES OF THE DUCTLESS GLANDS 
not as a rule, recur, but the myxedema is favorably influenced by thyroid 
extract continually administered. Just so soon as it is discontinued, the 
symptoms recur. My series includes one case. (Moebius reports similar 
experiences.) 
Acromegaly.—When thyroid overactivity is associated with acro- 
megaly, the latter, as in uncomplicated cases, remains uninfluenced by 
any known treatment. One of our cases of goiter with mild hyperthy- 
roidea developed acromegaly and syringomyelia. The patient is still 
living after many years of continuous and uninfluenced symptoms though 
she has since had a hysterectomy and oophorectomy for fibromyoma of 
the uterus and ovarian cyst; she also has a ranula, pigmentation of the 
skin and multiple skin fibromata. 
Blood Picture.—In the average advanced case there is a reduction 
of erythrocytes; there is leukocytic decrease with monolymphocytic in- 
crease, eosinophilic increase, reduction of mast cells. Transitional forms 
may he either increased, normal or reduced. 
Grawitz offers an unfavorable prognosis in cases in which there is an 
absolute lymphocytosis. Kocher has found, after operation, a fall of 
lymphocytosis from 48 to 2.7 per cent and a return of neutrophilic 
leukocytosis. Such results are not surprising and are found after other 
operations (laparotomies). The consensus of opinion justifies the con- 
clusion that the prognosis of the disease is more unfavorable in cases with 
marked leukocytosis and high absolute lymphocytosis. Coagulation time 
is prolonged and autolysis is increased on the addition of the blood serum 
of the hyperthyroideic patient (Kottmann, Blumenthal). 
Kostlivy concluded from his surgical material (already mentioned) 
that radical intervention was exceedingly grave with absence of mono- 
nucleosis (lymphocytosis). 
Grave or secondary anemia in all cases adds to the danger; ultimately 
the outcome must depend upon the cause of the added anemia and the 
resistance of the patient. 
ii. Atypical Exophthalmic Goiter 
The preceding pages include the consideration of the prognostic sig- 
nificance of the separate symptoms of hyperthyroidea. In the atypical 
type of the disease there are, as a rule, fewer grave symptoms and com- 
plications; while the course is often chronic, the patient bears the toxemia 
fairly well and is less likely to fall into the asthenic state characteristic 
of the grave type. 
Atypical exophthalmic goiter may merge into the typical complex 
without more than a short period of increasing symptoms, or the meta- 
morphosis may be gradual. Close watch will unearth a large number of 
unsuspected atypical hyperthyroideas in which the cardiovascular symp- THYROID DISEASES 
1149 
toms will remain in the ascendency. It is an established fact that atypical 
cases are likely to prove chronic, and with one or two syinptoms many 
continue uninfluenced by medical treatment. The surgical treatment of 
these cases does not in the majority of cases entirely and permanently 
relieve the leading subjective complaints. 
Stern’s basedowoid disease deserves to be classified among the atypical 
hyperthyroideas. In these, the symptoms can be easily traced to early 
life though the complex remains undeveloped and decades may pass before 
its leading features are developed. In these cases the trophic disturb- 
ances are in the foreground—the typical types of Basedow’s disease de- 
velop in only 3 per cent before the twentieth (20th) year, while 60 per 
cent of atypical, or basedowoid, cases are found before that time. 
The atypical types develop in those with neuropathic tendencies and 
marked heredity. The basedowoid cases are less likely to suffer from 
continuous tachycardia than are the atypical cases which are more closely 
related to the genuine degenerative types. Tachycardia recurs during 
acute exacerbations—in paroxysms. The atypical cases of the basedowoid 
type do not as a rule develop marked exophthalmos, while the Graeffe 
phenomenon is not constant, the Moebius is frequent, the Stellwag is 
usually present, the goiter small and soft and the systolic bruit over it 
absent, tremor is present and choreatic. The heart is arhythmic, not 
enlarged; often a systolic bruit is heard; respiration is irregular. The 
reflexes are exaggerated. The basedowoid type is obstinately chronic 
but its mortality is low. The operative results are not favorable in this 
class of cases. 
Goiter Heart {Kraus) 
Atypical Hypertiiyroidea 
The so-called goiter heart of Kraus in which cardiovascular symptoms 
are added to a preceding symptomless goiter or a suddenly appearing 
goiter, is considered among the atypical types of the disease, depend- 
ent upon perverted thyroid function or hyperthyroidea, in which the 
prognosis for life is good but complete relief from tachycardia is hardly 
to be expected. These patients show “irritable hearts” on slight cause, 
perspire freely and are likely to show marked tremor. The ocular symp- 
toms are variable but not persistent. These cases may develop the typical 
complex on comparatively slight cause: after profound shock or emotion, 
infection, pregnancy, gynecological operations, or the administration of 
large doses of thyroid extract (Kraus, Barker, Kocher, Ball, Riedel, Wells, 
Gitterman, Auld, Rogers). 
Goiter and Ilyperthyroidea 
When a goiter (uncomplicated) in an adult has remained unchanged 
many years and enlarges perceptibly without known cause (pregnancy 1150 
DISEASES OF THE DUCTLESS GLANDS 
occasionally), hyperthyroidea may he expected to develop and the symp- 
toms are likely to he typical. 
There is no time in the history of ordinary goiter when either typical 
or atypical exophthalmic goiter may not develop. Billings reports 20 
years of uncomplicated goiter with final hyperthyroidea. Kocher (A.) 
reports cases in which exophthalmic goiter developed after from 3 to 12 
years of small or large goiters, and Kocher (W.) reports 72 cases of this 
kind of which 60 were operated without a single fatality. Of 53 cases 
followed, 51 were permanently cured and two improved. 
Relapse in both typical and atypical cases apparently cured is not 
unusual and attention in offering prognosis should he called to this possi- 
bility. Some relapses are mild and evanescent, others are severe, acute, 
and may promptly lead to death, especially in those who have been weak- 
ened by repeated exacerbations. Relapse may follow radical operation 
for exophthalmic goiter; Kocher believes that in these cases insufficient 
thyroid was removed. My experience has not always corroborated this 
conclusion; I have met relapses after both ligation and radical operation. 
Thyroid Neoplasm and Ilyperthyroidea 
Sudden development of symptoms of hyperthyroidea in adenoma or 
malignant neoplasm of the thyroid is possible and usually leads to pro- 
gression of'both physical and mental weakness, and does not improve. 
Nodular masses in the enlarged thyroid are always of serious import, 
for degenerative change or perversion of function leading to persistent 
and threatening hyperthyroidea must he expected. There are cases of 
goiter with multiple adenoma in which periods of exacerbation are fol- 
lowed by relief, hut in the end particularly in men who continue to over- 
work, sudden and severe cardiac insufficiency may cause dilatation and 
death. 
Hard thyroids with multiple nodular deposit and erratic heart demand 
close watching; such combination is serious. 
Self-limitation and Spontaneous Cure 
In a large number of cases hyperthyroidea proves to be a self-limited 
process, and approximate cure in the presence of all of the striking 
symptoms of the disease is by no means infrequent. Spontaneous cure 
may include the disappearance of exophthalmos and tachycardia as well 
as tremor. 
In these cases added insult—emotional factors—will he likely to pro- 
voke short periods of symptoms or recurrence of all symptoms, or there 
may he hut short periods of symptoms during acute exacerbations. Some 
of the hasedowoid cases, a few of the typical chronic cases may to all THYROID DISEASES 
1151 
appearances remain perfectly well and die of intercurrent disease. One 
of my typical cases ran its course to full recovery in two years; she 
remained well fifteen years, when a myoma uteri which was present early 
in her history degenerated and she died of cancer of the uterus. Preg- 
nancy influences the disease unfavorably, aggravates it and may cause 
such alarming acute hyperthyroidea as to threaten life. 
The psychic element (suggestion) enormously influences hyperthy- 
roidea. There are cases in which, under favorable surroundings with 
rest and healthy suggestion, the improvement of all symptoms follows 
promptly. There are a number of recorded cases in which systematic 
hypnotic suggestion has led to full recovery. 
Rest, freedom from care, wholesome living and change of scene are 
powerful factors and influence prognosis favorably. 
Children rarely develop the disease, with them the acute types are 
usually fatal, though recoveries are recorded without recurrence (Sattler). 
My series does not include a single case. In dispensary and hospital 
practice an occasional typical chronic case presents in which the heart 
lesions are usually advanced. 
Leonard Williams in considering the results of the operative treat- 
ment of exophthalmic goiter has recently said: “The truth is, these opera- 
tive procedures in Graves’ disease represent the heroid application of 
loose conclusions from insufficient data.” lie believes that “the produc- 
tion of the symptoms” is not due to the goiter but “the evidence points 
strongly—even overwhelmingly—in the direction of showing that the 
thyroid is merely an unwilling agent” . . . “and reflects reluctantly 
enough a disturbance which originates elsewhere.” We do not commend 
this statement as justified without qualification and amplification but 
give it to prove that in spite of brilliant results the last word has not been 
written on the influence of surgical operation for the relief of thyroid 
anomalies. 
Mortality 
It is exceedingly difficult, in fact, impossible to give a figure which 
even approximates the truth concerning the mortality of the disease. 
There are so many factors to be considered and so many complications 
which influence the issue that no statistics can be considered reliable. 
The author can simply offer those which he has and must look to the 
future for more reliable data. Mortality in my cases has not been high. 
In central Hew York we rarely record a death due to uncomplicated 
hvperthyroidea. Eight per cent is a high figure to offer and it is unques- 
tionably above the average of treated cases in Hew York State. 
Sattler gives his mortality at 11 per cert. 
Kocher 22 per cent. 
Mackenzie 30 per cent. 1152 
DISEASES OF THE DUCTLESS GLANDS 
Operated Cases.—Kocher reports 7G per cent cured (with persistence 
of exophthalmos in one-fourth of these). His mortality was 3.9 per cent; 
one-third of his cases were repeatedly operated. 
Eiselberg’s Klinik: in 45 cases there were 3 deaths among the first 
four operated; in all he had 6 deaths. Eighteen of his patients were 
permanently cured, 8 improved. 
Mayo, Charles H.—1 to 3 per cent mortality following operation. 
Tinker, Martin—less than 1 per cent mortality following operation. 
Schultze—72 per cent cured, 12 per cent improved, 2 per cent abso- 
lute failures or accidents, 12 per cent deaths. 
Rehn—75 per cent cured, 9.8 per cent improved. 
The ultimate influence on symptoms in Tinker’s and Mayo’s cases, as 
I interpret their reports, are possibly more encouraging than are those 
of the Continental operators. 
Capelle reports that 100 per cent of operated cases which ended fatally 
showed enlarged thymus glands, and Kostlevy holds that in the absence 
of mononuclear lymphocytosis the prognosis for surgical intervention is 
exceedingly grave. 
There are occasional cases of hyperthyroidea in young subjects (usu- 
ally males) with large goiter and a remnant of thymus gland which at 
times cause acute and threatening attacks of asphyxia. These cases are 
always serious and when massaged the symptoms of hyperthyroidea may 
be promptly aggravated; the pressure may cause cyanosis, the cardiac 
asthenia is extreme and death may follow. Such cases justify thyroidec- 
tomy even in young subjects; for the prognosis is surprisingly favorable 
following the operation. 
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a, 111. 
Sattler. Die Basedow’sche Krankheit. Leipzig, 1909-1910. 
Schmidt (H. E.). Forlsch. auf d. Geb. d. Roentgenstrahlen., xiii, 324• 
Steinlechner. Wiener med. Wchnschr., ix, 5, No. 1. 
Stern. Jahrb. f. Psychiatrie., Bd. xxix. Leipzig, 1909. 
Mitth. aus d.Grenzgeb. d. Med. u. Chirurg., 1912-1913. 
Stumme. Deutsch. Ztschr. f. Chirurg., xc, 265. 
Tinker {Martin B.). Transact. Am. Acad, of Ophthalmology, 1912. 
Wells {B. H.). Am. Med. News, June 25, 1905. 
Williams {Leonard). The practitioner. London, Jan., 1915. 
(6) Myxedema—Cretinism 
(Thyroid Insufficiency, “Cretinoid Change,” Cachexie Pachydermique) 
Thyroid Insufficiency.—The abolition of function of the gland or 
partial or complete reduction of the parenchyma of the thyroid leads to 
a complex of symptoms which is easily recognized because of character- 
istic myxedematous infiltration of the subcutaneous connective tissue. 
There is dry skin, subnormal temperature, mental tardiness, often atrophy 
of the thyroid gland and marked reduction of vital processes—metabolic 1154 
DISEASES OF THE DUCTLESS GLANDS 
particularly—reduction of animal lieat; trophic changes in the skin are 
prominent, as are those in the nails, hair and teeth. There is marked 
tendency to early arteriosclerosis—to infection and death from tuber- 
culosis. 
The “maximal thyroid insufficiency” is found when there is complete 
absence of development of the gland or in cases in which the entire struc- 
ture has been removed surgically (Operative myxedema). 
Leopold-Levi has recently dilated on the functions of the gland in 
considering its insufficiency and for purposes of prognosis I quote the 
following: “The function of the thyroid gland is manifold. It con- 
trols the nervous system, the nutritional exchanges and the humoral 
equilibrium.” “There is increasing evidence to show that it is in part 
responsible for the process which I propose to describe as thermogenic, 
oregogenic, morphogenic, antigenic and prophylactic.” 
In the consideration further of the influence of the gland and the 
dangers of its insufficiency, the clinician should remember that its two 
main functions include the “promotion of cell growth, and the elimination 
of the waste material which results from the destruction of the tissues” 
(Hertoghe). Its disturbance affects the “chemistry of the entire organ- 
ism” unfavorably. Hypothyroidea reduces the normal resistance to 
infection and invites blood changes—hemophilia, anemia and lympho- 
cytosis. 
The English school has done more than any other to base our knowl- 
edge of hypothyroidea upon a solid foundation. In 1873 Sir William 
Gull called attention to a condition which he termed “cretinoid change.” 
In 1877 Ord spoke of the same condition as myxedema; about the same 
time Charcot noted the complex and named it “cachexie pachydermique” ; 
Schiff and George Murray immortalized their names by proving experi- 
mentally that the removal of the gland and its grafting into the animal 
produced symptoms in direct proportion as they supplied or removed 
thyroid substance. The removal or destruction of the gland produces a 
characteristic cachexia which is fatal unless the continuous administration 
of the thyroid extract or substance compensates for the loss. 
In the consideration of thyroid insufficiency I adopt the classifica- 
tion of the Commission of the London Clinical Society: 
I. Operative Myxedema (cachexia strumipriva) 
II. Sporadic Cretinism or myxedema of the child 
III. Endemic Cretinism (ordinary myxedema or myxedema of the 
adult) 
IV. Cretinoid State due to complete loss of gland function. 
Deficient or reduced thyroid function from whatever causes produces 
practically parallel symptoms and tissue changes. In children it is 
safe to forecast more or less arrest or inhibition of the normal proc- THYROID DISEASES 
1155 
esses of growth and the subcutaneous changes may vary, while in the 
adult there is usually greater infiltration of the skin—face and hands 
particularly—in proportion to the gland insufficiency. The prognosis is 
in occasional cases favorably influenced by the compensatory hypertrophy 
of the gland or accessory thyroid if present. 
Hertoghe calls attention to “those fortunate instances in which preg- 
nancy is accompanied by resorption of the infiltrates.” . . . “The favor- 
able phenomena in such cases are due to the hypertrophy of the thyroid, 
by which pregnancy is accompanied.” Such patients again lapse into the 
subthyroid condition after pregnancy or lactation. 
i. Operative Myxedema 
(Cachexia strumipriva) 
Total extirpation of the thyroid gland invariably leads to myxedema. 
When the parathyroids are completely removed at the same time, tetany 
promptly develops and in almost all cases causes death. Operative myx- 
edema will in the future demand little consideration from the surgeon 
for he has learned the effect of total thyroidectomy and is governed 
accordingly in his work. Occasionally malignant growths demand the 
total removal of the gland, in which cases the prompt administration of 
the thyroid extract prevents operative myxedema. 
Accessory thyroid tissue after operation may hypertrophy and com- 
pensate for the loss of the gland. 
In complete removal of the gland it may occasionally cause mild 
cachexia which is promptly relieved by the organic extract and does not 
return if its use is continued. 
ii. Sporadic Cretinism—Congenital Cretinism—Myxedema of the Child 
Congenital cretinism uncontrolled, unrecognized early, will invariably 
lead to developmental faults, both physical and mental. 
The evidences of hypothyroidea appear after the first few months of 
life. The conditions which are uniformly present in all varieties of myx- 
edema soon follow. Growth is stunted; the mental status at times in 
severe cases shows the cretin with hut few or no human attributes; the 
skin is dry; the tongue large, thick, heavy, protruding continually with 
persistent drooling; the eyes are half closed, the face expressionless. All 
these children look alike and remain oblivious to their surroundings, rest- 
less and crying much of the time, often developing hernia. As they grow 
older it is noted that there is no hairy growth, the teeth usually fail to 
develop; if they do develop they promptly decay and break. The hands 
become more and more “spadelike,” the eyebrows thin or absent, the lids 
puffy, the myxedematous tissue persists boggy, more or less resistant. 
The untreated cretin who lives, at sixteen years of age is no larger than 1156 
DISEASES OF THE DUCTLESS GLANDS 
a babe of two years. There is persistent mental torpor; these subjects 
learn nothing, they grasp nothing and are of the Mongolian type; they 
are idiotic. Life may be prolonged until thirty-five or forty years in some 
cases, though the majority die young of intercurrent infection, tubercu- 
losis, pneumonia, etc. I saw one male, aet. 35, a typical cretin without 
sexual development who resisted a severe pneumonia. Untreated cases 
are likely to die within the first two years of life. The blood shows 
anemia, lymphocytosis and eosinophilia. Reaction to pilocarpin is low- 
ered while adrenalin glycosuria is also reduced, but less than in adult 
myxedema. 
Prognosis.—The inhibition of growth in all directions persists in all 
cases of congenital myxedema so long as the condition remains undetected 
or untreated. Sporadic cretinism, treated early offers a good prognosis. 
The marvelous and prompt effect of a few grains of the thyroid extract 
in these cases is surprising; the introduction of the organic extract for the 
treatment of this anomaly is at once the greatest advance of modern medi- 
cine. The prognosis formerly absolutely bad is now encouraging; it 
requires only early recognition and persistent treatment to keep these 
patients comparatively normal. No myxedematous child or adult, unless 
there is thyroid growth or the organic extract of the gland is given as is 
his ordinary food in sufficient doses at stated intervals, can be expected 
to remain normal. There will always be a tendency to the subthyroid 
state. It is surprising to note how small the dosage needs to he to hold 
the cretin and promote growth. 
The congenital cretin who escapes treatment during the first decade 
of his life may he materially benefited by treatment, but his growth will 
not become normal; neither will he develop mentally as he would had he 
been given the food early (organic extract) which the athyroidea or 
hypothyroidea demanded. 
Treatment of the cretin after the tenth year is not encouraging, and 
the prognosis grows more unfavorable with increasing years and neglect. 
Congenital defects, unfavorable surroundings, faulty feeding and a variety 
of factors are paramount in the prognosis of these children. The removal 
to well-appointed institutions where treatment can be systematically fol- 
lowed increases the chances materially. 
iii. Endemic Cretinism 
(Ordinary Myxedema—Adult Myxedema) 
Adult myxedema is more frequent in women than in men. The close 
relation of the thyroid and organs of generation, leading often to exhaus- 
tion of the functionating ability of the gland, may account for the greater 
frequency of the disease in women. 
The symptoms develop insidiously, with the changed features and THYROID DISEASES 
1157 
characteristic skin changes; there is mental lethargy, including slow and 
monotonous speech. The mental processes in most cases are accurate but 
slow; the patients are able to think but thinking is exasperatingly tardy. 
The thick tongue of the congenital type is almost constant. The untreated 
cases develop moderate deafness, changes in the vocal organs, and ocular 
disturbances; besides the usual skin changes there are sluggish circula- 
tion and subnormal temperature.. There is often reduced electric excita- 
bility of the pneumogastric and sympathetic. Early arteriosclerosis in 
this form of hypothyroidea is an annoying and serious complication. 
Uncontrolled myxedema in the adult leads to intestinal paralysis—chronic 
constipation. 
Blood changes are the same as in the infantile form of the disease. 
Myxedematous anemia and blood changes are favorably influenced by 
thyroid administration as are also the metabolic processes which without 
such treatment remain subnormal. 
Myxedematous adults show a high tolerance for grape sugar while the 
ability to cause adrenalin glycosuria is also reduced. Severe cases may 
show genital anomalies—amenorrhea, sexual weakness. 
Hypophyseal lesions are not uncommon and unfavorably influence 
prognosis. 
Prognosis.—Myxedema may develop in the adult after a period of 
exophthalmic goiter, and offers a favorable prognosis (See Exophthalmic 
Goiter). In the absence of complications the prognosis of adult myxedema 
is good under rational organotherapy. Advanced arteriosclerosis and 
added infection, tuberculosis, pneumonia, myocardial disease and nephritis 
naturally deserve consideration in the individual cases and influence prog- 
nosis unfavorably. 
The use of the x-ray for diagnostic and prognostic purposes in all 
forms of myxedema offers valuable data; bone growth, hypophyseal in- 
volvement and other processes may be thus followed. 
Probably in most cases of cretinoid degeneration there is some rem- 
nant of thyroid function. The cretinoid degenerate is found oftener in 
Switzerland (Central Alps), Carpathia, in the Pyrenees and in the middle 
mountainous regions of Germany, than anywhere else. Unquestionably 
infected or tainted water holds the pathogenic toxin. These unfortunates 
are poorly housed, most are dwarfs, mentally dull, sexually undeveloped, 
and inefficient with goiters of varying size—“Degenerative histologically” 
(Falta). 
To these cases only the earliest recognition and treatment offer hope 
of any improvement. The majority live on aimlessly, develop cardio- 
vascular lesions, tense arteries and infections. 
iv. Cretinoid State Due to Complete Loss of Gland Function 1158 
DISEASES OF THE DUCTLESS GLAHDS 
Heredity.—In all forms of myxedema heredity is an important factor 
in etiology. Syphilis and tuberculosis, gout or diabetes and syphilis or 
tuberculosis, alcoholism and syphilis are paramount, for as Hertoghe has 
taught, “true congenital myxedema is the outcome of the superposition 
of two grave blemishes in the parent.” 
Prognosis.—It may he assumed that the average subject of myxedema 
—whether congerlital or acquired—always remains myxedematous so long 
as the gland structure fails to functionate or the absence of thyroid secre- 
tion is not compensated by the administration of the organic extract. The 
prognosis of all forms of myxedema is therefore good so far as life is 
concerned, and will, as already suggested, continue favorable with thyroid 
administration in the absence of complication. 
References 
Biedl. Innere Sekretion. Berlin & Wien, 1910, i, 2. Aufl., 1913. 
Charcot. Cachexie pachydermique. Gaz. des Hopit., Paris, 1881, No. 10. 
Falta. Handb. d. inner. Med. Mohr u. Staehelin. Berlin, 1912, Bd. iv. 
Gull (Sir William). On a cretinoid state, etc. Clinical Soc. of London, 1873. 
Hertoghe. The practitioner. London, Jan., 1915. 
Horsley (Victor). Report, etc. London Clin. Soc. Tr. 
Report on Myxedema, Supp. to vol. xxi, London, 1888. 
Leopold-Levy. The practitioner. London, Feb., 1915. 
Murray (G. W.). Twentieth century practice. New York, 1895. 
Ord. On myxedema, etc. 
Royal Med. & Chir. Soc. of London, 1877. 
Reverdin. Soc. Med. de Geneve, 1882. 
Schiff. Report on myxedema. Clin. Soc., London [l. c.), 1873 & 1888. 
Semon (Sir Felix). Clin. Soc., London, 1880-1881, xiv. 
Virchow (R.). Berl. klin. Wchnschr., 1887. 
B. Diseases of the Pituitary Gland 
(Dyspituitarism ) 
1. Hypopituitarism 
Infantilism 
The subject of infantilism never lifts himself above the physical and 
mental status of childhood. There is faulty or no sexual development in 
the majority of cases. There is in all direction an inferiority, a lack of 
the normal ability to produce or serve, or even an approach to the lowest 
ordinary mental or physical standard. 
Cause.—Probably we shall ultimately find that whether general or DISEASES OF THE PITUITARY GLAND 
1159 
partial, infantilism is primarily due to some faulty internal secretion, 
hypopituitarism. Even in those cases in which long-continued disease 
early in life has led to the cachectic type, it may be assumed that the 
faulty development is consecutive to changed relations of one or more 
ductless glands or direct change in histologic build and consecutive per- 
verted function of the pituitary gland. Cachetic types of infantilism are 
found in hereditary syphilis, the tuberculous, the otfspring of morphinists 
and alcoholics. 
Types.—Freund and von den Velden have recently classified all in- 
fantilism as either 
(a) General 
(b) Partial. 
(a) General Infantilism may be an accompaniment of myxedema 
■—cretinism, monogolism, absence of or miniature genital organs; it may 
accompany suprarenal, thymus or pancreatic disease. Syphilis, alco- 
holism, lead or mercurial poisons or morphinism in either parent, tuber- 
culosis, chlorosis, congenital heart anomalies, pellagra, faulty hygienic 
surroundings or underfeeding may lead to infantilism in the offspring. 
(b) Partial Infantilism includes: 
Infantilism with abnormally small and undeveloped sexual organs, 
cardiovascular congenital faults. 
Infantilism with faulty vocal organs—high-pitched speech, with faulty 
growth of hair (face and pubes) or with the mental attributes of the infant, 
during life (Freund, and von den Velden). 
Cretinoid infantilism may show some improvement when early de- 
tected, when sexual organs are present and complete and when treated 
with thyroid substance (See Myxedema and Cretinism). Those cases 
of the Frohlich type (dystrophia adiposo-genitalis) are not influenced by 
treatment; they are obese, awkward, with genitals undeveloped. In these 
cases there are positive evidences of pituitary disturbance (dyspituitarism 
of Cushing). 
Marburg has divided the cases of general adiposity and underdeveloped 
genitals into (1) simple adiposity, (2) adiposity with genital atrophy 
and (3) simple genital atrophy; and Church adds a (4) type of infan- 
tilism in which there is a lack of physical and sexual growth. Marburg 
insists that hyperfunction of the pituitary ends in acromegaly, that hypo- 
pituitarism or hypofunction causes general adiposity and genital dys- 
trophy while entire destruction or defect or complete loss of function 
produces a cachectic condition much like cachexia strumipriva. 
The subjects of infantilism may show all of the features of continuous 
youth (ateliosis), or wrinkled and inferior they present the picture of 
premature old age (progeria). Gilford has called attention to these two 
types. The ateliotic cases are either asexual or sexual. The asexual type 1160 
DISEASES OF THE DUCTLESS GLANDS 
is more a developmental fault than cretinoid or specific, while in the 
sexual form the development of the sexual organs begins at puberty and 
the body remains dwarfed (Tom Thumb type). 
Outlook.—All subjects of infantilism, whatever the type, always re- 
main inferior, ready to yield to traumatism, particularly liable to injury 
of the genitalia, subject to infection and without resistance. The cell 
resistance is never normal and complete recovery from diseases, consti- 
tutional or infectious, is not to be expected. There is never a moment 
when the subject is not to be considered pathologic. The daily tax, as 
Freund has well said, cannot be met and tuberculous infection finds a 
ready habitat in the lungs and other organs of these subjects. There is 
no treatment which favorably or permanently influences the mental or 
physical status of these unfortunates, though some cases have been reported 
improved by pituitary administration. The majority die young. 
References 
Church. J. Am. Med. Ass., 1910. 
Gilford. Lancet, London, 1913, 1, 412. 
Freund u. von den Velden. Mohr u. Staehelin’s Handb. d. inner. Med., 1912. Bd. iv. 
Frohlich. Wien. klin. Rundschau, 1901. 
Marburg. Deutsch. Ztschr. f. Nervenheilk., 1908. 
2, Hyperpituitarism 
Acromegaly 
(Pierre Marie, 1886) 
Diagnostic Factors.—In the consideration of acromegaly the reader 
is reminded of the facts upon which we base onr modern conception of 
the disease. In abstract they are the following:. The pitnitary body 
consists of three parts: 
(a) The anterior lobe or glandular portion 
(b) The middle portion 
(c) The posterior lobe or nervous portion. 
In true acromegaly the change is probably limited at first to the 
anterior or glandular lobe and the pathologic lesion is, as a rule, the 
growth of adenomatous tissue—true adenoma. The anterior lobe per- 
forms an important function in its relation to body growth, more par- 
ticularly the osseous system, and there seems further to he a strong rela- 
tion between this lobe and the sexual organs. 
The intermediate or middle portion is not related to skeletal growth DISEASES OF THE PITUITARY GLAND 
1161 
but exercises an important function in keeping up blood pressure, slowing 
the heart, “increasing the activity of smooth muscles and causing in- 
creased secretion of the urine, the gastric juice and the milk” (Vincent). 
This lobe also exerts an important influence over carbohydrate metab- 
olism. Vincent and others hold that the secretions of the middle lobe 
are passed on into the “nervous” portion proper (posterior lobe) where 
they become converted into more active forms, or become concentrated. 
Association.—I have, in other chapters, called attention to probable 
reciprocal relations of the ductless glands and to the frequent association 
of lesions in two or more at the same time and compensatory changes 
after removal of one ductless gland. The hypertrophy of the pituitary 
body after thyroidectomy is an example. Diabetes is frequent with dys- 
pituitarism, which as the disease progresses, often yields and surprising 
tolerance for sugar develops (See Diabetes Mellitus, also Exophthalmic 
Goiter). Goiter and acromegaly are comparatively frequent in the same 
subject; in one of my cases goiter, acromegaly and syringomyelia were 
found with a number of other lesions. (Eisner). 
Importance of Pituitary Gland.—The pituitary gland is essential for 
life and the anterior or glandular position is most important. 
Characteristic Features of Acromegaly.—Acromegaly is a condition 
in which there is hyperpituitarism, which leads to marked increase in the 
size of the face, broadening and prominent jaw and overgrowth of the 
extremities—the hands and feet particularly. If acromegaly develops 
before epiphyseal union gigantism results. When, as in the adult, the 
bones of the face and extremities are mainly involved the picture of acro- 
megaly is presented. 
Cushing’s conception of acromegaly is expressed in the following 
paragraph: 
“The disease, in short, is the expression of a functional instability of the pars 
anterior, doubtless brought about by some underlying biochemical disturbance 
which leads to the elaboration of a perverted or exaggerated secretion containing 
a hormone that accelerates skeletal growth (of the long bones if epiphyseal union 
is incomplete, of the acral parts if epiphyseal ossification has taken place).” . . . 
“A subsequent recrudescence with resumption of the perverted functional activity 
will then serve to superimpose acromegalic manifestations on primary gigantism.” 
“Acromegaly cannot precede gigantism” but “always occurs as gigantism which 
has become acromegalized.” 
The disease is not frequent. In an active hospital and consulting 
experience of over thirty-five years I have seen less than ten cases. 
Operative Treatment.—The question of the primary change which 
leads to acromegaly is of vital importance for prognosis; if it can be 
established that B. Fischer is correct that the complex is due to hyper- 
function dependent upon adenoma and that no other growth causes hyper- 
thyroidea, then operative treatment—the removal of the enlarged gland— 1162 
DISEASES OF THE DUCTLESS GLANDS 
offers the only hope of relief or cure. The disease is progressive and in 
the end fatal, though years of latency have prolonged the lives of the 
majority of cases seen in Central Hew York. Ocular symptoms—optic 
atrophy—are due to pressure of the growing adenoma. 
Schloffer first suggested operative interference as a means of checking 
acromegaly and his case was relieved of its discomforts, and the acrome- 
galic manifestations also showed marked improvement. Hochenegg has 
reported similar experiences. 
Cushing’s experience which is large should influence our conclusions 
in this country. Ilis views are conservative, and he is opposed to operative 
interference in the absence of progressive symptoms (“degree of hyper- 
plasia sufficient to cause neighborhood symptoms”). He believes that it is 
doubtful whether operative measures “can hold out any promise of per- 
manently controlling the disorder.” On the other hand, he believes that 
with “neighborhood symptoms” (pressure) due to “extreme enlargement 
of the gland due to the formation of an adenomatous struma whether or not 
there have been antecedent symptoms of acromegaly, the surgical aspects 
of the matter stand on a firmer basis.” 
Course of the Disease.—The rule may he accepted that with the 
gradual advance of the disease the facies in all acromegalies are similar, 
the bony growth is characteristic, the chin advances more and more, the 
teeth are widely separated, kyphosis is always prominent, the larynx en- 
larges, the nose broadens, lips are thick, tongue abnormally large, sexual 
function is likely to suffer—impotence is the rule in the male, in the 
female amenorrhea is frequent and there is involution of the uterus and 
its appendages. 
The symptoms referable to the nervous system which show progression 
are increasing apathy, changed reflexes with increasing pressure symp- 
toms, headache, vertigo, convulsions at times, optic atrophy, choked disk 
with increasing atrophy, amblyopia, bitemporal hemianopsia and cardio- 
vascular changes, arteriosclerosis, dilatation of the ventricles and myo- 
cardial degeneration. 
In the advanced cases there is enlargement of the liver and spleen. 
The blood shows eosinophilia and monolymphocytosis. There are acute 
cases which run a comparatively short course. Sudden exacerbation of 
symptoms is unfavorable and may lead to rapid growth and grave nervous 
manifestations—coma, meningeal symptoms, cerebral edema. Sudden 
heart weakness or death after several years of gradually increasing symp- 
toms may follow acute infection. 
Prognosis.— In the present state of our knowledge I am forced to 
offer a doleful prognosis for cure—medicine is of no avail; surgery offers 
only the hope of symptomatic relief during varying periods, though with 
our present experiences as a basis for surgical treatment the outlook for 
the future is reasonably encouraging. Animal experimentation and close DISEASES OF THE THYMUS GLAND 
1163 
clinical study with the laboratory as a helpmate are demanded to bring 
us to the scientific solution of this subject. 
References 
Cushing. The pituitary body. Philadelphia, 1912. 
Eiselberg. Wien. klin. Wchnschr., 1909, xxii, 287. 
Am. Surg. Ass., 1910, xxviii. 
Fischer (B.). Hypophysis, Akromegalie u. Fettsuche. Wiesbaden. 
Hirsch. Arch. f. Laryngolog. u. Rhinol., 1910, xxi, 129-177. 
J. Am. Med. Ass., 1910, Iv, 772-774. 
Berl. klin. Wchnschr., 1911, xlviii, 1933. 
Hochenegg. 37th Kongress d. Gesellsch. f. Chir., 1908. 
Wien. med. Wchnschr., 1908, 5, 891. 
Ztschr.f. Chir., No. 100. 
Horsley. Brit. Med. J., 1906, ii, 411-423. 
Marie (P.). Rev. de Med., 1886, vi, 297. 
Schloffer. Beitr. z. klin. Chir., 1906, i, 767-817. 
Wien. klin. Wchnschr., 1907, Hi, 1177. 
Vincent. London practitioner. Jan., 1915. 
For full literature see 
Biedl. Inner Sekretion. Berlin u. Wien, 1913, Zweiter Teil. 
Cushing. The pituitary body. Philadelphia, 1912. 
Falta. Mohr & Staehelin’s Handb. d. inner. Med., Bd. iv, 530. 
C. Diseases of the Suprarenal Gland 
Addison’s Disease 
See Tuberculosis of the Suprarenal Bodies 
D. Diseases of the Thymus Gland 
1. Hypertrophy 
2. Atrophy 
3. Status thymo-lymphaticus. 
1. Hypertrophy 
In the consideration of the diseases of the ductless glands I called 
attention to the frequent enlargement of the thymus with goiter, exophthal- 
mic goiter, acromegaly, suprarenal diseases, rachitis, and with myasthenia 
gravis in which various observers have found infiltration of the gland and 
the skeletal muscles with lymphoid cells and marked productive change in 
the thymus tissue. I have seen sudden and fatal enlargement of the 
thymus with acute hyperthyroidea, also in one case of Ebstein’s glandular 1164 
DISEASES OF THE DUCTLESS GLANDS 
fever. There are cases of asthma of thymic origin which have been re- 
lieved by surgical intervention. 
In children sudden hyperplasia of the gland with oi without other 
lesions may promptly cause death (thymus death). When the enlarged 
thymus compresses the trachea (substernal struma) asphyxia may cause 
death. Sarcoma—lymphosarcoma—may invade the thymus, also car- 
cinoma. Enlarged thymus with Hodgkins disease occasionally leads to 
prompt death. 
Surgical intervention offers a fair prognosis in substernal struma and 
innocent thymus hyperplasia. The prognosis is absolutely bad in second- 
ary enlargement which, when present, hastens the end. 
2. Atrophy 
Atrophy of the thymus is not of great clinical significance, so far as we 
know at the present time. It has been found with wasting of other organs, 
marasmus after gastro-intestinal drain and with syphilis (congenital). 
The clinician will not be called upon to offer prognosis based on atrophy 
of the thymus, for the condition is not diagnosticated intra vitam. 
3. Status thymo-lymphaticus 
Kopp, in 1855, called attention to sudden death in young subjects with 
cyanosis and stridor in which the post mortem showed only the enlarged 
and hyperplastic thymus. In 1889, Paltauf called attention to sudden 
death in which there was, with hypertrophy of the thymus gland, lym- 
phatic enlargements throughout the body and abnormally small arteries. 
In all of these cases death resulted in a few minutes. 
The “status lymphaticus” has been established by Paltauf—a lym- 
phatic diathesis which may lead to sudden death in children under a va- 
riety of conditions. Such children may die suddenly while under an anes- 
thesia or from insignificant causes. There is a familial type of the status 
thymo-lymphaticus in which it is found that several children of a family 
die suddenly with like symptoms on slight cause. The status lymphaticus 
and enlarged thymus are intimately associated and the abnormal growth of 
the latter in a child ought always to he considered in connection with 
surgical or other risks, von Sury has found bronchiolitis (“capillary 
bronchitis”) (?) a frequent accompaniment of thymus death. Sudden 
death during thyroidectomy is usually due to the status thymo-lymphaticus 
(See Exophthalmic Goiter). 
There is a tendency to separate the status lymphaticus and the status 
thymo-lymphaticus; if differentiation is indicated, it is practically im- 
possible because the status lymphaticus cannot be recognized by the 
Lymphatism DISEASES OE THE PARATHYROID GLAND 
1165 
clinician as a clinical entity ante mortem, and the enlarged thymus and 
status lyinphaticus are almost always found together. In both death is 
sudden; in both there is lymphatism. 
The blood picture which is characteristic of most deep changes of the 
ductless glands is found with the lymphatic diathesis—relative and abso- 
lute reduction of neutrophvlic leukocytes and increase of mononuclear 
lymphocytes; in severe cases increase of preceding eosinophilia. 
Biedl. Innere Secretion. Wien, 1912. 
Falta. Mohr u. Staehelin’s Handb. d. inner. Krankh., 1912, Bd. iv. 
Grawitz. Deutsch. med. Wchnschr., 1888, No. 22. 
Kopp. Quoted by Falta. 
Mohr u. Staehelin’s Handb. d. inner. Krankh., 1912, Bd. iv, 4-74. 
Paltauf. Wien. klin. Wchnschr., 1889, No. 46; idem, 1890, No. 9. 
von Sury. Vierteljahrsschr. f. d. ges. Med., 1908, Bd. xxxvi. 
See literature in 
Biedl [Z.c.]. 
Falta [l.c.]. 
Index Catalogue, Surgeon-General’s Library, 1913, xviii. 
References 
E. Diseases of the Parathyroid Gland 
Tetany 
(Tetanilla, Tetanie, Intermittent Tetanus, Status parathyreoprivus, 
Hypoparathyreosis) 
Definition.—Frankl-Hochwart’s definition of the disease has been gen- 
erally adopted by the profession. lie considered its leading manifesta- 
tions “tonic, intermittent, bilateral, often painful cramp, which without 
(as a rule) loss of consciousness, involve the muscles of the arms and hands 
particularly, which latter are held ‘wedge shaped’ or in the obstetrical 
position.” The cramp is not always limited to the upper extremities but 
may include the legs, at times the jaw, the larynx, the face, rarely the 
thorax or other parts of the body (abdomen, neck, diaphragm or tongue). 
We now lean to the theory that tetany is often due to altered function 
of the parathyroid bodies. 
Characteristic Features.—The bilateral symmetrical tonic spasm of 
the muscles associated with pain and paresthesias are the characteristic 
features, with the obstetrical hand, the Trousseau phenomenon (reproduc- 
tion of the spasm by applying pressure to the arm above the elbow), the 
Chvostek phenomenon (producing muscular contractions of the facial 
muscles by tapping over the branches of the facial nerve) the Hoffman’s 
symptom (abnormal hypersensitive sensory nerves as shown by the produc- 1166 
DISEASES OF THE DUCTLESS GLANDS 
tion of severe pain on tapping the Valleix’s points) and Erb’s phenome- 
non (hyperexcitability of the motor nerves to electrical stimulation). 
Occurrence.—True tetany is an exceedingly rare disease in the United 
States. I have met but four cases in adults—three of which were 
secondary and due to gastro-intestinal lesions. Most cases seen in this 
country are of secondary and gastro-intestinal origin to which condition 
Kussmaul called attention in 1872. 
Forms.—In considering the prognosis of tetany, the division of the 
separate forms in the adult by Frankl-Hochwart, the leading authority on 
the subject, may be safely followed: 
(a) Idiopathic tetany 
(b) Gastric-gastro-intestinal tetany 
(c) Tetany associated with the acute infections 
(d) Tetany of the poisons 
(e) Tetany of maternity 
(f) Tetany of parathyroid disturbance 
(g) Tetany of various nervous diseases. 
MacCallum and Voegtlin conclude that in all of these forms the 
essential factor of tetany is found in the relation of the parathyroid 
to the calcium metabolism of the body; their researches which bear on the 
role which the calcium salts exert in connection with tetany are of exceed- 
ing importance, for they tend to prove that the “salts have a moderating 
influence on the nerve cells” and that the “parathyroid secretion in some 
way controls the calcium exchange of the body.” 
(a) Idiopathic Tetany 
Characteristic Features.—This is the so-called primary tetany of the 
Germans—the tetany found in otherwise healthy individuals—the work- 
man’s tetany and the epidemic tetany. The tetanic spasm is limited to 
shoemakers, tailors and handworkers. It is acute at times with remissions, 
and these are likely to make the disease chronic. With return to the usual 
work of the patient there is, after a time, recurrence of the characteristic 
symptoms of the disease. It is particularly frequent among shoemakers 
—in Vienna 60 per cent of all adult tetany is found among them. The 
disease among artisans afflicted selects the months from January to April 
by predilection. Among workmen, if this disease is primary it appears 
between the twentieth and thirtieth year; if later it is not likely to be 
primary. There are occasional acute forms of primary tetany which yield 
to rest and treatment. 
Remissions.—Frankl-Hochwart found 32 of 37 cases of primary (oc- 
cupation) tetany, chronic and subject to relapse. Curschmann reports the 
case of a tailoress whom he treated after twenty years of remission. Re- DISEASES OF TIIE PARATHYROID GLAND 
1167 
missions and exacerbations are materially and favorably influenced by 
change of occupation. 
Frankl-Hocliwart has recently given a less favorable prognosis than 
formerly in this form of tetany which seems to recur in epidemic form. 
In his further observation of the cases he found that many had died di- 
rectly or indirectly as a result of tetany or the primary disease in from 
four to eleven years after the initial symptoms. The resistance of the 
patients was reduced and they yielded more readily to acute disease than 
do normal individuals. Of 264 cases originally observed 55 were traced 
ten years or more. Of these 11 died early; of the remaining 44 but 9 
were in good health; 37 were examined personally; 7 had chronic tetany; 
19 had tetanoid symptoms and 2.3 of all had persistent tatany phenomena. 
(6) Gastric and Gastro-intestinal Tetany 
The mortality of tetany secondary to gastric or gastro-intestinal dis- 
turbance in which the underlying factors persist (dilatation, ulcer, etc.) is 
between 45 and 15 per cent. Naturally the underlying disease must re- 
main the paramount factor in prognosis. I have found that in recurring 
and severe tetany in which there seemed to me to be a toxemia from dilated 
viscera, the daily lavage and emptying of the intestinal tract and the 
stomach prevented the threatening spasm. 
Suddenly arising cardiac asthenia may prove fatal. This condition 
is always a serious complication and should be so regarded in the selection 
of therapy which, as a rule, needs to be radical—i. e., surgical. 
(c) Tetany Associated With The Acute Infections 
Among the acute infections which may occasionally be complicated 
with tetany are typhoid fever, cholera asiatica, measles, scarlet fever, ton- 
sillitis, acute tracheal catarrh, laryngitis, polyarthritis and malaria, rarely 
influenza. 
In the majority of these cases the infections are benign and the out- 
come favorable. In most cases there is but one seizure and the prognosis 
of the primary disease is not influenced thereby. 
(d) Tetany of Poisons 
The physiologic effect of poisons including chloroform, morphin, ergot, 
phosphorus, lead, urea and other renal and genital intoxicants may in- 
clude tetanic symptoms. Tetany is mentioned in connection with novocain 
poisoning (Curschmann), cocain and atropin. Chvostek has seen tetany 
after tuberculin injection. Curschmann doubts Frankl-Hochwart’s con- 
clusion that tetany may be caused by alcoholism. 
Prognosis.—The prognosis of this type of tetany must naturally depend 1168 
DISEASES OF THE DUCTLESS GLANDS 
upon the ability of the attendants to combat the acute poisoning promptly. 
In occasional cases lead may cause tetany. The prognosis of such cases is 
not materially influenced by the presence of tetany, unless the patient is 
already reduced or there are other grave effects of the poison. 
(e) Tetany of Maternity 
The tetany of maternity is more frequently met than was formerly 
supposed. This form of tetany is never to be lightly regarded. It is 
always a serious complication and is most frequent during the sixth to 
the eighth month of pregnancy. Once established the condition may per- 
sist until delivery; most women who recover are similarly afflicted during 
succeeding pregnancies. Occasionally a woman dies suddenly during an 
acute exacerbation. 
(/) Tetany of Parathyroid Disturbance 
(Tetania strumipriva) 
The consideration of this form of tetany belongs to the surgeon. 
Tetania strumipriva is the gravest of all forms and may lead to death 
after thyroidectomy and the removal of the parathyroid bodies in a few 
days or weeks. Tetany may follow thyroidectomy within a few hours, or 
several days may lapse before the strumipriva is fully developed. If the 
entire parathyroid substance has been removed the prognosis is almost uni- 
formly bad. von Eiselberg claims that partial thyroidectomy may occa- 
sionally cause tetany and reports 2 cases among 356 partial extirpations 
(See Exophthalmic Goiter). 
(g) Tetany of the Various Nervous Diseases 
Primary Disease.—Tetany occasionally accompanies epilepsy, Base- 
dow’s disease (hyperthyroidism) myxedema (hypothyroidism) tumor of 
the brain, syringomyelia and cysticerci. 
The presence of tetany when limited to the hands and arms, without 
cardinal symptoms and without respiratory spasm, is not per se of grave 
moment; the prognosis should be based on the nature and extent of the 
primary disease. Attention should be called to the possibility of latent 
tetany with hypothyroidism. In such cases the Chvostek phenomenon is 
present. Such cases usually yield to treatment with the organic (thyroid) 
extract—the tetany disappearing as the myxedema is relieved. 
Prognosis.—The prognosis of tetany in suckling children and during 
early life is, as a rule, favorable. The complication is likely to be acute 
and disappears after a limited period—usually several weeks, occasionally 
one or two months. DISEASES OE THE SPLEEH 
1169 
Chronicity may follow but is exceedingly rare. When associated with 
grave nutritional faults the prognosis is correspondingly grave. Spasm 
of the larynx may prove threatening. 
Infantile convulsions are separately considered. 
References 
Chvostek. Wien. klin. Wchnschr., 1907, 487, etc. 
Curschmann. Mohr u. Staehelin’s Handb. d. inner. Medizin. Berlin, 1912, Bd. v. 
von Eisenberg. Mohr u. Staehelin [l. c.]. 
Escherich. Tetanie, etc., 1909. 
Frankl-Hochivart. Die Tetanie. Wien, 1907. 
Kussmaul. Berl. klin. Wchnschr., 1872, No. 27. 
MacCallum & Voegtlin. J. of Exper. Med., 1909, ix. 
F. Diseases of the Spleen 
The larger number of lesions of the spleen are of secondary origin, are 
associated with the infections, constitutional and toxic states, each of 
which demands separate consideration; to each I give due consideration 
with the separate diseases. 
The great importance of the spleen as a hemolytic organ receives sepa- 
rate consideration in connection with the primary anemias, splenic anemia, 
Banti’s disease and liver cirrhosis. 
1. Secondary Splenomegaly 
(Enlarged Spleen) 
The acute enlargements of the spleen are practically constant with the 
infections: typhoid, malaria, sepsis, pyemia, pneumonia, recurring fever, 
kala-azar and a variety of other conditions including the acute congestions 
associated with the acute forms of disease of the blood-producing organs 
(See Infections). 
The chronic enlargements of the spleen are rarely primary as, is 
abundantly demonstrated by the study of the essential anemias, syphilis, 
tuberculosis, chronic malaria, various liver changes, chronic portal obstruc- 
tion, with the various types of cirrhotic liver. To all of these separate 
conditions the reader is referred. 
In almost all diseases in which there is secondary splenomegaly, there 
are no subjective evidences of its presence; the diagnosis is only made 
after physical examination of the patient. The prognostic significance of 
the enlargement taken alone is not as a rule paramount. There are grave 
infections in which the spleen is but slightly enlarged, while in mild infec- 
tions the enlargement may often be surprisingly great. 1170 
DISEASES OF THE DUCTLESS GLANDS 
Prognostic Factors.—(a) Passive Congestion.—Passive congestion 
of the spleen and consecutive enlargement may be associated with valvular 
diseases of the heart, emphysema, cirrhosis of the liver, leukemia with 
final proliferation and leukemic infiltrate. Leukemic spleens may hasten 
death by their enormous growth and the pressure which results. 
(b) Abscess.—Abscess of the spleen may be encapsulated, there may 
be small multiple abscesses or there may be purulent breakdown of the 
enlarged organ with pyemic or septic infection. These forms of splenic 
abscess are associated with the graver pyemic conditions, sometimes with 
puerperal phlebitis or pyemia, erysipelas or infectious endocarditis. 
(c) Perforation.—Perforation through the capsule may lead to 
fulminating septic peritonitis. In all of these conditions the prognosis is 
grave in accordance with the seriousness and extent of the primary infec- 
tion. 
(d) Perisplenic Abscess.—Perisplenic abscesses may invade the 
spleen, cause disorganization and seriously complicate conditions. Most 
of these cases are due to the perforation of ulcers of the stomach or duode- 
num, traumatism at times, with or without subphrenic abscess. The prog- 
nosis is always grave. 
(e) Perisplenitis or Capsulitis.—This is secondary to syphilitic 
infection, leukemia, chronic malarial poisoning or polyseroritis (Pick’s 
disease, multiple serositis, zuckergusskrankheit) in which the serous cover- 
ings of these organs—liver, peritoneum, pericardium—are involved, with 
enlarged spleen and fluid in the serous cavities. These patients may live 
for years but the fluid reforms and they finally die after repeated tappings 
of exhaustion or intercurrent infection (See Polyserositis). 
(f) Tuberculous Spleen and (g) Amyloid Spleen have been 
separately considered. The former is comparatively rare when we con- 
sider the large number of tuberculous subjects. Amyloid spleen is a part 
of a general amyloid degeneration in which the blood vessels (arteries) 
are primarily involved after long-continued drain due to suppuration, 
tuberculosis, syphilis, bone disease or other infection. The kidney and 
vital organs are insufficient, and death is the rule in all such cases. 
(g) Syphilis of the Spleen.—Syphilis of the spleen (See Syphilis) 
may cause enlargement. Gummata are not infrequent. Syphilis of the 
spleen is more frequent than is generally supposed and offers a favorable 
prognosis. 
(h) Uncomplicated enlargement of the spleen in otherwise 
healthy subjects without subjective symptoms, accidentally discovered, 
will often remain unexplained. This condition is permanent and does not 
interfere with the general condition; neither does it cause discomfort or 
shorten life. 
(i) Chronic enlargement of the spleen with polycythemia is 
separately considered (See Polycythemia—Osier’s Disease). DISEASES OF THE SPLEEN 
1171 
(j) Enlargement with liver cirrhosis.—The prognostic signifi- 
cance of secondary enlargement of the spleen with alcoholic cirrhosis of 
the liver, syphilis of that organ and hypertrophic cirrhosis of Hanot, is 
separately considered (See Diseases of the Liver). 
(k) Rupture of the Spleen.—Rupture of an enlarged and infected 
spleen may occasionally happen with typhoid or malarial infection. In 
these cases the prognosis is bad. 
The larger number of ruptured spleens follow traumatism and if 
promptly recognized and surgically treated offer an encouraging prognosis. 
Peritonitis and depletion are the leading dangers in neglected cases. 
(l) Cyst of the Spleen.—This is a surgical condition which, 
when innocent, offers a favorable outlook after radical treatment (See 
Echinococcus Disease). Operations for splenic cysts are almost uni- 
formly successful. 
(m) Infarct.—Enlargement of the spleen with hemorrhagic compli- 
cations, multiple infarct, more or less involvement of the sensorium, is 
always indicative of malignant infection. In all such cases malignant 
endocarditis should be suspected; coagulation necrosis leads to disorgan- 
ization and perisplenitis may complicate unfavorably. Recession of the 
enlarged spleen with acute or chronic conditions may, in the majority of 
cases, be interpreted as being favorable. 
2. Primary Splenomegaly 
(a) Splenomegaly of the Gaucher Type or Gaucher Disease 
(.Primary Endothelioma of the Spleen) 
Gaucher, in 1882, first called attention to splenomegaly of familial 
type in which the pathology has since been firmly established by the pains- 
taking work of Stengel, Brill, Mandelbaum and Libmann, proving it to 
be primary endothelioma. Brill insisted that the Gaucher type of spleno- 
megaly ought not to be considered in the category of splenic anemia be- 
cause of its “unique and typical” pathology and “destructive clinical 
picture.” In all cases of familial splenomegaly of the Gaucher type the 
splenomegaly is associated with corresponding increase in the size of the 
liver. Brill, Mandelbaum and Libman "reach the following conclusions 
and I quote these because I have had no personal experience with the 
disease: 
“Splenomegaly (Gaucher type) is a distinctive disease starting in early life, 
often affecting several members of a family and running a chronic course. It 
may be recognized by a great enlargement of the spleen, which precedes a similar 
enlargement of the liver, and is unaccompanied by jaundice or ascites; by the dis- 
coloration of the skin, especially where exposed to the light; and by the absence 
in the blood of any characteristic findings. The disease has none of the charac- 1172 
DISEASES OF THE DUCTLESS GLANDS 
teristics of malignancy and usually terminates as the result of an intercurrent 
infection. The organs affected are the spleen, liver, lymph nodes and bone marrow. 
Histologically these organs show the presence of large cells with small nuclei and 
a peculiar hyaline cytoplasm which arises from the endothelium or normal 
reticulum and the presence of pigment containing iron. The etiology is unknown, 
though a peculiar susceptibility of the endothelium or reticulum of the hemapoietic 
apparatus to some unknown toxic agent is most likely present.” 
There was nothing in the cases reported which suggested tuberculosis, 
“when found in cases of this disease, it must be considered as a superimposed 
process.” 
The chronicity of Gaucher’s disease is striking. Naegele reports a 
case which had existed 39 years. Anemia is the fate of these spleno- 
megalies with a strong tendency to leukopenia. 
(6) Banti’s Disease—Splenic Anemia 
Characteristic Symptoms.—Banti’s disease is characterized by en- 
larged spleen of unknown origin associated with splenic anemia, marked 
tendency to hemorrhages, esophageal varices, in most cases cirrhosis of 
the liver with jaundice and ascites in which the anemia is due to the 
hemolytic action of the spleen and in which the progress of the disease 
is readily controlled by early splenectomy. The splenomegaly is marked, 
the spleen is hard and smooth, painless and continues so throughout the 
disease. 
Blood.—The blood count in the average case shows the characteristic 
features of secondary anemia, marked hemoglobin loss and striking 
leukopenia. In two of my cases the white count was as low as 800 and 
1,500 per c. mm. respectively. My average red count has been between 
2,500,000 and 3,000,000 per c. mm. After hemorrhages the erythrocytes 
reach low levels, while the leukocytic count is raised. One of my cases 
died of esophageal hemorrhage. At post mortem a varix was found 
eroded. Repeated gastric and intestinal hemorrhages influence the fore- 
cast unfavorably. The prognosis is bad in the cases which are far ad- 
vanced and show hemorrhagic tendenciesv with cutaneous and visceral 
purpura* In favorable cases the splenomegaly persists during many years 
without liver cirrhosis (these are the cases of uncomplicated splenic 
anemia), moderate anemia with leukopenia and without hemorrhage. 
Beep jaundice is rare; when present is an unfavorable symptom and 
is coincident with either marked degeneration of liver cells or the destruc- 
tion of large numbers of red blood corpuscles. Moderate jaundice does 
not influence prognosis unfavorably and may persist with enlarged spleen 
and moderate splenic anemia during long periods. The growth of con- 
nective tissue in the liver may be exceedingly slow and is often without 
increase of subjective symptoms—during many years. DISEASES OF THE SPLEEN 
1173 
Ascites is never to be interpreted as favorable. It usually proves the 
presence of portal obstruction dependent on advanced liver cirrhosis. 
Albuminuria with casts or positive evidences of nephritis, toxic symp- 
toms (involvement of the sensorium), myocardial weakness or degenera- 
tion are all unfavorable. 
In the present state of our knowledge I would include all forms of 
splenomegaly of primary origin not due to new growths (carcinoma, 
sarcoma or the Gaucher endothelioma) in the class of splenic anemias of 
which Banti’s disease with advance to liver cirrhosis represents the full 
development; in other words, splenic anemia is a chronic primary spleno- 
megaly of the infant (von Jaksch anemia splenica infantum) or adult, 
associated with marked anemia and striking leukopenia. 
Prognosis.—All splenic anemias are persistently chronic and all offer 
a good prognois when the hemolytic organ—the spleen—is removed, with- 
out its removal the prognosis for cure is bad—not always fatal. It is of 
the utmost importance for the clinician to appreciate the fact that the 
cirrhosis of the liver with splenomegaly or splenic anemia is of secondary 
origin, dependent in some way upon the primary disease of the spleen. 
Splenic anemia in children may prove to be self-limited and may lead 
to full recovery with recession of the spleen. The author has seen several 
such cases and medical literature offers abundant examples (See Refer- 
ences). The degree of the anemia should not always be taken as the 
guide for prognosis. 
3. Mobile Spleen 
Movable or mobile spleen may give rise to no symptoms and is often 
accidentally discovered. It is more frequent in women than in men and 
is usually a part of Glenard’s process with enteroptosis, gastroptosis and 
gastrectasia—often mobile liver as well. Mobile spleen may cause dis- 
comfort but never seriously interferes with the normal processes of the 
individual. Mechanical devices and, in extreme cases, surgical inter- 
ference will bring relief. 
References 
Banti. Ziegler's Beitr. 1898, Bd. xxiv, 40. 
Bovaird. Am. J. Med. Sci., 1900, cxx, 377. 
Brill, Mandelbaum & Libman. Am. J. Med. Sci., 1905, cxxix, 491. 
Idem, 1909, 849, No. 137. 
Idem, April, 1910. 
Bull, de la Soc. de Pediatrie. Paris Journal, xv, 1913, 337-413, No. 7. 
IReporting cases of recovery from splenic anemia without surgical interfer- 
ence in children.) 
Gaucher. These de doctoral, 1882. 
Epitheliome primitif de la rdte. 1174 
DISEASES OF THE DUCTLESS GLANDS 
hippy. Am. J. Med. Sci.} Nov., 1899, 443; also Dec., 1899, 570. 
Litten. Die Krankheiten der Milz. In: NothnageVs Ilandb., Bd. viii. 
Marchand. Munch, med. Wchnschr., 1907, liv, 1102. 
von Mehring u. Krehl. Lehrbuch d. inner. Med. Jena, 1913. 
Naegeli (O.). Blutkrankheiten, etc. 2. Aufl. Leipzig, 1912. 
Osier (Sir William). Am. J. Med. Sci., May, 1899. 
Idem, Nov., 1902. 
Discussion on splenic enlargement. Brit. Med. J., Oct. 17, 1908. 
Pfaundler & Schlossman. Handbuch d. Kinderkr. 2. Aufl., Bd. ii. 
Stengel. Am. J. Med. Sci., Sept., 1904. Section XI 
Intoxications 
1. Alcoholism 
(a) General Consideration of the Alcohol Habit 
Excessive Use of Alcohol 
Intoxication Impulse (Lambert) 
(b) Acute Alcohol Poisoning 
(c) Chronic Alcoholism 
(d) Delirium Tremens. 
(a) Alcohol Habit 
Intoxication Impulse 
(Lambert) 
General Considerations.—In the preparation of this chapter the author 
has been materially assisted by Alexander Lambert, of Hew York, who, 
in the management of his large material at Bellevue Hospital, has demon- 
strated his superior knowledge of the subject, his tact and humanity. The 
author wishes to thank Doctor Lambert for his assistance which he gladly 
acknowledges, and feels at liberty to base his conclusions as they affect 
prognosis upon data liberally supplied by Doctor Lambert and the result 
of his own hospital and private experiences. 
We assume that the alcohol habitue has, as the result of his habit, dis- 
turbed “the equilibrium of health,” that his tissues are so changed as to 
justify the conclusion that he is out of health; in other words, after the 
excessive and continued use of alcohol as it is taken by the chronic drinker, 
a changed condition of the central nervous system—more particularly the 
brain—develops which robs the victim of will power sufficient to resist 
the impulse ivhich leads him to drink. Without the assistance which the 
physician extends to every human being whose will power is paralyzed 
or who is suffering from a disease which makes it impossible for him to 
help himself unaided, and without sufficient remnant of will power to 
1175 1176 
INTOXICATIONS 
make the victim will and divorce himself from the slavery which holds 
him, there can he no hope of emancipation. 
No victim of the alcoholic habit can be cured permanently who is so 
blunted, so diseased that he remains absolutely passive, without the desire 
to he cured. The perverted mind—changed psychic function—must be 
brought under control before lasting benefit from any form of treatment 
can he expected. The brain cells are altered by the long-continued or even 
periodic use of the poison—as Lambert says: “If we fail to unpoison the 
individual, we will surely fail in our cure of him.” 
Personality and will are both poisoned; the mind thus poisoned can- 
not act normally; it is without will power and must remain so until 
unpoisoned—when the foundation for release has been established. 
The use of alcohol in small doses by the worker in any field of activ- 
ity will ultimately lead to larger doses (in most cases) and the develop- 
ment of the alcohol habit. Chronic alcoholism often follows the re- 
peated convivial drinking in those “who drink to increase the joys of 
life.” Lambert does not believe that this tends to chronic alcoholism so 
often as do other forms of drinking, but we are agreed that it does finally 
lead to steady drinking which becomes excessive and in many, chronic 
alcoholism follows. There is a third and large class which we meet in 
hospital and private practice in which because of inherent weakness— 
bad heredity—the slightest disappointment or extra tax, physical or 
mental, leads to the use of alcohol. The added reserve which may fol- 
low the initial small dose encourages repeated drinking until the habit is 
fastened, the mental processes grow more and more satisfactory to the 
deluded victim, while in truth, judgment, memory, expression and physical 
force are all influenced unfavorably and in the end, the subject is so 
enslaved that he does nothing without alcohol and becomes a chronic alco- 
holic. 
This is the history of the development of the alcohol habit in doctors 
and lawyers. The former, wearied by long vigil, drinks to gain “arti- 
ficial stimulation” that he may finish the day’s work; the latter in the 
trial of a case, seeks the “brace” which he believes will carry him through. 
In all of these, the psychic element becomes the paramount issue. “Judg- 
ment, reasoning, memory” and will power one after the other depart 
and there is left “an emotional creature” no longer dominated by normal 
psychic processes—sound reasoning—but swayed by sentiment with in- 
creasing mental decay, without initiative, who falls and feeds his diseased 
nervous system with the poison which his perverted appetite craves. 
Alcoholics, like all who are enslaved by other narcotics, are ready to 
subject themselves to the influence of any drug which will bring that 
exhilaration or paralysis so much enjoyed when the brain has become 
thoroughly poisoned. Mental breakdown with alcohol and morphin or 
\vith both and cocain is prompt, the entire personality is changed and INTOXICATIONS 
1177 
the moral sense blunted. Hope of release is offered by eliminating from 
the memory of the habitue the continuous physiologic and pathologic effect 
which creates the appetite for the drug. This can only be accomplished by 
thorough divorce from the poison. The physical and mental restoration 
are often slow—for there is in all that psychic state which is persistent, 
full of torture, with a panoramic view of the hours of dream which invite 
recourse to alcohol, against which a strong will is needed. Once released 
or “unpoisoned” much depends upon the physical status of the patient, 
the environment, the social condition and above all, upon the assistance 
which the habitue gives himself. 
Influencing Factors.—Heredity is an important factor; it influences 
the resistance, the amount of mental vigor and the personality of the 
individual and affects the basis on which the addiction is built. I am 
fully agreed with Lambert that a weak personality poisoned by any drug 
will be a difficult subject to release. The prognosis is unquestionably in- 
fluenced unfavorably by alcoholic inheritance. “It would seem that we 
should find an expression in the individuals of today in their actions 
toward alcohol and their reaction to the impulses leading to intoxication 
which shows the development and racial use of alcohol in the past.” The 
“intoxication impulse” is “an expression of the social instincts of the 
individual,” “an expression of vigorous youth straining to enjoy the teem- 
ing abundance of sensations” (Lambert). Uncontrolled, this impulse, in- 
herent in the race, “drives the individual on and overpowers often the 
instincts of self-preservation and self-interest.” 
In early vigorous manhood (early twenties) excessive drinking in 
those not burdened with an unfavorable heredity or provoking factors, as 
seen “in college students and in youths of that age” is not as a rule an 
expression of paralyzed will, and in the end, before there is addiction, 
the majority escape. The prognosis depends largely on the personality 
and many factors in these subjects. Early training—discipline—proves 
of enormous prognostic influence. The man, who in middle life drinks 
deliberately that he may become intoxicated, who seeks periods of efface- 
ment, is among the most hopeless of all drinkers. He seeks the narcotic 
and soon he longs for its continuous effect. 
Periodic drinkers are among the most unfortunate of drinkers. In 
them, the intoxication impulse is sustained by the memory of past de- 
bauches and an eager desire to escape from their surroundings. Their 
psychic anomalies are often remedied with the greatest difficulty. The 
will seems to be paralyzed in cycles and there is an instability which is 
easily recognized, the features of which it is difficult to explain. Many 
periodic drinkers are physically sick; they are often poisoned by toxins 
which they elaborate or which they add. Lambert believes that “the ma- 
jority of periodic drinkers who are endeavoring hopelessly to cease their 
periodic sprees are really cases of chronic tobacco poisoning.” Cigarettes 1178 
INTOXICATIONS 
more frequently than the pipe or cigars are the cause. “Double narcotic 
poisoning” is often cured by release from the primary poison which leads 
to the final intoxication. 
Psychoses are often responsible for periodic drunkenness. The manic- 
depressiVe condition, which is recurrent, invites that indulgence which 
divorces the diseased mind from a state of depression and one of less 
gloom to practical oblivion. The prognosis of such conditions naturally 
depends upon the ability to control the mental element (alienation). 
Lambert reports 1,019 patients treated for alcoholism (habit) with 105 
relapses—10 per cent. Some of these relapsed once or twice and are 
now permanently released, having returned to their occupations “sober 
members of the community.” He reports 80 per cent successes in his final 
analysis—20 per cent failures. In my own experience, I have, because of 
a different clientele, been less successful. Many of my cases have, come 
from country districts and not a few have been addicted to the use of 
morphin, cocain, one or both with alcohol. I have found the element of 
time of great importance in prognosis. Those cases which have left the 
hospital or observation before restoration of physical strength or the 
relief of diseased conditions or who have returned to be subjected to 
annoying and complicating problems have lapsed early and have continued 
unrelieved. 
Excessive Use of Alcohol as Exciting Factor in Many Diseases.— 
The prognosis of many diseases is materially influenced by the excessive 
use of alcoholic drinks. This is particularly true of tuberculosis and 
syphilis (See Section I—Tuberculosis and Syphilis). There are sud- 
denly arising complications in which alcohol finally proves to be the 
exciting factor, in which the habit had never been suspected. 
Tolerance.—The daily quantity of alcohol which may be taken without 
bad effect varies with different individuals; this variation is influenced 
by the general condition of the subject and varies at different times under 
changed conditions in the same individual. Sedentary occupations reduce 
the tolerance for alcohol and invite consecutive chronic changes. In my 
consideration of acute and chronic alcohol poisoning mention is made of 
the organic changes which influence the clinical history. 
Conclusions.—In my practice I have learned to place the greatest reli- 
ance on the results of a thorough investigation of the life history of 
patients, a study of their antecedents, their environment, a full under- 
standing of their social and daily problems. In hospital practice this is, 
as a rule, impossible, but it becomes the function of the social worker to 
lead in this crusade which promises to save a large number of these unfor- 
tunates. In private practice*the prognosis of the alcohol habit is better in 
proportion to the ability to supervise the life of the patient. The strong 
personality of the physician will always prove a powerful factor in leading 
the victim. The diseased mind and body demand surveillance and treat- INTOXICATIONS 
1179 
ment; each case becomes a psychic study; each life demands that rear- 
rangement which will lead to mental and physical health in an environ- 
ment which will be most likely to reduce depressing factors during long 
periods. This is a monumental task but with proper organization it prom- 
ises sufficient success to justify the trial. 
(b) Acute Alcohol Poisoning 
Ordinary acute intoxication following the nse of alcohol as seen in the 
average case of drunkenness after a period of cerebral paralysis (stupor) 
following psychic excitation, increased frequency of the pulse (as a rule), 
involuntary discharge of urine and feces, disturbed respiration, dilatation 
of the pupil, cyanosis, clearing of the sensorium, leaving the victim 
with tremor, headache, nausea, muscular weakness, gastro-intestinal dis- 
turbance during periods varying from a few hours to several days—all 
depending largely upon the size of the dose, idiosyncrasy, age, the dura- 
tion of the habit and the extent of secondary changes which follow long 
periods of preceding inebriety with repeated acute exacerbations (poi- 
soning) . 
Associated Conditions.—The leading dangers are due to exposure, 
accident, infection, cardiovascular disease and complications referable to 
the central nervous system, liver and kidneys. In hospital practice drunk- 
ards are often brought in with frozen extremities, final deep sloughs, and 
in bad cases loss of fingers, toes and occasionally one or more extremities. 
In these cases convalescence is slow and exposure is not infrequently fol- 
lowed by alcoholic pneumonia associated with meningismus, often with 
delirium tremens. As a rule with alcoholic pneumonia there is extensive 
infiltration; the prognosis of pneumonia with acute alcohol poisoning is 
had—over 80 per cent die. 
Alcoholic Poisoning.—There are but few deaths following acute alco- 
holic intoxication in which the lungs are found without evidences of in- 
flammation—infection. Many are brought into hospitals with acute de- 
lirium and with injuries sustained while intoxicated. In these, there is 
danger of infection; erysipelas, sloughing, gangrene and reparative proc- 
esses are tardy. In one case, which had been acutely poisoned during sev- 
eral days a hernia became strangulated, remained unrecognized and led 
to death. Acute alcoholic poisoning may lead to sudden death in the 
subjects of chronic cardiovascular disease, often with fibroid or fatty 
hearts, or with degenerated hearts in chronic nephritics. In one of 
my hospital cases a young woman who had been acutely poisoned, 
who was not addicted to the use of alcohol, I found after a few days of 
wet brain fully developed multiple neuritis with quadriplegic paralysis 
and before the end of the seventh day she died of acute atrophy of the 
liver. 1180 
INTOXICATIONS 
Changes Due to Poisoning.—The development of acute nephritis or 
acute exacerbations of chronic nephritis following alcohol poisoning may 
seriously menace life. In those suffering from chronic disease of the 
nervous system, acute poisoning produces profound changes, often threat- 
ening. Epileptics are promptly affected and unfavorably; idiots develop 
alarming meningeal and peripheral symptoms; acute poisoning in the in- 
jured is always of serious significance, while the prognosis in those con- 
valescent from the infections or from surgical operations is always grave. 
Small doses of alcohol are often sufficient in these to promptly provoke 
symptoms; in health large doses would be required to cause the same 
results. 
The drinking at once of a large quantity of alcohol may promptly cause 
collapse and death. In some cases death may not follow; in such cases for 
several hours during which the local effect of alcohol on the gastric mucosa 
leads to vomiting, retching and increasing heart weakness results. 
In cases in which either with suicidal intent, by accident or to pro- 
duce a prompt drunk, the victim swallows a large quantity of alcohol, the 
prognosis will depend very largely upon the promptness with which the 
stomach is emptied and absorption prevented. 
Cerebral apoplexy and thrombosis may develop during acute alcohol 
poisoning, as may uremia in cases of chronic nephritis. I have seen 
death from coronary spasm, thrombosis of the coronaries, and unrecognized 
dilatation of the stomach during acute alcohol poisoning. 
Symptoms referable to the nervous system (neuritis and meningitis), 
the gastro-intestinal tract, the genito-urinary and cardiovascular organs, 
may persist during long periods after acute poisoning; these in the pre- 
viously healthy usually yield (See Alcoholic Neuritis—Section VII). 
(c) Chronic Alcoholism 
Psychic Element as Leading Factor.—In the general consideration of 
this subject I insisted that the alcoholic habit is nurtured and sustained 
by an abnormal psychic state. Whatever the conditions which lead to the 
formation of the habit—and it is more likely to develop in those with 
lowered resistance, inherent weakness (hereditary influences)—ultimately 
the psychic element in all stands prominently in the foreground and as 
already suggested (general considerations) the prognosis depends upon 
the recognition of this fact. 
Productive and Degenerative Changes.—The chronic alcoholic is per- 
sistently below par. He is without normal resistance to disease, is more 
subject to all diseases—constitutional, local and infectious—than is the 
normal individual, and when the habit has existed during a considerable 
period there are productive and degenerative changes which increase in- 
sidiously, often unnoticed during long periods, because of the absence of INTOXICATIONS 
1181 
subjective symptoms, which are often so deep and far-reaching as to make 
restitution impossible. The leading changes produced by chronic alco- 
holism are referable to 
(a) The gastro-intestinal tract 
(b) The nervous system 
(c) The liver 
(d) The circulatory system 
(e) The genito-urinary system 
(f) The organs of special sense 
(g) The respiratory system. 
(a) Gastro-usttestinal Tract.—But few chronic drinkers are with- 
out change in the gastric mucosa. This may be productive, atrophic; 
and, when the habit has not continued long, subacute gastritis with or 
without proliferative change may he present. The intestinal changes are 
less marked, but in advanced cases, atrophy of the follicles and irregularly 
distributed hyperplasia are not uncommon. The prognosis of alcoholic 
gastritis and enteritis is good in cases which can be controlled. It is 
surprising to find how promptly the “morning vomiting” of the chronic 
drunkard yields (See Gastritis—acute and chronic). 
In chronic cases polypoid growth and pyloric hyperplasia (stricture) 
may lead to continuous symptoms which refuse to yield, and for surgical 
interference offer an unfavorable outlook. In all forms of surgical com- 
plications the prognosis is unfavorable, compared with the non-alcoholic 
subject. 
The chronic pharyngitis of the drunkard does not yield to local treat- 
ment, it does yield to discontinuance of the poison. Duodenal and gastric 
ulcers may develop during active gastro-intestinal symptoms or may have 
existed before the alcoholic gastritis. I have no case of perforation to 
report. The prognosis of the stomach lesion per se has been the same as 
without alcoholism. Hone of my cases were operated. 
(h) Nervous System.—The complications referable to the nervous 
system have been separately considered in the various chapters of Section 
VII, dealing with alcoholic multiple neuritis, amblyopia, optic neuritis as 
well as other changes in the cranial nerves, the meningitides, also wet brain 
and encephalitis; to these the reader is referred. The general statement 
may be made, that in favorable surroundings with corrected habits the 
prognosis of these conditions is often surprisingly good. This however 
is only a general conclusion and in each of the conditions mentioned de- 
mands such modification as is fully considered in the separate chapters 
to which I refer. 
The psychic disturbances depend for their prognosis upon the extent 
of the organic change which the long-continued use of alcohol has caused 
(See Encephalitis, Wet Brain, Epilepsy, Neurasthenia, Hysteria, etc.). 1182 
INTOXICATION S 
In hospital practice long-continued psychoses may finally yield perma- 
nently; in some there is a remnant of symptoms which remains. 
Korsakoff’s 'psychosis may complicate delirium tremens or chronic 
alcoholism without marked mania. Patients with the complex are usually 
delirious, have multiple neuritis and the characteristic memory defect. 
There is inability to orient, failure to retain new facts or impressions, 
loss almost entire of the recent past and in some cases retention of only 
isolated events of the remote past. The loss of memory of the day’s 
events is prompt and early demonstrated in a test of but a few minutes. 
The psychosis is usually chronic, the polyneuritis is likely to mend before 
the memory improves. In subjects who recover it is often noticeable 
that they retain their habitual social forms, while their real personality 
is burnt out; you seek for it in vain. It is a curious condition. Talking 
to them superficially, to. be with them in superficial things, they appear 
perfectly normal, but try to reach the mainsprings of their personality 
and you find that it has been destroyed. Years may elapse before there 
is full return of memory—in some cases the normal may never be reached. 
The attending conditions (heart, arteries, kidneys, etc.) are paramount 
in the prognosis of the Korsakoff syndrome. 
Oppenheim found 30 per cent of all alcoholics admitted to the Charite 
(the ward in which the delirious were confined) suffering from epilepsy 
(See Delirium Tremens). 
(c) The Liver.—The lesions referable to the liver and their prog- 
nostic import are fully considered in connection with the various types 
of cirrhosis. Advanced cirrhosis is usually complicated with organic 
changes in other vital organs (stomach, kidney, heart and arteries) and 
materially influences the prognosis (See Liver Cirrhosis). 
(d) Circulatory System.—The influence of alcohol on the heart 
and arteries has also been separately considered. Whether these changes 
are produced directly or indirectly their results are the same and prog- 
nosis is unfavorably influenced by their presence. Much can be done 
to influence these cases favorably in the presence of far-reaching changes 
in the circulatory organs mentioned. The cooperation of the patient 
with rational living is the important factor. 
Degenerative heart changes (myocarditis—coronary sclerosis) with 
chronic alcoholism seriously complicate the forecast (See Diseases of 
the Heart, Arteries, etc.). The complication of syphilis with alcoholic 
change in the cardiovascular system and alcoholism is often provocative 
of lesions which involve the nervous system (paresis, tabes, etc.). 
(e) Genito-urinary System.—Changes of organic nature involving 
the genito-urinary system often add a large element of danger. This is 
particularly true of cases with enlarged prostate and urinary retention 
in which cystitis results from neglect, in cases of ascending infection, with 
calculosis—either bladder or kidney—and with all forms of nephritis, INTOXICATIONS 
1183 
particularly the chronic interstitial, in which there are at the same time 
advanced heart and arterial changes or in those forms of secondary con- 
tracted kidney with chronic uremia or recurring poisoning (See separate 
chapters—the Hephritides—Nephropathies). 
(f) Organs of Specific Sense.—Organic or functional changes in 
the organs of special sense may cause prominent symptoms. Ocular dis- 
turbances are most frequent. The functional disturbances yield to rational 
treatment. Optic neuritis, partial optic atrophy, central scotoma for colors 
(red and green) and loss of pupillary light reflex in advanced cases may 
remain unchanged, though improvement may follow with the disappear- 
ance of separate symptoms in the less chronic cases under favorable con- 
ditions. 
(g) The Respiratory System.—I have elsewhere referred to the 
bad prognosis of all pneumonias in alcoholics (See Pneumonia) and to 
the fact that pneumonic infiltrate is found in most alcoholics who die with 
either acute or chronic symptoms. The tuberculization of the alcoholic is 
comparatively easy. Many finally yield to this infection (See Tubercu- 
losis). 
In alcoholics disseminated bronchitis, grippal infection, acute ca- 
tarrhal invasion of any part of the respiratory tract are easily complicated 
by broncho-pneumonia—always serious. The chronic bronchitis of the 
alcoholic is persistent and never yields until he has reformed during a 
sufficiently long period. In some, it persists in spite of the discontinuance 
of liquor; the same is true of alcoholic laryngitis and tracheitis. 
(d) Delirium tremens 
(Mania a potu) 
Symptoms.—Habitual drinkers are subject to a complex of symptoms 
known as delirium tremens. This includes active delirium associated 
with muttering, continuous incoherent talking with hallucinations—almost 
always visual and aural—increasing terror as the condition develops, trou- 
blesome insomnia—often controlled with great difficulty—persistent 
tremor of all muscles and tongue increased by movement, rapid pulse (100- 
130 per minute) often dicrotic, usually febrile movement (101°-104° F.) 
and albuminuria in over 60 per cent of all cases. 
Recurrence.—Delirium tremens once developed is likely to recur if 
the habit is continued. In my hospital service I have alcoholics who 
for years have returned to the wards as often as once in two months, usu- 
ally leaving the hospital restored physically but with their psychic being 
unchanged. 
Prognosis.—The prognosis of uncomplicated delirium tremens is rela- 
tively good. A mortality of 15 per cent represents the average of hos* 1184 
INTOXICATIONS 
pital practice. Statistics vary from 2 to 15 per cent (Oppenheim). In 
709 cases of delirium tremens in Bellevue Hospital there were 143 deaths 
or about 20 per cent (Lambert) ; G1 of these died of pneumonia. There 
were 125 cases of pneumonia in the 709 cases. Deducting the pneumonias 
there were 584 remaining, with a death rate of 14 per cent. It is use- 
less to compare the mortality of hospital with private practice. The for- 
mer include the worst possible timber, the latter, well-housed, early escape 
the exposure and infection which kills. Moderate drinkers who develop 
delirium tremens easily, offer an unfavorable prognosis. 
Persistently high temperature with delirium is unfavorable; if the 
pulse continues rapid and small with evidences of dilated heart and 
cyanosis, particularly in the plethoric, the prognosis is bad. Obesity is 
unfavorable in such cases. Wild delirium with rapid pulse, dry tongue, 
albuminuria with casts and uncontrolled insomnia is an unfavorable com- 
bination. Involuntary discharge of urine and feces is not necessarily 
significant though it attends the more serious cases. 
Collapse at any time usually leads to death because of its primary 
cause (dilated heart, myocardial degeneration). Infections of any hind 
are serious, the more alarming as already mentioned, are pneumonia, ery- 
sipelas, meningitis and suppurative otitis. 
Patients with “wet brain” who live beyond the second week, in my 
service as a rule make slow, but good, recoveries. With retraction of head 
and stiff neck, the prognosis is not good (Dana). We have only rarely 
committed a patient to a state institution from our wards, who on ad- 
mission failed to show some evidences of preceding mental alienation. 
Mild delirium persisting during several weeks does not affect prognosis 
unfavorably if without complications. 
Duration.—The length of the average delirium is about 4 days; no 
time limit can he given. 
References 
Curschmann. Lehrb. der Nerverikr. 1909. 
Dana. Diseases of the nervous system, 1915. 
Kraepelin. Psychiatrie. 8. Aufl. 
v. Jaksch. NothnageVs Spec. Path. u. Therap. (Vergiftungen). 
Lambert (Alexander). New York State J., 1910. J. Am. Med. Ass., Feb. 18, 1911, Ivi. 
Boston Med. & Surg. J., April 25, 1912, cixvi. J. Am. Med. Ass., June 
21, 1913, lx. New York Med. Rec., Feb. 18, 1915. Osier’s Modern 
medicine. Philadelphia, 1907, i. 2d ed., 1913, 
von Mehring & Krehl. Lehrb. der inner. Med. Jena, 1913. 
Meyer. Mohr u. Staehelin’s Handb. der inner. Med. Bd. v. 
Oppenheim. Lehrb. der Nervenkrank. Berlin, 1913. 
Osier (Sir William). Practice of medicine. New York, 1913. 
Wassermeyer. Delirium tremens. Arch. f. Psychiat. Bd. xliv. INTOXICATIONS 
1185 
2. Morphinism 
What has been written in this section of the underlying psychic anom- 
aly in alcoholism is equally true of the morphin habit and it is also true 
that no morphinist can be saved from the bondage which holds him who 
does not earnestly assist in his own emancipation. Unquestionably re- 
cently enacted federal and state laws will prove powerful factors, if rig- 
orously enforced, in reducing the number of drug habits; the medical pro- 
fession has a large responsibility to shoulder in this connection. When we 
consider that one-third, at least, of all morphinists are physicians, we 
find ourselves face to face with a problem which should enlist our most 
careful study. 
Prognosis.—Prognosis in the majority of those treated early, before 
the nervous system lias been functionally ungeared, is good; it is discour- 
agingly bad in the majority of chronic cases, particularly in those asso- 
ciated with central nervous disease, with sensory symptoms (tabes dor- 
salis, chronic neuritis) and with gastro-intestinal or any other disease in 
which pain started the use of the drug, including cholecystitis and renal 
calculosis. The prognosis of the morphin habit is always improved by 
the radical removal of the factor which causes pain, unless the habit has 
been long formed; it is always worse when morphin is taken without sen- 
sory symptoms demanding relief. 
Course of Intoxication.—Like alcohol, the early small dose is grad- 
ually increased. In rare cases the initial dose is not increased during 
considerable periods and the general appearance of the patient and his 
health are not noticeably changed; sooner or later all morphinists increase 
the dosage and show the earmarks, promptly recognized by the experienced 
eye, which brands them as slaves to the drug. The physiological effect 
of the drug is sought; the color remains persistently sallow, the eye dull 
and pupils contracted; marked restlessness continues unless the fading 
effect of the preceding dose is met by a fresh injection or dose; the men- 
tal vigor for a time is increased, as the dose is increased and narcosis, more 
or less continuous, begins to fail; the moral sense is blunted, truth is no 
longer respected; the being is metamorphosed and often physically and 
mentally unrecognizable. Unkempt and neglected they live, often many 
years, always deceiving, untruthful, absolutely undependable. 
I met one country physician in consultation who took a level teaspoon- 
ful of morphin sulphate in a single dose. He lived to be almost eighty 
years of age. 
Influencing Factors.—The size of the dose and the quantity taken 
during twenty-four hours varies with the duration of the habit and with 
the individual. Lambert does not believe that the size of the dose has 
any settled ratio to the duration of the habit. The sudden withdrawal 
of all morphin from the chronic habitue may lead to collapse—alarming, 1186 
INTOXICATIONS 
even fatal. I have seen gastric symptoms and diarrhea during treatment 
and the withdrawal of morphin prove threatening and controlled with 
great difficulty. Most of my cases of morphinism have fallen into 
wretched states, have developed intercurrent disease—often infection. 
The majority of habitues are handicapped by an unstable nervous sys- 
tem or bad heredity. This fact makes prognosis graver. Psychopathic 
states invite the habit and make the release exceedingly difficult. 
The development of the habit among medical students is encouraged 
by a desire to learn the physiological effect of the drug; this practice 
should be vigorously discouraged. Successful issue demands months of 
surveillance and control, without which the prognosis for lasting cure is 
bad and relapse is the rule. 
Meyer (E.) places the percentage of permanent cure at only 1 to 2 
per cent. Levinstein reports 82 patients (males) ; of these 61 relapsed; 
of 28 women, 10 relapsed; of 32 physicians only 6 were released, 26 
relapsed. The prognosis among physicians is discouraging. Hirt reports 
27 of 35 morphinists cured. This is an unusually favorable outcome and 
has not often been equalled by the treatment of an equal number of aver- 
age cases in America. Suicidal mania develops in a comparatively large 
number of cases. 
I have been more successful in my cases, probably because many 
have been placed in hospitals, taken from depressing environments and re- 
mained under strict surveillance; then too, the cases which I have seen 
in private practice have been treated early. The material which we 
have in our wards is not favorable for ultimate cure; this includes many 
who are alcoholics, tobacco and cocain fiends, and among the women, a 
large proportion of prostitutes. They are without the remnant of moral 
force which is so necessary for success. 
Accompanying Conditions. — Arteriosclerosis, chronic constipation, 
other gastro-intestinal symptoms, myocardial insufficiency, sexual anomal- 
ies (perversion), irregular types of fever, final emaciation (marasmus) 
with terminal infections—septic, pyemic, tuberculous and pneumonic— 
complicate chronic morphinism. 
Crothers. Med. Rec., New York, 1899. 
Frlenmeyer. Die Morphinsucht, etc. 3d ed. 1887. 
Uirt. Neurol. Centralbl., 1898. 
Lambert (Alexander). Osier’s Modern medicine. Philadelphia & New York, 1907, i. & 1913. 
Levinstein. Die Morphinsucht. 3d ed. 1883. 
Meyer (E.). Mohr u. Staehelin’s Handb. der inner. Medizin. Berlin, 1913, Bd. v. 
Oppenheim. Lehrb. der Nervenkr. Berlin, 1913, Bd. ii. 
Schroeder. Berl. klin. Wchnschr., 1911. 
Weber. Deutsch. med. Wchnschr., 1910, 1^3. 
References INTOXICATIONS 
1187 
3. Cocainism 
Cocainism which has not persisted during a long time is more success- 
fully treated than morphinism; if the drug has been used long, complete 
or lasting cure is unusual. Cocainism and morphinism are twin sisters 
—they frequently rule together, and alcoholism completes a trio of habits 
from which escape is exceedingly rare and difficult. 
Cocainism which has continued during months drags the victim to 
the lowest level of morality; the change is so complete as to leave but 
little of his original brain power or personality. Hallucinations, paranoic 
symptoms and insane jealousies develop which with marked emaciation, 
occasional jaundice, persisting insomnia, pigmentation, optic disturbances, 
cardiac anomalies (tachycardia), irregular respiration, spasm of the neck 
muscles (oftener in acute cases), anomalies of the sweat glands and utter 
disregard for order, discipline, cleanliness, truth or tact often continue 
during months or years, the victim awaiting intercurrent disease, infec- 
tion, accident or suicide to end his days. 
T have seen a number of advanced cases of cocainism permanently 
cured. The struggle in such cases is fierce and the forces which invite 
relapse are powerful and usually conquer. 
References 
Briand & Virchow. Ztschr. f. d. gesamt. Nervenheilk., vi. 
Erlenmeyer. Morphinism and cocainism. 4- Aufl. 
Handb. der Therapie. Jena, 1909. 
Higier. Munch, med. Wchnschr., 1911. 
Meyer (E.). Mohr u. Staehelin’s Handb. der inner. Krank. Berlin, 1913, Bd. v. 
Oppenheim. Lehr, der Nervenk. Berlin, 1913, ii. 
4. Lead Poisoning 
Acute Poisoning 
The acute poisoning due to lead, usually the acetate and oxid, is in- 
frequent, leads to gastro-intestinal of an irritating character, 
rarely to subacute or chronic symptoms and in almost all cases offers a 
good prognosis when rationally treated. 
Chronic plumbism includes— 
(a) Constitutional symptoms with lead colic, 
(b) Saturnine arthralgia 
(c) Lead palsy 
Chronic Plumbism 1188 
INTOXICATIONS 
(d) Lead encephalopathy 
(e) Saturnine anemia 
(f) Saturnine arteriosclerosis 
(g) Saturnine nephropathy (Chronic interstitial nephritis). 
Influencing Factors.—The influence of heredity on the development 
of lead poisoning has not been satisfactorily settled. It may be assumed 
however, that in cases where several members of a family or succeeding 
generations have been poisoned that all were exposed to corresponding con- 
ditions. We have positive evidences at our command which prove that 
children are less easily 'poisoned than are adults (shown by poisoned drink- 
ing water, cider, etc.) but when once surcharged they yield with greater 
difficulty—often resist cure during long periods more obstinately than do 
adults. In children diarrhea, a frequent symptom early, has a favorable 
effect. 
Oliver proved that women were more susceptible than men and it has 
been noticed that their suffering is more acute. Improper feeding, filth, 
carelessness in the care of hands, teeth and utensils, alcoholism, nephritis, 
sexual excess and faulty ventilation are all inviting factors and increase 
symptoms. 
(a) Constitutional Symptoms with Lead Colic 
Occupational Influence.—Painters, carriage rubbers, lead workers, 
plumbers, potters (china workers), tea tasters, typesetters, polishers and 
glaziers are among the most frequent occupations which cause lead poi- 
soning. 
Constitutional Symptoms.—In all lead poisoning, whatever the symp- 
toms, there are constitutional anomalies which are characteristic with 
changes in the blood of a degenerative character demanding consideration 
in offering prognosis. In my treatment of the subject I refer to the 
leading clinical pictures upon which prognosis may he safely based. The 
constitutional symptoms in cases with lead colic are less developed than 
with some of the other clinical types. This is so because in most cases of 
lead colic the poisoning has not become chronic and colic is one of the early 
manifestations. 
Colic is due to spasmodic contraction of the intestinal musculature. 
While most cases show moderate saturnine anemia, it is not profound: 
as a rule, the cardiovascular changes in early cases are not developed, the 
blue line is likely to he present, the pulse shows some abnormal slowness, 
is tense, and lethargy is more or less marked. The colic itself is often 
severe and is associated with obstipation. There is vomiting, and the 
pain of the tense abdomen is often relieved by pressure and opium and 
in almost all uncomplicated cases, is cured when recognized and the 
source of poisoning is removed. Where the water supply is “lead charged” INTOXICATIONS 
1189 
and the source is unrecognized, colic will return and other symptoms of 
plumbism develop. I have never seen death result directly from uncom- 
plicated lead colic; cure has been the rule. 
(b) Saturnine Arthralgia 
Severe and persisting pains in the joints and neighboring muscles may 
complicate any of the clinical types of lead poisoning. It may however, 
be the only subjective complaint in occasional cases; it is usually asso- 
ciated with anemia, tense and sloiv pulse, often elevated blood pressure 
and occasional albuminuria. The knee is the favorite seat of arthralgia. 
The outcome of most saturnine arthralgias included in this type, associ- 
ated with some of the less threatening organic changes of chronic plumb- 
ism, is good. It requires only the recognition of the cause and source 
of the pains and poison and common sense treatment. 
More than one-half of the cases of lead poisoning which enter the 
hospital for treatment show evidences of lead paralysis and the majority 
of these have double ivrist drop. 
(c) Lead Palsy 
I have separately considered the peripheral paralysis and neuritis 
due to lead (See Section VII). 
The prognosis of most cases is good though in chronic cases remnants 
of paralysis may remain. 
(d) Lead Encephalopathy 
The cerebral disturbances dependent upon lead poisoning are included 
in the lead encephalopathies. There are cases in which the sensorium 
is never disturbed; others in which lead causes early brain symptoms, 
sometimes mild, in some severe and threatening. In some with colic or 
other positive organic changes moderate psychic disturbances are transi- 
tory, while in others—and these are graver types—after long periods 
of plumbism there are psychoses or delirium, coma and death. 
In the majority of fatal cases the encephalopathies have been found 
in chronic conditions with cardiovascular and renal changes and usually 
with profound anemia. Subacute poisoning with anemia gravis and 
marked morphologic change of cellular elements of the blood, leukocytosis 
and abundant basophilic bodies have been most intractable and I have 
lost a number of these patients within the first two or three months fol- 
lowing recognition and treatment. Long-continued plumbism with arterial 
change in subjects who continue at their work is often sudden, followed 
by encephalopathies, active mania, wild delirium and with evidences of 
failing heart, preceded by hypertension, these patients die. 1190 
INTOXICATIONS 
Encephalopathies (psychoses) which persist during long periods, un- 
less they show some improvement following institutional treatment early, 
may never fully recover though there may be sufficient change to justify 
discharge from state surveillance. In all encephalopathies the associated 
conditions and lesions must influence prognosis powerfully. Xhe delirium 
of profound saturnine anemia and the muttering or occasional delusions 
with lead colic and constitutional symptoms usually yield as the general 
status is improved. 
Recurrence.—Encephalopathies are likely to recur with fresh poison- 
ing and in such cases are obdurate, persist long after the more acute 
symptoms yield. There may never be a return to the normal standard. 
Associated Conditions.—Convulsions of an epileptic nature are not in- 
frequent and recur especially in the more chronic cases. In subacute and 
chronic cases tremor is often a prominent and occasionally remains a per- 
manent symptom. I have seen a number of cases without encephalopathy 
in which tremor was associated with colic, hypertension or peripheral 
neuritis and palsy, in which with full recovery the tremor disappeared 
entirely. Ocular symptoms may develop with or without encephalopathies, 
including optic neuritis, optic atrophy, neuro-retinitis, and with advanced 
arterial change choroidal hemorrhage. In these cases the prognosis should 
be guardedly given, the case should be observed by the ophthalmologist. 
These complications are likely to accompany the more chronic types with 
cardiovascular and renal changes. Serious eye lesions are not frequent. 
De Schweinitz found only three in 15,000 eye cases. The addition of an 
emotional element—hysteria and neurasthenia—does not materially com- 
plicate the outcome, so far as life is concerned. 
(e) Saturnine Anemia 
Moderate saturnine anemia, as already stated, complicates most, 
chronic lead poisonings. The milder anemias promptly improve under 
treatment and do not lead to persisting blood changes. The graver ane- 
mias are found in the more serious cases with mental torpor, often de- 
lirium, hallucinations and encephalopathies. These graver anemias are 
among the more serious complications of lead poisoning. 
The Blood Picture of Lead Poisoning 
Stengel, White and Pepper 3d, have after painstaking study of the 
blood concluded that there is no other poison which so regularly and 
promptly causes degeneration as does lead. 
hfaegeli believes that the pallor of the poisoned is due largely to vas- 
cular spasm and bases that opinion upon the frequent absence of chloro- 
sis and low red count. My cases have usually shown moderate oligemia INTOXICATIONS 
1191 
during the early stages, and increasing anemia as the condition became 
more chronic. 
In chronic lead poisoning the average red count in severe cases will 
be found below 2,000,000—mild poisoning 3,000,000 to 4,000,000 with 
leukocytes between 10,000 and 20,000. Many normoblasts indicate se- 
vere anemia—.5 to 3.4 per cent (Becker, Limbeck and Malassey). 
Cadwalader has demonstrated the presence of nucleated red corpus- 
cles even in mild cases of plumbism; taken alone the presence of nucle- 
ated reds does not materially affect prognosis. In a recent fatal case 
in our hospital we found with abundant basophilic bodies a red count 
below 1,000,000 and hemoglobin 20. 
Grawdtz, in 1889, called attention to the presence of basophilic bodies 
in the erythrocytes with lead poisoning. The detection of basophilic 
bodies is of some importance for prognosis; more important is the fact that 
it makes the early recognition of the disease possible in lead workers who 
are watched. 
Schmidt contends that 100 basophilic bodies in 1,000,000 erythrocytes 
demands removal from lead. Grawitz holds that all poisoned with lead 
show basophilic erythrocytes and that this fact is of the utmost importance 
for diagnosis and prognosis. ISTaegeli has seen cases of severe poisoning in 
which there has been lead in the urine and “marked blue line” without 
basophilic bodies. The presence of basophilic bodies one day may be fol- 
lowed by their absence the next, and during several subsequent days. 
In the present state of our hematologic knowledge we must conclude 
that while basophilic bodies are present at some time, and usually early, 
neither their number nor their presence are to be depended upon for 
prognosis alone; the low erythrocyte count, the presence of large numbers 
of normoblasts, the positive evidences of hemolysis and morphologic change 
are more dependable when coupled wffth the clinical picture than the con- 
sideration of a single blood change. 
Leukocytosis is usual, and with the grave anemias the count is high—at 
times there is myelocytosis. The lower the red count with involvement of 
the central nervous system, delirium, encephalopathies and nephropathies, 
the ivorse the outlook. Extreme myasthenia in these cases often precedes 
death. 
Subacute cases in which there has been sudden poisoning and in which 
there is daily accession, have been associated with marked hemolysis, low 
counts and death. My last cases, two brothers, were brought to the hos- 
pital from the country where during a number of months they drank cider 
which was drawn through a corroded lead pipe. Both showed marked 
anemia and basophilia, one was myasthenic with marked encephalopathy 
including continuous delirium. He died without showing regeneration, 
while his brother recovered and with a low blood state, promptly improved. 
The initial blood picture in these cases was not materially different. 1192 
INTOXICATIONS 
(f) Saturnine Arteriosclerosis 
I have separately considered the influence of lead on the arterial tree 
and the arteriosclerotic changes resulting (See Arteriosclerosis and Blood 
Pressure Study), also the influence of lead on gout (See Gout). 
Advanced and chronic cases show arteriosclerosis disseminated and a 
hypertensive condition with aortic lesions and high pulse amplitude. In 
most of these, there is also interstitial change in the kidneys. Once estab- 
lished, the arteriosclerosis remains though in young subjects, under favor- 
able conditions and treatment, it may not advance. When renal lesions are 
present and the heart is markedly hypertrophied, toxic symptoms may 
complicate or sudden myocardial changes are responsible for a fatal termi- 
nation. Limited arteriosclerosis, i. e., even thickening of the arteries with- 
out other complications—even with moderate hypertension, may not per se 
shorten life when the patient is removed from the source of poisoning. 
(£) Saturnine Nephropathy 
Chronic Interstitial Nephritis 
Lead is a frequent factor in producing chronic renal change. It is 
never in such cases, dissociated from arteriosclerosis; in fact the arterial 
degeneration of the renal vessels and ultimate connective tissue prolifera- 
tion with marked hypertension are the leading accompaniments of sat- 
urnine nephropathy—usually there is a complete picture of chronic inter- 
stitial nephritis with ventricular hypertrophy. 
The reader is referred to Section VI—2—Chronic Interstitial Nephri- 
tis—for a fuller consideration of the outcome of chronic kidney changes 
with lead poisoning. 
Moderate changes early recognized, without marked or advanced 
cardiovascular lesions and removal from the poison often remain station- 
ary. The chronic and advanced nephropathies are among the most serious 
of all lesions and do not yield to treatment, though they too may remain 
stationary under favorable conditions during many years. The cases with 
degenerative blood changes, myocardial lesions and coronary or cerebral 
complications (hemorrhage, miliary aneurism, vascular spasm, thrombosis, 
uremia) are always life-threatening. 
Wickham Legg reports 264 cases of lead poisoning with 32 deaths from 
some form of encephalopathy; in 43 there was nephritis, in 47 cerebral 
apoplexy, in 43 paralysis, 38 were tuberculous and 40 died of pneumonia. 
Among the other causes of death were heart lesions, aneurism, and in 44, 
“lead poisoning” (probably without evident complication) was given as the 
cause of death. 
References 
Becker. Deutsch. med. Wchnschr., 1900, Nos. 35 & 36. 
Cadwalader. Fol. haemal. 1905, ii, 808. 
Idem, Hi, 621. INTOXICATIONS 
1193 
Edsall (D. L.). Osier’s Modern medicine. Philadelphia, 1907, i, 84-113. 
Goodby. Brit. Med. J., 1904, i, 654- 
Grawitz. Blut, etc. 4th ed., 753. 
Berl. klin. Wchnschr., 1905, 1438. 
Hamilton (Alice). The economic influence of lead poisoning. Bull. Am. Acad. Med., 
Easton, Pa., 1914, xv, 297-304- 
Clin. Path. Soc., Chicago, 1909-12, viii, 293-311. 
J. Am. Med. Ass., 1914, vol. 59, p. 777. 
Legg (Wickham). Quoted by Tyson and Fussell, Philadelphia, 1914. 
Legge & Goodby. Lead poisoning. London, 1912. 
International Med. Monograph. 
Limbeck. Klin. Path, des Blutes. 2. Aufl., 1896. 
Malassez. Gaz. med de Paris, 1874, 615. 
Naegeli. Blutkrank., etc. Leipzig, 1912. 
Oliver (Thomas). Lancet, London, 1913, ii, 527. 
Brit. Med. J., London, 1911, i, 1096-1098. 
Goulstonian lectures on lead, etc. Lancet, London, 1891, i, 530-588. 
Industrial diseases, etc. London, 1904. 
Stengel, White & Pepper, 3d. Am. J. Med. Sci., May, 1902. 
Thompson (W. G.). Occupational diseases. New York, 1914. 
5. Arsenical Poisoning 
Acute Arsenical Poisoning 
Acute arsenical poisoning interests us only in this work as it leads to 
symptoms after the initial features have passed and there are evidences 
of peripheral neuritis, usually multiple or degenerative changes of the 
liver and other organs which may prove serious. The peripheral poly- 
neuritides associated with arsenical poisoning are separately considered 
(See Multiple Neuritis). 
The poisoning may lead to arsenical tabes in which there are motor 
and sensory symptoms, absence of patella tendon reflex and ataxia, re- 
sembling true tabes. Such symptoms with ocular manifestations or more 
pronounced evidences of polyneuritis with ocular disturbances may follow 
the use of salvarsan. 
Prognosis.—The prognosis of most peripheral disturbances and ocular 
changes following acute arsencial poisoning is good. Recovery is often 
slow, but in the end the majority recover with occasional sensory remnants. 
Chronic Arsenical Poisoning 
Arsenical poisoning follows the use of many articles in domestic use 
which contain arsenic. Wall paper, (green coloring mainly) has heen 
proven by Gmelin (1839), Basedow (1846) and later Draper, Wood and 
others to he a source of danger. Articles of clothing, playing cards, carpets, 
rugs, furs, foods and adulterated drugs (bismuth) have caused isolated 
arsenical poisoning. 1194 
INTOXICATIONS 
I have seen a number of cases in which the long-continued use of arsenic 
for medicinal purposes as a tonic, also for psoriasis, has led to chronic 
poisoning. One case was reported to me in which an arsenic-charged fluid 
in the dissecting room used to prepare and preserve material led to alarm- 
ing symptoms, hyperesthesias and motor insufficiencies. Arsenic eaters 
(mountain climbers) may develop chronic poisoning. 
Prognosis.—The prognosis of most chronic arsenical poisonings is good. 
After the withdrawal of the drug and rational treatment the sensory, motor 
and gastro-intestinal symptoms gradually disappear. Paresthesia and an- 
esthesia with slight motor remnant of peripheral neuritis may continue 
during several months, but cure is the rule. In old subjects who are 
slowly poisoned I have seen some symptoms of neuritis remain throughout 
life. If the cord degeneration in any case is far advanced there will be 
persisting symptoms. 
Skin Changes.—The skin changes following excessive sweating (hyper- 
idrosis), maceration with ultimate exfoliation may recur during several 
months; painful neuralgia or symptoms resembling erythromalalgia are 
not infrequent. Most of these conditions are accompaniments of arsenical 
neuritis as is also the characteristic arsenical herpetiform eruption. In 
chronic cases, the 'pigmentation and keratosis may remain permanent and 
final epithelial thickening (localized) develops. In most cases pigmenta- 
tion gradually disappears after the supply of arsenic has been cut off. The 
leading manifestations of chronic arsenical poisoning are referable to the 
peripheral nerves and cord. 
Prognosis.—The prognosis is good (See Peripheral Neuritis and 
Peripheral Paralysis—Section VII). 
Accompanying Conditions.—The associated atrophy may continue 
troublesome during discouragingly long periods, but finally there is in most 
cases gradual return to an approximately normal condition. The knee jerk 
may remain blunted during years or may never reappear; normal reflex is 
the rule after reasonable periods. In cases which have been undetected 
during long periods in which arsenic is added from day to day, the condition 
may be one of extreme weakness with marked anemia and final cachexia. 
In one of my cases due to wall paper, nephritis developed with duodenal 
ulcer, death resulted from subphrenic abscess following perforation. 
Psychic disturbances are frequent in the chronic and more severe 
types; dementia is rare but it may develop. The leading symptoms refer- 
able to the brain are amnesia (forgetfulness), mental lethargy, and occa- 
sionally hallucinations. With psychic symptoms the prognosis is graver 
than without them. Ocular lesions have increased since the introduc- 
tion of salvarsan and its use for the intensive treatment of syphilis— 
amblyopia, amaurosis and opacities of the crystalline lens. 
Prognosis.—Death due directly to chronic arsenical poisoning is rare 
and need not be expected unless there are grave complications. INTOXICATIONS 
1195 
References 
For full bibliography see References to Arsenic—Index Medicus; also References under 
Arsenic in both the original and second series of the Index Catalogue of the Surgeon-General’s 
Office. 
Dana. Arsenical tabes. Brain, 1886-7, ix. 
Draper. Report of State Board of Health, Massachusetts, 1872. 
Edsall (D. L.). Osier’s Modern medicine. 1907, i. 
Wood. Report of State Board of Health, Massachusetts, 1884. 
6. Mercurial Poisoning 
Occupational Influence.—Chronic mercurial poisoning is exceedingly 
rare in the United States. The chief industries which lead to the poison- 
ing are mining and smelting of mercury, the manufacture of thermometers 
and barometers, instruments of precision in which mercury is used, the 
production of mercury salts by chemists and the manufacture of felt hats. 
Occasionally in practice the long-continued and careless use of mercury for 
medicinal purposes leads to chronic poisoning. Poisoning among miners 
and workmen is encouraged by carelessness, poor ventilation and lack of 
cleanliness. 
Prognostic Symptoms.—Stomatitis with degeneration of the teeth, 
extensive ulceration of the gums and buccal mucosa and occasional caries 
of the jaw are the leading early symptoms. With these symptoms early or 
later, gastro-intestinal symptoms and a characteristic cachexia (cachexia 
mercurialis—von Mehring u. Krehl) develop with a peculiar bluish gray 
or ashen color of the face. The leading and often persistent symptoms arc 
tremor, erethism (marked irritability) and insomnia. These latter symp- 
toms when coupled with psychic disturbances—mania, hallucinations or 
mental torpor—brand the case as serious. In grave cases the tremor may 
be universal; it remains uncontrolled, and is associated with characteristic 
cachexia and anemia; it continues until death. Mercurial neuritis is an 
occasional accompaniment; per se it does not add to the danger. 
In the extreme cases the symptoms which threaten life are the uncon- 
trolled cachexia, anemia, tremor, diarrhea and extreme asthenia. 
Moderate albuminuriai in cases which do not present malignant features 
is not unfavorable. Most chronic cases make satisfactory recoveries unless 
the poisoning has continued uncontrolled and has been neglected too long. 
References 
Edsall (D. L.). Osier’s Modern medicine. Philadelphia, 1907, i. 
von Mehring u. Krehl. Lrhrh. der inner. Medizin. Jena, 1913, Bd. ii, 347. 1196 
INTOXICATIONS 
7. Carbon Monoxid Poisoning 
Illuminating gas poisoning is never anything but a serious incident. 
It may be acute, or in occasional, cases there may be the inhalation of a 
small quantity of gas due to a continuous small leak which causes positive, 
but mild and chronic discomfort. In these latter cases, headache, nausea, 
anorexia, giddiness, somnolence and dyspnea with some cyanosis in the 
more severe cases, are the leading symptoms. Removal from the gas 
promptly leads to permanent recovery. The prognosis is less favorable if 
mental or peripheral symptoms exist. 
In acute 'poisoning unless relief is prompt and an abundant supply of 
oxygen (fresh air) supplied, or if the victim remain in the vitiated atmos- 
phere, the prognosis is absolutely bad. 
Symptoms.—Loss of consciousness, with the congested face, irregular 
respiration, subnormal temperature and disorganized blood are among the 
unfavorable symptoms. Coma may continue during prolonged periods and 
yet recovery may follow. 
The blood picture is characteristic. The degeneration or dissolution of 
the red blood corpuscle in profound poisoning is prompt; there is concen- 
tration of the blood, (polycythemia—polyglobulia) the carbon monoxid 
combines with the hemoglobin for which it has a strong affinity, and makes 
the latter useless as an oxygen carrier. Death results therefore from 
asphyxia. If there is marked leukocytosis the prognosis is bad. There is 
always some increase of polymorphonuclear cells (Gilman Thompson). 
Prognostic Factors.—The dangers from both coal gas and water gas 
are greater in proportion to the amount of carbon monoxid contained in the 
atmosphere breathed. An atmosphere which contains one per cent of 
carbon monoxid breathed during a considerable period proves fatal; if the 
per cent were larger, death would result correspondingly sooner. Coal gas 
contains from 4 to 8 per cent of carbon monoxid, while water gas contains 
between 35 and 45 per cent (40 per cent average). The dangers are not 
always ended with the disappearance of the acute symptoms, for purpuric 
conditions, hematogenous jaundice, lesions including bullous eruptions 
(pemphigus), bed sores and grave central and peripheral disturbances may 
follow days or weeks after the initial poisoning. 
Naturally the great factor in prognosis is the early discovery of the 
poisoned subject and immediate treatment. It is not unusual for sudden 
death to follow return of consciousness. 
Complications.—Focal softening of the lenticular nucleus or other 
portions of the brain have been found post mortem (Poetchen). Multiple 
neuritis and neurosis (psychoneuroses) are not infrequent sequelae in cases 
which live beyond the acute period (Oppenheim, Lippmann, Stierlin). 
Bronchopneumonia occasionally complicates recovery; if extensive, 
with high fever, the prognosis is bad. The sequelae referable to the lung INTOXICATIONS 
1197 
(pneumonia) may cause death early, i. e., within the first ten days follow- 
ing the poisoning, or several weeks may lapse before the lungs are attacked. 
Arhythmias and cardiac weakness may follow or accompany the acute 
symptoms. In some cases the symptoms resemble Landry’s paralysis; 
there is ascending motor paralysis and death may follow from respiratory 
or cardiac involvement. 
Chorea, tremor, scanning speech and involuntary discharge of urine 
may develop (Edsall). Symptoms of multiple sclerosis have developed, as 
have also ocular symptoms including transitory blindness, also aural symp- 
toms—tinnitus and deafness. 
Prognosis.—In offering prognosis it must be remembered that any of 
the above mentioned sequelae may develop long after (several weeks) the 
subsidence of the acute symptoms. Patients may die months after the 
poisoning from any one of the sequelae mentioned or they may gradually 
lift themselves back to comparative health. 
Patients who develop psychic disturbances (dementia) which continue 
uninfluenced during several months are not likely to recover completely. 
Of the cases promptly treated 80 per cent live. Of the 20 per cent who die 
a number yield to complications. Young subjects offer a more favorable 
prognosis than do the aged. 
References 
Edsall. Osier’s Modern medicine. Philadelphia, 1907, i. 
Lippmann. Arzt. Sachverstand. 1908. 
Oppenheim. Lehrh. der Nervenkrank. Berlin, 1913. 
Poetchen. Virchow’s Arch. Berlin, Bd. cxii. 
Stierlin. Zurich, 1909. 
Thompson (Gilman). New York Med. Rec., July 9, 1904. 
Occupational diseases. New- York, 1914. 
Westphal (A.). Arch.f. Psychiat., Bd. xlvii. 
8. Pellagra 
(Maidismus) 
Pellagra is a disease of unknown origin which is as a rule chronic, 
but which may be acute; it is associated with early gastro-intestinal 
symptoms, cutaneous lesions (early erythema), marked nervous mani- 
festations including great unrest, mental disturbance, depression, suicidal 
mania, convulsive movements, contractures and paralyses—trophoneuroses 
and characteristic cachexia in the terminal stages. 
Geographical Distribution.—The disease is more prevalent in South- 
ern Europe, Italy and Roumania than on the western continent, though 
jt is at present more frequent in the United States than formerly. It is 1198 
INTOXICATIONS 
found in country districts oftener than in the city. In central New York 
it was never known to exist until within the past three years. I know 
of two deaths, both in country districts, one of which suicided after 
about fourteen months of continuous symptoms. The other ran a more 
rapid course to a natural death from asthenia. Neither of these patients 
ate corn; they were widely separated. 
Etiology.—There is no positive proof that the disease is a food intoxi- 
cation, neither has the recent suggestion of Sambon been accepted by the 
profession that it is due to an infection of protozoan origin transmitted 
by sand dies (Genus Simulium). 
There is no proof of the contagious character of the disease. The 
literature of pellagra has grown enormously, but after its thorough review 
we do not feel that there are any data which establish its etiology beyond 
doubt. 
We have not yet been able to divorce ourselves from the suspicion of 
the pathogenic influence of maize (spoiled corn or corn products) in the 
causation of the disease but there are innumerable cases in which corn 
products have never been used. 
Sambon’s contention, above mentioned, that the Simulium reptans 
(sand fly) carries an infecting protozoa has been surrendered; the Thoinp- 
son-McFadden Commission has pretty thoroughly weakened that theory. 
Jennings and King after considering insects as a factor in pellagra and 
the Thornpson-McFadden Commission throw a suspicion upon the stable 
fly (Stomoxvs calcitrans) as the carrier of the infection. The entire 
question of etiology must remain sub judice until more convincing proof 
is offered. 
Niles, who has had an enormous experience with pellagra, basing his 
conclusions on the treatment of over six hundred cases admits that “the 
etiology of pellagra is unknown.” 
Prognostic Symptoms and Factors.—The symptoms of pellagra are 
usually typical, though there have been no characteristic anatomic lesions 
to brand the disease save as they are found in the skin and rest upon a 
fundament of trophoneurosis “similar to the degenerations incident to 
senility” (Niles). 
The leading symptoms and factors which influence prognosis are: 
(a) Ilabits (including diet) 
(b) Location 
(c) Course (acute, subacute, chronic) 
(d) Age, race, sex 
(e) Gastro-intestinal symptoms 
(f) Skin lesions 
(g) Psychic disturbances 
(h) Central and peripheral lesions of the nervous system. INTOXICATIONS 
1199 
(a) Habits 
Intelligent living favors pellagrins very materially; in the present 
state of our knowledge corn should be interdicted—at any rate it should 
be fresh and “should not have undergone heating” (Niles). 
In countries where pellagra is endemic there is no doubt of the bane- 
ful effect of alcohol. The increase of the disease in Italy (1908-1911) 
over a preceding equal period is in all probability due to the abuse of 
alcohol. In all cases, alcohol increases the psychoses'. 
Pellagrins in order to improve must take advantage of right living, 
eating, and drinking; their environment exerts an enormous influence 
on the course of the disease. 11 eat provokes the skin lesions and aggra- 
vates subjective symptoms of irritation. Direct sun rays are detrimental, 
as is also excessive heat from stoves or furnaces. Hot weather invites 
pellagra; it is less prevalent or troublesome during the winter months or 
in a cool atmosphere. 
(b) Location 
In countries where pellagra has been endemic during long periods 
the prognosis seems more favorable than in America. This is particu- 
larly true of Spain and some parts of Italy where the endemic was wide- 
spread, early and severe; later there was a marked drop in the severity 
of the disease and its incidence. All agree that the disease as seen in the 
United States offers a graver prognosis than in Europe. The death rate 
in America varies between 25 and 65 per cent. In Italy and Spain the 
mortality at times falls to 4 per cent. 
(c) Course 
Acute and Subacute Cases.—The acute cases with typhoid condition, 
high temperature, rapid pulse and delirium, intestinal symptoms (diar- 
rhea and vomiting) are exceedingly grave. They may die in the course 
of a few days or weeks and demand differentiation from typhoid fever. 
In this type as well as with the subacute, deep invasion of the sensorium 
is always of serious significance. 
Chronic Cases.—The prognosis of the chronic cases largely depends 
upon many separate factors including habits, environment, age and symp- 
toms specially considered. In all of these cases rational and intelligent 
treatment and persistence, materially improve the chances of the patient. 
(d) Age, Race, Sex 
Age.—Most cases are found during the active .years of life (18 to 
45). Young subjects offer a better prognosis than do those beyond 50. 1200 
INTOXICATIONS 
In all, the factors above mentioned (particularly habits—alcohol, environ- 
ment, etc.) remain powerful. 
Race.—The negro is more susceptible than the white but under the 
same conditions the prognosis is not materially different. 
Sex.—Women are more frequent victims than are men. 
(e) Gastro-intestinal Symptoms 
In chronic or acute cases, persistent gastro-intestinal symptoms— 
diarrhea, vomiting, anorexia, ulcerative or catarrhal gingivitis, glossitis 
and stomatitis-—and persistent abdominal pain add to the extreme exhaus- 
tion and lead to such weakness as we often find associated with cachexia. 
The dryness of the mouth and glazed tongue with dysphagia in my case, 
which finally suicided, threatened life during several weeks. Progressive 
cachexia and persistent diarrhea are always grave. 
(f) Skin Lesions 
Erythema and bullous eruptions with persistent moisture are evidences 
of severe disturbance. Moist eruptions have been noted by most observers 
in the most threatening cases Symmetry of lesions, particularly of the 
forearms, is striking but is of no prognostic significance. Skin lesions 
should be considered in connection with the other features for prognosis, 
and not alone. 
(if) Psychic Disturbances 
The deeper and more persistent the psychic manifestations of toxemia 
the worse is the prognosis. 
Mania with the refusal of food and gastro-intestinal symptoms threat- 
ened my case during several weeks, during which a cachectic condition 
developed, from which the patient finally rallied; there was a manic- 
depression which was never relieved and which led to suicide. Mental 
alienation demanding removal to a state institution is not uncommon. 
The prognosis in those committed to public asylums is very bad. 
Conclusions.—It may he safely concluded that the most serious cases 
are those with profound mental disturbances in which there are also gastro- 
intestinal symptoms which lead to cachexia and marasmus. 
(h) Central and Peripheral Lesions of the Nervous System 
There are cases in which, besides psychic disturbances there are symp- 
toms which can only be explained on the basis of organic change in the 
central or 'peripheral nervous system. These refer to the cord, in which 
there is sphincter involvement with Hunted deep and superficial reflexes 
and spastic paralysis, or there are symptoms of peripheral neuritis. INTOXICATIONS 
1201 
Cases in which these lesions are not deep-seated and are without 
profound psychoses, the prognosis is not necessarily bad. Niles says: 
“If the patient is under 50, and has sufficient intelligence and perse- 
verance to adhere to a fixed line of treatment and will faithfully cooperate 
with the physician, a permanent cure may be expected in the majority 
of cases.” 
References 
Pellagra. In: Index Catalogue, Library of the Surgeon-General’s Office, 
vol. xii, 2d series, 724. 
Jennings & King. Am. J. Med. Sci., Aug., 1913. 
J. Am. Med. Ass., Jan. 25, 1913, lx. 
Niles. J. Am. Med. Ass., Jan. 24, 1914. 
Sambon. La pellagra. Bull., Acad, de Med., Paris, 1914. 3d ser., Ixxi. 
J. Trop. Med. A Hygiene, Oct., 1910, xii, No. 19. 
Brit. Med. J., 1905, ii, 1272. 
Singer. (Report) Pellagra Commission, State of Illinois, 1911. 
Strumpell. Bibliography. New York, 1913. 
Thompson & McFadden Commission. New York Postgraduate School, 1913. 
Tizzoni. La pellagra. Torino, 1913. 
Willcocks. Practitioner. London, 1914, xciii, 106-112. 
9. Beriberi 
(Kakhe) 
Symptoms.—Beriberi, or kakke, is a polyneuritis associated with fever, 
in some cases edema or anasarca, and in the subacute and chronic types 
more or less muscular degeneration causing atrophy. 
Etiology.—The disease is due in all likelihood to the eating of pol- 
ished rice. The disease is invited by faulty housing and is frequent in 
barracks, asylums, on shipboard, in prisons—wherever people are massed 
in unsanitary quarters among whom polished rice furnishes the larger 
portion of sustenance. The phosphorus compounds of the pericarp are 
removed in the process of polishing. 
Most cases which come to America are imported from India, China, 
Japan or from South and Central America. The cases which are found 
in America are mainly those which have lived through the early stages 
and present with the clinical picture of multiple neuritis fully established. 
The number of beriberi patients among the Japanese during the Japanese- 
Bussian war was astounding (over 50,000). Many cases are complicated 
with intestinal parasites. 
Wright believes that the disease is positively infectious, “due to a 
specific organism not yet certainly determined; the organism is not one 
whose special habitat is any food such as fish or rice, but one that may 
nevertheless be ingested in any food and drink accidentally contaminated.” 1202 
intoxications 
Tsuzuki lias (he claims) isolated a germ from the urine and feces of 
beriberi patients; a diplococcus which in inoculation experiments has 
reproduced the symptoms of the disease. At present, the. consensus of 
opinion is in favor of a faulty dietary as the etiologic factor. 
Forms of the Dieease.—The forms accepted as representing the dis- 
ease are conceded by clinicians to he the following. 
(a) Incomplete or rudimentary form 
(b) The atrophic form 
(c) The wet form 
(d) The cardiac or pernicious form. 
(a) Incomplete on Rudimentary Form.—Relapses are frequent in 
the incomplete or rudimentary form. The patient usually recovers after 
a catarrhal period which is associated with and followed by pains and 
marked myasthenia with some paresthesia in the legs and edema—not 
great, as a rule. Respiratory embarrassment, rapid heart and extreme 
mental and physical exhaustion gradually improve in from a few days 
to as many months. With the return of warm weather the exacerbations 
renew the original symptoms in many cases. 
(b) Atrophic Form.—With the atrophic form there are marked and 
persisting symptoms of polyneuritis. The loss of motor power of the 
legs is prompt and the‘arms are usually involved—true quadriplegic 
paralysis (multiple neuritis). The atrophy of the muscles is marked. 
The face is also involved. 
(c) Wet Form.—The wet form—dropsical form—is associated with 
general edema, including dropsies of the serous cavities. The cardio- 
respiratory symptoms are more prominent than is the atrophy. With 
the disappearance of the dropsy the extent of atrophy is apparent. 
(d) Cardiac or Pernicious Form.—The cardiac or pernicious form 
represents the most serious type of the disease. In these cases there is 
often acute cardiac dilatation, myocardial degeneration or weakness. Tt 
may complicate the other forms, and either independent or in combina- 
tion with the rudimentary or wet form, it may lead to death within a 
day or two. 
The mortality varies from a comparatively insignificant percentage 
to a high figure. Thus Osier places the mortality “from 2 or 3 per cent 
to 40 or 50 per cent among the coolies in certain of the settlements of the 
Malay Archipelago.” The average mortality of cases which go beyond 
the acute stage is 20 per cent. 
In some the course is acute, the onset sudden with gastro-intestinal 
symptoms, prompt heart weakness, sensory and motor paralysis, pulmonary 
edema and death. These are the acute pernicious cases of Wright. They 
all die within a few days. 
Our experience with beriberi is so limited in the inland cities of the INTOXICATIONS 
1203 
United States that we are dependent entirely for our data upon the study 
of its literature. The severe polyneuritides which live often leave rem- 
nants which never entirely disappear in individual cases. 
Church & Peterson. Nervous and mental diseases. Philadelphia, 1914. 
Oppenheim. Lehrh. der Nervenk. Berlin, 1913, i. 
Osier. Practice of medicine. 8th ed. New York, 1914. 
Schaumann & Moszkowski. Berl. klin. Wchnschr., 1911. 
Tsuzuki. Arch. f. Schiffs- u. Tropen-Hygiene. July, 1906. 
Wright (H.). Brain, 1903. 
Brit. Med. J., June 29, 1901; idem, Nov. 1], 1905. 
Studies from the Institute for Medical Research, Federal Malay States, 1902- 
1904. 
References 
10. Food Poisoning 
Ptomain and Leukomain Poisoning 
Ptomain ‘poisoning depends upon the putrefaction of food in which 
alkaloidal substances are formed. 
Leukomain poisoning depends upon the development of animal poisons 
in the body, during life. 
Food poisons may be either endogenous, when, without added con- 
tamination the poisonous element is always present, or exogenous when 
the poison is accidentally present or acquired. The majority of food 
poisons are exogenous. Epidemics of food poisoning from bacterial con- 
tamination are frequent, and usually offer a fair prognosis. Poisoning 
of severe types may follow the eating of tainted meats or meat products. 
Bacterial Invasion of Meats.—The bacterial invasion of meats 
(colon bacillus, paratyphoid or intermediate bacilli) may lead to grave 
symptoms within a limited time after eating the contaminated meat, and 
gastro-intestinal and cardiovascular symptoms with collapse may threaten 
life. Collapse with symptoms of cholera, muscular cramps, concentrated 
blood, cyanosis, may lead to death in two or more hours, or the patient 
may gradually rally to remain exhausted during a number of days or 
weeks. 
Contaminated sausage or pork, with the Bacillus enleritidis of Gaert- 
ner, may cause death in a few days after symptoms of gastro-enteritis, 
collapse with thin small pulse. Recovery from meat poisoning is the 
rule, but there are separate poisonings in which many victims are claimed. 
In America veal contamination is a frequent cause of gastro-intestinal 
symptoms; while the pains are often severe and collapse frequent, most 
patients recover. When the meat has undergone putrefaction the alka- 
loids (cadaverin, sepsin and putrescin) are present, and the poisoning 1204 
INTOXICATIONS 
may prove severe and threatening. The resistance of the patient is often 
taxed and proves a valuable guide in giving a forecast. Many of these 
patients may fall into extreme conditions of weakness from which recov- 
ery is finally slow, but full. 
The poisonings due to milk products, i.e., milk, cheese, custard and 
ice cream, are often grave but rarely lead to death. The colic, with 
gastro-intestinal symptoms, vomiting, diarrhea, exhaustion, rapid pulse, 
may continue during from one to four or five days. I have rarely lost 
a patient from this form of poisoning. Weak subjects, children, the sick 
who are poisoned while passing through acute or chronic illness are bad 
subjects and a few of these die as the direct result of the added insult. 
Many of these cases are examples of tyrotoxicon poisoning. 
Poisoning from fish, also shell fish including oysters, clams and mus- 
sel cause gastro-intestinal symptoms and extreme heart weakness in occa- 
sional cases—but recovery is the rule. 
Conclusions.—The contamination of all kinds of food by poisons or 
bacteria is possible; each case demands separate consideration; but few 
who are attended and receive rigorous treatment early will lose their lives, 
though many make very slow recoveries and the weak may continue 
below par. 
Whatever the source of infected food, it should be remembered that 
the effect is dependent upon the presence of a specific germ and its toxin, 
an organic chemical poison of basic nature. Different patients are dif- 
ferently affected during the same poisoning; much often depends upon 
the prompt emptying of the stomach and intestinal tract, much upon 
inherent strength and resistance and on the amount and nature of the 
ptomain taken. Free vomiting and diarrhea early without collapse are 
favorable. Grave poisoning often develops from twenty-four to forty 
hours after taking the food. Section XII 
Diseases Due to Physical Agents 
1. Sunstroke 
{Heatstroke, Insolation) 
With periods of long-continued and inordinate heat and exhausting 
humidity, sunstroke is relatively frequent in the Northern States, par- 
ticularly in large cities along or near the Atlantic Coast (New York, 
Philadelphia, etc.) in those who are exposed to the sun or who work in 
close quarters, in shops, under tin roofs, in engine rooms, among stokers 
on ocean steamers, also farm hands and diggers. 
Contributing Factors.—Plethora and alcoholism predispose to sun- 
stroke and thermic fever. 
Dangers.—The dangers from sunstroke are either (a) immediate or 
(b) remote. 
(a) Immediate Dangers.—Sudden vertigo before marked rise of 
temperature in workmen on roofs or elevations may lead to fatal accidents 
or injuries. 
IIyperpyrexia is at once the most dangerous and life-threatening 
symptom. The relief of hyperpyrexia depends largely upon early, prompt 
and radical treatment. Hyperpyrexia (106°-108° F.) while always seri- 
ous, is by no means fatal. I have in hospital practice repeatedly saved 
such cases by energetic and persistent hydrotherapy. 
Hyperpyrexia, which refuses to yield after a reasonable period of 
treatment with deep coma, at first full tense pulse, then small rapid pulse, 
is unfavorable. Hyperpyrexia with convulsions and persistent coma is 
also grave. Hyperpyrexia during a limited period with profuse perspi- 
ration and but little conjunctival engorgement, few cerebral symptoms 
after the first two hours is a favorable combination. 
Irregular respiration (Cheyne-Stolces), hurried respiration, halting or 
abnormally slow breathing, are all unfavorable—more serious when found 
in alcoholics and beer drinkers and with chronic nephritis or arterial 
change. 
1205 1206 
DISEASES DUE TO PHYSICAL AGENTS 
Deep coma persisting with or without hyperthermia during unreason- 
able periods often leads to meningitis and death. 
Paralyses, hemiplegia, focal symptoms early are unfavorable. Per- 
sistent delirium and psychopathic types of heat delirium among stokers 
may lead to suicide. Cases which begin with pronounced delirium are, 
as a rule, among the most serious. Symptoms of meningitis, encephalitis 
are always of grave moment. Evidences of invasion of the pons or medulla 
are also serious. Obese patients succumb more promptly and easily than 
do thin subjects. Once the sensorium begins to clear, the chances of 
recovery are enormously improved. Relapse into coma and the develop- 
ment of meningitis and encephalitis are possible—not always fatal. 
Atmospheric Influence.—Different seasons offer varying results. 
Some days of the same season, with equally high temperature, show higho 
mortality than do other days. 
Mortality.—The mortality of sunstroke varies between 5 and 25 per 
cent, the average in the Eastern States is not far from 12 per cent. 
(b) The Remote Dangers.—These include the tendency to recur- 
rence of hyperpyrexia on slight cause. These patients are often repeat- 
edly overcome by heat and may develop alarming symptoms, though they 
rarely die as the direct result of subsequent heatstroke. 
Epilepsy has been a remote complication in a small proportion of my 
cases. Psychoses have also followed sunstroke. Meningitis has been a 
late complication in cases after they have lifted themselves out of the 
primary coma. Mental lethargy, laziness, loss of memory and changed 
disposition occasionally persist and follow during long periods, sometimes 
indefinitely. 
Ocular disturbances and deafness, partial or complete, are sequelae 
which are rebellious to treatment. 
Asthenia and myasthenia during the summer months are not infre- 
quent sequelae. I have seen two hospital cases in which peripheral 
neuritis complicated convalescence during many months—full recovery 
never followed in either case. 
Thermic Fever 
Thermic fever offers a good prognosis in most cases. The symptoms 
are less deep than with sunstroke; the temperature is more easily con- 
trolled ; the cerebral manifestations also yield more promptly. Faulty 
clothing or dress, excessive indulgence in spirits and working during hot 
weather in unfavorable surroundings are inviting factors. In both sun- 
stroke and thermic fever, degenerative changes in the kidneys and liver 
as well as myocardial degeneration with meningeal or brain invasion are 
among the immediate dangers and add to the possibility of remote com- 
plications. DISEASES DUE TO PHYSICAL AGENTS 
1207 
2. Caisson Disease 
(Divers’ Paralysis) 
Caisson disease, or divers’ paralysis, includes the development of a 
train of nervous symptoms referable more particularly to the spinal cord 
—rarely to the brain at the same time—which develop after divers, bridge 
builders or other workers in caissons under high pressure return to the 
surface. Sudden decompression is the important factor in the production 
of the disease. The increased pressure leads to characteristic changes 
which are found in most cases in the brain and cord, at times in the 
internal organs. In the acute cases there is marked hyperemia; in chronic 
cases disorganization of nerve tissue, with consecutive softening is the 
rule. The latter lesions resemble those found in the advanced types of 
myelitis, and are incurable. 
Thompson says that those who die “comprise” two classes of cases—• 
practically these may be classified as acute and chronic. The acute cases 
are found “with blood and tissues saturated with gas; in these cases 
death occurs before organic changes have developed; in the second, or 
chronic cases, death results after a protracted course with spinal symp- 
toms; the lesions of disseminated and transverse myelitis with hemor- 
rhages are present.” 
Complications in Chronic Cases.—The complications of these chronic 
cases include pneumonia, bed sores, hemorrhagic conditions (purpura), 
bladder infection, ascending infection of the kidney (pyelitis and pyelo- 
nephritis), and at times embolic infarct of the brain and other vital organs. 
Influencing Factors.—Naturally the amount of pressure, length of 
exposure and suddenness of return to the surface, are important factors in 
producing lesions and influencing prognosis. Because of the increased 
atmospheric pressure, bubbles of air are forced into the blood, and on 
reaching the surface these are liberated suddenly. Paul Bert proved that 
increased atmospheric pressure up to eight atmospheres “is harmless to 
the circulation and other functions, after which the partial pressure of 
the oxygen of the absorbed air may exercise toxic effects upon the tissues.” 
Too rapid decompression is now generally recognized as the cause of the 
symptoms of divers’ paralysis. 
The symptoms develop after the patient leaves the caisson—as a rule, 
suddenly. The report of Keays which includes the study of 3,692 cases 
in 10,000 workers which he had the opportunity to study as physician to 
the Pennsylvania Bailroad Tubes, shows but 20 deaths—.54 + per cent. 
Cases in which the paralysis—usually referable to the dorsal cord— 
is of moderate severity, may recover fully after several weeks or a few 
months. Recovery often follows paralysis which may continue a few 
days. Hemiplegia often yields but is not as a rule permanent. 1208 
DISEASES DUE TO PHYSICAL AGENTS 
In occasional cases death may promptly follow the initial symptoms. 
Deep involvement of the sensorium, including coma, delirium and respira- 
tory invasion, is unfavorable. 
Allen Starr reports a large experience with caisson disease without a 
single death. Some patients drag out a wretched existence of chronic 
invalidism with the unrelieved symptoms of myelitis, arthritis deformans 
or aural complications. 
The 20 fatal cases reported by Keays included 6 cases “with pain 
and prostration,” 5 cases showing “symptoms referable to the central 
nervous system” and 9 cases “showing partial or complete unconscious- 
ness with collapse.” 
Recovery is often prompt and complete. 
Paraplegia may be followed by full or only partial recovery; some 
of these cases are associated with paralysis of the bladder. Those cases 
in which symptoms of myelitis persist, develop the same complications as 
are found with the ordinary types of transverse and disseminated myelitis 
(spastic paraplegia, cystitis, bed sores, pneumonia, and sepsis). 
The collective investigation of von Schroetter shows 137 fatal cases 
of the disease between 1854 and 1897. 
Prophylactic measures exert an enormous influence on prognosis. 
Keays in his service during the construction of the Pennsylvania tun- 
nels subjected all new caisson workers to a preliminary test. He exposed 
the workman to thirty pounds of pressure for ninety minutes without 
exertion of any kind, followed by decompressing the men at the rate of 
two pounds per minute, i. e., fifteen minutes for the entire time of decom- 
pression. If after this test the applicant develops even mild symptoms, 
insignificant pains, fatigue or weakness in the legs, it may safely be 
concluded that the workman is below the standard and therefore unfit. 
The prognosis is also influenced by the habits of the workman. 
Those who are below par, muscularly enfeebled, who have arterial, 
kidney or heart disease, or live in an unfavorable environment, are handi- 
capped and are more likely than those in better general condition to 
develop the disease. 
Frequent shifts and proper feeding after emerging from the caisson 
are also important in connection with gradual decompression in prevent- 
ing the development of the disease. Immediate recompression has in many 
cases proved a powerful factor in preventing the full development of the 
disease. 
References 
Bert (Paul). La pression borometrique. 1879. 
Keays. Report, Physician to Pennsylvania Railroad Tunnels. 
Van Rensellaer (H.). Med. Rec., New York, 1891, xl. 
von Scliroetter. Die Luftdruckerkrankung. Wien, 1900. 
Starr (Allen). New York Med. Rec., 1909. DISEASES DUE TO PHYSICAL AGENTS 
1209 
Thompson. Occupational diseases. New York, 1914. 
Med. Rec., New York, 1894, xiv. 
Additional References 
For the fuller clinical study of Caisson Disease the reader is referred to: 
Smith, Andrew H. Prize Essay for the Alumni Association of the College of Physicians & 
Surgeons, New York, 1873. 
Hill {Leonard). Caisson disease. 1895. 
Leyden. Arch. f. Psychol., ix, 316. 
For fuller bibliography see also: 
Index Catalogue, Library of the Surgeon-General’s Office, U. S. Army, 2d ser. ,i, 
180-181. 
3. Mountain Sickness 
(Bergkrankheit, Mai des montagnes) 
Causes and Dangers.—True mountain sickness, from which we now 
exclude “mountain fever” (which is usually typhoid or paratyphoid), and 
secondary anemia (due to ankylostoma duodenale), is due to diminished 
atmospheric pressure, insufficient oxygen, to which “all men are subject 
in an altitude of 16,500 feet and upwards” (Allbutt). 
The great danger is due to cardiac insufficiency in those who have 
myocardial weakness or degeneration with either hypo- or hypertension, 
advanced arteriosclerosis with or without coronary narrovoing. In those 
suffering from cardiovascular disease, added fatigue and overeating, before 
entering a high altitude, add to the danger of sudden death. 
Sudden entrance into high altitudes adds materially to the risk of 
heart weakness and syncope. 
“Toleration in the healthy can be easily established when there are 
compensatory changes in the blood and the readaptation of the respira- 
tory neuromuscidar apparatus” (Allbutt). As the process of acclimatiza- 
tion is established there are likely to be high hemoglobin readings and 
polycythemia. 
The prognosis of mountain sickness in those persons who were 
perfectly healthy before its development is good; the period of acclima- 
tization varies, but is followed by normal function, comfortable breathing, 
and as above mentioned, blood changes, including increase in the number 
of erythrocytes and blood coloring matter. 
Allbutt. System of medicine. 2d ed., iii, 243. 
References INDEX 
Abscess, perisplenic, 1170. 
retropharyngeal, 560. 
subphrenic, in cholelithiasis, 730. 
of brain. See Brain Abscess, 
of kidney, 833. 
of liver, in amebic dysentery, 79. 
of lung, 386. 
in influenza, 127. 
in pneumonia, 165. 
of spinal cord, associated symptoms of, 
914. 
course of, 914. 
in typhoid fever. 106. 
Acetone, test for, Garrod’s modification of 
Rothera’s, 1115. 
Achondroplasia, 1131. 
Achylia gastrica, with pernicious anemia, 
522. 
stomach contents in. 574-575. 
Achylia gastrica nervosa, 618. 
Acidosis, in diabetes mellitus, 1115. 
chronic, 1116. 
in young subjects, 1115. 
profound, 1116. 
in gastric ulcer, 596. 
Acromegaly, and goiter, 1161. 
association of, 1161. 
characteristic features of, 1161. 
course of, 1162. 
diagnostic factors of, 1160. 
in exophthalmic goiter, 1148. 
operative treatment of, 1161. 
prognosis of, 1162. 
syringomyelia with, 918. 
Acroparesthesia, 415. 
associated conditions in, 1075. 
causative factors in, 1075. 
nature and symptoms of, 1074-1075. 
Actinomycosis, 301. 
alimentary, 302. 
cerebral, 302. 
character of, 301. 
of liver, 302. 
of respiratory tract, 302. 
of skin, 302. 
prognosis of, 303. 
with brain tumor, 988. 
Acute abdomen, 591-592. 
in intestinal obstruction, 635. 
Acute indigestion, angina pectoris mis- 
taken for, 458. 
arteriosclerosis mistaken for, 409. 
Adams-Stokes phenomenon, 29. 
Addison’s disease, causes of, 263. 
duration of, 264. 
symptoms of, 263. 
Adenia. See Hodgkin’s Disease. 
Adenitis, in measles, 345. 
in scarlet fever, 332. 
Adenoids, influence of, on growing child, 
299. 
pharvngeal, catarrhal condition due to, 
358. 
Adherent pericardium, associated condi- 
tions of, 431-432. 
cause of, 430. 
prognosis of, 431. 
results of, 430-431. 
X-ray for, 431. 
Adhesions, perigastric, in gastric ulcer, 
595. 
Adiposis dolorosa, 1078. 
Adiposity, in infantilism, simple, 1159. 
with genital atrophy, 1159. 
Adrenalin, glucosuria produced by, 1107. 
in sympathicotonia, 1083. 
Adynamia, 634. 
Aerophagia, 617. 
Ageusia, 870. 
Akinesia algera, extreme pain of, 1086- 
1087. 
hysterical, 1017. 
mental condition in, 1087. 
prognosis of, 1087. 
Albuminuria, casts in, 744. 
cyclic, 744. 
definition of, 741. 
false, 742. 
febrile, 746. 
in typhoid fever, 108. 
with non-malignant infections, 746. 
following surgical operations, 748. 
hematogenous, 742. 
in aged and young, 746. 
in appendicitis, 654. 
in cerebral hemorrhage, 970. 
in cholera, 746. 
in diphtheria, 139. 
in erysipelas, 176. 
in influenza, 747. 
in nephritis, 741, 743, 793. 
in new born infants, 743. 
in pneumonia, 160. 
1211 INDEX 
1212 
Albuminuria, Leube’s rule in, 742. 
of nephritis, in typhoid, 108. 
of pregnancy, 747, 794. 
orthostatic, as suggesting tuberculosis, 
745. 
continued beyond puberty, 745. 
persistent, 745-746. 
postural, 744. 
provoked by spinal curvature, 745. 
parenchymatous, 742. 
physiological, 742. 
and nephritis, 743. 
as misnomer, 743. 
prognostic importance of, 741, 748. 
recurring, 744. 
renal, with casts, 744. 
without casts, 744. 
toxic, 747. 
transitory, 743. 
true, 742. 
vascular, 742. 
with catarrhal influenza, 125-126. 
with constitutional diseases, 747. 
with glycosuria. See Diabetes mellitus. 
with nervous diseases, 747. 
Avith scarlet fever, 746. 
with tonsillitis, 747. 
Albuminuric retinitis, in chronic intersti- 
tial nephritis, 809. 
Albumosuria, Bence-Jones, 1134. 
detection of, 1134. 
myelopathic, 1134. 
Alcoholic enteritis, 1181. 
Alcoholic gastritis, 571. 
Alcoholic meningitis, with alcoholic mul- 
tiple neuritis, 849. 
Alcoholic multiple neuritis, 849. 
Alcoholic poisoning, acute, 1179. 
in cirrhosis, 694. 
Alcoholics, poor surgical subjects, 1181. 
Alcoholism, acute poisoning of, associated 
conditions with, 1179. 
causes of death in, 1179-1180. 
changes due to, 1180. 
symptoms of, 1179. 
arteriosclerosis due to, 405-406. 
associated Avith cardiovascular disease, 
1179. 
associated Avith chronic laryngitis, 361. 
associated with drug habit, 1176. 
chronic, associated Avith chronic laryn- 
gitis, 361. 
degenerative heart changes in, 1182. 
effect of, on circulatory system, 1182. 
on gastro-intestinal tract, 1181. 
on genito-urinary system, 1182. 
on liver, 1182. 
on nervous system, 1181. 
on respiratory system, 1183. 
Korsakoff’s psychosis complicating, 
1182. 
ocular disturbances due to, 1183. 
productive and degenerative changes 
in, 1180. 
psychic disturbances due to, 1181. 
psychic element as leading factor in, 
1180. 
Alcoholism, delirium tremens, collapse in, 
1184. 
duration of, 1184. 
infections with, 1184. 
prognosis of, 1183. 
pulse and temperature in, 1184. 
recurrence of, 1183. 
symptoms of, 1183. 
“wet brain” in, 1184. 
epilepsy due to, 1050. 
erysipelas in, 174. 
exciting factor of disease in, 1178. 
formation of habit of, 1176. 
general considerations of, 1175. 
glucosuria with, 1118. 
habit of, 1175. 
in syphilis, 41. 
in tabes dorsalis, 58. 
in tuberculosis, 242. 
influencing factors in, early training and 
discipline, 1177. 
heredity, 1177. 
intoxication impulse, 1177. 
narcotic poisoning, 1178. 
periodic drinking, 1177. 
personality, 1177. 
psychosis, 1178. 
time, 1178. 
tolerance, 1178. 
intestinal changes in, 1181. 
loss of will power in, 1175. 
pachymeningitis due to, 935. 
perverted mind in, 1176. 
relapses of, 1178. 
supervision of life of patient in, 1178. 
with nephritis, 1180. 
Aleukemic lymphadenomata, 538. 
Algid pernicious malaria, 75. 
Alimentary actinomycosis, 302. 
Alimentary canal, disturbances of, in ty- 
phoid, 101. 
Alkaptonuria, 786. 
Alopecia, in syphilis, 19. 
and atrophic changes, in typhoid fever, 
106. 
Amaurosis, 857. 
Amblyopia, 857. 
crossed, 859. 
functional, of one eye, 857. 
hysterical, 1012. 
in epilepsy, 1051. 
Amebic dysentery, acute, gangrenous type 
of, 79. 
manifestations of, 78-79. 
causes of death in, 80. 
chronic, 79. 
complications in, 79-80. 
manifestations of, 78-79. 
mortality from, 80. 
myocardial degeneration in, 80. 
specific origin of, 78. 
symptomatic, 80. 
Amenorrhea, in obesity, 1128. 
American disease. See Neurasthenia. 
Amnesia, in epilepsy, 1053. 
in hysteria, 1009. INDEX 
1213 
Anemia, pernicious, tongue in, 527. 
urine in, 527. 
with fatty liver, 712. 
primary or essential, chlorosis, 517. 
pernicious, 519. 
primary hemolytic, 523. 
saturnine, 1190. 
secondary, to cirrhosis, 693. 
splenic, 1172. 
symptomatic secondary, 514. 
syphilitic, 524. 
with chronic nephritis, 799. 
Anesthesia, glucosuria due to, 1110.. 
hysterical, 1009-1010. 
Aneurism, age and sex considered in, 421. 
death due to, 426. 
definition of, 420. 
dissecting, 421. 
due to infectious processes, 422. 
embolic detachments from walls of, 422. 
greater frequency of, in England and 
United States than in Europe, 421. 
mycotic-embolic, 422. 
of aorta, descending thoracic and ab- 
dominal, 424. 
of ascending portion of arch, 423. 
of descending portion of arch, 424. 
of transverse portion of arch, 423. 
of brain. See Cerebral Aneurism, 997. 
of celiac axis, 425. 
of coronary artery, 425. 
of heart, 467. 
of hepatic artery, 680. 
of pulmonary artery, 425. 
of subclavian artery, 425. 
pathogenic factors of, 421. 
prognosis for life of, 421. 
rupture of wall of, 422. 
stationary, 422. 
syphilitic, 421. 
tendency of, toward progression, 422. 
thrombosis with, 422. 
X-ray examination of, 422. 
Angina, Ludwig’s, 560. 
pectoris, among professional men, 456. 
and nephritis, 807. 
associated conditions of, 455, 458, 459. 
causes of, 455. 
causes of death from, 458. 
exhausted left ventricle of, 455. 
family tendency to, 456. 
increase of, 456. 
large attack of, 457. 
latent, 455. 
nature of, 454. 
of syphilitic origin, 456. 
prognosis of, 458-459. 
self-cure of, 460. 
small attack of, 457. 
symptoms without actual lesion of, 
456. 
uncertainty of, 457. 
pseudo-angina, 456. 
Vincent’s, 298. 
Angioneural arthroses, 1079. 
Amorphous urates, precipitation of, 785. 
Amygdalitis, 293. 
Amyloid degeneration of other organs 
than liver, 713. 
Amyloid kidney, albuminuria of, 741. 
associated diseases of, 814. 
characteristic symptoms of, 814. 
course of, 814. 
origin of, 814. 
urine of, 815. 
vomiting in, 815. 
with operable diseases, 815. 
Amyloid liver, primary diseases of, 713. 
Amyloid spleen, 1170. 
Amyotrophic lateral sclerosis, 890. 
Anacidity, 618. 
Anadenia gastrica, stomach contents in, 
574-575. 
Anemia, achylia gastrica with, 522. 
acute (hemorrhagic), 514. 
blood regeneration in, 515-516. 
danger point in, 515. 
due to malignant growths, 515. 
during menstruation, 515. 
Biermer’s progressive, 520. 
bothriocephalus, 521. 
chronic (hemorrhagic), blood changes 
of, 516. 
causes of, 516. 
operable cases of, 517. 
definition of, 514. 
due to malignant growths, 515. 
during menstruation, 515. 
general, 514. 
idiopathic, 520. 
in chronic interstitial nephritis, 809. 
in congenital syphilis, 66. 
in exophthalmic goiter, 1148. 
in malarial cachexia, 76. 
in nephritis, 799-809. 
in trypanosomiasis, 81. 
local, 514. 
neuralgia due to, 838. 
of brain. See Cerebral Anemia, 
of spinal cord. See Spinal Anemia, 
pernicious, acute, 524. 
blood picture of, 519-521. 
blood vessels in, 526. 
causation of, 522. 
cerebral toxemia in, 526. 
complications with, 528. 
diarrhea with, 523. 
glossitis with, 528. 
heart condition in, 526. 
heredity in, 520. 
history of, 520. 
influence on, of splenectomy, 523. 
manner of death from, 528. 
oral sepsis provocative of, 527. 
remissions and periods of latency in, 
525. 
retinal hemorrhages with, 527. 
salvarsan for, 528. 
symptoms of, 519. 
Lichtheim, 520, 526. 
nervous, 520, 526. 
temperature in, 527. 1214 
INDEX 
Angioneurotic edema, intermittent dropsy 
of joints, as atypical types of, 
1079. 
life-threatening features of, 1076. 
Meni&re complex due to, 869. 
prognosis of, 1076. 
symptoms of, 1075-1076. 
Ankylostomiasis, 310. 
Anorexia, hysterical, 1017. 
Anosmia, causes of, 856. 
Anterior crural paralysis, 880. 
Anthracosis, 380. 
Anthrax, character of, 209. 
external, malignant anthrax edema, 210. 
malignant pustule, 210. 
infection of, 209. 
internal, gastro-intestinal, 210. 
respiratory, 211. 
serum for, 211-212. 
splenic, 211. 
Antitoxin for diphtheria, 142-143-144. 
Anuria, 765-766. 
calculous, surgical treatment of, 824. 
complete, in hydronephrosis, 817. 
obstructive, 766. 
scarlatinal, 766. 
“Anxiety neurosis” of Freud, 1029. 
Aortic aneurism, hemoptysis of, 377. 
of ascending portion of arch, 423. 
of descending portion of arch, 424. 
of descending thoracic and abdominal 
aorta, 424. 
of transverse portion of arch, 423. 
Aortic insufficiency, associated conditions 
of, 502.' 
blood pressure in, 501. 
endocarditic form of, 501. 
functional form of, 500. 
of syphilitic origin, 500. 
organic form of, 500. 
prognosis of, 501. 
pulse in, 502. 
Aortic stenosis, 438, 499. 
unfavorable cases of, 499. 
Aortic tuberculosis, 274. 
Aortitis, syphilitic, 27, 423. 
in tabes dorsalis, 58. 
Aphasia, in cerebral hemorrhage, 969-970. 
in cerebral hyperemia, 951. 
in encephalitis of children, 979. 
optic, 859. 
with facial paralysis and hemiplegia, 
866. 
Apoplectic attack, in cerebral hemor- 
rhage, 963. 
Apoplectic habit, 962. 
Apoplectiform seizures, in multiple sclero- 
sis of brain and cord, 910. 
Apoplexy, and paralysis, table of deaths 
from, 959. 
cerebral, 957. 
meningeal, 930. 
pulmonary, 378. 
Appendicitis, 644. 
abnormal position of appendix in, 646. 
and typhoid fever, 657. 
Appendicitis, catarrhal, apparent im- 
provement of subjective symp- 
toms in, 648-649. 
effects of, 649. 
fulminating, 649. 
nature and symptoms of, 648. 
perforation of, 649. 
spreading symptoms of, 648, 
surgical treatment of, 648. 
ulcerative and gangrenous, 649. 
chronic, conditions caused by, 656. 
danger of intestinal obstruction from, 
656. 
symptoms of, 656. 
Complications in, cardiac, 658. 
nephritis, 657. 
pulmonary, 658. 
septic phlebitis, 658. 
factors in prognosis of, age, 647. 
albuminuria, 654. 
effacement of liver dullness, 655. 
facies and general appearance, 654. 
heart condition, 651. 
hiccough, 653. 
indicanuria, 654. 
leukocytosis, 651. 
obstipation, 653. 
pain, 653. 
physical signs, 654. 
pulse, 652. 
size and physical signs of tumor, 655. 
temperature, 652. 
vomiting, 653. 
fatty degeneration of liver with, 712. 
favorable forecast of surgical treatment 
for, 644. 
fecal concretions in, 646. 
fibrinoplastic, 649. 
history of, 644. 
infectious nature of, 645. 
irregular and anomalous course of. 646. 
metastatic, 651. 
perforative, 650. 
fate of pus accumulation in. 651. 
general diffuse peritonitis due to, 
650. 
general septic peritonitis due to. 650. 
presence of previous disease in. 651. 
retroperitoneal abscesses in, 651. 
perforative peritonitis in, prognostic 
factors of, 652. 
peritonitis, acute diffuse, with, 661. 
purpuric, 649. 
recurring, 655. 
reflex symptoms in, 647. 
special considerations of, 645. 
with rheumatic fever, 289. 
Appendix, abnormal position of, 646. 
cancer of, 656. 
diseases of, 644. 
hemorrhage into, in purpura hemor- 
rhagica, 545. 
tuberculosis of, 656. 
ulcers, typhoid, 650. 
Appetite, in diabetes mellitus, 1113. 
perverted, of hysteria, 1017. INDEX 
1215 
Aprosexia, 299. 
Arhytlimias, auricular fibrillation, 450. 
due to depressed conductivity, 447. 
due to extrasystoles, 448. 
pulsus alternans, 449. 
sinus, 447. 
Windle’s table of, 450. 
Arsenical multiple neuritis, 852. 
Arsenical poisoning, accompanying condi- 
tions of, 1194. 
acute, prognosis of, 1193. 
symptoms of, 1193. 
tabes due to, 1193. 
chronic, causes of. 1193. 
prognosis of, 1194. 
skin changes in, 1194. 
encephalitis following, 976. 
Arsenical tabes, 1193. 
Arterial degeneration, 402. 
Arteries, aortic and pulmonary, transposi- 
tion of, 439. 
diseases of, aneurism, 420. 
arteriosclerosis, 402. 
effect on, of typhoid fever, 95-96. 
of spinal cord, changes in, 928. 
physiological hyperplasia of intima of, 
403. 
Arteriocapillary fibrosis, 402. 
Arteriorenal disease, 411. 
Arteriosclerosis, advanced, 402. 
causative factors of, 403. 
character of, 402-403. 
dictum of Bruce on, 402. 
factors in prognosis of, age, 404. 
alcohol, 405. 
aneurismal dilatation, 413. 
blood pressure study, 416. 
cardiac asthenia and pulmonary 
edema, 413. 
chemical and toxic, 409. 
condition of peripheral arteries, 413. 
coronary lesions, 411. 
endocardial changes, 413. 
gangrene, 414. 
heredity, 405. 
hypertension, 410. 
hypertrophy of left ventricle, 412. 
increase of physical signs, 414. 
infection, 407. 
intermittent claudication, 414. 
kidney invasion, 411. 
lead poisoning, 406. 
mechanical, 409. 
myocardial degeneration, 412. 
occupation, 407-408. 
ocular changes, 415, 418. 
overeating, 409. 
pulse, 413. 
pulse pressure, 417. 
thrombosis, 418. 
tobacco, 407. 
vascular crises, 414. 
effects of, 415. 
worry and stress, 405. 
X-ray, 419. 
hemoptysis of, 377. 
in aged, 403. 
Arteriosclerosis, in chronic nephritis, 
802. 
in tabes dorsalis, 58. 
mortality from, 402. 
of hepatic artery, 680. 
of syphilitic origin, 67, 404, 405. 
period of hypertension in, 403, 410. 
appropriate treatment during, 408. 
saturnine, 1192, 
spinal, 929. 
with cholelithiasis, 730. 
with cirrhosis, 086. 
with paralysis agitans, 1033, 
Arteriosclerotic endocarditis, 504. 
Arteritis, due to congenital syphilis, 67. 
due to syphilis, 26. 
blood pressure in, 27. 
in tabes dorsalis, 58. 
with cerebral syphilis, 40, 43. 
Artery, coronary, aneurism of, 425. 
pulmonary, aneurism of, 425. 
subclavian, aneurism of, 425. 
Arthritis, acute, bacteriology of, 279. 
and chorea, 1039. 
and meningitis, 287. 
endocarditis due to, 283. 
gonococcus, 192. 
in cerebral hemorrhage, 970. 
in pneumonia, 167. 
in scarlet fever, 332. 
myocarditis due to, 285. 
with varicella, 342. 
Arthritis deformans, absence of symptoms 
with streptococcus in focus. 
1089. 
age in, 1090. 
atrophic type of, 1091. 
beginning at menopause, 1091. 
blood and urine in, 1092. 
causes of, 1089. 
causes of death from, 1092. 
climatic conditions in, 1092. 
definition and process of, 1088. 
etiology and pathology of, 1088. 
general condition of patient in, 1091. 
Heberden’s nodes in, 1091. 
hypertrophic, 1091. 
hypertrophic hip changes in, 1092. 
in hysterical and neurasthenic patients, 
1091. 
in non-resistant, 1091. 
infectious nature of, 1089. 
occupation in, 1090. 
pathological similarity of, to chronic 
articular rheumatism, 1088. 
prognosis of, 1091-1092. 
race in, 1090. 
sex in, 1089. 
source of infection causing, 1089. 
traceable to dental alveoli, 1089. 
Arthropathies, in tabes dorsalis, 57. 
Arthropathy, hypertrophic pulmonary, 
1096. 
Ascaris lumbricoides, 309-310. 
Aschoff’s hemorrhagic erosions in gastric 
ulcer, 586. 1216 
INDEX 
Ascites, in cancer of liver, 710. 
in cirrhosis, 691. 
in perihepatitis, 702. 
Asiatic cholera, blood picture in, 200. 
complications in, 201. 
conclusions on, 201. 
diarrhea of, 199. 
history of, 197-198. 
prognosis by stages of, 199. 
stages of, cold or algid, 199. 
reaction, 200. 
symptoms of, 198. 
in pernicious malaria, 75. 
Astasia-abasia, hysterical, 1016. 
Asthenia, due to sunstroke, 1206. 
Asthenopia, hysterical, 1012. 
Asthma, bronchial. See Bronchial Asthma, 
cardiac, 370. 
reflex from genito-urinary disturbance, 
371. 
renal, 370. 
thymic, 1164. 
vagotonic, 371. 
Ataxia, Friedreich’s hereditary, symptoms 
of, in poliomyelitis, 323. 
hereditary. See Hereditary Ataxia. 
Marie’s hereditary, 888. 
vasomotor, 1079. 
Ataxic paraplegia, associated diseases of, 
901. 
character of, 901. 
course of, 902. 
duration of, 902. 
forecast of, 902. 
Atelectasis, in bronchiectasis, 367. 
in bronchitis, 364. 
in pleurisy, 391. 
Ateliosis, in infantilism, 1159. 
Atheromatous degeneration, 402. 
Atrophic muscular dystrophy, 897. 
Atrophy, genital, in infantilism, 1159. 
muscular, in cerebral hemorrhage, 968. 
in syringomyelia, 915. 
of gall-bladder, due to cholelithisis, 
726. 
of heart, brown, 454. 
starvation, 454. 
of liver, acute yellow, differentiated 
from phosphorus poisoning, 
674. 
duration of, 675. 
nature of, 673. 
origin of, 674. 
prognosis of, 675. 
symptoms of, 673. 
optic, 858. 
progressive central muscular, 888. 
amyotrophic lateral sclerosis, 890. 
bulbar paralysis, 891. 
duration of, 890. 
juvenile or family type of, 890. 
spinal, adult type of, 889. 
progression of, 889. 
remissions of, 890. 
reverse in, 889. 
symptoms of, 889-890. 
unfavorable cases of, 889. 
Atrophy, progressive neural muscular, 
character of, 894. 
course of, 894. 
senile cerebellar, 1003. 
Atropin, vagotonia due to, 1082. 
Auditory nerve, paralysis of, 868. 
associated symptoms of, 868. 
aural vertigo with, 869. 
causes of, 868. 
degree of deafness in, 868. 
invasion of cochlear and facial nerves 
by, 868. 
involvement of vestibular nerve in, 869. 
labyrinthine invasion by, 868. 
tinnitus aurium with, 868. 
Aural disturbances, in diabetes mellitus, 
1119. 
in neurasthenia, 1030. 
Aural vertigo, 869. 
apoplectiform type of, 869. 
chronic course of, 869. 
definition of, 869. 
due to angioneurotic edema, 869. 
epileptiform seizures in, 869-870. 
hemorrhagic cases of, 870. 
in neurasthenia and hysteria, 869. 
lesions and symptoms of, 869. 
prognosis of, 869. 
Auricular fibrillation, conclusions of Goa- 
sage and Hicks in, 451. 
fatal, 450. 
favorable cases of, 451. 
nature of, 450. 
prognostic significance of atropin reac- 
tion in, 451. 
of digitalis treatment for, 451. 
B 
Babinski phenomenon, in epilepsy, 1052. 
Bacillary dysentery, bacillus of, 193. 
character of, 193. 
complications in, 195-196. 
general considerations of, 193. 
incubation period of, 194. 
mortality from, 193. 
occurrence of, 193. 
symptoms of, 194. 
Bacilluria, pathogenic bacteria causing, 
775. 
symptomatic, 774. 
Bacterial diseases, anthrax, 209. 
Asiatic cholera, 197. 
bacillary dysentery, 193. 
diphtheria, 134. 
epidemic cerebrospinal meningitis, 177. 
erysipelas, 173. 
glanders, 212. 
gonococcus infections, 189. 
influenza, 124. 
leprosy, 214. 
Malta fever, 196. 
metastatic parotitis, 30ft, 
paratyphoid, 121. 
plague, 201. INDEX 
1217 
Bacterial diseases, pneumococcus infec- 
tion, 145. 
pyogenic infections, 130. 
rheumatic fever, 278. 
tetanus, 206. 
tonsillitis, 292. 
tuberculosis, 216. 
typhoid fever, 84, 117. 
Bacteriuria. See Bacilluria. 
Banti’s disease, 1172. 
Barlow’s disease. See Scorbutus, infantile. 
Basedowoid disease, 1149. 
Basedow’s disease, 1142. 
in tabes dorsalis, 58. 
Beard’s disease. See Neurasthenia. 
Bedsores, acute, in cerebral hemorrhage, 
966. 
in typhoid fever, 106. 
Bell’s palsy, causes of, 864. 
symptoms of, 864. 
Beriberi, course of, 1202. 
etiology of, 1201. 
forms of, atrophic, 1202. 
cardiac or pernicious, 1202. 
incomplete or rudimentary, 1202. 
wet, 1202. 
intestinal parasites in, 1201. 
mortality from, 1202. 
pernicious cases of Wright, 1202. 
symptoms of, 1201. 
Bile, secretion of, at low pressure, 665. 
Bile passages, acute catarrh of (cholan- 
gitis, 714. 
and gall bladder, diseases of, 718. 
Bilharzia hematobia, 316. 
Biliary calculus. See Cholelithiasis. 
Biliary colic, acute, adhesions due to lo- 
cal inflammation in, 721. 
blood picture in, 723. 
fever with, 721. 
gall-bladder enlargement in, 722. 
hyperpyrexia in, 721. 
initial attack of, 721. 
jaundice with, 721. 
liver enlargement in, 722. 
prognosis of, 723. 
severity of, 722. 
splenic enlargement in, 722. 
vomiting in, 722. 
with relative mitral insufficiency, 720. 
with weak myocardium, 720. 
x-ray in, 723. 
Biliary fistulae, with gall-stones, 730. 
Biliary system, 734-735. 
Birth palsies, 978. 
“Black death,” 202. 
Black vomit, 347. 
Black water disease, 76. 
“Bleeders.” See Hemophilia. 
Bleeding, extragastric, 613. 
intragastric, 614. 
Blepharospasm, with tic convulsive, 867. 
Blindness, bilateral, 857. 
due to hemianopia, 859. 
complete, 857. 
hemianopia, 858. 
hysterical, 857, 1012. 
Blindness, partial, 857. 
unilateral, 857. 
Blood and hemapoietic organs, diseases of, 
anemia, primary or essential, 
517. 
symptomatic or secondary, 514. 
erythremia, 549. 
leukemia, 530. 
lymphoblastoma, 536. 
purpura, 542. 
Blood casts, 750. 
Blood condition, in Asiatic cholera, 200. 
in bronchial asthma, 370. 
in cirrhosis, 693. 
in diabetes mellitus, 1117. 
in epidemic cerebrospinal meningitis, 
182. 
in epilepsy, 1056. 
in erysipelas, 176. 
in exophthalmic goiter, 1148. 
in genital tuberculosis, 271. 
in gonococcus endocarditis, 191. 
in hay fever, 358. 
in lead poisoning, 1190. 
in malaria, 73-74. 
in measles, 343. 
in paratyphoid, 123. 
in pernicious anemia, 519, 521. 
in purpura hemorrhagica, 545. 
in scarlet fever, 330. 
in splenic anemia, 1172. 
in trichinosis, 314. 
in tuberculosis, 235. 
in whooping-cough, 189. 
Blood flukes, 316. 
Blood poisoning, 130. 
Blood pressure, in arteriosclerosis, 416. 
in chronic interstitial nephritis, 806 
in chronic nephritis, 801. 
in myocardial insufficiency, 445. 
Blood vessels, in pernicious anemia, 526. 
of spinal cord, affections of, 927. 
Bones, changes in, due to syphilis, 67. 
diseases of, fragilitas ossium, 1097. 
hypertrophic pulmonary arthropathy, 
1096. 
leontiasis ossea, 1095. 
osteitis deformans, 1093. 
Bothriocephalus latus, 305. 
Brachial neuralgia, 843. 
Brachial paralysis, anesthesia in, 877. 
of circumflex nerve, 878. 
Duchenne, 877. 
infraclavicular, 877. 
motor point in, 877. 
musculospiral, 878. 
of median nerve, 878. 
of posterior thoracic nerve, 877. 
prognosis of, 877. 
subscapular, 877. 
supraclavicular, 876. 
ulnar, 879. 
Brachial plexus, paralysis of, 875. 
due to cervical rib, 876. 
involving all nerves, 876. 
involving two or more nerves, 876 1218 
INDEX 
Bradycardia, causes of, 511. 
false, 511. 
hysterical, 1019. 
in typhoid fever, 95. 
prognosis of, 512. 
true, 511. 
Brain, actinomycosis of, 302. 
anemia of. See Cerebral Anemia, 
circulatory disturbances of, abscess of 
brain (suppurative encephalitis), 
980. 
anemia, 947. 
aneurism. See Cerebral Aneurism, 
cerebral hemorrhage, 957. 
cerebral paralysis of childhood, 977. 
encephalitis, 973. 
hyperemia, 949. 
occlusion of cerebral vessels, 953. 
congestion of. See Cerebral Hyperemia, 
cysticercus in, 304. 
hydatid disease of, 308. 
hyperemia of. See Cerebral Hyperemia, 
in measles, 345. 
parasites of, 1002. 
tumors of, 988. 
Brain abscess, bacterial infections causing, 
981. 
cases of self cure in, 987. 
chronic, 987. 
conclusions on, 986. 
duration of. 986. 
extradural pus in, 986. 
in amebic dysentery, 80. 
infectious origin of, 980. 
influenzal, 129. 
Jacobson’s classification of, metastatic, 
984. 
otitic, 982. 
rliinologic, 985. 
traumatic, 981. 
location and primary cause of, 981. 
lumbar puncture in, 986. 
metastatic, infections causing, 985. 
location of, 985. 
prognosis of, 894. 
multiple, 986. 
operation for, importance of, 986. 
statistics on, 986. 
otitic, complications in, 983, 984, 986. 
direction of infection in, 982. 
with double otitis media suppurativa, 
983. 
location of, 983. 
ophthalmoscopic examination in, 984. 
perforation of, 984. 
pyemia due to, 984. 
single, 983. 
symptoms of, focal, 984. 
pulse and heart, 984. 
various, 984. 
prognostic factors in, 986. 
rhinologic, development of, 985. 
primary causes of, 985. 
rupture into lateral ventricle in, 987. 
traumatic, causes of, 982. 
development of, 981. 
location of, 982. 
Brain abscess, traumatic, with purulent 
leptomeningitis, 982. 
tuberculous, 981. 
without known cause, 985. 
“Brain fag,” in neurasthenia, 1031. 
Brain membranes, diseases of, cerebro- 
spinal meningitis. See Cere- 
brospinal Meningitis, 
leptomeningitis, 937. 
pachymeningitis, 934. 
syphilitic cerebral meningitis. See 
Syphilitic Cerebral Meningitis, 
tuberculous meningitis. See Tuber- 
culous Meningitis. 
Brain parasites, cysticercus cellulosae, 
1002. 
echinococcus, 1002. 
involvement of cranial nerves by, 1002. 
lumbar puncture for, 1002. 
symptoms of, 1002. 
Brain tumor, 988. 
additional considerations of, 998. 
age in, 988. 
aneurismal dilatation in, 990. 
choked disk with, 994-995. 
decompression in, 999. 
degeneration of, 998. 
due to traumatism, 990. 
duration of, 999. 
heredity in, 990. 
hydrocephalus simulating, 943. 
localization of, 998. 
location of, 990. 
lumbar puncture in, 998, 1000. 
meningeal hemorrhage in, 1000. 
meningitis with, 994. 
metastases, 990. 
occurrence of, statistics of, 988. 
table on, 989. 
operation for, factors influencing result 
of, 1000. 
hyperpyrexia following, 1000. 
mortality following, 1000. 
palliative, 1000. 
percentage of recoveries from, 998. 
periods of latency in, 999. 
pituitary, 1000. 
prognostic factors in, 988. 
prognostic influence of nature of, 996. 
pseudo, 998. 
removable, table on, 989. 
rupture of, 998. 
simulated by hydrocephalus, 943. 
social status in, 990. 
subcortical, 992. 
symptomatic improvement in, 998. 
symptoms of, focal, 991. 
complex, 991. 
hemiplegia, 991. 
mental disturbances, 991. 
paralysis of two or more cranial 
nerves, 991. 
with spasmodic contractions, 998. 
general, constipation, 996. 
emaciation. 995. 
epileptic seizures, 994. 
fever, 993. INDEX 
1219 
Brain tumor, symptoms of, general, 
headache, 992. 
optic atrophy, 994-995. 
optic neuritis, 994-995. 
pulse, 993. 
psychic, 993. 
remission and exacerbation of, 996. 
spasms and convulsions, 994. 
venous obstruction, 996. 
vertigo, 992. 
vomiting, 992-993. 
weakness, 996. 
unilateral, 991. 
syphilitic cases of, vomiting in, 993. 
tolerance of brain in, 990. 
varieties of, 988. 
abscess. See Brain Abscess, 
aneurism, 997. 
carcinomatous deposits, 997. 
entozoa, 997. 
glioma, 997. 
sarcoma, 996. 
syphilomata gummata, 997. 
tubercle, 996. 
with actinomycosis, 988. 
without operation, 999. 
X-rav in, 999. 
Breakbone fever, 356. 
Bright’s disease, acute, 788. 
chronic, 797. 
Brill’s disease, 120-121. 
Brinton’s disease, 572. 
Bronchi, dilatation of, 366. 
diseases of, asthma, 368. 
bronchiectasis, 366. 
bronchitis, acute, 363. 
chronic, 365. 
fibrinous, 373. 
whooping-cough. See Pertussis, 
syphilis of, 33. 
Bronchial asthma, age in, 369. 
and tuberculosis, 371. 
alternating and intercurrent, 372. 
antitoxins for, 372. 
associated conditions of, 369. 
blood picture in, 370. 
character of, 368. 
“fixed thorax” with emphysema in, 372. 
general considerations on, 370. 
heredity in, 369. 
length of life in, 371. 
location and climatic conditions in, 370. 
Meltzer’s theory of, 368. 
occupation considered in, 369. 
postural change for, 370. 
secondary, 372. 
sex in, 369. 
sputum of, 368. 
symptoms of, 368. 
Bronchial catarrh, 364. 
dry, of Laennec, 365. 
Bronchial lymphadenitis, 265. 
Bronchial tuberculosis, 252. 
Bronchiectasis, acquired, 366. 
associated symptoms of, 367. 
atelectasis in, 367. 
causes of, 367. 
Bronchiectasis, congenital, 366. 
development of, 367. 
in influenza, 127. 
symptoms and course of complications 
in, 367. 
Bronchiolitis, in pneumonia, 165. 
Bronchitis, acute, atelectasis with, 364. 
primary, 363. 
secondary, 364. 
symptoms of, 364. 
bronchopneumonia with, 364. 
capillary, 169. 
chronic, associated conditions of, 365- 
366. 
dependent on chronic heart lesions, 
365. 
effect on, of climatic conditions, 365. 
hemoptysis of, 377. 
nature of, 365. 
purulent, with asthma, 366. 
putrid or fetid, 366. 
complications in, 364-365. 
. croupous, 373. 
fibrinous, 373. 
in influenza, 127. 
in measles, 344. 
in pneumonia, 165. 
in typhoid fever, 98. 
with cirrhosis, 693. 
with malaria, 77. 
Bronchobiliary fistulae, with gall-stones, 
730. 
Bronchopneumonia, character of, 169. 
complications in, 170-171. 
significance of, 171-172. 
fibrinous, 169. 
in measles, 344. 
lesions of, in contradistinction to lobar 
pneumonia, 170. 
primary, 169. 
with bronchitis, 364. 
Bronchorrhea, in pneumonia, 165. 
purulent, 366. 
types of, 365. 
Bruce, dictum of2 402. 
Bubonic plague, 203. 
Buccal psoriasis, 555. 
Bulbar neuritis, acute, 892. 
Bulbar paralysis, acute, 892. 
asthenic, 893. 
degenerative type of, 891. 
hemiplegics with, 892. 
hemorrhagic cases of, 892. 
infantile form of, 892. 
myasthenia gravis, 893. 
progressive infantile, 892. 
pseudo, 893. 
symptoms of, 891. 
with facial involvement, 865. 
Byssinosis, 380. 
C 
Cachexia, chronic malarial, 76. 
due to malaria, 76. 
neuralgia due to, 839. 1220 
INDEX 
Cachexia strumipriva, 1155. 
Cachexie pachydermique. See Myxedema. 
Caisson disease, acute, 1207. 
cause of, 1207. 
chronic, 1207. 
complications in, 1207. 
definition of, 1207. 
habits of workman in, 1208. 
immediate death from, 1208. 
influencing factors in, 1207. 
prophylactic measures in, 1208. 
paralysis, symptoms of, 1207. 
paraplegia, 1208. 
time of development of, 1207. 
Calculi, biliary. See Cholelithiasis, 
hepatic. See Cholelithiasis, 
pancreatic, 738. 
renal, 820. 
cystin stones, 821. 
large, 821. 
multiple, 821. 
sand or gravel, 821. 
single, without infection, 821. 
varieties of, 821. 
xanthin stones, 821. 
ureteral, 822. 
Calculosis, of kidney and ureter, 820. 
Calculous anuria, surgical treatment of, 
824. 
Calculous pyelitis, 831. 
Camp fever. See Typhus Fever. 
Cancer, cholangitis with, 714. 
hysterical, 1017. 
metastases to spine and cord due to, 
919-920. 
of appendix, 656. 
of brain, 997. 
of esophagus, 567. 
of gall-bladder, 717. 
of intestines, appearance of subjective 
symptoms in, 642-643. 
cachexia in, 643. 
profound blood changes in, 643. 
surgical treatment of, 643. 
symptoms of, 643. 
of kidney, 825 
of liver, acute course of, 711. 
encephaloid, 711. 
heredity in, 711. 
mortality from, 710. 
primary, 709. 
prognostic factors in. ascites, 710. 
edema of extremities, 709. 
fever, 710. 
jaundice, 709. 
spleen, 710. 
spontaneous recovery from, 710. 
usual secondary nature of, 709. 
of pericardium, 434. 
of peritoneum, 664. 
of spinal cord, 924. 
of stomach, age in, 603. 
complications in, hypostatic conges- 
tion of lung, 612. 
metastases, 606. 608. 
thrombotic processes, 611. 
Cancer of stomach, complications in, tu- 
berculosis, 612. 
death rate from, 600. 
duration of, 612. 
early diagnosis of, its difficulty, 601. 
Graefe-Rohmer test for, 601. 
importance of, 601. 
Leube rule for, 603. 
Oppenheimer test for, 601. 
for prompt surgical treatment, 608. 
Solomon test for, 601. 
stomach contents in, 602. 
tests for, 601. 
by x-ray, 602. 
fatality of, 601. 
glycyltryptophan test for, 605-606. 
general considerations of, 600. 
heredity in, 603. 
in early life, 603. 
incurability of, 608. 
infiltrating, without palpable tumor, 
608. 
latency of, 607. 
metastases in, 606, 608. 
origin of, in ulcer, 592. 
perforation of, 607. 
primary, 601. 
prognostic significance of leading 
symptoms of, 604. 
race in, 603. 
secondary, 603. 
sex in, 603. 
surgical treatment for, statistics on, 
609, 610, 611. 
symptoms of, acidity in stomach con- 
tents, 605. 
blood picture, 606. 
disturbance of stomach function, 
604. 
dropsy, 607. 
emaciation, 604. 
fever, 606. 
hematemesis, 604. 
latent, bloed picture in, 607. 
pain, 604. 
ulcerative stomatitis, 607. 
urinary, 606. 
vomiting, 604. 
tryptophan test for, 605-606. 
types of, their relative frequency, 603. 
pulmonary, 387. 
Cancer-free islands, 601. 
Cancerous degeneration, in gastric ulcer, 
593. 
of organ harboring gall-stones, 731. 
Cancerous infiltration, in cirrhosis, 687. 
Cancrum oris, 555. 
in measles, 344. 
Capsulitis, 1170. 
Caput medusae, in cirrhosis, 689. 
Carbon monoxid poisoning, acute, symp- 
toms of, 1196. 
chronic, symptoms of, 1196. 
complications in, 1196. 
prognosis of, 1197. 
prognostic factors in, 1196. INDEX 
1221 
Carbuncles, with diabetes mellitus, 1118. 
Carcinoma. See Cancer. 
Cardiac asthma, 370. 
and obesity, 1127. 
influence of, on endocarditis, 489. 
Cardiac complications, in appendicitis, 658. 
Cardiac neuroses, in neurasthenia, 1029. 
Cordiopathia chronica, 477. 
Cardiovascular disease, death due to, in 
alcoholism, 1179. 
arteritis, 26. 
due to syphilis, aortitis syphilitica, 27. 
heart syphilis, 28. 
myocarditis, 29. 
in scarlet fever, 330. 
increase of, in past two decades, 403. 
tuberculosis, 274. 
Caries of spine, with syringomyelia, 917. 
Casts, associated conditions of, 752. 
bacterial, 753. 
blood, 750. 
definition of, 749. 
epithelial, 750. 
fatty and granular, 751. 
fatty or oily, 750. 
granular, 749-750. 
hyaline, 749, 751. 
prognostic significance of, 751. 
in albuminuria, 744. 
prognostic significance of, 749. 
promptly disappearing, 749. 
pus, 750. 
waxy or amyloid, 750. 
Catalepsy, hysterical, 1016. 
Catarrh, autumnal, 358. 
bronchial, 364. 
dry bronchial, of Laennec, 365. 
epidemic. See Influenza. 
Catarrhal conditions, in typhoid fever, 97. 
Catarrhal influenza, 125. 
Catarrhal tuberculosis, 250. 
Cauda equina, paralysis of, 882. 
Cecum mobile, 632. 
Celiac disease, 629. 
Cerebellar disease, ataxia, 1003. 
congenital defects in, 1003. 
hemiataxia with, 1004. 
hemihypotonia with, 1004. 
hemorrhage in, 1003. 
invasion of pons by, 1004. 
neoplasms, 1003. 
nystagmus with, 1004. 
of middle peduncle, 1004. 
optic neuritis with, 1004. 
polioencephalitis hemorrhagica superior, 
1004. 
reflexes in, 1004. 
senile atrophy, 1003. 
staggering, 1003. 
thrombosis, 1004. 
Cerebellar staggering, in Marie’s heredi- 
tary ataxia, 888. 
Cerebral anemia, associated symptoms of, 
947. 
delirium of inanition in, 948. 
due to vascular spasm, 947. 
Cerebral anemia, faint spells of, 948. 
localized, 947. 
paralyses with, 948. 
secondary origin of, 947. 
secondary to other controllable hemor- 
rhages, 947. 
with convulsions, 948. 
with lead poisoning, 948. 
with unconsciousness, 948. 
with uremic intoxication, 948. 
Cerebral apoplexy, 957. 
Cerebral embolism, and diphtheria, hemi- 
plegia due to, 954. 
breaking away from aneurismal coagu- 
lum, 954. 
chrome, 954. 
due to mitral stenosis, 953. 
due to septic or malignant endocarditis, 
953. 
fat, following trauma, 954. 
onset of, 954. 
origin of, 953. 
prognosis of, dependent on area involved, 
953. 
in thrombosis of pulmonary vein with 
pneumonia, 954. 
recovery from, 954. 
seat of, 954. 
septic, 954. 
with puerperal infection, 954. 
Cerebral hemorrhage, age considered in, 
959. 
and paralysis, table of deaths from, 
959. 
apoplectic attack in, acute bed-sores in, 
966. 
Cheyne-Stokes breathing in, 964. 
coma in, 963. 
duration of, 966. 
ophthalmoscopic examination in, 966. 
pulse in, 965. 
pupils in, 965. 
temperature in, 965. 
apoplectic habit in, 962. 
associated symptoms of, 957. 
bed-sores in, 966. 
causes of, 958. 
Cheyne-Stokes breathing in, 964. 
climatic influence in, 962. 
coma in, 963. 
duration and depth of, 964. 
complicating constitutional disease, 958. 
due to endocarditis, 960-961. 
due to increased blood pressure, 957. 
due to syphilis, 960-961. 
duration of life in, 972. 
following infantile convulsions, 960. 
general considerations of, 957. 
hemiplegias supposed to be due to, 958. 
heredity in, 962. 
in early life, 960. 
in puerperal period, 961. 
influence of special symptoms on prog- 
nosis of, apoplectic attack, 963. 
period of paralysis, 968. 
period of reaction, 967. 1222 
INDEX 
hemorrhage, mental conditions 
following, after coma, 971. 
cerebral apoplexy in insane, 972. 
change of disposition, 971. 
dementia, 971. 
in young subjects, 972. 
maniacal disturbances, 972. 
Weakening of intellect, 972. 
mortality from, 959-960. 
occupation in, 963. 
period of paralysis in, albuminuria, 970. 
arthritis, 970. 
atrophy of muscles, 968. 
Babinski phenomenon, 968. 
exalted knee reflex, 968. 
hemianesthesia, 969. 
hemianopsia, 970. 
inclusion of medulla oblongata, 970. 
posthemiplegic motor complications, 
970. 
secondary contractures, 968. 
transitory cases, 969. 
period of reaction in, 967. 
aphasia, 969-970. 
hemiplegia, 969. 
improvement of motor function, 969. 
symptoms during, 967. 
pneumonia with, 972. 
prodromata of, 963. 
recurrence of, 972. 
rupture in, 957-958. 
sex considered in, 962. 
spontaneous, 961. 
traumatic, 959. 
Avith chronic interstitial nephritis, 
958. 
Cerebral hyperemia, active, 950. 
assumptions in prognosis of, 950. 
cases suggesting, due to chronic con- 
stipation, 952. 
classification of, 949. 
due to toxemia, 949, 951. 
leading causes of, 950. 
merging of forms of, 951. 
passive, 950, 951, 952. 
pathology of, 949. 
prodromal stage of, 952. 
prognosis of, 952. 
secondary origin of, 949. 
soporific, with apoplectiform symptoms, 
951. 
symptoms of, aphasic, 951. 
apoplectiform, 950. 
convulsive, 951. 
paralytic, 951. 
soporific, 951. 
with mania, 951. 
Cerebral neurasthenia, 1028. 
Cerebral paralysis, choreatic paresis with, 
980. 
of childhood, acute encephalitis of chil- 
dren, 979. 
birth palsies, causes of, 978. 
Oppenheim-Vogt type of, 978. 
symptoms and prognosis of, 978. 
differentiation of acquired and con- 
genital, 978. 
Cerebral paralysis, of childhood, due to 
intra-uterine anomalies, ar- 
rested development of cortex 
cerebri, 977. 
cysts developed in fetus, 977. 
influence of heredity on produc- 
tion of epilepsy after, 977. 
prognosis of, 977. 
uremic, 764. 
Cerebral polioencephalitis, 322. 
Cerebral softening, 953. 
Cerebral syphilis, 38. 
arteritis in, 40, 43. 
degeneration of brain tissue in, 40. 
deposits in, 42. 
epilepsy in, 42. 
examination of spinal fluid in, 40. 
genera] considerations of, 39. 
globulin reaction in, 40. 
gummatous lesions in, 40. 
hemiplegia in, 43. 
interval between specific infection and 
development of, 41. 
lumbar puncture in, 38. 
malignant types of, 41. 
meningitis, specific localized with, 42. 
paralysis of motor oculi in, 43. 
primary, 42. 
prognosis of, 41. 
relapse of, 41, 43. 
secondary, 41. 
single gumma in, 42. 
specific endarteritis in, 42-43. 
Cerebral thrombosis, about an embolus, 
956. 
anemias and leukemias ending in, 955. 
coma with, 956. 
due to blood changes and weakened 
heart, 956. 
during puerperal period, 956. 
following otitis, 955. 
frequency of, 955. 
in senile subjects with arteriosclerosis, 
956. 
multiple “marantic” thrombi, 955. 
of small arteries, without symptoms, 
956. 
pathologic conditions predisposing to, 
955. 
primary, of longitudinal sinuses, 955. 
prognosis of, 956. 
seat of, 955. 
slow formation of, 955. 
symptoms of pseudobulbar paralysis in, 
956. 
with chronic alcoholism, 956. 
with paralysis, 956-957. 
with specific endarteritis, 956. 
Cerebral toxemia, in pernicious anemia, 
526. 
Cerebral vessels, occlusion of, by embol- 
ism, 953. 
by thrombosis, 955. 
Cerebral vomiting, 993. 
Cerebrospinal meningitis, 932. 
epidemic, hydrocephalus due to, 182. INDEX 
1223 
Cerebrospinal syphilis, hereditary, 37. 
Cervical lymphadenitis, 265. 
Cervical nerves, paralysis of, hiccough- 
spasm of diaphragm, 875. 
phrenic, 874. 
Cervical pachymeningitis, hypertrophic, 
bladder symptoms in, 933. 
prognosis of, 933. 
symptoms of, 932. 
syphilitic cases of, 933. 
Cervical rib, paralysis due to, 876. 
sensory and motor disturbances due to, 
876. 
surgical removal of, 876. 
Cervical sympathetic, irritation of, 1082. 
paralysis of, 1081. 
Cestodes, Bothriocephalus latus, 305. 
Tenia echinococcus, 306. 
cysts of, 306-307. 
in brain, 308. 
in heart, 466. 
in kidney, 308. 
in liver, 307. 
in lung, 308. 
in other organs, 309. 
in spleen, 308. 
Tenia mediocanellata, 305. 
Tenia saginata, 305. 
cysticercus of, 305. 
Tenia solium, character of, 304. 
cysticercus of, 304-305. 
seats of, 304-305. 
symptoms of, 304. 
Chalicosis, 380. 
Charcot, “grande hysterie” of, iOlO. 
hysterical stigmata of, 1005. 
Cheyne-Stokes breathing, in cerebral hem- 
orrhage, 964. 
Chicken pox. See Varicella. 
Chloroleukemia. See Leukemia, lym- 
phatic. 
Chloroma, with lymphatic leukemia, 533. 
Chlorosis, blood picture of, 517. 
causes of. 518. 
chronic, 519. 
complications with, 518. 
nature of, 514, 517. 
oligocythemia with, 518. 
subjective symptoms of, 518. 
Choked disk, with brain tumor, 994-995. 
Cholangitis, acute, 714. 
chronic, nature of, 714. 
produced by gall-stones, 715. 
with cancer, 714. 
suppurative, 715. 
Cholecystitis, acute, 715. 
acute phlegmonous, 717. 
chronic, 716. 
in typhoid fever, 105. 
obliterative, 716. 
and cholangitis. 716. 
with gangrene, 717. 
Cholelithiasis, absence of svmptoms in. 
718, 728. 
acute biliary colic in, adhesions due to 
local inflammation in, 721. 
blood condition of, 723, 
Cholelithiasis, acute biliary colic in, en- 
largement of gall bladder 
with, 722. 
enlargement of liver with, 722. 
enlargement of spleen with, 722. 
fever with, 721. 
hyperpyrexia with, 721. 
initial attack of, 721. 
jaundice with, 721. 
prognosis of, 720. 
relative mitral insufficiency in, 720. 
severity of, 722. 
small stones in intestines in, 723. 
vomiting with, 722. 
with weak myocardium, 720. 
x-ray examination for, 723. 
adhesions in, protection offered by, 729. 
adhesions of gall bladder and duodenum 
or pylorus in, 729. 
age in, 719. 
arteriosclerosis with, 730. 
associated infection in, 719, 728. 
associated with malignant disease, 719. 
associated with metabolic faults, 719. 
cancerous degeneration in, 731. 
cholesterin, main constituent of, 718. 
chronic, adhesions in, 724. 
effect on patient, 723. 
location of stones in, 723. 
prognosis of, 724. 
pyloric obstruction in, 724. 
secondary changes due to, 724. 
with added chronic infection, 730. 
complications in, 728. 
due to diet, 719. 
endocarditis with, 731. 
fistulae in, 728. 
biliary, 730. 
bronchobiliary, 730. 
urinary, 730. 
frequency of, in internal diseases, 719. 
gangrenous gall-bladder in, 728. 
hemorrhage in, 732. 
interstitial nephritis with, 730. 
intestinal obstruction in, 729, 731. 
migration of stones into right kidney 
in, 730. 
myocarditis with, 731. 
nervous system in, 732. 
obstruction of common duct by, “adven- 
titious outlets” for bile in, 725. 
ball valve action of stone in, 726. 
changes caused by, 725. 
complete, 725. 
Courvoisier’s law, 725. 
effect of, on gall-bladder, 725. 
liver abscess due to, 726. 
partial, 725. 
serious complications of, 725. 
source of, 725. 
ulceration in, 725. 
obstruction of cystic duct by, atrophy 
of gall-bladder with, 726. 
dilatation of gall-bladder with, 726. 
duration of, 726. 
source of, 726. 
symptoms of, 726, 1224 
INDEX 
Cholelithiasis, obstruction of hepatic and 
intra-hepatic ducts by, causa- 
tion of, 727. 
coincident with stones in other pas- 
sages, 727. 
prophylaxis in, 727. 
stones in liver substance in, 727. 
pancreatic disease with, 731. 
passing of stones by rectum in, 729. 
perforation of gall-bladder in, 728. 
perforation into peritoneum in, 729. 
process of, 719. 
protective factors in, 728. 
sex considered in, 719. 
solubility of stones in, 719. 
spontaneous solution of, 720. 
subphrenic abscess in, 730. 
surgery in, 733. 
ulceration into portal vein and into 
hepatic artery in, 730. 
vagaries of, 718, 729. 
wanderings of stones in, 729. 
Cholera asiatica. See Asiatic Cholera. 
Cholera morbus, 623. 
Cholera nostras, 623. 
Cholerine, 200. 
Cholesterin, 718. 
Chondrodystrophy, fetal, 1131. 
Chorea, acute hereditary, 1043. 
associated conditions of, grippal infec- 
tion, 1040. 
associated diseases of, arthritis, 1039. 
gonorrhea, with endocarditis, 1040. 
polyarthritis, with endocarditis, 1040. 
purpura rheumatica, 1039. 
streptococcus viridans infection, 1039. 
tonsillar, 1039. 
chronic, 1043. 
chronic progressive, 1044. 
complications in, cardiac, 1042. 
conditions influencing, age, 1038. 
heredity, 1038. 
moisture and exposure, 1038. 
psychic disturbances, 1038. 
race, 1038. 
sex, 1038. 
unhygienic conditions, 1038. 
definition of, 1037. 
Dubini’s, 1046. 
electrical, 1046. 
endocarditis in, 1042. 
endocarditis and rheumatism with, 284. 
family, 1044. 
foudroyant cases of, 1043. 
history of, 1038. 
Huntington’s, 1044. 
in aged, 1043-1044. 
latent, 1041. 
mortality from, 1043. 
myocarditis in, 1042. 
nature of, 1037. 
problematic nature of, 1037. 
prognostic factors in, heart anomalies, 
1042. 
loss of flesh. 1041. 
mental symptoms, 1040. 
motor disturbances, 1041. 
Chorea, prognostic factors in, muscular 
weakness, 1041. 
ocular errors in, 1040. 
sensory disturbances, 1041. 
sphincter involvement, 1041. 
psychic disturbances in, improvement of, 
1042. 
recurring, and endocarditis, 1043. 
relapse of, 1043. 
subacute, 1043. 
symptoms of, eosinophilia, 1041. 
Chorea gravidarum, 1040. 
Chorea minor, 1037. 
Choreatic paresis, 980. 
Chylous urine, 776. 
Chyluria, non-parasitic, 776. 
parasitic, 776. 
Circulatory disturbances, in typhoid fever, 
93. 
of lung, congestion, 373. 
Circulatory system, diseases of, aneurism, 
420. 
arteriosclerosis, 402. 
congenital defects of heart, defective 
intraventricular septum, 438. 
dextrocardia, 438. 
insufficiency and stenosis of mitral 
and tricuspid valves, 439. 
perforate foramen ovale, 438. 
stenosis of aortic orifice, 438. 
stenosis of pulmonary orifice, 435. 
transposition of aorta and pulmon- 
ary artery; perforate and pre- 
mature closure of ductus ar- 
teriosus, 439. 
endocardial, acute, 468. 
chronic, 477. 
functional heart disorders, 506. 
bradycardia, 511. 
neurasthenic state, 512. 
palpitation, 507. 
tachycardia, paroxysmal, 508. 
tachycardia, simple, 510. 
gastric, enteroptosis, 579. 
myocardial, 441. 
aneurism, 467. 
chronic insufficiency, 443. 
heart weakness due to insufficient 
exercise, 464. 
hypertrophy and dilatation, 460. 
inherent muscular weakness, 465. 
insufficiencies with anemias, meta- 
bolic faults and toxic states, 
465. 
myocarditis, acute interstitial, 443. 
myocarditis, acute purulent, 442. 
neoplasms, 465. 
parasites, 466. 
rupture, 466. 
Stokes-Adams disease, 463. 
syphilis. See Cardiovascular 
Disease. 
pericardial, adherent pericardium, 
430. 
hemopericardium, 433. 
hydropericardium, 433. 
neoplasms, 434. INDEX 
1225 
Circulatory system, diseases of, pericar- 
dial pericardioperitonitis, 432. 
pericarditis, 426. 
pneumopericardium, 434. 
in alcoholism, 1182. 
in erysipelas, 175. 
in pneumonia, 153. 
Circumflex nerve, paralysis of, 878. 
Cirrhosis, and nephritis, 685. 
biliary, 698. 
capsular, 701. 
associated symptoms of, 701. 
fatal terminations of, 703. 
tapping in, 702. 
complications with, alcoholic poisoning, 
694. 
arteriosclerosis, 686. 
bronchitis, 693. 
cerebral, 695. 
coma, 694. 
convulsions, 695. 
delirium, 694-695. 
gout, 695. 
invasion of nervous system, 694. 
pleurisy, 694. 
pneumonia, 694. 
progressive lenticular degeneration, 
695. 
renal insufficiency, 694. 
terminal infections, 695. 
tuberculosis, 693. 
uremia, 694. 
Hanot’s hypertrophic biliary, 698-699. 
Laennec’s, duration of, 698. 
late operation for, 697. 
malarial, cases of, 696. 
mortality from, 683. 
multilobular, 682. 
alcoholic history of, 682. 
etiology of, 683. 
faulty diet as factor in, 682. 
prognostic factors of, 682. 
spleen as factor in, 682. 
splenectomy for, 682. 
obstructive biliary, 698-699. 
of liver, chronic gastritis associated 
with or secondary to, 573. 
enlargement of spleen with, 1170. 
nature of, 681. 
with tuberculosis, 255, 258. 
of lung, 379. 
of stomach, 572. 
pericellular, 701. 
pigmented, 696. 
hemachromatosis, 696. 
prognostic factors of, arteriosclerosis, 
686. 
cancerous infiltration, 687. 
esophageal lesions, 685. 
heart condition, 687. 
individual symptoms, 687. 
intestinal lesions with, 685. 
kidney lesions, 685. 
latency, 684. 
latency and complications, 685. 
lesions in other organs, 685. 
peritonitis, 686. 
Cirrhosis, prognostic factors of, pulmon- 
ary tuberculosis with, 686. 
stomach lesions with, 685. 
progressive, secondary anemia with, 
693. 
surgical treatment for, 696-697. 
symptoms of, ascites, 691. 
blood condition, 693. 
caput medusae, 689. 
change in size of liver, 690. 
epistaxis, 690. 
facies, 688. 
gastro-intestinal, 688. 
general dropsy, 691. 
heart, 696. 
hematemesis, 689. 
hematuria, 690. 
hemoptysis, 690. 
ill defined, 687. 
jaundice, 692. 
melena, 690. 
pulse, 695. 
respiration, 696. 
skin lesions, 696. 
splenic, 689. 
temperature, 695. 
urinary secretion, 691. 
venous obstruction, 688. 
weight, 688. 
syphilitic, 701. 
unilobular, 698. 
blood condition in, 700. 
causes of, 699. 
complications with, 699. 
conclusions on, 701. 
course of, 700. 
general statements on, 698-699. 
jaundice in, 700. 
joint changes in, 700. 
myocardial insufficiency in, 700. 
size of spleen in, 700. 
urine in, 700. 
Claw hand, 879. 
Clubbed fingers, 1096. 
Cocainism, effects of, 1187. 
prognosis of, 1187. 
Cochlear nerve, invasion of, in auditory 
paralysis, 868. 
Colitis, acute membranous, secondary, 623. 
membranous, in pneumonia, 161. 
mucous, infantile, 623. 
infectious, 622. 
nervous or hysterical, 622. 
secondary, 622. 
Colitis cystica, 624. 
Colles-Baume law, 65. 
Colon, dilatation of, 640. 
Color perception, faulty, hysterical, 1012. 
Coma, in cerebral hemorrhage, 963. 
in cerebral thrombosis, 956. 
in cirrhosis, 694. 
in malarial fever, 75. 
Common duct, obstruction of, 725. 
occlusion of, 715. 
Compensatory hypertension, in chronic 
nephritis, 802. 
Compensatory hypertrophy, 582. 1226 
INDEX 
Compensatory hypertrophy,, in chronic 
nephritis, 797, 802. 
Concussion of spine, 1021-1022. 
Congested kidney, acute, as secondary 
condition, 811. 
associated with acute infections, 811. 
heart lesions provoking, 812. 
prognosis of, 812. 
chronic, causes of, 812. 
due to heart lesions, 812. 
condition of urine in, 813. 
conditions associated with, 813. 
due to local obstruction, 813. 
due to pulmonary obstruction, 813. 
due to venous stasis, 813. 
prognosis of, 813. 
Congestion, pulmonary, 373. 
of brain. See Cerebral Hyperemia, 
of liver, 676. 
Conjunctival diphtheria, 138. 
Conjunctivitis, in measles, 343. 
Constipation, 630. 
and hemorrhoids, with obesity, 1127. 
atonic form of, due to insufficient ex- 
pulsive strength, 631. 
due to reduced intestinal peristaltic 
activity, 631. 
cathartics for, 633. 
causes of, 630-631. 
due to cecum mobile, 632. 
due to habits, 630, 632. 
hysterica], 1017. 
in brain tumor, 996. 
organic causes of, 631. 
spastic, 632. 
with neurasthenia, 1031. 
Contractures, hysterical, 1014. 
Convergent strabismus, 861. 
Convulsions, in brain tumor, 994. 
in cerebral anemia, 948. 
in cirrhosis, 695. 
in malarial fever, 75. 
infantile. See Infantile Convulsions. 
Coronary disease, due to arteriosclerosis, 
411. 
with chronic nephritis, 802. 
Coronary sclerosis, 454. 
Coryza. See Rhinitis, Acute Catarrhal, 
in congenital syphilis, 66. 
Cough, hysterical, 1018. 
in pneumonia, 155. 
in pulmonary tuberculosis, 229. 
Courvoisier’s law, 725. 
Cranial nerves, paralysis of, abducens, 861. 
auditory, 868. 
Bell’s palsy, 864. 
facial, 863. 
due to pontine disease, 864. 
facial or mimic spasm, 866. 
facial hemiatrophy, 863. 
glossopharyngeal, 870. 
hypoglossal, 873. 
motor oculi, 860. 
ocular, 860. 
ophthalmoplegia, 861. 
optic, 857. 
pneumogastric, 871, 
Cranial nerves, paralysis of, spasm of 
spinal accessory muscles, 872. 
spinal accessory, 871. 
tic convulsive, with, 867. 
trigeminal, 862. 
trochlear, 861. 
peripheral paralysis of, olfactory, 856. 
Cretinism, congenital, 1155. 
prognosis of, 1155. 
symptoms of, 1155. 
thyroid treatment for, 1156. 
due to complete loss of gland function, 
1157. 
endemic, 1156. 
fetal, 1131. 
heredity in, 1158. 
prognosis of, 1158. 
sporadic, 1155. 
Cretinoid change. See Myxedema. 
Crural neuralgia, 844. 
Crural pains, 840. 
Cylindroids, 750. 
Cystic duct, obstruction of, 726. 
Cysticercus. See Cestodes. 
Cysticercus cysts, in tumors of spinal 
cord, 924. 
Cystinuria, conditions indicated by, 785. 
Cystitis, in typhoid, 109. 
Cystoscopic examination, in pyelitis, 832. 
Cysts, pancreatic, 738. 
renal, 826. 
splenic, 1171. 
D 
Dandy fever, 356. 
Deafmutism, due to epidemic cerebrospinal 
meningitis, 868. 
Deafness, 868. 
Decubitous ulcers, of esophagus, 564. 
Decubitus, in acute myelitis, 905. 
Delirium, epileptic, 1053. 
in cirrhosis, 695. 
of inanition, 948. 
Delirium cordis, 510. 
Delirium tremens, collapse in, 1184. 
duration of, 1184. 
infections with, 1184 
prognosis of, 1183. 
pulse and temperature in, 1184. 
recurrence of, 1183. 
symptoms of, 1183. 
“wet brain” in, 1184. 
with alcoholic multiple neuritis, 849. 
Dementia, in cerebral hemorrhage, 971. 
in epilepsy, 1053. 
in paresis, 64. 
Dementia paralytica. See Paresis. 
Dengue, 356. 
Dercum’s disease, 1078. 
Dextrocardia, 438. 
Diabetes, glucosuria and, in exophthalmic 
goiter, 1147. 
in tuberculosis, 242. 
neuralgia due to. 839. 
Diabetes bronze, 1107. INDEX 
1227 
Diabetes insipidus, as incurable complex, 
1124. 
backache in, 1124. 
blood picture in, 1123. 
characteristic features of, 1122, 
heart and blood pressure in, 1123. 
heredity in, 1123. 
idiopathic, 1122. 
influence of hypophysis in, 1123, 
primary, 1124. 
quantity of urine secreted in, 1123. 
secondary, 1122. 
urine in, 1123. 
Diabetes mellitus, acute, 1113. 
chronic, 1113. 
acidosis in, 1115. 
and gout, 1119. 
aural disturbances in, 1119. 
blood condition in, 1117. 
carbuncles in, 1118. 
emaciation in, 1114. 
furuncles in, 1118. 
gangrene in, 1118. 
hunger in, 1113. 
infections complicating, 1117. 
mental state in, 1115. 
muscular weakness in, 1116. 
nervous system in, 1118. 
ocular infections with, 1119. 
pneumonia with, 1117. 
polyuria in, 1114. 
pulse and blood pressure in, 1114. 
pruritus with, 1118. 
relative value for prognosis, of indi- 
vidual symptoms in, 1113. 
sexual anomalies in, 1117. 
skin lesions in, 1118. 
thirst in, 1114. 
tuberculosis with, 1118. 
urine in, 1116. 
eternal vigilance in, 1121. 
fasting method of treatment for, 1121. 
general considerations of, 1106. 
glucosuria in, alimentary, 1108. 
due to adrenalin, 1107. 
due to disease of hypophysis, 1107. 
due to liver disease, 1107. 
due to pancreatic disease, 1106. 
due to skeletal muscles, proteid and 
fat, 1108. 
due to surgical lesions, 1119. 
due to thyroid extract, 1107, 
due to traumatism, 1108. 
glucosuric condition in, 1106. 
impossibility of cure in, 1121. 
in infancy and childhood, 1112. 
in obese, 1112. 
increase of cellular resistance in, 1120. 
negative factors in, contagion, 1108. 
kidney, 1108. 
pancreatic disease with, 1106. 
process of, 1106. 
prognostic factors in, age, 1110. 
control of hyperglycemia, 1111. 
heredity, 1110. 
race and geographic location, 1111. 
sex, 1110. 
Diabetes mellitus, relation to, of lacto- 
suria, 1109. 
surgery for, 1119. 
in presence of acetone or diacetic acid, 
1120. 
preliminary treatment, 1120. 
vulnerability of tissue in, 1118. 
with syringomyelia, 917. 
Diaphragm, spasm of. See Hiccough, 
Diarrhea, acute. See Enteritis, acute, 
chronic, 623. 
gastrogenic, 624. 
gastro-intestinal, 624. 
hysterical, 1017. 
in pernicious anemia, 523. 
in pulmonary tuberculosis, 232. 
in typhoid fever, 102. 
secondary chronic, primarv causes of, 
625. 
with exophthalmic goiter and Addison’s 
disease, 625. 
Diarrhea alba, 629. 
Diarrhea chylosa, 629. 
Diarrheal diseases, of early childhood, 
mortality from, 627-628-629. 
prophylaxis against, 627. 
Schmidt’s bile test, 629. 
symptoms of, affecting prognosis, 629. 
Diazo-reaction, 234. 
Dietl’s crises, in gastroptosis, 580. 
with nephroptosis, 829. 
Digestive system, diseases of, appendiceal, 
appendicitis, 644. 
cancer, 656. 
tuberculosis, 656. 
bile passages and gall-bladder, chol- 
angitis, 714. 
cholecystitis, 715. 
cholelithiasis, 718. 
esophageal, cancer, 567. 
dilatation, 568. 
diverticula, 569. 
esophagitis, 562. 
rupture, 568. 
spasm and paralysis, 565. 
stricture, 566. 
gall-bladder, cancer of, 717. 
intestinal, cancer and other growths, 
642. 
celiac disease, 629. 
constipation, 630. 
diarrheal diseases of early child- 
hood. 627. 
dilatation of colon, 640, 
diverticulum, 641, 
enteritis, acute, 619. 
enteritis, chronic, 623, 
enteroptosis, 579. 
obstruction, 633. 
liver, abscess, 704. 
acute yellow atrophy, 673, 
amyloid, 713. 
circulatory disturbances, 676. 
cirrhosis, 681. 
echinococeus. See Echinococcus dis- 
ease, 1228 
INDEX 
Digestive system, diseases of, liver, fatty, 
712. 
jaundice, 664. 
neoplasms, 709. 
syphilis of. See Syphilis, 
tuberculosis of. See Tuberculosis, 
mouth, stomatitis, 553. 
pancreatic, calculi, 738. 
cysts, 738. 
hemorrhage, 737. 
necrosis, 738. 
neoplasms, 739. 
pancreatitis, 734. 
peritoneal, new? growths, 663. 
peritonitis, acute diffuse, 659. 
peritonitis, chronic, 662. 
tuberculosis. See Tuberculosis, 
pharyngeal, circulatorv anomalies, 
559. 
pharyngitis, 559. 
salivary glands, Mikulicz disease, 557. 
mumps. See Parotitis, epidemic, 
parotitis, 557. 
stomach, cancer of, 600. 
dilatation, 576. 
gastric and duodenal ulcer, 585. 
gastric neuroses, 615. 
gastritis, acute, 570. 
gastroptosis, 579. 
gastrorrhagia, 613. 
hematemesis, 613. 
pyloric obstruction, 581. 
tonsillar. See Infectious Diseases, 
syphilis of, 34. 
tuberculosis of, 252. 
Dilatation of colon, due to gas, 640. 
due to organic stricture, 640. 
idiopathic, 640. 
with solid matter within it, 640. 
x-ray in, 640. 
of esophagus, 568. 
of stomach, acute, 576. 
involvement of innervation in, 577. 
with pneumonia, 577. 
with pneumonia and chronic valvu- 
lar disease, 577. 
atonic, 578. 
primary myasthenic, 577. 
congenital, 578. 
secondary chronic, obstruction as 
cause of, 578. 
tetany in, 579. 
Diphtheria, and cerebral embolism, hem- 
iplegia due to, 954. 
and hemiplegia, 954. 
antitoxin for, blood counts after injec- 
tion of, 142. 
conclusions on, 144. 
mortality statistics on, 144. 
serum sickness, 142-143. 
bacteriology of, 134. 
carriers of, 136. 
complications in, heart, 139-140. 
nephritis, 139. 
otitis media suppurativa, 142. 
paralysis, 140. 
Diphtheria, complications in, parotitis, 
142. 
pleurisy, 142. 
pneumonia, 142. 
conjunctival, 138. 
endocarditis with, 140. 
factors influencing growth of, 135. 
history of, 134. 
in measles, 345. 
in scarlet fever, 329. 
laryngeal, 136, 138. 
liver and spleen in, 142. 
myocarditis in, 139. 
nasal, 138. 
of vulva, 138. 
paralysis in, 140. 
asphyxia in, 141. 
facial, 865. 
glossopharyngeal, 141. 
hemiplegia in, 141. 
ocular, 141. 
of extremities, 141. 
pneumogastric, 141. 
simple uncomplicated, of soft palate, 
141. 
von Behring antitoxin for, 141. 
pharyngeal, gangrenous, 137. 
mild infection without severe gen- 
eral toxemia, 136. 
with severe toxemia, 137. 
relapses of, 142. 
skin, 138. 
sudden death from, 140. 
vomiting with, 142. 
Diphtheritic dysentery, 194. 
Diphtheritic enteritis, 621. 
Diphtheritic esophagitis, 564. 
Diplegia, spastic, 978. 
Diplopia, in paralysis of sixth nerve, 861. 
Divers’ paralysis. See Caisson disease. 
Diverticulum, of intestines, 641. 
effects of, 642. 
false, 641. 
true, 641. 
“Drop-foot,” 881. 
Drop wrist, in lead multiple neuritis, 850. 
in musculospiral paralysis, 879. 
Dropsy, and obesity, 1128. 
in chronic interstitial nephritis, 807. 
in chronic nephropathies, 800. 
in cirrhosis, 691. 
in endocarditis, 492, 496. 
of gall-bladder, 726. 
of joints, intermittent, 1079. 
Dubini’s disease, 1046. 
Duchenne paralysis, 877. 
Ductless glands, diseases of, parathyroid, 
1165. 
pituitary, 1158. 
splenic, 1169. 
suprarenal, 1163. 
thymus, 1163. 
thyroid, 1136. 
Ductus arteriosus, perforate, and prema- 
ture closure of, 439. 
Duke’s disease, 352. INDEX 
1229 
Duodenal ulcer, alcoholic, 1181. 
and gastric, relative frequency of, 587. 
due to surface burns, 588. 
hyperchlorhydria symptomatic of, 588. 
indicanuria in, 588. 
perforation of, 590. 
subphrenic abscess formed by, 591. 
with chronic nephritis, 588. 
Duodenitis, acute, 620. 
Duodeno-cholangitis, 714. 
Duodenum, adhesions of, in cholelithiasis, 
729. 
Dura mater, inflammation of, 934. 
Dysentery, amebic. See Amebic Dysentery, 
bacillary, 193. 
diphtheritic, 194. 
with malaria, 77. 
Dyspepsia, chronic, 574. 
of Leube, 574. 
without stomach lesions, 576. 
gastro intestinal, chronic, 624. 
intestinal, dependant upon fermenta- 
tion, 624. 
motor, due to hypermotility, 617. 
due to hypomotility, 617. 
nervous, due to neurasthenia, 615. 
due to organic diseases, 615. 
sensory, appetite in, 616. 
gastralgia in, 616. 
mental condition in, 616. 
psychic influences in, 616. 
symptoms of, due to organic constric- 
tion at pylorus, 579. 
Dysphagia, 870. 
Dyspituitarism, 1158. 
Dyspnea, in nephritis, 807. 
in pleurisy, 391. 
influence of, on endocarditis, 489. 
with uremia, 765. 
Dystrophia adiposo-genitalis, 1159. 
Dystrophy, muscular. See Muscular Dys- 
trophy. 
E 
Ear, affection of, by influenza, 128. 
effect on, of scarlet fever, 329. 
of congenital syphilis, 66. 
involvement of, in typhoid, 113. 
paralysis of auditory nerve, 868. 
Echinococcus. See Cestodes. 
Eclampsia, mortality from, 795. 
symptoms in prognosis of, 795-796. 
Eclampsia infantum. See Infantile con- 
vulsions. 
Ectasia, 726. 
Eczema, associated with bronchial asthma, 
369. 
Edema, acute circumscribed. See Angio- 
neurotic edema, 
in chronic nephritis, 802. 
of extremities, in cancer of liver, 709. 
of glottis, in syphilis, 33. 
of larynx, 362. 
of leg, persistent hereditary, 1080. 
of pharynx, 559. 
Edema, pulmonary, 375. 
Ehrlich, therapy of, 35. 
Electrical choiea, 1046. 
Elephantiasis, due to filariasis, 316. 
Elephantiasis neuromatosa, 884. 
Elephantoid fever, due to filariasis, 316. 
Emaciation, in brain tumor, 995. 
in diabetes mellitus, 1114. 
Embolic infarcts, in diphtheria, 140. 
Embolism, cerebral, 953. 
of hepatic artery, 680. 
spinal, 929. 
Emphysema, pulmonary, associated condi- 
tions of, 383-384. 
atrophic, 385. 
compensatory, 382. 
fixed thorax in, 383. 
heredity considered in, 383. 
hypertrophic, 383. 
occupations in, 383. 
surgical, 382. 
sex considered in, 383. 
Empyema, 392. 
and pneumonia, 164, 165, 393. 
double, 394. 
general statements on, 393. 
lung abscess with, 393. 
parapneumonic, 394. 
prognosis of, during early life, 394. 
time of complication in, 394. 
with metastases, 393. 
with rheumatism, 288. 
Empyema necessitatis, 394. 
Encephalitis, acute, 974. 
following arsenical poisoning, 976. 
of children, 977. 
aphasia with, 979. 
causes of, 979. 
contractures in, 979. 
epilepsy in, 979. 
symptoms of, 979. 
causative origin of, 973. 
chronic, 974. 
due to arsenical poisoning, 976. 
due to influenza, 129. 
due to salvarsan, 976. 
hemorrhagic, 974. 
cure of, 974. 
influenza hemorrhagic, 975. 
lumbar puncture in, 975, 977. 
meningo-encepbalitis, 974. 
paralysis with, 975. 
polioencephalitis superior, 975. 
polioenceplialomyelitis, 976. 
primary acute hemorrhagic, 976. 
prognosis of, 974. 
purulent. See Brain Abscess, 
secondary to acute infections, 973. 
suppurative. See Brain Abscess, 
traumatic, 974. 
with small brain abscesses, 974. 
Encephalopathy, in lead multiple neuritis, 
851'. 
lead, 1189. 
Endarteritis, specific, cerebral thrombosis 
with, 956. 1230 
INDEX 
Endarteritis, specific, in cerebral syphilis, 
42-43. 
spinal, 929. 
Endarteritis chronica deformans, 402. 
Endarteritis chronica nodosa, 402. 
Endocarditis, acute septic, avenues of en- 
trance of infecting agent, 472. 
benign and malignant types of, 473. 
cerebral form of, 476. 
chronic cardiac, 476. 
fulminating intermittent type of, 475. 
intermittent or pyemic form of, 474- 
475. 
involvement by, 473-474. 
origin of, 472. 
preceding valvular disease, 472. 
process of, 471-472. 
typhoid form of, 476. 
acute simple, 469. 
bacterial invasion of, 469. 
complications of, 470. 
duration of, 471. 
extent of damage done by, 469. 
involvement of, 469. 
physical signs of, 470-471. 
prominent lesion of, 469. 
relapses of, 470. 
and pneumonia, 167, 485. 
arteriosclerotic, 504. 
cerebral hemorrhage due to, 960-961. 
chronic, age in, 484. 
anatomic cure of valvular lesions in, 
493. 
blood condition in, 491. 
decompensation in, 482. 
degenerative process of, 478. 
dilatation in, 480. 
blood pressure in, 481. 
conditions of, 481. 
hypertrophy of left ventricle, 481. 
of left ventricle, 481. 
with aortic insufficiency, 481. 
dropsies in, 492. 
duration of, 494-495. 
frequency of valvular lesions in. 483. 
heredity and family history in, 483. 
inflammatory process of, 478. 
influence of treatment on prognosis 
of, 493. 
influence on, of cardiac asthma and 
dyspnea, 489. 
of erysipelas, 486. 
of induration of lung, 490. 
of infections, 485. 
of intercurrent diseases, 486. 
of marriage and pregnancy, 486-487. 
of pericarditis, 489. 
of pneumonia, 485. 
of respiratory diseases, 489. 
of tuberculosis. See Cardiovascular 
Tuberculosis, 
nature of, 477. 
nephritis with, 491. 
nervous system in, 492. 
occupation and social conditions in, 
484. 
prognosis of, 478. 
Endocarditis, chronic, prognosis of, com- 
pensatory hypertrophy, 479- 
480. 
reserve force of heart, 479. 
prognostic significance of physical 
signs, 494. 
psychic element in, 492-493. 
pulse in, 492. 
reaction of, to digitalis, 494. 
sex in, 483. 
skin condition in, 491. 
sudden death from, 493. 
valvular anomalies in, 493. 
with hypertrophy, 478. 
x-ray examination in, 492. 
due to arthritis, 283. 
gonococcus, 132, 190, 476. 
in chorea, 1042. 
in typhoid fever, 96. 
infections in, 471, 485. 
liver complications with, 491. 
malignant, 131, 284, 471, 486. 
mild, in children, with chorea and rheu- 
matism, 284. 
non-septic malignant rheumatic, 473. 
origin of, 468. 
pathology of, 468. 
scarlatinal, 330. 
severe, in children, with chorea and 
rheumatism, 284. 
syphilitic, 504. 
tuberculous, 275. 
ulcerative, 471. 
varieties of, 468. 
with cholelithiasis, 731. 
with diphtheria, 140. 
Endocarditis verrucosa, 469. 
Endothelioma, 999. 
primary, 1171. 
Enteric fever. See Typhoid Fever. 
Enteritis, acute, cholera morbus, 623. 
acute catarrhal, 619. 
constipation with, 620. 
diarrhea with, 620. 
due to ptomaine poisoning, 620. 
primary, 620. 
prognosis of, 620. 
recovery from, 620. 
secondary, 620. 
acute croupous, 621. 
acute diphtheritic, 621. 
acute membranous, 622. 
infantile, 623. 
infections in, 622. 
nervous or hysterical, 622. 
acute phlegmonous, 621. 
acute ulcerative, 621. 
constriction due to, 621. 
alcoholic, 1181. 
chronic, causes of, 623, 625. 
due to opium, 625. 
gastrogenic diarrhea, 624. 
intestinal dyspepsia dependent upon 
fermentation in, 624. 
of nervous origin, 625. 
of warm countries, 626. INDEX 
1231 
Enteritis, chronic, sprue, 626. 
croupous, 621. 
secondary chronic, primary causes of, 
625. 
tuberculous, 253. 
ulcerative tuberculous, 233. 
Enteropathia dyspeptica chronica, 624. 
Entozoa, of brain, 997. 
Eosinophilia, in chorea, 1041. 
Ephemeral fever, 350. 
Epidemic cerebrospinal meningitis, 177. 
Epilepsy, abortion of seizures in, 1052. 
amblyopia in, 1051. 
amnesia in, 1053. 
and pregnancy, 1051. 
and vertigo, 870. 
aura in, 1052. 
Babinski phenomenon in, 1052. 
complications in, 1052. 
convulsions of, 1047. 
course of, 1052. 
definition of, 1046. 
delirium of, 1053. 
dementia in, 1053. 
due to acute infections, 1051. 
due to alcoholism, 1050. 
due to cortical irritation, 1047-1048. 
due to dietetic errors, 1051. 
due to fright. 1051. 
due to sunstroke, 1051. 
due to syphilis, 1050. 
due to traumatism, 1050. 
essential or idiopathic, surgery for, 
1058. 
focal. See Secondary Epilepsy, 
jacksonian, 1047. 
following cerebral palsies of childhood, 
influence of heredity on produc- 
tion of, 977. 
grand mal, 1046. 
dislocation of humerus in, 1053. 
postepileptic period, 1054. 
recurrence of, 1054. 
in encephalitis, acute, of children, 979. 
insanity in, 1053. 
jacksonian, 1055. 
loss of self-control in, 1053. 
mania, with homicidal tendencies in, 
1053. 
mental lethargy in, 1053. 
merging of forms of, 1047. 
migraine with, 1062. 
nocturnal, 1054. 
ocular anomalies in, 1051. 
pathogenesis of, 1048. 
petit mal, 1046, 1055. 
postepileptic period in, 1054. 
posthemiplegic, 1050. 
primary, 1047. 
age in, 1048. 
due to alcoholism, 1050. 
due to syphilis, 1050. 
due to traumatism, 1050. 
family, 1049. 
heredity in, 1049. 
prognostic factors in, 1048. 
sex in. 1050. 
Epilepsy, prognostic factors in, diet, 1051. 
disordered nutrition, 1052. 
psychic, 1046, 1055. 
secondary, 1055. 
blood condition in, 1056. 
bromid treatment for, 1057. 
complicated by meningitis or men- 
ingo-encephalitis, 1055. 
complications in, 1056. 
course of, 1056. 
cure of, 1057. 
danger of death in attacks of, 1050. 
general condition of patient in, 
1057. 
manner of death in, 1056. 
operation for, 1055. 
pneumonia with, 1056. 
pulmonary edema with, 1056. 
pulmonary tuberculosis with, 1056. 
remissions and relapses in, 1057. 
with organic nervous disease, 1056. 
senile, 1049. 
status epilepticus in, 1054. 
syphilitic, 42, 1050. 
with hydrocephalus, 945. 
Epileptic convulsions, in lead enceph- 
alopathy, 1190. 
Epileptic equivalent, migraine with, 1062. 
Epileptic equivalents, 1046, 1055. 
in brain tumor, 994. 
Epileptiform seizures, 1047. 
hysterical, 1014. 
in multiple sclerosis of brain and cord, 
910. 
in tabes dorsalis, 59. 
Epinephritis, 835. 
Epistaxis, causes of, 359. 
in children, 360. 
in chronic interstitial nephritis, 809. 
in cirrhosis, 690. 
in typhoid fever, 97. 
Epithelial casts, 750. 
Erb’s paralysis, 876. 
Erb’s syphilitic spinal paralysis, 37. 
Erysipelas, albuminuria in, 176. 
and endocarditis, 486. 
blood condition in, 176. 
circulatory disturbances in, 175. 
complications influencing growth of, 
174. 
conclusions on, 176. 
etiology of, 173. 
in alcoholics, 174. 
in typhoid fever, 107. 
manifestations of, general, 175-176. 
local, 174. 
meningitis, purulent, with, 176. 
of aged, 174. 
of newborn, 174. 
parotitis, metastatic, with, 176. 
period of incubation of, 174. 
port of entry of, 173. 
puerperal, 174. 
respiratory system in, 176. 
streptococcus erysipelatis of, 173. 
with chronic disease, 174. 1232 
INDEX 
Erythema multiforme, alternation of 
chronic purpura with, 546. 
Erythema nodosum, 289. 
resemblance to, of purpura rheumatica, 
544. 
Erythremia, primary, associated condi- 
tions of, 550. 
blood picture of, 550. 
nature of, 549. 
symptoms of, 549. 
secondary, leading primary diseases of, 
551. 
prognosis of, 551. 
Ervthromelalgia, 415. 
and Raynaud’s disease, 1067. 
associated symptoms of, 1067, 1068. 
characteristic symptoms of, 1066. 
chronic, 1068. 
course of, 1068. 
definition of, 1066. 
destructive processes in, 1067. 
duration of, 1068. 
morphinism due to, 1069. 
pathological findings of, 1066. 
prognosis for life in, 1069. 
Esophageal stricture, benign, 566. 
congenital, 567. 
extra-esophageal, 566. 
malignant, 566. 
symptoms of, 567. 
Esophagismus, 565. 
hysterical, 1014. 
Esophagitis, acute, 562. 
catarrhal, acute, 562. 
chronic, 563. 
corrosive, 564. 
croupous, 564. 
diphtheritic, 564. 
phlegmonous, 563. 
pustular, 563. 
ulcerative, 564. 
Esophagus, cancer of, 566. 
dilatation of, 568. 
diverticula of, pressure or pulsation, 
569. 
traction, 569. 
diseases of, cancer, 567. 
dilatation*, 568. 
diverticula, 569. 
rupture, 568. 
spasm and paralysis of, 565. 
fibrous thickening of, 568. 
inflammatory or ulcerative changes of, 
562. 
lipomata of, 568. 
neoplasms of, 567. 
paralysis of, 565. 
polypi of, 568. 
rupture of, 568. 
spasm of, 565. 
syphilis of, 34. 
tuberculosis of, 253. 
varices of, 565. 
Estivo-autumnal fever. See Malaria. 
Exophthalmic goiter, atypical, 1148. 
relapse in, 1150. 
Exophthalmic goiter, clinical forms of, 
1140. 
compression of, for treatment, 1142. 
heredity in, 1141. 
in tuberculosis, 242. 
manipulation of, 1142. 
minimum symptoms of, cardiovascular, 
1139. 
sympathetic, 1139. 
tremor and singular ocular symptom, 
1139. 
mortality from, 1151. 
in operated cases, 1152. 
myxedema in, 1147. 
ocular symptoms in, 1145. 
operative treatment of, 1151. 
size of swelling in, 1145. 
symptoms of, 1139. 
typical, relapse in, 1150. 
typical acute, 1141. 
development of, 1141. 
gastro-intestinal symptoms in, 114w. 
mental torpor in, 1141. 
symptoms of, 1141. 
x-ray in, 1142. ' 
typical and atypical types of, 1140. 
typical chronic, acromegaly in, 1148. 
blood picture in, 1148. 
blood pressure study of, 1144. 
cardinal symptoms of, 1142. 
cardiovascular symptoms in, 1143. 
complications referable to nervous 
system in, 1143, 1146. 
digestive disturbances in, 1146. 
eye symptoms in, 1145. 
genito-urinary organs in, 1147. 
glucosuria and diabetes in, 1147. 
leading clinical manifestations of, 
1142. 
loss of weight in, 1146. 
mental state in, 1146. 
Musset’s phenomenon in, 1144. 
myxedema in, 1147. 
prognostic significance of leading 
clinical features in, 1143. 
pulse amplitude in, 1144. 
respiratory symptoms in, 1146. 
skin changes in, 1147. 
spasm in, 1144. 
sweating in, 1146. 
tremor in, 1144. 
Extensor paralysis, in lead multiple neu- 
ritis, 851. 
Extragastric bleeding, 613. 
Extrasystoles, irregularities due to, 448. 
Eye, affection of, in tabes dorsalis, 54, 
56. 
effect on, of arteriosclerosis, 415, 418. 
of cerebral syphilis, 43. 
of juvenile tabes, 47. 
of measles, 345. 
involvement of, in typhoid, 113. 
lesions of, in congenital syphilis, 67. 
Eye complications, in gout, 1105. INDEX 
1233 
Fibroid phthisis, chronic, non-tubercu- 
lous fibrosis with final tubercu- 
lization, 245. 
tuberculosis ab initio, 244. 
due to occupation, 380. 
in pneumonia, 166. 
Filariasis, 314-315. 
Filaton-Duke’s disease, 352. 
Fistulae, biliary, with gall stones, 730. 
bronchobiliary, with gall-stones, 730. 
in cholelithiasis, 728. 
urinary, with gall-stones, 730. 
Fixed thorax, in emphysema, 383. 
Flexner serum, for cerebrospinal menin- 
gitis, 184-185. 
Flint murmur, 501. 
Food poisoning, bacterial invasion of 
meat, contaminated sausage or 
pork, 1203. 
contaminated veal, 1203. 
symptoms of, 1203. 
conclusions on, 1204. 
due to fish and shell fish, 1204. 
due to milk products, 1204. 
endogenous, 1203. 
epidemics of, 1203. 
exogenous, 1203. 
leukomain, 1203. 
ptomain, 1203. 
Foot and mouth disease, conveyance of, 
349. 
healing process of, 349-350. 
nature of, 349. 
symptoms of, 349. 
Foramen ovale, perforate, 438. 
with pulmonary stenosis, 436. 
Friedreich’s disease. See ' Hereditary 
Ataxia. 
Fright, epilepsy due to, 1051. 
Fungus infections, non-bacterial, 301. 
Furuncles, in diabetes mellitus, 1118. 
in paratyphoid, 123. 
G 
Gall-bladder, acute inflammation of, 715. 
adhesions of, in cholelithiasis, 729. 
cancer of, 717. 
cholecystitis of, 715. 
dilatation of, due to stone in cystic 
duct, 726. 
dropsy of, 716, 726. 
enlargement of, in acute biliary colic, 
722. 
gangrene of, 717. 
in cholelithiasis, 728. 
perforation of, 717. 
in cholelithiasis, 728. 
tuberculosis of, 256. 
Gall-stones. See Cholelithiasis, 
bronchobiliary fistulae with, 730. 
cholangitis due to, 715. 
chronic cholecystitis due to, 716. 
Ganglionitis, acute posterior. See Herpes 
zoster. 
F. 
Facial hemiatrophy, causes of, 863. 
nature of, 863. 
Facial paralysis, 847. 
causes of, 863. 
character of, 863. 
crossed with hemiplegia, 866. 
double, 866. 
due to pontine disease, associated condi- 
tions of, 864. 
causes of, 864. 
in children, 866. 
location of, 863. 
peripheral, 864. 
reaction of degeneration in, 865. 
right-sided, with aphasia and hemi- 
plegia, 866. 
with family neuropathic tendencies, 866. 
Facial spasm, in neurasthenic and hyster- 
ical children, 866. 
in women, 867. 
tic habit due to, S66. 
Faint spells, of cerebral anemia, 948. 
Falling sickness, 1046. 
Fallopian aqueduct, hemorrhage into, 865. 
Fallopian tubes, tuberculosis of, 272. 
Famine fever. See Typhus Fever. 
Farcy. See Glanders. 
Fat deposits, in adiposis dolorosa, 1078. 
Fatty heart, associated conditions of, 453. 
causes of, 452. 
prognosis of, 453. 
Fatty liver, and enlargement, with per- 
nicious anemia, 712. 
degeneration of, 712. 
infiltration in, 712. 
with appendicitis, 712. 
with infectious diseases, 712. 
Febris epidemica. See Influenza. 
Febris recurrens. See Relapsing Fever. 
Fecal vomiting, hysterical, 1018. 
Fetal chondrodystrophy, 1131. 
Fetal cretinism, 1131. 
Fever, breakbone, 356. 
dandy, 356. 
enteric. See Typhoid Fever, 
ephemeral, 350. 
estivo-autumnal. See Malaria, 
glandular, 353. 
herpetic, 352. 
hysterical, 1018. 
intermittent. See Malaria. 
Mediterranean, 196. 
Neapolitan, 196. 
relapsing, 82. 
symptomatic, 350. 
thermic, 1206. 
typhoid, 84. 
typhus. See Typhus Fever, 
undulant, 196. 
Fibrinous bronchitis, 373. 
Fibroid degeneration, of myocardium, 443. 
Fibroid phthisis, 379. 
acute, 244. 
chronic, interstitial pneumonia, 246. 1234 
INDEX 
Gangrene, angiospastic. See Raynaud’s 
disease, 
diabetic, 1118. 
in cholecystitis, 717. 
in pharyngeal diphtheria, 137. 
pulmonary, in cancer, 387. 
in influenza, 127. 
in pneumonia, 164. 
in tuberculosis, 242. 
symmetrical. See Raynaud’s disease. 
Gangrene of vulva, in typhoid, 110. 
Garrod’s modification of Rothera test, for 
acetone, 1115. 
Gastralgia, 616. 
in dyspepsia, 616. 
Gastrectasia, 576. 
Gastric neuroses, general considerations 
on, 615. 
motor, due to hypermotility, 617. 
due to hypomotility, 617. 
psychic element in, 615, 619. 
psychoses with, 615. 
secretory anomalies of, 618. 
hyperacidity, 618. 
hypersecretion, 618. 
sensory, 616. 
Gastric tetany, 1167. 
Gastric ulcer, acid condition in, 587. 
acute and chronic, 587. 
age and type most affected by, 587. 
alcoholic, 1181. 
and duodenal, relative frequency of, 587. 
Aschoff’s hemorrhagic erosions in, 586. 
blood picture of grave anemia in, 596. 
carcinomatous, 589. 
carcinomatous degeneration in, 593. 
chronicity and resistance to treatment 
of, 588. 
complete, 590. 
complications in, acidosis, 596. 
carcinomatous degeneration, 593. 
cicatricial distortion and stenosis, 
595. 
exhaustion, 596. 
hemorrhage, 592. 
parotitis (metastatic?), 596. 
perforation, 590. 
perigastric adhesions, 595. 
tetany, 596. 
examination of stomach contents in, 
589. 
frequency of complications in, 598. 
hemorrhage in, large, into mucosa, 586. 
occurrence of, 592. 
repeated, 592. 
history of, 585. 
hourglass contraction in, 595. 
hyperchlorhydria symptomatic of, 588. 
indicanuria in, 588. 
mortality from, 597-598. 
paramount factors in cure of, 599. 
partial, 590. 
perforation of, “acute abdomen” in, 591- 
592. 
early operation for, 59\, 592, 599. 
frequency of, 590. 
Gastric ulcer, perforation of, importance 
of early diagnosis in, 591. 
into pleural cavity, heart sac or lung, 
591. 
prognosis of, 590-591. 
protective localized peritonitis in, 
591. 
protective processes in, 591. 
recovery after operation for, 592. 
symptoms of, 591-592. 
periods of remissions of symptoms, 
without healing of, 588. 
prognosis of, facts influencing, 587. 
general facts for, 586. 
significance of age and surgical treat- 
ment in, 597. 
proliferative changes produced by, 
588. 
symptoms of, 585. 
vomiting in, 589. 
with nephroptosis, 829. 
without subjective symptoms, 587. 
x-ray for, 589. 
Gastritis, acute, with organic diseases of 
stomach, 571. 
recurring, 572. 
acute forms of, acute catarrh, 570. 
corrosive, 571. 
of fungus origin, 572. 
infectious, 570. 
membranous, 571. 
phlegmonous, 570. 
suppurative, 572. 
toxic, 571. 
alcoholic, 575, 1181. 
chronic, associated with or secondary to 
cirrhosis, 573. 
blood picture in, 575. 
complications of, 576. 
examination of stomach contents in, 
574-575. 
mucosa in, 575. 
nervous symptoms of, 575. 
secondary to cirrhosis of liver, 573. 
symptoms of, 574. 
chronic forms of, cirrhotic, 572. 
interstitial, 573. 
mixed, 573. 
parenchymatous, 573. 
influenzal type of, 570. 
occult blood in stool in, 588. 
primary, 573. 
secondary, 573. 
severe, 576. 
Gastritis acida, 573. 
Gastroduodenitis, 620. 
Gastroduodenocholangitis, 665. 
Gastro-enteritis, in measles, 345. 
Gastrogenic diarrhea, 624. 
Gastro-intestinal diarrhea, 624. 
Gastro-intestinal influenza, 128. 
Gastro-intestinal symptoms, in alcoholism, 
1181. 
in neurasthenia, 1031. 
of pellagra, 1200. 
Gastro-intestinal pernicious malaria, 75. INDEX 
1235 
Gastro intestinal tetany, 1167. 
Gastroptosis, absence of tenth costal car- 
tilage in, 580. 
associated conditions in, 580-581. 
causes of, 580. 
Dietl’s crises in, 580. 
mobile kidney in, 580. 
nature of, 579. 
predisposition to, 579. 
prognosis of, 581. 
symptoms of, 580. 
Gastrorrhagia, 613. 
primary causes of, 614. 
Gastrostasis, 615. 
Gastrosuccorrhea, suggestive of ulcer, 
589. 
Gaucher’s disease, 1171. 
Genital atrophy, in infantilism, 1159. 
Genital tuberculosis, in females, blood 
condition of, 271. 
menstrual irregularities in, 271. 
of fallopian tubes, 272. 
ovarian, 272. 
primary, 272. 
uterine, 273. 
vaginal, 273. 
Genito-urinary system, in alcoholism, 
1182. 
in exophthalmic goiter, 1147. 
in typhoid fever, 107. 
Genito-urinary tuberculosis, 267. 
blood pressure in, 270. 
factors in prognosis of, 267. 
persistent fever with, 270. 
pregnancy and childbirth with, 270. 
German measles, complications in, 346. 
nature of, 346. 
Gibson’s rule, on blood pressure in pneu- 
monia, 148. 
Gingivitis, ulcerative, in scorbutus, 
1133. 
Glanders, acute, 212-213. 
chronic, 213. 
infection of, 212. 
prophylactic methods against, 213. 
Glandular fever, 353-354. 
Glenard’s disease, 579. 
Glioma, 924-925. 
of brain, 997. 
Gliomatosis, spinal, 925. 
Gliosis of spinal cord. See Syringomyelia. 
pseudotabetic, 917. 
Glomerulonephritis, chronic, 797. 
Glossitis, with pernicious anemia, 528. 
Glossopharyngeal paralysis, 870. 
Glottis, edema of, 362. 
in syphilis, 33. 
stenosis of, in syphilis, 33. 
Glucosuria, in alcoholics with polyneuritis, 
1118. 
alimentary, following anesthesia, 1110. 
following drinking of beer, etc., 1110. 
functional origin of, 1109. 
relation of, to diabetes, 1109. 
tolerance to sugar assimilation, 
1108, 
Glucosuria and diabetes, in exophthalmic 
goiter, 1147. 
due to adrenalin, 1107. 
due to anesthesia, 1110. 
due to hypophysis disease, 1107. 
due to liver disease, 1107. 
due to skeletal muscles, proteid and fat, 
1108. 
due to surgical lesions, 1119. 
due to thyroid extract, 1107. 
due to traumatism, 1108. 
in diabetes bronzg, 1107. 
in diabetes mellitus, 1106. 
in pancreatic disease, 1106. 
negative factors in, contagion, 1108. 
kidney, 1108. 
phloridzin, 1108. 
Gluteal nerves, paralysis of, 881. 
Goiter, acromegaly and, 1161. 
and hyperthyroidea, 1149. 
association of, 1137. 
with soil and water, 1138. 
complications in, 1138. 
distribution of, 1137. 
endemic, 1137. 
endemic areas in, 1137. 
exophthalmic. See Exophthalmic goiter, 
frequency of, 1137. 
heredity in, 1137. 
infections in, 1138. 
influencing factors in, 1137. 
return of, 1138. 
spontaneous recovery from, 1138. 
with lymphatic and nervous tempera- 
ment, 1138. 
Goiter heart, 1139-1149. 
Gonococcus arthritis, 192. 
Gonococcus endocarditis, 132, 190, 476. 
blood condition in, 191. 
clinical manifestations of, 190. 
complications in, 191-192. 
types of, intermittent or pyemic, 190. 
irregular, 191. 
typhoid, 190. 
Gonococcus infection, 132. 
gonococcemia, 189. 
gonococcus arthritis, 192. 
gonococcus endocarditis, 190. 
Gonorrhea, myelitis secondary to, 906. 
multiple neuritis, 855. 
rheumatism, 192. 
Gout, abarticular, 1103. 
acute, course of, 1102. 
determining symptoms of, 1102. 
duration of, 1102. 
evidences of approaching remission in, 
1102. 
initial symptoms of, 1101. 
monarthritic cases of, 1102. 
causative factors of, age, 1100. 
diet, 1101. 
habits, 1100. 
heredity, 1100. 
lead poisoning, 1101. 
lowered standard of health, 1101, 1236 
INDEX 
Gout, causative factors of, sex, 1100. 
chemical conclusions in, 1099. 
chronic, extent of joint changes in, 1103. 
limitation of, to joints, 1103. 
ulcerative articular processes in, 1103. 
chronic articular, 1103. 
complications in, cardiac, 1104. 
dyspepsia, 1104. 
gastro-intestinal, 1104. 
kidney, 1104-1105. 
liver, 1105. 
of eye, 1105. 
of nervous system, 1104. 
pulmonary, 1105. 
skin lesions, 1104. 
definition of, 1099. 
diabetes mellitus and, 1119. 
history of, 1099. 
in cirrhosis, 695. 
irregular, 1103. 
complications in, 1104. 
theories on, Brugsch, 1099. 
Epstein, 1098. 
Gar rod, 1098. 
Haig, 1098. 
Klemperer, 1098. 
Kolisch, 1098. 
Luff, 1099. 
Mordhorst. 1098. 
von Noorden, 1098. 
Roberts, Sir William, 1098. 
Schittenhelm, 1099. 
uric acid phenomenon in, 1099. 
Gouty conditions, in tuberculosis, 242. 
Grand mal, 1046. 
humerus in, 1053. 
Granular casts, 749-750. 
Granuloma, syphilitic, 541. 
Graves’ disease, 249, 1142. 
Green sickness, 517. 
Grippe. See Influenza. 
H 
Habit paralysis, 847. 
Hay fever, blood picture of, 358. 
nature of, 358. 
surgical treatment for, 359. 
use of cocaine for, 359. 
vaccination against, 359. 
Headache, bilious. See Migraine, 
blind. See Migraine, 
hysterical involvement of, 1011. 
in brain tumor, 992. 
sick. See Migraine. 
Heart, aneurism of, 467. 
congenital defects of, defective inter- 
ventricular septum, 438. 
dextrocardia, 438. 
insufficiency and stenosis of mitral 
and tricuspid valves, 439. 
perforate and premature closure of 
ductus arteriosus, 439. 
perforate foramen ovale, 438. 
stenosis of aortic orifice, 438. 
Heart, congenita] defects of, stenosis of 
pulmonary orifice, 435. 
transposition of aorta and pulmonary 
arteries, 439. 
delirious, 510. 
fatty, 452. 
functional disorders of, bradycardia, 
511. 
causes of, 506-507. 
neurasthenic state, 512. 
palpitation, 507. 
tachycardia, simple, 510. 
hypertrophy and dilatation of, 460. 
hypertrophy of, idiopathic, 441. 
inherent muscular weakness of, 465. 
irritable, 510. 
palpitation of, 507. 
parasites of, 466. 
senile, 460. 
syphilis of, 28. 
Heart anomalies, in chorea, 1042. 
Heart block. See Stokes-Adajns disease. 
Heart changes, degenerative, in al- 
coholism, 1182. 
in chronic interstitial nephritis, 806- 
807. 
in gout, 1104. 
in measles, 345. 
Heart condition, in appendicitis, 653. 
in cirrhosis, 687. 
in leukocytic leukemia, 532. 
in pernicious anemia, 526. 
Heart disease, hemoptysis of, 376. 
causing congested kidney, 812. 
Heart weakness, due to insufficient ex- 
ercise, 464. 
Heatstroke. See Sunstroke. 
Heberden’s nodes, in arthritis deformans, 
1091. 
Heine-Medin disease. See Poliomyelitis, 
317. 
Hemachromatosis, with pigmented cir- 
rhosis, 696. 
Hematemesis, hysterical, 614. 
in cancer of stomach, 604. 
in cirrhosis, 689. 
primary causes of, 613-614. 
Hematoma, spinal, 931. 
Hematomyelia, 930. 
spontaneous, 930. 
Hematorrhachis, 930. 
Hematuria, conditions indicated by, 755. 
acute and chronic primary infections, 
759. 
constitutional diseases, 760. 
echinococcus disease. See Cestodes. 
hemorrhagic, with infections, 760. 
nephritis, tuberculous, 759. 
acute tubal, 756. 
chronic interstitial, 756. 
chronic tubal, 756. 
new growth of kidney, 760. 
paroxysmal hematuria following chill- 
ing of surface, 758. 
pyelitis, non-calculous, 759. 
renal epistaxis, 757. INDEX 
1237 
Hematuria, conditions indicated by, renal 
hematuria with gouty diath- 
esis, 758'. 
renal infarct, with septic fever, 758. 
rupture of kidney, 760. 
stone in kidney, 759. 
cystoscopic examination in, 753. 
effects of, 754. 
essential, 757. 
in cirrhosis, 690. 
origin of, 753. 
paroxysmal, following chilling of sur- 
face, 758. 
with chronic nephritis, 801. 
renal, 754. 
with gouty diathesis, 758. 
Hemianesthesia, hysterical, 1009-1010. 
in cerebral hemorrhage, 969. 
Hemianopia, bilateral vertical, 858. 
binasal, 859. 
bitemporal, 858. 
blindness due to, 859. 
double, 858. 
functional, with migraine or hysteria, 
859. 
in cerebral hemorrhage, 970. 
lateral or homonymous, 859. 
one-sided, 858. 
temporal, 858. 
Hemiataxia, in cerebellar disease, 1004. 
Hemiatrophy, facial, 863. 
Hemicrania. See Migraine. 
Hemicrania sympatheticotonica, 1062. 
Hemicrania sympatheticoparalytica, 1062. 
Hemihypotonia in cerebellar disease, 1004. 
Hemiplegia, cerebral hemorrhage sup- 
posed cause of, 958. 
due to cerebral embolism and diphtheria, 
954. 
in brain tumor, 991. 
in cerebral hemorrhage, 969. 
in cerebral syphilis, 43. 
in diphtheria, 954. 
in diphtheritic paralysis, 141. 
in syphilis, 43. 
spastic infantile, 977. 
with aphasia and facial paralysis, 866. 
Ilemocytozoa, 72. 
Hemoglobinuria, paroxysmal, 761. 
periodic, 761. 
toxic, 761. 
Hemopericardium, 433. 
Hemophilia, 548. 
hemoptysis of, 377. 
Hemoptysis, in cirrhosis, 690. 
of bronchitis, 377. 
of heart disease, 376. 
of hemophilia, 377. 
of hyperemia, 376. 
Hemorrhage, anemia due to, 514. 
cerebellar, 1003. 
cerebral, 957. 
danger point in, 515. 
extragastric, 614. 
in cholelithiasis, 731. 
in gastric ulcer, 586-592. 
Hemorrhage, into spinal membranes and 
cord. See Spinal hemorrhage, 
intragastric, 614. 
pulmonary. See Pulmonary Hemor- 
rhage. 
regeneration from, 515-516. 
retinal, with pernicious anemia, 527. 
Hemorrhagic diathesis. See Purpura. 
Hemorrhagic pancreatitis, 737. 
Hemorrhagic pleurisy, 396. 
Hemorrhagic symptoms, of pharynx, 559. 
Hemosporidia, 72. 
Henoch’s purpura, 547. 
Hepatic and intra-liepatic ducts, obstruc- 
tion of, 726. 
Hepatic artery, diseases of; aneurism, 
680. 
arteriosclerosis, 680. 
embolism, 680. 
enlargement, 681. 
thrombosis, 680. 
Hepatic calculi. See Cholelithiasis. 
Hepatic vein, diseases of, complete oc- 
clusion, 679. 
thrombosis, 679. 
Hepatitis, suppurative, 704. 
Hereditary ataxia, complications in, 888. 
course of, 887. 
Marie’s, 888. 
nature of, 887. 
symptoms of, 887. 
Hernia, hiccough with, 875. 
Herpes labialis, in pneumonia, 161. 
Herpes zoster, accompanying symptoms 
of, 886. 
classification of, 885. 
confluence in, 886. 
course of, 886. 
definition of, 885. 
duration of, 886. 
epidemics of, 885. 
hemorrhagic form of, 886. 
malignant, 886. 
sacral, 886. 
vesicles and inflamed base of, 885. 
Herpetic fever, 352. 
Herxheimer reaction, in edema of glottis, 
33. 
Hiccough, causes of, 875. 
easily controlled, 875. 
hysterical, 875. 
in appendicitis, 653. 
indicative of virulent infection, 875. 
with deep coma, 875. 
with hemorrhagic pancreatitis, 875. 
with hernia, 875. 
with inflammatory disease, 875. 
with peritonitis, 875. 
with toxemia, 875. 
with typhoid fever, 875. 
Hippocrates, aphorisms of, 2. 
genuine treatises of, 3. 
rules of practice of, 2. 
Hirschsprung’s disease, 632, 640. 
Hodgkin’s disease, acute, 538. 
latent type of, 539. 1238 
INDEX 
Hodgkin’s disease, acute, non-relapsing, 
538. 
Pel and Ebstein’s process of, 538.. 
relapsing, 538. 
chronic, blood picture in, 539. 
bronzing of skin in, 539. 
duration of, 540. 
hemorrhagic symptoms of, 541. 
mediastinal glands in, 539. 
periode cachectique of, 540. 
periode latente of, 540. 
periode progressive of, 540. 
remissions in, 540. 
definition of, 536. 
diphtheroid organism in, 537. 
distinguished from tuberculous lymph- 
adenitis, 266. 
leading causes of death from, 541. 
pathologic changes in lymph glands in, 
537. 
resemblance of, to tuberculosis, 537. 
surgical treatment of, 541. 
symptom-complex of granuloma, 538. 
symptom-complex of lymphocytoma, 
537. 
Hookworm. See Ankylostomiasis. 
Hourglass stomach, in gastric ulcer, 595. 
Huntington’s chorea, 1044. 
Hutchinsonian teeth, 67. 
Hyaline casts, 749, 751. 
Hydatid disease, cause of, 306. 
cysts of, 306. 
of brain, 308. 
of kidney, 308. 
of liver, death due to, 308. 
latent, 307. 
perforation in, 307. 
suppuration, 307. 
of lung, 308. 
of other organs, 309. 
of spleen, 308. 
Hydrocephalus, acquired, acute exacerba- 
tions with, 943. 
chronic, 943. 
simulating brain tumor, 943. 
symptoms of, 943. 
congenital, 67. 
appearance of, 944. 
arrested, 944. 
causes of, 944. 
complications in, 945. 
death due to intercurrent disease in, 
945. 
duration of, 944. 
effect of, on intelligence, 945. 
family type of, 944. 
menstrual anomalies in. 945. 
moderate, 945. 
spinal fluid in, 945. 
spontaneous rupture of, 944. 
syphilitic, 944-945. 
due to epidemic cerebrospinal menin- 
gitis, 182. 
epilepsy with, 945. 
idiopathic internal, 943. 
Hydromvelus, 914. 
Hydronephrosis, acquired, 816, 817, 
Hydronephrosis, acute infection with, 818. 
advanced, prognosis of, 819. 
anuria in, 817. 
bilateral, 817. 
causes of, 815. 
cause of death in, 817. 
chronic, 818. 
complications in, 818. 
congenital, causes of, 816, 
operation for, 819. 
prognosis of, 818. 
definition of, 815. 
early recognition of, 818. 
genera] condition of patient in. 818. 
intermittent, 820. 
nephrectomy for, 819. 
prognostic conclusions on, 819. 
prognostic factors in, 810. 
purulent, 818. 4 
rupture of, 818. 
secondary bladder and ureteral changes 
in, 820. 
unilateral, condition of second kidney 
in, 818. 
prognosis of, 819. 
uremia due to, 818. 
with nephroptosis, 829. 
Hydropericardium, 274. 433. 
Hydrophobia, nature of, 354. 
Pasteur treatment of, 355. 
period of incubation of, 354-355. 
prognosis of, 355. 
stages of, 355. 
statistics on, 356. 
symptoms of, 355. 
Hydropneumothorax, 396. 
Hydrops articulorum, 1079. 
Hydrops articulorum intermittens, 1079. 
Hydrothorax, 396. 
associated symptoms of, 396. 
causes of, 396. 
Hyperacidity, 618. 
Hyperchlorhydria, 618. 
Hyperemia, hemoptysis of, 376. 
of brain. See Cerebral Hyperemia, 
of kidney, 811. 
of liver, active, 676. 
passive, 676. 
of pharynx, 559. 
of spinal cord, 928. 
Hyperesthesia, 616. 
Hyperesthetic areas of Head, 840. 
Hypermotility, belching of gas in, 617. 
nervous vomiting in, 617. 
peristaltic unrest of Kussmaul in, 617. 
pylorospasm in, 617. 
rumination in, 617. 
Hypernephroma, 826. 
Hyperosmia, 857. 
Hvperostoses, diffuse, 1094. 
of skull, 1095. 
Hyperpeptica, 573. 
Hyperpituitarism, 1160. 
Hyperpyrexia, in acute biliary colic, 721. 
in sunstroke. 1205. 
with arthritis, 286. INDEX 
1239 
Hypersecretion, 618. 
Hypertension, compensatory, in chronic 
nephritis, 802. 
in chronic interstitial nephritis, 806- 
807-808. 
Hyperthyroidea, atypical, 1148-1149. 
clinical features of anomalous types of, 
1140. 
chronic typical, 1142. 
due to degeneration of innocent small or 
large chronic goiters, 1140. 
exophthalmic goiter, 1139. 
goiter and, 1149. 
in children, 1151. 
mortality from, 1151. 
in operated cases, 1152. 
myxedema-cretinism, 1153. 
protean character of, 1140. 
psychic element in, 1151. 
self-limitation of, 1150. 
spontaneous cure of, 1150. 
symptoms of, without goiter, 1139. 
thymus enlargement in, 1145. 
thyroid neoplasm in. 1150. 
Hypertrophic muscular dystrophy, 896. 
Hypertrophy, and dilatation of heart, due 
to hypertension, 461. 
due to overstrain, 460. 
compensatory, in chronic nephritis, 802. 
of heart, due to masturbation, 462. 
due to uterine fibroids, 462. 
idiopathic, 441. 
secondary to other conditions, 462. 
of left ventricle, in chronic interstitial 
nephritis, 806. 
Hypnosis, for hysteria, 1009. 
Hvpochlorhydria, 618. 
Hypochondriasis, sexual, 1028. 
Hypoglossal paralysis, causes of, 873-874. 
symptoms of, 873. 
Hypomotilitv, 617. 
pyloric insufficiency with, 617. 
Hypoparathyroidism, 1035. 
Hypophvsis, disease of, glucosuria due to, 
1107 
Hypopituitarism, 1158. 
Hvpostatic congestion, in typhoid fever, 
98. 
Hypotonia, in tabes dorsalis, 56. 
Hysteria, acquired predisposition to, 1007. 
akinesia algera in, 1017. 
amnesia in, 1009. 
anomalous mental states of, 1015. 
appetite in, perverted, 1017. 
associated with organic disease, 1019. 
atasia-abasia in, 1016. 
bradycardia of. 1019. 
cataleptic conditions in, 1016. 
“cathartic method” of Freud for, 1008. 
constipation of, 1017. 
contractures of, 1014. 
contradictory nature of symptoms of, 
1009. 
cough of, 1018. 
death never due to, 1020. 
diarrhea of, 1017. 
Hysteria, duration of psychoses in, 1009. 
element of suggestion in, 1007. 
emotional element in, 1009. 
favorable influence of change on, 1020. 
fecal vomiting of, 1018. 
fever of, 1018. 
forecast of behavior of individual 
symptoms in, 1007, 1008. 
general prognosis of, 1020. 
“grande hysterie” of Charcot, 1010. 
hearing, involvement of, 1011. 
hypnosis for, 1009. 
hypnotic conditions of, 1016. 
improvement of social status in, 1015. 
in tabes dorsalis, 59. 
influence of etiology on control of symp- 
toms in, 1006. 
inherited predisposition to, 1007. 
internal organs in, 1017. 
joint manifestations of, 1015. 
latency of symptoms in, 1008. 
loss of muscular sense in, 1016. 
membranous colitis of, 1018. 
Meniere symptoms in, 869. 
menstrual anomalies of, 1018. 
mimicry of cancer by, 1017. 
monoparalysis of, 1013. 
mutability of symptoms in, 1006. 
ocular anomalies of, amblyopia, 1012. 
asthenopia, 1012. 
blindness, 1012. 
contractures of ocular muscles, 1013. 
contraction of visual field, 1011. 
errors of accommodation, 1012. 
faulty color perception, 1012. 
palpebral and bulbar, 1013. 
paralysis of eyelids, 1013. 
paralysis of ocular muscles, 1013. 
pupillary phenomenon, 1013. 
organic disease following, 1020. 
pains of, simulating organic disease, 
1010. 
paralysis of, 1013. 
of vocal cords, 1014. 
previous history in, 1007. 
psychic disturbances or events in, 1007. 
psychical nature of, 1005-1006. 
psychic-sexual factors in, 1007-1008. 
psychopathic and neuropathic condition 
in, 1006. 
recurring autosuggestion in, 1005. 
reflex excitability in, 1015. 
secretory dsturbances of, 1018. 
sensory disturbances due to anesthesia, 
1009-1010. 
hemianesthesia, 1009-1010. 
pain, 1010. 
special senses, 1011. 
various, 1009. 
sexual anomalies of, 1018. 
simulating organic diseases, 1005, 1019. 
smell, perversion of, 1011. 
spasms of, epileptic, 1014. 
esophagismus, 1014. 
various forms of, 1014. 
special senses in, hearing, 1011. 1240 
INDEX 
Hysteria, special senses in, sight, 1011. 
smell, 1011. 
taste, 1011. 
stigmata of Charcot in, 1005. 
sudden cessation of svmptoms in, 1007- 
1008. 
tachycardia of, 1019. 
taste, perversion of, 1011. 
torticollis in, 1019. 
traumatic. See Traumatic Neurosis, 
1021. 
trophoneuroses of, 1018. 
vasomotor disturbances of, 1018. 
vomiting of, 1017. 
Hysterical temperament, 1015. 
grave mental disease with, 1016. 
social status in, 1015. 
Hystero-epilepsy, 1014. 
I 
Icterus, 664. 
Icterus gravis, 674. 
Icterus neonatorum, grave familial, 671. 
infections, 671. 
mortality from, 672. 
obstructive, due to organic lesions in 
duct or liver, 671. 
physiologic, 670. 
Idiocy, amaurotic family, cause and pa- 
thology of, 903. 
symptoms of, 903. 
Idiopathic hypertrophy of heart, 441. 
Indian Kala-azar, 83. 
Indicanuria, and constipation, 781. 
associated with gastro intestinal indi- 
gestion, 780. 
auto-intoxication, 780. 
bacterial action in, 782. 
conditions indicated by, 781. 
due to lesions of intestinal mucosa, 781. 
in appendicitis, 654. 
in duodenal ulcer, 588. 
process of, 780. 
prognostic significance of, 780. 
Infantile convulsions, causes of, 1065. 
cerebral hemorrhage due to, 960. 
influence of, on acute infections, 1065. 
predisposition to, 1065. 
serious nature of, 1066. 
symptomatic natur.e of, 1065. 
Infantile Kala-azar, 83. 
Infantile paralysis. See Poliomyelitis, 317. 
Infantilism, adiposity in, 1159. 
ateliosis in, 1159. 
cause of, 1158. 
cretinoid, 1159. 
general, 1159. 
general adiposity and undeveloped gen- 
itals in, 1159. 
genital atrophy in, 1159. 
of Frohlich type, 1159. 
partial, 1159. 
prognosis of, 1160. 
progeria in, 1159. 
types of, 1159, 
Infections, acute, congested kidney due to, 
811. 
tetany associated with, 1167. 
acute and chronic primary, hematuria 
due to, 759. 
influence of, on endocarditis, 485. 
neuralgia due to, 839. 
Infectious diseases, specific, bacterial, an- 
thrax, 209. 
Asiatic cholera, 197. 
bacillary dysentery, 193. 
diphtheria, 134. 
epidemic cerebrospinal meningitis, 
177. 
erysipelas, 173. 
glanders, 212. 
gonococcus infections, 189. 
influenza, 124. 
leprosy, 214. 
malta fever, 196. 
metastatic parotitis, 300. 
paratyphoid disease, 121.# 
plague, 201. 
pneumococcus infection, 145. 
pyogenic infections. 130. 
rheumatic fever, 278. 
tetanus, 206. 
tonsillitis, 292. 
tuberculosis, 216. 
typhoid fever, 84. 
typhus fever, 117. 
of doubtful or unknown origin, dengue, 
356. 
ephemeral fever, 350. 
foot and mouth disease, 349. 
fourth disease, 352. 
German measles, 346. 
glandular fever, Pfeiffer’s disease, 353. 
herpetic fever, 352. 
hydrophobia, 354. 
infectious jaundice, 350. 
measles, 342. 
parotitis, epidemic, 352. 
poliomyelitis, 317. 
scarlet fever, 327. 
smallpox, 333. 
sweating sickness, 351. 
varicella, 341. 
yellow fever, 347. 
due to metazoan parasites, cestodes, 
303-304. 
nematodes, 309. 
irematodes, 316. 
non-bacterial fungus, actinomycosis, 
301. 
protozoan, amebic dysentery, 78. 
Leishmaniasis, 83. 
malaria, 72. 
relapsing fever, 82. 
syphilis, 15. 
trypanosomiasis, 81. 
Infectious jaundice, 350. 
Inflammatory rheumatism. See Rheu- 
matic Fever. 
Influenza, and neurasthenia, 1027, 
bacteriology of, 125. INDEX 
1241 
Influenza, catarrhal, 125. 
albuminuria with, 125-126. 
bronchiectasis with, 127. 
bronchitis with, 127. 
complications in, 125-126. 
ear complications in, 128. 
enlarged spleen of, 125. 
gangrene of lung with, 127. 
pleurisy with, 127. 
pneumonia with, 126. 
pulse and heart changes with, 127. 
tuberculosis with, 127. 
character of, 124. 
epidemics of, 124. 
gastro-intestinal, 128. 
mortality from, 125. 
of nervous system, complications due to 
organic change in, 129. 
primary invasion by, 129. 
respiratory, 125. 
Influenzal brain abscess, 129. 
Influenzal fever, 130. 
Influenzal meningitis, pneumonia with, 
126-127. 
Influenzal pneumonia, 126-127. 
chill with, 151. 
migratory type of, 126. 
Infraclavicular paralysis, 877. 
Insanity, due to psychasthenic states, 
1030. 
in epilepsy, 1053. 
Insolation. See Sunstroke. 
Intercostal neuralgia, 842. 
Intermittent claudication, 414. 
Intermittent fever. See Malaria. 
Interventricular septum, 438. 
Intestinal changes, in alcoholism, 1181. 
Intestinal dyspepsia, dependent upon fer- 
mentation, 624. 
Intestinal hemorrhage, in amebic dysen- 
tery, 80. 
in paratyphoid, 123. 
in typhoid fever, 102, 103, 104. 
Intestinal obstruction, complete acute, 
635. 
complete, causes of, 634-635. 
extra intestinal pressure, 639. 
fecal accumulations, 639. 
intussusception, 637. 
strangulation, 636. 
stricture, 638. 
tumors or foreign bodies in bowels, 
638. 
volvulus, 637. 
of large intestine, 634. 
of small intestine, 634. 
symptoms of, 635. 
due to appendicitis, 656. 
in cholelithiasis, 729, 731. 
nature of, 633. 
partial, causes of, 633-634. 
chronic adynamic, 634. 
symptoms of, 633. 
Intestinal parasites, in beriberi, 1201. 
Intestinal stricture, due to carcinoma, 
638. 
Intestinal stricture, due to cicatrization, 
638. 
due to congenital defects, 638. 
due to multiple ulcers, 621. 
Intestinal toxemia, chronic, 781. 
Intestinal tuberculosis, 253. 
primary, 253. 
secondary, 254. 
Intestines, affection of, in congenital 
syphilis, 67. 
diseases of, cancer and other growths, 
642. 
celiac disease, 629. 
constipation, 630. 
diarrheal, of early childhood, 627. 
dilatation of colon, 640. 
diverticulum, 641. 
enteritis, acute, 619. 
enteritis, chronic, 623. 
enteroptosis, 579. 
obstruction, 633. 
new growths of, 642. 
polypoid growths of, 644. 
sarcoma of, 644. 
strangulation of, 636. 
syphilis of, 34. 
Intoxication impulse, 1175, 1177. 
Intoxications, alcoholism, 1175. 
arsenical poisoning, 1193. 
beriberi, 1201. 
carbon monoxid poisoning, 1196. 
cocainism, 1187. 
food poisoning, 1203. 
lead poisoning, 1187. 
mercurial poisoning, 1195. 
morphinism, 1185. 
pellagra, 1197. 
Intra-esophageal stenosis, 566. 
Intussusception, 637. 
Invagination, 637. 
Iodin, purpura from administration of, 
543. 
Iodothyroidism, acute, 1142. 
Irritation of cervical sympathetic, 1082. 
Ischemia, 514. 
Ischio-reetal tuberculosis, 257. 
J 
Jacksonian epilepsy, 1055. 
Jail fever. See Typhus Fever. 
Jarisch-Herxheimer reaction, in svphilis, 
21. 
Jaundice, associated conditions of, 666- 
667. 
black, 667. 
catarrhal, 665. 
chronic, prognosis of, 667. 
deep, 666. 
epidemic catarrhal, 350, 667. 
hemo-hepatogenous, 668. 
causes of, cerebral, 669. 
infectious diseases, 669. 
poisons and drugs, 669. 1242 
INDEX 
Jaundice, hemo-hepatogenous, causes of, 
splenomegaly, 669. 
sudden hemolysis, 669. 
conditions indicated by, 669. 
hemolytic, 668. 
influence of spleen on, 668. 
hepatogenous, causes of, 664. 
hereditary splenomegalic, 670. 
in cancer of liver, 709. 
in cirrhosis, 692, 700. 
infectious, 350. 
in newly born, grave familial, 671. 
infections, 671. 
mortality from, 672. 
obstructive, due to organic lesions 
in duct or liver, 671. 
physiologic, 670. 
in syphilis of liver, 30. 
in typhoid fever, 105. 
malignant, 673. 
nature of, 664. 
obstructive, 664. 
primary diseases of, 666. 
prognostic factors in, feces, 666. 
urine, 665. 
syphilitic, 670, 672. 
toxic, 668. 
with biliary colic, 721. 
Joint complications, in amebic dysentery, 
80. 
Joints, diseases of, polyarthritis, de- 
structive chronic, 1088. 
hysterical, 1015. 
intermittent dropsy of, 1079. 
Juvenile paresis, 65. 
K 
Kahler’s disease, 1134. 
Kala-azar, 83. 
Kidney, abscess of, 833. 
amyloid, 814. 
arteriosclerotic, 805. 
benign growths of, 827. 
congested, 811. 
contracted, 805. 
contracted granular, 804. 
cyanosed, 811. 
effect of, 813. 
urine of, 813. 
cysts of, 827. 
diseases of, amyloid kidney, 814. 
anomalies of urinary secretion, al- 
buminuria, 741. 
alkaptonuria, 786. 
bacilluria (bacteriuria), 774. 
casts, 749. 
chyluria, 776. 
cystinuria, 785. 
hematoporphyrinuria, 787. 
hematuria, 753. 
indicanuria, 780. 
lipaciduria, 787. 
lipuria, 777. 787. 
lithuria, 785. 
melanuria, 786. 
Kidney, diseases of, anomalies of urinary 
secretion, oxaluria, 779. 
phosphaturia, 777. 
pneumaturia, 787. 
uremia, 762. 
urobilinuria, 782. 
congested kidney, 811. 
movable, 828. 
neoplasm, 825. 
nephritis, acute parenchymatous, 
788. 
chronic interstitial, 804. 
chronic parenchymatous, 797. 
perinephric abscess, 834. 
pyelitis, 829. 
fibrosis of, 804. 
floating, 828. 
gouty, 804. 
hydatid cysts of, 308. 
hyperemia of, 
in scarlet fever, 331. 
large white, 797. 
malignant growths of, carcinoma, 825. 
prognosis of, 826. 
sarcoma, 825. 
congenital, 826. 
movable, 828. 
neoplasm of, 825. 
new growths of, hematuria with, 760. 
papilloma of, 826. 
polycystic, leading symptoms of, 827. 
nature of, 8£7. 
operation for, 827. 
unilateral, 827. 
pus in, 832. 
drainage of, 834. 
red granular, 805. 
rupture of, hematuria with, 760. 
secondary contracted, 797, 804. 
senile, 805. 
surgical diseases of, hvdronephrosis, 
815. 
nephrolithiasis, 820. 
syphilis of, 31. 
waxy, 814. 
Kidney complications, in gout, 1104-1105. 
Kidney fixation, 828. 
Kidney invasion, in arteriosclerosis, 411. 
King’s evil, 265. 
Klebs-Loeffler Bacillus, 134. 
Klumpke’s paralysis, 877. 
Korsakoff’s psychosis, in alcoholic multi- 
ple neuritis, 849. 
in alcoholism, 1182. 
Kossel’s conclusions, on tuberculosis, 219. 
Kundrat’s disease, 538. 
Kussmaui. unrest of, in hypermotility, 
617. 
L 
Labyrinthine disease. See Aural Vertigo. 
Lactosuria, relation of, to diabetes, 1109. 
Landry’s paralysis, 322, S54. 
Lardaceous disease, 814. 
Laryngeal diphtheria, 136, 138. INDEX 
1243 
Laryngeal lupus, 252. 
Larvngeal tuberculosis, and pulmonary, 
251. 
chronic, 251. 
early recognition of, 251. 
miliary deposit in, 251. 
pregnancy in, 251. 
primary, 250. 
secondary process of, 250. 
tendency to infiltration in, 250. 
“tuberculoma” in, 251. 
ulcerations in, 251. 
Laryngismus stridulus, deaths from, due 
to status thvmolymphaticus, 
363. 
in adults, 363. 
in children, 362. 
Larvngitis, acute, catarrhal, in children, 
360. 
factors in relief of, 361. 
primary, 360. 
catarrhal, in typhoid fever, 97. 
causes of, 360. 
chronic, 361. 
associated conditions of, 361. 
primary, 361. 
edematous, 362. 
in measles, 344. 
secondary, 360-361. 
spasmodic, 362. 
syphilitic. See Syphilitic Laryngitis, 
tuberculous, 234, 241, 251. 
Laryngoscope, use of in edema of larynx, 
362. 
Larynx, diseases of, edema, 362. 
laryngismus stridulus, 362. 
laryngitis, acute, 360. 
chronic, 361. 
syphilitic. See Syphilitic Laryngi- 
tis. 
tuberculous, 363. 
edema of, causes of, 362. 
laryngoscope in, 362. 
Lateral and posterior disease, combined. 
See Ataxic Paraplegia, 901. 
Lead encephalopathy, associated condi- 
tions of, i 190. 
recurrence of, 1190. 
symptoms of, 1189. 
Lead multiple neuritis, 850. 
Lead palsy, 1189. 
Lead poisoning, acute, 1187. 
arteriosclerosis due to, 406. 
blood picture in, 1190-1191. 
chronic, 1187. 
chronic nephritis due to, 798. 
colic of, 1188. 
conditional symptoms with, 1188. 
encephalopathy, 1189. 
gout due to, 1101. 
influencing factors in, age, 1188. 
heredity, 1188. 
sex, 1188. 
occupational influence in, 1188. 
palsy, 1189. 
saturnine anemia in, 1190. 
saturnine arteriosclerosis in, 1192. 
Lead poisoning, saturnine arthralgia in, 
1189. 
saturnine nephropathy in, 1192. 
with cerebial anemia, 948. 
Lenticular degeneration, progressive, 695. 
Leontiasis ossea, 1095. 
Leprosy, anesthetic type of, 215. 
history of, 214. 
infection of, 214. 
mixed type of, 216. 
non-hereditary character of, 214. 
period of incubation of, 214. 
relapse of, 216. 
sexual intercourse in, 215. 
tubercular, fever in, 215. 
skin and hair in, 214-215. 
Wassermann reaction in, 215. 
Leptomeningitis, 277. 
purulent, as complication of disease, 
938. 
basilar, 939. 
causes of, 938. 
duration of, 942. 
lumbar puncture in, 941. 
metastatic, 938. 
microorganisms causing, 938. 
postbasilar, 939. 
prognosis of, 939-940-941. 
symptoms of, 939-940. 
with metastatic parotitis, 939. 
serous, chronic, 946. 
hydrocephalus, acquired, 943. 
congenital, 944. 
serous meningitis, 943. 
spinal. See Spinal Leptomeningitis, 
symptoms of, in poliomyelitis, 323. 
Leube rule, for early diagnosis of cancer, 
603. 
Leukanemia, 534. 
Leukemia, acute, 534. 
complications in, 535. 
influence of treatment on prognosis of, 
535. 
leukanemia (Leube), 534. 
leukocytic, blood picture of, 530. 
definition of, 530. 
myelocytic count in diagnosis of, 532. 
symptoms of, 532. 
cardiac, 532. 
in final stages, 532. 
priapism, 532. 
splenic, 531-532. 
urinary, 532. 
lienal. See Leukemia, Leukocytic, 
lymphatic, blood picture in, 533. 
chloroma with, 533. 
essential features of, 533. 
symptoms of, 533. 
mixed forms of, 535. 
myelocytic. See Leukemia, Leukocytic, 
myeloid. See Leukemia, Leukocytic, 
remissions of, 535. 
resemblance to, of lymphoblastoma, 537. 
splenectomy in, 535. 
splenomyelogenous. See Leukemia, Leu- 
kocytic. 
transition of pseudo leukemia to, 541. 1244 
INDEX 
Leukemia, x-ray in, 535. 
Leukocythemia. See Leukemia, Lym- 
phatic. 
Leukocytosis, in appendicitis, 651. 
Leukomain poisoning, 1203. 
Leukoplakia buccalis, 555. 
Lichtheim symptoms, of pernicious ane- 
mia, 520. 
Lion face. See Leontiasis ossea. 
Lipaciduria, 787. 
Lipomata, of esophagus, 568. 
Lips, tuberculosis of, 252. 
Lipuria, 777, 787. 
Lithuria, 785. 
Little’s disease. See Sclerosis, congenital 
lateral. 
Liver, actinomycosis of, 302. 
amyloid, 713. 
amyloid degeneration of, in tuberculosis, 
255. 
and spleen, in tuberculosis, 234. 
atrophy of, in syphilis, 30. 
benign growths of, 711. 
chancroid, 713. 
circulatory disturbances of, congestion, 
676. 
diseases of hepatic artery, 680. 
diseases of hepatic vein, 679. 
diseases of portal vefti, 678. 
cirrhosis of, and tuberculosis, 255. 
complicated by syphilis, 31. 
enlargement of spleen with, 1171. 
diseases of, abscess, 704. 
acute yellow atrophy, 673. 
amyloid, 713. 
cancer, 709. 
circulatory disturbances, 676. 
cirrhosis, 681. 
echinococcus. See Echinococcus Dis- 
ease, 
fatty, 712. 
glucosuria due to, 1107. 
jaundice, 664. 
syphilis. See Syphilis of Liver, 
tuberculosis. See Tuberculosis of 
Liver. 
effect on, of malaria, 73, 74, 77. 
enlargement of, in acute biliary colic, 
722. 
fatty degeneration of, 712. 
in tuberculosis, 255. 
fatty infiltration of, 712. 
hydatid cysts of, 307. 
hyperemia of, active, 676. 
passive, 676. 
in alcoholism, 1182. 
lardaceous, 713. 
multiple adenomata of, 711. 
syphilis of, congenital, 30. 
waxy, 713. 
Liver abscess, causes of, 705. 
due to cholelithiasis, 726. 
due to infection, 704. 
general considerations of, 704. 
in amebic dysentery, 79. 
Liver abscess, multiple, accompanying 
symptoms of, 707. 
causes of, 707. 
course of, 707. 
secondary anemia and leukocytosis 
with, 708. 
single or tropical, blood count in, 706. 
complications in, 706. 
course of, 707. 
duration of, 705. 
mortality from, 706. 
primary diseases causing, 705. 
rupture of, 706. 
spontaneous cure of, 705. 
without symptoms, 705. 
Liver complications, in gout, 1105. 
in typhoid fever, 105. 
with endocarditis, 491. 
Liver congestioh, causes of, 676. 
Liver flukes, 317. 
Lockjaw. See Tetanus. 
Locomotor ataxia. See Tabes dorsalis, 
vertigo with, 869. 
Locomotor system, bone diseases of, fra- 
gilitas ossium, 1097. 
hvpertrophic pulmonary arthropathy,- 
1096. 
leontiasis ossea, 1095. 
osteitis deformans, 1093. 
joint diseases of, polyarthritis, destruc- 
tive chronic, 1088. 
muscular diseases of, akinesia algera, 
1086. 
myalgia, 1084. 
myositis, 1084. 
paramyoclonus multiplex, 1086. 
progressive myositis ossificans, 1085. 
Thomsen’s disease (myotonia), 1085. 
Ludwig’s angina, 560. 
causes of, 561. 
definition of, 561. 
mortality from, 561. 
symptoms of, 561. 
Lues. See Syphilis, 15. 
Lues hereditaria tarda, 30-31. 
Lues maligna, 20. 
in syphilis of liver, 30. 
Lumbago, 1084. 
Lumbar neuralgia, 844. 
Lumbar puncture, for brain parasites, 
1002. 
in brain abscess, 986. 
in brain tumor, 998, 1000. 
in encephalitis, 975. 
in leptomeningitis, purulent, 941. 
in poliomyelitis, 323. 
in serous meningitis, 943. 
in tumors of spinal cord, 926. 
Lumbosacral paralysis, causes of, 879- 
880. 
of anterior crural nerve, symptoms of, 
880. 
of external popliteal nerve, 881. 
of gluteal nerves, 881. 
of internal popliteal nerve, 881. 
of obturator nerve, 880. INDEX 
1245 
Lumbosacral paralysis of sciatic nerve, 
880. 
Lung abscess, 386. 
in influenza, 127. 
in pneumonia 165. 
in typhoid fever, 98. 
Lung fever. See Pneumonia, Lobar. 
Lungs, cirrhosis of, 379. 
diseases of, abscess, 386. 
cancer, 387. 
congestion, 373. 
emphysema, 382. 
gangrene, 385. 
hemorrhage, 376. 
neoplasms, 387. 
non-tuberculous pneumonia, 379. 
fibrosis of, due to occupation, 380. 
in pneumonia, 166. 
gangrene of, in influenza, 127. 
in pneumonia, 164. 
hydatid cysts of, 308. 
induration of, and endocarditis, 490. 
neoplasms of, 387. 
purulent infiltration of, in pneumonia, 
166. 
syphilis of, 33. 
Lupus, of tongue and lips, 252. 
Lymphadenitis, bronchial, 265. 
cervical, 265. 
Lymphadenoma. See Hodgkin’s Disease. 
Lymphangitis, due to filariasis, 316. 
Lymphatic glands, tuberculosis of, 265. 
Lymphatics, enlargement of, in congenital 
syphilis, 66. 
Lymphatism, 1164. 
Lymphemia. See Leukemia, Lymphatic. 
Lymphocytoma, 537. 
Lymphogranuloma. See Hodgkin’s Dis- 
ease. 
Lymphosarcoma, 1164. 
Lymphosarcomatosis, 538. 
Lymph-scrotum, due to filariasis, 316. 
M 
Maid ism. See Pellagra. 
Malaria, black water fever, 76. 
bronchitis with, 77. 
cachexia in, chronic, 76-77. 
from neglected treatment for, 76. 
cause of lesions of, 72. 
chronic cachexia in, 76. 
complications in, 77-78. 
enlargement of spleen in, 73. 
factors in malignancy of, 73. 
hemorrhagic, 76. 
intermittent, 73. 
irregular, 73. 
quartan type of, 73. 
quotidian type of, 73. 
relapses of, 74. 
spontaneous recovery from, 74, 
tertian, 73. 
miscarriages in, 78. 
mixed types of, 77. 
Malaria, neuralgia due to, 77, 839. 
pigmentation of organs in, 72. 
remittent, algid pernicious, 75. 
black water disease, 76. 
cerebral pernicious, 75. 
coma type of, 75. 
forecast in, 75. 
gastro-intestinal pernicious, 75. 
mania and convulsions in, 75. 
manifestations of, 74-75. 
paroxysms of, 74-75. 
pernicious, 74. 
pulmonary pernicious, 75. 
purpuric complications in, 76. 
specific origin of, 72. 
Malignant granuloma. See Hodgkin’s Dis- 
ease. 
Malignant growths, anemia due to, 515. 
Malignant pustule. See Anthrax. 
Malleus. See Glanders. 
Malta fever, diagnosis of, by blood culture, 
197. 
etiology of, 196. 
period of incubation in, 196. 
prognosis of, 197. 
symptoms of, 197. 
Mania, in cerebral hemorrhage, 972. 
in cerebral hyperemia, 951. 
in malarial fever, 75. 
suicidal, in morphinism, 1186. 
with homicidal tendencies, in epilepsy, 
1053. 
Marie’s disease, due to traumatism, 1090. 
importance of early detection of, 1091. 
prognosis of, 1091. 
symptoms of, 1090. 
tuberculosis with, 1090. 
Marie’s hereditary ataxia, 888. 
Mastodynia, 843. 
Maternity, tetany of, 1168. 
Measles, complications in, brain, 345. 
bronchitis, 344. 
cancrum oris, 344. 
diphtheria, 345. 
ear, 344. 
eye, 345. 
gastro-enteritis, 345. 
glandular, 345. 
heart, 345. 
pulmonary, 344. 
scarlet fever, 345. 
tuberculous meningitis, 345. 
contagion of, 342. 
German, 346. 
malignant, 342. 
mortality from, 344. 
nature of, 342. 
period of incubation of, 342. 
period of invasion of, 342. 
symptoms of, blood, 343. 
conjunctiva, 343. 
skin, 343. 
temperature, 343. 
urine, 343. 
Median nerve paralysis, causes of, 878. 
symptoms of, 878, 1246 
INDEX 
Mediastinum, diseases of, associated symp- 
toms of, 400. 
tumors of. 399. 
Mediastinopericarditis, 430. 
Medulla oblongata, invasion of, in tabes 
dorsalis, 58. 
Melanosis, 786. 
Melanuria, 786. 
Melena, in cirrhosis, 690. 
Membranous colitis, hysterical, 1018. 
Membranous croup, non-diphtheritic, Vin- 
cent’s angina in, 298. 
Meniere’s disease. See Aural Vertigo. 
Meningeal apoplexy, 930. 
Meningismus, 931. 
Meningismus typhosus, 111. 
Meningitis, alcoholic, with alcoholic mul- 
tiple neuritis, 849. 
and epilepsy, 1055. 
basilar, 224. 
cerebrospinal, 932. 
epidemic cerebrospinal, abortive cases of, 
182. 
blood picture of, 182. 
character of, 177. 
chronic cases of, 181. 
complications in, 183-184. 
factors influencing severity of, 179. 
Flexner serum for, 184-185. 
foudrovant cases of, .181. 
general symptoms of, 179-180. 
hydrocephalus due to, 181-182. 
lumbar puncture in, 182-183. 
mortality from, 177-178. 
occurrence of, 178-179. 
due to influenza, 129. 
pneumococcus, 1591 
postbasilar, 934. 
purulent, with erysipelas, 176. 
septic, 133. 
serous, course of, 943. 
diseases complicated by, 943. 
primary, 943. 
specific localized, in cerebral syphilis, 42. 
spinal. See Spinal Meningitis, 
tuberculous, 224, 242, 277. 
with arthritis, 287. 
with brain tumor, 994. 
Meningo-encephalitis, 974. 
and epilepsy, 1055. 
Menstrual anomalies, hysterical, 1018. 
in typhoid, 110. 
palpitation of heart with, 508. 
sudden anemia during, 515. 
with tuberculosis, 271. 
Mental anomalies, in cerebral hemorrhage, 
971. 
in chorea, 1040. 
in diabetes mellitus, 1115. 
in epilepsy, 1053. 
in exophthalmic goiter, 1146, 
in multiple sclerosis of brain and cord, 
910. 
in neurasthenia, 1031. 
Mercurial poisoning, occupation influence 
in, 1195. 
prognostic symptoms of, 1195. 
Mesenteric tuberculosis, 266. 
Metabolic faults, achondroplasia, 113j 
diabetes insipidus, 1122. 
diabetes mellitus, 1106. 
gout, 1098. 
hereditary tendency to, 1125. 
multiple myeloma, 1134. 
obesity, 1124. 
osteomalacia, 1131. 
rachitis, 1129. 
scorbutus, 1132. 
Metastases, empyema with, 393. 
in cancer of stomach, 606. 
to brain, 990. 
to spine and cord, 925. 
due to carcinoma elsewhere in body, 
919, 920. 
Metastatic abscess of brain, 984. 
Metastatic parotitis, 300. 
Metasyphilitic disease, 44. 
tabes dorsalis, 45. 
Metazoan parasites, cestodes, 303. 
nematodes, 309. 
trematodes, 316. 
Meteorism, in typhoid fever, 102. 
Mexican tabardillo. See Typhus Fever. 
Migraine, abortive, 1062. 
classification of, 1060. 
climacteric period in, 1060. 
definition of, 1059. 
exciting factors of, 1059. 
hemicrania svmpatheticotonica, 1062. 
hemic rania sympatheticoparalytica, 
1062. 
influencing factors in, heredity, 1059. 
infection and other toxic states, 1060. 
traumatism, 1060. 
tuberculosis, 1060. 
various, 1060. 
nature of, 1059. 
ophthalmic, 1060-1061. 
prognosis of, 1063. 
red, 1062. 
symptomatic, 1063. 
symptoms of, general, 1059. 
white, 1062. 
with epilepsy, 1062. 
with epileptic equivalent, 1062. 
Mikulicz’s disease, associated conditions 
of, 558. 
Brunn’s classification of, 557-558. 
hereditary influence in, 558. 
nature of, 557. 
types of, 557. 
Miliary eruption, in typhoid fever, 106, 
Miliary tuberculosis, 222. 
Milk, infected, epidemic tonsillitis due to, 
294. 
Milroy’s disease, 1080. 
Milzbrand. See Anthrax. 
Mimic spasm. See Facial Spasm, 
Miscarriages, in malaria, 78. 
Mitral insufficiency, favorable cases of, 
497. 
unfavorable cases of, 497. 
valvular lesions due to, 495. INDEX 
1247 
Mitral stenosis, cerebral embolism due to, 
953. 
hemoptysis of, 376. 
of early life, 498. 
unfavorable features of, 498. 
valvular lesions due to, 497. 
Mitral and tricuspid valves, insufficiency 
and stenosis of, 439. 
Mobile spleen, 1173. 
Mollifies ossium, 1131. 
Mononeuritis, 846. 
Monoparalysis, hysterical, 1013. 
Morphinism, accompanying conditions in, 
1186. 
course of intoxication in, 1185. 
due to erythromelalgia, 1069. 
effects of, 1185. 
in tabes dorsalis, 54. 
influencing factors in, bad heredity, 
1186. 
development of habit in medical stu- 
dents, 1186. 
psychopathic states in, 1186. 
quantity taken, 1185. 
sudden complete withholding of drug 
from victim, 1185. 
unstable nervous system, 1186. 
percentage of permanent cures in, 1186. 
prognosis of, 1185. 
psychic anomaly in, 1185. 
suicidal mania in, 1186. 
Morvan’s disease, 916. 
Motor oculi, paralysis of, 860. 
Mountain sickness, causes of, 1209. 
dangers of, 1209. 
prognosis of, 1209. 
toleration in, 1209. 
Mouth, diseases of, stomatitis, 553. 
effect on, of typhoid fever, 101. 
Mouth breathing, 299. 
Movable kidnev, associated symptoms of, 
829.* 
operation for 828. 
mortality following, 828. 
prognostic factors of, 829. 
Multiple myeloma, 1134. 
of brain and cord, age considered in, 
908. 
apoplectiform seizures in, 910. 
atypical types of, 911. 
bulbar involvement in, 910, 912. 
cause of, 909. 
characterization of, 908. 
complications in, 913. 
course of, 908. 
cutaneous reflexes in, 911. 
diagnosis of, 911. 
duration of, 911-912. 
epileptiform attacks in, 910. 
mental deterioration in, 910. 
ocular changes in, 909, 910, 912. 
periods of latency in, 909, 911, 912. 
prognosis of, 911-912. 
resemblance of, to transverse myelitis, 
912. 
scanning speech in, 910. 
Multiple myeloma, of brain and cord, 
seats of predilection of, 908. 
symptoms of, 909. 
vertigo in, 910. 
with ataxic symptoms in ascending, 
912. 
vertigo with, 869. 
Mumps. See Parotitis, epidemic. 
Muscles, diseases of, akinesia algera, 1086. 
myalgia, 1084. 
myositis, 1084. 
paramyoclonus multiplex, 1086. 
progressive myositis ossificans, 1085. 
Thomsen’s disease (myotonia), 1085. 
Muscular atrophy in cerebral hemorrhage, 
968. 
Muscular dvstrophy, complications of, 
898. 
course of, 896. 
hereditary, 895. 
juvenile, characteristics of, 897. 
Erb-Landouzy-Dejerine, 897. 
of childhood, atrophic, 897. 
hypertrophic, 897. 
pseudohypertrophic, 896. 
prognosis of, 898. 
progression of, 895. 
symptoms of, 895. 
Muscular rheumatism. See Myalgia. 
Muscular spasm, in myotonia, 1085. 
Muscular system in typhoid, 113. 
Muscular weakness, in chorea, 1041. 
in diabetes mellitus, 1116. 
Musculospiral paralysis, causes of, 879. 
common form of, 878. 
complete, 878. 
symptoms of, 879. 
Musset’s phenomenon, in exophthalmic goi- 
ter, 1144. 
Myalgia, causes of, 1084. 
lumbar, 1084. 
occupation 1084. 
prognosis of, 1084. 
Myasthenia, 1030. 
with chronic nephritis, 799. 
Mvasthenia gravis, associated conditions 
of, 894. 
symptoms of, 893. 
Mycosis intestinalis, 210. 
Myelemia. See Leukemia, leukocytic. 
Myelitis, acute, cervical, 906. 
chronic stage on removal of cause of, 
905. 
compression or disorganization in, 
905. 
decubitus in, 905. 
diffuse, 906. 
due to traumatism, 905. 
early symptoms of sepsis in, 905. 
extent of paralysis in, 905. 
foudroyant cases of, 906. 
lumbar cord involvement in, 906. 
primary causes of, 905. 
prognosis of, 905-906. 
secondary, 905. 
secondary to gonorrhea, 906. 1248 
INDEX 
Myelitis, acute, syphilitic, 906. 
transverse, 906. 
with unrecognized cause, 906. 
chronic, associated diseases of, 907. 
causes of, 907. 
compression, 907. 
of pregnancy, 907. 
periods of latency in, 907. 
prognosis of, 907. 
classification of, bulbar, 904. 
central, or poliomyelitis, 904. 
diffuse or general, 904, 906. 
due to influenza, 130. 
focal, 904. 
transverse or compression, 904, 906, 
907. 
unilateral, 904. 
compression, in tumors of spinal cord, 
925. 
definition of, 904. 
funicular, 927. 
post-typhoid, 112. 
subacute, 905, 907. 
transverse, from extradural tumors of 
cord, 925. 
resemblance to, of multiple sclerosis, 
912. 
tuberculous, 277. 
Myelocytes, in leukemia, leukocytic, 530. 
Myeloma, multiple, 1134. 
Myelopathic albumosuria, 1134. 
Myocardial degeneration, 443. 
in amebic dysentery, 80. 
in arteriosclerosis, 412. 
in scarlet fever, 330. 
Myocardial insufficiency, angina pectoris, 
454. 
blood pressure study in, 445. 
brown atrophy, 454. 
chronic, cause of, 443. 
complex conditions in, 444-445-446. 
depressing factors from, 452. 
factors in prognosis of, 444-445-446. 
fatty heart, 452. 
fibroid degeneration, 443. 
irregularities of, auricular fibrilla- 
tion, 450. 
due to depressed conductivity, 447. 
due to extrasystoles, 448. 
pulsus alternans, 449. 
sinus, 447. 
Windle’s table of, 450. 
nature of, 443. 
sudden death from, 446. 
symptoms of, 444-445-446. 
coronary sclerosis, 454. 
fragmentation and segmentation, 454. 
in cirrhosis, 700. 
senile heart, 460. 
with anemias, metabolic faults, and 
toxic states, 465. 
Myocarditis, acute interstitial, septic, 443. 
simple, 443. 
acute purulent, 442. 
associated with pericarditis, 428. 
due to arthritis, 285. 
Myocarditis, due to arthritis, blood pres- 
sure in, 286. 
sudden death from, 286. 
due to syphilis, 29. 
in chorea, 1042. 
in diphtheria, 139. 
parenchymatous, 443. 
post-typhoid, 95. 
with cholelithiasis, 731. 
Myocarditis hemorrhagica, 1085. 
Myocardium, diseases of, aneurism, 407. 
chronic insufficiency, 443. 
fibroid degeneration, 443. 
heart weakness due to insufficient ex- 
ercise, 464, 
hypertrophy and dilatation, 460. 
inherent muscular weakness, 465. 
insufficiencies with anemias, meta- 
bolic faults and toxic states, 
465. 
myocarditis, acute interstitial, 443. 
myocarditis, acute purulent, 442. 
neoplasms, 465. 
rupture, 466. 
Stokes-Adams disease, 463. 
syphilis. See Cardiovascular syphilis, 
influence of, on prognosis, 441. 
obesity with, 1126. 
parasites of, 466. 
tuberculosis of, 275. 
Myoclonia, 1086. 
Myogenic hypothesis, of paralysis agitans, 
1035. 
Myositis, 32. 
Myositis ossificans, progressive, 1085. 
Myotonia, 1085. 
Myotonia congenita, 898. 
Myotonic reaction of Erb, 1086. 
Myxedema, adult, 1156. 
prognosis of, 1157. 
symptoms of, 1156-1157. 
classification of, 1154. 
congenital, prognosis of, 1156. 
symptoms of, 1155. 
thyroid treatment for, 1156. 
due to complete loss of gland function, 
1157. 
heredity in, 1158. 
in exophthalmic goiter, 1147. 
operative, 1154. 
prognosis of, 1158. 
thyroid insufficiency in, 1153. 
thyroid insufficiency in, dangers of, 
1154. 
maximal, 1154. 
N 
Narcotic poisoning, double, with alcohol- 
ism, 1178. 
Nasal diphtheria, 138. 
Nasal tuberculosis, 250. 
Naso-pharyngeal obstructions, 299. 
Necator americanus of Stiles, 310. 
Neisser’s Statistics, on tertiary svphilis, 
25. INDEX 
1249 
Nematodes, ankvlostomiasis, character of, 
310. 
clinical manifestations of, 311. 
incidence of, 311. 
infection of, 310. 
occurrence of, 310. 
prognosis of, 311. 
ascaris lumbricoides, 309-310. 
filariasis, 314-315. 
oxyuris vermicularis, 309-310. 
trichinosis, cause of, 312. 
duration of, 315. 
factors in prognosis of, 313. 
infection of, 312. 
mortality from, 315. 
symptoms of, blood, 314. 
intestinal, 313. 
respiratory, 313-314. 
trichocephalus dispar, 312. 
Neoplasms, pancreatic, 739. 
pulmonary, 387. 
thyroid, 1136. 
and hyperthyroidea, 1150. 
Neoplasms of esophagus, 567. 
Neoplasms of heart, primary, 465. 
secondary or metastatic, 466. 
Neoplasms of pericardium, 434. 
Neoplasms of peritoneum, 663. 
Nephritis, acute, complications in, 794. 
glomerular type of, 789. 
mortality from, 793-794. 
symptoms in prognosis of, 790. 
alluminuria, 793. 
blood, 793. 
cardiac, 791. 
peritonitis, 792. 
pulmonary edema, 792. 
uremia, 792. 
urinary, 791. 
vomiting, 792. 
acute croupous, 788. 
acute non-suppurative, of Councilman, 
789. 
acute parenchymatous, 788. 
in typhoid, 108-109. 
acute syphilitic, 790. 
acute tubal, 788. 
indicated by hematuria, 756. 
aggravation of, by pregnancy, 796. 
albuminuria and, 743, 744, 793. 
albuminuria of, in typhoid, 108. 
alcoholism with, 1180. 
and appendicitis, 657. 
benign, albuminuria in, 741. 
chronic, arteriosclerosis with, 802. 
coronary disease with, 802. 
due to bacillary dysentery, 196. 
duodenal ulcer with, 588. 
chronic catarrhal, 797. 
chronic diffuse, 797. 
chronic interstitial, Adams-Stokes phe- 
nomenon in, 807. 
albuminuric retinitis in, 809. 
anemia in, 809. 
angina pectoris in, 807. 
arteriosclerotic kidney, 805. 
Nephritis, chronic interstitial, blood pres- 
sure in, 806. 
cerebral hemorrhage with, 958. 
cerebral symptoms in, 807. 
complications in, 809. 
contracted kidney in, 805. 
digestive symptoms in, 808. 
dropsy in, 807. 
duration of, 810. 
dyspnea in, 807. 
epistaxis in, 809. 
headache in, 806-807. 
heart changes in, 806-807. 
hemoptysis of, 377. 
heredity in, 805. 
hypertension in, 806-807-808. 
hypertrophy of left ventricle in, 806. 
indicated by hematuria, 756. 
infections in, 80. 
in lead poisoning, 1192. 
leading features of, 804. 
ocular disturbances in, 806-807. 
orthopnea in, 807. 
polyuria in, 807. 
prognosis of, 805. 
purpura in, 809. 
red granular kidney, 805. 
renal insufficiency in, 806. 
respiratory symptoms in, 807. 
secondary contracted kidney, 804. 
senile kidney, 805. 
stasis in, 807. 
surgical operations in, 809. 
tachycardia in, 807. 
thick artery in, 806. 
urine in, 808. 
with cholelithiasis, 730. 
chronic parenchymatous, 797. 
anemia with, 799. 
arteriosclerosis in, 802. 
associated conditions of, 797. 
blood pressure in, 801. 
compensatory hypertension in, 802. 
compensatory hypertrophy in, 797, 
802. 
complications in, 803. 
coronary disease with, 802. 
digestive derangement with, 798. 
due to chronic lead poisoning, 798. 
due to cold or exposure, 798. 
due to malarial infection, 798. 
duration of, 804. 
edema in, 802. 
faulty living in, 802. 
following nephritis of scarlatina, and 
pregnancy, 798. 
immediate causes of death from, 804. 
myasthenia with, 799. 
origin of, 798. 
paroxysmal hematuria with, 801. 
process of, 797. 
prognosis of, 797, 798, 803. 
prolonged surgical conditions, asso- 
ciated with, 789. 
pulse in, 802. 
renal sufficiency test for, 800. 1250 
INDEX 
Nephritis, chronic parenchymatous, retinal 
changes in, 803. 
surgical treatment in, 804. 
uremia with, 799. 
urine in, 800. 
vomiting with, 798. 
chronic tubal, 797. 
indicated by hematuria, 756. 
diffuse interstitial, 873. 
hematuria due to, 754-755. 
in measles, 345. 
in syphilis, 31. 
interstitial, with cholelithiasis, 730. 
in pneumonia, 160. 
in varicella, 342. 
of pregnancy, 794. 
albuminuria in, 794. 
diet and treatment for, 795. 
eclampsia in, 795. 
mortality from, 795. 
prognostic factors in, 795. 
post febrile, in typhoid, 109. 
renal asthma with, 370. 
saturnine chronic, retinal hemorrhage 
with, 798. 
scarlatinal, 331. 
septic, 131. 
suppurative, 833. 
tuberculosis, hematuria due to, 759. 
tubular, renal sufficiency test for, 769. 
urinary casts with, 750-751-752. 
vascular, renal sufficiency test for, 769. 
with arteriosclerosis, 411, 802. 
with cirrhosis, 685. 
with diphtheria, 139. 
with endocarditis, 491. 
with malaria, 78. 
Nephrolithiasis, calculous anuria in, 824. 
cause of, 820. 
conditions associated with, 823-824. 
diathesis in, 823. 
mortality following operations for, 824. 
operation for (nephrolithotomy), 824. 
prognostic features of, 821. 
reaction of urine in, 821. 
renal colic in, 823. 
renal lithiasis in, 823. 
size and number of stones in, 821. 
stone in pelvis of kidney in, 822. 
symptoms of, 823-824. 
ureteral stones in, 822. 
varieties of, 821. 
x-ray in, 821. 
Nephropathies, acute, duration of, 793. 
infectious history of, 790. 
amyloid kidney, 814. 
chronic, 797. 
complications in, 803. 
dropsy in, 800. 
nephritis, chronic interstitial, 804. 
congested kidney, 811. 
malignant toxemia in, 788. 
nephritis, acute parenchymatous, 788. 
non-malignant toxemia in, 789. 
origin of, 788. 
prognostic factors in, 788. 
Nephropathies, saturnine, 1192. 
symptoms of, 788-789. 
tuberculous kidney. See Tuberculous 
kidney. 
Nephroptosis, associated symptoms of, 
828. 
Dietl’s crises in, 829. 
hydronephrosis with, 829. 
operation for, 828. 
mortality following, 828. 
prognostic factors in, 829. 
Nephrotyphoid, 108. 
Nerves, anterior crural, paralysis of, 880. 
auditory, paralysis of, 868.' 
brachial, paralysis of, 875-876. 
cauda equina, paralysis of, 882. 
circumflex, paralysis of, 878. 
cochlear, invasion of, in auditory pa- 
ralysis, 868. 
gluteal, paralysis of, 881. 
hypoglossal, paralysis of, 873. 
median, paralysis of, 878. 
musculospiral, 878. 
obturator, paralysis of, 880. 
peripheral, tumors of, 883. 
phrenic, paralysis of, 874. 
popliteal, paralysis of, 881. 
sacral, paralysis of, 882. 
sciatic, paralysis of, 880. 
spinal accessory, paralysis of, 871. 
ulnar, paralysis of, 879. 
vestibular, involvement of, in auditory 
paralysis, 869. 
Nervous dyspepsia of Leube, 574. 
Nervous exhaustion. See Neurasthenia. 
Nervous prostration. See Neurasthenia. 
Nervous system, anomalies of, in malaria, 
78. 
complications of, in gout, 1104. 
diseases of, anterior—of efferent or mo 
tor tract, 888. 
brain parasites, 1002. 
cerebellar disease, 1003. 
circulatory disturbances of brain, 947. 
of brain membranes, 934. 
of spinal membranes, 930. 
peripheral, neuralgia, 837. 
neuritis, 845. 
paralysis, 856. 
tumors, 883. 
sympathetic, 1081. 
diseases of spinal cord, indiscriminate, 
904. 
lateral, 899. 
of afferent or sensory system, 885. 
diseases of sympathetic system, vaso- 
motor and trophic disturbances, 
1066. 
effect on, of congenital syphilis, 67. 
functional and general diseases .of, 
chorea, 1037. 
epilepsy, 1J46. 
hysteria, 1005. 
infantile convulsions, 1065. 
migraine, 1059. 
neurasthenia, 1025. INDEX 
1251 
Nervous system, functional and general 
diseases of, occupation paraly- 
sis and neurosis, 1064. 
paralysis agitans, 1033. 
tetany. See Tetany, 
traumatic neurosis, 1021. 
functional heart disorders due to, 507. 
in alcoholism, 1181. 
in cholelithiasis, 732. 
in diabetes mellitus, 1118. 
in endocarditis, 492. 
influenza of, 129. 
in typhoid, 111. 
in tuberculosis, 235. 
invasion of, in amebic dysentery, 80. 
in cirrhosis, 694. 
in pellagra, 1200. 
in pneumonia, 158. 
symptoms of, in exophthalmic goiter, 
1143-1146. 
syphilis of, 35. 
tuberculosis of, 277. 
Neuralgia, age in, 838. 
arteriosclerotic, 842. 
brachial, 843. 
brachial, 843. 
associated conditions of, 843. 
causes of, 843. 
ciliary, 841. 
climate considered in, 838. 
conditions indicated by, 844. 
conditions responsible for, 837. 
crural, 840, 844. 
definition of, 837. 
due to anemia, 838. 
due to bad habits, 839. 
due to cachexias, 839. 
due to caries of teeth, 840. 
due to diabetes, 839. 
brachial, 843. 
due to infections, 839. 
due to malaria, 839. 
due to poisons, 839. 
due to syphilis, 839-840. 
due to tumors of spinal cord, 921. 
epidemics of, 839. 
“fixed,” 840. 
hyperesthetic areas of Head in, 840. 
idiopathic, 837. 
intercostal, conditions indicated by, 842. 
lumbar, 844. 
persistent double, 844. 
malarial, 77. 
mastodynia, 843. 
mild paroxysms of, 840. 
occipital, conditions indicated by, 841. 
persistent or recurring, in extremities, 
840. 
phrenic, 843. 
predisposition to, 838. 
red. See Erythromelalgia. 
relapses of, 841. 
sex in, 838. 
sciatic, 844. 
acute idiopathic, 845. 
causes of, 845. 
chronic neuritic, 845. 
Neuralgia, sciatic, conditions symptoma- 
tic of, 844. 
double, 845. 
neuropathic tendency of, 844. 
results of long-continued, 845. 
subacute secondary, 845. 
symptomatic, prognosis of, 845. 
senile, 842. 
supra-orbital, causes of, 841. 
treatment for, 842. 
symptomatic, 837. 
intercostal, 843. 
with flabby and atrophic muscles, 840. 
with transitory tenderness, 840. 
trifacial, 841. 
associated symptoms of, 841. 
causes of, 841. 
Neuralgia of stomach, 616. 
Neuralgic pains, about head and jaw, 840. 
due to incipient brain disease, 840. 
nasal and frontal, 840. 
of herpes zoster, 885-886. 
persistent or recurring, in abdomen, 840. 
in thorax, 840. 
radiating along intercostal, and lumbar 
nerves, 839. 
with hysteria, 841. 
Neurasthenia, age in, 1026, 1032. 
“anxiety neurosis” of Freud, 1029. 
associated conditions of, cardiac neuro- 
ses, 1027. 
gastro-intestinal disturbances, 1027. 
infections, 1027. 
influenza, 1027. 
traumatism, 1027. 
aural symptoms of, 1030. 
“brain fag” in, 1031. 
cardiac neurosis in, 1029. 
causes of, faulty hygiene with improper 
education, 1027. 
high altitudes, 1026. 
idleness, 1026. 
insufficient early discipline, 1026. 
occupation, 1027. 
cerebral, 1028. 
clinical varieties of, 1028. 
constipation with, 1031. 
cooperation of physician and patient in, 
1032. 
course of, 1032. 
definition of, 1025. 
due to alcoholic history, 1027. 
due to diabetic history, 1027. 
due to gouty history, 1027. 
due to influenza, 129. 
dyspepsia due to, 615. 
emaciation with Glenard’s process in, 
1031. 
exogenous nature of, 1026. 
factors influencing course of, 1029. 
faulty nutrition in, 1031. 
fear and imagination in, 1030. 
gastro-intestinal anomalies in, 1031. 
heart complaints of, 513. 
history of, 1025. 
inherent weakness in 1032. 1252 
INDEX 
Neurasthenia, insanity due to psychasthe- 
nic states in, 1030. 
melancholy of, 1028. 
Meni&re symptoms in, 869. 
mental character in, 1025. 
muscular weakness in, 1030. 
ocular symptoms in, 1030-1031. 
operative treatment for varicocele in, 
1029. 
phobias of, 1030. 
predisposition by heredity to, 1026, 
1028. 
predisposition of race to, 1026. 
primary, 1025. 
reflexes in, 1030. 
removal of cause of, 1032. 
secondary nature of, 1025. 
sensory symptoms in, 1030. 
sex in, 1026. 
sexual, 1028-1029. 
spinal, 1028. 
urinary anomalies in, 1029. 
Neurasthenic habits, 1030. 
Neuritis, bulbar, acute, 892. 
due to influenza, 129. 
in pneumonia, 168. 
in rheumatic fever, 287. 
multiple, symptoms of, in poliomyelitis, 
323. 
tuberculous, 278. 
optic, 858. 
peripheral. See Peripheral Neuritis, 
sciatic, 844. 
syphilitic peripheral, 37. 
tuberculous, 278. 
Neuritis-polyneuritis, 1119. 
Neurofibromata, disseminated, with central 
deposits, 883. 
chronic, 883. 
congenital, 883. 
involving subcutaneous branches of 
sensory nerves, 884. 
multiple, 883. 
plexiform, 884. 
size of, 883. 
symptoms of, 883. 
Neuromata, false, 883. 
following amputation, 883. 
true, 883. 
Neuropathic predisposition, 838. 
Neurorecidive, polyneuritis due to salvar- 
san, 852. 
Neurosis, traumatic, 1021. 
Noma, 555. 
Nose, diseases of, acute catarrhal rhinitis, 
357. 
hay fever, 358. 
effect on, of congenital syphilis, 66. 
syphilis of, 32. 
Nosebleed. See Epistaxis. 
Nutrition, disordered, in epilepsy, 1052. 
faulty, in neurasthenia, 1031. 
with cerebellar disease, 1004. 
Nystagmus, in ophthalmoplegia, 861. 
0 
Obesity, acquired, causes of, 1125. 
treatment for, 1125. 
age considered in, 1120. 
cardiac insufficiency and death due to, 
1125. 
causes of, 1124. 
change by decomposition and reforma- 
tion of fat deposits, 1126. 
complications in, acute hemorrhagic 
pancreatitis with, 1127. 
amenorrhea, 1128. 
angina pectoris, 1127. 
arteriosclerosis with myocardial 
change, 1127. 
cardiac asthma, 1127. 
constipation with hemorrhoids, 1127. 
dropsy, 1128. 
dystrophia adiposo-genitalis in, 112S. 
emphysema with bronchitis and insuf- 
ficient heart muscle, 1127. 
in asthenic or anemic cases, 1128. 
interference with locomotion, 1127. 
interstitial nephritis, 1127. 
myocardial insufficiency, 1127. 
plethora, 1127. 
constitutional inclination to, 1126. 
dangers of, 1126. 
thyroid extract in large doses, 1128. 
unscientific dieting in, 1128. 
diabetes mellitus with, 1112. 
effect of relief of sexual anomalies on. 
1125. 
fatty degeneration of myocardium in, 
1125. , 
fatty heart with, 1126. 
heart weakness in, 1126. 
hereditary, 1125. 
at menopause, 1125. 
at puberty, 1125. 
hypoplasia in, 1128. 
in anemic subjects, 1125. 
in tuberculosis, 242. 
poor insurance risks, 1128. 
poor surgical subjects, 1128. 
pregnancy in, 1128. 
prognosis of acute infections in, 1126. 
sudden death from, 1127-112S. 
treatment for, 1128. 
tumor of hypophysis in, 1128. 
Obstipation, in appendicitis, 653. 
organic causes of, 631. 
Obturator nerve, paralysis of, 880. 
Occipital neuralgia, 842. 
Occupation, arteriosclerosis due to, 407- 
408. 
Occupation diseases, pneumonia, 3S0-381. 
Occupation neuroses, 1064. 
Occupation paralyses, chronic, 1064. 
pathologic basis for, 1064. 
relief from, 1064. 
symptoms of, 1064. 
ulnar, 879. 
various, 1064. 
writers’ cramp, 1064. TNDEX 
1253 
Ocular anomalies, hysterical, amblyopia, 
1012. 
asthenopia, 1012. 
blindness, 1012. 
contraction of visual field, 1011. 
contracture of ocular muscles, 1013. 
errors of accommodation, 1012. 
faulty color perception, 1012. 
palpebral and bulbar, 1013. 
paralysis of eyelids, 1013. 
paralysis of ocular muscles, 1013 
pupillary phenomenon, 1013. 
due to alcoholism, 1183. 
in arteriosclerosis, 415-418. 
in chorea, 1040. 
in chronic interstitial nephritis, 806- 
807. 
in epilepsy, 1051. 
in lead encephalopathy, 1190. 
in neurasthenia, 1030-1031. 
supra-orbital neuralgia due to, 841. 
with hydrocephalus, 945. 
Ocular infections, with diabetes mellitus, 
1119. 
hysterical paralysis of, 1013. 
Ocular nerves, paralysis of, 860. 
in tabes dorsalis, 56. 
Olfactory nerve, paralysis of, 856. 
Oligemia, 514. 
Oligochromemia, 514-517. 
Oligocythemia, 514. 
in chlorosis, 518. 
Ophthalmic migraine, 1060. 
of Charcot, 860. 
Ophthalmoplegia, 861. 
acute, 862. 
associated symptoms of, 861. 
in tabes dorsalis, 56. 
nystagmus in, 861. 
recurrent, 862. 
Ophthalmoscopic examination, in cerebral 
hemorrhage, 966. 
in otitic brain abscess, 984. 
Opium, enteritis due to, 625. 
Oppenheim’s disease, 898. 
Optic aphasia, 859. 
Optic changes, in multiple sclerosis of 
brain and cord, 909, 910, 
912. 
Optic nerve, atrophy of, 858. 
in tabes dorsalis, 54. 
hereditary family, 858. 
with brain tumor, 994-995. 
disseminated sclerosis of, 858. 
paralysis of, 857. 
Optic neuritis, conditions indicated by, 
858. 
syphilitic, 43. 
with brain tumor, 994-995. 
with cerebellar disease, 1004. 
Oral sepsis, provocative of pernicious 
anemia, 527. 
Orchitis, in typhoid, 110. 
Orthopnea, in nephritis, 807. 
Osier’s disease. See Erythremia. 
Osseous system, in typhoid, 113. 
Osteitis deformans, duration of, 1095. 
malignant growths with, 1094. 
pathology and symptoms of, 1093-1094. 
skull involvement in, 1094. 
Osteoarthropathy, hypertrophic pulmon- 
ary, 1096. 
Osteochondritis syphilitica, 67. 
Osteogenesis imperfecta, 1097. 
Osteomalacia, characteristics of, 1131. 
early recognition and treatment of, 
1132. 
puerperal, 1132. 
symptoms of, 1132. 
uncontrolled cases of, 1132. 
Otitis, brain abscess following, 983. 
cerebral thrombosis due to, 955. 
Otitis media suppurativa, diphtheria in, 
142. 
in measles, 344. 
in pneumonia, 167. 
Ovarian tuberculosis, 272. 
Oxalic acid diathesis, 779. 
Oxaluria, 779. 
Oxyuris vermicularis, 309-310. 
P 
Pachymeningitis, cervical hypertrophic, 
with syringomyelia, 917. 
hypertrophic cervical, 932. 
spinal. See Spinal Pachymeningitis, 
tuberculous, 277. 
Pachymeningitis externa, development of, 
937. 
nature of, 936. 
primary and secondary, 937. 
prognosis of, 937. 
Pachymeningitis interna, acute hem- 
orrhagic, 931. 
paresis with, 935. 
causes of, 935-936. 
chronic form of, 936. 
development of, 935-936. 
due to chronic alcoholism, 935. 
due to infections, 936. 
due to purpuric conditions, 935. 
due to syphilitic infections, 936. 
due to traumatism, 934-935. 
general considerations of, 934. 
prognosis of, 935. 
senile dementia with, 935. 
symptoms of, 935-936. 
Pachymeningitis spinalis hemorrhagica, 
930. 
Paget’s disease. See Osteitis deformans. 
Pains, hysterical, simulating organic dis- 
ease, 1010. 
Palsies. See Paralysis. 
Paludism. See Malaria. 
Pancreas, cancer of head of, 739. 
simulation of, by gall-stones, 730. 
diseases of, calculi, 738. 
cysts, 738. 
hemorrhage, 737. 
necrosis, 738. 1254 
INDEX 
Pancreas, diseases of, neoplasms, 739. 
pancreatitis, 734. 
relation of, to diabetes mellitus, 1106. 
sclerosis of head of, 737. 
tuberculosis of, 262. 
with cholelithiasis, 731. 
with diabetes mellitus, 1106. 
Pancreas-achylia, functional, 625. 
Pancreatic apoplexy, 737. 
Pancreatitis, acute, gall-stone provoking 
factor of, 734. 
acute hemorrhagic, 734. 
due to traumatism, 735. 
Cammidge test for, 736. 
chronic, associated conditions of, 737. 
causes of, 736. 
hemorrhagic gangrenous, 735-736. 
hemorrhagic, hiccough with, 875. 
secondary, 736. 
suppurative, 736. 
Papilloma of kidney, 826. 
Parageusia, 870. 
Paralysis, anterior crural, 880. 
auditory, 868. 
bulbar, 891. 
cerebral, of childhood, 977. 
circumflex, 878. 
crossed, hypoglossal and hemiplegia, 874. 
crossed facial, with hemiplegia, 866. 
deaths from, and apoplexy, table of, 959. 
diphtheritic, 140. 
Duchenne, 877. 
due to cervical rib, 876. 
Erb’s, 876. 
extensor, in lead multiple neuritis, 851. 
facial, 847, 863. 
due to pontine disease, 864. 
glossopharyngeal, 870. 
habit, 847. 
hysterical, 1013. 
influence of traumatism on development 
of, 1024. 
infraclavicular, 877. 
Klumpke’s, 877. 
Landry’s, 854. 
lumbosacral, 879. 
musculospiral, 878. 
obstetrical, 978. 
ocular, 860. 
in tabes dorsalis, 56. 
of cauda equina, 882. 
of cervical sympathetic, causes of, 1081. 
prognosis of, 1081. 
symptoms of, 1081. 
of external popliteal nerve, 881. 
of eyelids, hysterical, 1013. 
of fifth (trigeminal) nerve, 862. 
of fourth (trochlear) nerve, 861. 
of gluteal nerves, 881. 
of hypoglossal nerve, 873. 
of internal popliteal nerve, 881. 
of median nerve, 878. 
of nerves of brachial plexus, 875-876. 
of obturator nerve, 880. 
of phrenic nerve, 874. 
of posterior thoracic nerve, 877. 
of sacral plexus, 882. 
Paralysis, of serratus magnus, 877. 
of seventh (facial) nerve, 863. 
of sixth (abducens) nerve, 861. 
of spinal accessory nerve, 871. 
of sternomastoid, 872. 
of third nerve (motor oculi), 860. 
ophthalmoplegia in, 861. 
peripheral. See Peripheral Paralysis, 
peripheral facial, 864. 
pneumogastric, 871. 
pseudobulbar, 893. 
quadriplegia, due to alcoholic multiple 
neuritis, 849. 
radial, 878. 
rheumatic facial, 848. 
sciatic, 880. 
spastic, 899. 
spastic family type of, associated with 
idiocy, 903. 
subscapular, 877. 
supraclavicular, 876. 
trapezius, 872. 
ulnar, 879. 
vagus, 871. 
with cerebral anemia, 948. 
with cerebral hemorrhage, 968. 
with cerebral thrombosis, 956-957. 
Paralysis agitans, age in, 1033-1034. 
arteriosclerosis with, 1033. 
complications in, bed-ridden cases, 1036. 
fractures and other trauma, 1036. 
infections, 1036. 
nervous, 1036. 
course of, 1035. 
factors in prognosis of, 1034. 
frequency of, 1034. 
general symptoms of, 1033. 
heredity in, 1034. 
in tabes dorsalis, 58. 
inviting factors of, 1034. 
juvenile forms of, 1033. 
mental condition in, 1036. 
myogenic hypothesis of, 1035. 
parathyroid therapy, 1035. 
pathogenesis and pathology of, 1034. 
periods of latency in, 1036. 
premature decay in, 1033. 
sex in, 1034. 
symptoms of, facial expression, 1036. 
hold of hand and arm, 1036. 
muscular rigidity, 1035. 
reflexes, 1036. 
sphincter, 1036. 
stooping posture, 1036. 
“trotting gait,” 1036. 
tumor, 1035. 
Paralysis cliiropodale, due to arsenical 
multiple neuritis, 852, 
Paramyoclonus multiplex, 1086. 
Paranephritic abscess, 834, 
Paranephritis, 834. 
Paraplegia, ataxic, 901. 
secondary spastic, causes of, 903. 
course of, 902. 
senile, 929. 
spastic. See Sclerosis, primary lateral. INDEX 
1255 
Paraplegia, sudden, with embolism of 
cord, 929. 
Parasites, intestinal, in beriberi, 1201. 
of brain 1002. 
metazoan, 303. 
Paratyphlitis, 644. 
Paratyphoid disease, bacilli of, 122. 
complications in, 123. 
puerperal, 124. 
relapses of, 123. 
symptoms of, 123. 
Parathyroid disturbance, tetany of, 1168. 
Parathyroid therapv, in paralysis agitans, 
1035. 
Paresis, and pachymeningitis interna, 935. 
as syphilitic lesion, 35. 
average duration of, 62. 
causes of death in, 64. 
choreatic, 980. 
effect of treatment in, 64. 
juvenile, 65. 
manifestations of, 63-64. 
periods of latency in, 63. 
predisposing factors to, 62. 
prevention of, in syphilis, 39. 
remissions in, 63. 
simulation of symptoms of, in cerebral 
lesions, 63. 
trophic changes in, 63. 
Wassermann reaction in, 63. 
Parkinson’s disease. See Paralysis agitans. 
Parosmia, causes of, 857. 
Parotid tuberculosis, 249. 
Parotitis, chronic, 557. 
epidemic, complications in, 353. 
mortality from, 353. 
nature of, 352. 
symptoms of, 353. 
in gastric ulcer, 596. 
in typhoid fever, 101. 
infections, 300. 
metastatic, 300. 
in pneumonia, 168. 
with erysipelas, 176. 
secondary, 300. 
with diphtheria, 142. 
Parry’s disease, 1142. 
Pasteur treatment, of hydrophobia, 355. 
“Patchy tongue,” 555. 
-Pellagra, acute and subacute, 1199. 
associated symptoms of, 1197. 
chronic, 1199. 
etiology of, 1198. 
geographical distribution of, 1197. 
origin of, 1197. 
prognostic factors and symptoms in, 
1198. 
age, 1199. 
central and peripheral lesions, of ner- 
vous system, 1200. 
course of, 1199. 
gastro-intestinal, 1200. 
habits, 1199. 
location, 1199. 
psychic disturbances, 1200. 
race and sex, 1200. 
skin lesions, 1200. 
Pelvis, pus in, 832. 
Pemphigus syphiliticus, early, 66. 
Peptic ulcers, of esophagus, 564. 
Perforating ulcer, in tabes dorsalis, 57. 
Perforation of intestine, in amebic dysen- 
tery, 80. 
Peri-arteritis, 402. 
Pericardial pseudocirrhosis of liver, 432. 
Pericarditis, acute, adhesions of, 428. 
and diphtheria, 140. 
and endocarditis, 489. 
and myocarditis, 428. 
definition of, 426. 
effusions of, blood stained, 428. 
fibrinous, 428. 
purulent, 428. 
serofibrinous, 428. 
in chorea, 1042. 
in pneumonia, 166. 
in typhoid fever, 96. 
mortality from, 427, 430. 
primary infections of, 426-427. 
prognostic significance of, 427. 
associated conditions of, general, 429. 
valvular, 430. 
calcareous, 428. 
chronic, 430. 
due to arthritis, 285. 
idiopathic, 427. 
prognosis of, 429-430. 
symptoms of, 429. 
tuberculous, 274. 
x-ray examination in, 428. 
Perieardioperitonitis, chronic, associated 
conditions of, 432-433. 
character of, 432. 
symptoms of, 432-433. 
Pericardium, adherent, 430. 
diseases of, adherent pericardium, 430- 
hemopericardium, 433. 
hydropericardium, 433. 
neoplasms, 434. 
perieardioperitonitis, 432. 
pericarditis, 426. 
pneumopericardium, 434. 
Perigastric adhesions, in gastric ulcer, 
595. 
Perihepatitis, ascites with, 702. 
associated symptoms of, 701. 
chronic hyperplastic, 702. 
fatal terminations of, 703. 
tapping in, 702. 
Perinephric abscess, definition of, 834- 
definition of, 829. 
due to kidney disease, Guiteras’ classifi- 
cation of, 835. 
in renal tuberculosis, 269. 
nature of primary lesion of, 835. 
occurrence of, 836. 
origin of, 835. 
perforation of, 836. 
primary case of, 836. 
prognostic factors in, 835. 
timely recognition of, 835. 
Perinephritis, 835. 
Perineuritis, 846. 1256 
INDEX 
Peripheral nerves, elephantiasis neuroma- 
tosa, 884. 
neuralgia, 837. 
neuritis, 845. 
paralysis, 856. 
tumors of, benign solitary, 883. 
malignant, 883. 
neurofibromata, 883. 
neuroma, 883. 
Peripheral neuritis, chronic and progres- 
sive forms of, 846. 
degenerative changes in, 846. 
diabetic. See Diabetes Mellitus. 
general considerations on, 845. 
habit paralysis in, 847. 
Landry’s paralysis, classification of, 
854. 
complications in, 854. 
mononeuritis, 846. 
multiple, 846. 
causes of, 848. 
forms of, 848. 
with leprosy. See leprosy, 
multiple alcoholic, 849. 
acute, of ascending type, 850. 
in delirium tremens, 849. 
Korsakoff’s psychosis in, 849. 
meningeal symptoms in, 849. 
quadriplegic paralysis due to, 849. 
with myocarditis, 850. 
multiple arsenical, acute and chronic, 
852. 
associated symptoms of, 852. 
bulbar symptoms with, 853. 
causes of, 852. 
complications in, 853. 
due to salvarsan, 852. 
paralysis with, 852. 
pseudotabetic symptoms with, 852. 
trophic symptoms of, 853. 
multiple gonorrheal, 855. 
multiple idiopathic, associated symp- 
toms of, 853. 
infections, 853. 
prognosis of, 853. 
reaction of degeneration in, 854. 
temperature in, 853. 
types of, 853. 
multiple lead, 850. 
in children, 851. 
chronic, 851. 
encephalopathy in, 851. 
partial recovery from, 851. 
reaction of degeneration in, 851. 
relapses of, 851. 
severity of poisoning in, 851. 
multiple, postdiphtheritic. See Diph- 
theria, Paralysis, 
multiple puerperal, 854. 
preaxial, of Gombaults, 846. 
prognosis of, 846. 
reaction of degeneration in, 847. 
secondary forms of, origin of, 845. 
single, 846. 
acute, 848. 
course of, 846. 
due to exposure to cold, 847. 
Peripheral neuritis, single, due to infec- 
tions, 847. 
due to occupation palsies, 847. 
due to pressure of crutches, 847. 
postoperative, 848. 
prognosis of, 846-847. 
secondary, 847. 
syphilitic, 37. 
traumatic single, 84G. 
tuberculous. See Tuberculous neuritis. 
Peripheral paralysis associated with cere- 
bral and spinal lesions, 856. 
brachial, 875. 
circumflex, 878. 
due to cervcal rib, 876. 
infraclavicular, 877. 
median, 878. 
musculospiral, 878. 
of posterior thoracic nerve, 877. 
supraclavicular, 876. 
ulnar, 879. 
cauda equina, 882. 
cause of, neuritis, 856. 
cervical, hiccough-spasm of diaphragm 
in, 875. 
cervical, phrenic, 874. 
cranial, of auditory nerve, 868. 
Bell’s palsy, 864. 
facial, due to pontine disease, 864. 
facial or mimic spasm, 866. 
facial hemiatrophy, 863. 
glossopharyngeal, 870. 
hypoglossal, 873. 
of fifth (trigeminal) nerve, 862. 
of fourth (trochlear) nerve, 861. 
of ocular nerve, 860. 
of olfactory nerve, 856. 
of optic nerve, 857. 
of seventh nerve (facial), 863. 
of sixth (abducens) nerve, 861. 
of spinal accessory nerve, 871. 
of third nerve (motor oculi), 860. 
ophthalmoplegia, 861. 
pneumogastric, 871. 
spasm of spinal accessory muscles, 
872. 
tic convulsive with, 867. 
location of lesion causing, 856. 
lumbosacral, 879. 
sacral, 882. 
Peripylephlebitis syphilitica, 702. 
Periserositis, 662. 
Perisigmoiditis, 642. 
Perisplenic abscess, 1170. 
Perisplenitis, 1170. 
Peritoneum, diseases of, new growths of, 
663. 
peritonitis, acute diffuse, 659. 
peritonitis, chronic, 662. 
tuberculous. See Tuberculosis, 
endothelial degeneration of, 663. 
fatty deposits of, 663. 
innocent cysts and echinococcus of, 663. 
imitation of bacterial virulence and 
proliferation by, 660. 
neoplasms of, 663. INDEX 
1257 
Peritoneum, secondary carcinomata of, 
664. 
Peritonitis, acute diffuse, with appendici- 
tis, 659, 661. 
early control of, 662. 
kidney and liver in, 661. 
temperature in, 661. 
acute localized, 662. 
associated conditions of, 659-660. 
chronic, 662. 
pus accumulation in, 662. 
chronic nodular proliferative, 663. 
deforming and obliterating, 662. 
favorable cases of, 661. 
general, 660. 
hemorrhagic, 663. 
hiccough with, 875. 
idiopathic, 659. 
in nephritis, 792. 
localized and protective, 660. 
origin of, 659. 
perforative, gravity of, 660. 
in typhoid fever, 104-105. 
puerperal, 661. 
rheumatic, 659. 
suppurative, in pneumonia, 167. 
tuberculous, 257. 
with cirrhosis, 686. 
with rheumatic fever, 289. 
Peritonsillitis, acute suppurative, 297. 
Perityphlitis, 644. 
Pertussis. See Whooping-cough. 
Pestis minor, 205. 
Petit mal, 1046-1055. 
Pfeiffer’s disease, 353. 
Pharyngitis, acute catarrhal, 559. 
catarrhal, in typhoid fever, 97. 
chronic, 560. 
chronic alcoholic, 1181. 
phlegmonous, 560. 
ulcerative, 560. 
Pharyngitis sicca, 560. 
Pharynx, diseases of, circulatory anoma- 
lies, 559. 
pharyngitis, 559. 
edema of, 559. 
hemorrhagic symptoms of, 559. 
hyperemia of, 559. 
Phlebitis, sinus, following otitis, 955. 
septic, in appendicitis, 658. 
Phlebitis cruralis, in typhoid fever, 
95. 
Phlegmons, in typhoid fever, 107. 
Phobias, of neurasthenia, 1030. 
Phosphates, triple, in urine, 778. 
Phosphaturia, 777. 
Phosphorus poisoning, differentiated from 
acute yellow atrophy of liver, 
674. 
Phrenic neuralgia, 843. 
Phrenic paralysis, bilateral, 874. 
causes of, 874. 
prognosis of, 875. 
Phthisis, See Pulmonary Tuberculosis, 
fibroid, 244. 
Physical agents, diseases due, to caisson 
disease, 1207. 
mountain sickness, 1209. 
sunstroke, 1205. 
Pia mater and arachnoid, inflammation of, 
937. 
Pick’s disease, 432, 702. 
Pilocarpin, in sympathicotonia, 1083. 
vagotonia due to, 1082. 
von Pirquet’s test, 239. 
Pituitary gland, diseases of, hyperpitui- 
tarism, 1160. 
hypopituitarism, 1158. 
importance of, 1161. 
Plague, bubonic, 203. 
character of, 201. 
complications in, 206. 
general considerations of, 205. 
history of, 202. 
mode of entry of, 203. 
pestis minor, 205. 
pneumonic, 204. 
septicemic, 204. 
symptoms of, 205. 
transmission of, 202. 
Plethora, and obesity, 1127. 
Plethora vera. See Erythremia. 
Pleura, diseases of, hydrothorax, 396. 
mediastinal, 399. 
pleurisy, 389. 
pneumothorax, 396. 
Pleurisy, atelectasis in, 391. 
chronic, fibroid pneumonia due to, 395. 
nature of, 395. 
serofibrinous cysts with, 395. 
with multiple adhesions, 395. 
with proliferative changes, 395. 
differentiation of tuberculous and non- 
tuberculous, 392. 
dry, 248, 389. 
fibrinous, 389. 
associated symptoms of, 389. 
primary, 389. 
secondary, 389. 
hemorrhagic, 396. 
in cirrhosis, 694. 
in influenza, 127. 
in pneumonia, 165. 
in scarlet fever, 330. 
interlobular, 391. 
in typhoid fever, 98. 
pneumococcus, 389-390. 
purulent, 392. 
associated symptoms of, 393. 
general statements on, 393. 
in typhoid fever, 99. 
secondary, 392. 
virulent types of, 393. 
serofibrinous, 389. 
associated symptoms of, 390. 
double, 391. 
general considerations on, 391. 
mortality from, 392. 
persistent dyspnea with, 391. 
symptoms of, 390-391, 
temperature in, 390. 1258 
INDEX 
Pleurisy, serofibrinous, tuberculous. See 
Tuberculous pleurisy, 
unfavorable, 391. 
with diphtheria, 142. 
with effusion, 389. 
with endocarditis, 491. 
with rheumatism, 288. 
Pleuropneumonia. See Pneumococcus in- 
fection. 
Plumbism. See Lead poisoning. 
Pneumaturia, 787. 
Pneumococcus infection, general, manifes- 
tations of, 146. 
lobar pneumonia, 145. 
pneumococcemia, 146. 
Pneumococcus meningitis, 159. 
Pneumogastric paralysis, associated condi- 
tions of, 871. 
compression of nerve at base in, 871. 
primary, 871. 
Pneumonia, acute dilatation of stomach 
with, 577. 
and tuberculosis, 163-164. 
blood condition in, bacteremia, 156. 
blood-plates, 158. 
coagulation time, 158. 
diminution of carbon dioxid, 156. 
eosinophilia, 157. 
increase of fibrin, 158. 
leukocytosis, 156-157. 
lymphocytes, 157. 
myelocytes, 158. 
urobilin, 158. 
blood-pressure in, Gibson’s rule, 148. 
catarrhal, 169. 
chronic non-tuberculous, fibrinous or 
catarrhal, 379. 
general conclusions on prognosis of, 
380-381. 
interstitial, 379. 
pneumonokonioses, 280. 
tuberculosis developed from, 381. 
circulation in, collapse, 154. 
cyanosis, 153. 
influence of toxemia on heart and 
vasomotors, 147-153. 
irregularities of heart, 154. 
previous disease of heart, 153-154. 
complications in, arthritis, 167. 
bronchitis, 165. 
bronchorrhea, 165. 
emphysema, 166. 
empyema, 164-165. 
endocarditis, 167. 
fibrosis of lung, 166. 
gangrene of lung, 164. 
lung abscess, 165. 
metastatic parotitis, 168. 
neuritis, 168. 
otitis media suppurativa, 167. 
pericarditis, 166. 
peritonitis, 167. 
pleurisy, 165. 
pulmonary edema, 164. 
purpura, 167. 
purulent infiltration of lung, 166. 
Pneumonia, croupous, 146. 
clinical varieties of, 162. 
afebrile, 162. 
alcoholic, 162. 
aspiration, 163. 
asthenic, 162. 
bilious, 162. 
embolic, 163. 
hypostatic, 163. 
influenzal, 163. 
migratory, 163. 
complications in, tuberculosis, 163- 
164. 
pneumococcemia in, 146. 
desquamating, 169. 
due to occupation, 380-3S1. 
empyema with, 393. 
factors in prognosis of, age, 148. 
alcoholism, 149. 
association of diseases, 149. 
blood pressure study, 147-148. 
condition of life, 149. 
effect of toxemia and associated 
lung lesion on cardiovascular 
system, 147. 
extent of pulmonary and associated 
lesions, 150-151. 
malignancy of infecting organism, 147. 
predisposition to, 150. 
pregnancy, 150. 
race, 149. 
resistance of patient, 148. 
seasonal influences, 150. 
sex, 150. 
traumatism, 150. 
fibroid, due to chronic pleurisy, 395. 
fibrosis of lung in, 166. 
gangrene due to, 385. 
gastro-intestinal system in, dilatation of 
stomach, acute, 157, 161. 
hiccough, 161. 
membranous colitis, 161. 
meteorism, 161. 
vomiting, 161. 
greater frequency of, among men, 150. 
hemoptysis of, 376. 
herpes labialis in, 161. 
immunity following, 150. 
in congenital syphilis, 67. 
in diabetes mellitus, 1117. 
influence of, on endocarditis, 485. 
influence on, of prophylactic vaccination, 
169. 
in scarlet fever, 329. 
insular, 169. 
in tabes dorsalis, 58. 
lobar, 145. 
symptom complex of, 145. 
lobular, 169. 
membranous colitis in, 161. 
meningococcus, in cerebrospinal men- 
ingitis, 184. 
mortality from, among mental defec- 
tives, 150. 
nervous system in, of alcoholics, 159. 
convulsions, 159. INDEX 
1259 
Pneumonia, nervous system in, delirium, 
159. 
headaches, 159. 
lumbar puncture, 159. 
meningismus, 159. 
pneumococcus meningitis, 159. 
postpyrexial delirium, 160. 
spinal fluid, 159. 
toxemia of, 158. 
physical signs of, 162. 
post scarlatinal, 332. 
respiratory system in, cough, 155. 
frequency of respirations, 154-155. 
severe pain in pleura, 154. 
sputum, 155. 
symptoms of, 154-155. 
secondary, 169. 
skin in, 161. 
spleen in, 162. 
statistics and results of treatment in, 
168. 
sweating in, 161. 
temperature in, chill, 151. 
fever, 151-152. 
tuberculosis, 244. 
urinary system in, albuminuria, 160. 
chlorid excretion, 160. 
nephritis, 160. 
quantity of urine, 160. 
sugar, 160. 
urea and uric acid, 160. 
with cerebral hemorrhage, 972. 
with cirrhosis, 694. 
with diphtheria, 142. 
with epilepsy, 1056. 
with influenza, 126-127. 
with influenzal meningitis, 126-127. 
with malaria, 77. 
with pyemia, 133. 
with rheumatism, 288. 
with sepsis, 133. 
Pneumonic plague, 204. 
Pneumonic tuberculosis, 228. 
chronic interstitial, 244, 245, 246. 
Pneumonokonioses, 380. 
Pneumopericardium, 434. 
Pneumothorax, considerations in prognosis 
of, 397-398. 
dangers of, 397. 
due to empyema, 398. 
general considerations on, 397. 
in typhoid fever, 99. 
in tuberculosis, 397. 
statistics on, 397-398. 
with pus (pyopneumothorax), 396. 
with serum (hydropneumothorax), 
396. 
Poisoning, tetany due to, 1167. 
Poisons, neuralgia due to, 839. 
Polioencephalitis, 322, 975. 
Polioencephalitis inferior, 976. 
Polioencephalitis superior, of alcoholic 
origin, 975. 
psychic disturbances with, 975. 
respiratory paralysis with, 975. 
Polioencephalomyelitis, 976. 
Poliomyelitis, 854. 
acute anterior, abortive type of, 320. 
ataxic type of, 323. 
bulbar and pontine types of, 322. 
cerebral type of, 322. 
conclusions on, 324. 
electrical reactions in, 323. 
general considerations of, 323. 
Landry type of, 322. 
lumbar puncture for, 323. 
meningitic type of, 323. 
mortality from, 324-325. 
polyneuritic type of, 323. 
prodromal period of, 311). 
spinal, 321. 
sporadic cases of, 324. 
stage of paralysis in, 320. 
chronic, 326. 
encephalitic, 975. 
Flexner’s and Noguchi’s findings on, 
318. 
“healthy carriers” of, 319. 
increase in number of cases of, 318. 
increase in severity of, 319. 
nature of, 317. 
pathologic area of, 318. 
period of incubation of, 319. 
port of entry of, 319. 
“rudimentary,” 320. 
Pollantin, 359. 
Polyarthritis, acute. See Rheumatic fever, 
destructive chronic, arthritis deformans, 
1088. 
rheumatism, chronic articular, 1088. 
non-suppurative, in scarlet fever, 332. 
Polycystic kidney, leading symptoms of, 
827. 
nature of, 827. 
Polycythemia, symptomatic. See Ery- 
thremia, secondary. 
Polycythemia vera. See Erythremia, pri- 
mary. 
Polyneuritis, 848. 
acute febrile, 853. 
glucosuria in alcoholics with, 1118. 
tuberculous, 278. 
Polypi, of esophagus, 568. 
Polypoid growths, 358. 
of intestines, 644. 
Polyplasma, 518. 
Polyserositis, chronic, 432. 
Polyuria, in chronic interstitial nephritis, 
807. 
in diabetes mellitus, 1114. 
Pontine disease, facial paralysis due to, 
864. 
Popliteal nerve, external, paralysis of, 
881. 
internal, paralysis of, 881. 
Portal pyemia, 678, 679, 707. 
Portal vein, diseases of, pylephlebitis, 
678. 
thrombosis, 678. 
Postbasic meningitis, 934. 
Posterior disease, combined lateral and* 
901. 1260 
INDEX 
Posterior thoracic nerve, paralysis of, 
877. 
Postpyrexial delirium, 160. 
Pregnancy, albuminuria of, 794. 
and epilepsy, 1051. 
and obesity, 1128. 
and pneumonia, 150. 
chorea due to, 1040. 
in paratyphoid, 123. 
in tuberculosis, 241-251. 
in typhoid, 110. 
myelitis of, 907. 
nephritis of, 794. 
nephritis aggravated by, 796. 
Priapism, in leukocytic leukemia, 532. 
Profeta law, 65. 
Prognosis, Alpinus, Prosper, on, 4. 
Chauffard on, 5. 
collective investigation of disease in, 
9. 
definition of, 1. 
Duckworth, Sir Dyce, on, 5. 
endogenous influences in, 6, 7, 8, 9. 
exogenous influences in, 6-7. 
factors in, after effects of disease, 7-8. 
age, 6. 
constitution, 7. 
diathesis, 7. 
early diagnosis, 6. 
general survey of patient, 11-12. 
influence of acute infections, on exist- 
ing chronic diseases, 8-9. 
latency of symptoms, 11. 
localization of lesions, 6. 
neuropathic tendencies, 8. 
occupation, 6. 
phagocytosis, 8. 
race, 7. 
tolerance of organs to pathologic 
change, 6. 
varying character of epidemics, 7. 
giving of, to patient, 10-11. 
Harvey, J., on, 4. 
Hippocrates on, 2-3. 
honest suggestion with, 11. 
in acute infections, 7. 
in bacterial disease, 8. 
in contagious diseases, 7-8. 
in epidemics, 7. 
in infectious diseases, 8. 
Munk on, 4. 
optimism in, 10, 11. 
Paget, Sir James, on, 8. 
publications dealing with, 4-5. 
requirements for, 9. 
setting of time limit in, 11. 
Progeria, in infantilism, 1159. 
Protozoan infections, amebic dysentery, 
78. 
Leishmaniasis, 83. 
malaria, 72. 
relapsing fever, 82. 
syphilis, 15. 
trypanosomiasis, 81. 
Pruritus, in diabetes mellitus, 1118. 
Pseudo-angina, 456. 
Pseudobulbar paralysis, causes of, 893. 
course of, 893. 
infantile, 893. 
symptoms of, 893. 
Pseudoleukemia. See Leukemia, lymphatic. 
See Hodgkin’s disease, 
transition of, to leukemia, 541. 
Pseudomultiple sclerosis, 913. 
Pseudotabetic gliosis, 917. 
Pseudotabetic symptoms, in arsenical mul- 
tiple neuritis, 852. 
Psilosis, 626. 
Psychalgia, 841. 
akinesia algera, 1086. 
Psychasthenia, 1030. 
Psychic disturbances, in brain tumor, 993. 
in chorea, 1040. 
in pellagra, 1200. 
Psychoneurosis. See Hysteria. 
Psychoses, due to influenza, 129. 
Ptomain poisoning, 1203. 
enteritis due to, 620. 
Ptyalism, 556. 
Puerperal erysipelas, 174. 
Puerperal multiple neuritis, 854. 
Pulmonary abscess, associated with em- 
pyema, 393. 
hemoptysis of, 378. 
Pulmonary apoplexy, 378. 
Pulmonary cancer, 387. 
Pulmonary complications, in appendicitis, 
658. 
in gout, 1105. 
Pulmonary congestion, active, 373. 
edema, 375. 
hypostatic, 374, 375. 
passive, 374. 
Pulmonary edema, 375. 
in nephritis, 792. 
in pneumonia, 164. 
in typhoid fever, 99. 
with epilepsy, 1056. 
Pulmonary embolism, with chlorosis, 518. 
Pulmonary emphysema, caused by chronic 
bronchitis, 365. 
Pulmonary gangrene, due to infarct, 378. 
hemoptysis of, 377. 
in pulmonary carcinoma, 387. 
primary infections of, pneumonia, 385. 
thrombosis or embolism of branch of 
pulmonary artery, 386. 
Pulmonary hemorrhage, hemoptysis, by 
aspiration to other parts of 
lungs, 378. 
due to aortic aneurism, 377. 
due to chronic bronchitis, 377. 
due to gangrene, 377. 
due to heart disease, 376-377. 
due to hemophilia, 377. 
due to hyperemia, 376. 
due to malignant growths, 376. 
due to malignant purpura, 377. 
due to mitral stenosis, 376. 
due to pneumonia, 376. 
due to syphilitic ulceration of air 
passages, 377. INDEX 
1261 
Pulmonary hemorrhage, due to ulcera- 
tive disease of upper air pas- 
sages, 376. 
due to vicarious menstruations, 376. 
due to Avhooping-cough and measles, 
377. 
in arteriosclerosis, 377. 
in nephritis, chronic interstitial, 377. 
into air cells, 378. 
Pulmonary infarct, 378. 
in typhoid fever, 98. 
Pulmonary insufficiency, 504. 
Pulmonary neoplasms, primary, 387. 
secondary, 388. 
Pulmonary obstruction, congested kidney 
due to, 813. 
Pulmonary pernicious malaria, 750. 
Pulmonary stenosis, and associated condi- 
tions, 436-437. 
compensatory hypertrophy, 435. 
nature of, 435. 
Pulmonary tuberculosis, age as factor in, 
238. 
and laryngeal, 251. 
calcification or fibroid change in, 227. 
caseous, 229. 
cavity formation in, 230. 
chronic, 229. 
diazo-reaction in, 234. 
disappearance of, due to, raised resist- 
ance of patient, 218-227. 
due to measles, 344. 
factors in, 226. 
gangrene due to, 386. 
incipient cases of, 237. 
limited expansion of thorax in, 233. 
lobar or pneumonic, 228. 
lobular pneumonic, 227. 
misshapen or retracted thorax in, 233. 
physical signs of, of advancing disease, 
238. 
in incipient cases, 237. 
in last stage, 238. 
rheumatoid form associated with, 234. 
rontgenoscopy in, 239-240. 
symptoms of, blood conditions, 235, 236, 
237. 
cough, 229-230. 
diarrhea, 232. 
digestive, 234. 
dyspepsia, 228. 
expectoration, 229-230. 
fever, 227, 231, 232. 
heart, 233. 
hemoptysis, 227-231. 
hoarseness, 234. 
infiltration of lung tissue, without 
cough, 230. 
liver and spleen, 234. 
loss of weight, 233. 
nervous, 235. 
nummular expectoration, 230. 
pain, 233. 
shortness of breath, 230. 
urinary, 234. 
tuberculin tests for, 238-239. 
Pulmonary tuberculosis, ulcerative, 229. 
with chlorosis, 518. 
with cirrhosis, 086. 
with defect in intraventricular septum, 
436. 
with epilepsy, 1056. 
with perforate foramen ovale, 436. 
Pulmonary valve, defects of, 503. 
Pulse, alternate, 449. 
Pupillary phenomenon, hysterical, 1013. 
in cerebral hemorrhage, 965. 
Purpura, chronic, alternation of, with ery- 
thema multiforme, 546. 
blood picture of, 547. 
continuous, 546. 
intermittent, 546. 
mode of termination of, 547. 
nature of, 546. 
rebe’lion of, to treatment, 546. 
due to iodin, 543. 
Henoch’s, 547. 
in congenital syphilis, 67. 
in nephritis, 809. 
in rheumatism, 290. 
malignant, hemoptysis of, 377. 
primary, chronic, 546. 
hemophilia, 548. 
Henoch’s, 547. 
purpura hemorrhagica, 545. 
purpura rheumatica, 544. 
purpura simplex, 543. 
secondary, associated conditions of, 
542. 
prognostic import of, 543. 
symptom complex of, 542. 
Purpura fulminans, of adults, 545. 
of infants, 544. 
Purpura hemorrhagica, 545. 
blood picture of, 545. 
hemorrhage into appendix in, 545. 
in typhoid fever, 106. 
Purpura rheumatica, 544. 
chorea with, 1039. 
resemblance of, to erythema nodosum, 
544. 
Purpura simplex, 543. 
Purpuric appendicitis, 649. 
Pus casts, 750. 
Pyelitis, acute, 831. 
ascending, 832. 
blood examinations in, 832. 
calculous, 824, 831. 
catarrhal, 830. 
recurrence of, 831. 
chemical and bacteriological examina- 
tions in, 832. 
chronic, 831. 
chronic cystitis with, 831. 
cystoscopic examinations in, 832. 
danger of neglected, 831. 
definition of, 829. 
distinguished from renal tuberculosis, 
268. 
gonorrheal, 832. 
in enfeebled subjects, 830. 
in typhoid, 110. 1262 
INDEX 
Pyelitis, lack of bacteriological cure of, 
832. 
non-calculous, with hematuria, 759. 
prognosis of, after local treatment, 833. 
after operation, 831. 
prognostic factors of, 830. 
pyelography for, 832. 
repeated chills and fever in, 834. 
surgical treatment for, 831. 
urine in, 833. 
with tuberculosis of genito-urinary 
tract, 830. 
x-ray in, 832. 
Pyelocystitis, infection of, 830. 
toxic symptoms of, 830. 
Pyelography, in pyelitis, 832. 
Pyelonephritis, acute, nephrotomy for, 831. 
definition of, 829. 
nephrectomy for, 831. 
Pyemia, 131-132. 
and pneumonia, 133. 
due to aural and brain abscess, 984. 
in actinomycosis, 301. 
Pyemic infections, mixed with septic, 131. 
Pylephlebitis, 678. 
suppurative, 679, 704, 707. 
Pylethrombosis, 678. 
in amebic dysentery, 80. 
Pyloric spasm, 581. 
causes of, 582. 
in hypermotility, 617. 
Pyloric stenosis, benign acquired, acute 
inflammatory, 583. 
chronic cicatricial, 583. 
complete, 585. 
dependent on active ulcer, 583. 
dependent on non-malignant growths, 
584. 
due to distortion or traction, 584. 
fibrotic, 583. 
general fibrotic, 583. 
hypertrophic, of Cruveilliier, 583. 
localized fibrotic, 583. 
syphilitic, 583. 
tuberculous, 584. 
benign functional, 581. 
benign organic, 582. 
acquired, 583. 
congenital, 582. 
extrapyloric, 584. 
Pylorus, adhesions of, in cholelithiasis, 
729. 
Pyonephrosis, 815. 
definition of, 829. 
Pyopneumothorax, 396. 
Pyothorax, 392. 
Pyrexia, post-typhoid, 93. 
Q 
Quadriplegia, 846. 
due to alcoholic multiple neuritis, 849. 
Quincke’s disease. Sec Angioneurotic 
edema. 
Quinsy. See Peritonsillitis. 
R 
Rabies. See Hydrophobia. 
Rachitis, acute, 1131. 
advanced, 1129. 
bony changes in, 1129. 
causes of, 1129. 
course of, 1129. 
deformities of, 1130. 
due to congenital syphilis, 67. 
due to hereditary syphilis, 1129. 
due to patent foods, 1129. 
enlarged spleen and liver in, 1130. 
excessive sweating of head in, 1130. 
faulty diet in, 1130. 
Harrison’s sulcus in, 1130. 
heredity in, 1129. 
Hutchinson teeth in, 1130. 
in poorer classes, 1129. 
late, 1129. 
persistent improper respiration in, 1130. 
predisposition to, 1129. 
“rosary” in, 1130. 
severe cases of, 1130. 
severity of infections in, 1130. 
tardiness of walking in, 1130. 
tendency to recovery in, 1130. 
Radial paralysis, 878. 
Railroad spine. See Traumatic neurosis. 
Ray fungus, 301. 
Raynaud’s disease, age in, 1070. 
and erythromelalgia, 1067. 
characteristic symptoms of, 1069. 
complications in, 1072-1073. 
family predisposition to, 1070. 
first stage of, local syncope, 1070. 
frequency of,-1070. 
gangrenes not included in, 1070. 
prognosis for life in, 1074. 
seasonal influences in, 1070. 
second stage of, local asphyxia or cyan- 
osis, 1071. 
sex influence in, 1070. 
third stage of, symmetrical gangrene, 
1072. 
thyroid treatment for, 1073. 
Reaction of degeneration, in facial paraly- 
sis, 865. 
in idiopathic multiple neuritis, 854. 
in lead multiple neuritis, 851. 
in peripheral neuritis, 847. 
Reactions, electrical, in poliomyelitis, 323. 
von Recklinghausen’s disease, 883. 
Rectum, syphilis of, 34. 
Reflex excitability, hysterical, 1015. 
Refraction, errors of, 857. 
Reichman’s disease, 618. 
suggestive of ulcer, 589. 
Relapsing fever, 82. 
Relapsing typhus. See Relapsing fever. 
Renal asthma, 370. 
and nephritis, 370. 
Renal calculi, cystin stones, 821. 
hematuria due to, 759. 
large, 821. 
multiple, 821. INDEX 
1263 
Renal calculi, sand or gravel, 821. 
single, without infection, 821. 
varieties of, 821. 
xanthin stones, 821. 
x-ray examination in, 821. 
Renal cirrhosis, 804. 
Renal colic, in nephrolithiasis, 823. 
Renal epistaxis, indicated by hematuria, 
757. 
Renal function, estimation of, 770. 
Renal growths, 825. 
Renal infarct, hematuria with, and septic 
fever, 758. 
Renal insufficiency, in chronic interstitial 
nephritis, 800. 
in cirrhosis, 694. 
Renal sclerosis, 804. 
Renal sufficiency test, early application 
of, 773. 
diagnostic and prognostic value of, 768. 
for chronic nephritis, 800. 
for estimation of incoagulable or non- 
protein nitrogen of blood, 771. 
phenolsulphonephthalein, of Rowntree 
and Geraghty, 770. 
of Thayer and Snowden, 772. 
results of, 773. 
Schlayer’s, 769-770. 
ureteral catheterization with, 773. 
Renal system, diseases of, nephropathies, 
amyloid kidney, 814. 
congested kidney, 811. 
nephritis, acute parenchymatous, 
788. 
nephritis, chronic interstitial, 804. 
nephritis, chronic parenchymatous, 
797. 
tuberculous kidney. See Tuber- 
culous kidney. 
suppurative, perinephric abscess, 834. 
pyelitis, 829. 
surgical, hydronephrosis, 815. 
movable kidney, 828. 
neoplasm, 825. 
nephrolithiasis, S20. 
Renal tuberculosis, bladder invasion in, 
269. 
blood pressure in, 270. 
distinguished from pyelitis, 268. 
early hematuria in, 269. 
extent of, 269. 
factors influencing prognosis of, 268. 
perinephric abscess with, 269. 
pregnancy and childbirth with, 270. 
reduced functional activity in, 268. 
surgical removal of primary focus in, 
269. 
with advanced pulmonary, 269-270. 
with miliary infection, 268. 
Respiratory symptoms, in exophthalmic 
goiter, 1146. 
in typhoid fever, 96. 
Respiratory system, actinomycosis of, 302. 
anthrax, 211. 
diseases of, bronchial, asthma, 368. 
Respiratory system, diseases of, bronchial, 
bronchitis, acute, 363. 
bronchitis, chronic, 365. 
bronchitis fibrinous, 373. 
syphilis, 33. 
whooping-cough. See Pertussis, 
laryngeal, edema, 362. 
laryngismus stridulus, 362. 
laryngitis, acute, 360. 
laryngitis, chronic, 361. 
laryngitis, syphilitic. See Syph- 
ilitic laryngitis. 
laryngitis, tuberculous. See Tuber- 
culous laryngitis, 
syphilis, 33. 
nasal, acute catarrhal rhinitis, 357. 
epistaxis, 359. 
hay fever, 358. 
nasal, 32. 
pleural, hydrothorax, 396. 
mediastinal, 399. 
pleurisy, 389. 
pneumothorax, 396. 
pulmonary, abscess, 386. 
congestion, 373. 
emphysema, 382. 
gangrene, 385. 
hemorrhage, 376. 
neoplasm, 387. 
non-tuberculous pneumonia, 379. 
syphilis, 33. 
effect on, of trichinosis, 313-314. 
in alcoholism, 1183. 
influence of, on endocarditis,, 489. 
in measles, 344. 
in pneumonia, 154. 
in scarlet fever, 329. 
Retina, lesions of, causing blindness, 857. 
in chronic nephritis, 803. 
Retinal hemorrhages, with pernicious ane- 
mia, 527. 
Retinitis, albuminuric, in chronic intersti- 
tial nephritis, 809. 
Retrobulbar disease, 858. 
Retropharyngeal abscess, 560. 
Rheumatic fever, bacteriology of, 279. 
complications in, appendicitis, 289. 
blood, 287. 
brain and nervous system, 287. 
heart, bradycardia, 286. 
endocarditis, 283. 
myocarditis, 285. 
pericarditis, 285. 
tachycardia, 286. 
hyperpyrexia, 286. 
kidney, 288. 
lung and pleura, 288. 
peritonitis, 289. 
purpura, 290. 
rheumatic nodules, 289. 
septic, 289. 
skin, 289. 
duration of, 290. 
factors influencing prognosis of, 279. 
age, 281. 
character of onset, 281. 1264 
INDEX 
Rheumatic fever, factors influencing 
prognosis of, coincident dis- 
ease, 282. 
environment and social conditions, 
291. 
preexisting diseases, 281. 
resistance of patient, 280. 
sex, 280. 
immunity to, 291. 
mortality from, 279. 
nature of, 278. 
number of joints inflamed in, 290. 
recurring, 290. 
relapses of, 291. 
symptoms of onset of, 281. 
Rheumatic nodules, 289. 
Rheumatism, chorea and endocarditis 
with, 284. 
chronic articular, pathological simi- 
larity of, to arthritis defor- 
mans, 1088. 
gonorrheal, 192. 
inflammatory. See Rheumatic fever, 
muscular. See Myalgia, 
pleurisy and, 288. 
Rhinitis, acute catarrhal, extension of, 357. 
primary, 357. 
secondary, 357. 
syphilitic, 357-358. 
Rhinologic abscess of brain, 985. 
Rickets. See Rachitis. 
Romberg symptoms, of tabes dorsalis, 55. 
Rontgenoscopy, for tuberculosis, 239-240. 
Rose cold. See Hay fever. 
Roseola, epidemic, 346. 
in typhoid fever, 106. 
See Measles. 
Rothera test, for acetone, Garrod’s modifi- 
cation of, 1115. 
Round worms, 315. 
Rubeola, 346. 
Rubeola scarlatinosa, 352. 
Rupture of esophagus, 568. 
Rupture of heart, 466. 
Rupture of valves, 500. 
S 
Sachs’ disease. See Idiocy, amaurotic 
family. 
Sacral plexus, paralysis of, 882. 
Salivary glands, diseases of, Mikulicz’s 
disease, 557. 
mumps. See Parotitis, epidemic, 
parotitis, 557. 
Salivary swellings, bilateral, 557. 
Salvarsan, encephalitis due to, 976. 
in pernicious anemia, 528. 
polyneuritis due to, 852. 
Sarcoma, of brain, 996. 
of intestines, 644. 
of kidney, 825. 
of liver, 709-711. 
of spinal cord, 923. 
infiltration in, 924. 
Sarcoma, of spinal cord, multiple, 924. 
Saturnine anemia, 1190. 
Saturnine arteriosclerosis, 1192. 
Saturnine arthralgia, 1189. 
Saturnine nephropathy, 1192. 
Scanning speech, in multiple sclerosis of 
brain and cord, 910. 
Scarlatinoid, 352. 
Scarlet fever, albuminuria with, 746. 
and measles, 345. 
character of, 327. 
classification for prognosis, 332. 
complications in, adenitis, 332. 
arthritis, 332. 
endocarditis, 330. 
myocardial degeneration, 330. 
nephritis, 331. 
nephritis, with endocarditis, 330. 
respiratory, 329. 
uremic poisoning, 331. 
mild, 328. 
pleurisy in, 330. 
prognosis of, 828-329. 
symptoms of, 330. 
cardiovascular, 330. 
diphtheritic, 329. 
ear, 329. 
general, 328-329. 
increasing anemia with eye symp- 
toms, 332. 
pulse, 330. 
renal, 331. 
without rash and with slight tonsillitis, 
328. 
Schmidt’s bile test, in summer diarrhea of 
infants, 629. 
Schoenlein’s disease, 544. 
Sciatic neuralgia, 844. 
Sciatic pain, with tumors of spinal cord, 
921. 
Sciatic paralysis, 880-881. 
Sciatica, 844. 
Sclerodactylia, 1077. 
Scleroderma, acute, 1077. 
causes of, 1077. 
circumscribed, 1077. 
definition and nature of, 1077. 
duration of, 1077. 
heredity in, 1077. 
intercurrent disease in, 1078. 
joint changes in, 1077. 
pigment deposit and bronzing in, 
1077. 
prognosis of, 1078. 
recession of lesions in, 1077. 
typical cases of, 1077. 
Sclerosis, amyotrophic lateral, 890. 
congenital lateral, cause of, 900. 
diplegic character of, 901. 
prognosis of, 901. 
symptoms of, 900. 
coronary, 454. 
disseminated nodular. See Multiple 
sclerosis of brain and cord, 
disseminated, of optic nerve, 858. INDEX 
1265 
Sclerosis, multiple, of brain and cord. 
See Multiple sclerosis of brain 
and cord. 
primary lateral, advanced, symptoms of, 
900. 
character of, 899. 
course of, first stage, 899. 
second stage, 900. 
terminal or third stage, 900. 
stationary periods of, 900. 
weakness of legs in, 900. 
pseudomultiple, 913. 
Sclerosis en placque. See Multiple sclero- 
sis of brain and cord. 
Scorbutus, adult, causes of, 1132. 
endemic, 1133. 
malignant, 1133. 
origin and association of, 1132. 
symptoms and infections of, 1133. 
infantile, causes of, 1133. 
symptoms of, 1133. 
Scrivener’s palsy, 1064. 
Scrofula, 265. 
Scurvy. See Scorbutus. 
Secretory disturbances, hysterical, 1018. 
Senile heart, 460. 
Senile kidney, 805. 
Sensory disturbances, in chorea, 1041. 
in neurasthenia, 1030. 
Sepsis, 130, 131, 132, 133. 
duration of, 133. 
in rheumatism, 289. 
Septic meningitis, 133. 
Septic thrombosis, 132. 
Septicemia, character of, 130-131. 
Septicemic plague, 204. 
Septicopyemia, 130. 
Serratus magnus, paralysis of, 877. 
Seventh nerve, paralysis of, 863. 
Sexual anomalies, hysterical, 1018. 
in diabetes mellitus, 1117. 
Sexual hypochondriacs, 1028. 
Sexual neurasthenia, 1028-1029. 
Shaking palsy. See Paralysis agitans. 
Shingles. See Herpes zoster. 
Ship fever. See Typhus fever. 
Siderosis, 380. 
Silicosis, 380. 
Sinus phlebitis, following otitis, 955. 
Sixth nerve, paralysis of, 861. 
Skin, actinomycosis of, 302. 
in paratyphoid, 123. 
in typhoid fever, 106. 
Skin changes, in arsenical poisoning, 1194. 
in diabetes mellitus, 1118. 
in exophthalmic goiter, 1147. 
in gout, 1104. 
in measles, 343. 
in pellagra, 1200. 
Skin diphtheria, 138. 
Sleeping sickness. See Trypanosomiasis. 
Smallpox, age in, 334. 
black, 337. 
classification of, 335. 
variola without eruption, 337. 
variola hemorrhagica, 337. 
Smallpox, classification of, variola vera, 
336. 
varioloid, 337. 
complications in, 338. 
confluent, 337. 
discrete, 336. 
epidemics of, 334. 
general considerations on, 333. 
general statement on, 336. 
hemorrhagic, 337. 
historical data for, 333. 
immunity to, 334. 
nature of, 333. 
pustular hemorrhagic, 336. 
race in, 334. 
sex in, 334. 
stage of eruption of, 335. 
stage of incubation of, 334. 
stage of invasion of, 334. 
symptoms of, backache, 334. 
blood, 336. 
cerebral invasion, 334. 
enlarged spleen, 335. 
eruptions, 335. 
pulse, 335. 
pustulation, 335. 
temperature, 336. 
vaccination against, 333. 
influence of, on prognosis, 340. 
rules for, 339-340. 
Smell, hysterical perversion of, 1011. 
loss of, 856. 
perversion of, 857. 
Spasm, facial, 866. 
hysterical, 1014. 
in brain tumor, 994. 
in exophthalmic goiter, 1144. 
mimic, 866. 
muscular, in myotonia, 1085. 
of sternocleidomastoid, 872. 
of trapezius, 872. 
Spasm of diaphragm. See Hiccough. 
Spastic paralysis, 899. 
family type of, associated with idiocy, 
903. 
with hydrocephalus, 945. 
Spastic paraplegia. See Sclerosis, primary 
lateral, 
secondary, 902. 
Spinal accessory, neuritis, 872. 
paralysis, causes of, 871-872. 
Spinal anemia, complete, 928. 
due to arterial obstruction, 927. 
effect of, on primary disease, 928. 
local, 927. 
prognosis of, 928. 
secondary, 927. 
symptoms of, 928. 
Spinal arteriosclerosis, 929. 
Spinal congestion, passive, 928. 
Spinal cord, abscess of. See Abscess of 
Spinal Cord. 
affections of blood vessels of, 927. 
anemia of. See Spinal anemia, 
carcinoma of, 924. 
changes in arteries of, 928. 1266 
INDEX 
Spinal cord, gliosis of, 914. 
hyperemia of, 928. 
sarcoma of. See Sarcoma of Spinal 
Cord, 923. 
tubercle of, 924. 
tumors of. See Tumors of Spinal Cord. 
Spinal cord diseases, afferent or sensory 
system, general paralysis of in- 
sane. See Paresis, 
hereditary ataxia, 887. 
herpes zoster, 885. 
Marie’s hereditary ataxia, 888. 
tabes dorsalis. See Tabes dorsalis, 
taboparesis. See Taboparesis, 
anterior of efferent or motor tract. Lan- 
dry’s ascending paralysis. See 
Landry’s Paralysis, 888. 
muscular dystrophies, 895. 
myotonia congenita, 898. 
poliomyelitis anterior, 854. 
progressive central muscular atrophy, 
888. 
progressive neural muscular atrophy, 
894. 
indiscriminate, abscess, 914. 
of blood vessels, 927. 
caisson disease. See Caisson disease, 
multiple sclerosis of brain and cord, 
908. 
myelitis, 904. 
pseudomultiple sclerosis, 913. 
syringomyelia, 914. 
tumors, 918. 
lateral, amyotrophic lateral sclerosis. 
See Amyotrophic lateral sclero- 
sis. 
ataxic paraplegia, 901. 
congenital lateral sclerosis, 900. 
Erb’s syphilitic spinal paralysis. See 
Syphilis of cord, 
idiocy, amaurotic family, 903, 
paraplegia, secondary spastic, 902. 
primary lateral sclerosis, 899. 
Spinal embolism, 929. 
Spinal endarteritis, 929. 
Spinal fever, sporadic, 934. 
Spinal fluid, in epidemic cerebrospinal 
meningitis, 182-183. 
Spinal hematoma, 931. 
Spinal hemorrhage, causes of, 930. 
prognosis of, 931. 
spontaneous, 930'. 
symptoms following, 930. 
traumatic cases of, 931. 
Spinal leptomeningitis, acute, 933. 
chronic, 933. 
Spinal membranes, diseases of, hematoma, 
931. 
hemorrhage, 930. 
spinal meningitis, 931. 
most frequent forms of, 931. 
Spinal neurasthenia, 1028. 
Spinal pachymeningitis, definition of, 932. 
external, diseases primary to, 932. 
following surgical operations, 932, 
lumbar fluid in, 932. 
Spinal pachymeningitis, external, prog- 
nosis of, 932. 
internal, 932. 
Spinal paralysis, due to syphilis, 36. 
Spinal syphilis, 35. 
effects of, 36. 
Erb’s syphilitic spinal paralysis, 37. 
paralysis due to, 36. 
reactions in, 36. 
relapse of, 37. 
symptoms of, 35-36. 
without cord involvement, 36. 
Spinal thrombosis, 929. 
Spinal vessels, advanced change in, 929. 
Spine, concussion of, 1021-1022. 
railroad, 1021. 
typhoid, 112. 
Spleen, abscess of, 80, 1170. 
amyloid degeneration of, 34, 1170. 
changes in, due to malaria, 73, 74, 77. 
condition of, in leukemia, 531-532. 
cyst of, 1171. 
diseases of, mobile spleen, 1173. 
splenomegaly, primary, 1171. 
splenomegaly, secondary, 1169. 
enlargement of. See Splenomegaly, 
gummata of, 33. 
hydatid cysts in, 308. 
in erythremia, 550. 
infarct of, 1171. 
influence of, on hemolytic jaundice, 668. 
in lymphatic leukemia, 533. 
in pneumonia, 162. 
in typhoid fever, 107. 
mobile, 1173. 
perforation of, 1170. 
rupture of, 1171. 
syphilis of, 33, 1170. 
tuberculous, 262, 1170. 
Splenectomy, in cirrhosis of liver, 682. 
in leukemia, 535. 
in pernicious anemia, 523. 
Splenic abscess, in amebic dysentery, 80. 
Splenic anemia, characteristic svinptoms 
of, 1172. 
in children, 1173. 
prognosis of, 1173. 
Splenic anthrax, 211. 
Splenomegaly, of Gaucher type, 1171, 
primary, 1171. 
secondary, abscess with, 1170, 
acute, 1169. 
amyloid, 1170. 
chronic, 1169. 
with polycythemia, 1170. 
cyst with, 1171. 
infarct with, 1171. 
in otherwise healthy subjects, 1170. 
in syphilis, 34. 
passive congestion with, 1170. 
perforation in, 1170. 
perisplenic abscess in, 1170. 
perisplenitis or capsulitis with, 1170, 
prognostic factors in, 1170. 
rupture in, 1171. 
syphilitic, 1170, INDEX 
1267 
Splenomegaly, secondary, tuberculous, 
1170. 
with liver cirrhosis, 1171. 
splenic anemia in, 1172. 
Spondylitis. See Marie’s disease. 
Sporadic spinal fever, 934. 
Spotted fever. See Typhus fever. 
Sprue, 626. 
St. Vitus’ dance. See Chorea. 
Staggering, cerebellar, 1003. 
Staphylococcus infection, 131. 
Stasis, in chronic interstitial nephritis, 
807. 
Status epilepticus, 1054. 
Status thymo-lymphaticus, 363, 370, 1164. 
Stegomyia fasciata, 347. 
Stenosis, extrapyloric, 584. 
intra-esophageal, 566. 
intrapyloric, 583. 
tricuspid, 503. 
Stenosis of aortic orifice, 438. 
Stenosis of glottis, in syphilis, 33. 
Stenosis of mitral and tricuspid valves, 
439. 
Stenosis of pulmonary orifice, 435. 
Sternomastoid, paralysis of, 872. 
spasm of, 872. 
Stern’s basedowoid disease, 1149. 
Still’s disease, 1092. 
Stokes-Adams’ disease, associated condi- 
tions of, 463. 
deaths due to, 464. 
duration of, 464. 
mercury and neosalvarsan, treatment of, 
464. 
phenomena of, 463. 
prognosis of, 464. 
Stomach, catarrh of, 570. 
chronic catarrh of, 572. 
cirrhosis of, 572. 
diseases of, cancer, 600. 
dilatation, 576. 
enteroptosis, 579. 
gastritis, 570. 
gastroptosis, 579. 
gastrorrhagia, 613. 
hematemesis, 613. 
pyloric obstruction, 581. 
syphilis of, 34. 
tuberculosis of, 253. 
Stomach contents, examination of, in gas- 
tritis, 574. 
in early diagnosis of cancer, 602. 
in gastric ulcer, 589. 
Stomach lesions, in cirrhosis, 685. 
Stomachal vertigo in chronic gastritis, 
575. 
in dilatation of stomach, 578. 
Stomatitis, aphthous, 553. 
aphthous, epidemic. See Foot and 
Mouth Disease, 
causative relations of, 555. 
causes of, 553. 
erythematous, 553. 
extent of inflammation in, 553. 
gangrenous, 555, 
Stomatitis, herpetiform, 554. 
mercurial, 556. 
simple catarrhal, 553. 
ulcerative, in cancer of stomach, 607. 
in measles, 344. 
primary, 554. 
secondary, 554. 
symptoms of, 554. 
Stomatitis neurotica chronica, 554. 
Stomatitis parasitica, 556. 
Strangulated intestines, due to false liga- 
ments, 636. 
due to hernia, 637. 
due to incarceration through slits and 
apertures, 637. 
due to isolated bands and adhesions, 637. 
due to Meckel’s diverticulum, 636. 
due to normal structures abnormally at- 
tached, 637. 
due to omental cords, 636. 
Streptococcus erysipelatis, 173. 
Streptococcus infection, 131, 132, 133. 
Streptococcus tonsillitis, 293. 
Streptococcus viridans infection, with 
chorea, 1039. 
Streptotlirix, 301. 
Stricture. See Stenosis. 
Subphrenic abscess, in cholelithiasis, 730. 
Subscapular paralysis, 877. 
Substernal struma, 1164. 
Sunstroke, atmospheric influence in, 1206. 
contributing factors to, 1205. 
dangers of, immediate, 1205. 
remote, 1206. 
effects of, asthenia and myasthenia, 
1206. 
changed disposition, 1206. 
epilepsy, 1051, 1206. 
meningitis, 1206. 
mental lethargy and loss of memory, 
1206. 
ocular disturbances and deafness, 
1206. 
psychoses, 1206. 
tendency to recurrence of hyper- 
pyrexia, 1206. 
mortality from, 1206. 
occurrence of, 1205. 
symptoms of, deep coma, 1206. 
delirium, 1206. 
focal, 1206. 
hemiplegia, 1206. 
hyperpyrexia, 1205. 
in obese patients, 1206. 
irregular respiration, 1205. 
meningitis and encephalitis, 1206. 
paralysis, 1206. 
sudden vertigo, 1205. 
thermic fever due to, 1206. 
Supraclavicular paralysis, 876. 
Supra-orbital neuralgia, 841. 
Suprarenal gland, diseases of, Addison’s, 
See Tuberculosis of Suprarenal 
Bodies. 
Suprarenal tuberculosis, chronic, 264. 
duration of, 264. 1268 
IKDEX 
Suprarenal tuberculosis, chronic, symp- 
toms of, 263. 
syphilitic deposit in, 264. 
Swallowing, difficult, 870. 
Sweating, in exophthalmic goiter, 1146. 
Sweating sickness, 351. 
Sydenham’s chorea, 1037. 
Sympathetic nervous system, diseases of, 
irritation of cervical sympa- 
thetic, 10S2. 
paralysis of cervical sympathetic, 
1081. 
vagotonia, 1082. 
influence of, 1081. 
Sympathicotonia, 1083. 
Syphilis, 15. 
acquired, 16. 
alopecia in, 19. 
aortitis syphilitica due to, 27. 
arteritis and, 19, 26. 
blood changes during early stages of, 
17. 
blood changes during tertiary stage 
of, 24. 
cardiovascular lesions due to aortitis 
syphilitica, 27. 
cardiovascular lesions due to arteritis, 
26. 
cardiovascular lesions due to endar- 
teritis, specific obliterating, 27. 
heart syphilis, 28. 
latent, 29. 
myocarditis, 29. 
cerebrospinal fluid in, second stage of, 
22. 
during tertiary stage of, 24. 
condylomata in, 19. 
constitutional symptoms in, 18. 
ear changes in, 20. 
endarteritis, specific obliterating in, 
27. 
eye affections in, 20. 
fever in, 19. 
galloping, 20. 
gummata in, 23. 
gummata of nose in, 23. 
gummata of scalp in, 23. 
gummata of tongue, tonsils, soft pal- 
ate and buccal mucosa in, 24. 
Jarish-Herxheimer reaction, 21. 
joint invasion in, 20. 
leukocytosis in, 24. 
lues maligna in, 20. 
complicated with visceral lesions, 
20. 
lues maligna of liver in, 30. 
lymphocytosis in, 24. 
manifestations of, early, 16-22. 
late, 23. 
myocarditis, early, in, 19. 
nephritis in, 19, 31. 
of digestive tract, 34. 
of liver, 30. 
of nervous system, 35. 
of respiratory organs, 33. 
of spleen, 33. 
Syphilis, acquired, optic, 43. 
period of latency in, second stage 
of, 21. 
phlebitis syphilitica in, 29. 
previous disease in, 17. 
primary stage of, 16. 
“saddle-nose” in, 23. 
secondary stage of, 18. 
length of, 22. 
skin lesions of, gummatous syphilids. 
23. 
in tertiary stage of, 23. 
lues maligna, 20. 
mucous patches, 18. 
papular and pustular eruptions, 18. 
papular syphilids, 23. 
pustulation, early, 18. 
roseola eruption, 18. 
rupia syphilitica, 20. 
in secondary stage of, 18. 
squamous syphilids, 18. 
ulceration, 20. 
specific amyloid degeneration in, 27. 
tabes dorsalis due to, 45. 
tertiary stage of, 23. 
metasvphilitic manifestations of, 
44. 
Neisser’s statistics on, 25. 
visceral syphilis in, 25. 
tertiary lesions, frequency of, 24-25. 
visceral, in tertiary stage, 25. 
Wassermann reaction in, during pri- 
mary stage, 18. 
alcoholism in, 41. 
and life insurance, 68. 
and marriage, 68. 
aneurysm due to, 421. 
angina pectoris due to, 456. 
aortic insufficiency due to, 500. 
arteriosclerosis due to, 67, 404, 405. 
arteritis due to, 26. 
bronchial, 33. 
cardiovascular, 26. 
cerebral, 38. 
cerebral hemorrhage due to, 960-961. 
cerebrospinal, hereditary, 37. 
classification for prognosis of, 15-16. 
congenital, anemia of, 66. 
arteriosclerosis in, 67. 
arteritis due to, 67. 
bone changes in, 67. 
changes in nails and skin in, 66. 
characteristic manifestations of, 66- 
67. 
Colles-Baume law for, 65. 
destructive disease of skin, nose and 
soft palate in, 67. 
early pemphigus syphiliticus, 66. 
effect of, on growth of child, 66. 
on mental progress, 66. 
on nervous system, 67. 
enlargement of lymphatics in, 66. 
eye lesions in, 67. 
Hutchinsonian teeth in, 67. 
hydrocephalus, 67. 
intestinal lesions with, 67. INDEX 
1269 
Syphilis, congenital, juvenile paresis due 
to, 65. 
juvenile tabes dorsalis due to, 45-47. 
latent, 65. 
maternal transmission of, 65. 
non-transmission of, to child, 66. 
of liver, 30. 
of spleen, 34. 
pneumonia with, 67. 
Profeta law for, 65. 
purpura, 67. 
rachitis due to, 67, 1129. 
transmission of, to third generation, 
68. 
conjugal nervous lesions due to, 69. 
edema of glottis in, 33. 
epilepsy due to, 42, 1050. 
Herxheimer reaction, in edema of glot- 
tis, 33. 
immunity of affected child to, 66. 
immunity of mother of syphilitic child 
to, 65. 
in tuberculosis, 242. 
laryngeal, 33. 
manifestations of, early, 1622. 
metasyphilis, 44. 
paresis, 62. 
tabes dorsalis, 45. 
taboparesis, 61. 
mortality among offspring of, 69. 
myocarditis due to, 29. 
nasal, 32. 
neuralgia due to, 839. 
of bones and joints, 32. 
of cord and brain, 44. 
of digestive tract, 34. 
of esophagus, 34. 
of intestines, 34. 
of kidney, 31. 
gummatous deposit in, 31. 
of liver, acquired, 30. 
acquired, jaundice, 30. 
atrophy acute, 30. 
cirrhosis complicated by, 31. 
congenital, 30. 
gummata, 30. 
lues hereditaria tarda, 31. 
lues maligna, 30. 
specific treatment in, 31. 
of muscles, 32. 
of nervous system, 35. 
of respiratory organs, 33. 
of spleen, 33, 1170. 
of stomach, 34. 
of testicle, 32. 
paresis as lesion of, 35. 
paresis due to, 62. 
pulmonary, 33. 
rectal, 34. 
shortening of life in, 68. 
spinal, 35. 
spinal leptomeningitis due to, 934. 
stenosis of glottis in, 33. 
tabes as lesion of, 35. 
tertiary, Neisser’s statistics on, 25. 
tracheal, 33. 
Syphilis, traumatic neurosis associated 
with, 1024. 
Wassermann reaction in, negative, 19-21. 
positive, 15, 18, 21, 22, 28. 
Syphilitic anemia, 524. 
Syphilitic aortitis, aneurism due to, 423. 
Syphilitic brain tumor, 993. 
Syphilitic cirrhosis, 701. 
Syphilitic coryza, 358. 
Syphilitic endocarditis, 504. 
Syphilitic epilepsy, 42. 
Syphilitic granuloma, 541. 
Syphilitic hydrocephalus, 944, 945. 
Syphilitic jaundice, 070, 671, 674. 
Syphilitic myelitis, 906. 
Syphilitic nephritis, 790. 
Syphilitic peripheral neuritis, 37. 
Syphiiltic pyloric stenosis, 583. 
Syphilitics, fate of, 69. 
offspring of, 69. 
Syphilomata, of brain, 997. 
Syringomyelia, classification of, 915. 
congenital, 914-915. 
diabetes mellitus with, 917. 
direct causes of death from, 918. 
due to pressure from tumors, 915. 
due to traumatism, 914. 
duration of, 918. 
futility of treatment for, 917-918. 
muscular atrophy in, 915. 
spinal curvature in, 917. 
symptoms of, 914. 
bulbar, 917. 
muscular atrophy, 915. 
psychic, 917. 
sensory disturbances, 915-916. 
trophic, 916. 
tabes dorsalis and paresis with, 917. 
tabes of spine with, 917. 
with acromegaly, 918. 
with pachymeningitis, cervical hyper- 
trophic, 917. 
Syringomyelic symptoms, in hemato- 
myelia, 930. 
T 
Tabes, arsenical, 1193. 
Tabes dorsalis, 45. 
as syphilitic lesion, 35. 
blood and fluid during initial stage of, 
50. 
causes of, 46. 
causes of death in, 58, 59, 60. 
causes of rapid progression of, 56. 
complications in, alcoholism, 58. 
aortitis, 58. 
arteriosclerosis, 58. 
arteritis, 58. 
Basedow’s disease, 58. 
epileptiform seizures, 59. 
hemorrhagic conditions, 60. 
hysteria, 59. 
infections, 58. 
invasion of medulla oblongata, 58. 1270 
INDEX 
Tabes dorsalis, complications in, paralysis 
agitans, 58. 
pneumonia, 58. 
septic conditions, 59. 
surgical operations, 58. 
trauma, 58. 
tuberculosis, 58. 
vertigo, 59. 
duration of, 60. 
effect of trauma in, 58. 
general conclusions on, 60. 
influence of treatment, on various 
stages, ataxic, 52. 
incipient, 48-51. 
paralytic, 52. 
juvenile, 45-47. 
manifestations of, 45-46. 
morphin habit in, 54. 
ophthalmoplegia in, 56. 
pneumonia in, 58. 
predisposing factors to, age, 47. 
complications, 58. 
location and extent of degeneration, 
48. 
prognostic significance of separate 
symptoms, 53-57. 
prophylaxis, 47-48. 
sex, 47. 
social status, 58. 
treatment, influence of, on various 
stages of disease, 48-53. 
prevention of, in syphilis, 39. 
prognosis of life of patient in, 60-61. 
prognostic conclusions, of initial stage, 
51. 
psychic element in, 56-59. 
single symptom, without progression, 
49. 
social status of patient in, 59. 
stages of, ataxic, 52. 
initial or neuralgic, 48-51. 
paralytic, 52. 
stationary, 49-50. 
symptoms of, Argyll-Robertson pupil, 
56. 
arthropathies, 57. 
ataxia, 55. 
ataxic stage, 52. 
atrophy of optic nerve, 54. 
bladder, 55. 
gastric crises, 49-53. 
hypotonia, 56. 
impotence, 56. 
initial stage, 49-51. 
multiplicity of, 53. 
ocular paralysis, 56. ' 
ophthalmoplegia, 56. 
paralytic stage, 52. 
. perforating ulcer, 57. 
prognostic significance of, 53. 
rectal, 55. 
Romberg, 55. 
Westphal, 55. 
treatment of, Donath’s conclusions on, 
52-53. 
Dreyfus report on, 52. 
Tabes dorsalis, treatment of, Wassermann 
reaction in, 57. 
with syringomyelia, 917. 
Tabes inversa, 55. 
Tabes mesenterica, 260. 
of childhood, 260. 
Taboparesis, 01. 
Tachycardia, hysterical, 1019. 
in diphtheria, 140. 
in nephritis, 807. 
paroxysmal, duration of, 509. 
fluoroscope in, 509. 
heart rate of, 509. 
in women, 509. 
symptoms of, 509. 
simple, 510. 
causes of, 510. 
physiological, 510. 
Tapeworm. See Cestodes. 
Taste, hysterical perversion of, 1011. 
loss of, 870. 
perverted, 870. 
Tenia echinococcus, 306. 
mediocanellata, 305. 
saginata, 305. 
solium, 304. 
cysticercus of, in myocardium, 466. 
Testicle, syphilis of, 32. 
Tetanoid chorea, 695. 
Tetanus, bacillus of, 206. 
conveyance of, 206. 
factors influencing prognosis of, 207-208. 
injection in, 206. 
injections of magnesium sulphate in. 
209. 
symptoms of, 207-208. 
Tetany, associated with acute infections. 
1167. 
characteristic features of, 1165. 
definition of, 1165. 
essential factor of, 1166. 
forms of, 1166. 
from poisons, 1167. 
prognosis of, 1167. 
gastric, 1167. 
gastro-intestinal, 1167. 
idiopathic, 1166. 
characteristic features of, 1166. 
prognosis of, 1167. 
remissions of, 1166. 
in gastric ulcer, 596. 
occurrence of, 1166. 
of maternity, 1168. 
of nervous diseases, 1168. 
of parathyroid disturbance, 1168. 
Thermic fever, 1206. 
Third nerve, paralysis of, 860. 
Thirst, in diabetes mellitus, 1114. 
Thomsen’s disease, 1085. 
Thrombo-endocarditis septica, 471. 
Thrombo-endocarditis simplex, of Ziegler, 
469. 
Thrombomyoendocarditis, 285. 
Thrombosis, and liver cirrhosis, 697. 
cerebellar, 1004. 
cerebral, 953. INDEX 
1271 
Thrombosis, in arteriosclerosis, 418. 
in typhoid fever, 95. 
of hepatic artery, 680. 
of hepatic vein, 679. 
of marasmus, 679. 
pulmonary, with chlorosis, 518. 
septic, 132. 
spinal, 929. 
tuberculous, 275. 
Thymic asthma, 1164. 
“Thymus death,” 1145-1164. 
Thymus gland, disease of, atrophy, 1164. 
hypertrophy, 1163. 
in hyperthyroidea, 1145. 
with Hodgkin’s disease, 1164. 
status thymo-lymphaticus, 1164. 
sarcoma of, 1164. 
Thyroid extract, glucosuria produced by, 
1107. 
in Raynaud’s disease, 1073. 
Thyroid gland, complete loss of function 
of, 1157. 
function of, 1154. 
goiter, 1137, 1139. 
insufficiency, 1153. 
classification of, 1154. 
dangers of, 1154. 
in adults, 1155. 
in children, 1154. 
maximal, 1154. 
total extirpation of, 1155. 
tuberculosis, 249. 
tumors, 1136. 
and hyperthyroidea, 1150. 
inflammatory conditions of, 1136. 
Thyroiditis, 1136. 
acute swelling with, 1137. 
productive or sclerotic, 1137. 
Tic convulsive, blepharospasm with, 867. 
clonic and tonic spasms in, 867. 
definition of, 867. 
following trigeminal neuralgia, 867. 
longevity in, 867. 
other neuroses with, 867. 
Tic douloureux, causes of, 842. 
operative interference and injections 
for, 842. 
Tic habit, due to facial spasm, 866. 
Tinnitus aurium, with aural paralysis, 
868. 
Tobacco, arteriosclerosis due to, 407. 
Tongue, tuberculosis of, 252. 
Tonsillitis, acute follicular, 293. 
epidemic, 294. 
sporadic, 293. 
albuminuria with, 747. 
chronic, 299. 
complications in, arthritis, 296. 
heart, 294. 
kidney, 296. 
paralysis, 296. 
pneumonia, 297. 
septicemia, 296. 
various, 297. 
epidemic, complications in, 294-295. 
Tonsillitis, epidemic, course of, 295. 
due to infected milk, 294. 
phlegmonous, 297. 
septic, 297. 
streptococcus, 293. 
accompanying other diseases, 294. 
endemic and epidemic, 294. 
mortality from, 297. 
symptoms of, in acute follicular, 293. 
Vincent’s angina in, 298. 
Tonsils, acute infections of, 293. 
as port of entry for infection, 292. 
disease, and chorea, 1039. 
enlarged, influence of, on growing child, 
299. 
enucleation of, 292-293. 
in tuberculosis, 292. 
mortality due to diseases of, 300. 
primary focus for disease, 292. 
tuberculosis of, 252. 
Torticollis; causes of, 873. 
congenital, 873. 
tenotomy for, 873. 
course of, 873. 
functional or spasmodic, 872. 
hysterical, 1019. 
organic, 872. 
psychic influence of, 873. 
symptoms of, 873. 
Toxinemia, 133. 
Trachea, syphilis of, 33. 
tuberculosis, 252. 
Trapezius paralysis, 872. 
spasm of, 872. 
Traumatic neurosis, complex of symptoms 
in, 1021. 
convulsive tic in, 1023. 
death never due to, 1024. 
diagnosis of, 1021. 
due to electric shock, 1024. 
due to railroad accidents, 1022. 
heart affections in, 1023. 
honest cases of, 1021. 
leading to suicide, 1024. 
litigated cases of, 1021-1022. 
localized muscular spasm in, 1023. 
mental attitude in, 1023. 
multiple and single symptoms, 1023. 
neurotic-psychic symptoms of, 1022. 
persistent melancholia of, 1023. 
prognosis of, principal facts in, 
1022. 
psychic attacks in, 1023. 
psychic disturbances in, 1024. 
surgical conditions in, 1023. 
syphilis associated with, 1024. 
with organic injury, 1023. 
without litigation, 1023. 
vasomotor symptoms in, 1023. 
Traumatism, epilepsy due to, 1050. 
glucosuria due to, 1108. 
influence of, on development of general 
paralysis, 1024. 
migraine due to, 1060. 1272 
INDEX 
Trematodes, 316. 
complications with, 316. 
nature of, 316. 
symptoms of, 316. 
Tremor, in exophthalmic goiter, 1144. 
in lead encephalopathy, 1190. 
Treponema pallidum, 15. 
carriers of, 70. 
excursion of, through blood, 19. 
in metasyphilitic disease, 44-45. 
Trichinosis, 312. 
Trichocephalus dispar, 312. 
Tricuspid insufficiency, 503. 
Tricuspid stenosis, 503. 
Trigeminus, neuralgia of, 841. 
paralysis of, 862. 
symptoms of, 862. 
Trophedema, hereditary, 1080. 
Trophoneurosis, hysterical, 1018. 
Tropical sore or ulcer, 83. 
Tropical splenomegaly, 83. 
Trypanosomiasis, 81. 
Tube casts, 749. 
Tubercula dolorosa, 884. 
Tuberculin, 225. 
in pulmonary tuberculosis, 238-239. 
Tuberculoma, 251. 
Tuberculosis, abortion in, 241. 
acute miliary (general), meningeal 
form of, 224-225. 
primary focus for, 223. 
pulmonary form of, 224. 
secondary character of, 222. 
spread of, 223. 
typhoid form of, 223. 
advance in study of, 217-220. 
and malaria, 78. 
and marriage, 241. 
and pneumonia, 163-164. 
bacillus of, 216. 
bovine, 219. 
bronchial, 252. 
bronchial asthma and, 371. 
cardiovascular, 274. 
catarrhal, 250. 
complications in, alcoholism, 242. ' 
diabetes, 242. 
exophthalmic goiter, 242. 
gangrene of lung, 242. 
gouty conditions, 242. 
meningitis, 242. 
obesity, 242. 
syphilis, 242. 
diminished mortality from, 218-219. 
fibroid phthisis in, 244. 
galloping, 227. 
genital, in female, 271. 
genito-urinary, 267. 
heredity as factor in, 220, 221, 241. 
history of, 217-220. 
immunity of normal tissue to, 218. 
in early life, 240-241. 
in influenza, 127. 
in tabes dorsalis, 58. 
infection of child with, by mother, 220, 
241. 
Tuberculosis, inviting conditions for, 221- 
222. 
ischiorectal, 257. 
Kossel’s conclusions on, 219. 
laryngeal, 250. 
mesenteric, 266. 
migraine and, 1060. 
nasal, 250. 
nursing of baby by mother with, 241. 
of aorta, 274. 
of appendix, 656. 
of brain, 996. 
of digestive tract, esophagus, 253. 
intestinal, 253. 
lips, 252. 
stomach, 253. 
tongue, 252. 
tonsils, 252. 
of gall-bladder, 256. 
of liver, amyloid degeneration, 255. 
cirrhosis of liver and, 255. 
fatty degeneration, 255. 
primary tubercle nodule, 256. 
of lymphatic glands, 265. 
of myocardium, 275. 
of nervous system, 277. 
of pancreas, 262. 
of parotid, 249. 
of spinal cord, 924. 
of thyroid, 249. 
predispositions to, 220-221. 
pregnancy in, 241. 
pulmonary. See Pulmonary Tubercu- 
losis. 
in typhoid fever, 99. 
in whooping-cough, 188. 
renal, 268. 
resemblance to, of lymphoblastoma, 537. 
rontgenoscopy for, 239-240. 
spinal leptomeningitis due to, 934. 
splenic, 262. 
suggested by orthostatic albuminuria, 
745. 
suprarenal, 263. 
symptoms of, blood pressure, 276. 
constriction of veins, 276. 
dyspepsia, 253. 
heart, 276. 
pulse, 276. 
tests for, lumbar puncture, 225-226. 
tuberculin, 225. 
tonsils in, 292. 
tracheal, 252. 
transmission of, 219-220. 
tuberculin tests for, 238-239. 
with cirrhosis, 693. 
with diabetes mellitus, 1118. 
Tuberculous abscess of brain, 981. 
Tuberculous endocarditis, 275. 
Tuberculous enteritis, chronic, 254. 
intestinal stricture with, 255. 
primary, 253. 
secondary, 254. 
Tuberculous laryngitis, 234, 241, 251. 
Tuberculous meningitis, 277. 
in measles, 345. INDEX 
1273 
Tuberculous meningitis, invasion of cra- 
nial nerves in, 278. 
Tuberculous myelitis, 277. 
Tuberculous nephritis, hematuria due to, 
759. 
Tuberculous neuritis, 278. 
Tuberculous pachymeningitis, 277. 
Tuberculous pericarditis, 274. 
Tuberculous peritonitis, chronic, 259. 
chronic fibroid, 260. 
focus of, 257. 
miliary, 258. 
surgical treatment of, 260-261. 
Tuberculous pleurisy, 389. 
adhesions in, 248. 
complications in, 248-249. 
development of, 247. 
dry, 248. 
frequency of effusion in, 248. 
history of, 247. 
Tuberculous pneumonia, 244. 
Tuberculous pyloric stenosis, 584. 
Tuberculous spleen, 1170. 
Tuberculous thrombosis, 275. 
Tumors, of brain. See Brain Tumor, 
of cauda equina, 926. 
of conus, 926. 
of peripheral nerves, 883. 
of spinal cord, classification of, 918. 
differentiation between extra- and in- 
tra-medullary, 923. 
due to carcinoma elsewhere in body, 
919-920. 
early diagnosis of, 924. 
extramedullary, benign and slow 
growth of, 920-921. 
cervical invasion by, 922. 
focal symptoms of, 921. 
in dorsal region, 922. 
intervertebral, extradural, 919. 
intradural, 919. 
laminectomy for, 922. 
neuralgia with, 921. 
paralyses with, 921-922. 
reflexes in, 921. 
sciatic pain with, 921. 
sensory symptoms of, 921. 
vertebral, 919. 
without cachexia, 921. 
intramedullary, 919. 
carcinoma, 924. 
compression myelitis in, 925. 
direction of growth of, 922. 
early diagnosis of, 922. 
echinococcus and cysticercus cysts, 
924. 
glioma, 924-925. 
infiltrating and limited, 923. 
metastasis to spine and cord, 925. 
multiple neuromata, 924. 
primary or secondary, 924. 
sarcoma, 923. 
secondary chronic, 925. 
spinal gliomatosis in, 925. 
surgical removal of, 922-923, 925. 
transverse myelitis in, 925. 
Tumors, intramedullary, tubercle, 924. 
lumbar puncture in, 926. 
necessity of surgery for, 918. 
relation of trauma to, 925. 
x-ray in, 925. 
Tympany, in typhoid fever, 102. 
Typhlatonia, 632. 
Typhlectasia, 632. 
Typhlitis, 644. 
Typhlitis stercoralis, 635. 
Typhoid appendix ulcers, 650. 
Typhoid fever, abortive, 90. 
afebrile, 92. 
age in, 87. 
albuminuria of nephritis in, 108. 
alcoholics with, 111. 
alimentary disturbances in, diarrhea, 
102. 
gastric, 102. 
intestinal hemorrhage, 102, 103, 103. 
of mouth, 101. 
parotitis, 101. 
peritonitis, 104. 
tympany, 102. 
ambulatory, 91. 
appendicitis with, 657. 
blood in, 99-100. 
blood count in, 88. 
“carriers” of, 85. 
cause of infection by, 84. 
causes of death in, 114-115. 
cerebral invasion by, 111. 
circulatory disturbances in, accented 
aortic II sound, 95. 
blood pressure, 94. 
bradycardia, 95. 
cyanosis, 93. 
endocarditis, 96. 
heart, 94. 
pericarditis, 96. 
post-typhoid myocarditis, 95. 
pulse, 93. 
sudden death from, 94. 
thrombosis, of arteries, 96. 
gangrene from, 96. 
phlebitis cruralis, 95-96. 
deaths from sequelae of, 115-116. 
ear complications in, 113. 
encephalitis in, 974. 
epidemics of, 88. 
eye complications in, 113. 
factors influencing prognosis of, 86. 
genito-urinary disturbances in, albumi- 
nuria, 108, 109, 110. 
cystitis, 109. 
gangrene of vulva, 110. 
menstruation, 110. 
nephritis, 108-109. 
orchitis, 110. 
pregnancy, 110. 
pyelitis, 110. 
urine, 107. 
immunity to, through vaccination, 85, 
influence of complications of, 88. 1274 
INDEX 
Typhoid fever, intestinal hemorrhage in, 
102. 
death due to, 104. 
prognostic significance of, 103. 
relapses of, 103. 
liver and bile passages in, cholecystitis, 
105. 
jaundice, 105. 
malignant infection of, 88. 
manifestations of, circulatory, 93. 
general, 87-88. 
temperature and pulse, 89. 
mild irregular, 90. 
mortality from, 86. 
muscular system in, 113. 
nervous system in, central, 111. 
convulsions, 112. 
delirium, 111. 
peripheral, 112. 
reflexes, 112. 
treatment of, 112. 
osseous system in, 113. 
peritonitis in, 104. 
perforative, 104-105. 
post-typhoid pyrexia from, 93. 
protracted fever in, 89-90. 
pulse in, 89-97, 93. 
reactions in, 110. 
relapses of, 114. 
resistance of patient to, 87. 
respiratory disturbances in, bronchitis, 
98. 
catarrhal pharyngitis and laryngitis, 
97. 
epistaxis, 97. 
hypostatic congestion, 98. 
lung abscess, 98. 
pneumonia, 98. 
pneumothorax, 99. 
pulmonary edema, 99. 
pulmonary infarct, 98. 
pulmonary tuberculosis, 99. 
purulent pleurisy, 99. 
respiration, 96. 
severity of infection in, 87-88. 
skin disturbances in, abscesses, 106. 
alopecia and atrophic changes, 106. 
bedsores, 106. 
erysipelas, 107. 
miliary eruption, 106. 
phlegmons, 107. 
purpura hemorrhagica, 106. 
roseola, 106. 
spleen in, 107. 
sudden death in, 94. 
symptoms of perforation in, 93. 
temperature in, 89-97. 
sudden fall of, 92-93. 
Typhoid spine, 112. 
Typhoid symptoms, in gonococcus endocar- 
ditis, 190. 
in influenzal fever, 130. 
in malarial fever, 74. 
in tuberculosis, 223. 
Typhus abortions, 91. 
Typhus exanthematicus. See Typhus fever, 
blood in, 119. 
general symptoms of, 119-120. 
history of, 117, 118, 119. 
prevention of, 118-119. 
pulse in, 119. 
urine in, 120. 
without intestinal lesions, 114. 
Typhus levissimus, 90. 
U 
Ulcers, catarrhal follicular, 621. 
decubitus, of esophagus, 564. 
peptic, of esophagus, 564. 
gastric, 585. 
Ulnar paralysis, causes of, 879. 
Uremia, acute, abnormally high temper- 
ature with, 764. 
active mania with, 764. 
cerebral paralysis with, 764. 
chronic nephritis with severe head- 
aches and, 765. 
diarrhea with, 765. 
hemiplegia with, 764. 
dyspnea with, 765. 
prognosis of, 763. 
pulmonary edema with, 764. 
pulse condition in, 765. 
renal sufficiency tests in, 763. 
retinal hemorrhages with, 765. 
sudden blindness before attack of, 
764. 
symptoms of, 763. 
test for impairment of function in, 
771. 
typhoid state associated with, 765. 
vomiting with, 764. 
with chronic nephropathies, 763. 
with respiratory paralysis, 764. 
chronic, diagnosis of, 767. 
symptoms of, 766-767. 
due to hydronephrosis, 818. 
in cirrhosis, 694. 
in chronic nephritis, 799. 
in nephritis, 792. 
in scarlet fever, 331. 
latent, anuria with, 765. 
leading features of symptom-complex of, 
762. 
nature of, 762. 
Uremic breath, 767. 
Ureter, stones in, 822. 
Uric acid diathesis, 785. 
Urinary fistulae, with gall-stones. 730. 
multiple, due to trematodes, 317. 
Urinary secretions, anomalies of, albumi- 
nuria, 741. 
alkaptonuria, 786. 
bacilluria (bacteriuria), 774. 
casts, 749. 
chyluria, 776. 
cystinuria, 785. 
hematoporphvrinuria, 787. 
hematuria, 753. INDEX 
1275 
Urinary secretions, anomalies of, hemo 
globinuria, 761. 
indicanuria, 780. 
lipaciduria, 787. 
lipuria, 777-787. 
lithuria, 785. 
melanuria, 786. 
oxaluria, 779. 
phosphaturia, 777. 
pneumaturia, 787. 
uremia, 762. 
urobilinuria, 782. 
Urine, albumin in, 741. 
alkaptonic, 786. 
ammoniacal fermentation of, 778. 
black, 786. 
blood in, 753. 
casts in, 749. 
complete suppression of, 766. 
cryoscopy, 774. 
cystin in, 785. 
disease-producing germs in, 774. 
fat in, 776, 777, 787. 
gas in, 787. 
hematin in, 787. 
hemoglobin in, 761. 
indican in, 780. 
in amyloid kidney, 815. 
in chronic interstitial nephritis, 808. 
in chronic nephritis, 800. 
in diabetes mellitus, 1116. 
indol in, 780. 
indoxylsulphate of potassium in, 780. 
in leukocytic leukemia, 531. 
in measles, 343. 
in neurasthenia, 1029. 
in paratyphoid, 123. 
in pernicious anemia, 527. 
in pyelitis, 833. 
in tuberculosis, 234. 
in typhoid fever, 107. 
methemoglobin in, 761. 
oxalic acid in, 779. 
phosphates in, 777. 
serum albumin in, 741. 
serum globulin in, 741. 
triple phosphates in, 778. 
uric acid in, 785. 
urobilin in, 782. 
volatile fatty acids in, 787. 
Urobilinuria, clinical significance of, 782. 
conditions associated with, 783-784. 
prognostic significance of, 782-783. 
Urogenital disease, renal sufficiency tests 
for, 768. • 
Urticaria, bronchial asthma with, 369. 
giant. See Angioneurotic edema. 
Uterine tuberculosis, 273. 
V 
Vaccination, against hay fever, 359. 
against smallpox, 333. 
influence of, on prognosis, 340. 
rules for, 339-340. 
Vaccination, in typhoid fever, 85. 
Vaccine treatment, for gonococcus arthri- 
tis, 192. 
Vaccinia, for smallpox, 339. 
Vaginal tuberculosis, 273. 
Vagotonia, due to atropin, 1082. 
due to pilocarpin, 1082. 
prognosis of, 1083. 
symptoms of, 1082. 
Vagotonic asthma, 371. 
Vagus paralysis, 871. 
Valvular disease, aortic insufficiency, 
500. 
aortic stenosis, 499. 
blood pressure in, 496. 
chronic, prognosis of, 495. 
combined, 504. 
defects of pulmonary valve, 503. 
due to mitral insufficiency, 495. 
due to mitral stenosis, 497. 
general considerations, in prognosis of, 
478. 
influence on, of marriage and preg- 
nancy, 486, 487, 488. 
localization of, 495. 
lung complications in, 497. 
pulmonary insufficiency in, 504. 
rupture in, 500. 
tricuspid insufficiency, 503. 
tricuspid stenosis, 503. 
Vaquez disease. See Erythremia. 
Varicella, complications in, 342. 
death due to, 341. 
nature of, 341. 
nephritis in, 342. 
prognosis of, 341. 
Varicocele, operation for, in neurasthenia, 
1029. 
Variola hemorrhagica, purpura variolosa, 
337. 
pustulosa, 337. 
Variola vera, 336. 
Varioloid, 337. 
Vascular spasm, anemia of brain due to, 
947. 
in arteriosclerosis, 414. 
in lead poisoning, 1190. 
Vasomotor and trophic disturbances, acro- 
paresthesia, 1074. 
adiposis dolorosa, 1078. 
angioneurotic edema, 1075. 
ataxia, 1079. 
dropsy (intermittent) of joints, 1079. 
edema of legs, persistent hereditary, 
1080. 
erythromelalgia, 1066. 
hysterical, 1018. 
in traumatic neuroses, 1023. 
Raynaud’s disease, 1069. 
scleroderma, 1077. 
Venous obstruction, in brain tumor, 996. 
Venous stasis, congested kidney due to, 
813. 
Vertigo, acute, of gastrohepatic and in- 
testinal origin, 870. 
aural, 869. 1276 
INDEX 
Vertigo, due to constitutional disease, 
870. 
due to organic brain disease, 870. 
epilepsy and, 870. 
essential, 870. 
general considerations of, 870. 
in brain tumor, 992. 
in multiple sclerosis of brain and cord, 
910. 
in tabes dorsalis, 59. 
ocular associated with diplopia, 870. 
petit mal with, 870. 
stomachal, in chronic gastritis, 578. 
in dilatation of stomach, 578. 
of Trousseau, 870. 
Vestibular nerve, involvement of, in audi- 
tory paralysis, 869. 
Vicarious menstruation, pulmonary hem- 
optysis of, 376. 
Vincent’s angina, 298. 
Visceroptosis, 579. 
Visual field, hysterical contraction of, 
1011. 
Vocal cords, hysterical paralysis of, 1014. 
Volvulus, 637. 
Vomiting, in acute biliary colic, 722. 
cerebral, 993. 
fecal hysterical, 1018. 
hysterical, 1017. 
in brain tumor, 992. 
in amyloid kidney, 815. 
in nephritis, 792, 798. 
in pneumonia, 161. 
nervous in hypermotility, 617. 
of cancer, 604. 
Vulva, diphtheria of, 138. 
gangrene of, in typhoid, 110. 
W 
Walking typhoid, 91, 92. 
Wassermann reaction, in paresis, 63. 
in syphilis, negative, 19, 21. 
positive, 15, 18, 21, 22, 28. 
in tabes dorsalis, 57. 
Weil’s disease, 350. 
Werlhof’s disease, 544. 
Westphal symptom, of tabes dorsalis, 55. 
“Wet brain,” in delirium tremens, 1184. 
Whip worm, 312. 
Whooping-cough, blood condition in, 189 
character of, 186. 
complications in, 186, 189. 
conclusions on, 189. 
stages of, 186. 
uncomplicated, 186. 
with measles, 344. 
Woolsorters’ disease. See Anthrax. 
Writers’ cramp, 1064. 
Wryneck. See Torticollis. 
X 
X-ray for adherent pericardium, 43L 
in aneurism, 422. 
in arteriosclerosis, 419. 
in biliary colic, 723. 
in brain tumors, 999. 
in dilatation of colon, 640. 
in early diagnosis of cancer, 602. 
in endocarditis, 492. 
in gastric ulcer, 589. 
in leukemia, 535. 
in nephrolithiasis, 821. 
in pericarditis, 428. 
in pyelitis, 832. 
in pyloric obstruction, 584. 
in tumors of spinal cord, 925. 
Y 
Yellow fever, conveyance of, 347. 
epidemics of, 347. 
factors in prognosis of, 347-348. 
nature of, 347. 
prophylaxis against, 347. 
racial insusceptibility to, 348-349. 
symptoms of, 347-348. '