NATIONAL LIBRARY OF MEDICINE NLn D010727b D NATIONAL LIBRARY OF MEDICINE Washington V Founded 1836 U. S. Department of Health, Education, and Welfare Public Health Service NLM001072760 * A TEXT-BOOK OF PRACTICAL MEDICINE DESIGNED FOR THE USE OF STUDENTS AND PRACTITIONERS OF MEDICINE ALFRED L. LOOMIS, M.D., LL.D., Professor of Pathology and Practical Medicine in the Medical Department of the Univer- sity of the City of New York; Visiting Physician to Bellevue Hospital, Etc. REVISED AND ENLARGED WITH TWO HUNDRED AND SEVEN ILLUSTRATIONS ELEVENTH EDITION \ J $ I (*7 :■■ a NEW YORK WILLIAM WOOD AND COMPANY 1895 Copyright, 1895, By WILLIAM WOOD & COMPANY, PRESS OF THE PUBLISHERS' PRINTING COMPANY 132-136 W. FOURTEENTH ST. NEW YORK. PREFATORY NOTE. Dr. Loomis was actively engaged in the revision of the present vol- ume at the time of his last illness, and had completed the greater por- tion of the work. Since his death only such alterations and additions have been made as seemed necessary. Dr. C. G. Coakley, Clinical Professor of Laryngology in the Medi- cal Department of the University of the City of New York, has revised, and largely rewritten, at Dr. Loomis' request, the section devoted to Diseases of the Nose and Throat, and Diphtheria. At Dr. Loomis' request, Dr. E. D. Fisher, Professor of Mental and Nervous Diseases in the Medical Department of the University of the City of New York, has revised the section on Nervous Diseases. Dr. Warren Coleman, Instructor in Pathology at the Loomis Lab- oratory, assisted Dr. Loomis in the revision and has corrected the proof-sheets. September, 1895. PREFACE TO THE EIGHTH EDITION. In the progress of medical sciences during the four years since the third edition of this treatise was published, many unsettled questions have received definite answers, and numerous theories have crystallized into definite forms of fact or fancy. The author has always sought to maintain a conservative yet liberal attitude in his consideration of any statements emanating from recognized authorities. The contributions of intelligent observers, both in this country and Europe, have been care- fully studied, and it is believed that the present edition, much of which has been rewritten, and all of which has undergone careful revision, will be found abreast with the present position of conservative scientific medi- cine ; that its dogmatic affirmations will be found reliable, and its state- ments of still debatable questions will prove unbiassed and just to both sides, although intended to be conservative rather than radical. Such changes as are at variance with former editions have been made as the result of more exact knowledge of the etiology and pathology of disease, and from a more extended experience in its treatment. The important additions include brief descriptions of the more frequent path- ological processes, and a detailed statement of the methods employed in bacteriological study, with an enumeration of the distinguishing charac- teristics of those micro-organisms which at the present time are regarded as pathogenic. Several additions also have been made to the list of dis- eases considered. In the revision, Phthisis has been classed as an infec- tious disease, although retained among pulmonary diseases for description, and its pathology and etiology rewritten in conformity with its bacillary nature, adopting the name pulmonary tuberculosis. The pathological term nephritis has been substituted for the indefinite one Bright''s disease, with a view of making a more exact classification of renal diseases. The methods advised to be pursued in bacteriological studies are those now employed in the " Loomis' Laboratory," the details of which have been furnished by J. D. Byron, M.D., Instructor in the Bacteriological Department of the Laboratory. The changes and additions which have been made in the plates have been furnished by H. P. Loomis, M.D., Director of the Pathological Department of the Loomis Laboratory. C. E. Quimby, M.D., Assistant Professor of Practice in the Medical Department of the University of the City of New York, has rendered me valuable assistance in the prep- aration of this edition. A. L. L. 19 West 34th Street, New York, August, 1889. PREFACE TO FIRST EDITION In- the preparation of a Text-book of Practical Medicine, my experience as a medical teacher has led me to employ, quite extensively, plates illus- trating the morbid changes and objective symptoms of disease. The present work, both in text and illustration, is practically a revision and an elaboration of lectures given during the past eighteen years in the Medical Department of the University of the City of New York. I have avoided, as far as possible, the discussion of unsettled questions, and in order to economize space have made reference to many of these only in brief foot-notes. The Classification adopted is that which it has been my custom to fol- low in teaching, and is based on our present knowledge of the etiology of disease. It is well known that many diseases present very different types in differ- ent countries, and I have selected for description those types commonly observed by the American physician. I have considered only those diseases which come strictly within the province of Practical Medicine, and have endeavored to indicate the treatment usually followed in this country. The illustrations, with but few exceptions, have been made by my assist- ant, Dr. Maurice N. Miller (Instructor in the Laboratory of Normal and Pathological Histology, University Medical College). The microscopical drawings were, in most instances, made from sections prepared in the Lab- oratory by Dr. Miller, especially for this work, and they will, I believe, aid in the appreciation of the actual morbid processes and conditions. In the consultation of Authorities, particularly the German and French, in the reading of the proof, and in the preparation of the Index, I have been assisted by Dr. Leigh Hunt, Assistant Instructor in the Pathological Laboratory of the University. If I have failed to give credit—either in the text or in foot-notes—to those from whom many of the facts stated have been drawn, it has been an unintentional omission. 19 West 34th Street, New York City, July, 1884. CONTENTS. INTRODUCTION. GENERAL PATHOLOGY. INFLAMMATION. 1.—Inflammation of Serous Surfaces. 2.—Inflammation of Mucous Surfaces. (a) Croupous Inflammation of Mucous Surfaces. (b) Diphtheritic Inflammation of Mucous Surfaces. (c) Ulceration of Mucous Surfaces. 3.—Parenchymatous Inflammation. 4.—Interstitial Inflammation. 5.—Fate of Pus................................................Pages 1-8 HYPERTROPHY.-ATROPHY.........................................9-10 DEGENERATIONS. 1.—Parenchymatous Degeneration. 2.—Fatty Infiltration. 3.—Fatty Degeneration. 4.—Colloid Degeneration. 5.—Mucoid Degeneration. 6.—Calcareous Degeneration. 7.—Pigmentation. 8.—Amyloid Degeneration. 0.—Necrosis.........................................................11-20 TUBERCLE.—TUBERCULOSIS.........................................21-23 BACTERIOLOGY. l.—Technology. 2.—Examination and Staining. 3.—Biology. 4.—Classification__..............................................24-34 SECTION I. DISEASES OF THE RESPIRATORY ORGANS. DISEASES OF THE NASAL PASSAGES. Acute Rhinitis.—Hypertrophic Rhinitis.—Atrophic Rhinitis.— Tubercular Rhinitis..............................................35-42 Vlll CONTENTS. DISEASES OF THE LARYNX. Acute Laryngitis—Chronic Laryngitis.—Tubercular Laryn- gitis.—Syphilitic Laryngitis.—Membranous Laryngitis.—Ede- matous Laryngitis.—Laryngeal Ulcers.—Neuroses of the Larynx.—Tumors of the Larynx...........................Pages 43-67 BRONCHITIS. Acute Bronchitis.—Chronic Bronchitis.—Bronchiectasis.—Croup- ous or Plastic Bronchitis.—Bronchial Asthma.—Bronchial Hemorrhage.—Hemoptysis...................................... 67-91 DISEASES OF THE LUNGS AND PLEURA. Acute Lobar Pneumonia.—Lobular Pneumonia.—Interstitial Pneu- monia.—Pneumonokoniosis.—Pulmonary Hyperemia.—Pulmo- nary OZdema.— Pulmonary Infarction.—Pulmonary Apoplexy. —Pulmonary Gangrene.—Pulmonary Anemia.—Pulmonary Collapse.—Pulmonary Emphysema.—Pulmonary Tumors.—Other Neoplasms in the Lung and Pleura.—Syphilitic Disease of the Lung.—Atrophy of the Lung.—Parasitic Diseases.— Pleu- risy, (a) Plastic.—(&) Serofibrinous.—(c) Suppurative.—(d) Interstitial. Cancer of the Pleura.—Pyopneumothorax.—Hydrothorax.— Hemothorax.—Pulmonary Tuberculosis, (a) Acute Tuberculosis. —(b) Chronic Tuberculosis...........................................02-227 SECTION II. DISEASES OF THE DIGESTIVE SYSTEM, INCLUDING DISEASES OF THE LIVER, SPLEEN, AND PANCREAS. DISEASES OF THE MOUTH. Stomatitis, (a) Catarrhal—(b) Follicular.—(c) Gangrenous.—(d) Vleer- ative.—Thrush.—Diseases of the Tongue, (a) Glossitis.—(b) Can- <*r.................................................................228-237 DISEASES OF THE PHARYNX. Tonsillitis.—Peritonsillar Abscess.—Inflammations.—Retropha- ryngeal Abscess............................................. 237-247 DISEASES OF THE CESOPHAGUS. Inflammations.—Cancer................................... 248-251 DISEASES OF THE STOMACH. Inflammations. (a) Acute.—(b) Sub-acute—(c) Chronic—(d) Phlegmo- nous—Dyspepsia.—Cancer and Ulcer.—Neuroses.—Nervous Dyspepsia.—Hematemesis.—Dilatation.......................252-283 CONTENTS. IX DISEASES OF THE INTESTINES. Enteritis.—Diarrhoea.—Cholera Morbus.-Cholera Infantum.—In- testinal Dyspepsia.—Typhlitis.—Appendicitis.—Perityphlitis. —Intestinal Ulcers.—Intestinal Hemorrhage.—Intestinal Ob- struction.—"Waxy Degeneration.— Cancer. — Rectitis.—Peri- proctitis.—Hemorrhoids.—Intestinal Parasites.—Intestinal Colic.—Constipation.—Peritonitis.—Ascites...........Pages 284-359 DISEASES OF THE LIVER. Hyperemia, (a) Actire.—(6) Passive.—Inflammations, (a) Interstitial Hepatitis or Cirrhosis.—(6) Circumscribed Hepatitis or Abscess.—(c) Diffused Hepatitis or Acute Yellow Atrophy.—Perihepatitis.—Py- lephlebitis.—Degenerations, (a) Amyloid.—(b) Fatty.—(c) Pig- mentary.—(d) Atrophic.—New Growths, (a) Cancer.—(b) Gummata. —(c) Hydatids.—(d) Tubercle.—Jaundice...........................359-417 DISEASES OF THE GALL BLADDER AND DUCTS. Inflammations, (a) Catarrhal.—(b) Exudative.—Cancer.—Enlarge- ment.—Gall Stones.—Functional Derangements.............417-431 DISEASES OF THE PANCREAS. Pancreatic Hemorrhage.—Acute Pancreatitis.—Degenerations. (a) Fatty.—(b) Waxy.— Morbid Growths {Cancer, Tubercle, etc.)— Cysts.—Calculi................................................432-435 DISEASES OF THE SPLEEN. Hyperemia.—Inflammation, including Embolism and Infarction.— Hypertrophy.—Degenerations.—Morbid Growths.—Parasites. 435-441 SECTION III. DISEASES OF THE HEART, BLOOD-VESSELS, AND KIDNEYS. DISEASES OF THE HEART. Pericarditis.—Endocarditis.—Valvular Lesions.—Hypertrophy.— Dilatation—Diseases of Myocardium.—Degenerations.—Atro- phy.—Rupture.—Thrombosis.—Aneurism.—Morbid Growths and Parasites.—Tuberculosis of the Pericardium.—Neuroses.— Hydropericardium.—Pneumohydropericardium.—Syphilitic Dis- ease of the Heart.—Basedow's Disease.........................442-534 DISEASES OF THE BLOOD-VESSELS. DISEASES OF THE ARTERIES. Acute Endarteritis.—Chronic Endarteritis.—Periarteritis.—De- generations, (a) Fatty.—(b) Waxy.-(c) Calcareous— Syphilis- Hypertrophy, Atrophy, and Narrowing.—General Arterial Fibrosis.......................................................... 535-542 X CONTENTS. DISEASES OF THE VEINS. Acute Phlebitis.—Chronic Phlebitis—Varix.—Thrombosis.—Em- bolism.—Thoracic Aneurism.—Abdominal Aneurism".—Medias- tinal Tumors................................................Pages 542-55: DISEASES OF THE KIDNEYS. THE URINE. Normal Constituents.—Urinary Sediments.—Uremia ...........557-571 THE KIDNEYS. Renal Hyperemia.—Renal Hemorrhage.—Nephritis, (a) Acute Nephritis, Parenchymatous and Interstitial.—(b) Chronic Nephritis, Parenchymatous and Interstitial.—(c) Amyloid Degeneration.—Pye- litis.—Hydronephrosis.—Cystic Kidney.—Renal Calculi.—New Growths, (Cancer, etc.).—Parasites.— Perinephritic Abscess.— Floating Kidney.—Hematuria.—Chyluria.—Cystitis.........571-634 SECTION IV. ACUTE GENERAL DISEASES. Fever.—Typhoid Fever.—Yellow Fever.—Cholera.—Dysentery. —Cerebro-spinal Meningitis.—Septicemia.—Pyemia. Diphtheria.—Erysipelas.—Acute Miliary Tuberculosis.—Typhus Fever.—Relapsing Fever.—Small-Pox.—Inoculation and Vac- cination. — Varicella. — Scarlet Fever. — Measles. — German Measles.—Miliary Fever.—Influenza.—Whooping-cough.—Hy- drophobia.—Acute Infectious Jaundice. Intermittent Fever.—Remittent Fever.—Continued Malarial Fever.—Pernicious Fever.—Dengue Fever.—Chronic Malarial Infection..........................................................635-892 SECTION V. CHRONIC GENERAL DISEASES. Rheumatism.—Gout.—Lithemia.— Diabetes.—Anemia.—Chlorosis.-- Progressive Pernicious Anemia.—Leucocythemia.—Pseudo- Leukemia. — Addison's Disease. — Ammonemia. — Hemophilia.— Scurvy.—Purpura.—Myxcedema.—Scrofula.—Rickets.—Alcohol- ism. —Trichinosis.—Syphilis.............................. oqq contents. XI SECTION VI. DISEASES OF THE NERVOUS SYSTEM, INCLUDING DISEASES OF THE BRAIN, SPINAL CORD, AND FUNCTIONAL NERVOUS DISEASES. GENERAL SYMPTOMATOLOGY. Of Nervous Diseases.........................................Pages 963-969 DISEASES OF THE BRAIN. Cerebral Hyperemia (Active or Passice.)—Cerebral Anemia.—Men- ingitis.—Syphilis of the Dura Mater.—Cerebral Thrombosis and Embolism.—Cerebral Softening.—Cerebral Apoplexy.— Abscess of the Brain.—Cerebral Tumors.—Sclerosis of the Brain.—Hypertrophy of the Brain.—Atrophy of the Brain. 970-1030 DISEASES OF THE SPINAL CORD AND ITS MENINGES. Spinal Hyperemia.—Spinal Meningitis.—Acute Myelitis.—Chron- ic Myelitis.—Non-inflammatory Softening.—Acute Bulbar Paralysis.—Progressive Bulbar Paralysis.—Infantile Spinal Paralysis.—Acute Spinal Paralysis of Adults.—Chronic An- terior Myelitis.—Syringo-Myelia.—Progressive Muscular Atrophy.—Muscular Dystrophy.—Cerebro-spinal Sclerosis.— Locomotor Ataxia.—Spasmodic Tabes Dorsalis.—Amyotrophic Lateral Sclerosis.—Chronic Muscular Dystrophy.—Pseudo Hypertrophic Paralysis.—Acute Ascending Paralysis.—Spi- nal Apoplexy.—Tumors of Spinal Cord.—Spina-Bifida and Hydrorachis.— Acromegaly..................................1030-1076 DISEASES OF THE PERIPHERAL NERVES. Peripheral Neuritis.—Localized Spasm and Paralysis.—Chronic Lead Poisoning.—Chronic Mercurialism.—Paralysis Agitans. —Facial Paralysis.—Eclampsia and Infantile Convulsions- Tetanus.—Neuralgia.—Megrim.............................1076-1096 FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM. Epilepsy.—Hysteria.— Hystero-Epilepsy.—Catalepsy.—Neurasthe- nia.— Chorea.— Sunstroke.— Spinal Irritation.— Vertigo.— Sea-Sickness......................................................1096-1124 DESCRIPTION OF PLATE. No. 1. Bacillus Anthracis.—Section of liver of a white mouse inocu- lated with a pure culture of anthrax bacilli. Gram's method. Bismarcfc brown, x 500. No. 2. Bacillus Typhosus.—From a cover-glass preparation of spleen pulp. Loffler's solution and acetic acid, x 700. No. 3. Gonococcus Neisserii.—From a cover-glass preparation of gonor- rhceal discharge. Aqueous solution of methyl blue, x 1000. No. 4. Bacillus Tuberculosis (tissue).—Giant cell of a miliary tubercle of liver, containing bacilli. Erlich-Koch method. Methyl blue and Bis- marck brown staining, x 900. No. 5. Bacillus Tuberculosis (sputum). — Cover-glass preparation. Erlich-Koch method, x 900. No. 6. Spirillum Oholerm Asiatics.—Cover-glass preparation of intes- tinal discharge. Aqueous solution of methyl blue, x 900. No. 7. Spirochete Obermaieri.—Cover-glass preparation of blood, from case of relapsing fever. Aqueous solution of Bismarck brown, x 900. No. 8. Actinomyces.—Prepared from tumor of jaw of calf. Gram's method and Bismarck brown, x 850. LIST OF ILLUSTRATIONS. Fig. Page l. Inflammation of omentum............................................ 2 2. Granulation cells, in various stages..................................... 3 3. Inflammation of a serous membrane.................................... 5 4. Inflammation of a mucous membrane.................................. 6 5. Diphtheritic inflammation of a mucous surface......................... 8 6. Parenchymatous degeneration in cells.................................. 13 7. Fatty infiltration of cells............................................... 14 8. Fatty degeneration of muscle fibres..................................... 15 9. Amyloid degeneration.............................. .................. 18 10. Miliary tubercle....................................................... 22 11. Tuberculosis of liver................................................... 24 12. Diagram showing position of the vocal bands in abductor and adductor paralysis as seen with the laryngoscope................................ 62 13. Multiple papilloma of the right vocal cord as seen with the laryngoscope 65 14. The trachea laid open, showing the same tumor as seen in Fig. 13....... 65 15. Transverse section of a portion of a medium-sized bronchial tube in acute catarrhal bronchitis................................................... 68 16. Diagram illustrating the physical signs of bronchitis.................... 70 17. Various forms of bronchiectasis........................................ 78 is. Mould of bronchi in sputum of plastic bronchitis...................... 80 19. Morbid anatomy of first stage of acute lobar pneumonia................. 92 20. Morbid anatomy of second stage of acute lobar pneumonia................93 21. Morbid anatomy of second stage of pleuro-pneumonia................... 93 22. Morbid anatomy of third stage of acute lobar pneumonia................ 95 23. Morbid anatomy of purulent infiltration................................ 07 24. Temperature record in acute lobar pneumonia in an adult............... 103 25. Temperature record in acute lobar pneumonia, observations every six hours................................................................ 104 26. Temperature record in acute lobar pneumonia ending in purulent infiltra- tion ................................................................. 105 27. Physical signs of the three stages of acute lobar pneumonia............. 112 28. Morbid anatomy of lobular pneumonia................................. 123 29. Temperature record in lobular pneumonia in a child.................... 125 30. Morbid anatomy of interstitial pneumonia.............................. 130 31. Morbid anatomy of brown induration of the lung....................... 137 32. Hemorrhagic infarctions............................................... 143 33. Morbid anatomy of emphysema of the lung............................ 154 34. Hydatids of lung...................................................... 165 35. Temperature record in acute pleurisy.................................. 167 36. Physical signs in acute pleurisy with a small amount of effusion........ 168 37. Physical signs in pleurisy with effusion...............................• 1''4. 38. Physical signs of pyopneumothorax..................................... 1°' 39. Lung in acute tuberculosis............................................. 194 40. Acute tuberculosis : alveolus filled wtih fibrin and cells................. 195 41. Tubercle bacilli from phthisical sputum................................ 199 xiv list of illustrations. Fig. Page 42. Temperature record in a case of acute tuberculosis...................... 200 43. Morbid anatomy of pneumonic tuberculosis............................. 202 44. Lung cavity........................................................... 203 45. Miliary tubercle in disseminated tuberculosis........................... 205 46. Tubercular nodule..................................................... 206 47. Physical signs of first stage of chronic tuberculosis..................... 214 48. Physical signs of cavities in third stage of chronic tuberculosis.......... 216 49. Oidium albicans....................................................... 233 50. Stricture of the oesophagus............................................. 249 51. Stomach wall in sub-acute gastritis..................................... 254 52. Mucous membrane and stomach-tubules in chronic gastritis............. 256 53. Sarcinae ventriculi from vomit of chronic gastritis...................... 258 54. Cancer of pyloric end of stomach....................................... 266 55. Perforating ulcer of stomach.......................................... 272 56. Dilatation of stomach................................................. 282 57. Acute enteritis, small intestine near middle of ileum.................... 284 58. Acute follicular enteritis ; transverse colon showing ulceration.......... 285 59. Tubercular ulcers ; ileum.............................................. 308 60. Intussusception (intestinal obstruction)................................ 312 61. Head of taenia solium (tape-worm).................................... 329 62. Mature segment of taenia solium....................................... 329 63. Head of taenia saginata................................................ 330 64. Oxyuris vermicularis with ovum ; and ascaris lumbricoides............. 331 65. Passive hepatic hyperaemia............................................ 362 66. Interstitial hepatitis................................................... 365 67. Interstitial hepatitis, same as Fig. 66 : more highly magnified.......... 366 68. Circumscribed suppurative hepatitis (pyaemic abscesses)................ 373 69. Cells from a lobule in acute yellow atrophy of the liver.................. 380 70. Amyloid degeneration of the liver...................................... 391 71. Three intralobular zones ; waxy, fatty and pigment degenerations of the liver.................................................................. 392 72. Chronic atrophy of the liver............................................ 395 73. Fatty infiltration of the liver........................................... 396 74. Fatty degeneration of the liver........................................ 397 75. Pigmentary degeneration of the liver................................ 399 76. Same as Fig. 75 : more highly magnified............................... 400 77. Cancer of the liver.................................................... 403 78. Diagrammatic enlargements of liver.................................... 405 79. Hydatids of omentum.................................................. 409 80. Hydatids of liver : head of echinococcus................................ 411 81. Gall-bladder filled with calculi........................................ 423 82. Section of a large gall-stone showing layers............................. 424 83. Crystals of cholesterin................................................. 424 84. Areas of splenic enlargement as shown by percussion.................... 438 85. Morbid anatomy and physical signs of sero-plastic pericarditis.......... 443 86. Physical signs of pericarditis with effusion............................. 447 87. Changes in mitral valve in diphtheritic endocarditis.................... 453 88. Changes in aortic valves in diphtheritic endocarditis.................... 454 89. Section of aortic valve in acute endocarditis........................... 454 90. Diagram showing the mode of production of cardiac murmurs........... 464 91. Diagram showing area of cardiac murmurs............................. 466 92. Vegetations on aortic valves in aortic obstruction....................... 467 93. Sphygmographic tracing of pulse in aortic obstruction.................. 468 94. Morbid anatomy of aortic insufficieucy................................ 470 95. Sphygmographic tracing of pulse in aortic regurgitation............... 472 96. Morbid anatomy of mitral stenosis..................................... 475 97. Mitral orifice snowing button-hole slit in stenosis....................... 476 98. Sphygmographic tracing of pulse in mitral stenosis..................... 477 LIST OF ILLUSTRATIONS. XV Page View of left heart in mitral regurgitation.............................. 480 Sphygmographic tracing of pulse in mitral regurgitation................ 482 Physical signs in left ventricular hypertrophy.......................... 500 Physical signs in right ventricular hypertrophy......................... 500 Chronic endarteritis : " atheroma"...................................... 536 Section of kidney in general arterial fibrosis............................ 539 105. Diagrammatic representation of formation of thrombi and emboli....... 544 106. .Re-establishment of circulation by anastomosis after embolism.......... 546 107. Morbid anatomy of spontaneous arterial aneurism...................... 548 108. Hippuric acid......................................................... 558 109. Fat globules from chylous urine........................................ 559 110. Leucin and tyrosin..................................................... 559 111. Uric acid crystals..................................................... 560 112. Urate of soda......................................................... 560 113. Urate of ammonia crystals............................................. 560 114. Oxalate of calcium crystals............................................ 561 115. Ammonio-magnesian, or triple phosphate.............................. 561 116. Phosphate of calcium.................................................. 561 117. Cystine............................................................... 562 118. Epithelium from urinary deposits...................................... 562 119. Blood in the urine..................................................... 563 120. Pus in the urine....................................................... 563 121. Epithelial casts in the urine............................................ 564 122. Hyaline casts in the urine............................................ 564 123. Granular casts in the urine............................................ 564 124. Fatty casts in the urine............................................... 564 125. Blood casts in the urine................................................ 564 126. Spermatozoa in the urine............................................... 565 127. Torula cerevisiae ; penicilium glaucum ; and sarcinae ventriculi.......... 565 128. Section from Malpighian pyramid in passive renal hyperaemia.......... 572 129. Hemorrhage from tbe vascular tuft of a glomerulus in renal hemorrhage. 576 130. Renal hemorrhage and renal infarction................................. 577 131. Cortex of kidney showing cloudy swelling in acute nephritis............ 581 132. Glomerulonephritis, scarlet fever...................................... 581 133. Cortex of kidney showing advanced degenerative changes in acute ne- phritis ............................................................... 582 134. Cortex of kiduey in chronic parenchymatous nephritis.................. 593 135. Cortex of kidney in early cirrhotic nephritis............................ 599 136. Cortex of kidney in advanced cirrhotic nephritis....................... 600 137. Cortex of kidney showing commencing waxy changes.................. 605 138. Medullary portion of kidney showing advanced amyloid change.......... 606 139. Longitudinal section of cystic kidney................................... 617 140. A cyst of the kidney ; epithelial lining shown......................... 617 141. Renal calculi: an embedded mulberry calculus......................... 618 142. Mucous surface of ileum in first week of typhoid fever.................. 645 143. Mucous surface of ileum in second week of typhoid fever............... 646 144. Mucous surface of ileum in third week of typhoid fever................. 646 145. Enlarged mesenteric lymphatics in typhoid fever....................... 647 146. Temperature record in typical (mild) typhoid fever.................... 656 147. Temperature record in non-typical typhoid fever........................ 657 148. Temperature record in yellow fever.................................... 684 149. Temperature record in a case of acute dysentery....................... "00 149.\. Temperature record in septicaemia.................................... V:^, 150. Metastatic pyaemic abscesses of the lung................................ J}' 151. Temperature record in pyaemia........................................ I 152. Temperature record in a case of facial erysipelas........................ '** 153. Temperature record in a case of acute miliary tuberculosis.............. 7-15 154. Temperature record in severe typhus fever.............................. '" xv'l LIST OF ILLUSTRATIONS. Fig- ^ Pagb 155. Temperature record in a case of relapsing fever........................ 776 156. Temperature record in a case of discrete small-pox...................... 783 157. Temperature record in a case of confluent small-pox.................... 787 158. Temperature record in a case of varioloid............................... 796 159. Temperature record in a case of scarlatina............................. 805 160. Temperature record in a case of measles.......,........................ 820 161. Temperature record in a case of German measles....................... 827 162. Temperature record in a case of influenza............................... 832 163. Fever curve in quotidian intermittent................................. 848 164. Fever curve in tertian intermittent.................................... 849 165. Fever curve in quartan intermittent.................................... 850 166. Section of liver from a case of remittent fever.......................... 856 167. Temperature record in remittent fever.................................. 859 168. Temperature record»in a case of continued malarial fever............... 867 169. Temperature record in continued malarial fever (septic variety)........ 869 170. Temperature record in pernicious fever (comatose variety).............. 877 171. Temperature record in pernicious fever (algid variety)................. 879 172. Temperature record in a severe case of dengue fever..................... 886 173. Temperature record in a mild case of acute rheumatism................ 895 174. Temperature record in a fatal case of acute rheumatism................. 895 175. Deformity from articular rheumatism (hand).......................... 902 176. Section of a gouty cartilage........................................... 907 177. Vertical section of a Malpighian pyramid in gouty nephritis........... 908 178. Deformity from gout (hand)........................................... 910 179. Blood from a case of leucocythaemia.................................... 929 180. Section of leucocythaemic spleen....................................... 930 181. Encapsulated trichinae in voluntary muscle............................. 955 182. Trichinae with calcareous deposits and degeneration of the capsule...... 955 183. Temperature record in the fourth week of trichinosis.................... 956 185. Acute meningitis, showing also intact meninges........................ 976 186. Temperature record in a case of acute meningitis............'............ 977 187. Tubercular meningitis :—tubercular meningitis along blood-vessels...... 984 188. Temperature record in a case of tubercular meningitis.................. 985 189. Pachymengitis interna—vertical section of skull and cerebral meninges. 993 190. Cerebral softening..................................................... 1000 191. Small blood-vessels from a focus of yellow softening (cerebral thrombosis and embolism)..................................................... 1001 192. Cerebral apoplexy ; newly formed tract in the left optic tract............ 1004 193. Vertical section of the cerebrum........................................ 1009 194. Fibroma of the cerebellum............................................. 1013 195. Diagram showing connective-tissues of medullated nerve structure...... 1025 196. Sclerosis of the brain................................................... 1026 197. Acute myelitis....................................................... 1036 198. Chronic bulbar paralysis............................................... 1042 199. Muscle of the tongue in chronic bulbar paralysis contrasted with normal muscle.............................................................. 1043 200. Section of spinal cord in early stage of infantile spinal paralysis........ 1046 201. Same as 200 after establishment of sclerotic process..................... 1046 202. Teased fibers from abductor pollicis in progressive muscular atrophy .... 1053 203. Sketch of a hand in progressive muscular atrophy....................... 1054 204. Cerebro-spinal sclerosis................................................ 1057 205. Regions of degenerative changes in spinal cord.—Diagrammatic........ 1060 206. Locomotor taxia.—Section of cord in cervical region................... 1061 207. Spinal apoplexy : clot in the left anterior cornu......................... 1071 A TEXT-BOOK OF PRACTICAL MEDICINE. INFLAMMATION. According to the older writers the cardinal symptoms of inflammation are pain, heat, redness and swelling, features which are more striking in those forms of inflammation which come under the care of the surgeon than in those which the physician is called upon to treat. As the knowledge of tissues and processes became more detailed and complete, and as the hidden changes underlying these grosser ones were brought to light, pathologists sought to discover the essence of the inflammatory process, to find its cause, and to determine in which tissues or organs the primary change occurred. The history of the theories and definitions of inflammation is a record of the varying importance that has been attached to one or another of the changes observed. Into these theories, and the arguments by which they have been in turn supported and assailed, it is not desirable here to enter. It will be sufficient to describe the changes observed in the tissues, and to define the associated terms of which use will hereafter be made. The pathological results of inflammation are the product of three factors, com- bined in varying proportions, the vascular, the exudative and the paren- chymatous changes. According as one or another is prominent it deter- mines the character of the inflammation. Vascular Changes.—Except in the non-vascular tissues, as the cornea and cartilage, the earliest change observed is in the circulation, and this change is manifested by a change in the color of the affected part, which becomes 2 INFLAMMATION. red and congested. This redness is due to an increase of the quantity oi blood in the part; at first the hyperaemia is active, that is, blood is brought to the part and passed through the capillaries in larger quantities than before ; but it may become passive, a condition in which, while the quan- tity of blood present in the part is greater than usual, the current is much slower, the amount which actually passes through the capillaries in a given time being less than normal; finally, this retardation of the flow may end in actual arrest : stasis. That hyperemia is only an accompaniment, and Fig. 1. Inflamed Omentum from Human Subject. a, Normal fibrous trabecula ; b, normal endothelium ; c, small artery; d, vein with while blood-corpusdet peripherally disposed ; e, white blood-cells migrated or migrating ;f, desquamated endothelium ;ft, multi- nuclear cell ; g, migrated red blood.— Zeigler. not the essence, of inflammation, is shown by the fact that the hyperaemia which is caused by section of the sympathetic nerves is not accompanied by the other symptoms and changes observed in inflammation. Exudative Changes.—The swelling which has been mentioned as one of the four cardinal symptoms is due mainly to the presence of a liquid infiltrated through the tissues. This liquid comes from the blood by exudation through the walls of the capillaries ; but it is not simply the plasma or serum of the blood ; it contains large numbers of emigrated white blood-cells, which, with the fixed cells of the part, furnish those peculiar constituents of the exudation which distinguish this liquid from the normal juices of the part, or from that of oedema, and which make it an inflammatory exudation. The character of the exudation, whether it be serum, fibrin, or pus, is determined also by the cellular elements, and more especially by the emigrated white cells. Examination of fresh normal tissues shows, scattered through them, free INFLAMMATION. 3 cells which closely resemble the colorless corpuscles of the blood and lymph. Like them, they possess the power of amoeboid movement, of rapidly chang- ing their shape by throwing out processes, of moving from place to place by means of this change of form, and of multiplying by division. They are called " wandering cells,-' or leucocytes, because of their supposed identity with the colorless corpuscles of the blood. Under normal conditions the leucocytes contained within the blood-vessels may occasionally be seen to pass through the unbroken wall of a capillary by means of this power of amoeboid movement which they possess; when the tissue adjoining the capillary is inflamed, the number of cells "migrating" through its wall is notably increased. The emigrated white cells form the larger portion of the cellular part of inflammatory exudations, and play a most prominent part in both necrotic and reparative processes. The number of free cells is increased by the fixed corpuscles of the omnipresent connective-tissue, which swell, as has been described, and give rise by proliferation to other cells, which cannot be distinguished morpho- logically from the normal wandering cells or leucocytes. Parenchymatous Changes. — The cellular elements of the tissues undergo change in form and nutrition. The chemical inter- changes which constitute normal nutrition, and which are carried on between the cells of the tissues and the liquid furnished to the cells by the blood, are modified in character or extent, and the cells themselves are cor- Grairaiation-ceiin in various stages. respondingly modified in form. On the One a, uninuclear; a„ multinuclear migrated hand the cells may show a tendency to re- $yti%£fl2£Sd£ ZTcfZnZ turn to their earlier embryonal form, to be- tJ^^^Ze^f^^ come swollen, globular, pale and succulent, ^e^T^.-Zefglt^ cannective- perhaps to divide, to form new cells, by pro- liferation ; on the other hand, the exaggerated activity of the cell may prove too great a strain upon it, and it dies or becomes disabled by pas- sage into the condition known as fatty degeneration. The former of these two results is the one seen most commonly in the connective-tissue frame- work and envelopes of the various parts and organs, and the latter in the specific cells that constitute their parenchyma. These modifications of nutrition vary with the nature of the irritant, and the extent of the tissue compression from the exudation. Terminations of Inflammation.—The inflammatory process, as thus de- scribed, may be arrested at any point. If the irritation is slight or of short duration, if the change has not progressed to the point of tissue destruction and formation of pus, the withdrawal of the primary cause is followed by a diminution of the swelling and congestion, and by return to the normal state ;—this is called resolution. When, however, the vitality of the tissues is impaired, by prolonged irritation, by compression or by the action of specific poisons, parenchymatous degeneration or necrosis of Fig. 2. 4 INFLAMMATION. the tissues may occur. This necrosis may be preceded or followed by a localized or diffuse infiltration of the tissues by leucocytes. When these cells accumulate in great numbers (whether by transformation of connect- ive-tissue cells or by migration from the vessels), those which are in the necrotic area lose their vitality and constitute the cellular portion of pus, while those which fill the immediately adjacent parts pass on to the forma- tion of connective-tissue, producing the limiting wall of fibrin about the necrotic area. When this necrosis is gradual and attended by molecular disintegration of the tissues, it is called ulceration if upon a free surface, and abscess when the pus and necrotic tissue are retained in the substance of an organ. When necrosis affects palpable masses of tissue it is called sloughing. When necrotic changes have taken place, the simple arrest of the inflammation is not sufficient; the losses must be made good, the destruction repaired. This is cicatrization, and it is accomplished largely by cells of the connective-tissue. As the conditions become more favor- able, the cells newly formed by proliferation no longer remain stationary, lose their vitality, and become pus, but they progress in the direction of a normal development and form new tissue. The irregular pink granula- tions seen within a wound or upon an ulcerated surface are formed of masses of young cells crowded with capillary loops of new formation. The cells, at first large, soft, finely granular and juicy, become smaller and firmer, and the intercellular substance increases and becomes fibrous. If the inflammatory process has taken place in the interior of an organ, involving only a small portion of tissue, and has stopped short of the formation of a distinct collection of pus, the result of the reparative pro- cess is a mass of fibrous connective-tissue, a cicatrix ; and if a collection of pus has actually formed, but is only of small size, the pus may disap- pear by liquefaction of its cellular elements and absorption. If, on the other hand, a larger abscess has formed and has been opened, its cavity becoming filled by the granulations, the same change into fibrous tissue follows, and a cicatrix is again the result. The same is true of ulceration of a free surface, with the addition that the surface of the cicatrix is covered by a layer of epithelium resembling more or less closely the origi- nal layer which has been destroyed by the ulceration. When the irrita- tion has been less active but more prolonged, and has perhaps involved an entire organ, although the cellular development is abundant, the elements retain their vitality, and neither suppurative nor necrotic changes occur, but the effect again appears in an increase of the connective-tissue of the part involved ; the consequences of this increase are most serious. The origi- nal "fixed cells" of the connective-tissue multiply as in the other case mentioned, and develop into fully formed tissue, and the amount of this tissue becomes in consequence much greater than normal. In its natural evolution it retracts, and by its quantity and its retraction it presses upon, and interferes with the nutrition of the specific cellular elements of the organ, so that they become less fit to perform their functions. This change is called induration or cirrhosis ; common examples are cirrhosis of the liver, and " contracted kidney " or interstitial nephritis. INFLAMMATION OF FREE SURFACES. 5 INFLAMMATION OF FREE SURFACES. First: Serous Surfaces.—The most common form of inflammation of serous membranes is that which results in the production of serum, fibrin, or pus, in variable proportions ; these products may infiltrate the substance of the inflamed membrane, be poured out upon its free or attached surface, or collect in cavities lined by it. The first change in this inflammatory pro- cess is in the blood-vessels, which contain more than their normal quantity of blood, and it is from the blood circulating in f the vessels that most of the characteristic inflam- matory products are de- rived. After the initial hyperaemia, the fibrino- gen of the exudation comes in contact with the fibrino-plastic mate- g i^i rial of the cellular ele- ments (there being a ferment present), coagu- lation takes place, and layers of fibrin contain- ing few or many cells are formed on the free sur- face. These layers are called pseudo-mem- branes, or coagulable lymph. If the inflammation occurs in a membrane whose normal conformation makes a free effusion possible (as the pleura and peritoneum) some serum is always present. It may be only infiltrated through the meshes of the tissues, or it may accumulate at some point as a serofibrinous collection. When leucocytes are present in great num- bers, the exudation is fibrino-purulent. The greater the intensity of the inflammation, and the more enfeebled the patient, the greater is the liabil- ity to pus formation. In certain serous inflammations the exudation may be hemorrhagic ; the blood may come from a ruptured capillary vessel, or the coloring matter of the blood-corpuscle may be set free and color the exudation without vascular lesion. Such inflammation of serous mem- branes may end in necrosis or in resolution. If the inflammation is intense, and stasis occurs throughout a wide area of tissue, it will result in necro- sis. Stasis is the expression of a higher degree of injury than that which exists in simple inflammation.1 The intensity of the inflammation deter- 1 If inflammation is an arrest of function, and not diversion of agents of nutrition into new channels of activity, restoration of a part to the natural state must be as simple as its departure from it, and reso- lution of inflammation means,"either that the temporarily arrested process goes on again, or, if the process has proceeded to its ultimate issue (death of the affected part), that the destroyed part has to be repaired, not by a continuation of the morbid process, but simply by the restitution of the normal condition. Fig. 3. Inflammation of Serous Membrane. Section through the Pericardium and Overlying False Membrane, x 150. a, Visceral pericardium ; b, fibrinous false membrane; c, distended blood-vessel; d, leucocytes infiltrating tissues; e, lymphatics filled with cells ; f, formative cells within the false membrane.—After Zeigler. . 6 INFLAMMATION. mines whether the result shall be a return to the normal condition or a destruction of tissue. An uncomplicated serous inflammation is neither reproductive nor infective. It has no tendency except to stop as soon as its primary cause ceases to act. When resolution occurs, the emi- gration of leucocytes ceases, the serous fluid disappears, and the fibrin and the cell elements, after they have undergone molecular change, are absorbed. A second variety of inflammation of serous membranes is characterized by the production of new connec- tive-tissue cells either with or without a sero-purulent exuda- tion. It may be an acute or chronic process. The inflamed membrane becomes thickened, and there is abundant cell de- velopment in its substance and on its surface. If the inflamma- toryprocess is prolonged, orif the membrane becomes very much thickened, elevations are formed on the surface of the membrane, and thus adhesion takes place between opposing serous sur- faces, or the membrane be- comes thickened and indurated. If bands of adhesion form, they have the appearance of delicate membranes. This new tissue at first is exceedingly rich in capil- lary vessels, which are distin- guished from the normal capilla- ries of the membrane by their large calibre and thin walls. As the new tissue contracts, it may shut off its own blood supply, and then undergo fatty change and be absorbed, leaving no trace of its existence. Second: Mucous Surfaces.—Inflammation affecting mucous membranes may be either catarrhal, croupous, or diphtheritic. Catarrhal mucous inflammations are either acute, sub-acute, or chronic. In the acute variety the affected mucous membrane, at the very beginning of the process, is congested and dryer than normal, the functional activity of the mucous glands being diminished. After a time an abnormal quantity of mucus is poured out on its surface, the result of an increase in the functional activity of the glands. This mucus may be thicker or thinner than normal, and may have an acrid or irritating quality. Mucous exudations Fig. 4. Inflammation of Mucous Membrane. Vertical section of nasal septum. a. Pus corpuscles and degenerating epithelium on the free surface. b. Superficial layers of epithelium. c- Sub-epithelialtissue. In the submucous tissue beneath the last will be seen— ff. g g. Longitudinal and transversely divided arteries, increased in number and size. h h. Veins. i i. Portions of enlarged mucous glands. jj. Gland ducts. A portion of the cartilage of nasal septum is seen at (d). Kith its perichrondrlum (e). x 200. After Thierfelder. INFLAMMATION OF FREE SURFACES. 7 do not coagulate, but adhere somewhat closely to the surface of the inflamed membrane ; these changes are accompanied by desquamation of the superficial epithelial cells. If the catarrh assumes a purulent character in addition to the above changes, the mucous surface assumes a darker and livid hue, and pus cells are developed both in the mucous membrane and in the deeper substance. The amount of pus will indicate the intensity and character of the inflammation. In some cases there are very few pus cells, in others the quantity of pus is very large, and the tissues are extensively infiltrated. In chronic catarrh the blood-vessels of the inflamed membrane are either increased in size and number, or they are less numerous and more swollen than normal, giving to the mem- brane a grayish appearance. The production of mucus wTill be increased or diminished, according as the functional activity of the mucous glands is increased or diminished. When it is diminished, the membrane assumes a dry and shining appearance. The stroma of the affected membrane may be hypertrophied or atrophied. The mucous glands may also undergo hypertrophy or atrophy. If their ducts become obstructed they may suffer cystic change ; superficial erosions sometimes occur from a rapid epithelial desquamation. Croupous Inflammation of Mucous Membranes.—In croupous inflammation, the hypersemia is more intense than in catarrhal, so that the mucous sur- face usually assumes a dark livid color and becomes swollen ; soon its free surface is covered with a fibrinous exudation, which takes the place of the epithelium, and lies upon the sub-epithelial structures in the form of a network or in irregular masses. Enclosed in its meshes are epithelial and pus cells ; it varies in thickness from an exceedingly thin semi-trans- parent membrane to one that may be an eighth of an inch in thickness. This membranous exudation may be limited to small patches, or extend over a large surface. At first it is firm in consistency, and adheres closely to the tissues which it covers ; afterward it becomes soft, and is easily separated from the subjacent membrane; when fully formed it may be cast off in patches or shreds. Its separation is accomplished by the return- ing secretion of the follicles which have been obstructed, as well as by the serous effusion from the inflamed surface. It may sometimes undergo fatty, and more rarely a mucous degeneration, and so become a fluid re- sembling mucus. Generally in simple croupous inflammation the sub- mucous tissue is but slightly involved, and its meshes are rarely infiltrated. Diphtheritic Inflammation of Mucous Surfaces.—By some this is regarded as identical in character with croupous. It differs from it in a more intense hyperaemia, and a more extensive infiltration of the affected tissue. The fibrinous exudation is more abundant and granular, and there is a greater metamorphosis of the epithelial and tissue cells. The membranous exuda- tion seems to be a part of the mucous and sub-mucous tissues, and cannot be removed without the loss of their substance. In the surface exudation, and in the infiltrated tissues underlying it, are found multitudes of bacteria, especially the micrococci. When the mucous and sub-mucous tissues are so infiltrated as to cause undue pressure, and to cut off their nutritive sup- s INFLAMMATION. ply, the affected tissue dies and sloughs away. Between simple croupous and diphtheritic exudation there is every possible gradation. Some claim that the fibrinous de- eration, and ulcers formed by the bursting of small abscesses, are the chief varieties of necrosis, except in those catarrhal inflammations where the blood supply is so suddenly and completely shut off that the mucous mem- brane dies in bulk and sloughs away (as in acute dysentery). Most of the little abscesses that produce ulceration of mucous surfaces are due to obstruction of the follicles and lymph structures that lie in the sub- stance of the membrane ; in consequence of their obstruction their con- tents degenerate, an abscess is formed, and an ulcer is the result. Parenchymatous Inflammation.—In parenchymatous inflammation, the cells which perform the functions of the organ, the blood-vessels, and the stroma are in a greater or less degree involved in the inflammatory process; and this may pursue an acute or chronic course. In a mild type of paren- chymatous inflammation the cells are enlarged, granular, and opaque, and their functional activity is increased, the blood-vessels contain more than their normal quantity of blood, and the stroma is infiltrated with serum. The affected organ is slightly increased in bulk, but returns to its norma) size if the inflammation terminates by resolution. If the inflammatory process is very intense and prolonged, the cells are destroyed, the circula- tion is checked or arrested, and the stroma is extensively infiltrated with serum and pus. The inflamed organ is greatly increased in size, assumes a livid or purple hue, and its functional activity is arrested. In chronic parenchymatous inflammation the cells undergo fatty degeneration and HYPERTROPHY. 9 disintegration. The walls of the vessels undergo extensive thickening, their calibre is diminished, and they may be obliterated. The stroma is increased by the development of new tissue. The function of the affected organ is impaired, and never returns to its normal condition, as the result- ing changes are permanent. In interstitial inflammation the connective-tissue or stroma of the organ in the part involved is affected. If the inflammation is acute, it is usually suppurative. The pus formation may be limited to small areas, or it may be diffused. When the pus cells are few, resolution is possible, but if they are numerous and infiltrate a large area of the organ, abscesses are formed with dense, firm walls. If the inflammation is chronic, it ends in indura- tion and cirrhosis, by the formation of new connective-tissue, but does not form pus. The new tissue corresponds in kind to the original stroma of the organ, and is permanent. The affected organ never returns to its nor- mal condition. Fate of Pus.—Pus may undergo absorption, be evacuated, become inspis- sated, or undergo caseous transformation. To be absorbed it must undergo fatty degeneration and become converted into granular matter; its absorp- tion is accomplished by the lymphatics. Its evacuation is accomplished by an ulcerative process, established in the tissues which contain it. When it has been converted partly into fatty and partly into granular matter, it may become inspissated by the absorption of its liquid portion and remain unchanged for a long period. If it becomes incapsulated, it changes into caseous matter and remains as a cheesy mass. HYPERTROPHY. Hypertrophy is an enlargement of an organ or tissue, due either to an increase in the size of its elements or to an increase in their number. The former is called simple hypertrophy, and the latter numerical hypertrophy or hyperplasia. In most cases of hypertrophy these two forms are found associated. Examples of physiological hypertrophy are the enlargement of the uterus during pregnancy ; the increase in the size of the mammary gland in cer- tain uterine changes ; the hypertrophy of the prostate in old men, and the increase in size of muscles following persistent exercise. Causes of Hypertrophy.—1. Increased functional activity is a prominent cause of hypertrophy, as is shown in the heart when called upon to per- form extra work in overcoming obstructions at its orifices, or an impeded circulation from obliterating changes in the arteries. Also in long-continued obstruction to the outflow of urine from the bladder, requiring an increase of force to overcome the obstruction, the muscular coat of the bladder becomes hypertrophied, and in the same way the coats of the stomach and intestines become hypertrophied above old obstructions. Hypertrophy of one kidney after removal or destruction of the other 10 ATROPHY. is the result of enforced functional activity thrown upon the remaining organ to enable it to carry on the normal elimination. All these are examples of what may be called conservative hypertrophy. 2. Increased supply of nutrition caused by augmented blood supply is a less frequent cause of hypertrophy. The formation of the corpus luteum of pregnancy, in contradistinction to what is known as the "false corpus luteum," is possibly the best example of this. The hypertrophy of the cheeks and nose, as seen in acne rosacea, is another illustration. On account of the excessive amount of blood which surrounds areas of long-continued inflammation, there is often an excessive outgrowth of tissue. This is seen in the well-marked hypertrophy of bone which follows inflammation of the periosteum. Another example is the rapid outgrowth of hair in the neighborhood of ulcers and diseased joints. 3. A partial arrest or delay of the normal retrograde changes in tissues may equally result in hypertrophy when the nutritive changes are not lessened. Many cases of obesity are thus induced. ATROPHY. Atrophy is either a diminution in the size of the histological elements of a part, or a decrease in their number. The former is called simple and the latter numerical atrophy. Simple atrophy occurs in ordinary emaciation, which affects first the sub- cutaneous adipose tissue, then the muscles, omentum, intestines, heart, and last of all the brain and skeleton. The fat is removed from the cells more or less completely, and they diminish in size, their walls and nuclei becom- ing more distinct. This process is a physiological one in certain tissues and organs, especially in those which have only a temporary function, as the supra-renal capsules, mammae, female genital organs, and thymus gland. In all pathological forms the simple atrophic tissue elements remain unchanged except in size. Degenerative changes are sometimes associated with this form of atrophy. Numerical Atrophy.—In numerical atrophy the elements of an organ or tissue are diminished, not only in size, but in number. Gradually, isolated elements or groups of elements of a part become involved. In many respects this change is quite as important as necrosis, and very much more so than simple atrophy, for it involves absolute loss of tissue, a loss which cannot be restored except by the production of new elements, which is very seldom, if ever, possible. Atrophied organs arc firmer and more anaemic than normal. The causes of atrophy may be either general or local. General atrophy may be due— First. To deficient supply of nutritive material. Second. To excessive waste. Third. To impaired nutritive activity. Deficient supply of nutritive material is present in cases of gradual DEGENERATIONS. 11 starvation, m obstruction in the alimentary canal (as occurs in cancer of the pylorus), in mal-assimilation due to diseases of the alimentary tissues, obstruction of the thoracic duct or lacteals, or disease of the mesenteric glands. Excessive waste is the exciting cause when it is due to prolonged hemor- rhages, suppurations, diarrhoeas, and the excessive loss of albumen or sugar. Impaired nutritive activity is an accompaniment of senile atrophy, where the vitality of the tissues gradually diminishes, and they Decome less able to assimilate the nutritive material brought to them by the blood. Sometimes general atrophy results from a combination of these causes, as occurs in chronic phthisis. The causes of partial atrophy are— First. Insufficient supply of blood. Second. Diminished functional activity. Tliird. Excessive functional activity. Fourth. Nervous influence. Insufficient supply of blood may be due to partial obstruction of an artery by pressure of a tumor, by the contraction of new connective- tissue on the smaller vessels, the result of an inflammatory process. Pressure upon the skull in hydrocephalus, upon bone by an aneurism, are also examples of local atrophy from pressure. Local or partial atrophy from diminished functional activity may be physiological or pathological. Examples of physiological atrophy are furnished by those parts which have a use only at certain periods of life, such as the ductus arteriosus, umbilical vessels, thymus gland, the mammae, the female sexual organs, and the jaw after the falling of the teeth. Pathological examples of atrophy depending upon diminished func- tional activity are seen in the wasting of muscles after paralysis, disloca- tions, anchylosis, or chronic disease of bone or joints, and in the rectum after establishment of an artificial anus. Examples of local atrophy from excessive functional activity are seen in the class of hyperkinetic diseases, of which writer's cramp, acute cardiac dilatation from violent exercise, and atrophy of the testicles from sexual excesses are examples. Nervous Influence.—Muscles which have been cut off from their trophic nerves, as in hemiplegia after injury of the anterior cornua, show atrophy depending upon this cause. The atrophy of the muscles which occurs after degeneration of the nerve-cells in the anterior horn of the spinal cord is also an example. It has also been proven that nerve fibres which are cut off from their ganglia all soon atrophy. DEGENERATIONS. The tissues of the body may undergo certain morbid processes charac- terized by alteration in their quality. They degenerate, and, as it were. take a step backward in their development. 12 DEGENERATIONS. These changes may lead to an impairment of their function, and often to a complete destruction of their elements. The term degeneration, in its strict sense, is synonymous with meta- morphosis, and implies a direct transformation of the albuminous elements of the tissues into a new material. It is often used, in a broad sense, to include infiltration; but, strictly speaking, infiltrations are characterized by the introduction into the tissues of a new material brought from without. There arc certain prominent types of degenerative changes whose histo- logical characteristics are much the same wherever they occur. All struc- tures of the body are more or less liable to them ; so that when one is famil- iar with one of these types of degeneration in one tissue, he is practically familiar with it in every tissue of the body, and has only to recall the histo- logical elements of a part, to understand the changes in any particular degeneration. TABLE OF DEGENERATIVE PROCESSES AND INFILTRATIONS. Name. Nature of Process. Parts Affected. Cause. Parenchymatous.. Fatty............ Fatty........... Colloid....... .. Mucoid.......... Calcareous....... Pigmentary...... Amyloid........ Degeneration. Infiltration .. Degeneration Degeneration Degeneration Deposit.... Deposit Infiltration Epithelium, muscle___ | Gland cells, connec- \ \ tive tissue. J I Gland cells, coats of < small arteries, mus- ( cle. Epithelial cells....... Connective-tissue......, ( Connective-tissue, epi { thelium............. j Normal situations. } (seats of hemorrhage, j Blood-vessels......... Fever, poisons, etc. Imperfect oxidation. Impairment of quality or quantity of blood, etc. Unknown. Unknown. fl. Excess of salts in the J blood. 1 2. Anaemic and atrophic I. tissues. Hemorrhage, stasis, ca- chexias. j Syphilis, prolonged sup- j puration. PARENCHYMATOUS DEGENERATION. (Cloudy Swelling.) Parenchymatous degeneration consists in an alteration of the anatomical elements of the body, especially the epithelial cells and muscle fibres, so that they appear swollen, cloudy, and filled with minute granules which look like fat granules, but differ from them in being soluble in acetic acid. This condition has also been called albuminous, serous, and granular degeneration. The name cloudy swelling is the one by which it is now generally designated. FATTY INFILTRATION. 13 The parenchymatous cells of the glandular organs—as the liver and kidneys—are especially liable to be affected with this • change. The organ becomes enlarged and of a pale color. If a microscopic exam- ination is made, the cells appear swollen and opaque ; the body of the cell is filled with albuminous granules, which give the appearance as if the cell was sprinkled with fine sand. The normal markings of the cell are lost, and the nucleus is obscured. Slight grades of this form of degen- eration are very difficult to appreci- ate, for many of the cells are normally granular, and we must not forget that all cells after death become somewhat granular. A cell which has undergone this form of degen- eration is not necessarily destroyed ; if the change is only transitory, the cell may return to its normal con- dition. As a result of this form of degeneration the cardiac muscle and the muscles of the skeleton undergo exactly the same change as the epi- thelial cells. Parenchymatous degeneration occurs in most febrile diseases, especially the specific fevers, as pyaemia, diphtheria, scarlet fever, typhus, and typhoid fevers. It is also seen after poisoning by arsenic, phosphorus, and the mineral acids. High temperature was at one time supposed to cause it, but this has lately been abundantly disproven. This form of degeneration was at first supposed to represent the first stage of inflammation, and hence was called parenchymatous degeneration. While in a certain number of cases it may be considered as the result of the action on epithelial cells of the same influence which, acting upon the blood-vessels and connective-tissue, pro- duces hyperaemia, exudation, and cell proliferation, still, in the majority of cases it cannot be considered a true inflammatory process. Fig. 6. Cloudy Swelling of Cells. a, Normal epithelium. b, Commencing cloudy swelling. c, d, Cells in extreme degeneration. FATTY INFILTRATION. In fatty infiltration, fat is deposited within the cells of a tissue in the form of distinct drops. In the earlier stages the drops are small, but as they increase in number they run together, and larger drops are formed, which gradually displace the nucleus of the cell and obscure more or less of its protoplasm. The vitality and function of the cell is but little impaired by the accumulation of fat; and the protoplasm, although compressed by the fat globule, is 14 DEGENERATIONS. still unaltered, and quickly assumes its normal condition when the fat is removed. Fatty infiltration is a normal physiological process under certain condi- tions, as during the growth of adipose tissue, or in the liver cells during the process of digestion. More or less fatty infiltration takes place in the liver of many healthy persons after a hearty meal, but in a few hours the fat is " burnt up," or oxidized, and the liver cells return to their normal condition. When for any reason the fat is not com- pletely oxidized, then it collects in the tis- sues. This occurs under two opposite conditions: the one associated with gen- eral obesity, where an excess of fat, or substances capable of being converted into fat, are taken into the system, while the amount of oxygen received is insufficient to oxidize the excess, and it consequently accumulates in the cells; the other, in which there is general emaciation and a consequent impairment of the oxygenating power of the blood. As a result of this imperfect oxidation the fat contained in the food is incom- pletely oxidized, and so accumulated. This is well illustrated by the fatty infiltration often present in chronic phthisis. Fatty infiltration usually begins and is most marked in those cellular elements which are adjacent to the radicles of the nutrient vessels. Fig. 7. Fatty Infiltration of Liver Cells. a, b. Early stages. c, Nucleus of cell displaced by fat glob- ule. d, Cells completely filled by fat globule. FATTY DEGENERATION. This differs from fatty infiltration in that the fat is derived from the albuminous constituents of the tissues themselves. It is a far more serious process, as it ends in the destruction of the cells; and, there being no provision for the production of new cells, the loss is a permanent one. The fat makes its appearance as minute globules or granules in the protoplasm of the cell, the cell itself furnishing the fat from its own sub- stance, and in time the cell is converted into a mass of granular fat, and is destroyed. In fatty infiltration the protoplasm is displaced by the fat which is deposited in the cell, but it does not suffer materially in its integrity; remove the fat, and the cell returns to its normal condi- tion. As, in fatty infiltration, the well-known physiological deposit of fat in the cells of the liver during digestion furnished a type of what might become a pathological process, so in fatty degeneration the secretion of milk illustrates a fatty degeneration which is perfectly normal. The COLLOID DEGENERATION. 15 young cells in the acini of the mammary gland become converted into fat, they break up, and the fatty matter constitutes the milk corpuscles. Fatty degeneration depends upon all those conditions which interfere with the quality of the blood, so that the tissues are imperfectly nourished j as a result there is an interference with the oxidizing process in the cell, which loses its vitality and undergoes this form of degeneration. The diseases in which this change is apt to occur are, acute yellow atrophy of the liver, chronic alcoholism, progressive pernicious anaemia, and pulmonary phthisis. It is also seen in poisoning by phosphorus, arsenic, and antimony. The tissues which are most commonly the seat of fatty degeneration when it depends upon a general condition are the liver, kidneys, glands, heart, walls of the arteries, and voluntary muscles. When the cause of this degeneration is local, it is due generally to an insufficient supply of blood to a part, as would result from narrowing of the nutrient blood-vessels. This is well seen in the heart, as the result of atheromatous changes in the coronary arteries. Nerves which have been separated from their nerve- centres undergo this degeneration. Organs and tissues which have been long disused, and in which, consequently, the quantity of circulating blood is diminished, also undergo fatty degeneration. This change is often seen in the tissues of old persons, especially in the cartilages, the walls of the arteries, the edge of the cornea (arcus senilis) and the lens (cataract). Cerebral softening is only fatty degeneration of brain tissue, caused by the cutting off of the normal blood-supply to the softened part. Fig. 8. Fatty Degeneration of Cardiac Muscle. COLLOID DEGENERATION. Colloid degeneration is closely allied to mucoid, but differs from it in affecting principally the epithelial cells. The cells become filled with colloid material, which is derived from their substance. This material appears at first as minute spherules in the body of the cells, but eventually it escapes or is set free by the breaking down of the cells, and then the globules coalesce and form colloid masses. Colloid matter resembles mucine, but differs from it. It is more dense, contains sulphur, and is not precipitated by acetic acid. As a physiological process, colloid material is deposited in the thyroid gland, especially in the aged. When there is a large accumulation of this material in the follicles of the gland, then a goitre is formed. Colloid change is met with in lymphatic glands, in the tubules of altered kidneys, in the choroid plexus, and in certain new growths, as compound ovarian cysts and colloid cancers. The cause of this change is unknown, 16 DEGENERATIONS. MUCOID DEGENERATION. Mucoid degeneration consists in a transformation of the albuminous elements of the tissues into a transparent, homogeneous, colorless, jelly. like material called mucine. Mucine is closely allied to albumen. Like albumen it is coagulated by acetic acid, but differs from it in not being redissolved by an excess of the acid, and in not containing sulphur. Mucoid change has its physiological prototype in the secretion of mucus by the goblet-cells of mucous mem- branes and the epithelium of certain mucous glands. The material is formed by metabolism from protoplasm of the cells. Mucoid degeneration affects both cells and intercellular substance. In epithelial structures mucoid degeneration can hardly be called a pathological process. In any catarrh of a mucous surface there will be found in the secretion cells which have undergone this degeneration. Fibrous,tissue is especially liable to undergo mucoid degeneration, and the albuminous intercellular substance is replaced by mucoid material. This is a return of the tissues to their foetal elements, for mucine is found distributed in foetal structures. Mucoid degeneration is frequently met with in the intervertebral and costal cartilages of old people, in certain tumors, in bone, and in the disease known as myxcedema. The causes of this degeneration are unknown. CALCAREOUS DEGENERATION. (Calcification.) This form of degeneration is characterized by an infiltration in the tissues of calcareous particles composed mainly of lime and magnesia salts. It occurs physiologically in the formation of the bones of the skeleton, preceding actual ossification, and also in the formation of a deer's-horn. It is often confounded with ossification, but must be distinguished from it, for it never results in the formation of true bone. The degeneration is common in old age in the coats of the arteries.' Tissues which have undergone calcareous degeneration are rendered hard and gritty. When the process has not advanced very far, the tissues feel as if they had been sprinkled with sand, as the deposit occurs in the form of irregular granules. At a later stage large masses are formed of a gray or whitish color, the% result of an increase in the number and size of these granules. Under the microscope the affected tissue appears as an opaque mass in which no trace of structure can be distinguished, or at an early period the tissue and cells can be recognized, filled with small dark particles. If the tissue be treated with dilute hydrochloric acid, the salts dissolve, bubbles of carbonic acid gas appear, and the original structure of the part may be recognized. PIGMENTATION. 17 The deposit occurs first and most abundantly in the intercellular tissue ; afterwards the epithelial cells are involved. The effect of this degeneration is to destroy the life of the part, which remains as an inert mass ; but the histological structure of the part is not destroyed ; the calcified cells remain, but they are dead ; no further change occurs, and there is no softening. In these respects it differs from fatty degeneration, and is in fact a favorable termination of the latter. The results of this change are very serious when it occurs in the arteries, for it destroys their elasticity and leads to rupture and aneurism ; so also when it takes place in the valves of the heart. It occurs as a conservative process when it checks the growth of tumors and renders pathological products' inert, as is often seen in the lungs in a case of arrested phthisis. Calcareous degeneration may occur under two conditions. 1. When there is an excess of salts in the blood. 2. When there is no such excess, and the deposit takes place when certain alterations have occurred in the blood or tissues. The first is by far the least frequent; it occurs in certain forms of soft- ening of bone, osteomalacia, and extensive caries. Apparently as the bone breaks down, its salts are taken up by the blood and deposited in other places. In such cases it is usually quite general, involving the kidneys, lungs, dura mater, liver, stomach, and intestines. In the second it is local and due apparently to a diminution of vitality in the tissues by which the normal relation between the tissues and the small amount of calcareous salts in the blood is destroyed. Atrophic and retrogressive processes are apt to be accompanied by it. The favorite seats of calcific deposits are tumors, in and about parasites, old blood clots in veins, cheesy deposits, false membranes, and other patho- logical products. PIGMENTATION. Pigmentation is characterized by the presence in the tissues of a colored substance, amorphous or crystalline, which is derived from the coloring matter of the blood. Normal pigmentation occurs in the choroid, rete mucosum, and in some motor cells of the cerebral peduncles. An absence of this normal pigment is seen in albinos; an increase in Addison's disease, freckles, melanotic tumors, and brown atrophy of muscle. Pathological pigmentation follows the extravasation of red blood-corpus- cles, and the escape of their coloring matter, which may also be liberated from the corpuscles while in the vessels. This coloring matter (haemoglobin) infiltrates the tissues and stains both the cells and intercellular substance. It becomes converted into haamatoidin, and appears as minute yellow and reddish-brown granules, or as orange-colored needles and rhombic prisms. S 18 DEGENERATIONS. Pigmentation occurs in most cachectic conditions ; especially in chronic malarial poisoning by a destruction of the corpuscles in the blood. Local causes are rupture of small vessels, and those which cause obstruction to the flow of the blood and favor diapedesis of the red blood-corpuscles, as in a nutmeg liver and brown induration of the lungs, dependent upon heart disease. The staining of the tissues yellow with the coloring matter of the bile, as occurs in "jaundice," is not true pigmentation. Pigmentation may follow the introduction of extraneous substances into the body, as occurs in the lungs by the inhalation of coal dust, soot, and particles of iron, and in the skin and lymphatic glands by tattooing. AMYLOID DEGENERATION. This form of degeneration is characterized by the presence in the tissues of a homogeneous, structureless, translucent substance, differing but little from albumen, and giving peculiar reactions with certain staining reagents. Iodine in solution gives it a mahogany brown color; io- dine and sulphuric acid a blue color; methyl blue, and gen- tian violet a bright red or pink color. The nature of this material is still in dispute. Virchow held it was starchlike, and gave it the name "amyloid ;" other writers, from its resemblance to wax or lard, have called this change " waxy " or " lar- daceous " degeneration. Amyloid material is an al- buminoid rich in nitrogen, and is in all probability derived from the fibrin of the blood by direct metamorphosis (amy- loid reaction having been ob- tained in the fibrin of a haema- tocele). As this material is found in its earliest stage in close proximity to the blood-vessels, it in all probability soaks out from the blood into the tissues and is in reality an infiltration. The change is a pathological one. There is no physiological analogue unless we consider senile changes physiological, for amyloid degeneration is an almost constant accompaniment of senility, in the cartilages of joints, especially the sterno-clavicular and vertebral. Fig. 9. Amyloid Degeneration of Kidney. a, Normal capillary loop. b, Amyloid capillary loop. c. Normal epithelium in tube. d. Hyaline tube cast. e, Amyloid arteriole. /, Amyloid capillary. g, Loosened fatty epithelium, x 300. NECROSIS. 19 Under other more strictly pathological circumstances, amyloid degenera- tion may involve almost every kind of tissue ; but the change shows itself at first always in the walls of the capillaries and the small arteries. They become thickened, have a homogeneous look, and their lumen is diminished. Not every vessel is affected, nor is the change regularly dis- tributed over the same vessel. In time, as the process advances, the con- nective-tissue may become involved, aud last of all, and this but seldom, the epithelial cells may show this change. Amyloid degeneration may be local, but usually a number of organs are affected at the same time. The affected organ is enlarged, and heavier (denser) than normal, its cap- sule is tense, its borders rounded, its surface paler and dryer than normal, and of a grayish appearance. The organs which are most frequently affected with this change, in the order of their frequency, are the spleen (sago-spleen), kidneys, liver, lym- phatic glands, mucous membrane of the stomach and intestines, and occa- sionally the pancreas, thyroid, lungs, ovaries, and supra-renal capsules. Although this degeneration is a constant accompaniment of old age, it occurs pathologically principally between the ages of twenty and forty. It depends upon some nutritive disturbance, and in a large proportion of cases is associated with prolonged suppuration of bone (out of 96 cases examined by Wilks, bone suppuration existed in 68 and had been present in 17 others). It is common in persons suffering from certain cachexias. Pulmonary phthisis is one of its most common antecedents. Syphilis and chronic malaria are apt to lead to it. The prognosis of the disease is very unfavorable, and, considering the resistance of this substance to all reagents, it seems improbable that we shall ever be able to combat it successfully. Corpora amylacea are concretions which have been supposed to be identi- cal with amyloid material ; they give the same color-reaction with iodine, and with iodine and sulphuric acid. It is now known that they have no relation to amyloid degeneration, and are of no special significance. They are hard, stratified concretions found in the prostate, seminal vesicles, and in the central nervous system, and are very common in the aged. NECROSIS. Necrosis is a term applied to the death of a portion of the body. In the soft tissues the process is mortification, and the dead tissue a slough. As soon as a tissue dies, it becomes subject to the conditions of inorganic bodies. Its materials are held together only by cohesion, and that cohesion usually yields promptly to the forces of decomposition due to the action of a ferment generated by certain bacteria. When the entire body dies, its component parts are no longer capable of taking up new material and changing it into living tissue ; as a result the body is unable to resist 20 DEGENERATIONS. decomposition, and this inability is made manifest when the first symp- toms of dissolution appear. All the elements of the body do not lose their vitality at the same time ; as a rule the epithelial cells die sooner than the connective-tissue framework. When a part of a living body dies (necrosis), it undergoes similar changes to those occurring after death of the whole body, being modified only by the locality in which it occurs. The causes of necrosis are: 1. Arrest of blood supply, caused by obstruction in the arteries, veins, or capillaries,—in the arteries by ligature, compression, embolism, thrombosis ; in the veins principally by pressure or thrombosis ; but the anastomoses are so free in the veins that death of the part seldom occurs from this cause alone. Obstruction in the capillaries is much more serious ; for when complete capillary stasis occurs,—as from pressure or diminished heart power,—the vitality of the capillary walls is destroyed, and necrosis results. 2. Direct Injuries to the Cells.—Such injuries are : a. Mechanical, as chemical corrosives, crushing, and animal poisons. b. Bacteria, setting up septic processes, as from putrid pus, dead tissue, decomposing urine, etc. 3. Abnormal Temperatures.—All changes which cause slight increase or decrease of temperature produce inflammation, but when the variations of temperature are excessive, necrosis is the result: this is seen after frost- bites or a burn. The above causes of necrosis do not always act singly, but are often combined ; for example, in a part which is imperfectly supplied with blood, only a slight injury to the cells may cause necrosis ; or, again, let the vitality of the tissues be weakened by an extreme cachexia, and a slight interference with the blood supply will cause necrosis. An illustration of the first is seen in senile gangrene, and of the second in gangrene in children (noma). Certain general pathological conditions may so lower the vitality of the whole body that slight causes will produce necrosis. This is illustrated by the sloughing bed-sores which form in adynamic fevers and exhausting diseases on parts of the body exposed to pressure, and in the liability to senile gangrene, which is increased by the diminished heart power and arterial changes that accompany old age. The rapidly forming bed-sores which result from injury to the spinal cord are regarded by some as due to special trophic changes, but it seems more probable that they are the result of a general vaso-motor disturbance, which produces paralytic hyperaemia, and so necrosis. Varieties of Necrosis.— Eestricting the term " necrosis " to a local death of tissue, the following varieties are met with : 1. Dry Gangrene or Mummification.—Ii tissues that are the seat of this change contain little water, and are composed largely of earthy matters, they may preserve their outline and appearance for a long time. If the water contained in them evaporates rapidly, they shrivel and become hard. TUBERCLE. 21 2. Moist Gangrene.—Tissues that are the seat of this variety of necrosis undergo putrefaction, and, as the evaporation of the water contained in them is prevented, they are moist, soft, and doughy, and in time gases are formed, and their color becomes dark. Such changes are similar to those that occur in the body after death. Moist gangrene always has its seat in parts which are exposed to the air. 3. Hospital Gangrene.—This is a progressive necrosis which affects wounds, and is due to a special micro-organism (septic). 4. Senile Gangrene.—It affects the aged, and is due to an impeded cir- culation from atheromatous, or calcareous changes in the arteries. 5. Coagulation Necrosis.—In this variety of necrosis the cells of a tissue undergo a change analogous to the coagulation of the fibrin of the blood. Their protoplasm becomes rigid and converted into a homogeneous hyaline substance ; their nuclei disappear, and finally the cell breaks up into a granular-looking debris. Coagulation necrosis may affect entire organs, or portions of organs or cells. It occurs in infarctions, tubercular nodules, tumors, waxy degeneration of muscles, and in diphtheria, typhoid and relapsing fevers. The terminations of necrosis, when putrefaction is absent, are : 1. Liquefaction.—In tissues where there is an abundance of liquid, and its removal is prevented by non-evaporation, or the action of the lymphatics is imperfect, the softened tissue becomes converted into a thick creamy fluid. This occurs especially in brain necrosis, and in the soften- ing of infarctions and thrombi. 2. Caseation.—This is a change which results in the formation of a more or less dry, whitish-yellow mass resembling cheese. It is met with most frequently in encapsulated collections of pus, in tubercular masses, and in inflammatory products of low vitality. As the cell elements of such masses die, their watery portions are absorbed, they become granular and dry up. The fat contained in them becomes partly saponified, and crys- tals of cholestrine are deposited. If there are any cells which have not been entirely destroyed, they shrivel and atrophy. This cheesy change is not always a final one, for the cheesy mass may become calcified, calca- reous matter (lime salts) being deposited in and about it. The physical organism behaves towards all necrotic tissues the same as it does towards foreign bodies. If possible, it removes them ; when unable to do this, it surrounds them with a fibrous capsule and so renders them inert. TUBERCLE. To-day experimental research teaches that tubercle is the result of an infectious inflammatory process, and that the infection which excites the inflammation is a specific vegetable parasite, the " tubercle bacillus," which gains entrance into the body through the respiratory and digestive tract, rarely through the genito-uriuary passages or wounds of the skin. Wherever the bacillus lodges and finds conditions suitable for its develop- 22 TUBERCLE. ment and multiplication, there are found in a short time small, gray, translucent nodules, looking like particles of coarse sand, which are called miliary tubercles. If a tubercle is examined microscopically before any degenerative changes have taken place, it will be found to be composed of a reticulated basement substance, lymphoid, epithelioid and giant cells arranged in the following manner : near its centre are one or more large branching cells, the processes of which blend with the surrounding growth. These are the giant cells, which have a homogeneous cell body and a number of nuclei arranged around the periphery like a belt or ring ; sur- rounding these giant cells are a large number of epithelioid cells with single nuclei, packed so closely together that it is almost impossible to distinguish individual cells. Beyond these cells, as one looks towards the periphery of the nodule, is seen a large number of lymphoid cells. These three varieties of cells are enclosed and supported by a fine reticular stroma, sim- ilar to that of a lymphatic gland. The explanation of the formation of a tubercle is as follows : The tubercle bacillus, acting as a specific poison, sets up an inflammatory process, which leads first to an accu- mulation of lymphoid cells with some proliferated fixed cells of the part; some of the lymphoid cells change into epi- thelioid cells, and a few of the latter become giant cells by the enlargement of the cell body and a repeated division of their nucleus. Tubercles are non-vascular structures, no vessels have ever been found in them ; sometimes they start from the wall of a ves- sel, and often, in early growth, the remains of a partially obliterated vessel are seen in them, which has given rise to a dispute whether they were vascular or non-vascular growths. The changes which take place in tubercles are as follows : 1st. They undergo caseous or cheesy degeneration. As they are non- vascular, their centres are shut off from nutrition, and as they are sub- jected to the necrotic action of the tubercle bacilli, in a short time they die and undergo what is called " coagulation necrosis," so that in old tubercles no cells can be found in the centre of the tubercular nodule. Just outside of the caseous centre will be found giant cells blended with a few epithelioid cells, while still further from the centre, constituting the peripheral zone of the nodule, are a large number of lymphoid cells. By special methods of staining the tubercle, bacilli may be found in the Fig. 10. Miliary Tubercle. o, Giant cell. b, Nuclei of giant cell. c, Epithelioid cells. d, Lymp/ioid cells. x TUBERCULOSIS. S3 caseous centre and often in the giant cells. The nltimate change in a tubercle which has undergone caseous degeneration is disintegration with the formation of an irregular abscess cavity. If a number of miliary tubercles are united to form a tubercular mass, as is often seen in the lungs, the union of several of these small abscesses forms cavities of con- siderable size, in the walls of which are generally found a large number cf tubercle bacilli. These cheesy masses may become encapsulated, calcified, and remain as inert masses for an indefinite period. 2d. Tubercle may undergo fibroid change. The tissues which surround the tubercle taking on a chronic fibroid inflammation, the newly formed connective-tissue contracts, and, compressing the tubercle, converts it into a fibrous nodule. This change is most likely to occur in the aged, and in those of a strong fibrous diathesis. The characteristics of a typical tubercle may be briefly summarized as follows : First, a non-vascular nodular growth ; second, a growth com- posed of reticular basement substance and giant epithelioid and lymphoid cells; third, this growth has a tendency to undergo coagulation necrosis due to its non-vascularity and the direct action of the tubercle bacillus; fourth, the special and distinguishing characteristic of this growth is the tubercle bacillus. TUBERCULOSIS. We now understand, by the term tuberculosis, a diseased condition caused by the introduction into the body of tubercle bacilli. Its anatom- ical characteristic is the development of specific nodules. Its clinical characteristic is the consecutive invasion of one organ or of the entire system. Tuberculosis may be local or general: local, when it is limited, and gradually destroys the organ or tissue primarily involved, as occurs in tuberculosis of the lungs, kidney, liver, or peritoneum ; general, when large numbers of tubercle bacilli gain entrance into the general blood current, and in a few weeks develop in the various organs of the body a multitude of miliary tubercles, called acute miliary tuberculosis. It has been shown by experiments on animals that the tubercle bacilli and their spores are alone the infectious agent, and that they travel in the blood current; and wherever they lodge, there the characteristic cellular changes take place, and a tubercle is developed. We consequently reach the conclusion that tuberculosis is an infectious disease, and that its cause is the tubercle bacillus. The danger of local tuberculosis is that it may become general; for the first irruption of tubercles in the neighborhood of an existing tubercular focus is usually followed, sooner or later, by the appearance of nodules in the lymphatic system. It is in the glands that these tubercular irruptions are most intense ; generally the process makes a kind of halt in these gland stations, but in time spreads onwards, and at length reaches the thoracic duct, and through it the general blood current. We therefore conclude that tubercular infection may take place in the 24 BACTERIOLOGY. 1 '^. a following way: First, by the blood, as when tubercular masses grow into ihe pulmonary veins. Second, by the lymphatic system. Third, by con- tinuity, as on the surface of mucous or serous membranes. Fourth, by the direct application of the bacilli to a part, as when a tubercular mass is coughed up, and, before it can be ex- ■ pectorated, falls back into an- other bronchus. At the present time the fol- lowing questions in the pathol- ogy of tuberculosis are being discussed by scientists : 1. Can man become infected with tubercle by eating tuber- cular meat, or by drinking the milk of tubercular cows ? 2. May not the tubercle ba- cilli contained in the sputum and other discharges from tubercular subjects be infect- ing agents, and thus rendei tuberculosis a contagious dis- ease ? . 3. As the tubercle bacilli preserve their vitality for a long time outside the body, may not those contained in the sputum of tubercular subjects, after the sputum is dried and becomes pulverized, be inhaled with the air as dust particles, and set up tubercular processes in the respiratory organs of non- tubercular subjects ? 4. As a preventive measure for the spread of phthisis, should not the sputum and other discharges be burned or disinfected in their fresh state ? Accepting the doctrine that the tubercle bacillus is the only cause of tuberculosis, we are compelled to answer these questions affirmatively, and to say that the doctrine of heredity of tuberculosis must be abandoned, the tubercular taint being nothing more than a hereditary enfeeblement, which furnishes a better soil for the lodgment and development of the tubercle bacilli, or a physical condition which is less able to resist their invasion. Fig. 11. Miliary Tnbercles in the Liver. x 250 drawn by camera lucida. a, Miliary tubercle. b, Giant cells. c, Tubercle with cheesy centre. d, Normal liver cells. BACTERIOLOGY. Bacteria are microscopic organisms belonging to the vegetable kingdom, whose characteristics are the absence of chlorophyl and their peculiar method of reproduction by transverse scission, or by means of small sphe- rules called spores. The science of bacteria is termed Bacteriology. To facilitate bacterial studies I shall divide the subject into four sections : ■■ / ' " *,!.'» -■* -a © ng.i. Fig 2. »-* «v , * * * * i\ f * » * » * * * * » !•> %5»* %* ***** *•••##''* * * ' Fi9A ^ <-'<<■'" y.=A Fig.6. * • Fig.7 PATHOGENIC BACTERIA. PREPARED IN THE LOOMIS LABORATORY BY J.M.BYRON. M.D. rPfR mCSfeRlFrVON SEE PAGE xii. TECHNOLOGY. 25 First. Their technology, or the consideration of the principal facts relating to cultures, staining, etc. Second. A consideration of their forms, dimensions, classification, etc. Third. Their biology, including their origin, nutrition, constitution, reproduction, and special action. Fourth. A description of those whose pathogenic action on man has been established. TECHNOLOGY. In order to study the life history of the different known organisms, pure cultures must be obtained. A pure culture is an artificial growth on nutrient media, of a single species of micro-organisms. Media.—Nutrient media are either artificial or natural. Natural media are obtained directly from man or animals, as blood serum, pleuritic fluid, hydrocele fluid, etc. Artificial media are prepared from different substances and in different ways. Media may be liquid or solid. All media must be sterilized before using for cultures ; that is, they must be made free of all germs that by contamination may be contained in them. This is accomplished by subjecting the media several times to a temperature ranging from 50° C. to 120° C. All vessels and instruments used must be sterilized by heating in dry air to a temperature of 150° C. for an hour. Natural Media.—Blood serum is obtained by leaving in a cool place, for twenty-four to forty-eight hours, the blood of an animal in a sterilized jar. The blood-corpuscles precipitate with the clot, and the clear serum is then transferred to test tubes plugged 'tdth cotton-wool, which have been previously submitted to a dry temperature of 150° C. for an hour. The tubes and serum are then submitted during eight days—one hour every day—to a temperature of 50° C. If solid blood serum is desired, af tei the eighth day the tubes are transferred to the serum inspirator, and the temperature slowly raised to 70 or 80° C, when the blood serum coagulates. Pleuritic and hydrocele fluids are treated in the saJie way. Potatoes and other vegetables, as well as eggs, can be used for cultures with advantage in some cases. They are sterilized by boiling them, or keeping them fifteen minutes a day, during three days, at a temperature of 100° C. Artificial Media.—Pasteur's, Cohn's, and other fluids classed as mineral media, are made by mixing certain salts and water. Bouillon is the principal ingredient used, either as a medium itself or in the preparation of the artificial media used in bacteriological culture. It is prepared by boiling one part of lean chopped beef and two parts water. Filter, and add peptone, lvery of ptomaines by Gautier, and the experiments made by inocu- ,g them in animals and producing the symptoms of the disease incited j|he specific bacteria, scientists are inclined to attribute to the pto- ses, and not to the bacteria, the direct action in the development of the ase symptoms. Such facts, however, do not affect the doctrine of para- pm, as many of those opposed to it thought. The microbes generate i.poison and are thus the cause of the disease. 'ost of the infectious diseases have been studied bacteriologically, and )y bacteria have been claimed as pathogenic of certain diseases which ther experiments have shown to be innoxious. ittenuation of Virus.—Bacteria are differentl/ affected in their vital 5; »o3° § 2 V 5* £ S /o // /-2 iliill & 106 DISEASES OF THE RESPIRATORY ORGANS. The skin is often hot and dry until the crisis ; but it may be bathed in perspiration from the onset. A moist surface is regarded as a favorable sign, but when, at the acme of the disease, the parched skin becomes moist and'the patient is not relieved, it is an unfavorable symptom. In most cases, the expression of the countenance is characteristic. The face is anx- ious/and over the malar bones is a mahogany flush, not diffused as in ty- phus fever, but well defined and circumscribed ; it is called the "pneu- monic spot." The rest of the face is pale.1 Usually, one cheek is more flushed than the other; this is due to disturbance of the vaso-motor sys- tem. When there is a great disturbance of the circulation, or when vaso- motor disturbance is excessive, the lips become cyanosed. At the time of the crisis the lips become pale. In about 50 per cent, of cases, pneumonia is attended by an herpetic eruption upon the cheeks, nose, lips or eyelids. It is rare before the second or third day, and it may not occur until the crisis is reached. Herpes occurs with varying frequency in different years, and is more commonly met with in pneumonia than in any other febrile disease. One winter, nearly every case of pneumonia in Bellevue Hospital was accompanied by " herpes labialis." Sudamina may accompany profuse sweatings. In children, while the surface of the body is hot and dry, the extremities are cool, and the pneumonic flush is bluish or violet-colored. Cyanosis of the extremities is more frequent than in adults, and herpes la- bialis is more constant. All the cutaneous symptoms are exaggerated in children. In old age the pneumonic flush is often the first objective sign of pneumonia. The eyelids alone are cyanotic. If the face is at first dusky, it later assumes a sallow hue, and the surface heat is succeeded by a cold, clammy perspiration. The cerebral symptoms are not very significant in the early stages of pneumonia. Headache is the first to occur, and may continue throughout the entire course of the disease. It usually diminishes after the third day. When severe in the evening there will be slight delirium at night, so slight as often to escape notice. Delirium and convulsions rarely occur except in the debilitated and in those of dissipated habits. It is most frequently met with in drunkards, and then assumes the character of delirium tre- mens. Sometimes in non-alcoholic pneumonia the delirium assumes an active, violent character. Whenever delirium is present it is important to make diligent search into the former habits of the patient. Pneumonia of the apex is oftenest accompanied by severe cerebral symptoms. The delirium may pass into coma. When delirium and headache are marked symptoms, muscular tremors ("subsultustendinum") are very apt to occur with insomnia and frightful hallucinations. These cerebral symptoms occur so early and are so marked in alcohol drinkers that they mask the pneumonia ; a physical exploration alone reveals the disease. When de- lirium is present in the weak and feeble it is of the low, muttering, " typhoid" type, and soon passes into a state of stupor. Photophobia, 1 Bouillard regards the flush as best marked in pneumonia of the apex. Some regard the flush as best marked, or existing solely, on the cheek corresponding to the affected side; others as on the opposite Bi&e.—Jaccoud. ACUTE LOBAR PNEUMONIA. 107 disturbances of vision, and deafness are rare. In children the cerebral symptoms are more prominent than in adults. Stupor and restlessness on the one hand, or headache, delirium and convulsions on the other, may usher in pneumonia in children, and they may rapidly pass into a semi- comatose condition. Convulsions are as common in children as they are rare in adults. They may be general, resembling those of epilepsy ("Eclamptic Pneumonia"), or they may attack single muscles or groups. Tetanus and opisthotonos are uncommon. Delirium and coma occurring late are usually followed by fatal coma. The cerebral disturbances often strikingly resemble those of acute meningitis. In senile pneumonia head- ache may persist throughout the disease. It is usually accompanied by mild delirium, especially when the pneumonia is at the apex. It is a busy, active delirium, and the patient has a constant desire to get out of bed. The symptoms referable to the digestive tract are not important. Nausea and vomiting are among the initial symptoms, and occur in about 75 per cent, of cases. At first the tongue is covered with a white fur; later it becomes dry. Anorexia is marked, and thirst is intense. The lips and tongue may become brown, dry and cracked, and sordes collect on the teeth. Diarrhoea may be an initial symptom ; it usually accompanies nausea and vomiting. The bowels are usually constipated. In children nausea and vomiting are not only common, but in 25 per cent, usher in the pneumonia. They usually cease by the second day. Persistent diarrhoea often precedes death. In senile pneumonia the tongue early becomes dry, brown and shrivelled, and is protruded with difficulty. Although these patients may not complain of thirst, they drink with avidity when fluid is placed to their lips. Dysphagia is frequent. At the crisis critical diarrhoea is more frequent than critical sweats. Loss of strength occurs early, and is more marked in pneumonia than in any other acute disease except typhus fever. Eecovery is rapid when convalescence begins. The urine in pneumonia is scanty, high colored and of high specific grav- ity. The amount of urea and uric acid excreted is two or three times more than normal; it increases until the crisis, and then suddenly dimin- ishes, falling below normal. Inorganic salts, chloride of sodium especially, are constantly diminished and may be wholly absent. Eeappearance of the chlorides marks the approach of convalescence. At the crisis they are present in excess. Urea and uric acid are also sometimes retained in the system ; and at the crisis there will then be a critical diarrhoea followed by prolonged convalescence. Bile pigment and sometimes the bile acids appear in the urine. Slight albuminuria is present in 35 per cent, of the cases. The severer the pneumonia the more marked the albuminuria. Epistaxis may occur at any time, but is most frequent at the onset and at the crisis. Swelling of the veins of the hands in children is an unfavor- able symptom. When pneumonia is to terminate fatally dyspnoea greatly increases, the patient suddenly " sinks," the pulse becomes small, rapid, intermittent and dicrotic ; moist rales are heard in the larger bronchi or trachea, and there are physical evidences of pulmonary oedema. The sputa 108 DISEASES OP THE RESPIRATORY ORGANS. become frothy, liquid, and blood-stained ; they may be entirely suppressed. The respirations are more and more hurried, and the radial pulse become? imperceptible. The face is sunken and livid ; the extremities become cold, and the capillary circulation more and more imperfect. The body is bathed in a profuse cold sweat. Death is usually preceded by a semi-coma- tose state. The temperature may steadily rise up to the time of death, or there may be " defervescence." Death may occur at any period of the dis- ease. In alcoholic pneumonia death is preceded by active brain symptoms. In children death is often preceded by convulsions or coma; sometimes exhaustion or collapse is most marked. Cyanosis and extreme rapidity of pulse are common in children before death. Senile pneumonia may end fatally within a few hours after the onset in a most unexpected and quiet manner. In other cases sallowness of the skin, cold, clammy sweat, working of the auxiliary muscles of respiration, a feeble, rapid, irregular and intermittent pulse, and a sudden rise or fall of the temperature may precede the fatal issue. Abscess.—Acute pneumonia terminates in abscess in 1£ to 2 per cent, of all cases. It is met with oftenest in debilitated weak subjects. The sputa are copious and fetid, yellowish in color, consisting almost wholly of pus. The fever is of the hectic type, and is accompanied by rigors and sweats. The patient grows weak and emaciated, death resulting from exhaustion, from asphyxia, or from discharge of the abscess into some neighboring cavity or organ.1 The physical signs of the cavity are the most reliable evidences of an abscess. Abscess is rare in children. In old age there are no well- marked signs. Gangrene as a termination of pneumonia has been found in about 14 per cent, of cases. This, however, is an exceptionally high percentage. Its occurrence is marked by signs of sudden collapse. The pulse is rapid, feeble and intermittent; the face is pale and " death-like ; " there is pro- fuse expectoration of blackish-green masses containing shreds of decom- posed lung substance having a gangrenous odor. The breath is offen- sive and the body has a cadaverous smell. The sickening odor of pul- monary gangrene is most perceptible after coughing. Gangrene has its seat in the lower lobes of the lung, and it is here we must search for its ill-defined physical signs. In old age when pneumonia is to terminate in gangrene typhoid symptoms are present early and death occurs in collapse, usually within five days from the onset. Purulent infiltration has symptoms that differ but slightly from those of the third stage of pneumonia. When resolution does not take place at the period of crisis and the temperature remains high, accompanied by symptoms of prostration and profuse purulent expectoration, purulent infiltration may be suspected. Somnolence and mild delirium are quite frequent during " purulent infiltration." The sputum contains a large number of cells in various stages of fatty degeneration. The fever has regular evening exacerbations, and it may range higher than at any other ' Fox and Green state that abscess is located preferably at the apex ; Da Costa says at the base.—Gnyl Bospital Reports. Ser. VII. 1848. ACUTE LOBAR PNEUMONIA. 109 period in the disease. The tongue becomes brown and dry, and sordes collect on the teeth and mouth. Kecovery is slow and convalescence tedious. Death results from exhaustion. Typhoid pneumonia is a term that has been applied to a pneumonia attended by typhoid symptoms. It has also been called "asthenic," " low," or '' nervous " pneumonia. It is marked by extreme prostration that may exist from the onset. In the majority of cases, well-marked pneumonic symptoms, after having been present for a short time, soon give place to intense nervous prostration and adynamic symptoms. There is no sputa, no dyspnoea, no pain, no cough. Scrdes collect on the teeth and gums. The tongue is thickly coated, and later, covered with black crusts. There is incontinence or retention of urine. The pulse is small and rapid. There is stupor, somnolence, and continual low, muttering delirium. This form is common in the aged. In some cases there is marked disturbance of the special senses—the speech being most affected. Tremor and subsultus tendinum are frequent. Typhoid pneumonia may be accompanied by glandular swellings, sharp and darting muscular pains, arthritic symptoms or vomiting. It is not infrequent in epidemics, and it may follow Bright's disease, erysipelas, alcoholismus, or phlebitis. Recovery is always possible, but is slow and tedious, and may not begin until the twelfth or fourteenth day. A modification of typhoid pneumonia sometimes accom- panies dysentery, intestinal catarrh or phlegmonous gastritis. There is great sweating, profuse colliquative diarrhoea and high fever. Bilious, or gastric pneumonia, is lobar pneumonia occurring in mala- rial districts, and accompanied by gastro-enteritis with hepatic symptoms. It is sometimes called "malarial pneumonia." It has the characteristics of a severe pneumonia, but the fever is paroxysmal. The tongue is heavily coated; nausea and vomiting are common and may be persistent. The epigastrium is distended and tender, the skin more or less jaundiced ; the liver is enlarged, and there is constipation or exhausting diarrhoea; the latter is accompanied by greenish-black, viscid and inodorous discharges. " Bilious" pneumonia may be sthenic or asthenic ; but prostration is apt to be nearly as marked as in the typhoid variety. The symptoms of bilious pneumonia have frequently led to the diagnosis of " typhoid gastric fever.'1'' It runs a much more protracted course and has a much longer period of convalescence than the typhoid variety ; vomiting is "bilious," and somnolence and stupor may indicate a fatal issue. Latent pneumonia seldom occurs in adults unless it complicates some disease whose symptoms are so severe that the pneumonia is obscured. Inter-current senile pneumonia is always latent; and Grisolle states that a physical exploration gives negative results in the majority of instances. Senile pneumonia may run its course without expectoration, dyspnoea, flushed face or physical signs. Its diagnosis is then difficult. It is to be remembered that of all phlegmasia? of advanced life, pneumonia is the most frequent; and of all the acute diseases of advanced life it causes the highest temperature range and the greatest prostration. When an old person has a slight rigor, followed by a febrile movement attended by great 110 DISEASES OF THE RESPIRATORY ORGANS. prostration for which there is no explanation, pneumonia may be suspected even though all its usual signs are absent. Intermit tent pneumonia, which is by some described as a distinct type, is a form of acute pneumonia in which a malarial element is so pronounced that all the subjective and even the physical signs undergo distinct inter- missions, returning each day with increased severity. It may assume the quotidian or the tertian type. During the intermission the temperature may fall to the normal. Eecurring chills and sweats are often present; and the pneumonia is not infrequently double. By some it is regarded as peculiar to old age; it is very rare at any other period. Those malarial influences that give rise to this type of pneumonia are more frequently met with in our Southern and Western States than in any other part of the world. Physical Signs.—First Stage, or Stage of Congestion.—The physical signs indicative of the first stage of lobar pneumonia are usually present within twenty-four hours after its invasion. If the pneumonia commences in the central portion of the lung their appearance may be delayed till the third day. By studying these signs in connection with the anatomical stages of the disease their importance in diagnosis and prognosis can best be appre- ciated. Inspection.—The movements of the affected side are more or less re- stricted. The unaffected side moves as in health. In double pneumonia the respiratory movements will assume the costal type, attended by increase in the abdominal breathing. Palpation.—There is more Or less marked increase in the vocal fremitus over the affected lung; the degree of increase corresponding to the extent of the congestion. Percussion.—There is slight dulness over that portion of the chest which corresponds to the affected portion of the lung. It is not well marked until the end of this stage, although the pulmonary capillaries are engorged with blood from the very first. Even at the end of this stage there some- times remains a slight tympanitic note. Very extensive central pneumonia may fail to give any signs until the second stage is reached. Absolute dulness in this stage is very rare. Auscultation.—During the "dry" stage—which, according to some, precedes the exudation—there will be noticed a feebleness and unnatural dryness of the respiratory murmur. This murmur is sometimes harsh, sometimes weaker than normal, losing the "breezy," rustling quality of normal breathing. Elsewhere it is exaggerated. As soon as the conges- tion is well marked, fine crackling sounds are heard at the end of inspira- tion—" crepitant rdles "—which have been regarded as characteristic of this first stage, but which are usually pleuritic crepitation. These sounds resemble those produced by throwing salt on hot coals or rubbing the hair between the fingers. They are as numerous as they are minute, are un- affected by coughing, and remain audible for from twelve to twenty-four hours. This rale is of an unvarying character, and continues, i. e., is not inter- or remittent. If the pneumonic stages succeed each other in rapid ACUTE LOBAR PNEUMONIA. Ill succession, the crepitant rale may not be heard. They are rare in pneumonia developed with acute articular rheumatism. The respiratory murmur is feeble or assumes a broncho-vesicular character. Bronchial breathing may be heard in this stage (Traube). The voice sounds are slightly increased in intensity over the engorged spot. In children the " pneumonic crepita- tion " is usually absent; and though it may be heard at the end of a full inspiration after crying, it is never as fine or as distinct as in adults. There will be no marked increase in vocal fremitus. In old age the physical signs are modified by a more complete bony union of the chest walls, by curvature of the spine, rigidity of the bronchial tubes, by the rounded form of the chest, and by senile rarefaction of the lungs. Second, or Stage of Red Hepatization.—The physical signs of this stage are more diagnostic than those of either of the other stages. Inspection shows the expansive movements of the affected side more markedly diminished than in the first stage ; while those of the other side are increased. There may be absolute loss of motion over the affected lung. Palpation.—There is usually marked increase in the vocal fremitus over the consolidation. In some instances this is so slight that no difference can be detected. Very rarely it is less than on the normal side. The heart may be slightly displaced. Rarely can pulsation be felt over the inflamed lung. The majority of authorities regard this pulsation as due to increased pulsation in the arteries of the inflamed spot, but there is no reason to doubt that the cardiac impulse itself can be transmitted through the solid- ified lung as well as the arterial impulse or the vibrations from the chordce vocales. In central pneumonia, vocal fremitus may be normal. Pleuritic effusions mask the signs. Percussion.—There is marked dulness over that portion of the lung which is the seat of the pneumonia. Over the unaffected lung there is ex- aggerated resonance. The nearer the hepatization to the surface the more marked the dulness. There is a sense of resistance accompanying the per- cussion. A pneumonic lung is more resistant than any other form of con- solidated lung. When an entire lobe is consolidated its exact outlines can be defined. The percussion may have a tympanitic quality anteriorly, but there will always be dulness posteriorly. There may be slight tympa- nitis just around the pneumonic spot. When an entire upper lobe is con- solidated a tympanitic percussion sound may be caused by vibration of the air in a large bronchus. The " cracked-pot sound " is occasionally met with in pneumonia over the relaxed and permeable parts of the lung in the immediate vicinity of the consolidation. When heard over the condensed portion it is caused by the sudden expulsion of air from the large bron- chus. This occurs most frequently in the young with thin chest walls. In basic pneumonia the percussion note under the clavicle of the affected side may be amphoric. Auscultation.—As soon as the air-cells are completely filled with the pneumonic exudation the crepitant rales cease, and bronchial respiration is heard over the affected lung. It often has a metallic character ; or it may sound like tearing a piece of linen. Bronchial respiration is more intense 112 DISEASES OF THE RESPIRATORY ORGANS. in pneumonia than in any other disease.1 At the commencement of the second stage tubular breathing attends expiration only. Later, it accom- panies both acts. Pleuritic exudation may mask the auscultatory signs. Plugging of a large bronchus will prevent tubular breathing ; a violent fit of coughing may allow it to occur when the mucus is dislodged. The voice sounds are increased in intensity, and bronchophony is heard over the whole of the consolidated lung. Bronchophony has the same diagnos- tic significance as bronchial respiration because it is produced by the same physical condition of the lung. When the pleural cavity is partly filled with fluid, bronchophony is indistinct or absent below the level of the fluid; while at the level the voice sounds may be aegophonie. Pectoriloquy may First stage. ' Diminished respiratory movements Slight dulness on percussion....... Broncho-vesicular Meathing....... Crepitant rales.................. , Slight increase of vocal resonance Second stage. - ' Lost movement................ Increased vocal fremitus...... Complete dulness on percussion Bronchial respiration......... [ Bronchophony................ ' Returning respiratory movement, Diminishing dulness............ Third stage. Bronchial, giving place to Broncho-vesicular breathing Baieredux................... Fig. 27, Diagram Illustrating the Physical Signs in the Three Stages of Lobar Pneumonia. be heard independent of fluid in the pleural cavity. The heart sounds art abnormally intense. In children dulness is especially marked in the infra- clavicular region. Some speak of a feeling of greater solidity below than above the scapula which can be perceived before the ear can detect dulness on percussion. Vocal fremitus may be increased, but this is not always to be expected. In old age, inspection and palpation give negative results. What is dull on percussion in old age might be regarded as resonant in 1 Laennec taught that bronchial respiration was due to the superior conducting power of condensed lung. Skoda combats this view, and says that bronchial respiration is generated or magnified in caverns and in the bronchi of condensed lung substance by the air in these cavities and bronchi vibrating in con- sonance with that of the trachea; the condition necessary for this consonance is provided in the circ«n» stance that the air is pent up in confined spaces whose solid walls reflect t>" sonorous undulations. ACUTE LOBAR PNEUMONIA. 113 adults. Hence dulness on percussion is a relative term in senile pneumo- nia. When the pneumonia is superficial there is actual dulness. Tubu- lar or bronchial breathing marks the second stage, and is even more intense than in adult life. Small gurgles or mucous rales are heard in this stage. Bronchophony is not very common, and never distinct. iEgophony is fre- quent. By causing the aged patient to cough and expire violently tubular breathing may be heard. Third, or Stage of Gray Hepatization.—There is no abrupt transition from the second to the third stage ; the physical signs of early gray hepati- zation are the same as in the second stage. Inspection.—As resolution progresses, expansive motion on the affected side becomes more and more apparent. Palpation.—Vocal fremitus gradually diminishes. Percussion.—Dulness becomes less and less marked. Of all the signs this is the last to disappear. As the percussion sound becomes more and more resonant the tympanitic note is again heard in spots. It is a long while before normal pulmonary resonance is re-established. The dulness may disappear in patches. As the dulness diminishes the pitch of the percussion note rises. Auscultation.—The bronchial respiration that was present in the second stage gives place to broncho-vesicular breathing, which soon becomes "blowing,''then indeterminate, and finally normal. Bronchophony gives way to exaggerated vocal resonance. In connection with these changes in the respiratory and vocal sounds the crepitant rale returns, but is soon obscured by larger and moister crepitating sounds—the "resolving sub- crepitant rale " of pneumonia—the " rdle redux." Large and small mucous, sibilant, and sonorous rales accompany the sub-crepitant sounds, to disap- pear only when resolution is complete. Not infrequently the bronchial rales that are developed during the stage of resolution are " consonant" or ringing.1 The physical signs of this stage are all retrogressive, and they disappear in the opposite order to that in which they appeared. In rare cases resolution is so rapid that the sub-crepitant rale is not developed. In this class of cases bronchial breathing and dulness on percussion continue for some time after the crisis. If the consolidated lung becomes the seat of purulent infiltration, the temperature remains high and symptoms of great prostration are developed. Bronchial breathing continues, and becomes more intense, dulness persists, and when rales occur they are high-pitched, sharp, and resemble fine gurgles. The occurrence of abscess and gangrene is indicated by the physical signs which attend the formation of a cavity in consolidated lung substance. No one of the physical signs present during a pneumonia is sufficient for a diagnosis; but the manner and order of their occurrence and their relation to the subjective symptoms enable one to reach a positive 8 1 Skoda and Traube. 114 DISEASES OF THE RESPIRATORY ORGANS. diagnosis in all typical cases. The only diagnostic symptom is the sputum. In children bronchial breathing rarely disappears before the seventh day; it is often accompanied by the sub-crepitant rale. When resolution takes place, bronchial breathing and the sub-crepitant rale will disappear simul- taneously. If purulent infiltration occurs, large gurgling crepitation will be heard.- Vesicular breathing is rarely heard before the eighth or ninth day. In Old atfe^ inspection, palpation and percussion give similar results to those in adult life. Auscultation shows the crepitating sounds to be louder, and gargles large and loud are often heard at a distance from the chest. "the tale redux is not distinctive of, or peculiar to the third stage of senile pneumonia. The sound heard at this stage is a muco-crepitating sound, i. eti a sound produced in bronchi of medium size. The physical signs of pulmonary abscess in the aged are very generally wanting. Distinctly local- ized gurgling and cavernous respiration may, with the rational signs of abscess, suffice for a diagnosis. The sputa will also aid, but the diagnosis is only approximate. In old age the physical signs are subject to greater variations than in adult life. BilFerential Diagnosis.—Lobar pneumonia may be confounded with pul- monary congestion and cedema, pleurisy, hypostatic congestion, catarrhal pneumonia (in children), pulmonary infarction, acute phthisis (especially in children), meningitis and. typhoid fever. Pneumonia begins with a chill, followed by a rapid rise in temperature and pain in the side ; in pulmonary congestion and cedema, there is no chill OT rise in temperature, and no pain. The sputum of pneumonia is viscid, rusty and (microscopically) diagnostic; in pulmonary congestion and oedema there is profuse watery, blood-stained expectoration. Pneumonia is com- rrionly unilateral, and may occur in any portion of the lung; pulmonary cedema is bilateral, and usually occurs in the most dependent portions of the lungs. In pneumonia there is complete dulness on percussion, crep- itant rales and bronchial respiration ; in pulmonary cedema the dulness is hot complete, there is no bronchial breathing, and there occur numerous large, liquid, sub-crepitant rales. Pneumonia is ushered in by a distinct chill followed by fever; acute pleu- risy begins with chilliness or several rigors, and the temperature rarely rises above 100° F. The dry, hacking cough of pleurisy is accompanied by slight mucous expectoration, and the characteristic pneumonic sputum is absent. In pleurisy the face is pale and anxious, and the pulse is firm, small, tense and wiry; in pneumonia the face has a mahogany flush, and the pulse is full and compressible. The breathing in pleurisy is "catch- ing;" in pneumonia it is " panting." There are no critical days in pleurisy. Vocal fremitus is diminished or absent in pleurisy with effusion, there is flatness on percussion, and the sound of the percussion changes with a change in position of the patient. In pneumonia vocal fremitus is in- creased, and there is dulness—not flatness—on percussion. In pleurisy the ACUTE LOBAR PNEUMONIA. 115 respiratory sounds are feeble, and a grazing, rubbing or sticky friction- sound is heard; in pneumonia there are crepitant rales and bronchial breathing. Bronchophony and bronchial breathing may exist in pleurisy, but they are always diffuse—never sharp and tubular as in pneumonia. Hypostatic congestion is accompanied by copious, watery, blood-stained expectoration; it occurs in the most dependent portions of the lungs, dis- appears when the patient sits up, and is accompanied by no rational symp- toms except dyspnoea and expectoration. Lobular pneumonia in children is always secondary ; it is not ushered in by a chill, usually follows a bronchitis, and is developed in both lungs. There are no days of crisis, and the physical signs of pneumonia are lim- ited to circumscribed spots. The range of temperature in the two forms of pneumonia differ; the two curves represented by Figs. 20 and 25 show the differences. Pulmonary infarction is rarely met with independent of cardiac disease or pyaemia. It is a non-febrile disease, and intense dyspnoea, coming on abruptly, is its prominent symptom. In pneumonia dyspnoea comes on slowly. The expectoration in infarction consists of small black coagula ; in pneumonia it is viscid and contains few blood-globules. The dulness of an infarction is circumscribed, and around it moist rales are heard ; in pneumonia the area of dulness is extensive, and there are no moist rales. There is a peculiar garlic-like odor to the breath, in pulmonary infarction, never present in pneumonia. When lobar pneumonia has its seat at the apex, it may be confounded with acute phthisis. But the history of a wTeil-marked chill, followed by the characteristic pneumonic symptoms, will enable one to exclude phthisis. Moreover, the fever in phthisis is subject to irregular exa- cerbations and remissions. If the signs of consolidation persist with lit- tle or no change, if the temperature at no time falls to normal, if there are night sweats, if emaciation is progressive—then the case is to be regarded as one of phthisis, even though pneumonia may have complicated it. In children pneumonia is so often accompanied by cerebral symptoms that it may be mistaken for meningitis. Meningitis comes on insidiously, the temperature rarely rises above 103° F., the pulse is often lower than nor- mal, there are no thoracic symptoms, no dyspnoea, the face is pale and anx- ious, and the physical signs of pneumonia are absent. Sometimes latent pneumonia may be mistaken for typhus fever, especially when typhus is prevailing. While in charge of the typhus fever patients on Blackwell's Island, I frequently saw cases where such a mistake had been made during a typhus epidemic. In these cases there will be dry tongue, delirium, and high temperature. The countenance resembles that of pneu- monia, but the presence of the typhus eruption and the absence of the physical signs of pneumonia will establish the diagnosis. Pneumonia with typhoid symptoms is sometimes mistaken for typhoid fever. The differential diagnosis is not difficult, if one remembers that the pneumonia which complicates typhoid fever does not come on until late in 116 DISEASES OF THE RESPIRATORY ORGANS. the fever, and the regular history of typhoid fever precedes its development. On the other hand, when the typhoid symptoms are present from the be- ginning, or come on at the end of the second stage of pneumonia, the phys- ical sig°ns of pneumonia will precede the typhoid symptoms. If a patient over sixty years of age, with this type of pneumonia, is not seen until the second or third week of his sickness, although evidences of lung consolida- tion may be found, it will be very difficult to decide whether the pneumonia is or is not complicating a typhoid fever, and under these circumstances the diagnosis will be difficult if not impossible. Prognosis.__The phenomena of the crisis of pneumonia are a sudden fall of temperature followed by profuse sweats and a diminution in frequency of respirations and pulse. The cough becomes loose, the dyspnoea abates, the flush disappears from the face, the sputum is more copious, loses its rusty hue, diminishes in viscidity and becomes "creamy," thin and watery. Thirst decreases, the appetite returns, pain ceases and the patient falls into a quiet sleep, waking extremely exhausted. Epistaxis, hae- maturia and hemorrhage from the bowels may occur at the cri- sis. After the crisis the amount of urea in the urine, which was aug- mented before, becomes normal and the chloride of sodium reappears. The crisis in children is marked by a greater fall in temperature and by a more profuse sweat. When children have been restless or delirious the crisis is marked by a state of stupor. In old age the crisis is marked by a critical diarrhoea rather than by a sweat. The fatality of pneumonia is shown by the following statistics: of 12,421 cases treated in the hospitals at Stockholm, 11 per cent. died. In the Vienna hospitals 24 per cent. died. The Basle Hospital Reports for thirty-two years give 23 per cent, of deaths. Grisolle reports 59 per cent, of deaths in those over sixty. In the "U.S. Medical Reports," May 1st, 1861, to July, 1866, of 61,202 cases which occurred among the white troops, 14,738 died—more than 24 per cent. ; and of 16,133 among colored troops, nearly 33 per cent. died. The deaths from all other inflammatory diseases of the respiratory system for the same time were only one-seventh as many as from pneumonia.1 Of 255 cases treated in Bellevue Hospital during a period of four years the rate of mortality was 34 per cent. The statistics of private practice are very different: of Lebert's 205 cases, only 7T3o per cent. died. Ziemssen lost only 3^ per cent, of his cases. Bennet lost none of his 105 cases. (He says, however, that no complications existed.) Brundes, of Copenhagen, lost over 21 per cent, of his 142 cases. Fox gives to pneu- monia the fifth, and Walshe the third place among fatal diseases. The average mortality-rate from all the published reports to which I have had access gives 20^ per cent, of deaths. But the rate varies in different years. The prognosis depends more on the age than on any other single ele- ment. In infancy the mortality is greater than in early childhood. Be- i The Confederate Hospitals' Reports give over 30 per cent, of deaths from pneumonia for the same period. ACUTE LOBAR PNEUMONIA. 117 tween the ages of forty and sixty the death-rate is from 10 to 25 per cent., while from ten to thirty years almost all of the uncomplicated cases recover. After sixty the prognosis is always unfavorable. Pneumonia is the most fatal of all acute diseases at this period of life; most " sud- den deaths" in the old are from acute lobar pneumonia. Some of the most reliable modern authorities state that nine-tenths of deaths after the seventy- fifth year are from acute pneumonia. It is more fatal in females than in males. In some years the proportion of deaths is far greater in summer than either in the spring or winter ; and certain—as yet unknown—atmos- pheric influences are of the utmost importance in determining the death- rate. The extent of lung involved influences the prognosis ; double pneu- monia is rarely recovered from. When an entire lung is involved, the prognosis is not as good as when only a single lobe is involved. Apical pneumonia—especially in the old and very young—is more often fatal than basic. The feebler the patient the more unfavorable the prognosis. Complications render the prognosis unfavorable : of 225 of my own cases, 87 were fatal and 168 recovered. Of these, 124 were complicated and 131 uncomplicated. Of the complicated cases, 75 died; of the uncomplicated, 12 died.1 The most dangerous complications are those which exert a direct influence on the heart, diminishing its power and obstructing the flow of blood from the right ventricle. Acute infectious diseases are dangerous complications because they hasten heart failure. Pneumonia may be regarded as mild when the temperature is below 104°. When the fever ranges above 106° for two days, the case is unfavorable. A gradual rise in temperature after the fourth day is always an unfavor- able sign. A low temperature is dangerous only when the respirations are greatly accelerated. When the pulse is 120 to 130 for two or three days, the prognosis is bad. If the pulse reach 150 per minute, or if it becomes irregular, intermitting, or dicrotic, the patient rarely recovers. In children a rapid pulse is of less significance, and in old age the pulse is never a reliable guide. Prune-juice expectoration is an unfavorable sign, indicating extensive blood changes. When expectoration is absent in the second or third stage, or if it become scanty and difficult, the prog- nosis is unfavorable. Sudden suppression of the sputa, with coincident tracheal rales, indicates impending death. Delirium coming on after the sixth day, convulsions in children, with jactitation and subsultus, or, in the aged, a tendency to coma, are unfavorable signs. Exhaustion and prostration, accompanied by a sunken pallid face and cold, clammy sweat, are always dangerous. In children, bronchial breathing, after the seventh day, numerous subcrepitant rales, copious and persistent diar- 1 Lebert states that he lost only 5% per cent, of his uncomplicated, and all of his complicated cases. Hues lost 6 per cent, of uncomplicated and 20 per cent, of complicated cases. Fox states that pneumonia com- plicated by endocarditis is fatal in 75 percent, of cases ; by pericarditis, in 54 per cent.; by Bright's disease, in 50 per cent.; and by alcoholismus, in 25 per cent. Brundes (of Copenhagen), in 120 uncomplicated cases, lost 6% per cent.; of 22 complicated, he lost all. The danger of complications is markedly shown by these statistics. 118 DISEASES OF THE RESPIRATORY ORGANS. rhcea, and swelling of the veins of the hands are bad symptoms. In old age a sudden rise or fall in temperature, apathy, somnolence, and a sallow, anxious countenance are dangerous symptoms. Pulmonary con- gestion and cedema in the unaffected part of the lung often precede a fatal issue. The occurrence of purulent infiltration, abscess, or gangrene ren- ders the prognosis unfavorable. In pneumonia the fibrin-factors of the blood are increased (often 400 per cent, more than normal), the heart-power is diminished, so that the ventricles cannot empty themselves, the columns and cords whip up the residual blood (already prepared for clotting), and "heart clots" always form when the death struggle is prolonged and cardiac contractions feeble. The "heart failure" is the beginning of death. Post-mortem results can never give all, or the true causes of death, but only the modes of death. If, on account of heart failure, pulmonary oedema and congestion occur and heart clots form, these clots cannot be called causes of death. Jiirgensen states that in fatal cases of pneumonia cedema of the lungs is probably always present, and heart clots are fre- quent. Death may occur, then, from heart-insufficiency, from complica- tions (cardiac especially), or from asphyxia. Fatal collapse may follow an apparently regular and well-marked crisis. Treatment.—If we regard pneumonia as a general disease with a charac- teristic local lesion, the treatment must be modified by the constitutional condition of each patient and by the type of the pneumonia. If it is un- complicated and occurs at certain periods of life, it will terminate spon- taneously in recovery by crisis ; but when certain complications exist, when certain conditions are present, and at certain ages, it is almost necessarily fatal. Any plan of treatment in such a disease, if resorted to indiscriminately, will prove unsatisfactory. Although a large proportion of cases will re- cover without treatment, yet well-directed therapeusis will save lives and render convalescence less tedious. The pneumonic lung no more requires treatment than the intestinal ulcers of typhoid fever. It is the general con- dition of the patient, not the local changes, which is to govern us in the management of each case. Agents for the arrest of local inflammation have no place here; hence venesection, once generally practised, has been almost entirely abandoned. A careful study of the pathology of pneumo- nia not only leads to the conclusion that bleeding does harm, but it strongly contra-indicates the use of all those agents which have been em- ployed for the arrest of simple pulmonary inflammation. Hence veratrum viride, aconite, antimony, calomel, the tartrate of potash and antimony, iodide of potassium, and all so-called "cardiac sedatives" have been dis- carded, for it is evident that they add a new load to an already overburdened heart. They may, for a time, lower temperature and pulse-rate, but this will be accomplished at the expense of heart-power. Cardiac insufficiency will therefore appear earlier and be more profound. Counter-irritation by blisters, or other irritants, to the chest (in the early stages) is apt to do harm ; but blisters may be applied during the third ACUTE LOBAR PNEUMONIA. 119 stage, to hasten resolution. The application of leeches, followed by a lin- seed-meal poultice or other soothing fomentation, will relieve the pain in the side, which is often so urgent at the onset, and, if the condition of the patient will allow, may be of service. If extensive pulmonary cedema oc- curs, dry cups applied to the chest will relieve the dyspnoea, and for a time dispel the cedema. It has come to be a rule to incase the chest in a cotton-batting or flannel jacket, covered with oiled silk. This has no influence over the course of the pneumonia, but it promotes diaphoresis, protects the surface from sudden changes of temperature, and it is always grateful to the patient. The "jacket " is especially beneficial in children. Absolute rest is important; the patient should be moved as little as possible, and should not be kept in a constrained posture. If signs of heart failure occur, he should not be allowed to sit up or talk. The sick room should be large, cheerful and well ventilated, and its temperature should range between 65° and 70° Fahr. A most important adjuvant is a carefully-regulated diet. The food should be fluid or semi-fluid, and highly nutritious, e. g., milk, eggs, beef-tea, and concentrated broths. Milk is preferable to all other nourishment. The nervous shock which attends the onset of acute lobar pneumonia is greater than in any other acute disease, except, perhaps, acute peritonitis, and the important question presents itself: what measures shall be em- ployed to counteract, or mitigate, the impression made on the nerve centres by the morbific agent which is operating to produce the pneumonia ? The experience of the last five years leads me to the conclusion that during the developing period of the disease, when the pneumonic blow is first struck, and until the infiltration is complete (usually for the first four days), the patient is to be brought under the full influence of opium and held in a state of comparative comfort, by hypodermic injections of morphia, re- peated at regular intervals ; and that by this course a pneumonic patient is placed in the best condition, not only for sustaining the primary shock, but for resisting the pneumonia. Thus given, opium does not interfere with the employment of any stimulating or anti-pyretic measures which may be demanded. And not only does it diminish the chances of the occurrence of heart failure, but the great relief and comfort which it gives to the sufferer in the first four days of his struggles are sufficient to com- mend its use. After the pneumonic infiltration is completed, opium should be discontinued, for paralysis of, and a consequent accumulation of secretion in the bronchi may greatly increase the already deficient respirations. In all severe types of pneumonia there are two prominent sources of danger—heart-insufficiency and high temperature. The two prominent indications for treatment are, therefore, to sustain the heart and to reduce the temperature. A large proportion of deaths in pneumonia directly result from heart failure; alcohol, judiciously used, is the most efficient means for preventing or overcoming it, but its indiscriminate use is more dangerous than indiscriminate bleeding. Only a few ounces of brandy may be re. quired to carry a pneumonic patient through a critical period ; or its free administration may be demanded to save life. In the old and feeble, and 120 DISEASES OF THE RESPIRATORY ORGANS. in those who have been accustomed to the use of alcohol, stimulation may be necessary from the very onset. The indications in each case demand careful study; in no disease is so much discretion required in the admin- istration of stimulants. The pulse is the indicator of the heart's con- dition. A frequent, feeble, irregular or intermitting pulse calls foi stimulants. The quantity required in any case is to be determined by its effects on the pulse. It is best to begin with small quantities, and care- fully note the effect of the first few doses. If it acts beneficially, a favor- able effect will be seen in a few hours ; and then the quantity administered must be varied to suit each case. It is seldom necessary to use more than six or eight ounces of brandy in twenty-four hours ; but, when demanded, it is to be unsparingly given. A dicrotic pulse is always an indication for its use. The period immediately following the crisis is the time when stimulants are usually most required. Delirium, muscular tremor and sub- sultus are indications for their use. Critical collapse in the aged must be combated by a very free use of stimulants. Carbonate of ammonia is extensively employed as a stimulant in pneumonia ;—it is claimed that its use diminishes the danger of heart clot, but there is no evidence in support of this statement;—and if given in sufficiently large doses to act as a stimulant it irritates the stomach. It is unquestionably inferior to alcohol as a cardiac stimulant. Camphor and musk are also inferior to alcohol, and digitalis is only of service when there are evidences of extensive renal congestion. There are two plans of treatment advocated for reducing temperature in pneumonia : (1) the application of cold in various ways to the surface of the body ; and (2) the internal administration of some one of the anti- pyretics. It is claimed that the temperature can be reduced by applying cold compresses to the chest; a cloth of some thickness is to be wrung from cold water and applied every ten or fifteen minutes to the affected side. This not only relieves the local symptoms, but it lowers the body temperature and hastens the day of crisis. Some prefer the " Esmarch ice-bag " to the cold compress. When cold is used at all, I prefer the coil. There is no doubt but that the pain in the side and fever will be relieved by this means, but the relief is only temporary; and my own experience leads to the belief that pneumonia treated in this way is more likely to extend, and, that there is great danger of chilling the patient. The other methods of applying cold to the surface for the reduction of temperature in pneumonia are the cold bath, the cold pack, and cold sponging. The experience of American practitioners is against the cold bath and the cold pack. The shock of cold causes depression, which the feeble or old cannot rally from. And though fever is lessened, heart-failure more rapidly follows, and is more difficult to overcome. My own experience is decidedly against the use of cold on the surface for the reduction of temperature in pneumonia. Cold " sponging " may be practised when it is grateful to the patient. Of the internal antipyretics, antipyrin and antifebrin are largely employed. Of these, antifebrin is to be preferred. In many instances it ACUTE LOBAR PNEUMONIA. 121 will effect a reduction of temperature not obtainable by other antipyretics. In the majority of cases of pneumonia, however, sulphate of quinine is more efficacious than either of the newer drugs. To act antipyretically it must be given in doses of from gr. x. to gr. xx. within a period of not more than two hours.1 The very large antipyretic doses of quinine which have been recommended seem to me to be attended with danger, for in such large doses it appears to act as a cardiac depressant, and I believe that with gr. x.-xv. given in one dose we obtain as certain an antipyretic result as with much larger doses. No one of the antipyretics should be long continued or given in large doses. If there is great restlessness or wakefulness during the third stage, hy- drate of chloral, or, better, small hypodermatics of morphia can be given. If there is even slight evidence of cyanosis, these remedies should be used with great care. When the pupils are small, belladonna or hyoscyamus may be given. For the relief of the distressing cough which is sometimes present, five grains of hydrate of chloral combined with one-twentieth of a grain of morphia, or twenty-five drops of chlorodyne every two hours, may be given. If expectoration is difficult from loss of muscular power, stimulating "expectorants," such as senega and turpentine, are useful. But if this difficulty arises from great viscidity of the sputum, alkalies will be found of service, and, as alkalies and neutral salines also have a diuretic and diaphoretic action, they are especially indicated just before the crisis. For the relief of the delirium of chronic alcoholism, tartar emetic and digitalis are highly recommended by English authorities. In the first stage of senile pneumonia an emetic, when not specially con- tra-indicated, is given in the " Salpetriere Hospital." Ipecacuanha is re- garded as especially indicated. The nitrate of potash and the hydro- chlorate of ammonia are also highly recommended in senile pneumonia. In children the chest should be thoroughly protected, the diet carefully regulated. Leeching and blistering are both harmful, and should never be employed. Stimulating expectorants are often indicated, and the mod- erate use of stimulants in feeble children is always required. During con- valescence, iron, quinine, mineral acids, cod-liver oil, and blood-making wines, should be given. Very recently there has been advocated an antiseptic treatment of pneu- monia, based upon the recognition of the specific character of the disease. Such treatment cannot be supposed to affect the local etiological element in the lung, but may have the effect of neutralizing poison elements in the blood and thus reducing the constitutional manifestations. It can- not be denied that a septic element exists in some if not in all cases; ' Liebermeister gives quinine until the temperature has been reduced by it to within i° of the normal Pew American practitioners carry the antipyretic effects of quinine so far. In Ringer and GUI's expert- meets upon " The Influence of Quinine on Temperature'1'' in health, it took at least gr. xx. to produce a fall of 1°. Prom fifty to eighty minutes elapsed before the fall occurred, and the effects lasted from forty-five minutes to three hours. Ringer states that in pneumonia (and some other diseases) quinine does not readUy pass out with the urine, but is delayed in the system for considerable time, and its antipyretic effects are continued longer than in other diseases. Prof. Flint states that he has seen pneumonia rendered abortive in a certain proportion of cases by xx. to xl. grains of quinine daily, and even when this result baa not followed, the disease has often been favorably modified in a greater degree than by smaller doses. 122 DISEASES OP THE RESPIRATORY ORGANS. hence the sulphites and hyposulphites (20 grain doses every three hours) are recommended. Carbolic acid, from 1 to 5 grains, sulpho-carbolate of soda (5 to 20 grains every two hours), have both been used quite extensively as antiseptics in the treatment of pneumonia. Thymol and salicylic acid have risen into favor because they are powerfully antiseptic and are almost physiologically inert. Quinine has also been advocated for its antiseptic power The antiseptic treatment of pneumonia has not yet assumed a definite aspect or been sufficiently tried for any definite statements to bo made concerning it. LOBULAR PNEUMONIA. Lobular, catarrhal, or broncho-pneumonia, is always secondary, oemg preceded by, or associated with, inflammation and obstruction of the smaller bronchi, which lead to the consolidated lobules. It may run an acute, sub- acute or chronic course, and differs very decidedly both in its clinical and pathological history from acute lobar pneumonia. Morbid Anatomy.—The anatomical changes in lobular pneumonia are confined to scattered groups of air-vesicles, hence the gross appearance of the portion of lung involved will vary with the duration and extent of the pneumonic process. In well-marked cases there will be found scattered throughout one or both lungs, small, circumscribed nodules of a light, deep-red, or bluish color, which do not inflate when the lung is inflated. If they are situated near the surface of the lung, they cause small, rounded elevations. When they are of considerable size, a reddish fluid oozes from their cut surfaces on section, and a small quantity of dark blood can be pressed from them. They are less tough than healthy lung substance, and break down easily on pressure. These nodules shade off into the surrounding zones of lung-tissue, which may be the seat of cedema, con- gestion, or emphysema. The nodules vary in size from that of a pea to that of a hazel nut, and are very rarely granular.1 When the lung is inflated these spots of consolidation are rendered more prominent, so that they stand out sharply defined from the adjacent lung-tissue. In some in- stances these isolated spots of consolidation become confluent and involve a large portion of lung—perhaps a whole lobe—and become pale, firm, and dry, resembling in color the gray hepatization of lobar pneumonia. The smaller bronchi are congested ; their walls are often thickened, and they may contain a thick, tenacious, puriform secretion which, later, may become dry and inspissated. When a section of the lung is made they often stand out prominently or even rise a little above the level of the cut surface. A peri-bronchitis is very often associated with these changes. Cylindrical and fusiform dilatations of the tubes are not infre- quent. Often, when a small patch of consolidation is cut across, there will be found at its centre a dilated bronchiole filled with pus. Discolora- tion begins at this point and extends toward the periphery. The con- nective-tissue of the portion of lung involved is increased, and this, in » Jiirgensen says: " Granulation is never observed." LOBULAR PNEUMONIA. 123 Fig long-standing cases, is often pigmented. Bronchiectasis may occur at various points. A microscopical examination of an affected lobule may distinguish three stages in the inflammatory process. First, the air vesicles maybe more or less completely filled with pus and serum, containing swollen and granular epithelium. The capillaries in the walls of the air vesicles are usually elongated, and red glob- ules may escape into the air-sacs. In the unaffected portions of lung- tissue the epithelial cells appear large and more distinct than in healthy lungs. In the second stage the affected lobules become solid and airless. Their color changes to a pinkish gray. The other changes are similar to those that take place in the stage of red hepatization in lobar pneumonia, except that less fibrillated fibrin is found in the exudation, the pus and epithelial cells are more Alveolus from a Lung in Lobular Pneumonia. r r The capillaries (a) are distended with blood, and ivithm abundant, and there are fewer red to alV^o are $een swoUen ep'lihelia (b) and pus cdls blood globules.l The anatomical differences between the second stages of acute lobar and acute lobular pneumonia are as follows : acute lobar pneumonia involves a whole lobe ; acute lobular only portions of a lobe. Lobar pneumonia advances steadily and uninterruptedly from one point, usually from the base upwards, until the whole lobe is involved; while lobular begins simultaneously in several lobules remote from one another. Moreover, these lobules are in different stages of the inflammatory process, e. g., one is dark, red and moist ; another is grayish and quite firm. In lob- ular pneumonia the small bronchi are more or less filled with catarrhal pro- ducts ; while in lobar pneumonia the exudation is fibrinous and does not extend beyond the infundibula and minute bronchioles. The third stage is the stage in which occurs either resolution, cheesy degeneration, or purulent infiltration. Abscess and gangrene may both occur, but they are very rare. When resolution occurs the contents of the alveoli become fatty and granular and are absorbed, and the pulmonary epithelium is restored. Large confluent spots of catarrhal pneumonia may undergo cheesy degeneration. And even solitary lobules may remain pale and yellow, looking like so-called cheesy tubercles; when cut into, a fluid escapes from their centres. Some lobules that look like cheesy • Many pathologists claim that the pulmonary alveolar epithelium takes no active part in the processes that result in the above-described consolidation. Rindfieisch asserts an active proliferation. 124 DISEASES OF THE RESPIRATORY ORGANS. masses are soft, never granular, and a purifo??n fluid flows from their cut surfaces. While the contents of the alveoli are undergoing cheesy changes, hyperplasia of the interstitial connective-tissue is taking place, which leads to more or less fibroid induration or " sclerosis" of the lung. On the pleura covering the superficial nodules an exudation of plastic lymph occurs; the bronchial glands are swollen and hyperaemic. Ca- tarrhal pneumonia in adults occurs independently of lobular collapse or atelectasis. Etiology.—Lobular pneumonia is always secondary to obstruction in the air passages, especially those of capillary size. It may be excited either by the gradual extension of inflammatory processes from the tubes to the air- cells, or by the entrance of inflammatory products from the tubes into the air-cells. It is most frequently met with between the ages of one and three. The senile period also seems to predispose to it. The more imperfectly nourished the child, the more anti-hygienic the air, surroundings and food, the more liable is it to develop lobular pneumonia. Debility and a long- continued recumbent posture predispose to it. Indirectly, any cause of bronchial irritation is a predisposing cause. The bronchitis of measles, whooping-cough, influenza, and that which accompanies the acute in- fectious diseases, often leads to lobular pneumonia. It occurs in lung- tissue adjacent to spots of hemorrhage, or pyaemic infarctions; trauma- tism may induce it. It is intimately associated with all varieties of acute and chronic phthisis. It is claimed by some authorities that caseous changes—whether primary, constituting caseous pneumonia, or secondary to a catarrhal process—are always dependent upon the presence of tuber- cle bacilli. Symptoms.—The phenomena which attend this form of pneumonia are always more or less obscured by those of the disease by which it has been preceded. It has no early distinctive symptoms. From an anatomical standpoint it is evident that its symptoms should resemble those of capillary bronchitis. It rarely runs a regular course,—terminating after a definite period in either death or resolution,—but may be protracted for weeks or months. A large number of cases occur in the course of whooping-cough and measles or other diseases complicated by bronchitis. The acute form is met with almost exclusively in children. In adults the disease usually runs a sub-acute or chronic course. After a diffuse capillary bronchitis has existed for a variable period, attended by its ordinary symptoms, such as a cough with muco-purulent expectoration, slight rise in temperature and labored breathing, if lobular pneumonia is developed the labored breathing becomes panting and ac- celerated ; the respiration may be 100 per minute. Dyspnoea is greatly increased. It is rarely ushered in by a rigor or a distinct chill. The tem- perature will gradually rise to 104°-105°, unlike the sudden rise of lobar pneumonia. It runs no typical course ; though exacerbations and remis- sions are marked, they have no regularity; sometimes the morning, some- times the evening temperature is the higher. It varies with the extent of lung involved, and also with the rapidity with which consolidation is LOBULAR TNEUMONIA. 125 developed. This steady rise in temperature, occurring in any disease in which lobular pneumonia is liable to be developed, is one of its most valuable diagnostic suggestive symptoms. When death occurs early the temperature may rise to* 108°. The pulse rate often reaches 140 to 150.l In twenty- four to forty-eight hours the pulse becomes small, compressible, and feeble, though at first it is full and hard. The cough, which during the bronchitis was loose, "bronchial," and paroxysmal, now becomes dry, hacking, and non-paroxysmal. It is usually very painful. The expectoration is seldom seen in children; but we may find in the matters vomited clumps of tena- cious, often blood-streaked muco-pus. V&v / A J 4 S * / t ----------«r = -- ---1 [—=H _ j 3 ~ f 4 ^ - [ 4 - 4 - - 3- I - 3 - 4- -. X I - 4\ — ■ 4- - H t I Z 4 - I- - 3r-t - it — - T— _tict i l t — _ - C- -tirtti- L-t - — - t- -X£a t- tct I _ :_st3 t: :tt- - t X- If -3 - . ^ Xi \/.r|. „■ , -U - ' Xi I zzt _ Xl J t :± : - X ■ -3 1 - -£-- 4 - _^ ±__ -t - - 4- ±-- _t . d" ± : j - 4 — 1 : ~ 4 B9-- C 3_ Z r 5-,- ------- Fig. 29. Temperature Record in a case of Acute Lobular Pneumonia in a child. (Recovery.) After a time the dyspnoea becomes constant. The breathing is shallow, inspiration is short, the chest expanding but very slightly. The auxiliary muscles are called into play, and there is marked expansion of the nares during inspiration. The pale and anxious face becomes cyanotic, and the restlessness and jactitation give place to a lethargic semi-comatose state, interrupted by occasional but ineffectual attempts to cough. Towards the end the cough almost entirely ceases. Diarrhoea frequently increases the exhaustion; and vomiting which may accompany or follow the cough, while rare at the onset of the disease, is frequent in its advanced stages. Anorexia is an early symptom, though young children will take the breast, while older children cannot be made to swallow even the blandest liquids. The tongue may become dry ; sordes collect on the lips and teeth ; aphthous stomatitis is common. Emaciation is rapid. The sub-acute form often occurs in the bronchitis of strumous children, and in that which accom- panies measles and whooping-cough. Its occurrence is marked by an elevation of temperature, but the rise is not so great nor so sudden as in acute cases; it rises gradually until it reaches 103° F. or 104° F. The cough becomes more severe and metallic in character, and the respira- 1 Jurgensen states that he has found the pulse often over 200 a minute. 126 DISEASES OF THE RESPIRATORY ORGANS. tion changes from the labored respiration of bronchitis, to the rapid pant- ing respiration of pneumonia. The patient begins to lose flesh, becomes pale, has profuse sweatings and fits of exhaustion; the appetite becomes capricious or is entirely lost; loss of strength and emaciation are progres- sive; the face appears bloated, small indolent abscesses appear on the nates and back, the patient assumes the appearance of extreme anaemia, and finally death slowly comes from wasting and exhaustion. Perhaps, when hope of recovery has been abandoned after a prolonged illness, resolution of the consolidated lung takes place, and a slow though complete recovery is reached. When the disease is to end fatally the tem- perature rises rapidly, cyanosis increases, the respiration becomes irregulai in rhythm, and the comatose state is interrupted by convulsions in which death occurs. Death may occur suddenly in the midst of a violent fit oi coughing. The disease may terminate with symptoms which resemble thosi of well-marked tubercular meningitis. When recovery occurs, it is very slow, pulse-rate, temperature,' cough, and dyspnoea all imperceptibly diminish- ing. There is no rapid fall in temperature, such as occurs in croupous pneumonia. In a few cases, especially in older children, slight delirium will occur at night. The urine contains chlorides and slight traces oi albumen. Chronic lobular pneumonia differs from acute in the severity rather than the character of its symptoms. When it supervenes upon some ca- tarrhal affection of the bronchi of moderate severity—a whooping-cough oi an attack of measles—the temperature gradually rises until it reaches 102° or 103° Fahr. Exacerbations and remissions then occur which are more irregular than in the acute or sub-acute variety. The respirations increase in frequency. The increase in the pulse-rate, the dyspnoea, the anorexia, the loss of flesh and strength—all are more marked than in the acute form and mucri more persistent. The interference with respiration is greater than in lobar pneumonia. As muscular weakness increases the auxiliarj and normal respiratory muscles become more and more enfeebled, and the supply of oxygen becomes, in some cases, so much diminished as to cause complete muscular paralysis. From all of these causes, and perhaps from the prolonged fever, the heart becomes feeble. Should recovery occur, the fall of temperature and the decline of the other symptoms are gradual, and there is great liability to a second attack during the protracted convalescence. A spot of consolidation often remains after recovery is apparently complete. Bronchiectasis, fibroid induration of the lung and emphysema are frequent sequelae ; and in children as well as in adults, phthisis is a not infrequent sequela. The pneumonic symptoms are much less pronounced in adults than in children, except when, in the latter, the disease supervenes upon diphtheria. In the old and feeeble, especially when they have lain in one position for a long time, lobular pneumonia occurs as the result of hypo- stasis, independent of bronchial catarrh. In senile bronchial catarrhs gravitation determines the lobular pneumonia, and it is not infrequentlj unilateral. If epidemic influenza is complicated by lobular pneumonia LOBULAR PNEUMONIA. 12? the sputa, in adults, may be quite free and blood-streaked, but never rusty. Physical Signs.—Inspection. In well-marked cases the expansive move- ment of the chest is diminished; the diaphragmatic depression is deepened and the lower ribs may appear retracted. Should there be extensive pulmo- nary collapse the chest walls will be retracted. Palpation.—Slight increase in vocal fremitus may exist over isolated spots, if the pneumonic nodules are large and near the surface. Percussion.—There is slight dulness over the consolidated spots. The diminished pulmonary resonance in lobular pneumonia is not easily distin- guished from lobular collapse, and since collapse is symmetrical, usually involving both posterior bases, the difficulty is increased. One should therefore percuss, in succession, over similar areas on either side of the chest, for if a spot of dulness on one side has no counterpart on the other, one may be sure that it corresponds to a spot of pneumonic consolidation, and not to collapse. The upper part of the chest may be extra resonant and even tympanitic if there is much emphysema. Auscultation.—On auscultation, small mucous rales resembling sub-crep- itant rales, having a fine, crackling and metallic character, are heard over the spots where there is dulness. These rales are audible both with inspi- ration and expiration. They are not as fine as, and are more superficial than ordinary pneumonic crepitation. In children, during and after a fit of crying, fine crepitating sounds may be heard which were not audible during quiet respiration. The breathing is less vesicular and may even be broncho-vesicular. There is increased vocal resonance and perhaps bron- chophony. The respiration in unaffected portions of the lung is more or less exaggerated. When there is an extensive bronchitis with the pneumo- nia, moist, dry and bubbling rales, varying from the finest to the coarsest, may be heard all over the chest. Differential Diagnosis.—Lobular pneumonia may be confounded with croupous pneumonia, acute tuberculosis and pulmonary collapse. The differentiation between lobar and lobular pneumonia has been given. '-'-'_ Acute tuberculosis is accompanied by a higher temperature than lob- ular pneumonia and the pyrexia precedes the physical signs of bronchitis; whereas in lobular pneumonia the signs of a bronchitis precede the physical evidences of consolidation. Lobular pneumonia occurs oftenest in the child (1 to 4 years); tuberculosis occurs in early adult life. Acute tuber- culosis is attended by more rapid exhaustion and emaciation, and haemop- tysis is not infrequent. The presence of brain symptoms is in favor of tuberculosis. The history of an inherited tendency to tubercular disease is rarely absent in tuberculosis. In collapse of the lung there is a tympanitic quality to the percussion note over the unaffected portions. The affected side is more retracted, Mid sinking of the ribs and elevation of the diaphragm arc more marked than in pneumonia. In collapse the respiratory murmur is feeble or absent 128 DISEASES OF THE RESPIRATORY ORGANS. and has no bronchial character. Eales are rare in a collapse, portion of lung. Vocal resonance and fremitus are diminished.1 Prognosis.—The prognosis in lobular pneumonia is determined almost entirely by the conditions which precede and attend its development. In children under five the average mortality is one in five. The younger and feebler the subject, the more unfavorable the prognosis. The prognosis is better when it follows measles than when it occurs after whooping- cough and scarlatina or when it complicates renal or heart disease. When the initial bronchitis is severe and extensive, when the temperature rises rapidly to 105° to 106° Fahr., when there is cyanosis, muscular paralysis, and the pulse is feeble and frequent, the prognosis is very unfavorable. Lobular pneumonia occurring in a rachitic subject is always grave. The greater the extent of lung involved the more unfavorable the prognosis. The more abrupt the onset the better the prognosis. The average duration of acute lobular pneumonia is from ten to fourteen days ; death may occur within the first week. Chronic lobular pneumonia may be complicated by capillary bronchitis, fibroid induration of the lung, tuberculosis, pleurisy, emphysema and pneumothorax. A very frequent complication is acute intestinal catarrh. It may be complicated by pyaemia and pulmonary infarcts non-pycemic in origin. Death may result from asthenia, asphyxia, or from complications. Treatment.—It must be borne in mind in the treatment of this affection, that it is a secondary disease and that its occurrence indicates that the pa- tient is in an enfeebled condition. All depressing remedies must be avoided; even when the disease assumes a very active form depletion is not allow- able. When the bronchitis is extensive, vapor inhalations and the internal use of muriate of ammonia are to be employed in accordance with the plan proposed in the treatment of capillary bronchitis in children. The patient should be kept in a warm room, the temperature of which should nevei fall below 60° F. The ventilation should be as thorough as possible, but all draughts and sudden changes of temperature should be avoided. The air should be kept moist and the body should be covered with flannel. Some recommend cold compresses to the chest; the cold pack is likewise advocated. Cold baths or baths from 77° to 86°, which are subsequently lowered to 60° Fahr., are also advocated even for young children. Jiirgensen recommends that a small stream of cold water be thrown just over the upper part of th" back of the neck, the irrigation of which produces the most violent respira- tory efforts. My experience has. been altogether against cold applications; and I regard the application of counter-irritants, blisters, etc., especially to young children, as productive of more harm than good. I prefer that the chest should be enveloped in linseed or mild mustard poultices. Or, in very young children, it may be rubbed two or three times a day with a stimulating liniment and wrapped in cotton-batting covered with oiled silk. 1 Jiirgensen states that the differential diagnosis between collapse and catarrhal pneumonia can be determined only in two ways : the diminution in volume of a certain portion of the lung, if distinctly demonstrated, is evidence of simple collapse, an increase in volume is evidence of infiltration. Ln pulmo nary collapse there is not the rise of temperature which always attends broncho-pneumonia. INTERSTITIAL PNEUMONIA. 129 During the whole course of the disease the food should be fluid, nutritious, and administered in small quantities and at short intervals. Brandy or gin in milk, ten to twenty drops every three or four hours, may be given to a very young infant, and the quantity may be increased until the pulse is increased in force, the respirations become less frequent, and the distress and cyanosis diminish. As a rule stimulants must be commenced at the very onset of the disease and continued throughout its entire course; the quantity to be administered is to be determined by the necessities of each case. The drug which has most power in reducing temperature and combating asthenia is the sulphate of qui- nine, which may be given in full doses during the period of fever; and as an aid to resolution it is most serviceable in small doses during the active period of the disease. If the attendant bronchitis is extensive, and the accumulation in the tubes obstructs the entrance of air into the lungs, emetic doses of ipecacuanha will often afford great relief. Apomorphia is advocated by some, but the danger of its producing collapse is very great in young children. Under no consideration is opium to be given. Oil of turpentine, five drops every four hours, is often beneficial in chronic cases. While a patient with acute lobular pneumonia should always be kept in bed, it cannot be too constantly borne in mind that he should not constantly lie upon his back, for collapse and hypostasis are apt to occur in a lung whose power of resistance is diminished. Convalescence should be managed with the greatest care, for fatigue and exposure may induce bronchitis, a second attack of lobular pneumonia, and quite probably the advent of phthisis will be hastened, if a tandency to that disease exists. If the disease is prolonged and emacia- tion is marked, cod-liver oil, iron by hydrogen, or the syrup of the iodide of iron should be given, with a change of air. ESTTEKSTITIAL PNEUMONIA. Interstitial pneumonia is a fibroid induration of the lung due to chronic inflammation involving its fibrous framework. Multiplication of the con- nective-tissue elements in the pulmonary septa takes place, which leads to progressive obliteration of the alveolar cavities and conversion of portions of the lung into callous fibrous masses. It has been called chronic fibroid, and chronic interstitial pneumonia ; also scirrhus and cirrhosis of the Morbid Anatomy.—The new tissue formation in this variety of pneumo- nia may involve the walls of the air-vesicles, the bronchi, the blood-vessels, and the pleura. It may be arranged in the form of nodules, bands, or ir- regular patches, and it may involve an entire lobe. The lung is sometimes shrunken from one-third to one-quarter its normal size. The first change is 1 Chomel and Grisolle state that it is very rare. Fox (Reynolds' Practice, p. 245) says it is rare excepl m connection with tubercles ; but Niemeyer (Practice Medicine, vol. i. p. 195) states that it is one of tha lost frequent pulmonary diseases. 130 DISEASES OF THE RESPIRATORY ORG.) hyperemia of the intercellular and interlobular tissue, followed by the de- velopment of fibro-nucleated tissue from the alveolar and bronchial walls, and from the interlobular connective tissue. At the same time the alveo- lar epithelium undergoes more or less pro- liferation. As the new tissue contracts, it slowly replaces and obliterates the alveolar structure. As a consequence, the calibre of the air-cells is diminished. The new tissue development may reach such an extent that all of the air-cells of that portion of the lung which is the seat of the process may be oblit- erated, and no trace of lung-tissue remain. This is not infrequently observed in the sub- pleural tissue, and at the apex of the lung in chronic pleuritis. The alveolar cavities, when not obliterated, are empty or contain ex- udation products. Frequently, dense fibrous bands pass in from a thickened pleura, and the changes are more localized. The nuclei of the capillaries participate in these fibroid changes.' In a few instances the proc- ess begins, and is chiefly located, in the tissue about the bronchi and the blood- vessels. On section of a lung or portion of a lung that is the seat of interstitial pneumonia, there is a creaking sound with the movement of the knife, ac- iompanied by a sense of resistance that normal lung never offers. The ,ung substance tears with difficulty. The cut portion is firm, dry, hard, solid and shining, its color varying: at times it is of a dull, glistening, slaty blue ; at others whitish, resembling an amyloid organ ; or it may be yellowish red.2 The bluish-colored lung is called by some "gray black- fibroid induration."3 Sometimes the cut surface presents a marbled appear- ance, due to the irregular pigmentation of the interstitial tissue. The bron- chi are usually dilated in those portions where the fibroid changes are well marked. The dilated tubes may form cavities of considerable size, and their mucous surfaces are often ulcerated, or the seat of intense passive hyperaemia. Bronchial dilatations rarely occur unless there has been a pre- ceding peri-bronchitis, which has diminished the elasticity of the bronchial tubes. As the new connective-tissue develops at different points, the weak- ened bronchi become constricted, and as a result of this constriction bron- chiectases form, the dilatation being increased by the violent inspiratory efforts that attend the fits of coughing which are so common in interstitial pneumonia. It has been maintained that with the diminution in size oi the lung, there is compensatory retraction of the chest-walls ; but that thii 1 Fox in "Reynolds' System." 8 " Red induration of chronic pneumonia."—Fox. 3 Reynolds' System. Art. Pneumonia. Interstitial Pneumonia. Section of Lung through one of the interlobular septa with the contiguous vesicular structure. A A. Band of new connective-tissue from an interlobular s Cornil and Ranvier thus explain the loss of substance in circumscribed gangrene: " putrefaction and molecular destruction commence at the point where the gangrened inflammation come* in contact with the external air." GANGRENE OF THE LTJNGS. 149 ocen, cough and pain. The two symptoms which most positively indicate the existence of pulmonary gangrene, are an extremely fetid breath, and the expectoration of gangrenous material; sometimes the fetid breath pre- cedes the characteristic expectoration. The expectoration has usually a dirty black or brown color, and contains small black masses, and in rare iustances wavy elastic fibres of lung-tissue are to be found in it; more or less blood is often present, and death may occur from hemorrhage. The sputa are yellow, or brown : i. e.y purulent or bloody ; alkaline at first, but acid on standing; and in a test tube they form three layers : an upper of gray froth ; a middle, clear and watery ; and a lower containing shreds of lung-tissue. In some cases there is but slight constitutional disturb- ance, and the gangrenous process goes on for weeks before there are any general symptoms to indicate its presence. In other cases the greatest prostration is experienced from the beginning, the pulse becomes small and frequent, and the vital powers rapidly give way before the septic fever. Dyspnoea is in proportion to the prostration. Occasionally, death takes place from the exhaustion resulting from slow hectic fever. When diffuse gangrene of the lung occurs in connection with pneumonia, its occurrence is marked by a sudden prostration, accompanied by a small irregular pulse, a disturbed, anxious countenance, a fetid breath, and a black liquid expec- toration having a gangrenous odor. If the gangrenous material is swal- lowed, as sometimes happens, severe diarrhoea and tympanitic distention of the abdomen occur. Gastritis sometimes results from swallowing putrid masses of sputa. In some cases of gangrene the temperature runs very high. Physical Signs.—The physical signs of pulmonary gangrene are often ob- scure, and never distinctive. They are those of local consolidation followed by the evidences of breaking down of lung-tissue, and the formation of cavi- ties in the lung substance. Percussion elicits a dull or tympanitic note; and after loose crepitation, gurgles and amphoric breathing are heard. There are no special signs indicating the nature of the disorganizing proc- ess ; sometimes it is preceded by the signs of pneumonia, generally it is accompanied by signs of bronchitis, and in the later stages of the disease there are physical evidences of the formation of cavities in the lung-sub- stance. Differential Diagnosis.—The diagnosis of gangrene of the lungs rests almost entirely on the characteristic odor and appearance of the expectora- tion ; prior to their occurrence the existence of gangrene cannot be deter- mined. Gangrenous expectoration, accompanied by the physical evidences of softening and excavation of pulmonary substance, is sufficient for its diagnosis. Certain conditions may arise in which it will be difficult to make a differential diagnosis; for example, in some cases of fetid bron- chitis there may be a profuse, greenish, sero-purulent expectoration, at- tended by an extremely fetid odor, not distinguishable from that of gan- grene, and yet no true gangrene of the lung exists. But as bronchiectasis is nearly always present with fetid bronchitis, the physical signs of the lat- ter would be very different from those of a gangrenous focus. (Vide p. 77.) 150 DISEASES OF THE RESPIRATORY ORGANS. Again, gangrene of the lung may exist without any perceptible fetor to the breath or expectoration, or any of the other attendant symptoms of gan- grene. Under such circumstances the gangrenous portion of the lung does not communicate with a patent bronchial tube. Again, local gangrene may occur in a phthisical cavity ; when it does it is very difficult to distin- guish it from true gangrene of the lung, especially if the patient is seen for the first time just as the gangrenous process is established. In this case' the previous history would alone enable one to make a diagnosis. A fetid abscess is generally distinguished from true pulmonary gangrene not by the character of the fetor, but by the fact that the signs of excavation precede the occurrence of the fetor, while in true gangrene of the lung the signs of excavation follow the gangrenous expectoration. The sputa in abscess are decidedly purulent, and fetor does not usually occur until some time after they are expectorated. In all cases, in order to make a correct diagnosis, it is necessary to have found, in addition to the fetid breath and expectora- tion, decomposed pulmonary tissue in the expectorated matter. Prognosis.—The prognosis is always unfavorable, although the circum- scribed form is not regarded as absolutely fatal. Eecovery can only take place in those cases where the gangrene is circumscribed and limited to a small portion of the lung-tissue. Under such circumstances it is possible for the slough to separate and be discharged, and induration and final cica- trization of lung-tissue to take place. Circumscribed gangrene may be latent, and it often progresses slowly, simulating anaemia. Diffuse pulmo- nary gangrene is always fatal. Sometimes death is the result of profuse hemorrhage; at other times it is due to perforation of the pleura ; but more frequently the patient dies from the exhaustion which attends the septic infection. Gangrene may terminate by an external opening. It may be complicated by emphysema of the cellular-tissue, hemorrhage, pneumothorax, or peritonitis. Death often occurs within three days after the first gangrenous expectoration. Treatment.—Under no circumstances are depressing remedies to be given. On the contrary, the vital powers of the patient must be sustained in every possible way by the administration of stimulants, tonics, and a most nutri- tious diet. Opium may be given in moderate doses to alleviate pain, allay the cough, and overcome constitutional irritation. Quinine is to be given for any fever that may exist. I have never found antiseptic inhalations to produce the beneficial effects claimed for them by some authorities, nor have I been able, by the internal administration of chloride of potash, to obtain satisfactory results. If antiseptic sprays are used, thymol and salicylic acid are the best. Traube gives acetate of lead and tannin preparations with opium. Charcoal, carbolic acid, creosote and chloride of sodium are recom- mended as deodorizers and internal disinfectants. Bromine, chlorine, oxy- gen, and permanganate of potash are similarly given. My own experience leads me to believe that all remedies of this class are powerless either to arrest the gangrenous processor even mitigate its unpleasant effects. It has been suggested that the lung-cavities should be tapped and washed out. Atelectasis. 151 PULMONARY ANAEMIA. Anaemia of the lungs may be due to local or general causes. In general anaemia from any cause, tne lungs are paler and lighter than normal. In- dependent of senile atrophy, it is never met with except in conditions of extreme general anaemia. Local pulmonary anaemia may be caused by the compression of local emphysema ; and by obstruction of the pulmonary artery or its branches. Symptoms.—Dyspnoea and palpitation are its only signs. atelectasis. (Pulmonary Collapse.) Pulmonary atelectasis is a condition of the lungs where there is partial or total absence of air in the alveoli. When acquired, it is denominated pulmonary collapse or compression of the lung. Atelectasis is physiolog- ical in foetal life, and may be described as absolute absence of air from the alveoli. Morbid Anatomy.—In the new-born, atelectasis is usually lobular; rarely is more than one-half of a lobe involved. The lower lobes are oftenest the seat of atelectasis, then the tongue-like prolongations of the upper left lobe and the middle lobe of the right lung. The affected portions appear as sunken masses of violet or blue-red color; they do not crepitate, have a soft feel, but are tough, and resistant, and sink in water. In the atelectatic spots little yellow tubercle-like masses are found,—so-called " bronchial abscesses," vesicular bronchitis, and granulations purulentes. On section, the atelectatic part is brownish-red, smooth (not granular), airless, and in the earlier stages dilatable ; later on, not. The walls of the alveoli are approximated, touch, and, according to some, grow together. Fatty degeneration and cell proliferation occur in the collapsed spots. A whole lung may be involved, but usually only a lobe or a portion of a lobe. The collapsed portions contrast strongly with the surrounding parts. Its seat is most often in the periphery and the lower lobes of the lung. The affected portion has the same tough, "liver-like" characteristics as in congenital atelectasis, the difference being that in acquired collapse the lobular points are disseminated. The collapsed portion maybe engorged and oedematous, a condition sometimes called "splenization." The bronchi leading to the collapsed lobules are usually congested and plugged. When collapse occurs from pressure—compression of the lung—the part involved and its extent depend on the site and extent of the pressure. The air cells in the collapsed portion may or may not be wholly void of air. It is flesh- like ; and for a time can be inflated and caused to return to its normal size and condition. If the inspiration is insufficient and the expiratory efforts normal in force, after a time all air will be expelled, and the dry, tough 152 DISEASES OF THE RESPIRATORY ORGANS. gray-red mass assumes a condition known as " carnification " ; and in time only a fibrous or connective-tissue cicatrix remains. Small blood-clots may be found in the affected lobes, that are frequently decolorized and perhaps adherent to the walls of the vessels, whose calibres are impervious or oblit- erated. ' Etiology.—Co7igenital atelectasis occurs in feeble infants, in those born prematurely, and in those whose bronchi, nares or other parts accessory to respiration are plugged with mucus. Pulmonary collapse is rarer in adults than in young children. Any disease or condition that weakens or ob- structs the power of inspiration may induce it. Brain diseases are some- times accompanied by it. Too tight clothing about the chest of feeble children may lead to it. Paralysis of the vagus is said to cause it, and muscular paralysis from disease of the cord may lead to it. The most frequent cause is some catarrhal condition of the respiratory tract that induces the formation of a plug in a small bronchus; e. g., capil- lary bronchitis, catarrhal pneumonia and bronchitis with tenacious secre- tion. Twenty-five per cent, of the total mortality of very young in- fants may be safely set down to pulmonary collapse, following bronchitis. Collapse from compression of the lung results from fluid, pus, air or blood in the pleural cavity ; from mediastinal tumors, from rachitic and spinal deformities, and, rarely, from abdominal tumors. Symptoms.—In the new-born, atelectasis is shown by feeble breathing, slight motion of the chest, a low, almost inaudible, "whining" cry, lividity and coldness of extremities, constant sleepiness, and often muscular twitch- ings and convulsions. The child cannot nurse. Since the foramen ovale and ductus arteriosus so often remain open in congenital atelectasis, anomalies of the circulation may cause asphyxia, convulsions, suffoca- tion and death. Blood clots may form in the cerebral sinuses.2 In collapse there is labored breathing, dyspnoea, frequent respirations (70 to 100 per minute), and a cough with muco-purulent expectoration. Chil- dren utter the low, whining cry. Passive hyperaemia and oedema of the ex- tremities and central organs are common results of pulmonary collapse. The pulse is small and feeble, the skin cool, the urine scanty. There is an interval between inspiration and expiration, instead of after expiration. The whole act is "shallow." Physical Signs.—Inspection shows compensatory retraction of the most yielding portions of the thorax during the act of inspiration, and the inter- costal spaces retract. On percussion precordial dulness is increased ; there may be dulness when there is much condensation, but if emphysematous patches develop about the collapsed lobules the dulness may have a tym- panitic quality. On auscultation respiratory sounds may be feeble or ab- sent. Later there may be bronchial breathing and bronchophony. Kales may be due to associated bronchitis ; they are coarse and sonorous. The » Lichtheim's recent experiments go to prove Virchow's assertion that air, shut in by closure of a bron- chus, is absorbed by the blood-vessels, and also that elasticity of the lung acts untU the air is completely absorbed.—Arch. f. exnev. T>nihrJnnin ■>, T>h„„~» ™i _ _ ** ° absorbed.—Arch.f. exper. Palhologie u. Pharm., vol. x., p. 54. » Virchow's Archiv., Bd. xi„ p. 840. PULMONARY EMPHYSEMA. 153 physical signs of compression are merely those of the causative condition, e. g., hydrothorax, pleurisy with effusion, etc., etc. Differential Diagnosis.—Pneumonia is distinguished by the fever, flushed face, fine rales, lobar instead of lobular outline of dulness, pain, and ab- sence of "inspiratory retraction." Miliary tuberculosis is distinguished by the fever, cough, and wasting, all of which will precede the physical signs. The history of the parents will here aid us. In pleurisy with effusion the flatness and change in line of flatness with a change in the patient's position will establish the diagnosis. Prognosis—Extreme atelectasis is rarely recovered from. Occurring with whooping-cough it is especially fatal. Emphysema, bronchitis, lobu- lar pneumonia, tuberculosis and pleurisy may complicate it. Asphyxia or complications cause death. When compression occurs from tumors, hydro- or pneumo-thorax the prognosis is more unfavorable than with other causes. Cheesy pneumonia or phthisis may follow atelectasis or collapse. Treatment.—In the new-born the treatment should be that described in works on diseases of children and obstetrics. Efforts at full inspira- tion should be encouraged. Cold water may be poured over the neck and chest. A stream of water thrown on the nuchal region is said to excite violent and strong inspiratory impulses. Counter-irritation and stimulating embrocations are recommended. The catarrh that induces collapse must be treated with stimulating expectorants, or, in children, with emetics. Arsenic, belladonna, and salts of potash and ammonia are recommended. In compression remove the cause when possible, e.g., the emphysema and hydrothorax. In all cases tonics and stimulants with good nourishment are demanded ; the " depletory " plan is never indicated. Inhalation of compressed air may do good. Never let the diaphragm's action be im- peded by clothing or a distended abdomen. PULMONARY EMPHYSEMA. Pulmonary emphysema is seldom met with unless associated with more or less bronchitis ; and emphysematous persons are especially liable to at- tacks of spasmodic asthma. Emphysema is essentially a chronic affection ; it comes on slowly, and when once developed is permanent. By the term is understood either an abnormal accumulation of air within the air-cells or an infiltration of air into the sub-pleural and inter- stitial connective-tissue. There are two recognized varieties, termed, first, vesicular emphysema ; second, interlobular emphysema. The first is by far the more frequent and more important affection. There are no definite rules for the diagnosis of interlobular emphysema, and it rarely occurs except in connection with advanced vesicular emphysema. When the unqualified term emphysema is used, reference is always had to the vesicular variety. Morbid Anatomy.—In emphysema, there may be simple dilatation of the 154 DISEASES OF THE RESPIRATORY ORGANS. air-cells without rupture of their walls; or there may be dilatation of the air-cells with rupture of their walls. The rupture of the air-cells leads to the formation of what may be called air-sacs, which vary in sire from that of a pin's head to that of a pigeon's egg, and even larger. Both forms of the affection, the vesicular and the interlobular, are generally present in cases in which these larger air-sacs have formed. The changes which take place in the anatomical structure of the lung in this affection are as fol- lows • in slight cases there is dilatation of the infundibula, and a dimin- ished prominence of the alveolar walls, followed, later by their rupture and partial disappearance ; as a result, a small air-sac is formed, in which lit- tie ledges and filaments of tissue alone mark the site of the alveolar septa. At this time there is no well-marked line of demarcation between he infundibulum and the alveoli. As the disease advances rupture of the walls of these little air-sacs occurs and establishes a communication between their cavities. The openings thus made between the air-sacs are at the very central portion of the sac, where the wall is thinnest. By this grad- ual enlargement and the union of many small sacs, a large air cavity is formed, across and along the walls of which exist remains of the original tissue These larger air-sacs communicate with the bronchi, which are sometimes enlarged. The result of this destruction of the alveolar septa is the abolition of the capillary plexus which is normally spread over the walls of the air-cells. At times ovoid collections of fat granules are seen in the thinned septa. Whether these fat cells are in the nuclei of the capillaries, or in the inter-capil- lary cells is undetermined ;—prob- ably they are in both. This fatty metamorphosis as a rule precedes the dilatation, and is not constant. Fatty granules are found in the protoplasm about the nuclei of the epithelial Ei?!^%!rR^S^^min^^ibu'a,a,a,m' cells taken from an emphysematous vesicle. The small branches of the pulmonary artery are the longest retained ; they become dilated and looped, and communicate by anastomosis with the pulmonary vein, and thus the circuit of the pulmonary circulation is kept up, but it is not nearly so free or abundant as that which exists normally. The pulmonary circulation is therefore materially interfered with by this structural change. Well-marked emphysema generally affects both lungs; it is most marked in the upper lobes, especially along their anterior borders. Emphysematous degeneration throughout both lungs is rare. If the emphysema is compensatory its site will vary with that of the produc- ing cause. When it is the result of strong pleuritic adhesions, it most fre- quently affects the anterior border of the lung. In partial collapse of the Pig. 83. Pulmonary Emphysema, first stage. PULMONARY EMPHYSEMA. 155 lung following obstruction of the bronchi, or in inexpansibility from disease of its structure, emphysema will usually be limited to the vicinity of the bronchial obstructions or the structural disease. When emphysema is the result of forced inspiration with closure of the glottis, as occurs in vio- lent spasmodic croup, etc., the apex and anterior borders of the lungs are mainly involved. Emphysematous lungs do not collapse when the thoracic cavity U opened. In well-marked cases, the lungs meet and overlap each other in the median line. The left overlaps the superficial cardiac region, both extend lower than normal, and the heart is pushed downwards and nearer to the median line than normal. The diaphragm may also be pushed below its normal position, and all of the abdominal viscera crowded out of their normal situations in consequence. In some cases the liver has been so displaced as to lie entirely below the free border of the ribs. The lungs removed from the thoracic cavity bear the imp'ress of the ribs as furrows on their surface. Indentations made by pressure of the fingers on the surface of the lung are permanent, showing a loss of elasticity. The dilated alveoli may at times be seen on the surface of the lung through the pleura, or on section maybe found distributed through its substance ; they are, however, much more apparent after the lung has been blown up and dried. They appear as whitish or gray prominences, or as spherical vesic- ular appendages filled with air. When the air-sacs are large they protrude beyond the surface of the lung, and generally have a globular form ; in some cases they seem to be separated by a neck from the rest of the lung, looking like appendages to it. In well-marked examples of emphysema, the whole anterior surface of the lungs may be covered over with air-sacs, sometimes resembling the lungs of reptiles. The color of an emphy- sematous lung is usually abnormally pale ; it is soft and cushion-like to the touch; it crepitates but little when pressed between the thumb and finger ; it sinks in water less readily than healthy lung-tissue, for though its volume is increased, its weight is diminished. By pressure the air can be forced out of the larger and smaller sacs into the bronchi. The evi- dences of bronchitis are usually present in the bronchial tubes. The pa- renchyma of the lung may present lesions which may be either a cause or a complication of emphysema. Phthisis and pneumonia, although of rare occurrence, are not as infrequent as many writers would have us suppose. As a rule in advanced cases of emphysema, the right heart will be found hypertrophied and dilated ; as soon as the systemic circulation is inter- fered with, the left ventricle becomes hypertrophied, and this hypertrophy will for a time compensate for the obstruction to the return circulation, hut as a result of this interference when it is long-continued, anatomical changes take place in the liver, kidneys and spleen, which are similar in character to those which occur in connection with valvular heart lesions, and give rise to general dropsy ; changes of this class, however, belong to the remoter lesions of emphysema. Senile emphysema differs from the variety which has just been described in the following respects : the lungs are not only diminished in weight but 156 DISEASES OF THE RESPIRATORY ORGANS. very markedly m size ; the lobes are usually united, and their fissures di- rected vertically instead of horizontally; the lower lobes having lost the most in bulk, their surface is irregular, and their structure is composed of enlarged air vesicles and sacs which are the result of the natural atrophy of the lung-tissue which takes place in old age. In the aged the walls of the emphysematous cavities are usually deeply pigmented. The lung often consists merely of a number of large cavities. In interlobubar emphysema an air-vesicle or sac ruptures, so that the air escapes into the interlobular cellular-tissue, forming sacs of large or small size. These sacs, or rather these collections of air, may form be- neath the pleura, or, extending between the lobules of the lung and along its vessels, reach its root, spread into the mediastinal cellular-tissue, and be distributed over the neck and subcutaneous cellular-tissue of the body. The size of the air-sacs beneath the pleura may be only that of small vesicles, and these limited to the circumference of a lobule, or they may reach the size of the stomach. " They look like a membrane uplifted by foam." They may be distinguished from the vesicular dilatations by being freely movable beneath the pleura. Perforation of the pleura, produc- ing pneumothorax, is a rare result of interlobular emphysema. More or less interlobular emphysema is always present in advanced vesicular emphysema. Etiology.—The causes of emphysema may be divided into primary and secondary, or compensatory. Primary emphysema may exist independently of, or be associated with bronchitis. Among its causes are forced expiratory efforts, the glottis being closed or narrowed as in violent coughing, strain- ing at stool, etc. In a few rare instances the emphysematous distention is produced during strong inspiratory efforts. In both instances the disease is developed in the upper lobes of the lung. Another cause of this variety of emphysema is, that there exists in many persons either an hereditary or an acquired impairment of the elasticity of the lungs which renders them more readily dilatable and more easily torn. There are three prominent theories which have been advanced to account for this : first, that it is due to fatty degeneration of the alveolar walls. The constancy of this change has not as yet been demonstrated. It is true that molecules of fat are sometimes seen in the alveolar septa, but they may be the result rather than the cause of the emphysema. Secondly, there is a theory that the weakness of the alveolar walls is due to the growth of the inter-capillary nuclei. Thirdly, that it is due to the fibroid degeneration of the alveolar septa. No one of these theories has as yet received full confirmation; a co-operation of all of them, more particularly of the last two, is necessary in many cases to satis- factorily explain the production of the disease. Kecently another cause for the development of this form of emphysema has been advanced, viz.: an abnormal increase in the capacity of the chest, due to excessive growth of its walls. This theory as yet lacks proof. The causes of secondary emphysema are conveniently considered under three subdivisions, in all of which the emphysema is best denominated com- pensatory. The first of these subdivisions comprises all cases in which the PULMONARY EMPHYSEMA. 157 emphysema is developed around small portions of lung rendered inexpansible by disease of its tissue, as, for example, lobular collapse from obstruction of a small bronchus, a lobular pneumonia, a pulmonary infarction, etc.; the lob- ules adjacent to those that are thus rendered inexpansible become over-dis- tended by a forced inspiration or a forced expiration during a violent fit of coughing. Some would make these obstructions, operating in different parts of the lung, a primary cause. A second subdivision comprises those cases where a large portion of lung, either from some internal cause, as pneumo- nia, hypostasis, atelectasis, etc., or, from some external cause, as pleurisy, etc., is rendered inexpansible, and emphysema is developed in healthy por- tions. In both of these subdivisions the capacity and mobility of the chest remaining normal, the usual, and especially forced, inspiratory efforts require extra distention of the alveoli to compensate for those rendered more or less useless. A third subdivision includes those cases secondary to croup, lobular pneumonia, whooping-cough, pressure on the trachea or main bronchi. The emphysematous distention in this class of patients is pro- duced during inspiration. It is questionable, however, whether compensatory emphysema is ever developed when the walls of the air-cells have not been enfeebled. Interlobular emphysema is produced by forced expiration with narrowed glottis, as during severe cough, parturition, straining at stool, etc. It is usually preceded by vesicular emphysema. It may also occur from perforation of the lung from without, as in fracture of the ribs. Senile emphysema is mainly an atrophy of the alveolar septa, which become obliterated, so that vesicles coalesce. It is due to impaired nutrition, which affects the lungs as well as other organs in old age. Symptoms.—The prominent and most constant subjective symptom of emphysema is dyspnoea. It is a dyspnoea which is increased by physical exercise, by the occurrence of fresh attacks of bronchitis, and by spasm of the bronchi, such as occurs in spasmodic asthma. When the emphysema is well marked, very slight exertion will give rise to dyspnoea; when the emphysema is slight, only violent exertion will be followed by it. It is mitigated by a warm atmosphere, and returns with increased severity during the cold of winter. There is often a "smothering" sensation in the chest, and when present it is constant. In congenital cases the only symptom during childhood and early adult life is a moderate degree of dyspnoea. In advanced cases of the disease the dyspnoea is liable to be paroxysmal, the paroxysms depending upon a tendency to spasm which emphysema in its development seems to impart to the bronchi. A cough is usually present, but it is due to bronchial irritation, and unless bronchitis exists the cough may be wanting. The expectoration varies with the extent and character of the,accompanying bronchitis, and it is not uncommonly a part of the his- tory of the emphysema; if it occurs independently of bronchitis it will have nothing characteristic about it. Usually there is no pain in the chest dependent upon the emphysema. In advanced cases the countenance is peculiar and somewhat characteristic ; it is of a dusky hue and has a puffy appearance which contrasts remarkably with the wasted appearance of the rest of the body. The nostrils are distended, thickened, and vascular, and 158 DISEASES OF THE RESPIRATORY ORGANS. expand with each inspiration; the angles of the mouth are drawn down- ward, the voice is feeble, the patient stoops in the act of walking, and his whole body has a cachectic appearance ; the capillary circulation of the extremities is markedly imperfect, as shown upon the slightest exertion. There is a gradual, though steady loss of flesh and strength. Usually, the disease is not attended by febrile excitement; the pulse is not accelerated, but is markedly feeble, and the temperature of the body sub-normal. The other symptoms observed in connection with emphysema are indirect, and due to interference with the circulation. Not only is there always dis- turbance of the capillary circulation in the extremities, but the face and neck present a fulness or even a turgidity of the blood-vessels altogether ab- normal. The distention of the jugular veins, and the lividity of the face and hands, are unquestionably due to the interference with the circulation through the right heart, but do not occur until that stage is reached in which there is more or less hypertrophy and dilatation of the right ven- tricle. Patients who have reached this stage become very purple iu the face after and during fits of coughing, often presenting the appearance of impending suffocation. The paroxysms are perfectly characteristic; an attack of coughing comes on, grows more and more severe, gathers more or less of the spasmodic element, and when it has reached its climax the face and hands become livid, and the patient is completely exhausted. Vertigo is a common symptom in advanced emphysema ; it is most apt to be developed during a fit of coughing, and depends upon the interference with the return circulation from the head. Slight haemoptysis may occur. Emphysema of itself does not give rise to dropsy, although in advanced cases the feet and ankles are almost always oedematous. The oedema is the result of cardiac or renal complications. Ordinarily, there is more or less disturbance of the digestive organs in these advanced cases ; the disturbance is due to catarrh of the stomach, the result of passive hyperaemia of the mu- cous membrane of the stomach from failure of the right heart. For a like reason other functions are more or less disturbed. Emphysematous patients are especially liable to hemorrhoids, and very often have profuse bleeding from the rectum. As has been already stated, the development of emphy- sema is almost always slow; in rare instances it advances rapidly, and it is then called acute. If, from the rational symptoms, there is any doubt as to the diagnosis of emphysema, the doubt will disappear after a physical exploration of the chest, for the physical signs in a well-marked case are characteristic. Physical Signs.—On inspection, it will be noticed that there are alterations in the shape and movements of the chest. There is an unnatural elevation and arching of the sternum (as if from congenital deformity), and an un- natural bulging of the infra-clavicular and mammary region, which gives to the chest a more rounded appearance than in health : this has been termed "barrel-shaped." The scapulae are brought forward, and there may be antero-posterior curvature of the spine, which gives to this class of pa- tients a stooping posture which is habitual. The muscles of the neck are unnaturally prominent. The lower portion of the chest seems contracted, PULMONARY EMPHYSEMA. 159 and the intercostal spaces are depressed and wider than above. If the em- physema is extensive, the apex of the heart will be found beating lower down than normal and more toward the median line ; if the right side of the heart is extensively dilated there will be an epigastric impulse__this impulse is due to an increase in the size of the heart, and to its being crowded to the right, and lower down in the thoracic cavity. In some in- stances, when the general symptoms of emphysema are well marked, the lungs are atrophied instead of abnormally dilated, and no bulging of the chest (either general or local) occurs. The movements of the chest walls are also altered and peculiar. At the upper portion expansion on inspira- tion is diminished or entirely wanting ; the whole chest moves vertically up and down with inspiration and expiration, as if it were passively lifted from the shoulders, and composed of one solid piece; while below, the chest, instead of being dilated with inspiration, is contracted. The respiratory efforts are labored, and the breathing is chiefly abdominal. The diaphragm seems to be more actively engaged than the chest walls in the process of respiration. In cases far advanced, the existence of emphysema can be made out by inspection alone. On palpation the vocal fremitus varies : it may fall below, or equal, or it may exceed that in health. In senile emphysema, the vocal fremitus is usually increased. The intensity of the percussion sound is increased, the pitch is lowered, the pulmonary quality of the sound is greatly diminished, and it becomes vesiculo-tympanitic—that is, there is added to the vesicular element a tym- panitic quality which is the characteristic percussion sound of emphysema, and is not met in connection with any other pulmonary disease. The per- cussion note is not materially affected, either by forced inspiration or by forced expiration. The precordial region is usually resonant, owing to the distended lungs coming between the heart and the wall of the chest. On auscultation, the inspiratory sound is either short or feeble, or act- ually suppressed, while the expiratory is greatly prolonged, the ratio of the two being as one to four instead of four to one. As a rule, the pitch of both the inspiratory and expiratory sound is lower than in health. In some extreme cases of emphysema, the respiratory sounds are of equal length, greatly exaggerated in intensity, and of a harsh, sibilant or sonorous quality, the harsh quality undoubtedly being due to diminution in the calibre of ths minute bronchial tubes. In some cases, when interlobular and vesicular emphysema are combined, a crumpling sound is heard, which has been des- ignated as the "crumpling sound of emphysema." This sound has been said to resemble the crepitant rale, but it more nearly resembles the sound of crumpling parchment, than the crackling sound of the crepitant rale; but " Laennec's rale "—a modification of the sub-crepitant rale—is very often heard. The vocal sounds vary greatly ; they may be diminished, or altogether absent, or their intensity may be greatly increased. The heart sounds are feeble. The sphygmograph may afford valuable information. Differential Diagnosis.—Slight emphysema cannot be diagnosticated with certainty; but those advanced emphysematous cases which give rise to se- 160 DISEASES OF THE RESPIRATORY ORGANS. vere dyspnoea and cyanosis are readily distinguished, by a physical exami- nation of the thorax, from other diseases which manifest similar symptoms. The disease with which emphysema is especially liable to be confounded is pneumothorax. If the physical signs of the two diseases are properly ap- preciated, it is not difficult to distinguish between them. In emphysema the percussion sound, although somewhat tympanitic in character, still re- tains a pulmonary quality, and there is a vesicular element to the respira- tory sound, while in pneumothorax the percussion sound has a well-marked purely tympanitic character, and the respiratory sound, if audible, is am- phoric in character with no vesicular element. Emphysema affects both sides, pneumothorax only one side. The symptoms of pneumothorax come on suddenly, while those of emphysema are slowly developed, and are never so urgent as those of pneumothorax. A diagnosis of compensatory em- physema may not be made out during life, but the fact being well estab- lished that it does almost invariably exist in certain conditions, the proba- bility of its existence should always be borne in mind in the study, exam- ination, and treatment of those pulmonary diseases in which it is liable to occur. Prognosis.—Emphysema rarely if ever destroys life ; but, when once de- veloped, is never recovered from, and incapacitates the person to a greater or less degree for active exercise, rendering life at least uncomfortable. It strongly predisposes to bronchitis and renders existing bronchitis severe. Acute bronchitis of the smaller tubes is an extremely grave affection when it occurs in an emphysematous person. Again, emphysema develops heart disease. The impediment to the pulmonary circulation, which exists as the result of emphysematous changes in the lung substance, gives rise to an overloaded state of the right cardiac cavities, which in time leads to their permanent dilatation and to hypertrophy of their walls ; insufficiency of the tricuspid valves follows, and the resulting regurgitation through the tricuspid orifice into the right ventricle causes obstruction to the systemic venous circulation, and as a result there is congestion and a permanent dis- turbance of the function of the kidneys, liver, etc. In giving a prognosis in any case of emphysema, the liability to this complication should be con- sidered. Emphysema also predisposes to fatty degeneration of the different organs and tissues of the body, the result of an impoverished state of the blood. The occurrence of these secondary affections renders emphysema a serious disease. It is undoubtedly a more serious affection when it occurs in childhood or adult life, than in old age. Pleurisy, asthma, bronchitis and anaemia are the most frequent complications. Treatment.—The treatment of this affection will be briefly considered un- der two heads : first, the treatment of the disease itself; secondly, the treatment of secondary changes in other organs, which changes are more or less directly induced by the emphysema. Accepting the view that the lesions in this disease in the lung-tissue are the result of imperfect or dis- ordered nutrition, we may reasonably expect that, by improving the nutri- tion, the progress of the degeneration may be checked or arrested, and per- haps even the elasticity of the unaffected portion of the lung may be re- PULMONARY EMPHYSEMA. 161 stored. The most rational method of treatment is that by which we aim to remedy faulty nutrition in other organs and tissues. With this object in view, the drug which is of the greatest service is iron. This remedy should be taken daily with meals, for a long period, by persons who have emphysema or in whom it is developing. In this class of cases, the prepa- ration which I prefer is the ethereal tincture of the acetate of iron; sul- phate of quinine in small doses may be given with the iron in most cases with benefit. Strychnia, which has some reputation in the treatment of this disease, I am confident has no power in arresting its development, and it has seemed to me to increase the frequency and violence of the parox- ysms of dyspnoea, and thus hasten rather than retard the emphysematous development. If an emphysematous patient has dyspeptic symptoms the mineral acids in combination with bitter vegetable infusions will be found of service. When there is a tendency to great emaciation, I have found cod-liver oil of service. Stimulants, vinous and spirituous, when taken in small quantities after or during meals, often give beneficial results, and when their use is followed by marked improvement in the general condition of the patient, they should be used in the treatment of the disease. The regulation of the diet, and the general management of the emphy- sematous patient is, however, of much greater importance than the medical treatment. The diet should be of the most nutritious character, and com- posed largely of animal food ; overloading the stomach should be especially avoided, as well as everything which has a tendency to produce flatulence. The food should not be bulky or watery in character, and should be as di- gestible as possible ; the quantity of liquids taken into the stomach should always be small. Exercise in the open air should be taken systematically, but fatigue should be avoided. All sudden, violent exercise, or great physi- cal exertion must be strictly prohibited. The condition of the skin should be carefully considered. Emphysematous patients should not expose them- selves to cold. All localities where attacks of spasmodic asthma are liable to be developed should be carefully avoided, as also everything which may develop dyspnoea or predispose the patient to asthmatic attacks. The rule for all emphysematous persons is to change their residence to that locality where they suffer the least and are not troubled with dyspnoea. The treat- ment of those complications which accompany, or are induced by, the em- physema is also of importance in arresting the progress of the disease. Of these accompaniments, bronchitis (generally chronic) stands first. There is one drug which I have found especially serviceable, viz., iodide of potassium. It should be given in doses varying from five to twenty grains, three times during the day, and its administration should be continued at intervals over a long period. The treatment of diseases of the heart, liver and kid- neys, which occur as complications or accompaniments of emphysema, will be considered in connection with the history of cardiac, renal and hepatic diseases. PULMONARY TUMORS. Carcinoma, sarcoma, endothelioma, and enchondroma are the tumors most frequently met with in the lungs. They may be primary or second- 11 162 DISEASES OF THE RESPIRATORY ORGANS. ary. Of these carcinoma is the most frequent. Endothelioma usually arises in the pleura or lymphatic vessels of the lungs. Morbid Anatomy.—Primary carcinoma appears at first as a single growth in one lung, though later it may extend by metastasis to the other. Secondary carcinoma occurs as disseminated nodules of varying size, which are scattered usually throughout both lungs. Small multiple growths may be found in the pleura, and the lung be unaffected. They are often accompanied by an abundant hemorrhagic effusion. Structurally, the secondary deposits resemble the original tumor from which they were derived. The same degenerative changes take place in cancers of the lungs as in other situations. The bronchial glands are often extensively involved. Further consideration of pulmonary neoplasms will be left to the special works on pathological anatomy. Etiology.—A few cases of primary carcinoma of the lungs have been re- ported. Its most frequent seat is in the lower lobe of the right lung. Pulmonary carcinoma, however, is usually secondary to a tumor elsewhere in the body, e.g., the mammary gland, genito-urinary tract, oesophagus, stomach, liver, etc. It occurs most frequently during and after middle life, and affects females more often than males. Symptoms.—Cancer of the lung usually comes on very insidiously, with few subjective symptoms. There is usually pain in the chest and a cough accompanied by a muco-hemorrhagic expectoration resembling currant-jelly, which occasionally contains cancerous elements. More or less dyspnoea is present, especially if mediastinal tumors co-exist. The cancerous cachexia may or may not be present. As the disease advances, emaciation, fever, night-sweats, with failure of strength, become more and more marked, and this steadily increasing weakness and emaciation is one of the most constant rational symptoms. The " pressure effects " producing lividity, oedema, dys- phagia, and laryngeal symptoms, are like those of a thoracic aneurism. The glands in the axilla and above the clavicle are nearly always enlarged. If dyspnoea, cough, haemoptysis, pain in the chest, rapid emaciation, and cachexia should come on in one from whom a carcinomatous breast had been extirpated, there would be reason to suspect the development of cancer of the lung. Signs of pleurisy, bronchitis, emphysema, or catarrhal pneu- monia, may mask the signs of pulmonary cancer. Physical Signs.—These will vary according to the seat and extent of the cancerous development. If the lung is extensively involved with nodular cancer, inspection will show enlargement of the affected side with widening of the intercostal spaces and deficiency or entire absence of respiratory motion. Vocal fremitus may be diminished or absent. On percussion there will be complete dulness attended by friction over the space corre- sponding to the cancer. The signs of a cavity are sometimes present. On auscultation the respiratory sounds may be feeble or absent, or, if a large open bronchus is intimately connected with the cancerous mas?, bronchial respiration may be heard. Disseminated cancer of the lungs cannot be distinguished, by physical examination, from general bronchitis. In the infiltrated form the lung is often contracted, and, as a consequence, there is retraction of the chest-walls on the affected side. SYPHILITIC DISEASE OF THE LUNG. 163 Differential Diagnosis.—Pulmonary cancer is liable to be confounded with pleurisy with effusion. In cancer, the percussion dulness usually begins at the upper portion of the chest, while in pleurisy it begins at the lower portion. In cancer the dulness is most marked in front, in pleurisy it is most marked behind. In cancer there are isolated spots of resonance in the area of dulness, while in pleurisy the dulness is uniform over all the space occupied by the fluid. In pleurisy the line of dulness changes with the position of the patient; this never varies in cancer. It may also be mistaken for thoracic aneurism and for phthisis. The his- tory, the long duration and the physical signs of the latter will soon enable a diagnosis to be made. It may also be mistaken for fibroid induration of the lung, but its secondary character, more rapid course, greater marasmus and emaciation, and the absence of wooden dulness over an extensive tract, with retraction of the chest-walls, will suffice to make a diagnosis. Prognosis.—The prognosis is always unfavorable, death occurs either from local or general causes in from six months to two years. Treatment.—This is altogether palliative, and is restricted to the relief of symptoms. SYPHILITIC DISEASE OF THE LUNG. The most common and certain changes in the lungs which can be ascribed to syphilis are gummata. Morbid Anatomy.—They vary in size from a pea to an egg, and are single or multiple ; they appear in the lungs as well-defined rounded tumors, often surrounded by a fibrous capsule, and are usually situated in the deeper pul- monary structures. Syphilitic fibroid infiltration originating about the interlobular blood-vessels, about gummata, or from an ulcerating peri- bronchitis does not become caseous, but may ulcerate or become gangre- nous. " Syphilitic pneumonia of the new-born," white hepatization, or " epithelioma,'' as it is variously called, is a diffuse infiltration of one or both lungs. The organ is heavy, enlarged, dense, resistant and indented by the ribs. White dry spots are seen on section. There is thickening of the alve- olar walls and minute bronchi, and thickening and obliteration of the pul- monary vessels. Syphilitic affection of the bronchial tubes is, in such cases, extensive. Gummata may be developed in the nodules of syphilitic pneu- monia. The bronchial glands are enlarged and often cheesy. Abscesses may form from suppuration in gummatous patches. The pleurae may show fibroid thickening. Senile syphilitic gummata bear a close resemblance to caseous tubercle, but are much less friable—syphilitic patients often become phthisical, and there are good grounds for the belief that the phthisical developments commence in a proliferation of the pulmonary connective- tissue which terminates in the formation of gummata, and that; these gum- mata have a course and results similar to those of tubercle. Symptoms.—The symptoms are either the physical signs of a tumor, or of interstitial pneumonia. The diagnosis is reached by exclusion. The treat- ment is antisyphilitic. 164 DISEASES OF THE RESPIRATORY ORGANS. ATROPHY OF THE LUNG. This may be general or partial. Morbid Anatomy.—An atrophied lung is small, dry, anaemic, and some- what pigmented ; it pits readily and can be compressed into a very small space. In extreme old age the lungs atrophy, they crepitate less, the pleura over them is less moist than normal, and they cannot be inflated as normal lungs can. They lie close to the vertebral column, and their surface is un- even and "crumpled ;" the fissures change their position ; the lobes may be attached to one another by pedicles ; the alveoli have no definite form: and the cells are enlarged. The change in the lobes may bring the apes down to the base of the thoracic cavity. Atrophied lungs are " marbled" by lines and dots. The pulmonary artery and its branches are diminished in size, and the bronchial tubes are thinned. The first step toward atrophy is a general disappearance of the capillaries in the alveolar septa. Some fatty degeneration is always present. When it is the result of pressure by tumors, or liquid in the pleural cavity, the atrophy is generally limited to one lobe, and the atrophied part presents the lesions of interstitial pneu- monia. Pigmentation and atrophy, whether local or general, are usually associated. It is commonly best marked in the superior lobes. Sometimes the lobes appear to be adherent to one another. The right heart is gen- erally found in a condition known as "brown atrophy." Bronchitis nearly always complicates it. The diaphragm is thin, flabby, and pale. Etiology.—Old age, pulmonary emphysema, and general marasmus are frequent causes of pulmonary atrophy. Pressure of a tumor or fluid ac- cumulation within the thoracic cavity may induce local atrophy.1 Symptoms.—Dyspnoea, cyanosis, and oedema and coldness of the extrem- ities are its only constant rational signs. Inspection reveals a small thorax ; the lower ribs are approximated, giv- ing a "pigeon-breasted" appearance. The whole thorax moves as if ifc were one piece, as in emphysema, and the chest movements are restricted. Percussion.—The percussion note is particularly loud, clear, and resonant; but the pulmonary area is less than normal. The extent of the precordial dulness is increased. Auscultation.—The respiratory sounds lose their vesicular character and are feeble. Atrophy of the lung admits of no treatment. HYDATIDS OF THE LUNG. In this country hydatids of the lung is a rare disease. There is usually one tumor, and its most common seat is the lower portion of the right lung. Morbid Anatomy.—The cysts vary in size from that of an egg to that of a cocoa-nut. They are usually single, but may be multiple. They may be situated wholly within the lung, or be an outgrowth from the liver into the pleural cavity. The walls of the cysts vary in thickness and density. They develop in the interstitial tissue to which the parent sac is firmly adherent. 1 Buhl (in Virchow's Archiv., Bd. XI., p. 275) describes an atrophy observed by him in three cases ol typhus fever analogous to acute yellow atrophy of the liver. He thinks It is due to a high grade of desqua- mative pneumonia, which latter disease wiU then come in the list of causes. HYDATIDS OF THE LUNG. 165 1 hese cysts may cause serious pulmonary complications by their pressure. They may suppurate and be discharged into the bronchi, and then a cavity may remain. In many cases a pulmonary hydatid cyst is the result of an hydatid of the liver which has ruptured through the diaphragm. Some authorities state that primary hydatids of the lung is a condition yet to be met with. General pleurisy is of rare occurrence ; for the slow growth of the tumor excites local adhesions rather than a general pleurisy. In some instances an hydatid cyst ruptures into the pleural cavity and causes empyema. Bronchitis, pneumonia, and gangrene may be excited in the surrounding tissue by the pressure of the hydatid tumor. Etiology.—Hydatids of the lung are nearly always secondary to hydatids of the liver. The affection is met with most in the Norse countries of Europe, where men and animals live together. Symptoms.—Hydatids of the lung, when small, give rise to no symptoms by which they can be detected ; but as they enlarge they excite bronchitis, attended by cough, with /srp>& * p, ^) mnco-purulent expectoration, pain in the chest, a Jw^V -2? »' , sense of suffocation, haemoptysis, night sweats, pallor y + ^A^ 9%^Jfw and emaciation. When blood is expectorated goose- IL> ® ^Jt^ioy- Jj berry-like skins (the sacs of echinococci) or hook- ^Z..?^ t * 3 **&• lets may be found in the expectorated matter. Unless !L *%$& % \ */J the daughter-cysts, or hooklets, are expectorated the -=m diagnosis can never be positive. When an hydatid jf_ attains any considerable size it may cause bulging FlQ 34 of the chest wall and displace the mediastinum and Hydatids of the Lung. diaphragm. The circumscribed dulness on percus- Microscopical appearance of . , . T,n • » elements found in the sputum. sion, which may extend to the right or left of the A Hookgfrom head 0/Tarda median line, with absence of respiratory sound and Echinococcm. vocal fremitus over the area of dulness, is a strong c.'flS&foKis**. x 250. evidence of pulmonary hydatids. Differential Diagnosis.—The rupture of the cyst and the escape of its con- tents into a bronchial tube are its only diagnostic features and will prevent it from being confounded with any other condition. If an hydatid is super- ficial a portion of the fluid may be withdrawn by aspiration, and a micro- scopical examination will establish the diagnosis. It is impossible to dis- tinguish between hydatid tumors at the base of the right lung and those in the right lobe of the liver. Prognosis.—These tumors sometimes disappear by spontaneous retrogres- sion, or by discharge into a bronchial tube ; or suppuration may be estab- lished in the cysts which afterward undergo calcification. Kecovery occurs in fifty per cent, of cases. Rarely do patients die from emaciation or ma- rasmus. They may die from suffocation, when the cysts rupture into the bronchi, from long-continued suppuration, or from an empyema estab- lished by the rupture of a cyst into the pleural cavity. Inflammation of any of the three adjacent serous membranes may cause death, or this may result from extensive hemorrhage and from gangrene. Treatment—They should be treated as hydatids of the liver. It is a question if they should be injected with iodine. 166 DISEASES OF THE RESPIRATORY ORGANS. PLEURISY. Pleurisy is a circumscribed or diffuse inflammation of one or both pleurae. Upon a clinical basis, it may be divided into acute and chronic. Acute pleurisy may be plastic, serofibrinous, ox purulent. Chronic pleurisy may he dry and adhesive or effusive. It is infrequent that the inflammatory products are confined to any one element. It is rather the preponderance of either the serous, fibrinous, or cellular element of the exudation that gives character to the disease. Most cases of pleurisy present at different stages, in varied proportions, all the inflammatory products except pus. ACUTE PLEURISY. Plastic Variety.—In this variety the symptoms are well defined, the course rapid, and the exudation principally fibrinous. Morbid Anatomy.—The first stage of the inflammatory process is marked by a reddening of some part of the pleural membrane from hyperaemia of the capillaries of the serous and sub-serous tissue with degeneration of the endothelial cells. The pleura loses its natural glistening appearance on account of a slight fibrinous exudation and the swelling and increase in number of its fixed connective-tissue cells. These changes take place dur- ing the first forty-eight hours. Following this, the fibrinous exudation increases and the free surface of the pleura assumes a rough, shaggy ap- pearance. If any serum exudes it gravitates to the most dependent por- tions of the pleural sac. In the substance of the pleura and in the fibrinous exudation new cells are now found which are young connective-tissue or pus cells. These cells are at first more numerous on the inner surface of the pleura. As the inflammation progresses they increase in number and collect on the free surface of the pleura under the fibrinous exudation. By the fifth day of the pleurisy new blood-vessels are formed in the fibri- nous exudation and become connected with the original vessels of the pleura. The nature of the subsequent changes will depend upon the intensity of the inflammatory process ; in the milder types the fibrin gradually dimin- ishes and disappears, some of the cells become fatty and are absorbed, and the remainder enter into the formation of a basement substance which grad- ually increases and finally a permanent new connective-tissue forms upon the inner surface of the pleura. If the inflammatory process subsides with- out much serous effusion, the opposing surfaces of the pulmonary and costal pleurae come into contact and adhesions are formed between them composed of permanent connective-tissue containing long, slender vessels. These adhesions follow the general law that governs all new connective-tissue: they may be permanent, or—their blood supply becoming insufficient—- they may undergo fatty degeneration and be absorbed, the thickened pleura alone remaining to tell of the past inflammation. When an individual has PLASTIC PLEURISY. 167 once had this form of pleurisy he will always have a permanent lesion. This pathological process may be completed in two weeks, or a serofibrin- ous effusion may not be absorbed for months, and then the pleuritic thick- ening becomes very extensive. Etiology.—The etiology of plastic pleurisy is sometimes very obscure. Exposure to wet and cold has been regarded as one of its most frequent causes, but it is very doubtful if it ever occurs as the result of simple expo- sure to wet and cold. In all cases that have come under my observation where it has followed such exposure, I have been able to find some previously existing predisposing cause. It may be the result of a penetrating wound, or blows upon the chest walls. Fracture of the ribs, if the broken ends of the ribs penetrate the pleura, may cause it. It is often a complication of other diseases, such as pyaemia, the exanthematous fevers, acute and chronic alcoholismus, acute rheumatism, Bright's disease, pneumonia, etc. Some- times it is the result of extension of inflammation from adjacent organs and tissues. While a certain proportion of cases of acute pleurisy are undoubt- edly of tubercular origin, the claim that all pleurisy is tubercular has not been sustained. It may occur at any age. Although it has been claimed that it never occurs in young children, my experience leads me to believe that it is of quite frequent occurrence in children of two or three years of age, and pus is usually formed in the pleurisies of children which occur as complications or sequelae of the exanthematous fevers. When- ever acute-pleurisy occurs on the right side, it is important to determine if it is, or is not, the result of an extension of inflammation from the liver. Symptoms.—Plastic pleurisy may be mild or severe ; in either case it is ushered in by well-marked symptoms. The most prominent and constant at its onset is a sharp stitch-like pain in some portion of the chest; it usu- ally is referred to the nipple of the affected side. Each inspira- tion increases its severity. The patient, to prevent motion of the affected side, assumes a pe- culiar position, leaning forward and toward that side. At first the countenance is pale and anxious; after a few hours it becomes flushed. The pulse is accelerated, beating from 90 to 120 per minute; it is firm, small and tense in character— in this respect differing from the pulse of all other pulmonary diseases. The respiration is Temperature in a case otAcuje Pleurisy. Patient set. 24. hurried and difficult; each in- spiration is jerking in character; as soon as the general symptoms of pyrexia are present, the pain, in most cases, diminishes—in a small pro- Da-x 7 2 <3 A 5 L, r 3 9 IO M E M E M E u E M E M E M e M E M B M B 103- =" «r A "* r ~ fJ ^ — \ f - ~ . soi- L — — f " , - r i * \ 99- i \ H /- ~ 168 DISEASES OF THE RESPIRATORY ORGANS. . portion of cases it maintains its intensity throughout the attack. The temperature follows no regular course and has no fixed relation to the pulse or respiration ; in ordinary cases it rarely rises above 100° F.; in very severe cases it may reach 104° F. There is a short, dry, tearing cough, which is very distressing ; the patient restrains it as much as possible on account of the intense pain which it produces. In very severe cases of acute pleurisy, where the fibrinous exudation is very abundant and takes place rapidly, causing compression of the lung, the primary symptoms are very violent, resembling those of pneumonia. A distinct chill is followed by high fever, the temperature often reaching 105° F. The countenance assumes an anxious expression, the pulse beats 120 per minute and is feeble, but the pain in the side is not so severe as in the milder cases. Under these circum- stances, at the onset of the attack it is difficult to distinguish it from croup- ous pneumonia. Such severe cases are rare ; when they do occur they are apt to prove fatal. There are occasionally very mild cases of acute pleurisy which are attended by few of the subjective symptoms of pleurisy : the febrile move- ment is slight, the pain in the side is not severe, and cough and dyspnoea may be entirely absent. These patients continue their ordinary occupations, com- plaining only of an uneasy sensation in the side, and the disease would pass unrecognized but for the physical signs. Although the rational symp- toms of plastic pleurisy may vary in different cases and in some be very obscure ; the physical signs at once dispel all doubts. Physical Signs.—During the first twenty-four hours of plastic pleurisy, inspection will show the movements of the chest wall on the affected side to be more or less restricted. Palpation, percussion, and mensuration will give negative results. On auscultation the respiratory murmur will be found feeble over the affected side, and jerking in character both on in- spiration and expiration, and a grazing friction sound will be heard ; this friction sound will be most intense ^^Fi at the end of inspiration. Normal respiratory sounds.........JB$^dffl$k A n +k„ ^i„^j.- j i- t 1 i„,,„ J0§j?j0&ism As tne plastic exudation takes place J^^^^^^M inspection will show a greater loss of JB^^^^^^ expansive motion on the affected Crepitating friction ^m^^^^^^0^e\ s^e 5 and on palpation there will be a sounds............. MKy/s Ja£'33?£&r!>3w? m j- • j_- i> , 1 -i » ■. mWJ^^^^m y diminution of the vocal fremitus over dm'^^^^^^^/ *^s seat- On percussion there will mim^^^^^^m ^e slight dulness over the seat of the ^ZurJeeblZ Sf^^^^^, Pleurisy- The amount and extent of absent..........fii^^^^^^^S\ dulness will correspond to the Flatness mpercus- H^^^^^^^^B amount of the plastic exudation. Absent vdc'aifre-''' W^^^^^^^^^ Upon auscultation the respiratory Absent voice'.'.'.'.'.'..'. TMmfSg^^ murmur will be distant and feeble ^"***'*ihe cM elements tuberculosis is the bacillus tuberculosis. This bacillus is received directly or indirectly from some other tuberculous subject. The channels of communication are numerous and varied. The most frequent are by particles of dried sputa floating in the air ; by the use of dishes, napkins, handkerchiefs, and other personal belongings of phthisi- cal subjects ; by the use of milk of tuberculous women or cows, and possibly by tuberculous meat. Other unique methods of contagion are occasionally noticed. Although the bacillus is accepted as the sole exciting cause of phthisis, its omnipresence, and the impossibility, under the present social condi- tions, of avoiding a more or less intimate contact with it, render the pre- disposing causes of its development, without which it is inactive, of paramount clinical importance. These causes are general and local. The Fig. 40. Acute Pulmonary Tuberculosis. Section of lung showing a single alveolus in stage of hepa- tization. A. Wall of alrenins, with infiltration of pus at B, B. C. CiirUy of alveolus, nearly filled with changed epithelia and it few pus-corpuscles. 300. 196 DISEASES OF THE RESPIRATORY ORGANS. most important general causes are an inherited or acquired feebleness of constitution, anti-hygienic influences, climate, and soil. The local causes are found in inflammatory conditions of the pulmonary Inherited Tendency.—M, present proof is wanting that the bacillus is ever conveyed to the foetus in utero, although some observations appear to show that such may exceptionally be the case. The supposition that the bacilli are present in the tissues at birth, and remain latent, to become active later in life, is based upon the frequent development, in children, of tuberculous lesions of the joints without previous disease of the lung. The fact of an inherited vice of constitution, and its influence in deter- mining tubercular growth, are so decided that many observers have claimed that phthisis can never be developed by those who have no such tendency. Every-day experience disproves such sweeping statements. We have no knowledge of what constitutes the tubercular diathesis, although it is grossly manifested by certain well-marked signs to which we give the name "scrofulous." My own statistics show that such a predisposition is inherited in more than eighteen per cent. Mothers transmit phthisical tendencies more certainly than fathers. But when one parent alone is affected, the mother is more apt to transmit to the daughters than to the sons, and vice versa. The stronger the hereditary predisposition, the earlier will be the development of the disease, and the more acute its course. A phthisical vice of constitution may be inherited by the children of the aged, of drunkards, of those enervated by excesses, and of those who at the time of the birth of their children were suffering from some form of constitutional disease, such as cancer, syphilis, or gout. It is therefore necessary, in order to fully determine the influence of an hereditary tendency in any given case, to know the condition of the parents at the time of the individual's birth. Children of consanguineous marriages are especially liable to pulmonary phthisis. Anti-hygienic Surroundings.—Second only to hereditary influence are anti-hygienic surroundings. Impure air, improper quality and insufficient quantity of nutritious food, are among the most prolific of this class of causes. Bad ventilation and impure air, an indoor life, especially when large numbers are crowded into a small space, are strong predisposing causes. The frequency of phthisis in clerks, printers, tailors, milliners, seamstresses, factory employees—who live in a hot, close, dust-laden atmos- phere—proves this. Of indoor workers those are most liable to phthisis who exercise least at their vocations. Compositors suffer oftener than the press-hands in the same room. Prison and cloister statistics show a mor- tality from phthisis of from forty to fifty per cent., while that among the people at large is only fifteen per cent. Careful examinations of the dust and air of prisons for bacilli have shown that this difference cannot be accounted for on the theory of contagion alone. The moister the air and the higher the temperature of the apartment, the more liable is phthisis to be developed. If, in addition to these anti-hygienic conditions, are added ACUTE PULMONARY TUBERCULOSIS. 197 insufficient and improper clothing, want of cleanliness, alcohol drinking, prolonged lactation, and repeated miscarriages, it is evident that the feeble- ness of constitution which predisposes to phthisis can be acquired as well as inherited. I am convinced, from a careful analysis of my records, that the phthisi- cal developments depend as much upon the anti-hygienic influences under which childhood has been passed as upon hereditary tendencies. These predisposing anti-hygienic influences embrace the important problem of infantile diet. Few mothers, especially among the wealthier classes, are in a condition properly to nourish their own offspring. The habit which pre- vails of feeding children until they are one, two, or even three years of age upon barley-water and pap, has a great influence upon the future physical development of the child. In determining the influences which have predisposed to phthisis in any case, it is important to consider not only the condition of the parents at the time of the birth of the individ- ual, but also the hygienic influences under which his childhood and early life were passed. One of the great objects of early physical training should be to overcome hereditary physical tendencies ; this can be accomplished, in the majority of cases, by good hygienic surroundings and systematic physical training during infantile and early life. It is especially important that the children of phthisical parents should be placed under such influ- ences, during iufancy and childhood, as shall ensure the greatest physical vigor. All these predisposing influences tend to arrest physical develop- ment. Climate has long been regarded as an important factor in the develop- ment of phthisis. We know of no climatic condition which renders its development a necessity, or that makes its development impossible ; yet there is no question but that.it occurs with greater frequency in one climate than in another. It is rare in the torrid and frigid zones, and frequent in the temperate. Altitude is more important than climate, for most high elevations are antagonistic to its development. The condition of the soil of a region or locality favors, or is antagonistic to, phthisis : light, sandy, porous soils are antagonistic ; while heavy, hard, clayey, and impermeable soils are favorable. A damp, cold atmosphere, an impermeable soil, and sudden changes in temperature, are the most favorable conditions for devel- oping phthisis. Want of sunlight acts also as a strong predisposing cause. It seems probable that the climatic and telluric conditions influence both the resisting power of the individual, and the vitality of such bacilli as are distributed through the air. Local Causes.—One who carefully studies the clinical features of a large number of cases of phthisis must be convinced that bronchitis of the smaller tubes and chronic lobular {catarrhal) pneumonia are the starting- points of a large number of cases of phthisis. Some call these " excep- tional " catarrhs.1 That an apparently simple catarrh leads to the devel- opment of tuberculosis in one case and not in another may be explained by 1 Williams found in 1,000 cases of phthisis that bronchitis was the origin in 12 per cent. Niemeyer regards bronchitis us the primary and essential developing cause in the majority of cases. 198 DISEASES OF THE RESPIRATORY ORGANS. the fact that one individual is in a condition to resist the bronchitis, while in another all the predisposing causes of tuberculosis are in operation, and the catarrh then furnishes the favorable soil for the development of bacilli, while it decreases the resisting power of the tissues. The relation which pneumonia bears to the development of phthisis has been sufficiently con- sidered under the head of its morbid anatomy. From a clinical standpoint there seems tfo be no question but that a non-resolved pneumonia is the starting-point of phthisis in quite a large proportion of cases. The ques- tion which it seems difficult to decide is, Are such pneumonias tubercu- lar ? That pulmonary phthisis not infrequently dates from a pleurisy is evi- dent to every careful observer. Phthisis which is preceded by pleurisy is often attended by an extensive development of fibrous tubercular tissue, and it may be assumed that the primary pleurisy in all such cases is also tubercular. Bronchial hemorrhage is frequently the first and only sign of phthisical developments. It is claimed that tuberculosis precedes and causes the hemorrhage. Unquestionably such bronchial hemorrhages indi- cate a vice of constitution which favors phthisical developments; but it requires no argument to prove that the hemorrhage is not of necessity an evidence that tubercles exist in the lung at the time of the hemorrhage The connection which exists between phthisical developments and bron- chial hemorrhage is not always clear. The mechanical irritation of the bronchi produced by the constant inha- lation of an atmosphere laden with dust leads to phthisis. The phthisis of knife-grinders, stone-cutters, potters, and coal-miners, are examples of this. It must be stated, however, that the primary fibroid changes in the lungs of such persons do not always become tubercular. The constant inhalation of noxious gases, such as are generated in over- crowded, badly ventilated apartments, is a frequent predisposing cause of phthisis. Pregnancy, instead of preventing phthisis, as was at one time supposed, predisposes to it, and renders its course more rapid in those who are already phthisical. Emphysema and goitre have been by some supposed to afford an immu- nity against phthisis, but my observations lead me to the conclusion that it is a very frequent attendant of both these conditions. The notion that malaria and marsh fevers are antagonistic to phthisis is disproved by every- day experience. The relation between diabetes mellitus and pulmonary phthisis is not well understood, but that one complicates the other very frequently is a clinical fact. The factors which determine whether a particular pulmonary tubercu- losis shall result in recovery, or acute or chronic phthisis, are found in the manner of the infectiou and the diathesis of the patient. Sufficient quan- tities of infective material may be received by those of high resisting power to develop an acute phthisis, and small amounts in those of strong tuber- cular tendency may induce a similar condition. Patients in whom all inflammatory processes tend to necrosis and suppuration are more liable ACUTE PULMONARY TUBERCULOSIS. 199 to acute phthisis, while those of a strong fibroid diathesis are not only less liable to tubercular disease, but, even when infected, quite certainly develop chronic forms of the disease. Symptoms.—A young adult who for some time has had a dry, hacking cough, with a gradual but steady emaciation, is suddenly seized with a sharp pain in the side ; the pulse becomes rapid and feeble, and the temperature rises to 104° in the evening, while the morning temperature may be normal. With increase in pulse-rate and temperature the skin becomes pungently hot. The fever alternates with night chills and pro- fuse sweats. The cough is soon accompanied Fig. 41, by an opaque, purulent expectoration, in which Tuberc,e uncim from Phthisical are found numerous tubercle bacilli and yellow sPutum- Staln*d with Fuchsin. elastic fibres. There is rapid loss of flesh and f ^oSofttfsame strength; the patient becomes extremely anae- J^Z^inTmlf^st^i mic ; and the constant harassing cough causes faintly at c, D. x 500. loss of sleep and extreme exhaustion. The expectoration is usually not abundant until after the breaking down of the lung-tissue has occurred. Patients ascribe the emaciation and weakness to the profuse sweats. The respirations and the pulse-rate increase in frequency with the fever. The pulse ranges from 120 to 135. Cardiac palpitation and sudden accelera- tion of the pulse-rate follow excitement. In some cases the chill, fever, and sweat occur with such regularity that malarial fever is suspected, or a malarial element is regarded as the prominent feature. Nausea, vomiting, and diarrhoea are often prominent symptoms, and greatly add to the ex- haustion which is so marked a feature of the disease. The skin assumes a pearly pallor, the hectic flush is present, and the eyes are bright and glistening. Haemoptysis may mark the advent of the disease and recur at intervals during its course. It is rarely absent during the entire course of the disease. Anorexia is always a marked symptom. Not infrequently the destructive processes are so rapid as to cause pneumothorax. Acute phthisis usually pursues a steadily progressive course, but it may assume an intermittent character, and have periods of arrest and apparent amend- ment followed by periods of exacerbation and rapid progress. Physical Signs.—The physical signs will vary with the seat and extent of pulmonary consolidation, and with the rapidity with which destructive processes are established. Inspection, during its early stage, shows rapid respiration and imperfect expansion of the upper part of the chest during a deep inspiration ; as the disease advances, the loss of expansion becomes more and more apparent, but there is no infra-clavicular retraction. On palpation the loss of motion in the infra-clavicular spaces is more apparent ; and if the pleuritic changes are not extensive, there will be increased vocal fremitus. 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Over small cavities with lax walls low-pitched, puffing, cavernous respiration will be heard. This is very frequently heard in acute phthisis where soft yielding walls result from rapid pulmonary necrosis. Amphoric breathing, gurgles, and metallic tinklings will be heard over large cavities which communicate freely with bronchial tubes. The sub-clavian murmur (discussed in chronic phthisis) is not so liable to be heard in acute as in chronic pbthisis. Differential Diagnosis.—Acute phthisis may be mistaken for croupous pneumonia, bronchiectasis, and acute general capillary bronchitis. In pneumonia the prolonged ushering-in chill, the continuous high temperature, the characteristic sputum, the dulness limited to a lobe, and the pneumonic countenance, are symptoms which readily distinguish it from acute phthisis. In some cases the differential diagnosis cannot be made during the first week. Bronchiectasis accompanied by wasting, fetid expectoration, haemoptysis, and night sweats, with the physical signs of consolidation, may well be mistaken for the advanced stage of acute phthisis. In phthisis the signs of consolidation precede those of cavities ;— in bronchiectasis they follow them. Fever and emaciation are always greater in phthisis than in bronchiectasis, and the symptoms are more steadily progressive. In capillary bronchitis there is no dulness on per- cussion, subcrepitant rales are heard on both sides of the chest, and there is no bronchial character to the respirations. The temperature range is lower than in phthisis. Emaciation is rapid in phthisis, and the signs of the formation of cavities occur early. Prognosis.—The prognosis in acute phthisis is always unfavorable. Its average duration is from five weeks to five months. A sudden ameliora- tion of the symptoms may occur before the cavities are formed, but the amelioration is one of short duration, and is usually followed by a more rapid progress of the disease. It may be complicated by pleurisy, pneu- mothorax, hydrothorax, peritonitis, and, rarely, by pericarditis. Death may occur from exhaustion, asthenia, or complications. Acute capillary bronchitis and pulmonary cedema and congestion often lead to a rapidly fatal termination. Treatment.—Most cases are hopeless ; the dietetic and climatic methods employed in chronic phthisis have no place in the management of acute phthisis.1 Morphia in small doses—one-twentieth of a grain hypoder- mically every six or eight hours—has, in my hands, been more satisfactory in staying the progress of the disease, prolonging life, and keeping the patient comfortable, than any other plan. CHRONIC PULMONARY TUBERCULOSIS. (Chronic Phthisis.) Chronic pulmonary tuberculosis presents, both clinically and anatomi- 1 Dr. McCall Anderson (in London Lancet, June, 1877) takes a more hopeful view of these cases, and claims that subcutaneous injections of atropia check the exhausting sweats ; and that quinine, digitalis, and opium reduce the temperature, and if they fail, ice-cloths to the abdomen will accomplish the desired result. His reported results are exceedingly encouraging, but the failure of his treatment as tried by others causes many to doubt his diagnosis. 202 DISEASES OF THE RESPIRATORY ORGANS. cally, three well-marked varieties, dependent upon the form of the tuber cular development and the character of the secondary inflammation. They may be designated as : 1. Pneumonic tuberculosis, caseous pneumonia, <>r catarrhal phthisis. 2. Disseminated tuberculosis. 3. Fibrous tuberculosis, or fibroid phthisis. Aside from these distinctive forms, many cases will be seen in which the several tubercular developments are variously commingled. Morbid Anatomy.—Pneumonic tuberculosis. The primary tubercular developments occur in the bronchi and alveolar cavities, and not only may be, but often are, preceded by localized bron- chitis or catarrhal pneumonia. The tubercular tissue fills the air-cells in one of two ways : (1) by poly- poid outgrowths from the alveolar walls, consisting of round and polyg- onal cells in a basement substance; (2) by masses of similar cells—with or without giant cells—not in connection with the alveolar walls, which partially fill the vesicles of the affected lobules, the intervening space being filled with inflammatory products. These masses vary in size. They may be limited tu a single lobule, or may attain the size of a walnut. After a time masses of cells obstruct the bronchioles. The nutrition of the bronchia] Avails at the seat of the ob- struction is interfered with, and they become attenuated, or a peribronchitis is developed. This peribronchitis is primarily tubercular, and secondarily necrotic and suppurative or fibrous. Early in the process lymphoid cells infiltrate the alveolar septa, the bronchial walls, and the alveolar contents. Pressure on the vessels in connection with endothelial proliferation in their lumen, and thrombosis, as well as the direct action of the bacilli, induce caseation of the tubercular and inflammatory products. As caseation advances, all the elements become granular and are agglutinated by a slightly transparent substance which glistens like fibrin upon the addition of acetic acid. These cheesy masses are found in patches; they are fri- able, and present a gray homogeneous appearance, forming the so-called yellow tubercle, and contain bacilli. Before distinctly necrotic processes supervene, ulcerations may occur in the bronchioles. Ulcers thus formed in the tubes are usually sharply defined and shallow : sometimes they involve adjacent lung tissue as well as the bronchial tubes. The gross appearance of lung-tissue involved in this form of phthisis, Fio. 43. Pneumonic Tuberculosis. Section of lung shoieing two alveoli. A,A. Wall of alveoli covered with changed epithe- lium. B. "Polypoid outgrowth" from the alveolar wall, nearly filling the air-vesicle—composed of a delicate, granular basement substance in which are imbedded round and polygonal cells. C, C. Epithelial cells between the last and wall of the air-vesicle. D. Alveolus partly filled with epithelial and lymphoid cells in the basement substance. PNEUMONIC TUBERCULOSIS. 203 before necrotic changes supervene, varies. It may be of a gray color, hard and glistening, described by Laennec as ''gray infiltration," * or it may appear as a colloid jelly-like mass ((e gelatin if or m infiltration" of Laennec, or the " colloid caseous pneumonia " of Thaon). When a few lobules only are involved, they may become encapsulated, or may undergo resolution. It is rare, however, for a lung to return to its normal condition unless the nodules are small and few in number. Even should the masses be removed, obliteration of the alveoli which they occupied is apt to occur. If a cheesy nodule is encapsulated, cretaceous or chalky material is found in the centre of the fibroid tissue. The lung- tissue between these nodules may be anaemic, hyperaemic, oedematous, or emphysematous, or the seat of atelectasis. The larger the nodule and the more rapidly it has formed, the more liable is it to soften. Cheesy masses may soften, and by a process of ulceration be removed through the bronchi. Absorption of caseous matter by the lymphatics is attended by more or less adenoid hyperplasia, and a group of miliary granules may be developed about a caseous centre, the remainder of the lung not being involved. Sometimes softening and ulceration are so rapid that the process becomes distinctly gangrenous. Cavities.—The walls of a phthisical cavity are always irregular. At first they are soft and friable ; later they become tough, smooth, and fibrous. Bands of dense connective-tissue traverse them, sometimes covered by a layer of granulation- tissue, and vessels and large bronchi often extend across them. Sharply "cut-off'' stubs of bronchi often project half an inch from their walls ; portions of the wall may stand out like the columnae carneae of the heart ; or the sur- face may be uneven or ragged. The connec- tive-tissue trabeculae ex- tending across a cavity frequently contain blood-vessels, whose rupture may cause fatal haemoptysis. When cavities are formed, the lung-tissue around the cavity will be indurated, and the cavities will be separated from one another by bands of firm 1 The infiltrated tubercle of Laennec is considered as desquamative jmevmonia by Buhl, and scrofulous inflammation by Rindfleisch. Pig. 44. A Lung Cavity. A. Stump of small bronchus.—B, B. Bands of fibrin.—C. Loop of blood-vessels in bed of cavity.—D. Smaller cavities opening into a larger one. 204 DISEASES OF THE RESPIRATORY ORGANS. fibrous tissue, and the peri-bronchial and peri-vascular connective-tissue sheaths and the thickened pleura will all be involved in an indurative process. Cavities increase in size by peripheral disintegration, or several small ones may coalesce and form one large, irregular excavation. Phthis- ical cavities contain air and a grumous purulent fluid of a yellowish or greenish color, with which shreds of lung-tissue may be mingled. If the growth of a phthisical cavity becomes arrested, a "limiting membrane forms on its inner surface." The purulent secretion from it at first is abundant, later it diminishes, and the case becomes one of a "quiescent cavity." A large cavity may, by contraction of the fibrous tissue around it, have its walls approximated, but not united. True cicatrization of a chronic cavity which has a distinct lining membrane rarely if ever occurs. Ulcerating cavities are those which, having been long quiescent, take on, for some reason, an ulcerative process. A small cavity at the surface of the lung, after having caused a localized pleurisy and a thinning of the friable wall of consolidated lung-tissue which separates the pleura from the cavity, may break through into the pleural cavity and cause pyopneumothorax. Pleurisy is rarely absent in this variety of chronic jdithisis ; firm adhesions form, and the pleura may be from three-quarters of an inch to one inch thick. These changes—pulmonary and pleuritic—are best marked at the apices. The bronchial glands may be softened, cheesy, chalky, pigmented, and enlarged. The right heart is frequently hypertrophied or dilated. Disseminated tuberculosis is characterized by gray tubercle granules scattered more or less abundantly throughout the affected portion of the lung, or by masses of them agglomerated by fibrous tubercle-tissue. The lungs are large, emphysematous, and pale, unless pneumonia, con- gestion, or cedema is present. The surface of the lungs is often marbled. Tl;e apex of the lung is studded with firm, hard, gray, or cheesy nodules, varying in size from a pin's head to that of a pea. Upon section of a lung which shows these changes, muco-pus flows from the cut bronchi. Peribronchitic and inter-alveolar interstitial pneumonia is developed to a greater or less degree around these nodules, with irregular dilatation of the alveoli. These nodules originate chiefly in the lymph- sheaths of the arterioles, in the peribronchial adenoid tissue, or in the small masses of cytogenic tissue in the alveolar walls.1 These bloodless nodules are incapable of suppuration, resorption, or organization. As the tubercle-tissue about the vessels increases, it causes occlusion of their lumen. The lumen of the occluded vessel is occupied by granular fibrin, and on transverse section a row of white blood-corpuscles and of endothe- lial cells is often seen between the coagulum and the vessel wall. In recent cases the walls of the vessels are very easily distinguished. But if the centre of the tubercle has become caseous, the vessel wall is also altered and is very indistinct. Thickening of the alveolar walls may also result « Rindfleisch states that the. points at which the smallest bronchioles become con tin nous with alveolar sac* are the situations of the first eruption of the tubercles, and that the first lesion is a tuberculous infiltration ol all the angles and projections situated at these points. DISSEMINATED TUBERCULOSIS. 205 from the development of tubercle-tissue in them. Many claim that the commencement of the process is a small cellular projection on one side of an alveolus, which, as it grows, pushes the capillaries and the epithelium with it into the alveolar cavity. The bron- chioles are thickened and di- minished in calibre; sometimes there are complete peribronchial cylinders of new embryonic or tubercle-tissue. The alveolar cav- ity may be filled by the new formation, the walls remaining intact; or the wall may be de- stroyed by the growth of the pro- jecting nodule, and thus com- munication opened between adjoining air-vesicles.' After coalescence of masses of tubercle-tissue, anaemic necrosis occurs; the cellular elements become granular, atrophied, and fatty, and form cheesy yellow masses. These caseous masses are easily removed from the parenchyma in which they are imbedded. Surrounding these masses are found groups of gray miliary tubercles. The mode of the formation of cavities and their appearance are the same as already described. Between the ulcerous cavities the lung-tissue may be emphysematous, engorged, or pneumonic. The bronchi are filled with muco-pus ; their mucous mem- brane is the seat of a catarrh, and is congested and trabeculated. Their walls are thickened, tubercle-tissue is found in them, and ulcers are not infrequent. The pleura is congested, and covered with fleshy, soft vegetations over the parts involved in the chronic phthisical processes. Organized adhe- sions are common ; in them tubercles may be found, and also in the pleura. Tubercles may be found in the larynx, trachea, mesenteric and lymphatic glands, and in the mucous surfaces of the alimentary tract, the perito- neum, spleen, kidney, liver, brain, bladder, and testes. Fatty heart is not uncommon. Thus a chronic local disease of slow and seemingly inter- mittent progress is found associated with evidence of general infection. The recent dictum is that chronic tubercular growths may heal. Many, however, believe that, once established, the process can never become quiescent.8 Ulceration, dilatation of the bronchi, and the formation of large cavities are not infrequent attendants on this process.3 1 Hamilton states that this appearance, which so lesembles the condition of the lobules in catarrhal pneumonia, has caused the mistake of regarding tubercle and catarrhal pneumonia as identical. 2 Rindfleisch advances a new doctrine of the >l healing processes in tuberculosis of the lung," viz.: it consists in a shrinkage of the infiltration, combined with a formiition of new vessels. These vessels do not penetrate deeply into the infiltration, but surround it and supply it with constant, though scanty, nourish- ment. It is a " fibrinous shrinkage ; " the capsule not only encloses, but nourishes. 3 In a variety called by O. Clark and Rindfleisch " Broncho-phthisis Pulmonalis " the central feature of the change is an extensive ulceration of all the bronchi of medium size down to the intra-lobular Fig. 45. Section of lung showing a small miliary tubercle, with surrounding pulmonary alveoli. A. Cheesy centre of tubercle. B. B. Trabecidai of the basement tissue of the tubercle, containing lymphoid elements, large cells, etc. C. C. Divided arteries with infiltration of their wall with tubercidar tissue. D.D.D. Lung alveoli filled with catarrhalproducts. x 50. 2(Hi DISEASES OF THE RESPIRATORY ORGANS. Fibrous tuberculosis, or interstitial tubercular pneumonia, is char- acterized by the diffuse development, in the lungs, of dense fibrous tissue associated with tubercles. The fibrous changes may be primary, an inter- stitial pneumonia, with subsequent tubercular infiltration, or the in- flammation secondary to tubercular develop- ment may assume the fibrous character, and involve not only the tubercle, but the pul- monary tissue as well. The affected lung is diminished in size. The pleural surfaces are adherent and greatly thickened. A section of a portion of lung that is the seat of this variety of phthisis presents a smooth or granular sur- face, or it has a stri- ated appearance. If granular, the granules are imbedded in the fibrous mass. The fi- brous tissue contains more or less pigment which. gives to the cut surface a bluish or gray color. If the process is old, the lung will be tough; if recent, it is less resistant and less leathery. When the disease has existed for a long time, the apex, and sometimes the whole lung, is converted into fibrous tissue, all traces of the normal lung-tissue being obliterated. The indurated tissue may be studded with nodules. The nodules may be small masses of dense fibrous tissue containing a few cells at their centre, masses of tubercular tissue, granulation-tissue enveloping tubercles, or cheesy masses with tubercles and interlacing fibrous bands. Giant cells may or may not be present in the nodules. The connective-tissue growths may begin in the walls of the bronchi, alveoli, or blood-vessels, in the septa, or in the pleura. The alveoli are at times dilated, at times nar- rowed ; they are always deformed. The alveolar epithelium undergoes slight multiplication and swelling. New cells also form in the walls. Cheesy masses, specks of cretaceous material, and cavities of varying size, are found in the hard lung. branches. Spaces of all sizes are seen—nn section—connected with one another. Rindfleisch states that a " desquamative pneumonic process " accompanies this peculiar form of tuberculosis of the lungs. Fig. 46. Section of lung showing a small tubercular nodule with surrounding alveoli. A. Cheesy centre of nodule. B, B. Fibrillar basement substance containing cells and nuclei. C, C. Giant cells. D. Vacuoles. E,E,E. Alveoli, surrounding the tubercle, containingpneumonic products, rr,„fp,.;,,i F. Part of wall of an artery infiltrated with tubercle-tissue, x 250. [ CHRONIC PULMONARY TUBERCULOSIS. 207 The bronchi are at times thickened, at times thinned. Bronchiectatic cavities (cylindrical, fusiform, or sacculated) are found, chiefly in the apex. The appearance of these cavities is similar to that described in chronic interstitial pneumonia. Through ulcerative processes, cavities, often of large size, result from these bronchiectases. As the disease progresses, more and more of the tubercle-tissue is changed into connective-tissue. But while the growth of connective-tissue is extra-alveolar, the tubercle- tissue is both extra- and intra-alveolar. The early stage of connective- tissue development consists in the accumulation of a large number of small cells looking like granulation-tissue and lymphoid cells ; while, in the later stages, we find dense fibrillated tissue containing a few cells—and those spindle-shaped—and an abundant supply of irregular blood-vessels. Tuber- cles may also be found in the pleura. Etiology.—The same factors are concerned in the development of chronic as of acute tuberculosis. Local inflammations, however, play a more prominent part in rendering the pulmonary parenchyma less resistant to bacillary invasion. Some authorities state that bronchitis, catarrhal pneumonia, or pleurisy do not predispose to phthisis. My own experience is to the contrary. The only possible inference to be drawn from the fact that, of two per- sons living under similar conditions, one suffers from phthisis and the other does not, is that the failure of the bacilli to develop in the one case, and their success in the other, depends upon the vital power of the tissues to resist their invasion and to prevent their growth. It is well determined that inflammatory processes decrease the power with which the tissues resist the invasion of other bacteria; and vX only analogy, but all the well-established principles of pathology as wo±i as clin- ical facts, prove beyond question that inflammatory, and particularly sup- purative processes, favor the development of tubercle bacilli. Pulmonary irritants which lead to fibrous formations are not only less liable to be attended by tuberculosis, but tend to prolong its course, and even to result in arrest or cure of the disease. Anthracotic changes show but little tendency to become tubercular, and when infection does occur fibrous phthisis results. Symptoms.—There are certain symptoms which characterize the early stages of each variety of tuberculosis. Pneumonic tuberculosis usually commences as a bronchial catarrh. The cough is paroxysmal and accompanied by tenacious muco-purulent sputa, now and then blood-stained. There is a gradual but steady loss of flesh and strength ; the patient grows pale and has an occasional night-sweat. These symptoms are accompanied by the physical signs of slight consolida- tion at the apex of one or both lungs, with those of localized bronchitis of the small tubes. A localized pleurisy is very certainly present in these cases. Sometimes this variety begins with more acute symptoms, and the physical signs of apical lobular pneumonia are present. In such cases the pneumonia does not resolve, and the fever takes on a distinctly remittent type, with a more rapid loss of flesh and strength, and a copious purulent 208 DISEASES OF THE RESPIRATORY ORGAN'S. expectoration, often blood-streaked. Night-sweats become profuse and exhausting, and there are the physical signs of progressive consolidation of lung-tissue. At any time during the early stage the physical processes may be arrested, and during the period of arrest there may be a great improve- ment in the general condition of the patient, and complete recovery is possible. But in a large proportion of cases a return to the anti-hygienic conditions in which its primary development occurred, or a fresh bron- chitis, lights up anew the phthisical process. Disseminated tuberculosis may for a long period give no distinctive signs; for interstitial pleurisy, chronic bronchitis, and emphysema nearly always accompany it, their prominent symptoms masking those of tuberculosis. Patients with this form become emaciated ; their dyspnoea resembles that of emphysema. The expectoration is in the earlier stages mucous, and later it becomes muco-purulent. Haemoptysis is common; and hectic fever is more pronounced than in any other variety. There are no periods of improvement, though there may be periods during which the disease remains stationary. Pleurisy, laryngitis, and intestinal catarrh are more marked than the pulmonary symptoms. As the disease advances, its symp- toms resemble those of fibroid phthisis. Fibrous tuberculosis—or fibroid phthisis—comes on very insidiously; it may be ushered in by one or more attacks of haemoptysis. In most cases it commences with the physical signs of a localized bronchitis and pleurisy at the apex of one lung. Cough, and a muco-purulent expectoration with more or less pain in the affected lung, may exist for a long time before there is any marked impairment of the general health. After a variable period the patient begins to lose flesh and strength, the cough increases, and the expectoration becomes more abundant. There is a progressive loss of appetite, but at no time is the temperature high or the pulse rapid. Dysp- noea becomes more and more marked, especially on exertion. Extraction of the chest walls under the clavicle commences quite early and is steadily progressive. The limited play of the chest walls is the most distinctive early sign. This variety of phthisis rarely occurs in young persons, and it is often associated with a rheumatic, gouty, or syphilitic taint, or is the result of mechanical irritation. Of the symptoms which are common to all varieties of tuberculosis, the significance which is to be attached to the presence or absence of bacilli in the sputa is of paramount importance. Without entering upon a discussion of this question it may be stated that single examinations of the sputa cannot determine either the presence or absence of tuberculosis. The presence of small numbers of bacilli may be possible after prolonged exposure to infection, when tubercle has not formed. Persistent absence or presence of bacilli, or large numbers in the sputa, however, are almost positive evidence of the character of any pul- monary disease. The number of bacilli in any given specimen has little or no diagnostic significance, since the rupture of a caseous focus may have filled the sputa temporarily when there is little actual disease in the lung. Few of those who rely least upon the presence of bacilli for prognosis would care to find their own sputa persistently loaded with them. On the CHRONIC PULMONARY TUBERCULOSIS. 209 other hand, bacilli may be absent for a considerable period from the sputa of those who are unquestionably suffering from extensive pulmonary tuber- culosis. They may be present at one time, and absent at another in any given case. We are often able to recognize phthisical consolidation before bacilli appear in the sputa. In analyzing the symptoms which are common in all varieties of chronic phthisis I shall first consider the cough. It is the earliest and most con- stant of all the phthisical symptoms. It is present early and continues throughout the whole course of the disease. At first it is dry and hack- ing. It may exist before there are any physical signs, and then there is little or no expectoration; it may amount only to a "clearing of the throat.'' The severity of the cough without expectoration is a measure of the extent to which the pleura is involved. The younger and more excit- able the patient, the more paroxysmal is the cough. It is usually worse in the morning on rising, or just after lying down at night. Lying on the affected side often brings on violent paroxysms. Some cough after the slightest exertion ; others have a varying number of paroxysms during the day, and can estimate how long an interval of rest they will'have between the paroxysms. The loss of sleep occasioned by the cough may add much to the discomfort and wasting of the patient. In advanced phthisis, when cavities have formed, the cough becomes " hollow " in character. Expec- toration may accompany cough from its commencement. At first it is tenacious, glairy, frothy, and mucous; then yellow purulent spots are found in it. It is always important to ascertain whether pallor, fever, and emaciation have been preceded by cough and expectoration, or whether emaciation was the primary symptom. The sputa are gelatinous and faintly pink when the infiltration is extensive. Vitreous, gelatinous, rounded masses may be mingled with yellow catarrhal expectoration, and these are evidences of a recent pneumonia. Dots and streaks of blood in catarrhal sputa indicate a lobular pneumonia; and when this occurs, fatty, swollen, and granular bronchial and alveolar epithelium will be found intermingled in the mass. The sputa in the earlier stages—often for months—are muco-purulent. When shreds of elastic tissue are found, it indicates softening and destruction of lung-tissue. Elastic fibres are gen- erally found in compact, airless, uneven masses, which readily sink in water. As cavities form, the sputa become more purulent, sometimes being wholly composed of fluid pus, which may be fetid and greenish, and contain elastic fibres coming from the alveolar wall, organic matter, fat- crystals, pigment, young cells, and small masses of cheesy matter, and the tubercle bacilli ; the latter are present in the sputa of all varieties of advanced phthisis. The quantity of matter expectorated varies with the extent of the bronchial catarrh and the number and size of the cavities. It may be expectorated readily, or only with difficulty. Usually, the more feeble the patient the more difficult the expectoration. In rapidly formed cavities the expectoration may contain fragments of bronchioles and blood- vessels, with shreds of lung-tissue. Hcemoptysis is a very important symptom of phthisis, and may occur during any stage of the disease ; the blood may simply streak the sputa, 1A 210 DISEASES OF THE RESPIRATORY ORGANS. or a pound or more may be expectorated at one time. Hemorrhages that occur in the early stage of pulmonary phthisis are, in the majority of instances, bronchial, and the blood expectorated is arterial in color. When streaks of blood appear in the sputa, the bleeding usually comes from the vessels of the alveolar walls. Profuse hemorrhages in the later stages of phthisis have their origin in cavities in the lung substance. Hemorrhages that occur in the early stages may be profuse, but they are rarely danger- ous ; hemorrhages in advanced phthisis may be the immediate cause of death. Haemoptysis usually comes on with coughing. There is a sen- sation as if a fluid were trickling underneath the sternum, and there may be violent cardiac palpitation, oppressed breathing, and a peculiar sweetish taste in the mouth. In profuse hemorrhage the rapid flow of blood into the mouth may excite vomiting and be mistaken for haamatemesis. For some time after the primary hemorrhage blood is coughed up, and the color of the spitting becomes darker and darker. Sometimes without warning there is sudden filling of the mouth with hot arterial blood. Many English writers describe a hemorrhagic phthisis. In this variety an apparently healthy man has a sudden and profuse hemorrhage, recurring daily for some time, and followed by cough and slight expectoration for a few days, with no physical signs of consolidation. These cases often continue for years without any other phthisical symptoms, but sooner or later phthisis is developed.1 Haemoptysis often occurs in those who have no physical or rational signs of phthisis at the time of its occurrence, and who do not become phthisical afterward. Although haemoptysis occurs more frequently in phthisis than in any other pulmonary affection, and there are few phthisical subjects who do not have one or more hemorrhages, yet its occurrence is by no means a certain indication that an individual afterward will develop phthisis. Fever.—Rise in temperature is so constant a symptom of phthisis that it has led to the expression, "there is no consumption without fever;" but in no two cases is the fever course exactly the same. In some cases the temperature in the morning may be subnormal, only reaching normal in the evening; in others the rise commences at 2 p.m., continues until 8 p.m., and then falls until 5 in the morning. Between 10 and 11a.m. the temperature is nearly normal. As cavities form, the post-meridian rise occurs later ; i. e., 10 to 12 at night. Toward the end of the disease the fever type resembles that of pyaemia. Night-sweats temporarily lower the temperature. When the alveoli are involved in tubercular pneumonic processes, the temperature rises rapidly to 103°-104° F. Hectic fever may occur in any stage of phthisis, but is usually confined to the stage of soften- ing and excavation. It has three stages : first, at some time during the day there is a well-marked chill or chilly sensation, which may last from half an hour to an hour, followed [second) by a dryness and heat of the surface, the temperature rising from 102° F. to 104° F., the face assuming a peculiar brilliant appearance, and the cheeks having a peculiar rosy tint called the " hectic flush." After a time the fever gradually subsides, and some time in the night (it may be toward morning), the third or sweat- 1 Tubercular disease of the vascular walls is the primary and chief event in such cases, CHRONIC PULMONARY TUBERCULOSIS. 211 ing stage comes on. The night-sweats are usually profuse and exhausting, and always indicate the existence of hectic fever. The chilly feeling may be absent, the subsequent fever may be so slight as to be overlooked, but sweats are constant. A steady and continuous low temperature indicates that the phthisical processes are retrogressive ; a steady and continuous high temperature indicates that they are progressive. In fibroid phthisis the temperature rarely rises more than a degree or two above the normal. In the absence of local symptoms, the thermometer alone may detect pul- monary phthisis in the aged.1 An intermittent temperature indicates a milder process than a remittent or continuous febrile action. The pulse in chronic phthisis bears no uniform relation to the temper- ature ; it is always feeble. It varies greatly in frequency and force, but rarely in rhythm ; it is accelerated by slight exciting causes. In the early stages its excitability is one of its most characteristic features. The arterial tension is below the normal. In the early stage of fibroid phthisis it is rarely over 100. In a few cases it is abnormally slow. An improve- ment in the other symptoms is not always accompanied by an improvement in the pulse. In the last stage of all varieties of phthisis the pulse becomes very rapid and feeble. The respirations are more or less accelerated, and after exertion there is dyspnoea. When the patients are quiet, unexcited, and resting in bed, the respirations may be normal or but slightly increased. But on ex- ertion the breathing becomes accelerated and labored. The accelerated breathing is due to the fever, the diminished breathing area, to bronchial obstruction, and to pain in the chest. Anaemia and heart failure may also contribute to it. In the absence of fever the dyspnoea and accelerated breathing diminish. The extent to which the lungs are involved influences the frequency of the respirations. In young subjects the dyspnoea is fre- quently periodical. During the whole course of fibroid phthisis, shortness of breath on exertion is a constant symptom. Pain in the chest is not a prominent or constant symptom of chronic phthisis, except in connection with pleuritic changes. Dry and inter- stitial pleurisies are common ; yet they seldom cause severe pam, but rather a sense of tightness and constriction on taking a full inspiration. Intercostal neuralgia is frequent and may be confounded with the pain of a localized pleurisy. Dragging pains in the side are most marked in fibroid phthisis. Pain on swalkwing should always cause one to carefully examine the larynx. It usually announces the co-existence of laryngeal phthisis. Emaciation is an early and constant symptom of phthisis; but it is no*; always progressive. Fever is the chief cause of the wasting and pallor that are so common in all varieties of phthisis. The higher the average range of temperature, the more rapid the emaciation. The pulmonary change may be preceded by progressive emaciation, but in all such cases 1 Sir William Jenner makes three clinical types of chronic phthisis in reference to temperature—tht insidious, the active febrile, and the adynamic. In the first the mornipg temperature is normal ; in the second, the morning temperature will be about 100° or 101°, and the evening temperature 103°-104°. In the third, morning and evening temperatures are both high and not very different; but between these times irregular fluctuations occur. 212 DISEASES OF THE RESPIRATORY ORGANS. the average temperature is a degree above the normal. Emaciation may be a part of the constitutional tendency of the individual, but such emaciation forms no part of the phthisical wasting. While emaciation, loss of strength, and progressive anaemia are recognized premonitory symptoms, they cannot be regarded as diagnostic. Emaciation may not be continuous in all cases; there are periods when the patient may even regain lost weight and muscular strength. The anorexia, dyspepsia, diarrhoea, profuse expectoration, and haemoptysis are all causes of the emaciation. Phthisical wasting occurs not only in the fat and muscle, but in the organs and blood as well.1 Slow, gradual wasting belongs to the history oi fibroid phthisis. The symptoms indicating disturbances in the alimentary tract are important. Anorexia is often for a long time one of the most promi- nent symptoms. It may be accompanied by nausea, vomiting, and pain in the stomach, due either to reflex causes or subacute or chronic gastric catarrh. At the autopsy we often find a normal gastric mucous membrane in one who during life gave the symptoms of acute gastric catarrh. The most common cause which acts in a reflex manner to produce vomiting is a violent fit of coughing. It is important to distinguish between the vomit- ing due to reflex causes and that due to gastric catarrh. With dyspeptic symptoms the tongue and pharynx are frequently covered with aphthae. The most important interference with digestion which occurs during the progress of phthisis is due to changes which take place in the small and large intestine. These intestinal changes are marked by more or less tympani- tis and by diarrhoea which is often very troublesome and difficult to relieve; few altogether escape these symptoms. Diarrhoea may occur in any stage, but it is more likely to occur during the later stages ; in some cases it alternates with hectic "fever. It is usually most severe at night. The profuse watery diarrhoea which comes on late in phthisis is called colliqua- tive diarrhoea. Hemorrhoids and fistulce in ano are frequent trouble- some complications of phthisis, and should always be relieved by surgical interference in the early stages of the disease. The cure of a fistula in ano or the healing of an old ulcer is often followed by phthisical de- velopments ; and scrofulous joint disease, psoas and lumbar abscesses in children are often followed by phthisis in early adult life. Cerebral symptoms are rarely pronounced in any stage of phthisis; there is no chronic disease in which the mind is so clear. The hopefulness and buoyancy of spirits which attend its development are remarkable. The least improvement is hailed by the patient as an indication of commencing recovery. He speaks lightly of his unpleasant symptoms, and is very reluctant to admit that his disease is of a serious nature; rarely will a phthisical patient admit that recovery is not possible. Laryngeal symptoms of phthisis have been considered under the head of Chronic Laryngitis. The pharynx is sometimes the seat of tuberculous processes. Arrest of menstruation is a very frequent occurrence in females 1 Malassez states that the red discs are diminished in number. The haemoglobin is also diminished. Leucocytes, fibrin, and calcic phosphate are in excess. Granular masses agglomerate into patches vary- ing greatly in size; and, on a warm stage, they appear to develop into or give rise to organisms which move about in the blood. CHRONIC PULMONARY TUBERCULOSIS. 213 who are consumptive. In young females this is sometimes the first noticeable symptom. Its occurrence in advanced phthisis indicates extreme exhaustion, and it is often followed by a more rapid progress of the disease. The skin is pale, and traversed by prominent blue veins. Sudamina and pityriasis versicolor are often observed. The nails curve and become claw- like. The terminal phalanges of the fingers become "clubbed," and this is by some regarded as an important diagnostic symptom, but it occurs fre- quently in other chronic thoracic affections. It has been regarded as (1) a form of scleroderma beginning in the phalanges and extending centrally over the body; (2) as due to interference with peripheral return circu- lation ; and (3) as an hypertrophy of connective-tissue.1 The hair becomes thin, dry, gray, and falls out. CEdema of the feet and legs is not an infre- quent symptom during the last stage, and its gravity is well recognized by the non-professional. Its occurrence indicates that a fatal issue is not far distant. It may be due to secondary changes in the vessels, but in a large proportion of cases it is due to thrombosis of the veins of the lower extrem- ities, the result of an enfeebled heart. Physical Signs.—There are two recognized stages in chronic phthisis : a stage of consolidation, and a stage of softening and excavation. As the disease advances, evidences of the two stages will be found in close juxtaposition, areas of consolidation surrounding cavities and points of commencing softening. The physical signs of the stage of consolidation vary with the extent of the consolidation according as it involves large areas or small disseminated patches. Inspection reveals diminished expansion—on inspiration—in the supra- and infra-clavicular regions of the affected side. If there are extensive pleuritic thickenings and adhesions, or if extensive fibroid changes exist, flattening and retraction, most marked at the end of a full inspiration, will be found on the affected side or over the seat of the phthisical devel- opment. Palpation shows more distinctly the loss of expansion on the affected side. Vocal fremitus is slightly increased over the affected lung, although extensive pleuritic changes may render the vocal fremitus less distinct. Percussion.—The percussion sound will vary with the extent of the consolidation and the condition of the lung-tissue surrounding the con- solidated portion. There is always more or less pulmonary resonance. If the consolidation is slight, the percussion sound may remain normal, and localized emphysema may give rise to exaggerated resonance even when consolidated lung-tissue exists. When practising percussion, to recognize a slight consolidation at the apex of the lung, it is important to percuss from the trachea rather than toward it. In all cases percussion should be performed at the end of a full inspiration and at the end of a full expi- ration. Dulness usually appears first under the scapula, next over the sternal end of the clavicle, and gradually extends down, being limited, for a long time, to the apex of the lung. If the dulness is slight at first, it gradually increases and may reach complete flatness. 1 la 1,776 cases Pollock found clubbing of the finger-ends in about 25 per cent. 214 DISEASES OF THE RESPIRATORY ORGANS. Auscultation.—The auscultatory signs vary greatly in different cases, and at different times in the same case. Over the affected portion the res- piratory sounds may be feeble or exaggerated, interrupted, " cog-wheeled," or wavy. The breathing may be rude or bronchial; or, when rude in character, it may be rude and wavy, rude and interrupted, at the same time being exaggerated, or it may be feeble and rude. At the commence- ment there may be only a loss in the vesicular character of the inspira- tions, with a slight rise in the pitch of the expiration. The pitch of expiration as compared with that of inspiration indicates the extent of the consolidation. Prolonged expiration, when high-pitched, is very significant. The expi- increased vocal fremitus.......................^r ration is prolonged in emphy- siight dulness on percussion................ ^i||jp sema, but low-pitched. Wavy or Exaggerated vocal resonance..............^gSM nM jerking respiration is regarded Rude or broncho-vesicular resjtiration. jmmM Hp> , „ „ £„;„*.; ™ cm*, A 1™ ,,.. ., ,. islsPgKHBS^ bv some as a inction sound, by Moist rales may or may not be pres- M&, mff "J » others as the result of a narrow- ,,...Jfjj!Biug of the bronchi which inter- sMw feres with the entrance of air into the lung substance. Accom- panying or preceding changes in ^;V^';;;; | the respiratory murmur, crepitat- IpMtl '^§M ing sounds are heard ; they may %MziMil$-{p%Wm^ he crumpling or creaking in character. Small mucous and sub-crepitant rales, if present, Fig. 47. are heard loudest after cough- IHngrdm fflnstratin^Pty^rifflgM of the First Stage of ^ andj jf ft>e consolidation is Partial infiltration at the apex of the lung. extensive, they have a metallic ring. It is claimed by some that all the rales that are heard in this stage of phthisis are produced upon the surface, and not in the sub- stance of the lung. This statement is too sweeping, for these sounds are usually circumscribed. They can be changed by coughing, and are often entirely removed by violent coughing, and can be heard before the inspiration is completed. If they were pleuritic, they would remain after coughing, and would retain their distinctly crepitating character at different examinations. Pleuritic sounds are present in a large proportion of cases, but they can be very readily distinguished from rales produced in lung substance. Carefully conducted post-mortem examinations show that, in a large proportion of cases of phthisis, the pleuritic changes are secondary to the changes in the lung substance. Besides, by inflating phthisical lungs after they are removed from the body, sounds similar to those heard during life are distinctly audible if a stethoscope is pressed firmly upon their surface. A systolic murmur over the subclavian artery of the affected side, heard loudest during expiration, indicates that the pleural surfaces at the apex of the lung on that side are adherent. Vocal resonance is usually increased in proportion to the percussion dulness. In the second stage, or stage of softening and excavation, the physical CHRONIC PULMONARY TUBERCULOSIS. 215 signs of consolidation become more marked, and new auscultatory signs are developed. Inspection shows a greater frequency of respiration and a more marked depression above and below the clavicle on the affected side, as well as an increased difficulty in local expansion. In fibroid phthisis the retraction is more marked than in any other variety. Palpation shows a more marked diminution in expansion of the affected side. On forced inspiration—both hands being placed on the ehest equally far from the median line—the fingers that rest over the affected lung will move but slightly compared with those on the opposite side. Vocal frem- itus is increased. Percussion elicits more uniform and widely-spread dulness, which assumes a wooden or tubular character. Auscultation.—Bronchial breathing and broncophony become more dis- tinct ; numerous moist, crackling rales, unchanged by coughing, are heard over a circumscribed space, and have a distinct, sharp, metallic character, unlike the crepitation and bubbling sounds which were heard during the first stage. As excavation becomes more marked, inspection shows greater depres- sion in the infra-clavicular region than existed in the preceding stage, and there is more complete absence of expansive movements during the respi- ratory acts. Palpation gives results similar to those of the early part of the second stage. Over large cavities containing air and communicating with a bron- chus, vocal fremitus is intensified. Percussion.—The percussion sound will vary according to the condition of the cavities and their surroundings ; over large superficial cavities partly filled with liquid there will be amphoric or " cracked-pot" resonance, if there is a free communication with a bronchial tube. Deeply-seated cavi- ties, when filled, will give deep-seated dulness, and, when empty, an exag- gerated percussion sound. A metallic amphoric note is obtainable only from a cavity whose transverse diameter is at least 1^ to \\ in.1 Occasion- ally, cracked-pot resonance will disappear and remain absent for some time, and no evidence of a cavity can be found where one was known to have previously existed. This happens when the bronchial tube which has communicated with the cavity becomes obstructed in such a manner as to prevent the ingress of air and the egress of fluid. Auscultation.—Over small cavities with lax walls, low-pitched, puffing, cavernous respiration will be heard. When cavities are surrounded by firm, tense walls, and are of large size, communicating freely with a larger bronchus and are situated near the surface, a musical, or amphoric, res- piration is heard. The amphoric echo is sometimes most marked on inspi- ration ; at other times on expiration. The clearness of the amphoric note is no way influenced by the presence of a moderate amount of fluid in the cavity. But when the fluid in the cavity has its level at or above the opening of the bronchus, the incoming air may bubble up and cause gurgles. These have a metallic quality, and vary according to the 1 Merbach and Leichtenstern. 216 DISEASES OF THE RESPIRATORY ORGANS. character of the fluid,—the thinner and more watery the fluid, the more bubbling the sounds; the thicker the fluid, the more crackling are the sounds. Gurgles are always most distinct and abundant during and after cough. When very large cav- ities with rigid walls contain thin liquid, metallic, tinkling sounds may be produced by coughing and speaking. The vocal sounds over large cavi- ties have a metallic or musi- cal quality. Whispering pec- toriloquy is a diagnostic sign of a cavity. Differential Diagnosis.—The early stage of chronic phthisis may be confounded with bron- chitis, pulmonary infarction, pleurisy, acute lobar pneu- monia, ancemia with cough and expectoration, and cancer of the lung. The evidence of consolidation of lung-tissue is essential to the diagnosis of phthisis. So long as bronchitis is accompanied by a tem- perature of 100° F., and the physical signs show that the bronchitis is general, phthisis is readily excluded ; but if the temperature rises to 103° F., and localized crepitant rales develop at the apex of either lung, accom- panied by dulness on percussion over the seat of the rales, with a bronchial character to the respirations, then there is reason to believe that phthisis is being developed. If, with these signs, there is gradual loss of flesh and strength, the cough becoming hacking in character, and the expectora- tion containing fine yellow streaks and blood-stains, it is almost certain that phthisis is developing. The diagnosis between chronic bronchitis and fibrous phthisis rests upon the evideuces of consolidation and retrac- tion in phthisis, and their absence in bronchitis. Infarctions are attended by haemoptysis and localized areas of dulness. Their etiology, however, is very different from phthisis, heart disease being their chief cause. The blood expectorated in phthisis is of a bright scarlet color ; in infarctions it is dark and in the form of coagula. Infarctions are most frequently situated in the lower lobes ; in phthisis the dulness is apical. The temperature in infarction is usually lower than in phthisis, seldom exceeding 102° F. In pleurisy with effusion, flatness will exist from the base of the lungs to the level of the fluid; the line of flatness will change with a change in the position of the patient; the breathing will be exaggerated above the line of dulness ; the range of temperature is lower and does not undergo such marked diurnal changes as in phthisis. The cough is more hacking and is not accompanied by expectoration, and vocal fremitus is dimin- ished or absent. If, after the disappearance of the fluid, the lung remains compressed and bronchial, or broncho-vesicular breathing is present, witr Cracked-pot resonance. Cavernous respiration. Cavernous whisper — Amphoric respiration. Gurgles............... Pectoriloquy.......... Fig. 48. Diagram illustrating Physical Signs of Cavities in the Third Stage of Chronic Phthisis. CHRONIC PULMONARY TUBERCULOSIS. 217 feebleness of the patient, hacking cough and "short breath," the differen- tial diagnosis between it and fibrous phthisis is difficult. A localized pleurisy at the apex of the lung, not the result of a general pleurisy, is indicative of tubercular developments. Anosmia with cough and expectoration is attended by no febrile symp- toms, and by none of the physical evidences of pulmonary consolidation. In cancer of the lung there is usually bulging of the chest at the seat of the cancerous development; in phthisis there is retraction. In cancer the temperature is often sub-normal, in phthisis it is more or less elevated. The currant-jelly expectoration of cancer is diagnostic. Pain is constant in cancer and intermittent in phthisis. The cancerous cachexia and swollen lymphatic glands also aid in the diagnosis of cancer. Whenever cavities have formed in phthisis the diagnosis is not difficult if the physical signs are properly appreciated ; they can be confounded only with those of bronchiectasis. The rules for the diagnosis of bronchiectatic cavities are given under the head of chronic bronchitis. In any case the presence of bacilli in the sputa renders the presence of phthisis probable, and their persistence establishes the diagnosis. Prognosis.—Chronic pulmonary phthisis is not necessarily a fatal disease. Its morbid processes may be arrested in their early stage in a large propor- tion of cases. In the advanced stage, or stage of cavities, proper treatment will prolong life, and in some cases permanently arrest the progress of the disease. Recovery has occurred in one-sixth of my recorded cases during the past ten years. Its duration depends on the variety and treatment. In Laennec's and Bayle's statistics, its average duration is from one to two years. My records of chronic phthisis give an average duration of three years and four months. The younger the subject, the shorter its dura- tion. Phthisis can in no sense be regarded as a self-limiting disease. Some cases, after a period of activity, become stationary and then slowly recover; others slowly but steadily progress to a fatal termination ; others, again, pursue a more rapid and fatal course. The course that any case will take is determined more by the conditions under which it is developed than by the natural history of the disease. If an individual has suffered from phthisical developments from which he has apparently recovered, his chances for recovery from a second attack are greatly diminished. The history of phthisical manifestations in early life renders the prognosis unfavorable when the disease develops during middle life. The prognosis is unfavorable when there is a strong hereditary tendency, when phthisis develops early in life, when scrofulous or glandular disease has existed in childhood, when the patient is narrow-chested, when the ordinary pulse-rate is high, and when there is great variation in weight without any apparent cause. Opinions in regard to haemoptysis vary. Many think its occurrence renders the prognosis favorable, and that there is a larger percentage of recoveries when frequent haemoptysis occurs. My own experience leads me to the opinion that frequent haemoptysis in an early stage of the disease is not unfavorable. When cedema of the feet and lower extremities comes on in advanced phthisis, the prognosis is very unfavorable, and a fatal issue is not far off. The following complications 218 DISEASES OF THE RESPIRATORY ORGANS. render the prognosis unfavorable : pleurisy, pneumothorax, emphysema, pneumonia, secondary irruptions of miliary tubercles, pericarditis, menin- gitis, diarrhoea, intestinal ulceration, peritonitis (with or without perfora- tion), sub-acute gastric catarrh, amyloid degeneration of liver, intestines, spleen, or kidneys, chronic laryngeal catarrh, and bronchitis. But there is no general law that can be applied to all cases. The general condition of the patient, the rapidity of the emaciation, the pulse-rate and temperature, the amount of consolidation, the age of the patient, a knowl- edge of the progress of the disease in other members of the family, and the character of the phthisical process, will indicate the probable course of the disease. In chronic phthisis of long standing the future course maybe determined in some degree by the past history of the case. It must be remembered that phthisical patients who seem to be progressing favorably may suddenly develop some complication which rapidly terminates the case. Again, a case that presents symptoms which indicate a rapid course may suddenly be arrested and a retrogressive process be established. Advanced cases may die suddenly from heart failure or syncope. The majority waste to a skeleton, but the mind is perfectly clear and the patient is hopeful of recovery, and makes plans for the future as if perfectly well. Treatment.—I shall consider the treatment of pulmonary phthisis under three heads, viz. : (1) Prophylactic; (2) Medicinal—internal and local (as inhalations); and (3) Hygienic, including the climatic treatment. Prophylactic. —During the period when prophylaxis can be successfully employed it is possible to prevent the development of phthisis. In one who is delicate and leads a sedentary life, or is engaged in an occupation where the surroundings are unhealthy and depressing, or whose family history strongly predisposes him to phthisical developments, the occurrence of emaciation or loss of strength should immediately lead to such a change in habit of life, occupation and surroundings as shall arrest defective nutri- tion, invigorate his constitution, and thus counteract his marked tenden- cies. Children born of phthisical or decrepit parents should not be nour- ished in infancy by their own mothers, but should be placed with healthy wet-nurses. During childhood they should be fed chiefly on good cow's milk, and the greatest care should be taken in their exercise and general hygiene. Change of climate and surroundings is often of the greatest pro- phylactic importance in this class of children—let the child be removed from the city to the country. There is no other agent so powerful in correcting phthisical tendencies in childhood as systematic physical exer- cise in the open air. This training should be commenced in infancy and continue to adult life. All those agencies which tend to develop pulmo- nary hyperaemia and bronchial catarrh should be avoided. Individuals with phthisical tendencies should not breathe air laden with foul vapors or fine particles of dust. Sudden changes in temperature must be avoided, also hot crowded apartments. They should have the largest amount of fresh air, not only during the day, but also at night; their sleeping apartments should be large and well ventilated. Pulmonary hyperemia may be the result of speaking a few hours in a crowded and badly ventilated apart- CHRONIC PULMONARY TUBERCULOSIS. 219 ment, and then may be followed by broncho- or lobular pneumonia and phthisis. Flannel should be worn next the skin the whole year. It is important that such individuals should not engage in excessive physical exercise—as jumping, running, and violent gymnastics. The diet should be simple and nutritious, and taken with regularity ; and the digestive process should never be overtaxed by taking a large quan- tity of food into the stomach at one time. Alcohol is not to be taken, except after severe mental or physical work, when there is a sense of exhaustion, or after the body has been chilled. The functions of the skin must be most carefully preserved. The soil on which the dwelling-house is built must also be carefully chosen; a sandy, porous earth is the best. All bronchial catarrhs must be carefully and promptly treated until com- plete recovery is reached. I know of nothing so certain to assist in the removal of bronchial catarrhs, in this class of subjects, as a change of climate. Those living in the mountains should go to the sea ; those at the sea to the mountains. The " milk-cure " and ie grape-cure," so strongly advocated by some for the arrest of early phthisis, will often be useful in those who have feeble digestive powers. The primary object of prophy- laxis is to sustain and improve the nutrition, and to guard against bron- chial, pleuritic, or pulmonary complications. At present we are unable to assure absolute immunity from the recep- tion of the bacillus, but all possible means should be employed to avoid contact with sources of infection. Unless its source is known to be abso- lutely free from contagion, all milk fed to children should be boiled, and they should not be allowed to come in contact with phthisical parents, except under the most guarded conditions. For older persons the air of crowded public places not only induces pulmonary hyperaemia, but. is peculiarly liable to be loaded with bacilli when dust is stirred up. A persistent use of a respirator by persons of a phthisical tendency is theo- retically desirable, but clinically it is found that only a few of those sub- jected to the worst forms of dusty occupations can be induced to submit to the annoyance. It may be remembered that the bacillus is not found in the breath of phthisical patients in appreciable numbers, or throvra off from moist sputa. The possibility of tubercular inoculation by wounds of the skin at once suggests the proper prophylactic measures. When a patient becomes affected, the face (in men) should be cleanly shaved, the expectoration received in paper cups or old cloths, and both burned after use. The dis- charges from the bowels should be disinfected, and the utmost cleanliness observed in every particular. Medicinal Treatment.—The most constant symptom of phthisis is fever, and its reduction is therefore one of the most important things to be ac- complished in the management of the disease, for the wasting, the cough, the expectoration, and the rapidity of the phthisical processes, are closely connected with the fever. In some cases sulphate of quinine is one of the most reliable and satisfactory anti-pyretics. I have often found that when quinine had little anti-pyretic power while the patient was "taking exer- cise," a reduction of temperature was effected by the same dose if he were 220 DISEASES OF THE RESPIRATORY ORGANS. put to bed. Even when cavities are forming, its administration will often be followed by a lower temperature. One-tenth of a grain of morphine combined with quinine increases its anti-pyretic power, so much so that now I rarely give quinine as an anti-pyretic to phthisical patients without it. Recently it has been my practice to give phthisical patients, whose temperature ranges much above the normal, five grains of auti-febrin two or three times in the twenty-four hours. I find that their appetites are improved during its use, and that they suffer very much less from those nervous symptoms which usually distress such patients. Digitalis exer- cises no anti-pyretic power, and only temporarily increases heart-power in phthisis. Salicylate of soda is recommended as an anti-pyretic by English physicians, but my experience does not favor its use. Arsenic will act as an anti-pyretic in some mild cases when all others fail, but it is mainly of service in combination with cod-liver oil as a tonic. Aconite, veratrum, gelsemium, and antimony I seldom use, on account of the disturbance of digestion which they cause. In many cases, after the disease has passed the first stage, the fever cannot be controlled. Another medicinal agent which has been extensively employed in the treatment of phthisis, and which, for the past twrenty years, has enjoyed the reputation of curing this disease, is cod-liver oil. It has been claimed that if this remedy is commenced very early it has the power of arresting the phthisical processes. I am not among those who advocate its indis- criminate use. I doubt if it exerts any specific influence upon the disease; it is more than probable that all its beneficial influence is due to the fact that it furnishes some element essential to the digestion and assimilation of certain nutritive elements. In very many cases the exact manner in which it acts remedially is not well understood. There are three facts which seem to me to afford some clue to the mode of its action : first, unless the patient gains in weight while using the oil, it seldom or never proves remedial ; secondly, flesh and weight may be gained during its administration, and still the phthisical processes steadily progress; and thirdly, when it does act remedially, the weight gained is far greater than would result from the oil as a mere element of nutrition. A great gain in weight will sometimes immediately follow the administration of a small quantity of oil. It always acts remedially with more certainty in young persons and children than in the aged ; generally, old persons are not much benefited by its use. Those patients who improve under its use take more food than they have been accustomed to previous to its employment, and digest it more perfectly. In some instances diarrhoea will be arrested by its use, and also vomiting of food after eating. In other cases the oil itself will be rejected and its administration rendered impos- sible. If possible, it should be given in connection with an alkali. At first small doses should be given, not often repeated. A teaspoonful once or twice a day is sufficient to commence with, the dose being gradually increased to a tablespoonful three times a day. No special benefit is to be derived from the administration of large doses. Most patients take the oil best immediately or soon after meals. If it disagrees with the stomach, lying down a short time after taking it will often prevent any disagreeable CHRONIC PULMONARY TUBERCULOSIS. 221 sensation. Some can better take it upon going to bed at night. It should not be administered in connection with stimulants unless the patient cannot take it in any other way. Regularity and perseverance in its use are essen- tial in order to obtain the full benefit it is capable of producing. If, at times, it seems to disagree with the digestive organs, it may be tempora- rily omitted, especially during the summer months. The best oil in the market is " Moller's," or what is termed Norwegian oil. Fish-oils of various kinds, cream, glycerine, oils from vegetables, kournyss, malt extracts, pancreatic and pepsin emulsions, etc., have all proved inferior to the simple cod-liver oil. Phosphorus, sulphur, the hypophosphites of lime, soda, and iron, sulphurous acid, the sulphites, are all excel- lent adjuvants to the oil, but cannot take its place. When intestinal digestion is imperfect, the hypophosphites are especially beneficial. When phthisical subjects become anaemic, iron may be given at each meal if the temperature is below 100° F. ; it may be combined with quinine, arsenic, and the mineral acids as tonics. There is a great diversity of opinion as regards the use of alcohol in the treatment of phthisis. Some claim for it a curative power ; others maintain that its daily use does harm. The question, therefore, arises, Under what circumstances has experience taught that it is of service, and when it is hurtful ? I am convinced that benefit may be expected from the use of alcoholic stimulants only when they increase the desire for food and assist digestion, or when their use is followed by an increase in strength and a disposition to take exercise. On the other hand, if their use causes a rise in temperature and an acceleration of the pulse, followed by a feel- ing of increased weakness and nervous depression, they will certainly do harm. The belief that alcohol has the power of arresting phthisical development is one which experience does not sustain. The daily use of alcohol for a time may mask phthisical symptoms, and the patient and his friends may fancy that the progress of the disease is stayed; but soon he reaches a condition in which the disease will make rapid^progress, and in which a large quantity of stimulants will not give relief. It is unfortu- nate for a phthisical patient to become addicted to the daily use of stimu- lants. If an individual with developed phthisis reaches complete recovery while taking alcoholic stimulants freely, I am confident that he would have reached it more rapidly and safely without them. The quantity and kini of stimulants to be used must be determined by the effects; no rule can be given; each case is a law unto itself. Malt liquors and wines do less harm than whiskey and brandy, and are usually more serviceable. Phthisi- cal patients tolerate alcohol to a marked degree. Cough-mixtures are prescribed by physicians to phthisical patients more frequently than any other medicinal agents. Such mixtures are usually composed of substances which are more or less nauseating ; and as the future well-being of every phthisical patient depends upon his powers of digestion, everything that may interfere with the healthy performance of this function must, as far as possible, be avoided. Although a distressing symptom may temporarily be relieved by a cough-syrup, its administration will certainly cause digestive disturbances which will do positive harm 222 DISEASES OF THE RESPIRATORY ORGANS. The relief obtained by cough-mixtures is due, for the most part, to the anodynes which they contain. This brings us to the question, Should opium be given to phthisical patients ? In answer to this question I would say that opium should never be given in any stage of phthisis, except as already noted in con- nection with quinine, unless the cough is distressing and the patient is unable to obtain the required amount of sleep. Under such circumstances the milder narcotics should first be tried. Opium should be reserved for the later stages of the disease. Its use should be commenced with the smallest dose that will give rest. In the majority of instances I have found that more speedy and satisfactory relief will be obtaiued from the cough and restlessness during the early stages of phthisis by the inhaln- tion of a few drops of chloroform than from the use of opium; besides, chloroform is less liable than opium to disturb digestion. One must be careful in the use of chloroform ; there is danger that phthisical patients may become addicted to its excessive use. Codeia, chloral hydrate, hydro- bromic acid, " chlorodyne," creosote, stramonium, and belladonna some- times act better than opium. All narcotics act only as palliatives, and should be employed only when the symptoms become sufficiently distress- ing to demand relief. In those cases where a constant hacking or violent paroxysmal cough is excited or kept up by an inflamed or irritable condi- tion of the fauces or larynx, the topical application of sedative or astrin- gent remedies by means of sprays will be found of great service. Of all topical applications for the relief of this condition, a solution of cocaine will be found the most efficacious. It is sometimes imperative to give a stimulating expectorant. Ammonium carbonate in the infusion of wild cherry bark is one of the best. It never nauseates. Night-sweats are a part of hectic. When quinine does not control them, quinine with opium may do so. Oxide of zinc (gr. ij-iv), gallic or sulphuric acids, arseniate of iron (gr. |--J), ext. of belladonna or sulphate of atropia (hypodermically), muscarine, picrotoxine, ergot,—all may be tried at different times. Atropia is the most reliable. Cold spongings and sponging with acidulated or astringent waters (alum in alcohol) are always agreeable and sometimes efficacious. Capsicum in the sponging water is sometimes serviceable. Gastric and intestinal disturbances are a part of the history of nearly every case of phthisis, and there are two conditions upon which the diar- rhoea and distress after eating may depend ; viz., either upon a hyperaemic condition of the gastro-intestinal mucous membrane, produced by indigesti- ble food, or upon ulceration of the large or the small intestine. If it depend upon gastro-intestinal hyperaemia, the quantity and quality of the food must be carefully attended to, and a mild saline laxative rather than an astringent must be administered ; this should be followed by the daily use of the lacto-phosphate of lime. If the diarrhoea is dependent upon catarrh with or without ulcerations in the small intestine, cod-liver oil and the hypophosphites of lime and soda will often be of service. Five grains of pancreatine given two hours after eating will often relieve the intestinal pain even in the later stages of the disease. If these fail to give relief, CHRONIC PULMONARY TUBERCULOSIS. 223 ten grains of bismuth, combined with the twelfth of a grain of morphine, after each movement, will almost certainly control the diarrhoea for a time. If the diarrhoea depends upon ulceration of the large intestine, all that can be done is to give temporary relief by opium suppositories. When diarrhu'a is persistent and accompanied by rapid emaciation, it is tubercular. Vomiting after meals is often a troublesome attendant of phthisis. Champagne with the food, hydrocyanic acid, pepsin, and a long list of other remedies are recommended for its relief. The most certain relief is obtained by giving the patient a glass of hot water every two hours, followed in half an hour by a teaspoonful of raw scraped beef made into a sandwich, at the same time keeping him absolutely quiet in a recumbent posture. The most valuable remedies for the arrest of hcemoptysis are rest and opium. Lead, ergot, ice, and a long list of astringents are recommended. Ergotin hypodermically is much employed. Turpentine is more relia- ble than any remedy except opium. Local pains in the chest may be re- lieved by blisters and counter-irritants; strapping the chest so as to render the chest walls immovable often gives marked relief from the pains caused by the circumscribed pleurisies which attend phthisical processes. Dry cupping often gives marked relief from the dyspnoea which accompanies acute phthisical processes. The antiseptic treatment of phthisis has not thus far given satisfactory results, although the recognition of its specific cause has led to the trial of innumerable remedies of this class. Carbolized inhalations have been quite extensively employed, with very favorable results, according to the statements of some observers; but, after quite an extensive trial, my experience is decidedly against their use. The internal or hypodermic use of antiseptics, notwithstanding the strong statements made in their favor by some of their enthusiastic advocates, I have found to fail not only in counteracting the sepsis of advanced phthisis, but in reducing the high temperature which so rapidly exhausts the phthisical patients. The injection of cavities through the chest walls has not been followed by satisfactory results.' More recently, favorable results have been reported by careful observers from the use of creosote, both internally and by inhala- tion. I believe that it is utterly futile to attempt to reach the bacilli imbedded in tubercular or caseous products. It is quite possible that antiseptic inhalations may decrease the infective power of the secretions, and retard secondary inoculations of adjacent lung, and thus be slightly adjuvant to other measures, but their use must be guarded. When used freely they have seemed to me to increase the tendency to hemorrhage. When employed, they are carried more deeply and applied more evenly by the vaporizer and the pneumatic cabinet than any other method of inhalation. The pneumatic treatment has also seemed to me to be of value in relieving pulmonary congestion, assisting the general circu- lation and promoting general nutrition. It is also an efficient measure 1 Or. Pepper, American Journal Med. Science. The modus operandi of washing out lung-cavities and the ase of drainage tubes in such cases, are fully discussed by Mosler in the October nuniber of the Ber, Klin. Woch., 1878. 224 DISEASES OF THE RESPIRATORY ORGANS. for arresting haemoptysis and freeing the bronchial tubes from accumula- tions. The Hygienic Treatment of Phthisis.—-The quantity and quality of the air habitually respired is a most important consideration in the hygienic treatment of phthisis. Phthisical patients should sleep in large, well- ventilated and well-lighted rooms with a southerly or westerly exposure. Flannels should be worn next the skin, and the surface must never be exposed to sudden changes of temperature ; cold sponging or baths often act as tonics when judiciously employed. The patient must live as much as possible in the open air, and should avoid sedentary occupations, taking systematic daily exercises, but never to fatigue. It is a very great mistake for a phthisical subject to exercise when his temperature is ranging from 102° F. to 104° F. The dietetic treatment is usually delayed, like most measures, until forced upon the attention by failing digestion. The most absolute rules should be given upon the earliest recognition of the disease, and a system of forced feeding instituted, in which the digestion may be aided by artificial fer- ments if necessary. The diet should be varied, and phthisical subjects should become accus- tomed to drink from one to three quarts of milk each day. The quan- tity of food taken should be determined by the power of digestion; a phthisical subject should never take more food at a time than can be easily digested. Peptonized foods and preparations of pancreatin will aid a feeble digestion, in the later stages as well as earlier. The climatic treatment of phthisis is a subject which has recently received much attention, but it is to be remembered that its usefulness is confined almost exclusively to the first stage of the disease, and that no absolute rules can be laid down in regard to it. It is well known that some consumptives thrive best in a warm, moist air, others in a cool, dry atmosphere; some are most vigorous in winter, others in midsummer. Each year's experience impresses on me the conviction that while climate, more than any other agent, has a controlling influence over phthisical developments,1 each case must be carefully analyzed before any definite directions can be given as to the climate best suited to it. Although we know of no climatic conditions which render phthisis a necessity or an impossibility, still there are conditions which are known to be antagonistic to its development as well as those which favor its development. Scarcely twenty years ago the great desideratum was thought to be a warm, dry atmosphere, but we now know that a cold climate not only does not hasten, but often arrests phthisical processes. The statement has been made that "the higher the altitude the less prevalent is phthisis," but the altitude at which such immunity exists varies with the latitude, and with the idio- syncrasy of the individual. Mountains and elevated districts were thought to be beneficial on account of their elevation alone. But recent investigations show that the absence of atmospheric impurities is the chief element, and that the purity of the 1 Laennec long ago wrote : " Of all the means hitherto recommended for the cure of phthisis, none bave been followed more frequently by complete cessation of the disease than change of climate." CHRONIC PULMONARY TUBERCULOSIS. 225 air is the chief reason that elevated regions are so beneficial in phthisis. Prof. TyndalPs experiments are of special interest in this connection.1 Organic germs are more abundant in the air in the city than in the coun- try. Rain and ozone free the air from them, the latter by oxidation. Rain cleanses the atmosphere of solid particles and purifies it by washing down ammonia and carbonic acid. The presence of ozone in the air is presump- tive evidence of its purity. The air of high mountains and plateaux and along the shore of the ocean is richer in ozone than that of the plains. Prof. TyndalPs experiments show that in early summer the mountains, and in late summer and fall the seashore, have their purest air. The benefit which phthisical patients derive from living near pine forests has long been known. Turpentine exhaled from pine or hemlock forests con- verts oxygen into ozone, and thus the air of pine forests becomes pure. Direct inhalatiou of ozone has little power over phthisis; hence it is not the ozone, but the purity of air it induces, that renders the air of certain localities so salubrious. It was formerly thought that resorts where no rain fell for weeks and months were the best suited to phthisical subjects, but experience has taught the reverse. Long-continued rains are certainly unfavorable, but cleansing showers act beneficially. The amount of rain- fall is not a sure indication of the amount of moisture in the air of any region, the latter depending more upon the dampness of the soil. The atmosphere of a region with a loose, porous, sandy soil, through which the water filters, and whose surface dries quickly, is never damp ; but hard, compact, rocky, or clayey regions, that drain but slowly and imperfectly, hold the moisture and cause a dampness which is a strong predisposing cause of phthisis.2 Atmospheric temperature is an important element in the climatic treat- ment of phthisis. Some patients thrive best in a warm sedative climate, others in a cool, stimulating climate. Extended clinical observation leads one to believe that it is neither the heat nor cold of a certain locality, but the absence of sudden and frequent changes, which makes it so beneficial to phthisical invalids. Altitude is regarded by many at the present time as of more importance than any other natural element. As a rule, the atmosphere at elevations of 1,500 or 1,800 feet is purer than on the plains ; yet all high altitudes are not thus pure; experiment has shown the atmosphere of some elevated regions to be impure, and that consumptives on such elevations do badly. Something more than altitude is needed to make a given locality suitable to phthisical subjects. Recent investigations show that the similarity in the composition of sea and mountain air at certain times of the year is far greater than was at one time supposed. Mountain air is less dense, less 1 After boiling, filtering, and evaporating a vegetable infusion, he hermetically sealed it in flasks, which he transported to the Alps, 7,000 feet above sea level. Some of the flasks were opened during transporta- tion, and in these millions of organisms developed in the fluid while the fluid in the flasks that were opened on the mountain remained free from such organisms. By further experiments he showed that dust-laden air was necessary to the procreation of these organisms, and they are diffused through the atmosphere, although the air in different localities may be infected in different degrees. 2 Laennec states that the dampness arising from such a condition of soil is one of the most certain devel- oping causes of phthisis, and lie makes mention of a locality having such a soil, in which the dampness was so constant and of such a character that two thirds of the resident population died of phthisis. 15 226 DISEASES OF THE RESPIRATORY ORGANS. humid, and lower in temperature than sea air, but in both we find excess of ozone and freedom from organic impurities. Both sea and mountain air are cooler and less subject to frequent variations in temperature than the air of the plains. A slight diminution in atmospheric pressure produces no palpable changes. But a great diminution (say one quarter) produces serious disturbances of nutrition, developing a condition which favors, rather than retards phthisical developments. The effects of diminished atmospheric pressure vary so greatly in different individuals that no prac- tical deductions can be made. The question arises, Will this patient be benefited by sea or by mountain air ? Beneke's experiments show that tissue changes take place more rap- idly on or by the sea than in the mountains. Hence those in whom the pro- cess of tissue change needs no hastening, and those with exhausted nervous systems, with an overtaxed brain from excessive mental labor or an all- absorbing business, and who still retain considerable muscular power, should go to the mountains ; while those past middle life, who have devel- oped phthisis late, who are incapable of much muscular activity, and who therefore require stimulation for the production of tissue change, do best in sea air. Sea air is better suited than mountain air to those who can- not bear sudden changes of temperature, while the susceptibility to such changes is greatly lessened by mountain air. On our own continent is found every variety of climate. Permanent im- provement only occurs after a prolonged residence in the place which experi- ence proves best suited to each case. A change of climate should not be made every year. The limited space which can be devoted to the con- sideration of the localities best suited to phthisical patients in this and other countries will only allow of mention of the most important ones. Every stage of fibroid tuberculosis, no matter how far advanced or where the fibroid developments began, is benefited in the high altitudes found in Colorado and about the Rocky Mountains. But there is one grave objec- tion to Colorado as a winter refuge : the enormous monthly, and also the diurnal, range of temperature must severely try any invalid. It is impor- tant that every phthisical patient who visits Colorado or any high altitude should place himself under the direction of an intelligent physician before he attempts any exercise. It is during or before the stage of consolidation that persons with pneumonic phthisis are to be benefited by climatic influences, and a care- ful analysis of each case is important before directions can be given as to the region most likely to suit his special requirements. The patient must not wander around till he hits upon the place which suits him; much valuable time is thus lost. Except in those who are convalescing from some acute lung disease, a sojourn in a southern climate during the winter seems, after a time, to hasten the degenerative processes. My favorite resorts in the winter, for those recovering from acute pulmonary diseases, are Aiken, S. C, Palatka, Enterprise, and Gainsville, Fla., Thomasville, Ga., and Nassau. These localities are also favorable for those in whom there are evident phthisical tendencies, but in whom, as yet, no physical evi- dences of pulmonary consolidation exist. My best results, when the evi- CHRONIC PULMONARY TUBERCULOSIS. 227 deuces of consolidation were present, have been obtained in those who have stayed from one to three years in mountain regions 1,500 to 2,000 feet above the sea. My most decidedly beneficial and permanent results have been obtained in Asheville, N. C, in New Mexico, and in the Adirondack region of New York State. The temperature, rainfall, and surroundings of the latter region are all at variance with preconceived notions of a proper "re- sort for consumptives," but results are strong in its favor. A camp or tent life in the open air is best for those who can enjoy such life. Excursions and cheerful social intercourse in the open air should always be an object. A dreary spot, even with the best hygienic conditions, will not give favora- ble results. I would advocate sanitariums for the phthisical. Not overcrowded hos- pitals, but cottages aud pavilions in sheltered spots, in appropriate climates, and at a given elevation, where privacy and quiet are possible, and where all shall be supervised by a capable and intelligent physician. Minnesota has a dry, cool, exhilarating climate. Southern California, Georgia, and South Carolina have a dry, warm atmosphere. The Bermudas, Bahamas, Florida, Turk's Island, Santa Cruz, and St. Thomas have a warm, moist, and usually healthy climate. The extraordinarily dry belt of country which runs northward from San Antonio, Texas, has begun to endanger the su- premacy of Florida as a winter health resort for the consumptive. That this belt offers some climatic advantages for weak lungs over the mild but rather humid air of Florida cannot be doubted. Nassau, the capital of the Bahamas, is a noted resort and one that suits most phthisical subjects past middle life; Matanzas, Cuba, has a dry, warm climate, suitable for a win- ter home for the enfeebled, but not for those who have developed phthisis. It may be that, for various reasons, a phthisical patient prefers a residence abroad. Dry climates near the sea are Malaga, Riviera, and Algiers. Egypt and South Africa are highly recommended by the English physicians for phthisis. Sea voyages to Australia and New Zealand are recommended in cases of "hemorrhagic phthisis." J. Hughes Beunett finds the lakes of Scotland the best resorts for consumptives in the summer. The Engadine has been strongly advocated by many. Within the past ten years, Davos am Platz, in the Swiss Alps, has been most extensively visited. Williams, Albutt, and other English physicians give very favorable reports of it, and from my limited experience I can fully indorse their statements. It is 5,200 feet above the sea, very dry, but not windy, and not changeable.1 Davos possesses, also, the unique climatic characteristic of freedom from high winds (the records showing that from October 1, 1880, to March 31, 1881, there were one hundred and thirty- four days with "no wind"), while its "sun temperature" rises even in January, as Dr. Franklin notes, as high as 150°—conditions which admit of much invaluable outdoor exercise by invalids. Some points in Colorado and New Mexico offer all the favorable climatic conditions which are to be found in Davos. > Lancet, 1878, i. 824. SECTION II. DISEASES OF THE DIGESTIVE SYSTEM. {Including Diseases of the Liver, Spleen and Pancreas.) DISEASES OF THE MOUTH. The following classification may be made of the diseases of the mouth L Stomatitis. II. The " thrush." a. Catarrhal. Ill- The tongue-diseases. b. Follicular. a. Glossitis. c. Gangrenous. b. Cancer. d. Ulcerative. CATARRHAL STOMATITIS. Catarrhal stomatitis is an inflammation of the whole, or a portion of the mucous membrane of the buccal cavity and tongue. It may be acute or chronic. Morbid Anatomy.—At its onset the mucous and submucous tissue of the tongue and inside of the mouth becomes tumefied, much redder than nor- mal, and dry. Later, the mucous and salivary secretions are very much increased. The swelling is greatest over those parts disconnected with bone, as the tongue and cheeks. The tongue becomes covered with a whitish coating, and the red papillae are visible through it. A copious glairy secretion, slightly acid in its reaction, containing pus and epithelial cells, covers its surface. This secretion has a sourish, but not a fetid odor. In some cases the changes are slight and superficial, in others the tongue is so swollen that it presses on the teeth and becomes indented by them, and the mucous membrane of the cheek and gums fills the space outside of them. The whole surface becomes covered with a tenacious, opaque secre- tion. If the process becomes chronic, the glands of the mouth become swollen and tender, the filiform papillae become elongated and pale, and give what is called the " hairy tongue." The tongue is less swollen than in the acute stage ; the secretions have a fetid odor. Occasionally, patches of exudation form over the tongue and sides of the mouth, which tend to collect about the teeth. Large diffuse ulcers sometimes occur in adults. Etiology.—The acute form occurs almost exclusively in children during the period of dentition. The chronic occurs mainly in adults. Decayed CATARRHAL STOMATITIS. 220 and ulcerated teeth, acid ingesta, and the taking frequently of too hot or too cold fluids, often excite it. The prolonged administration of mercury and preparations of iodine for their specific effect, causes a form which is termed mercurial stomatitis. The excessive use of tobacco is a frequent cause. Gastric catarrh may precede or follow it. It may be an ex- tension of inflammation from wounds of the tongue and fauces. More or less severe catarrhal inflammation of the mucous membrane of the mouth is present in most of the specific fevers, especially in scarlatina. Improper food, bad air, and bad hygienic surroundings will induce it in children. Symptoms.—The acute form commences with a burning, smarting pain in the mouth. The child refuses to take food, or allow the finger to be put in its mouth ; it will take freely of cold drinks, is fretful and sleep- less, and there is usually a slight rise in temperature. Vomiting and diar- rhoea often accompany it. The salivary secretion is increased, and flows from the corners of the mouth, excoriating the parts with which it comes in contact. It may extend into the larynx and cause laryngeal catarrh. When it occurs in adults, there is a slight rise in pulse and temperature, a general feeling of malaise and much difficulty in swallowing. The patient is constantly trying to get rid of the slimy coating on the tongue and mouth, by hawking and spitting. The sense of taste is blunted, and there is usu- ally an unpleasant bitter taste in the mouth. These symptoms are usually accompanied by a dull frontal headache. In chronic stomatitis the breath in the morning has a fetid odor, the taste is vitiated, and there is often great depression of spirits. Rarely is the digestion interfered with. Differential Diagnosis.—Catarrhal stomatitis may be mistaken for the changes which take place in the tongue and mouth in some of the specific fevers. In catarrhal stomatitis the coating of the tongue is soon followed by a copious salivary secretion; while in fevers the tongue becomes dry, and the detachment of brown crusts leaves a glassy, smooth surface. In catarrh, the appetite for solid food and the digestive functions are not much changed, while in fevers there is great thirst and repugnance for food. There are slight, if any, constitutional symptoms in catarrh, while in incipient fever there are marked constitutional symptoms. Prognosis.—The acute form generally terminates in recovery within a few days. Chronic oral catarrh is very persistent and stubborn, and rarely yields to treatment. Treatment.—In young children the diet should be cold milk with lime- water. The mouth should be washed with a slightly alkaline wash, and chlorate of potash given internally. In all cases the cause should be re- moved, and the bowels regulated with rhubarb and soda. In chronic catarrhal stomatitis, after the removal of its exciting causes, moderately strong alkaline washes should be frequently used, and in obsti- nate cases a weak solution of nitrate of silver will be found most effica- cious. Carbolic acid sprays relieve the offensive odor and other unpleasant symptoms. 230 DISEASES OF THE DIGESTIVE SYSTEM. FOLLICULAR STOMATITIS. Follicular, aphthous, sometimes called croupous, stomatitis is a vari ety of inflammation of the mouth, in which the mucous follicles are pri- marily and chiefly affected. Morbid Anatomy.—On the anterior portion of the tongue, and on the mucous surfaces of the gums and cheeks, there appear small vesicle-like elevations, semi-transparent, and having a red zone about their base ; these are called "aphthae ;" some regard them as a peculiar deposit, others as a local croupous exudation. They are often numerous ; after they have rupt- ured they leave an irregular gray surface, resembling a small ulcer, which heals slowly. Occasionally a number of aphthae coalesce and form irregular ulcer-like or excoriated patches. In the majority of cases the ulcers soon dis- appear, new crops appear and the disease may run a tedious course. Dirty white or yellow sloughs cover the ruptured aphtha?, and gradually separate, leaving no scar. Follicular ulcers on the inner side of the lips sometimes occur at the menstrual epoch, or during pregnancy and lactation; ulcers like these rarely occur in men. Etiology.—Aphthae may accompany any disease of the tongue or mouth. It is, like most oral diseases, chiefly prevalent among children during den- tition, and is rare after five years of age. It is idiopathic, or a sequela of one of the exanthemata. ITnripe fruit, candy, and indigestible food re- maining in the child's mouth will cause it. Bad hygienic surroundings and a weakly, badly nourished state of the body, are its principal predis- posing causes. It sometimes prevails epidemically. Symptoms.—Aphthous stomatitis shows itself in very young children by pain on taking the breast and in swallowing. Older children have pain on talking and masticating. There is a slight febrile excitement and enlarged and tender sub-maxillary glands. Salivation occurs, and the parts about the mouth and chin become excoriated by the saliva, which continually runs over them. Feculent diarrhoea is common, and there is more or less interference with digestion. Differential Diagnosis.—This cannot be confounded with any other dis- ease. Prognosis.—It is never fatal; it generally disappears as soon as the causes that produced it are removed. Treatment.—Correct any intestinal disturbance that may exist with small doses of rhubarb and magnesia, or mild salines ; restrict the diet to milk. Wash the mouth with a weak solution of glycerine and borax, or chlorate of potash. In severe cases the mouth should be washed every few hours with a dilute mineral acid, or nitrate of silver. In weak children, when the general health is impaired, stimulants may be given with benefit. GANGRENOUS STOMATITIS. 231 GANGRENOUS STOMATITIS. Gangrenous stomatitis, "cancrum oris," or sloughing phagedaena of the mouth, is a formidable disease of childhood, in which the tissues of the cheek are prominently involved. Morbid Anatomy.—There is first a hard swelling developed in the cheek, the skin over it being red, shining, tense, and brawny. In the mouth, at the side of the indenture, there is a deep, ragged, angry, unhealthy ulcer covered with a dark, ashy, or brown colored slough. The adjacent tissue is oedematous, and hemorrhage from the livid and swollen part sometimes occurs. The ulcer in the cheek rapidly extends and deepens, emits a very fetid odor, and often perforates the walls of the buccal cavity. The slough may occupy the whole of one side of the mouth, the teeth may become loosened, and caries, or necrosis of the inferior maxilla, result. If the ulcerative process is not extensive, separation of the slough may occur, and the ulcer heal by granulation and cicatrization. The facial vein may be implicated, and then pyaemia, with multiple abscesses, may result. Etiology.—This is a very rare disease. It occurs principally in debilitated children between two and five years of age who are convalescing from some form of acute disease, such as scarlet fever. Whether it is contagious or not has never been determined. It sometimes follows the prolonged use of mercurials. Bad air, insufficient food, and anti-hygienic surroundings, predispose to it. Symptoms.—It commences with pain in the mouth, which is increased by movement of the jaws. Then the local changes already described appear on the cheek and gums, and an abnormal quantity of saliva, mixed with a putrescent fluid, often with blood, flows from the affected side of the mouth. The breath has a peculiarly offensive odor. The adjacent glands become enlarged and tender. As the disease advances, the constitutional symptoms of septicaemia are developed. In most cases the child after a time becomes drowsy, passes into coma, and dies. Differential Diagnosis.—Cancrum oris maybe mistaken for "malignant pustule." Malignant pustule attacks the skin and exposed parts first, while gangrenous stomatitis begins in the mucous membrane of the cheek or about the gums, involving the skin secondarily. Malignant pustule is at once accompanied by constitutional symptoms, and soon followed by the phenomena of a septic or typhoid fever, while cancrum oris is without pyrexia or loss of appetite at its onset, and severe general symptoms do not come on till late. Prognosis.—This is an exceedingly fatal disease—nineteen out of twenty die. In the few cases where the process has been mild, recovery has occurred within two weeks from its commencement. The complications are pneumonia, bronchitis, and pyaemia. Death may occur from exhaus- tion or from one of the above named complications. Treatment.—Prompt measures are indicated at the onset of this affection. Nitrate of silver, and even strong nitric acid, should be thoroughly applied 232 DISEASES OF THE DIGESTIVE SYSTEM. to the slough, and the mouth frequently washed with solutions of carbolic acid and chlorate of potash. The best internal remedies are quinine and hydrochloric acid. The diet should be highly nutritious ; stimulants may be freely given, if indicated. When the child cannot swallow, beef tea and brandy enemata should be administered. ULCERATIVE STOMATITIS. Ulcerative stomatitis, or noma, is a variety of inflammation of the mouth chiefly affecting the gums and spreading over a large extent of surface. Morbid Anatomy.—The gums are hyperamiic and tumefied. Sometimes they assume a purplish color, separate from the teeth, and are covered with a pulpy gray-white material which disintegrates, becomes soft and dark, and gradually spreads to the lips and side of the cheek. This gangrene- like slough may gradually extend until the gums are destroyed. In some few instances little vesicles precede the slough. If the slough is removed as soon as it appears, the gums underneath will be found red, bleeding and granular. The teeth become loosened and often drop out, the tongue enlarges and has a sodden appearance, and the mucous membrane of the cheek swells so that it often receives the impression of the teeth. Some- times the bones about the face lose their periosteum and exfoliate. When recovery takes place deep cicatrices may remain and cause more or less distortion of the face. Etiology.—Noma, or ulcerative stomatitis, is met with only in children from one to ten years of age. It occurs among those who inhabit filthy localities, who are badly fed and compelled to breathe unwholesome air. Dampness seems to exert a predisposing influence, and the disease is most prevalent during the autumn months. It is probably contagious, for well- marked epidemics of it are recognized. It is common after asthenic in- flammation and the eruptive fevers. The prolonged use of mercurials will cause ulcerative stomatitis. Symptoms.—The mouth is hot and painful for some time, and then ap- pear the changes already described. There is pain on chewing or speaking, and there may be slight febrile excitement, although constitutional symp- toms are not prominent. There is an increased flow of saliva which has a very offensive odor, and is mixed with blood and shreds of the pulpy mass. There is enlargement and tenderness of the sub-maxillary glands. In some cases the child will pick at its mouth and throat, and very often loosens and swallows some of the shred-like sloughs. The appetite may not be impaired, though the bowels are disordered, and the child is restless and sleepless. The upper lip becomes swollen, dark-red, and projects out- ward, while the mouth is kept widely open to prevent painful contact with the lips or tongue. The excessive salivation soon decreases, but the un- pleasant fetor of it and of the breath persists. Late in the disease the adja- cent glands become enlarged and tender. Differential Diagnosis.—Ulcerative stomatitis maybe mistaken for "can- crum oris," or gangrenous stomatitis. It is a local disease, while cancrum THRUSH. 233 oris is attended by constitutional symptoms ; it begins in the gums, while gangrenous stomatitis begins in the cheek. The progress of noma is slow compared with the very rapid extension of cancrum oris. The livid red- ness, the dark swelling, and the ashy slough of cancrum oris are absent in ulcerative stomatitis. Prognosis.—This is good. Its duration is about eight days, but slough- ing about the gums may continue for weeks. Treatment.—The treatment is the same as in aphthous stomatitis. The chlorate of potash may be used as a wash or gargle and internally, and will usually arrest it. In many instances, fresh air, cleanliness and a restricted diet are all that is necessary to effect a cure. If the ulceration spreads, the application of nitric acid, and sometimes the employment of the ac- tual cautery, must be resorted to. For the profuse salivation which is sometimes so troublesome, belladonna has proved efficacious. THRUSH. Thrush, sprue or muguet is an aphthous disease of the epithelium of the mouth and tongue, due to the growth of the germs of the thrush-fun- gus, the oidium albicans. It was formerly classed as an exudative inflam- mation. Morbid Anatomy.—The mucous membrane of the mouth assumes a dark red color, and upon the most superficial layer of the epithelium there ap- pear numerous small, round whitish spots,—" aphthae,"—which give to it a flocculent or curdy appearance. These spots are often aggregated in groups of two or three ; at first, as they enlarge, they fall off or can be readily removed, but are soon reproduced and run together in patches. The development in thrush of the oidium albicans and of its frequent parasitic companion, the leptothrix buccalis, in and between the epithelial cells may continue until the mucous tissue is invaded. The epithelium becomes swollen and loosened, the tongue and inside of the mouth are covered with a yellowish pultaceous, creamy mass, underneath which the mucous membrane is of deep red color, and the papillae are enlarged. In the new-born it occurs most abundantly about the boundary line between the hard and soft palates ; in adults, on the mucous membrane of lips, cheek __j i » i ti • i ,i i Oidium Albicans. From the and end of tongue. It may invade the pharynx, tongue in a case of "Thrush." oesophagus and stomach. It has been found in the naUhreaZ^'^m^ My<* \ungs and air-passages and about the breasts and genitals of infants. A microscopic examination of a patch shows it to con- tain mucous and epithelial cells, fat spherules, and the spores and filaments of the oidium albicans. The spores are round or ovoid and form masses of varying sizes, while the filaments coming out of the spores are cylindrical, curved or branched, and consist of long cells, which are constricted where they join one another, each cell being filled with granules. 234 DISEASES OF THE DIGESTIVE SYSTEM. Etiology.—In children this disease occurs from birth to the second year, and is very rare after that time until adult life. These parasitic plants grow best in the presence of acids, hence the acid secretion of the mouth for the first six or seven months predisposes to it. All food or drink that will produce irritation of the stomach or intestines, and make the intestinal contents acid, predisposes to it. Want of cleanliness in the care of nursing- bottles, spoons, etc., is one of its principal causes, consequently it is more frequently met with in children brought up on the bottle, especially in asy- lums. In adults thrush occurs toward the end of any long exhausting disease, such as cancer, or consumption. Symptoms.—In children the mouth becomes hot and painful. The child will not allow its mouth to be touched. An examination shows the mu- cous membrane to be drier than natural; soon after, the peculiar thrush aphthae appear, and there is salivation, which is always markedly acid. The lips swell and become everted. Diarrhoea is frequent and the passages are often green and smell of fatty acids ; so acid are they at times that they cause an erythema about the anus. If this condition persists, the but- tocks and parts around the genitals become excoriated. Besides this diar- rhoea, vomiting and purging give additional evidence of gastro-intestinal disturbance. In adults suffering from exhausting disease, the mouth be- comes hot, dry and painful before the thrush appears, and there is diffi- culty in swallowing, after which the mouth and tongue soon present the characteristic appearance of the disease. Differential Diagnosis.—The presence of the parasite establishes the diag- nosis. Prognosis.—In vigorous children the average duration of this affection is from eight to ten days, but in feeble infants it often lasts for months. Its only serious complication is gastro-intestinal catarrh. Death may result from the exhaustion of the diarrhoea. Treatment.—The most important thing to be accomplished in the treatment of this affection is to arrest or counteract the acidity of the se- cretions of the mouth. After each feeding the mouth must be thoroughly cleansed with borax and glycerine, or a weak solution of carbolic acid, and sulphate of soda. The diet should be restricted to milk with lime-water; when there is emaciation, cod-liver oil and the lactophospbate of lime will be of service. The bowels must be regulated as in follicular stomatitis. GLOSSITIS. Glossitis is an inflammation of the parenchyma of the tongue. It may be acute or chronic, and when chronic, is generally circumscribed. Morbid Anatomy.—There is first intense hyperaemia, causing slight swell* ing and intense redness of the tongue. This is soon followed by so great an enlargement of the organ that it entirely fills the mouth and protrudes beyond the teeth. Its surface is covered by a thick secretion, and its sub- stance assumes a pale or grayish color. The oedematous condition may rapidly subside and leave the tongue in its normal state, or the inflamm* GLOSSITIS. 235 tion may be so intense that small abscesses form which leave deep cica- tricial depressions, giving the tongue an uneven and lobulated appearance. In some instances the tongue may remain enlarged and hardened for life. There is a rare variety of glossitis which does not invade the deeper struct- ure of the tongue, but is confined to its mucous and sub-mucous tissue, causing thickening and sloughing of its surface, with depressions similar to the cicatricial depressions of the parenchymatous variety. Chronic glossitis occurs chiefly in patches along the edges of the tongue ; the thickening, induration, and cicatricial depressions occur in circum- scribed spots. When chronic glossitis is general, the tongue is uniformly enlarged and its color is much redder than normal, some spots being darker than others ; its movements are interfered with, and its surface pre- sents the appearance of eczema of the skin. Etiology.—Acute glossitis may develop under the influence of mercurial poison, or as a consequence of direct injury. Croton oil and other acrid matters taken into the mouth may cause it; burns, blows, and the poison of insects have caused it. Chronic glossitis occurs in the old without any apparent cause. It maybe produced by disease of the teeth, or of the maxil- lary bones, and may, in some instances, result from the action of the mate- rials of which false teeth are made. Symptoms.—With the enlargement of the tongue in acute glossitis, there is great restlessness and anxiety, accompanied by an increase of the pulse- rate, and an elevation of the temperature. In some cases, there is profuse salivation, and the swollen tongue protrudes between the lips. There is a sensation of heat in the mouth, and the swelling often causes severe pain. The glands at the angle of the jaw are enlarged and tender, and all move- ments of the tongue in talking, chewing or swallowing become exceedingly painful and frequently impossible. Dyspnoea and inability to lie down are sometimes caused by the obstruction to the free entrance of the air into the lungs. When the veins in the neck are compressed, cyanosis of the face is marked. The patient is anxious, and very much depressed, and may show signs of asphyxia ; indeed death has occurred from suffocation in extreme cases. When it terminates in suppuration, the constitutional symptoms be- come severe, and all the oral symptoms are intensified. When clefts remain in the tongue after glossitis, the ulcers in them are painful, but otherwise there is no inconvenience. In superficial glossitis, which is apt to be pro- tracted, any movement of the tongue is painful, and there is constant sali- vation. In chronic glossitis patients sometimes complain of a dull aching in the tongue, and in some cases movements of the tongue induce pain of a burning character. Differential Diagnosis.—Chronic circumscribed glossitis may be mistaken for cancer. Cancer develops rapidly, and chronic circumscribed glossitis al- most imperceptibly. Cancer tends to speedy ulceration, and hemorrhage is frequent, while glossitis passes on to induration and there is no hemorrhage. Fetor of the breath is present early in cancer, while it is slight or altogether absent in glossitis. In cancer the pain is sharp and lancinating, running along the branches of the fifth nerve, while there is only a dull pain in 236 DISEASES OF THE DIGESTIVE SYSTEM. glossitis. In cancer the adjacent lymphatics are early involved, in glossitis they are uninvolved. In cancer, emaciation and cachexia are marked; these are absent in glossitis. A microscopical examination of a portion of the diseased tissue will establish the diagnosis. Prognosis.—In acute glossitis, the prognosis is uncertain, for suffocation may occur unexpectedly; generally it subsides in from three to seven days. Of the modes of termination, that of thickening and induration is the most common, and is rarely entirely recovered from. Treatment.—In acute glossitis, ice should be freely applied to the tongue and a mild cathartic administered. If the patient is not able to swallow castor oil, a turpentine enema may be given. If the swelling interferes with respiration, free and deep incisions on the upper surface must be at once made, and if abscesses form they should be promptly opened and washed out with some disinfectant fluid. The ulcerations occurring in glossitis should be treated in the same way as those of ulcerative stomatitis. In the chronic form, if possible, remove the cause. In superficial glossitis, the local application of carbolic acid will be found the best remedy. If suffo- cation becomes imminent in either variety, tracheotomy should be per- formed. CANCER OF THE TONGUE. The most common variety of cancer of the tongue is epithelioma. Morbid Anatomy.—At some point that has been subjected to constant irritation, or in some ulcerative cleft in the tongue, there appears a small unhealthy ulcer or a small deeply seated nodule. When appearing on an otherwise healthy tongue, its locality is usually on its edge. In whatever way it may begin, an ulcer quickly forms, circular in shape with ragged everted edges, and a wide indurated base. The surface of the tumor has a dirty white or grayish-red appearance, is papillated and friable, and com- monly of a firm consistency. As the disease advances, it may involve the whole tongue, which is then larger than normal, unevenly lobulated, and covered with small ulcerations. The mucous membrane on the floor and sides of the mouth may be secondarily invaded. As the deeper tissues are encroached upon, hemorrhages occur. The sub-maxillary and sub-lingual glands early take part in the cancerous development, and the oral cavity may be filled with the cancerous mass. On scraping the surface of an epi- thelial cancer, a grayish granular mass is found beneath, a portion of which under the microscope will show the characteristics of an epithelioma. Etiology.—Cancer of the tongue is met with most frequently in middle life, between the ages of thirty-five and sixty, and occurs in men more often than in women. Its chief exciting cause is some local irritation, as from a projecting or carious tooth. It may develop in syphilitic fissures. Oc- casionally it appears on a tongue whose mucous membrane has, for a long time, been thickened and indurated. Usually there is an hereditary pre- disposition to cancerous development. It may develop without any discov- erable cause. Symptoms.—In most cases, from the onset there is a sharp pain at the seal HYERTROPHY OF THE PHARYNGEAL TONSIL. 237 of the disease. This pain is aggravated by any movement of the tongue, and generally runs along the branches of the fifth nerve. Salivation is pro- fuse, and swelling of the lymphatics in the neighborhood is present early. Hemorrhages not infrequently occur, which increase the anaemia that at- tends the cancerous cachexia. The disease runs a very rapid course, the pain becomes agonizing, and a fatal termination may at any time occur from hemorrhage from the lingual artery, or suffocation may result from me- chanical interference with respiration. Differential Diagnosis.—This disease may be mistaken for syphilitic ulcer- ation. A syphilitic ulcer is long and oval or irregular in shape, while can- cer is circular. A syphilitic ulcer is developed slowly and with little or no localized pain, but cancer spreads rapidly and is accompanied by severe pam. The constitutional symptoms of syphilis are usually well marked, and the ulcer improves under anti-syphilitic treatment, while the evidences of syphilis are absent in cancer. A microscopical examination of a small portion of the ulcerating surface removes all doubt in diagnosis. Prognosis.—The disease advances rapidly; its average duration is about fourteen months. I have known cases to last two years. Death results from the cancer, marasmus, exhaustion from hemorrhage, or from starva- tion, as the intense pain in eating causes the patient to refuse food. The constant and long-continued pain hastens the fatal termination. If, after removal, it does not reappear, death may result from cancerous develop- ments in other parts of the body. Treatment.—The relief of pain and the maintenance of the vital powers are the principal indications. The hypodermic use of morphia is the best means of relieving pain. Antiseptic gargles are grateful, and counteract the offensive odor of the breath and the unpleasant taste. The checking of hemorrhage, removal of the growth, removal of the tongue, ligation of the lingual artery and division of the gustatory nerve, belong to the surgical rather than to the medical treatment of the affection. DISEASES OF THE PHARYNX. I. Hypertrophy of the Pharyngeal Tonsil. II. Inflammation of the Faucial Tonsil. a. Acute Tonsillitis. b. Peritonsillar Abscess. c. Chronic Tonsillitis. III. Pharyngitis. a. Catarrhal, which is either acute or chronic. b. Membranous, Croupous, or Diphtheritic. I\ . Retropharyngeal Abscess. HYPERTROPHY OF THE PHARYNGEAL TONSIL. {Adenoids.) Hypertrophy of the normal lymphoid tissue at the vault of the naso- pharynx. 238 DISEASES OF THE DIGESTIVE SYSTEM. Morbid Anatomy.—The growth is essentially a hyperplasia of the lymphoid tissue found in the naso-pharynx. In young children the mass is lobulated, of a soft consistence, and gives to the finger passed behind the velum the impression of a bunch of worms. When abundant they are found not only at the vault of the pharynx, but extend down along the posterior pharyngeal wall, so that they may project below the arch of the soft palate. They are more frequently found invading Rosenmiiller's fossae, where their pressure against the Eustachian orifices and the inflammation set up in them account for the deafness and middle-ear inflammations so frequent in tin's disease. Histologically, they are composed of islands of lymphoid tissue surrounded by or enclosed in a little areolar tissue. Their surface and also the sulci or grooves dividing them into lobules are covered by ciliated epithe- lium, except at those portions where from friction the cilia are rubbed off. The lymphoid tissue is situated not merely beneath the mucous membrane of the pharynx, but also deep down in the substance of the pre-vertebral fascia. This accounts for the inability to completely eradicate them and for their reappearance in some cases after removal. They usually undergo more or less complete atrophy shortly after puberty; in those cases where they do not, they become of a firmer consistence, owing to the increase in the amount of connective tissue. Etiology.—Age is one of the most important causative factors in this dis- ease. It is occasionally congenital, but it usually makes its appearance between the third and fifteenth year of life; it occurs as early as eight months, and it is rare to find a case beginning after the twenty-fifth year. Adults who for the first time consult a physician for this trouble will, on careful inquiry into the history, be found to have been suffering from this disease since childhood. It is undoubtedly hereditary, and in very many hereditary cases one finds a tubercular or syphilitic family history. It is said to be more common in boys than in girls. While no class is exempt from the disease, it is more common in those who live in unsanitary sur- roundings, especially in damp dwellings. It frequently follows the ex- anthemata, especially measles, scarlet fever, and whooping cough. It is associated with nasal obstructions very frequently; children with cleft palate almost invariably have more or less enlargement of the pharyngeal tonsil. It is intimately associated with chronically enlarged tonsils, and there are few cases of the latter disease which are not complicated with adenoids. Symptoms.—The symptoms of adenoids are very characteristic. The patient is an inveterate mouth breather, snores at night, is restless, and has bad dreams in the early part of the night, but becoming exhausted falls into a deep, heavy semi-asphyxiated sleep the latter part of the night. In the morning the child awakens tired, with perhaps a headache, the mouth dry and parched; these children are usually dull, stupid, and have a peculiar expressionless countenance, the nose broad, the lips thick and everted, and the mouth constantly open. At school they are usually less easy to learn than the average child, partly from the insufficient rest their sleep affords them at an age when they need such rest greatly, and partly from the impairment of hearing, so often associated with adenoids. Very frequently neither they nor their parents or teachers are aware of the impaired HYPERTROPHY OF THE PHARYNGEAL TONSIL. 230 hearing until they are examined by a physician, and this faculty is found diminished half, or more than half. The voice has a marked nasal twang, and they are unable to sound the letters m or n, these letters being replaced by b or d. They are particularly subject to attacks of acute rhinitis and laryngitis, and from the obstructions to nasal respiration cannot properly use a handkerchief; .as a result, a thick tenacious yellowish-white discharge comesfrom the anterior nares. This irritates the skin at the nostril so that it is frequently the s'ite of an eczema. A similar muco-purulent discharge can be seen to be pressed from the posterior nares when the throat is ex- amined, a tongue depressor being used to get a view of the posterior pharyn- geal wall. This in a child is almost pathognomonic of adenoids. Epistaxis is of frequent occurrence. A cough of a peculiar hacking or barkiug character independent of any laryngitis or pulmonary disease is very common. Various neuroses are ascribed to the disease, such as incontinence of urine, laryngismus stridulous, and chorea. Many cases are recorded where these conditions have been cured on the removal of the hypertrophies; rickets and various chest deformities are also ascribed to adenoids. Ou account of the small distance existing in children between the soft palate and the posterior pharyngeal wall, it is rare that one can see a hyper- trophied pharyngeal tonsil in a child under five years of age. Even in older children it is often difficult to inspect the naso-pharynx. One must, therefore, learn to rely on the finger as a means of diagnosis. The fore- finger protected by a bandage or shield to prevent its being bitten by the child, should be passed to the back of the throat, where one should feel for the tonsil. Having felt the tonsil, and keeping the finger well against the posterior wall and laterally turning the finger upward, it will be found to pass behind the posterior pillar of the fauces and into the naso-pharynx without any difficulty. If the finger is kept in the median line while attempting to reach the naso-pharynx, it will impinge upon the uvula and soft palate and press these against the pharyngeal wall, thereby shut- ting off the mouth from the naso-pharynx, and it will be almost impos- sible to make the examination. The feeling of a soft, spongy, slippery mass more or less completely filling the naso-pharynx renders the diagnosis sure. Differential Diagnosis.—There is hardly any disease of childhood that could be mistaken for adenoids. Post-nasal polypi and fibroids occupying a similar position are in children extremely rare. Sarcoma may occur, but the larger size, rapidity of growth, its greater vascularity, and the involve- ment of neighboring fossas are sufficient for a diagnosis. Prognosis.—In more than half the cases, children suffering from adenoids will be relieved of those symptoms when atrophy at puberty takes place; but in the mean time, such inroads upon the health, hearing, voice, and mental faculties may have taken place that these cannot be overcome in after-life. It is advisable, therefore, in all cases to have the lymphoid tissue removed iis soon as it is manifest by the foregoing symptoms. In a certain propor- tion of cases when they are removed they may return, especially in those cases where the removal has not been complete, and in those children who bave a natural tendency to enlargement of the lymphoid tissues in other portions of the body. 240 DISEASES OF THE DIGESTIVE SYSTEM. Treatment.—In slight cases where the obstruction to respiration is not complete and where the other symptoms are slight in degree, the admin- istration of syrup of the iodide of iron in large doses and of cod-liver oil will oftentimes suffice to tide the patient over till the time of puberty. But in severe cases, these drugs will be found to be of little service, and the only treatment that is to be considered is operative. The number of instru- ments devised for this purpose is very great, and of these that which it is safest for the general practitioner to use is Gottstein's curette. The patient should be etherized or chloroformed with the head low, the curette passed behind the soft palate, and the whole naso-pharynx thoroughly curetted, especial care being taken to examine Rosenmfiller's fossae and to remove from them any of the lymphoid tissue that may be found there. The patient should be kept in the house, preferably in bed, for two or three days subsequent to the operation, and at the end of that time, the naso-pharynx carefully washed out with some alkaline cleansing solution, as Dobell's or Seiler's. In older children who have been suffering from this disease for a long time, the mouth breathing may be found to persist and the voice have the same nasal twang that it had before; both of these are the result of habit, the former may be overcome by tying up the chin at night and placing a handkerchief or other pad across the mouth so that the child will be forced to breathe through the nose. As regards the voice, that will need careful and systematic training on the part of the parents and teachers with whom the child comes in contact, in order to overcome the disagreeable twang. ACUTE TONSILLITIS. {Lacunar Tonsillitis, Follicular Tonsillitis, and Amygdalitis.) An acute non-suppurative inflammation of the parenchyma of the tonsil. Morbid Anatomy.—The tonsil is swollen, the surface reddened and dotted over with yellowish-white specks the size of a pin's head or larger, these pro- ject from the mouths of the lacunae; they may run together and form a mem- brane which can usually be readily removed. The surface of the soft palate is reddened but slightly swollen, the uvula elongated and oftentimes oede- matous, curved upon itself laterally and touching one or the other of the enlarged tonsils. Microscopically, we find an increase in the lymphoid cells of the tonsil, and the cells exhibiting karyokinetic figures. There is very little increase in the connective tissue, unless the tonsil is already the seat of a chronic inflammation. The exudation filling up the crypts consists of broken-down epithelial cells, which have undergone fatty and glandular degeneration, and masses of micrococci. The latter consist principally of streptococci, occasionally of staphylococci, and in about twenty per cent, of the cases so-called pseudo-diphtheritic bacilli. The exact relation that these germs have to the production of the disease has not yet been determined. Sendziak has made some very interesting experiments in those cases where the pseudo-diphtheritic bacilli have been found. He inoculated guinea- pigs not only with the mass from the crypts, but also with pure cultures of i ACUTE TONSILLITIS. 241 the pseudo-diphtheritic bacilli, and in no instance did he get any reaction following such injections. Etiology.—The disease occurs most frequently between the ages of ten and thirty. There is a hereditary predisposition to it in many cases. Ex- posure to wet and cold, especially getting the feet wet, is an exciting cause, but usually careful inquiry will find that a predisposing cause is a run- down condition of the system. It not infrequently occurs epidemically, and it is more common in this country in the spring and fall months. The relation of tonsillitis to rheumatism is a much discussed question. Clinically, it is very frequent to find a rheumatic history, and not uncom- mon to find a case of rheumatism preceded by an attack of acute tonsillitis. The disease is more common in those who live in insanitary surroundings. The disease is sometimes infectious, and when it is so, both tonsils are usually equally involved. As an evidence of its infective character, one sees it occasionally in persons who are tending cases of scarlet fever and measles, and also following operations performed upon the nose or mouth. Most writers believe that the disease may at times be contagious, for it is not infrequent to find in a family of children one after another afflicted with this disease. One attack predisposes to another, and it is rare for a person to have one attack without having another. Patients with chroni- cally enlarged tonsils are also especially prone to the disease. Symptoms.—The disease is frequently ushered in by a rigor or a chill, the temperature rapidly rising to 103° to 105°, and the pulse is accelerated. There are headache, pain in the back and limbs, a pricking sensation in the throat; the enlarged tonsil, acting as a sort of irritation, causes a constant desire to swallow, but on account of the great pain there is a tendency to restrain this act as much as possible. During the act of swallowing pain frequently radiates to the ear. The lymphatic glands at the angle of the jaw are more or less enlarged. The tongue is coated, the breath very offensive, and speech thick. The bowels are usually constipated; the urine scanty and high-colored and may contain a trace of albumin. On exami- nation of the throat, the appearances described in the pathology will be seen. The disease lasts from three to six days usually, but may be pro- longed as long as two weeks—the gland usually remaining slightly enlarged for a somewhat longer period. Differential Diagnosis.—About the only disease which can be mistaken for this would be diphtheria. For the differential diagnosis between ton- sillitis and diphtheria, see "Diphtheria." Prognosis.—The prognosis in acute tonsillitis is invariably good. The disease, if occurring frequently, may leave a chronically enlarged tonsil, and one must invariably bear in mind the possibility of the attack being followed by rheumatism. Treatment.—If at the first symptom of the disease a few doses of tinc- ture of aconite be given, it may cut short the disease, but one does not usu- ally see a case sufficiently early to make the employment of this remedy effective. Where a history of rheumatism is found, either in the patient or in his family, an anti-rheumatic treatment will in most cases be found to give relief quickest. Salol given in doses of ten or fifteen grains, admin- istered in milk or a mucilaginous drink every two hours until the ears 242 DISEASES OF THE DIGESTIVE SYSTEM. begin to ring, is usually most efficacious. Some prefer salicylate of soda, others guaiacum. The latter is usually not well borne by the stomach, but those who can take the drug highly praise its action. The aching and the pains are best controlled by phenacetin. On account of the constipa- tion present in this disease, it is well to administer at the beginning ami at regular intervals throughout the disease doses of calomel or blue mass. Tinctura ferri chloridi, in five to twenty minim doses well diluted with water, often acts well as an astringent. Gargles are not usually very service- able in this disease. The act of gargling is extremely painful, and the fluid only reaches a small portion of the surface of the tonsil and does not usually benefit the patient very much. Painting of the tonsils with nitrate of sil- ver, while it may be of service in some cases, has in many cases seemed to me to cause the acute tonsillitis to change into or to be complicated by a peritonsillar abscess. The diet should be fluid and nutritious; milk will generally be found to be most acceptable. Should the tonsils be very large so as to prevent res- piration, they should be excised, but the excision of an inflamed tonsil is not to be advocated under any other circumstances. PERITONSILLAR ABSCESS. {Quinsy.) An inflammation of the connective tissue external to the tonsil. Morbid Anatomy.—There is a suppurative inflammation in the loose areolar tissue surrounding the tonsil. On account of the dense tissue at the lower anterior portion of the tonsil, the pus seldom burrows down along the side of the pharynx, but rather extends upward between the pillars of the fauces; it may burrow down along the posterior pillar of the fauces. Etiology.—All the causes of acute tonsillitis may be causes of periton- sillar abscess; but usually where it is infectious, there will fee found to be a more severe degree of infection. A person who has once had a periton- sillar abscess will seldom have merely an acute tonsillitis follow, but it will almost always be another attack of peritonsillar abscess. It not infre- quently results from a second infection, or an exposure to cold or wet on the part of the patient, not yet fully recovered from an attack of acute tonsillitis. Symptoms.—The symptoms of this disease are the same as those of acute tonsillitis, but of a more severe character. Rigors or chills are apt to recur while the pus is forming. The inability to swallow food is more marked, so that the patient will frequently abstain from taking any nour- ishment by mouth for three or four days, and even longer. The pain in the ear on the affected side is more constant and more severe than it is in acute tonsillitis. In attempting to examine the throat, it is found that the patient is unable to open the mouth sufficiently to allow of a very thorough examination. We may see on one side of the throat a large bright-red mass sparsely covered with mucus, with a bulging forward of the soft pal- ate on that side. If the abscess is about to open, there will be found at such part of the soft palate an extra prominence, with a deeper red or bluish tinge to the surface. In those cases where the abscess tends to spread down CHRONIC TONSILLITIS. 243 in the posterior pillar of the fauces, the finger alone will detect the swelling and fluctuation. It is easy to be mistaken in the sense of fluctuation given to the finger, for the tissue is so loose that an extensive oedema will often- times give one the sensation of fluctuation. Differential Diagnosis.—This disease is not likely to be mistaken for any other disease, unless it may be retropharyngeal abscess. Examination' of the pharynx with the finger ought to differentiate between these two. Prognosis.—The prognosis in this disease is somewhat more grave than that of acute tonsillitis, both on account of the greater interference with deglutition and respiration, and on account of the danger of the sudden rupture of the abscess with the patient in the reclining position and the en- trance of the pus into the larynx. A complication to be greatly feared is oedematous laryngitis. Treatment.—In addition to the treatment advised in acute laryn- gitis, we should, as soon as we decide that the case is one of peritonsillar abscess, make a free incision into the abscess at its most prominent point and evactuate the pus. Should the pus not as yet have formed, the inci- sion will relieve the tension, reduce the swelling, and form a channel through which the pus when formed can find its way to the surface more quickly than if left to itself to burrow out. To make an incision, wind a bistoury with cotton or gauze, so that only a cutting edge one-half inch from the point is left free. Plunge it straight antero-posteriorly one-quarter of an inch from the free margin of the soft palate, cutting vertically or slightly toward the median line, but never externally. CHRONIC TONSILLITIS. {Hypertrophy of the Tonsil.) Morbid Anatomy.—There is an increase in all the tissues of the tonsil, but more especially in increase in the number of lymphoid cells. In young children and in tonsils of a soft consistence, the connective tissue is still in a developmental stage and not so firm as in older people, or hypertrophy of long standing. The crypts are deepened and widened, while their mouths are readily visible as large depressions in the surface of the tonsil. These depressions are frequently filled with a yellowish-white secretion of a peculiar and foul-smelling odor. Etiology.—Chronic tonsillitis often follows repeated attacks of the acute, but in children there may be no history of an acute attack. It is most common between the ages of three and five. It may be hereditary, and is more frequent in families having a tubercular, rheumatic, or syphilitic history. It frequently follows diphtheria, measles, and scarlet fever. It is often associated with hypertrophy of the pharyngeal tonsil, and like the latter there is a tendency to atrophy after the fifteenth year. Symptoms.—The patient is frequently subjected to attacks of acute ton- sillitis; mouth breathing, snoring at night, the sleep restless and uurefresh- ing, difficulty in respiration, and on account of these and the poorly oxyge- nated blood, the general health of the patient is often markedly impaired. 244 DISEASES OF THE DIGESTIVE SYSTEM. It is often difficult for these patients to swallow, and there is a feeling as of a lump in the throat. The voice is thick and muffled, sounding as if the mouth were half filled with some substance. The breath is fetid, and the inspiration of air, which must be contaminated by the decomposing sub- stances coming from these crypts, must affect the general health. The dyspnoea produced by the enlarged tonsils, causing the extraordi- nary muscles of respiration to act, is a frequent cause of pigeon-breasted- ness in these children. The cervical lymphatic glands are usually enlarged. On examination, the appearances described in the pathology are observed. The tonsils may be enlarged to such an extent as to meet in the median line. Differential Diagnosis.—'The only disease likely to be mistaken for hyper- trophied tonsil is a malignant disease, and this in children is rare. Malig- nant growths of the tonsils begin on one side, grow rapidly, are pain- ful, bright-red in color, and in doubtful cases examination of a portion of the excised growth will be sufficient to determine between benign and ma- lignant enlargement of the tonsil. Prognosis.—As in adenoids, the enlarged tonsils may atrophy, yet the damage produced before they do so is so great and the operation of their removal so simple that it is not advisable to expose the patient to all the dangers of retaining enlarged tonsils. Undoubtedly there is grave liability in these patients, owing to the excellent channel that an enlarged tonsil affords for the introduction of germs, to contract the infectious diseases, as diphtheria, measles, and scarlet fever. If removed, the tonsils may return. One frequently hears the mother say that one child had his tonsils removed, and the symptoms were not relieved. In such cases, overlooked adenoids were still responsible for the symptoms. Treatment.—In slight enlargements of recent standing astringent sprays and gargles and the internal administration of syr. ferri iodi and cod-liver oil may be sufficient to counteract the hypertrophy. But in long-standing cases excision is the only treatment to be considered. This is best done by means of a Mathieu tonsillotome, the patient having first been anaesthe- tized, unless he is of such age as to be able to stand the pain of having the second one removed. The hemorrhage that follows the operation is usually slight where this instrument is used. CATARRHAL PHARYNGITIS. This is an inflammation of the mucous membrane of the tonsils, uvula, soft palate and pharynx. It may be acute or chronic, and may affect all or only portions of the pharynx. Morbid Anatomy.—The morbid changes in the mucous membrane are the same as in catarrhal laryngitis and stomatitis. The uvula is enlarged, and the calibre of the pharynx is lessened. In chronic catarrhal pharyngitis the mucous membrane is either generally thickened and indurated, or the thickening occurs in irregular patches. The uvula is relaxed, and the af- fected parts are covered with a viscid mucus of a slightly offensive odor. The lymphatics are enlarged, especially at the back part of the pharynx, CATARRHAL PHARYNGITIS. 245 and small round nodules (often aggregated into masses of considerable size) present the appearance called "follicular pharyngitis." The escape of secre- tions from the glands being prevented, the latter dilate and form cysts whose contents undergo cheesy degeneration, or, after forming vesicles, ul- cerate. The cheesy masses in the cysts may, after a time, become calca- reous, or undergo purulent change. Follicular pharyngitis may extend upward and involve the posterior nares, or downward and involve the larynx. Etiology.—The acute form occurs most frequently in children and in young adults. There seems to be a predisposition in some persons to this affection. One attack predisposes to others. The causes which predispose to quinsy induce acute pharyngitis. Chronic follicular pharyngitis may be produced by prolonged use of the voice in public speaking or singing, or by the excessive use of tobacco or of spirituous liquors. Weak, scrofulous persons, and those with chronic thoracic disease are frequently affected with it. Its chief cause is repeated acute attacks. Symptoms.—Slight fever may usher in an attack of acute pharyngitis, or precede the development of its local symptoms. The throat first becomes dry and redder than normal, and movement of the parts produces pain in the direction of the Eustachian tubes, so that swallowing and speaking be- come painful. The elongated uvula may induce violent fits of coughing. The local symptoms are very severe ; there will be more or less regurgita- tion of food through the nose. If particles of food do not readily pass into the oesophagus they may enter the larynx and cause severe fits of coughing. k In these severe cases there is a nasal twang to the voice, and any movement of the throat, tongue, or mouth is carefully avoided on account of the pain it produces. If the inflammation invades the Eustachian tube, deafness may result, and not infrequently the tympanum is perforated by the pus which collects in the middle ear. The extension is more often forward, so that the mucous membrane of the tongue and mouth presents the same condition as that of the pharynx. These symptoms may gradually subside, after a few days, and the viscid secretion disappear from the tongue, mouth and pharynx. If it becomes chronic, the voice becomes hoarse, and there is a stridulous cough accompanied by a thick, tough mucous expectoration, often containing small firm, yellow masses. There is constant irritation of the throat, which is variously described as dry, tick- ling or tingling, and the secretion may be so much diminished that slight hemorrhage may occur from the membrane when pressed upon. All these symptoms are most marked in the morning. The symptoms in a long standing case may lead to anxiety on account of the supposed existence of pulmonary phthisis. These are all aggravated by " catching cold," atmos- pheric changes, and the prolonged use of the voice. Differential Diagnosis.—Follicular pharyngitis may be mistaken for pul- monary disease, and the early stage of mild chronic catarrh often excites suspicion of syphilis. In the former case an exploration of the chest and an examination of the throat will at once decide, while the presence or ab- sence of the constitutional signs of syphilitic infection will establish the diagnosis in the latter instance. 246 DISEASES OF THE DIGESTIVE SYSTEM. Prognosis.—Acute catarrhal pharyngitis is a very mild disease, subsiding completely in most cases within one week from its onset, while chronic phar- ingitis is the most persistent of all catarrhal affections. Treatment.—In acute pharyngitis, ice-cold carbonated water affords the greatest relief during the first twenty four hours. The throat and mouth should be frequently sprayed with a solution of alum, tannin, or sulphate of zinc, and at the same time the wet pack should be applied to the throat either hot or cold, but they should not be alternated. In chronic pharyn- gitis, the first thing to be done is to remove the cause and live an out- door life. Spraying the parts two or three times a day with the astringent just named, or a mild solution of nitrate of silver, will generally afford temporary relief. In some cases capsicum or guiacum may be advan- tageously combined with the astringents, and in obstinate cases the local use of iodine or a twenty per cent, solution of carbolic acid may be resorted to. In chronic (follicular) pharyngitis a nutritious diet is especially im- portant. German physicians recommend very highly the use of mineral waters, but alkaline gargles are as effective as a residence at some "spring." MEMBRANOUS PHARYNGITIS. Under this head are included both croupous and diphtheritic inflamma- tions of the pharynx. Croupous inflammation may be primary, but diph- theritic inflammation is always secondary. This form of pharyngitis is considered in the history of membranous laryngitis and diphtheria. RETRO-PHARYNGEAL ABSCESS. Suppuration behind the pharynx, in the areolar tissue between it and the vertebrae, is known as retro-pharyngeal abscess. Morbid Anatomy.—This is a cellulitis, and its morbid anatomy is the same as that of cellulitis terminating in an abscess elsewhere. It belongs properly to the province of surgery. Etiology.—Retro-pharyngeal abscess occurs more frequently in children than in adults. It is developed during the progress of caries of the cervical vertebrae. It is rarely if ever due to the extension of inflammation from the pharynx. A strumous diathesis predisposes to it. Sometimes it appears late in pyaemia, septicaemia, typhoid, typhus, scarlet fever and measles. Now and then it occurs without any obvious cause. Symptoms.—The first symptom is dysphagia. With this there is stiffness of the neck, slight difficulty in articulation, and a change in the tone of voice, which becomes nasal in character. On examining the pharynx its calibre will be found diminished by a bulging from behind and perhaps a little to one side ; the pharyngeal mucous membrane is redder than normal, and there may be a slight swelling about the angle of the jaw. The head is thrown backward, and any attempt at flexion causes dyspnoea ; the jaws seem to be partially locked. There is regurgitation of food through the nose. In young children there may be snuffling, choking, coughing and great dyspnoea, with a certain hoarse tone to the voice. The mouth is filled with a mucous secretion. MEMBRANOUS PHARYNGITIS.—RETRO-PHARYNGEAL ABSCESS. 24? As the abscess increases in size the tumor may be seen nearly filling the space behind the soft palate. This swelling is soft, elastic and fluctuating, sometimes rupturing when pressed upon, and discharging an offensive pus. If it opens spontaneously the pus is vomited, swal- lowed, discharged through the nose, or is inspired into the trachea and may cause suffocation. Again, the abscess filling the pharynx may press on the rima glottidis and epiglottis and cause cedema glottidis. In rare instances the pus makes its way around to the opposite wall of tne pharynx, and then breaks into the oesophagus or trachea, or burrows into the pleural cavity or even the pericardium. It may burrow between the tracheal muscles and appear at the anterior part of the neck. Differential Diagnosis.—When fully developed, a careful examination of the pharynx will detect at once the existence of a retro-pharyngeal abscess. Prognosis.—The prognosis is bad whenever caries of the spine has caused the abscess. The complications which may cause death are cedema glot- tidis, pleurisy, pneumonia, and pericarditis. Death may result from suffo- cation from pressure. Treatment.—Open the abscess early, and never wait for its spontaneous rupture. The position of the child when the bistoury is used should be Buch that the escape of pus through the mouth is facilitated. 248 DISEASES OF THE DIGESTIVE SYSTEM. DISEASES OF THE OESOPHAGUS. The following diseases of the oesophagus will be considered : I. Inflammation, either catarrhal or membranous, including Stricture of the (Esophagus ; and, II. (Esophageal Cancer. OESOPHAGITIS. Oesophagitis, or inflammatory dysphagia, is a catarrhal inflammation of the mucous membrane of the whole or a part of the oesophagus. It is an exceedingly rare disease. Morbid Anatomy.—In the acute variety the mucous membrane is red, swollen, softened and covered with a layer of mucus containing epithelium and pus. In the chronic variety the mucous surface is of a dull pink or slaty blue color. The sub-mucous tissue is thickened, and a thick viscid mucus or pus covers its surface. It may cause dilatation of the oesopha- gus, which may affect the whole tube uniformly or form a pouch at its lower portion, or it may give rise to a hernial protrusion of the mucous mem- brane through the muscular coat. In all cases of oesophageal dilatation due to chronic catarrh, there is more or less thickening of the oesophageal walls. In some eases the thickening may diminish the calibre of the tube. Ulcer- ation of the mucous membrane at the seat of the catarrh sometimes occurs. The ulcer may be superficial, or extend through the walls of the tube. Membranous Inflammation of the oesophagus may be either croupous or diphtheritic. In either case the morbid changes are the same as in croup- ous or diphtheritic inflammation of other mucous surfaces. Etiology.—Acute oesophagitis has its most common cause in the irritation produced by acrid fluids or solids in their passage to the stomach. Irritat- ing drugs and corrosive poisons may excite it. Too frequent introduction of instruments into the stomach may cause it, and it may arise from the excessive use of alcohol. Extension of inflammation from the parts above or below it often induces acute oesophagitis. Chronic oesophageal catarrh may occur as part of a similar process affecting the whole alimentary tract It may develop as the result of a strumous or phthisical diathesis, or follow an acute attack. Membranous oesophagitis is always secondary and results from, or occurs with similar processes in the respiratory or other portions of the digestive tract. It also may appear after some of the eruptive fevers, cholera, pyaemia and septicaemia. Symptoms.—Varying with the intensity of the inflammation, an aching or severe burning pain is felt at the back, between the shoulders, or deep behind the sternum. Even the ingestion of fluids causes dysphagia, the pain being greatest as the fluids pass through the upper portion of the oesophagus. More or less febrile excitement and great depression and anxi- ety accompany the disease, and throughout its course the thirst is torment- ing. In severe cases there are paroxysms of coughing, and perhaps slight dyspnoea with hoarseness. Vomiting sometimes follows attempts at swal- lowing. All these symptoms gradually increase in severity. If extensive OESOPHAGITIS. 249 ulceration is present, sudden rupture of the oesophagus may occur during the act of deglutition. In chronic oesophagitis there is dysphagia and pain only on swallowing solids. If ulcers exist, there may be vomiting of viscid mucus tinged with blood, accompanied by the symptoms of oesophageal stricture. Stricture of the oesophagus is accompanied by gradually increasing dysphagia, emaciation and debility, which finally terminate in death from inanition. The most frequent seat of stricture of the oesophagus is at its cardiac extremity. It may be caused by structural changes in its wall, as in oesophagitis with or without ulceration, and cancer, or by compression from mediastinal and other tumors. As oesophageal strictures develop slowly, for a long time the only symptom is slight difficulty in swallowing solids, the patient usually referring the difficulty to a point behind the manubrium sterni. As the constric- tion increases there is difficulty in swallowing liquids. Food and drink collect in the oesopha- gus, and after a longer or shorter delay are re- gurgitated with the saliva through the mouth and nose. With oesophageal stricture there are usually painful eructations. Sometimes the pain is Ian- fig. m>. cinating in character, shooting from the region of Di^ran? showing stricture of the » ' ° ° (Esophagus near cardiac extrem- the oesophagus back to the spinal column. The ily- introduction of a bougie will determine the seat, £ S^K^S' extent, and form of the stricture.] % ^t'of the stricture. Uniform dilatation cannot be recognized dur- ing life. When dilatation is partial, or when pouches exist, there may be vomiting of undigested offensive food some hours after eating. In all cases of alteration in the calibre of the oesophagus, the oesophageal bougie will determine the amount of narrowing and the locality of the pouches. Membranous inflammations of the oesophagus cannot readily be determined during life. A portion of membrane may be vomited, but it cannot be determined whether it comes from the oesophagus, or has been swallowed and regurgitated. Differential Diagnosis.—This disease may be mistaken for cancer of the oesophagus; the diagnostic points will be considered in the history of oesophageal cancer. At the onset it may also be mistaken for hydrophobia, but the diagnosis is soon established by the development of the character- istic nervous phenomena of the latter disease. Prognosis.—The immediate prognosis in acute oesophagitis caused by chemicals or mechanical irritants depends more on the changes which have occurred around the larynx and in the stomach, than upon the oesophagitis. The prognosis in croupous and diphtheritic inflammations of the oesophagus is also determined by the conditions of the primary disease. In chronic oesophageal catarrh without stricture the prognosis is good. Treatment.—In acute oesophagitis, if the inflammation has been excited by foreign bodies lodged in the oesophagus, they must at once be removed; 1 The treatment of stricture of the oesophagus belongs to surgery. 250 DISEASES OF THE DIGESTIVE SYSTEM. if corrosive chemicals have been swallowed, the proper antidote must be ad- ministered. In severe cases, all movement of the parts must be prevented. Ice in the mouth is grateful and does no harm. Nutrient enemata may be given, and, if the pain is severe, hypodermics of morphine must be given in sufficient quantities to afford relief. Hot anodyne fomentations applied locally are usually of service. In chronic oesophageal catarrh, if ulcers ex- ist, spray the parts with astringent fluids, such as a solution of nitrate of silver. Surgery directs that if starvation seems imminent a gastric fistula should be made. In oesophageal stricture, bougies must be daily intro- duced for a long time, with the hope of dilating the stricture. No treat- ment is required in oesophageal dilatation. CANCER OF THE (ESOPHAGUS. The most frequent variety of oesophageal cancer is epithelioma, but scirrhus and medullary cancer are not unknown. It occupies the upper and middle third of the oesophagus more often than the cardiac portion ; in the former, it is associated with pharyngeal and laryngeal cancer, and in the latter with cancer of the cardiac extremity of the stomach. Morbid Anatomy.—Epithelioma begins in the mucous tissue, and pursues the same course as cancer of the tongue. The ulceration may be limited to a circular patch an inch in diameter, or may involve the whole circum- ference of the oesophagus. The growth after a time invades all the tissues of the oesophagus, and causes stricture of its calibre. Above the stricture there is either uniform dilatation or a pouch, sometimes as large as an orange. If the cancerous mass involves the entire oesophageal wall, it may press upon and destroy one or both pneumogastrics, and lead to the devel- opment of pneumonia or pulmonary gangrene. If the oesophagus is rupt- ured, openings may be made into the trachea, through the diaphragm into the peritoneal cavity, or into the posterior mediastinum. Cancer has some- times ulcerated into the aorta, pulmonary artery, and even into the right subclavian artery. Etiology.—Two-thirds of the cases of cancer of the oesophagus occur in males between the ages of forty and sixty. It is generally primary; it may be secondary to cancer of the mouth, pharynx, mediastinum, or stomach. Symptoms.—The first thing noticed in cancer of the oesophagus is difficult deglutition ; soon well-marked dysphagia occurs. Pain is present early, and may be dull, burning, or lancinating in character ; it is located about the centre of the sternum, in the throat, or in the interscapular space. It varies greatly in kind and degree, but it is greatly aggravated when food reaches that portion of the oesophagus which is the seat of the cancer. As the stricture grows narrower, flatulence, regurgitation of food and vomiting, with steadily increasing emaciation, become prominent symptoms, and a well-marked cachexia is developed. Cough, dyspnoea, and hoarseness some- times result from pressure of the cancerous tumor. As the disease advances, the pain becomes more constant, the cachexia is better marked, and hem- CANCER OF THE OESOPHAGUS. 251 orrhages are frequent; the bloody fluid vomited often contains shreddy masses which contain cancer elements and show the character of the dis- ease. The neighboring lymphatic glands may also be implicated, and, by pressure on a main bronchus, cause feeble respiration in the lung to which the bronchus is distributed. If rupture occurs, it is followed by a sudden sharp pain in the chest, fainting, and coldness of the extremities, followed almost immediately by death. Differential Diagnosis.—Oesophageal cancer may be mistaken for stricture of ihe oesophagus from chronic catarrhal inflammation. In cancer, pain is constant and greatly aggravated by taking food, while in non-cancerous oesophageal stricture pain is absent, or is only present on swallowing. The glands about the neck are early involved in cancer, but are normal with chronic catarrh. Chronic pulmonary disease is rarely absent when oeso- phageal cancer is present, but is never induced by non-malignant stricture. Hemorrhage is frequent in cancer, and does not often occur with stricture from chronic catarrh. The bougie may bring up shreddy masses, with evi- dences of cancer in the one case, but merely meets with obstruction in the other. Prognosis.—This is always a fatal disease. Its average duration is one year, but death may occur in a few weeks. The prognosis as to time varies with the presence or absence of complications. Death may result from any of the complications, from hemorrhage or septicaemia. Treatment.—Early in cancer let the food be finely chopped and taken in a semi-fluid state; later, it should be entirely fluid, and when the patient cannot swallow, nutrient enemata must be given. The diet in all cases must be nourishing in the highest possible degree, and stimulants can usu- ally be given with benefit. When the pain is intense morphia per rectum or hypodermically should be administered in doses sufficient to relieve it. Bougies should be used with great care ; early, they should only be used to locate and diagnosticate the disease ; later, tubes must only be used for the purpose of introducing food into the stomach, as fatal hemorrhage or rupt- ure has followed their use. The subject of gastrotomy comes within the domain of surgery. 252 DISEASES OF THE DIGESTIVE SYSTEM. DISEASES OF THE STOMACH. I. Inflammations of its mucous membrane and its submucous or areolm tissue. a. Acute or Toxic Gastritis. b. Sub-acute Gastritis, or Acute Gastric Catarrh. c. Chronic Gastritis, or Chronic Gastric Catarrh. d. Phlegmonous Gastritis. II. Dyspepsia. IV. Neuroses or Gastralgia. III. Cancer and Ulcer. V. Hwmatemesis. VI. Dilatation. ACUTE GASTRITIS. Acute or toxic gastritis is a general inflammation of the mucous and sub- mucous tissue of the stomach. It is of rare occurrence, unless the result of the introduction into the stomach of irritating poisons. Morbid Anatomy.—On opening a stomach which is the seat of toxic gas- tritis'a thick layer of tough, viscid mucus will be found spread over ita mucous surface. Beneath this there will be found an intense redness of the membrane, which is most marked along the edge of the rugae, near the car- diac orifice. The mucous and submucous tissues will be soft and oedema- tous. In some rare instances the whole or a portion of the mucous mem- brane will be found to present the appearance of a detached brown or black slough ; it may be entirely eroded. Fibro-plastic exudation may cause com- plete occlusion of its cardiac or pyloric orifices. When the muscular tissue is involved it becomes soft, easily torn, often gelatinous. In severe cases perforations may exist. Etiology.—Acute gastritis is almost always caused by the entrance into the stomach of irritant poisons, such as sulphuric, nitric, and oxalic acids, arsenic, the chloride of zinc, and large quantities of concentrated alcohol. Mechanical irritation, such as results from the introduction into the stomach of knives, pins, false teeth, etc., may produce a local acute gas- tritis. Introduction into the stomach of boiling water, hot lead, or steam may cause a most intense gastric inflammation, with extensive sloughing of its mucous surface. Symptoms.—Soon after the introduction of corrosive substances into the stomach, there will be a dull, uneasy feeling, sometimes one of warmth, over the epigastrium. This is rapidly followed by an intense burning pain shooting through to the back. The epigastric region becomes extremely ten- der. With, or preceding these symptoms, there is nausea, and vomiting of tenacious mucus ; the vomiting is very distressing; the ejected mucus often contains blood, and, at first, portions or traces of the substance which has caused the gastritis. As the pain becomes more severe the vomiting is more distressing ; there is intense thirst, and frequent spasms of the abdominal muscles. The temperature rapidly rises, sometimes to 105° F.; the pulse SUB-ACUTE GASTRITIS. reaches 120 or 140 per minute and is feeble and irregular. If the oesophagus is implicated, there is dysphagia. The urine becomes scanty ana" high colored, and is sometimes suppressed. These violent symptoms soon give place to a condition of general prostration, in which there is almost con stant hiccough. The surface becomes cold and clammy, the radial puis* grows feeble and finally imperceptible, while the respirations are hurried, short and irregular, the mind remaining clear to the last. There are cases on record of poisoning by chloride of zinc and sulphuric acid, in which there was no pain in the epigastrium during the whole course of the disease. Differential Diagnosis.—The diagnosis is not difficult. The history of its cause and the character of the vomiting establish it. Prognosis.—The prognosis depends upon the cause. The more intense the pain, the more extensive the gastric inflammation. Death may occur in a few hours, or it may be delayed two or three weeks. Acute gastritis may be complicated by analogous conditions of the mouth, pharynx, or oesophagus, by enteritis, laryngitis, or cedema glottidis, and as sequelae there may remain constrictions at the cardiac or pyloric orifices. Death may result directly from the shock of the gastritis, from the constitutional effects of the poison which produces it, or from resulting peritonitis. Treatment.—The first thing is to administer the proper antidote to the poison which has caused the gastritis, and thoroughly wash out the stom- ach, after which the gastritis should be treated as a local inflammation. Four or five leeches may be applied over the epigastrium, followed by warm poul- tices or fomentations. Some prefer the application of ice to the epigas- trium. Unless contra-indicated by the chemical constitution of the poison, the intense pain should be relieved by hypodermic injections of morphia. During the whole period the patient should be kept absolutely at rest in the horizontal position. SUB-ACUTE GASTRITIS. Sub-acute gastritis, or acute gastric catarrh, is always a secondary affec- tion. Morbid Anatomy.—The parts principally involved in this form of gas- tritis are the ridges between the depressions, the vessels which lie in imme- diate proximity to them, and the apertures of the tubules. The mucous membrane is mottled by red spots scattered over it in irregular patches; sometimes there are extensive ecchymoses and blood extravasations. The gastric juice is much diminished in quantity, and being mixed with much mucus loses its acidity and to a great extent its digestive power. The sur- face of the mucous membrane is covered with abundant, tenacious mu- cus ; there is also a moderate production of pus cells on the surface of the mucous membrane. The gastric tubules become filled with granular mat- ter. Late in the disease the solitary and lenticular glands, especially about the pylorus, increase in size and stud the surface as small white specks. The inflammatory processes are superficial and do not involve the deeper tissue of the mucous membrane. Superficial sloughs are some- 254 DISEASES OF THE DIGESTIVE SYSTEM. times formed varying in size from a pea to that of a three-cent piece ; they rarely involve the submucous tissue. Its most prominent lesion is the coating of the gastric mucous surface with tenacious mucus. Etiology.—No period of life is exempt from this form of gastri- tis. It occurs most frequently under two conditions :—first,with acute alcoholismus; secondly, with those diseases in which there is extensive blood-poisoning, as in scarlet fever, small-pox, measles, typhoid and typhus fevers, diph- theria, pneumonia, pyaemia and septicaemia. It sometimes com- plicates pulmonary phthisis, and may follow the disappearance of gout, rheumatism, or affections of the joints. Symptoms. — Vomiting is its first and most prominent symp- E. Mucous coat. The gastric follicles are shown filled tom. The matter Vomited COn- with granular detritus and covered with pus—O. . . , , F. Small vessels between the follicles, x 40. Sists of the Substances which have been taken into the stomach, mingled with a grayish, stringy mucus, and sometimes streaks of blood. When the vomiting is severe and prolonged, bright green, bitter fluid is often ejected. The fermentation which takes place in the fluid con- tained in the stomach sometimes develops gases which cause distention of the stomach and a prominence of the epigastrium. The patient has no desire for food, but constantly craves ice and cooling drinks. The thirst is intense. The smallest quantity of food taken into the stomach causes nausea and vomiting, which may be so severe as to induce extreme exhaustion or collapse. Accompanying the nausea and vomiting there is more or less pain at the epigastrium. This pain is sometimes intense, and shoots back- ward between the shoulders, but usually it is not severe unless firm pressure is made over the stomach. The tongue is coated with a yellow or ash-col- ored material, and becomes dry and red at the tip. The papillae are prom- inent. The breath has an offensive odor. Late in the disease, herpetic eruptions make their appearance about the lips and in the mouth. Often during its course there will be flashes of heat, with a burning sensation in the palms of the hands and the soles of the feet. The thermometer may indicate an axillary temperature of 103°, or even 105° F. The patient be- comes restless and irritable and often has attacks of syncope. In alcoholic cases the anorexia is absolute, and vomiting occurs mostly in the morning. Delirium tremens is often a complication. Its symptoms are always more or less varied by the diseases with which it occurs. In rare instances I have seen an icteric and sometimes a bronzed hue of the skin come on during a Fig. 51. A Vertical Section of the Stomach walls in Sub-acute Gastritis. A. Muscular fibres in longitudinal section. B. The same cut transversely. C. Submucous tissue, in which are seen at D, D. Blood-vessels enlarged and filled with blood. CHRONIC GASTRITIS. 255 prolonged attack of acute gastric catarrh. Diarrhoea is usually present, the stools having a very offensive odor. Obstinate constipation is rare. The urine is scanty and high colored, and in severe cases presents slight traces of albumen. Nitric acid gives a deep red color to it, or there is a copious deposit of lithates. Differential Diagnosis.—The diagnosis is easily made, and it is not likely to be confounded with any other affection, if its etiology and symptoms are carefully analyzed. Prognosis.—The prognosis is decided by the disease which it complicates. Unless associated with acute alcoholismus, it rarely becomes chronic. Its duration is from ten days to two or three weeks. It may be complicated by catarrhal conditions of the oral and pharyngeal mucous membranes, and in very rare instances by implication of the intestines (gastro-enteritis). It only causes death when it is extensive and complicates some grave acute general disease, as septicemia, pyaemia, typhoid or puerperal fever. Treatment.—The most important thing in the treatment of this affection is rest to the stomach. In mild cases, entire abstinence from food for twenty- four hours, and then peptonized milk, or milk with lime-water, in small quan- tities at stated intervals, is all that is required. In severe cases, and in all cases occurring in children, nourishment must be given per rectum as long as the gastric symptoms are urgent. One or two leeches applied over the epigastrium, followed by warm fomentations, usually afford marked relief. In adults, if the pain is so severe as to prevent sleep, or if there is great restlessness, small hypodermics of morphia may be administered. After the patient has passed twenty-four hours without vomiting, peptonized milk may be given in small quantities. In those cases in which vomiting is per- sistent, and there are symptoms of collapse, stimulants must be freely admin- istered by the rectum. None of the remedies which are so often employed for the relief of vomiting are serviceable in the treatment of this affection. During convalescence, if the stomach is in an atonic condition, mineral acids and the vegetable bitters will be found of service ; great care must be exer- cised in the diet during the whole period of convalescence. The improve- ment of the diet must be gradual, and those who have been spirit drinkers should be warned of their danger, and the use of stimulants prohibited. CHRONIC GASTRITIS. Chronic gastritis is known under the names of simple gastritis, chronic catarrh of the stomach, morbid sensibility of the stomach, and chronic in- flammatory dyspepsia. Morbid Anatomy.—The morbid appearances in chronic gastritis vary with its character and duration, and are usually best marked around the py- loric extremity of the stomach. Over all, or part of the mucous surface, there is a layer of gray mucus, varying in thickness and tenacity with the duration and character of the disease. On its removal the mucous mem- brane is seen studded with ecchymotic and pigmented spots, the result of small extravasations. In some cases the mucous tissue is oedematous and 25f. DISEASES OF THE DIGESTIVE SYSTEM. presents a well-marked granular appearance. The walls of the stomach ar« usually thickened and more or less indurated, especially about the pyloric orifice, which gives rise to more or less constriction, or "pyloric stenosis."' The thickened membrane is often "leathery" to the feel, and the indura- tion may be so great that it tear.j with difficulty and can be stripped off the submucous tissue. The submucous tissue may also be thickened and congested, the color varying from an inflammatory blush to a livid, al- most purple red. When the submucous tissue is involved, there is an infil- tration of cells into it; and upon their organization into new connective- tissue, and the subsequent contraction of this tissue, there will be more or less interference with the peristaltic motion of the stomach. Besides this there will be hypertrophy and distention of the gastric tubules, for their secretion is retained by the tissue-increase in the intertubular structure, which will cause them to stand out as small granulations in the atrophied tissue, presenting an appearance denominated "mammillation." This condi- tion may also be the result of hypertrophy of the glandular layer, which thus becoming too large for the basement muscular layer is corrugated and gives rise to another form of mammillation. It is only in rare instances that there is any mammillation about the cardia. In long-continued chronic catarrh of the stomach the muscular coat of the organ may become involved, and then the peristaltic movements will be still more impaired ; finally, the peritoneum may become thickened and adhesions take place between it and the adjacent parts. A microscopic examination of the gastric tubules in chronic gastritis will sometimes show that their epithelium has undergone granular degeneration, and in others there is a complete loss of epithelium, the tubules being filled with a granular detritus. Occasionally there will be found on the mucous membrane dirty white spots in irregular patches, which appear like de- pressions on the mucous surface. Under the microscope, there will be found in those spots some tubules completely filled with discrete fat spherules, and others whose epithelium has undergone fatty de- generation. If the tubules are constricted near their openings, cysts are formed from distention of the portion near the base by the secretion which cannot escape. In rare cases the fatty degeneration will in- volve the interstitial tissue as well. If hemorrhagic extravasation occurs into the gastric mucous membrane, the tubules will have their epithelium stained and their base blackened as a result of the sanguineous infiltration. Sometimes there is an increase in the intertubular lymphatic elements, with hyperplasia of tht nuclei in the sheath of the vessels. Fig. 5'-'. A. Vertical Section of Mucous Membrane of the Stomach, showing changes in the Tu- bules in Chronic Gastritis. A. Muscidaris mucosm. B. Smcdl blood-vessels around the follicles. C. Tubule with granular epithelium and fitted with granular detritus. D. Another tubule, in which the ejn/helium is lost—filled with fat globules. E. Gt (iimlar matter filling the follicles. F. A small cyst, formed by closing of themou/h of the follicle, wi/li proliferation of the epi- thelial wall, x 250. CHRONIC GASTRITIS. 257 In long-standing chronic gastritis there may be abrasions of the mu- cous surface and formation of ulcers (chiefly about the lesser curvature and the pylorus), circular in shape, varying in diameter from half an inch to an inch. These ulcers are very superficial, rarely extending beyond the mucous coat. They are pale in color, and their surface is covered with mucous cells, nuclei, and epithelium; between the ulcers'the rugae are con- gested. The intervening tissue is rarely normal. There may also be small follicular or punctate ulcerations, originating, it is supposed, in the enlarged solitary and lenticular glands. The base of these ulcers is infiltrated with lymph-cells and granular detritus ; they are never present except in the ad- vanced stage of chronic gastric catarrh. Chronic gastric catarrh may involve a large portion of the mucous surface of the stomach, and is gen- erally associated with a like condition of the intestinal mucous membrane. Waxy degeneration may be associated with these morbid changes, but in such cases other organs, as the liver and spleen, will have been primarily affected by the amyloid infiltration. The size of the stomach varies: some- times it is smaller than normal; at others it is dilated. Etiology.—Chronic gastric catarrh is essentially a secondary affection ; it is rarely the sequela of sub-acute, much less of acute, gastritis, unless the former has been caused by an abuse of alcoholic stimulants. In many persons there is an hereditary tendency, after middle life, to chronic gastric catarrh. The principal general cause of this affection is anaemia. The most common local cause is the daily use of alcoholic stimulants. Mechanical obstruction to the capillary circulation of the stomach, induc- ing continued passive hyperaemia (congestion) will cause it, and hence we find it associated with cirrhosis of the liver and other chronic hepatic affections where the blood is dammed back in the formative branches of the vena porta\ In the same way, valvular and other cardiac lesions, and pulmon- ary diseases, such as emphysema, chronic bronchitis, and phthisis, which offer an obstacle to the venous return, will induce chronic gastric catarrh. Pressure on the walls of the stomach by tumors produces first congestion, and then chronic catarrh. Degeneration of the capillaries—" arterio- capillaryfibrosis"—occurring in the cirrhotic form of Bright's disease, causes it, and it often accompanies ulcer and cancer of the stomach. Those causes which may be denominated recent are rapid ingestion of food, improper quality of food, or food which is known " to disagree with the stomach," and the sudden arrest of the digestive process after hearty meals. The prolonged use of arsenic, mercury, cubebs, and purgatives often causes it. Finally, scrofula, syphilis, and gout seem to predispose to it, and I am inclined to regard the chronic gastritis which is so often found associated with these diseases as the result of some degeneration of, or alteration in, the blood-vessels of the stomach. Symptoms.—The early symptoms of chronic gastric catarrh are chiefly those of indigestion. There is at first a sense of weight and fulness in the epigastrium, sometimes amounting to constriction, which comes on from naif an hour to an hour after meals. Later there is actual pain and heat iD the epigastrium (" heart-burn "). Pressure increases the pain and 258 DISEASES OF THE DIGESTIVE SYSTEM. causes it to shoot backward and upward toward the scapula1. Following, or with the advent of, these symptoms there is loss of appetite, first for solids such as meats; later there is complete anorexia. Nausea and eruc- tations accompany the anorexia ; the stomach, and often the intestines become distended with gas, but vomiting is not usually present unless pyloric stenosis exists. The most important of the dyspeptic symptoms are the acid risings after meals, and the vomiting or regurgitation of acid mucus in the morning, which may be regarded as characteristic, and with- out which the diagnosis is uncertain. It is this acid material belched up into the oesophagus that causes " heart-burn." If there is actual vomiting of food, traces of butyric acid are present, with the sarcince ventriculi, cuboid cells averaging 1-2500 inch in diameter, each being divided into four equal parts containing nuclei, usually heaped into large cubes. As the disease progresses, the feeling of malaise and un- easiness following meals changes to one of languor or ex- fig. 53. haustion, and there is a sensation of heat in the epigastrium; Sarcinw Venlri- , . , , ■ cuii. x 750. thirst becomes a prominent symptom, one person craving cold, another hot drinks. The thirst is greatest in the evening, but the taking of fluids is usually followed by a sense of weight in the epigastrium, and by acidity and flatulence. The appearance of the tongue varies : it may be normal, paler than normal, florid and " beefy," or may be covered with a white or brown coating. The general symptoms which accompany the anaemic condition which attends this disease are headache, vertigo, cardiac palpitation, a gradual loss of strength and emaciation. Constipation and hemorrhoids are usually present, and the stools are often coated with mucus. In the chronic gastric catarrh of phthisis, diarrhoea is present. In cases of long standing, the hair becomes harsh and loses its lustre or turns gray; the skin is dry, sallow, and shrivelled, sometimes covered with an eczematous eruption ; the nails are corrugated and exhibit a tendency to split, while in some there is premature caries of the teeth. Hypochondriasis, despondency, and irritability of temper are generally more or less marked. Haematemesis often occurs in that form of gastritis which accompanies cirrhosis of the liver, and the bleeding may for a time relieve the unpleasant gastric symptoms. Vomiting in the morning al- ways accompanies the gastritis of Bright's disease. The urine in chronic gastritis is cloudy, usually alkaline in reaction, depositing urates, phosphates and oxalates. Its specific gravity is highest at evening. The alkalinity is due either to imperfect gastric digestion or im- paired function of the liver and pancreas. The greater the mental depres- sion the more of earthy phosphates will be found in the urine. If hemorrhagic erosion exist in a stomach which is the seat of chronic catarrh, the pain in the epigastric region is constant, frequently shoot- ing back to the scapulae. Vomiting occurs not only in the morning, on rising and after meals, but also in the intervals. The vomited matter con- tains traces of blood, and bile mixed with mucus ; all of the gastric symp- toms are augmented in hemorrhagic erosion. Punctate or follicular vleet' CHRONIC GASTRITIS. 259 ation presents few, if any, symptoms differing from those of ordinary chronic catarrh. In most instances where a post-mortem has revealed this pathological state, there was vomiting of coffee-ground material during life. Differential Diagnosis.—Chronic catarrh of the stomach is to be differ- entiated from atonic dyspepsia, from cancer, and ulcer of the stomach. Atonic dyspepsia is associated with anaemic conditions dependent upon habits of life and an unhealthy occupation ; while chronic catarrh is asso- ciated with the immoderate use of alcoholic stimulants, or is secondary to chronic thoracic, renal, or hepatic disease. In atonic dyspepsia there is little or no pain or tenderness in the epigastric region, which is always present in chronic gastritis. In atonic dyspepsia the tongue does not present the coated appearance so constant in chronic gastritis, but is broad, pale, and flabby. In atonic dyspepsia there is loss of appetite, but never the complete anorexia and constant thirst which are present in chronic gastritis. Spices and stimulating ingesta often relieve the gastric symptoms of atonic dyspepsia, while in chronic gastritis they aggravate the gastric symptoms. The constitutional symptoms in atonic dyspepsia are slight, while in chronic gastritis they are marked and severe. The urine is altered in atonic dyspepsia only during the attack ; while it is cloudy and alkaline, and persistently deposits urates, oxalates, and phosphates in chronic gastritis. Nausea and vomiting are more apt to occur in chronic gastritis than in dyspepsia. In its earlier stages cancer presents no symptoms other than those of a chronic gastritis; later the vomiting and other evidences of obstruction will be persistent, and the vomited matters will more certainly be coffee- ground in character. Dilatation of the stomach is more frequent with cancer. The recognition of an abdominal tumor alone can render the diagnosis certain. The points in the differential diagnosis between chronic gastritis and ulcer of the stomach are given under the latter heading. Prognosis.—The duration of chronic gastric catarrh is variable ; it may last for months or years, and may terminate in ulcer or stenosis of the pyloric orifice. It is amenable to treatment except when associated with advanced hepatic, renal, or pulmonary diseases, or where stricture at the pyloric orifice exists. A not infrequent complication is disease of the suprarenal capsules, and the connection between the two diseases has by some been supposed to be a "sympathetic" one, but no rational explanation has yet been offered. Sub-acute gastric catarrh sometimes complicates chronic gastric catarrh and renders the prognosis unfavor- able. Gastro-enteritis is a very rare complication. Death may result from haematemesis or from stricture of the pylorus. The general fee- bleness which results from long-standing gastritis predisposes to acute disease. Treatment.—The most important thing to be accomplished in the treat- ment of chronic gastritis is the removal of its cause. Each case requires a special treatment suited to its special indications and to its complicating 260 DISEASES OF THE DIGESTIVE SYSTEM. causes. When alcohol is the cause, all stimulants must at once be pro- hibited, and the patient placed on a diet in which there are few fats or carbo-hydrates. The food should be taken slowly in small quantities, at shorter intervals than in health, and thoroughly masticated. I have found "underdone beef" and milk to be especially adapted to this class of cases. In catarrh induced by dram-drinking the best drug to allay morbid sensibility of the stomach and the morning sickness is opium, which also, by inducing sleep, relieves the nervous symptoms, which are always prominent. Strychnia and zinc in combination with min- eral acids have a wide reputation in this class of cases, acting favor- ably on both the nervous and digestive disturbances. The vegetable bitters as tonics are often serviceable when the craving for alcohol is excessive.1 Thorough washing of the stomach with an alkaline fluid used by the syphon tube is of great service in severe cases. In milder conditions the patient may drink a large glass of very hot alkaline water half an hour before eating. Such treatment is often combined with an exclusive meat diet. When there is marked anaemia, preparations of iron and pepsin may be given. When chronic catarrh is associated with cardiac disease, granules of digitaline, 1-50 of a grain each, may be given twice a day with advan- tage. When associated with pulmonary diseases, an out-of-door life in a' suitable climate not infrequently effects a cure. In phthisical gastritis, a form that is very obstinate, hydrocyanic acid with the alkaline carbonates combined with bismuth is often of service. If hepatic disease exists, the portal congestion may be relieved by leeches about the anus and an occasional brisk mercurial purge ; a course of mineral waters will in a large proportion of cases give temporary relief. The daily use of cold- water enemata will in these cases preclude the necessity of resorting to cathartics. Scrofulous subjects should be treated with iodine and cod-liver oil. The Vichy waters in combination with colchicum are indicated in gouty patients. Free purgation and warm alkaline baths are also serviceable in this class of cases. There is, perhaps, no remedy which will for a time relieve the irritability, pain, and acidity after meals as certainly as bis- muth. When it fails in cases of long standing, zinc, alum, tannin, or nitrate of silver may be tried. The habitual constipation which often com- plicates these cases will be relieved by daily use of aloes and strychnia, or rhubarb and soda. When there is evident deficiency of gastric juice, five or six drops of hydrochloric acid in a wine-glass of water, and ten or fifteen grains of saccharated pepsin, will greatly assist the digestive process. If there is an excess of gastric juice, alkaline waters should be freely used 1 I have found the following to allay this craving : R Tr. cinchonse comp...............................5 iv. Tr. capsici........................................ 3 ss. Tr. nuc. vomicae.................................3 ij. M. A teaspoonful every two or three hours. PHLEGMONOUS GASTRITIS. 261 during, and after meals. When fermentation is very active, and flatulence is annoying, sulphite and salicylate of soda or creosote, given after meals, are serviceable. If the stomach rejects food as soon as it is taken, rest is essential, and the patient must be nourished for a time by the rectum and then placed on a milk diet. Minute doses of arsenic and of belladonna have been recommended as curative agents, but there is no evidence that they have any such power. Blisters, moxae and issues over the stomach are sometimes of service in very chronic cases. PHLEGMONOUS GASTRITIS. Phlegmonous gastritis is a suppurative inflammation of the areolar (sub- mucous) tissue of the stomach ; it has also been called " suppurative lenitis." Morbid Anatomy.—The suppurative process may be circumscribed or diffused. On removal of the stomach its wall is found thicker than normal, and its substance oedematous and very friable. The submucous tissue is distended by, and infiltrated with fibrin and pus, which not infrequently accumulate in large quantities in the muscular tissue as well. The entire mucous coat is, in rare instances, very much thinned and undermined by the purulent accumulation which perforates it at different points; the email openings thus formed give exit to the pus from the spongy, irregular shaped cavities, or "abscesses," lying beneath. The raucous surface is /eddened in patches, or is of a deep purple color ; sometimes it is gangren- ous. If the peritoneal coat is involved it presents the usual appearance of acute peritonitis. The abscesses in the sub-mucous tissue tend to open into the cavity of the stomach, although they may perforate externally and be discharged into the peritoneal cavity. In circumscribed phlegmonous gastritis these pus cavities may be the starting-point of ulcers of the stomach. Etiology.—Phlegmonous gastritis is a very rare disease, usually occurring between the ages of twenty and forty years. It may occur idiopathically in previously healthy persons, without any assignable cause, or it may be secondary to pyaemia, septicaemia, puerperal fever, typhus fever, and diphtheria. Symptoms.—Phlegmonous gastritis is ushered in by a distinct chill, fol- lowed or accompanied by intense pain and tenderness over the region ol the stomach. Complete anorexia is an early symptom, and is accompanied by intense and constant thirst; there is persistent vomiting, which increases in severity with the advance of the disease ; the ejected matters are some- times purulent, but usually consist of a dark colored, bitter fluid. The pain increases in severity until it becomes as severe as in peritonitis. The temperature may reach 104° or 106° F. When the disease has reached its climax there is great depression and exhaustion ; the patient is anxious and fretful, not infrequently passing into active delirium, but, whether the latter is present or not, typhoid symptoms with low muttering delirium, jaundice, stupor, and collapse are rapidly developed, and the patient passe? into a state of coma and dies. 2G2 DISEASES OF THE DIGESTIVE SYSTEM. Differential Diagnosis.—The diagnosis of phlegmonous gastritis is only made by exclusion ; it often passes unrecognized during life. Prognosis.—The prognosis is always unfavorable. The majority die dur- ing the first week. When it is circumscribed its duration may be pro- longed to two or three weeks. Its only complications are secondary abscesses in other organs (as the liver) and peritonitis. When primary, the disease reaches a fatal termination either from peritonitis or from exhaustion with typhoid symptoms. Treatment.—When phlegmonous gastritis is secondary the primary dis- ease will demand attention; in all cases the treatment is merely palliative; stimulants are indicated very early, and the sufferings of the patient must be relieved by morphia hypodermically. GASTRIC DYSPEPSIA. Dyspepsia and indigestion are terms used to indicate a train of symp- toms caused by a functional derangement of the digestive processes. When these derangements are confined to the stomach they constitute gastric dyspepsia. Morbid Anatomy.—Strictly speaking, gastric dyspepsia has no morbid anatomy. If it has continued for a long time the walls of the stomach may be found thinned, the mucous membrane atrophied, and many of the gastric tubules shrunken and in a state of fatty degeneration. Not infre- quently the tubular structure of the stomach is replaced by a fibro-nucle- ated tissue. After death the power of self-digestion in such a stomach is markedly diminished or entirely lost. It is often met with as a part of senile decay. Etiology.—Dyspepsia is often an inherited condition and accompanies the changes of advancing age. There is no affection in which individual idiosyncrasies are so strongly marked. Its etiology can best be considered under the following heads :— First:—A class of cases in which there is a deficiency in the quantity of gastric juice secreted. Such deficiency often occurs in those disordered states of the blood which precede the onset of acute diseases. It occurs in enfeebled conditions, as the result of exhausting discharges, venereal excesses, masturbation, leucorrhoea and phthisis, and from the excessive use of narcotics, the tannin of tea, and the nicotine of tobacco. Second:—There is a class of cases in which there is an excess in the gas- tric secretion. This is most apt to occur in those suffering with chronic hepatic and cerebral diseases and in gouty subjects. It is sometimes changed in quality and in quantity in young persons who have grown rapidly, and in females at the menopause. Third:—There is a class of cases in which the gastric secretion is changed in quality. This occurs with ulcer and cancer of the stomach, gout, rheumatism, disease of the kidneys, uterus, and gall bladder. A lithic-acid diathesis is said to cause a change in the quality of the gas- tric juice. GASTRIC DYSPEPSIA. 263 Fourth:—There is a form of gastric dyspepsia due to impaired motion of the stomach, which may be the result of its adhesion to neighbor- ing parts, to an omental hernia dragging it out of its normal position, to cicatrices and new growths at its pyloric extremity, to thickening of its walls, or to a weak, flabby, enfeebled condition of its muscular coat, and to pressure on the stomach from tight lacing and from positions assumed by shoemakers, needlewomen, writers, etc. Fifth:—Mental emotion, prolonged mental labor, and anxiety rather than continuous and regular brain work, cause dyspepsia ; in such cases it is the sudden arrest of the digestive functions, especially after eating too much, which is the main etiological factor. Organic cerebral disease and pressure on, or disease of one or both pneumogastrics act in the same way. Sixth:—Deficient or excessive physical labor may be a cause of dyspepsia. Walking immediately after a full meal is a prolific cause of this variety, ex- amples of which are frequently met with in letter-carriers. Seventh:—Improper diet is a common cause of dyspepsia. It may arise from an excess of starchy materials, as potatoes ; or from deficiency of meats. Un- der improper diet may be included decomposing food, impure water, badly cooked food, too rapid eating, the food not being sufficiently masticated, or taken at too short intervals and irregularly. Articles of food that may be suited to one climate, season, or age may in another be wholly indigestible and cause dyspepsia. Symptoms.—The symptoms of dyspepsia are a series of phenomena which vary not only in different individuals, but in the same individual at differ- ent times; the most constant is an abnormal appetite : it may be lost, in- creased, or perverted. There is a weight, dull pain, and a sense of burning in the epigastrium after ingestion of food, accompanied by flatulence, heart- burn, gastralgia, constipation or diarrhoea, a dull headache, languor, de- pression of spirits and irritability of temper. Indiscretion in eating or drink- ing, and exercise or exposure in dyspeptic subjects are apt to bring on an at- tack of sick headache. There is frequently a bitter taste in the mouth, bilious vomiting and sluggish bowels ; this is called a bilious attach If these symptoms immediately follow the taking of food, it is called " inges- tive dyspepsia," or " morbid sensibility of the stomach." In some dyspep- tics the breath and faeces have a very offensive odor. Pyrosis, which is the chief symptom in another class of cases, is the regurgitation into the mouth of a large amount of thin, watery, saline fluid, preceded by a sense of constriction and pain in the epigastrium. This fluid consists mainly of saliva. Sometimes there is not only a feeling of oppres- sion in the thorax, but a severe pain is referred to the heart, accompanied by palpitation and dyspnoea. In such cases the patient is very apt to im- agine he has heart-disease. Accompanying some cases there is vertigo, ringing in the ears, spots before the eyes, and other sensations which together have been called "stomachic vertigo." These patients hear a buzzing sound and feel as if a vapor were enveloping them; they grow pale, and grasp for support through 264 DISEASES OF THE DIGESTIVE SYSTEM. fear of falling. When in any case the " indigestion" has lasted a long time, chronic gastric catarrh will almost always be developed, and evi- dences of mal-nutrition show themselves by anaemia, premature old age, corrugation of the nails, caries of the teeth, etc. At other times the patient will suffer from dyspnoea, with a short, dry cough, and occasional parox- ysms of an asthmatic character. The skin becomes sallow, dry, and rough, while various eruptions appear on it, and the abnormal contents of the urine show that the functions of the kidneys are disturbed. Often in long- standing dyspepsia in females there will be a feeble pulse, leucorrhcea, and irregularities in the menstrual functions. There is no characteristic change in the appearance of the tongue ; in one case it is white and heav- ily coated, in another it is clean, large, and indented. The urine often contains oxalate of lime ("oxaluria"). After the oxalates disappear, lithiates may appear for a time, soon to be followed by normal urine. Differential Diagnosis.—The phenomena of dyspepsia closely resemble those of chronic gastric catarrh. Eepeated attacks of dyspepsia are apt to result in a sub-acute or chronic gastric catarrh. Their differential diagnosis has already been considered. Acidity from hypersecretion may be confounded with acidity from fermentation, and stomachal may be confounded with cerebral vertigo. The following are the principal points in their differential diagnosis: pain in acidity from hypersecretion either immediately follows the taking of food, and is accompanied by "heartburn," or, quite as often, it is felt most when the stomach is empty, and is relieved by taking food ; but the pain from fermentation, due to obstruction to movements of, or to chronic inflammatory processes in, the stomach, comes on some time after eating, and is more a sense of weight or fulness in the epigastrium than pain. It is never present during the intervals between taking food. Vomiting is rare in acidity from fermentation, but if it does occur, the ejected materi- als will contain organic acids, torulae, and sarcinae; while with hypersecre- tion vomiting is a common symptom, and very frequently there is an excess of hydrochloric acid in the matter vomited. The constitutional symptoms, mental depression and emaciation, the sallow skin, etc., are much more marked in dyspepsia with fermentation than in dyspepsia with hypersecretion. In case of acid stomach from fermentation, flatulence is very common, while it rarely occurs with acidity from hypersecretion. The urine is alkaline or neutral in acidity from fermentation, while it is always acid with hypersecretion. Lastly, acidity from fermentation has a history of some cause or causes which interfere with digestion, while hyper- secretion is usually a reflex symptom, or occurs with ulcer of the stomach, or in perfectly healthy persons. With vertigo or dizziness from stomachal causes, there is a history of indi- gestion, and it usually occurs in middle life, while in cerebral vertigo the individual is beyond middle life, and there will be no history of difficult or impaired digestion. Vertigo from stomachal causes occurs during an attack of indigestion, or after some particular kind of food has been taken. Cere- bral vertigo occurs wholly independent of the state of the stomach. Con- CANCER OF THE STOMACH. 265 sciousness is never lost, nor are the special senses—sight alone excepted— involved in stomachal vertigo, while ringing in the ears, temporary deaf- ness, and often complete loss of consciousness occur in an attack of cerebral vertigo. A person suffering with stomach vertigo knows that the apparent motion of the surrounding objects is unreal—while a patient with cerebral vertigo believes the apparent movement of the objects to be real. Prognosis.—The prognosis varies with the etiology. Dyspepsia in most cases can be cured, but the cure depends for the most part on the will of the patient. The only danger is that the conditions induced by dyspepsia may predispose to organic diseases in other organs, as the lungs or kidneys, and that it may lead to a condition of melancholia. Treatment.—First, if possible, remove the cause. When the gastric juice is deficient in quantity, hydrochloric acid and pepsin are indicated. In these cases, also, the vegetable bitters are especially beneficial ; indeed, in most cases of dyspepsia they are valuable adjuvants to the other remedies. Tea and tobacco are always to be avoided ; alcoholic stimulants in moder- ate quantities may sometimes be combined with the vegetable bitters with advantage. When acid risings occur after ingestion of food, and are due to active fermentation, the sulphite of soda or salicylic acid imme- diately after meals may prevent such changes. When fermentation is present, these remedies, with alkalies, will relieve the heartburn and other gastric distress. A course of saline waters will be found, in such instances, to .aid the other remedies. When there is great irritability of the stomach, bismuth acts almost as a specific, and should be given in twenty-grain doses before eating. Creosote, codeia, oxalate of cerium, and morphia may be employed to arrest vomit- ing. If there is pain in the epigastrium, the local application of heat by means of the hot-water bag will relieve. Dyspeptics should never wear corsets or belts about the abdomen ; they should retire and rise early, and eat slowly, masticating their food thoroughly. The meals should be small and taken at stated intervals. The diet must be determined for each case. Most patients do best on a diet free from hydrocarbons, but many cases of a lithaemic diathesis must be deprived of meats. No mental or physical work should be performed directly after or before eating. Horseback- riding and walking in the open air should be insisted upon. A change of scene and climate works rapid cures in many instances. Dyspeptics should take plenty of rest, have their sleeping-rooms well ventilated, and take a cold sponge-bath morning and evening. The general principles of treat- ment in gastric dyspepsia are similar to those given in chronic gastric catarrh. CANCER OF THE STOMACH. The stomach, next to the liver, is the most frequent seat of internal cancerous developments ; one third of all the cases of primary cancer have their seat in the stomach. The varieties of cancer of the stomach, in the order of their frequency, are as follows : First, scirrhus; second, medullary; third, epithelial. Any one may 266 DISEASES OF THE DIGESTIVE SYSTEM. undergo colloid degeneration, and thus may appear as either villous or melanotic cancer. Morbid Anatomy.—Cancer has its seat at the pyloric extremity of the stomach in about three fifths of the cases. The next favorite seat is the cardia and the lesser curvature. When it is developed at the pylorus, it sometimes extends an inch or two into the duodenum ; cancer at the cardia usually involves the lower part of the aesophagus. Scirrhus of the stomach first appears as a small, grayish-white, opaque nodule in the submucous tissue, the normal structures of which arc en- closed by the new growth. These nodules are developed from off-shoots of the gastric tubules which have pushed their way through the mucous membrane into the loose submucous tissue. The primary change is thus epithelial in character.1 The fibrous stroma is far in excess of the cell- element ; it develops rapidly at the exterior of the mass, causing indura- tion and contraction of the surrounding structures. The mass sometimes extends inward toward the cavity of the stomach, causing flattened tu- mors which project into it. The contrac- tion of these nodules puckers the mucous surface, which be- comes immovably fixed upon them, and fibrous lines radiat- ing from the growth b. Pylorus. penetrate the mucous C. (Commencement of the Duodenum. -, , • > D. B. Vertical section of the cancerous mass. mem brane, W U 1 C Q IB, E. Internal surf ace of the cancerous infiltration encroaching on thtpy- £• j_ „„Anr.nnna a loricorifice. liraC unueigoeb A F. Small opening in the cancerous growth at the pyloric extremity. this cestoid can be said to have Tape-worm. a oeUy and a back. The eggs are oval, from l-350th to b b FoltrdisZs * 8. 1-550th inch, brown in color and at first ciliated. They possess six hooklets. This worm sometimes reaches sixty feet in length ; its color, unlike the others, is a dull bluish-gray. The seg- ments do not drop off when ripe, and have not an independent life. It is estimated that ten feet of this worm can produce twelve million ova. The development of this worm is unknown ; some suppose its embryo to be found in a fish or mollusk. It is found in the small intestine singly, or with the other two varieties ; several may inhabit the same individual. Round worms, or the nematodes, are more highly organized than the ces- toids; the common round worm, or A scar is lumbricoides, is of a brown color, with a cylindrical body, 10 x 1-8 inch in length and breadth in the male, and 15x1-4 in the female. The head terminates in three thick semilunar lips, each lip having about 200 teeth. The mouth opens into the alimentary canal, which can be seen through the transparent body. The tail is curved strongly toward the abdomen in the male, this, with its small size, distinguishing it from the female. The female contains two long coils of ovary and oviduct, the length of the generative tubes being eleven times the length of the animal. At the end of the tail, in the male, two projecting spiculae can be seen connected with the generative organs, which are coils of tubes eight times as long as the worm. The ova are oval in shape (1-340 to 1-440), are produced in immense numbers (sixty millions in a mature female), and are discharged with the feces. The vitality of these ova is wonderful. How they obtain entrance into man is not known, but it is probable that they previously pass through an intermediate state, and that they attain their full development after entrance. The worms inhabit the small intestine, and vary in numbers from one to thousands. They wander, however, through the tract, may pass through the nose or mouth, or may enter the hepatic, gall or pancreatic duct, into the gall- bladder, or into any fistulous channel, and reach the kidneys, spleen, lung, larynx, etc. The round worm occurs in the ox and pig as well as in man INTESTINAL PARASITES. 331 $d$ The "thread worm," "maw-worm," Oxyuris vermicularis, looks like an ordinary piece of thread ; the male (like the round worm) is smaller than the female, and is about one-sixth of an inch long. The fe- male is from one-third to one-half an inch long. The body is cylindrical,the tail is much sharper than the head. The head terminates in a mouth surrounded by three lips, from which extends the alimentary tract. The end of the tail, in the male, is curved up toward the abdomen. The eggs are oval, 1-100 to 1-500 inch, each female containing about ten thousand. They are very hardy, having a Btout envelope. All their stages of develop- ment take place within the intestinal canal. The "seat-worm," as its name indicates, has its habitat in the large intestine, especial- ly about the rectum, whence it may pass into the vagina or insinuate itself into narrow folds of skin in the anal region. Mature females especially inhabit the caecum. They vary in number: sometimes the mucous membrane is completely covered with them. The ova enter by means of the food or di- rectly through personal contamination ; they die in a few hours after th^y are placed in water. The Trichocephalus dispar, or " whip-tvorm," is a small worm about one and one-half to two inches in length, the female being the larger. It has been called the "hair-headed" worm because its head, which constitutes about two-thirds of its length, is thread-like. The thick body contains the genitals and the intestinal canal; the body of the male is curved into a spiral. The male organ presents a spicula projecting from the cloaca; it is set with numerous sharp points, and is surrounded by a sheath. The uterus, when distended with eggs (60 ova), fills nearly the whole posterior part of the body. The ^ggs are brown and oval (1-5,000—1-12,000 inch) with a nipple-like appearance at either pole. Its mode of entrance into the body is unknown. There is probably no intermediate state of the ova of T. dispar. The embryos are probably liberated in the stomach, and, developing as they travel onwards, reach the large intestine. Their numbers vary from fifty to one thousand. The T. dispar is found in some varieties of apes ; and the T. crenatus of the pig is probably the same as this worm. Trichina spiralis belongs to general diseases, and will not be considered here. The Anchylostomum duodonale, or dochmius duodenalis, is a small cylin- drical worm, the females being seven-tenths and the males four-tenths inch in length. It is thicker than the seat-worm, almost as thick as the body of Fig. 64. A. Oxyuris vermicularis, or thread worm, female. B, Same, male—both natu- ral size. C. Female of same, magnified about ten limes, containing bra. a, anus; b, vulva. D. Mature egg of the thread worm, x 250. E. Ascaris lurhbricoides, male, natural size. F, head, and O. tail of same, magnified about four diameters. 332 DISEASES OF THE DIGESTIVE SYSTEM. the whip-worm. The mouth is furnished with eight teeth. The armature of the mouth, and the capsule about the head are very complex. The male terminates in a lobate enlargement, but the female is pointed. The eggs are oval (1-350 to 1-1000 inch), have a very thin shell, but regarding their development little is known. It inhabits the lower part of the duodenum and the upper part of the jejunum. It probably has no intermediate bearer, but as soon as developed attaches itself to the villi and may become encysted between the mucous and muscular coats. It may cause intestinal hemorrhage. Etiology. —Worms develop in the intestines of man, either by the en- trance of ova which grow into the mother parasite; or by the entrance of what are called "intermediate parasites." Their entrance into the intestinal tract is only effected through food and drink. Butchers, and those who handle raw meat, are more subject to them than others. Filthy surroundings, squalor, and personal uncleanliness are conditions which favor their development. Cestodes occur at all ages ; tape-worm has been found in a five-day-old infant. Bothriocephalus latus is found chiefly in Scandinavia, Russia, and Poland. T. solium occurs wherever the pig is domesticated. T. saginata is found wherever raw beef is used for food. The Taenia are not found among Jews and those who eat no pork. The monks of the Carthusian order, who eat only fish, are free from worms. Iceland is the only country in which the haematoids are not found. The round worm occurs in warm climates oftener than in cold. Their number and extent are in direct pro- portion to the filth of the surroundings. They are more common in women and children than in men ; in those who live in the country than in those who live in cities. The oxyuris vermicularis is everywhere prevalent. It occurs especially in young children, but is not uncommon in adults. The itching which these worms cause, especially at night in a warm bed, induces so much scratching, that when two or more children sleep together the worms may be carried from one to another by the hands. Those who have charge of children, nurses, etc., often become infected in this way. T. dispar abounds in this country, Europe, Syria, and Egypt; it is present at all ages, but, strangely enough, in the first and second years of life it is rare. The whip-worm produces so few symptoms, and can be so readily overlooked at a post-mortem, that its etiology is obscure. The Anchylostomum duodenale (or the dochmiusor strongylus duodenalis) was discovered by Dubini in 1838, in Northern Italy. It prevails in Brazil and Egypt. The negro is oftener subject to it than the white ; but it can he shown that bad food and drink are of more importance in causing it than race. Women are affected oftener than men. The conditions known afi cachexia Africana, mal d'estomac, etc., are due to the presence of this parasite. Symptoms.—The only symptom which gives positive evidence of the ex- istence of intestinal worms or their ova is their discovery in the stools or about the anus. Ta-nia produces no constant symptoms. The bowels are usually irregular. There may be colicky pains in the abdomen ; the appe- INTESTINAL PARASITES. 333 tite is capricious, the face may be pale and the mouth drawn. Often the stomach feels weak, and there is nausea, perhaps vomiting. In some in- stances these stomach symptoms, with colic, occur after certain articles of food ; in others, certain kinds of food relieve them. Among the reflex symptoms are headache, dizziness, ringing in the ears, sudden sweatings, irregular attacks of palpitation, depression of spirits, lassitude, ocular spec- tra, sudden salivation, and itching about the nose and anus. Chorea, grinding the teeth, hysteria, anomalies in menstruation, epileptiform and maniacal actions have occurred in those in whom tape-worms were found to be present. The special senses may be temporarily involved : —deafness, blindness and loss of speech have occasionally occurred. All the senses are enfeebled to a marked degree. These symptoms are more those of hypo- chondria and hysteria than of taenia. The subjective sensations which one who believes he has taenia may describe are innumerable, and each patient will have his own peculiar group of special notions. Often patients with one large or several small taeniae enjoy perfect health so long as their exist- ence is not suspected. The diagnosis can only be made by the discovery of detached joints or segments of the worms in the faeces. The ascaris lumbricoides or round worm may be present in large num- bers, and yet give no symptoms of its presence. Usually, however, there are certain symptoms which are regarded as " signs of worms," such as itching and picking at the nose, foul breath, colicky pains, especially about the umbilicus, bloody mucous diarrhoea, perverted appetite, restless- ness, disturbed sleep in which the child grinds its teeth, with nausea and vomiting; which is regarded as evidence that the " worms have passed into the stomach." The vomiting, however, is reflex. The abdomen is usually tumid, distended, and doughy to the feel. The urine looks somewhat like rice-water, the lower eyelid is of a dark purple color, or there may be rings about the eyes ; the pupils are often unequal. Later there are hysterical convulsions, with choreal movements, and the child becomes emaciated. These worms, by coiling themselves into a bundle, have caused intestinal obstruction. They have entered the larynx and induced death by suffoca- tion, have reached the ductus communis and caused jaundice and hepatic abscess, and they may take their way through any artificial opening into the peritoneal cavity or bladder, but they cannot cause intestinal perfora- tion. It is a question if lumbrici can induce catarrh and ulceration of the intestine. At an autopsy, where large colonies of lumbrici have been found, the intestine has been intensely congested in the neighborhood, leaving no doubt as to the cause. Attacks of laryngismus stridulus are sometimes induced by lumbrici in highly nervous children. While the existence of these worms may be suspected, their diagnosis can only be made by their discharge from the stomach or intestine. The seat-worm, or oxyuris vermicularis, when present in small numbers, produces few symptoms. When they are numerous in nervous and suscep- tible patients, there is intense itching about the anus, especially on retiring, when the increased warmth causes them to be very active, and by this sleep is more or less disturbed. They often cause a frequent desire to go to stool, 334 DISEASES OF THE DIGESTIVE SYSTEM. and sometimes there is an abnormal amount of mucus mixed with the faeces showing that they have produced extensive local irritation. In such cases, there will be punctate redness about the anus, and in female children, where the worm wanders into the vagina, there will be irritation of the vulva, which leads to vulvitis. Sometimes with the itching there will be pain and tenesmus, and the fetid stools will be bloody and streaked. The genito- urinary disturbance may cause such abnormal excitement of the sexual organs, that it may lead to onanism, seminal loss, and nymphomania. Hys- terical, epileptiform, choreal, and cataleptic symptoms have been induced by the'irritation produced by these worms. On account of the local irrita- tion which they produce and their easy detection on careful examination, their diagnosis is not difficult, for their ova or the parasites themselves will be found in the faeces, or in the folds at the margin of the anus. A careful inspection of the rectum in those who suppose they are suffering from hemorrhoids will often disclose the presence of the seat-worm as the cause of the anal irritation. Trichocephalus dispar produces no symptoms. Either the worms or their eggs must be found in the faeces to establish a diagnosis. Anchylostomum duodenale induces a chlorosis-like anaemia; the skin and mucous membranes are pale, and the cardiac and venous murmurs of anae- mia are well marked. The loss of flesh and strength is constant and pro- gressive. Dyspepsia and anorexia, alternating with bulimia, and an appe- tite for certain and peculiar articles of food, are early symptoms. In most cases there is a sense of weight or pain in the abdomen ; the stools are fre- quently colorless, and the urine is pale and abundant. Sometimes slight intestinal hemorrhage will occur. Differential Diagnosis.—The diagnosis of the presence of intestinal para- sites is made by the discovery of the parasites or their ova in the stools or the matters vomited. Acute hydrocephalus may be mistaken for worms, but in hydrocephalus the projectile vomiting, the slowed pulse, the fever with irregular exacerbations and remissions, the constipation, the hydro- cephalic cry, and the retracted abdomen, all stand in marked contrast to the symptoms of intestinal parasites. Prognosis.—Intestinal parasites may cause death, first by their entrance into the larynx, the ductus communis (causing abscess of the liver), or when they collect in masses and cause fatal intestinal obstruction; secondly, when extreme anaemia and exhaustion are produced by anchylostomum duodenale. The prognosis in taenia is good, except in very young children, and in the enfeebled. When parasites have resided a long time in the in- testines, some of the reflex symptoms may remain after their removal. It is thought that the ascaris lumbricoides does not remain longer than a year in the human body, unless there is an exposure to new sources of infection. Death occurs with symptoms of exhaustion, greatly increased by the intes- tinal hemorrhage, profuse diarrhoea, and persistent vomiting. Treatment.—Prophylaxis demands that all raw or "underdone" meat shall be avoided. Measly pork should not be allowed to be sold in the markets, and wells and springs from which drinking water is obtained INTESTINAL PARASITES. 335 should be removed from the neighborhood of stockyards. A point in prophy- laxis that has never been mentioned is the washing of green vegetables, such as lettuce, as the Swiss and Germans sprinkle their growing vegetables with the water drained from human excrements. The means to be employed for the expulsion of the tape-worm have for their object the dislodgment of its head ; so long as this remains, it is use- less to hope for cessation of the symptoms. Whatever anthelmintic is administered for this purpose, the bowels must be thoroughly evacuated. This can be effected by some of the saline purges, or by a copious draught of some purgative mineral water. The diet should be restricted for two or three days before its administration, and then either pomegranate, Kousso, male fern, or pumpkin-seeds may be given in full doses. As the adminis- tration of anthelmintics may induce vomiting, a cup of black coffee may be given a few minutes before they are taken. The cortex radicis punicce granati is used in the form of a decoction (three ounces to a pint and a half of water). When boiled down one-half, it should be given in three divided doses. To this may be added filix mas, gamboge, or tansy; and in case the worm is not dislodged, a dose of castor-oil should follow. Kousso, the flower of the Brayera anthelmintica, is given in one-half oz. doses mixed with water ; or in an infusion (one-quarter oz. to four oz. of water). The odor of the Kousso is very offensive. The male fern {aspidium filix mas) is one of the oldest and best known vermifuges. The ethereal extract—oleoresin—is given in capsules ; dose, one-half drachm. It may be given as the powder of the rhizome, 60 to 100 grains. It should also be followed by a dose of castor-oil, gamboge, or cal- omel. Oil of turpentine, in one-half or one-ounce doses, is very effective; it may produce headache, giddiness, or a kind of intoxication. Petroleum, in 20 to 30-drop doses, has been used in Egypt. Kameela (Rottlera tinc- toria) is to be given in one-third drachm doses every three hours. Carbolic acid (5 grains) and salicylic acid (12 grains) have also been found efficacious. An emulsion of pumpkin-seeds frequently acts efficiently. The active prin- ciple of pomegranate-root bark, pelletierine, is thought by some to possess all the powers of the root. All the above-named drugs are efficacious, and when they fail it is usually because they are not properly administered. For round worms, besides the vermicides mentioned, santonin, spigelia, cal- omel, and chenopodium may be used. Santonin is by far the most reliable, but it requires care in its use, on account of the severe gastric and nervous symptoms which it causes ; one-half grain for a child and three to six grains for an adult is a maximum dose The oil of chonopodium is recommended, —dose, five to ten drops ; and the fluid extract of senna and spigelia is often effective. The thread or seat-worm may be destroyed and washed away by enemata of quassia, oak-bark, alum, salt and water, or carbolic acid. At the same time the vermifuges should be given, and the bowels gently moved by castor-oil. Thoroughly washing the anus and the parts around it with a one per cent, solution of carbolic acid, and subsequent attention to clean- liness, suffice in the majority of instances. It is said that turpentine and 33 INTESTINAL COLIC*. 341 stinately constipated, there is slight fever, the abdomen is tender and slightly distended, or it may be retracted. When prolonged, bilious colic may be accompanied by jaundice. Bilious colic occurs in summer and autumn, chiefly in malarial districts. A form of colic which is often a distinct " cramp," is obviously due to a gouty or rheumatic diathesis; beyond its etiology, it does not differ from flatulent colic. It may be metastatic. Of the metallic colics, lead colic, " colica pictonum," is far the most fre- quent ; it is a true colic, no lesions being found in the intestines of those who have died of it. The metallic colics are produced by the primary ac- tion of the metal on the nervous system, and are preceded by the general symptoms of the poisoning. Lead colic comes on with moderately se- vere paroxysms of pain, which gradually increase in severity until a series of intense paroxysms rapidly follow each other. The pain is located about the umbilicus, and is twisting or grinding in character. With the colic there may be cramps and pains in the extremities. The abdomen is con- tracted and hard ; knots of rigid intestine can sometimes be felt. The abdomen is not tender, and forcible pressure markedly relieves the pain. The bowels are obstinately constipated, but as the attack passes off diarrhoea often occurs. After the subsidence of the pain another attack may be ex- cited by taking food, or one may return without any apparent cause. The pulse is slow during an attack, and there is no rise of temperature. An individual suffering from lead poison is sallow, anaemic, and more or less enfeebled. The extensors of the fore-arm are often paralyzed (drop-wrist), and there may be amaurosis (due to optic neuritis) and epileptiform con- vulsions. Along the edge of the gums is a deep blue dotted line composed of lead, formed by the sulphuretted hydrogen produced by decomposing food lodged between the teeth reacting on the lead which circulates in the capillaries. This is the distinctive sign of lead poisoning. The pain in lead colic radiates in all directions, and its point of maximum intensity is located at different times in different regions of the abdomen. Copper colic may be distinguished from lead colic by the fact that the pain is increased by pressure, the abdomen is distended instead of retracted, and in place of obstinate constipation there is diarrhoea with greenish stools ; there is a purplish line about the gums, and there may be attacks of dysp- noea from laryngeal and bronchial spasm. Differential Diagnosis.—Intestinal colic may be confounded with peritoni- tis, intestinal obstruction, gall-stone colic, intestinal perforation, spinal disease, aneurism, labor-pains, hernia and muscular rheumatism. In peritonitis there is usually a distinct febrile movement, the pulse is accelerated and is tense and wiry in character. In colic there is no fever or increase in pulse-rate, the rule being rather a slowed pulse. In peritonitis the patient avoids the slightest motion of the body, and firm pressure over the abdomen increases the pain, while in colic the patient tosses from one side to the other, and firm pressure over the abdomen relieves the pain. The pain of peritonitis is constant, that of colic is paroxysmal. 342 DISEASES OF THE DIGESTIVE SYSTEM. Perforation of the intestine is to be distinguished by the intensity and rapidly increasing severity of the pain, rapidity of the pulse, rapidly de- veloping tympanites and collapse. In spinal disease the pain is along the course of the nerves and all the intestinal symptoms of colic are absent. Aneurism of the abdominal aorta is distinguished by the physical signs of aneurismal tumor, by the change in the femoral pulse, and by constant localized pain in the back. Hernia has an external tumor, there is stercoraceous vomiting, and only great carelessness in the examination will allow of error in the diagnosis. Labor-pains may simulate colic, and there are cases on record where- in concealed pregnancy—the true state of affairs was not recognized until labor was completed. Muscular rheumatism is attended by intense and constant pain, aggra- vated by motion and pressure, having its maximum intensity at the origin and insertion of the muscles. There will be a history of exposure, and also of frequent rheumatic attacks in other parts of the body. Prognosis.—The prognosis is always favorable. Death has occurred from rupture of the intestine from excessive gaseous distention, and from con- vulsions in very young children. Treatment.—The indications for treatment are to be found in the etiology of each attack. In flatulent colic, and in that from impacted faeces and undigested food, evacuants are indicated. The internal administration of castor-oil and an aperient enema generally give relief. If the colic is due to exposure of the feet or abdomen to cold, hot aromatic teas and diapho- retics are indicated. In all forms, opium, chloroform, hydrate of chloral, or ether may be given to relieve the pain and spasm. In hysterical and nervous subjects, at the onset of the attack, Hoffman's anodyne, musk. asafoetida, valerian, and the essential oils often quickly relieve the pain and remove the flatus. In children, bromide of potassium in carminative waters, often affords speedy relief. In some cases it will be necessary to re- lieve an overloaded stomach by administering an emetic. Malarial colics demand for their relief quinine combined with calomel. Gouty colic is best treated with oil of cajeput, Warner's cordial, and carminatives. The feet are to be placed in a mustard bath, and a mustard plaster is to be placed on the abdomen. Anti-gout remedies are to be given as soon as the sever- ity of the colic is relieved. In lead colic, opium is the most efficient remedy. It will often relieve the constipation. My rule is to combine it with belladonna and croton oil (1 grain of opium, l-6th grain of the extract of belladonna, and 1 drop of croton oil), every two hours, until relief is obtained. Sulphate of mag- nesia is preferred by some to the croton oil; a warm bath will often give immediate relief and hasten the action of the croton oil. As soon as the bowels are acted upon the pain disappears. Faradic electricity and pilo- carpin are advocated by some German authorities. A milk diet acts as a prophylactic and curative agent, and workmen in lead factories should drink large quantities of it-. It is claimed by some, that sulphuric-acid PERITONITIS. 343 lemonade is a good preventive, as it forms insoluble lead sulphate. A long time elapses before all the lead is removed from the system. In copper colic sulphur baths, turpentine stupes or sinapisms, ether and opium, and a milk diet, with the casual indications, are all that is ne- cessary for its successful management. In all forms there are two prom- inent indications for treatment, viz.: to relieve pain with opium, and to evacuate the bowels. Warm fomentations and sinapisms to the abdomen are always of service. Cold applications are contra-indicated. Always seek for, and, if possible, find the cause before cathartics are given. PERITONITIS. Peritonitis is an inflammation of the whole or a part of the serous mem- brane which lines the abdominal wall and covers the viscera contained in the abdominal cavity. It may be acute or chronic; local (circumscribed) or general. The acute form usually begins at one point and rapidly spreads over the entire membrane. The chronic may result from the acute, or it may be interstitial, hemorrhagic, tubercular or cancerous. Morbid Anatomy.—Acute, general (or diffused) peritonitis begins with an intense injection of the capillaries of some portion of the visceral or parietal layer of the peritoneum. Sometimes the injection is so intense that the capillaries rupture at points and cause small blood extravasations. The in- flamed portion at first presents a mottled appearance ; the redness is most intense at the starting point of the inflammation. With the capillary hyperaemia there is desquamation of the endothelial cells, and the perito- neum loses its natural glistening appearance, becomes dry and lustreless, and there is swelling and an increase in the number of its fixed connective- tissue cells. Following this, a more or less abundant exudation takes place upon its free surface, into its substance and underneath it. This exudation may be fibrinous, sero-fibrinous, or purulent. The changes in general peri- tonitis are usually most marked in the parietal portion of the peritoneum, in layers of the omentum, and in the meso-colon. With the advance of the disease, the fibrinous exudation increases in amount, and assumes a distinctly yellowish tinge ; as it increases in thick- ness it presents the appearance of a roughened false membrane, which may vary in thickness from a mere film to a quarter of an inch or more; its consistency varies from a pulpy mass to a coherent, elastic membrane. It may form a continuous layer over the visceral or parietal portion of the peritoneum, and agglutinate its opposing surfaces more or less firmly to each other. If a serous effusion occurs at the same time, it tends to gravitate to the most dependent portion of the peritoneal cavity ; it is usually small in quantity. After a time cells appear in the layer of fibrinous exudation, probably derived from the connective-tissue of the peritoneum, which cause the development of a layer of new connective-tissue, which may give rise to permanent thickenings and adhesions between the surfaces. Pap- illary connective-tissue growths may also form and cause adhesions; these adhesions are usually in patches. The new connective-tissue is most 344 DISEASES OF THE DIGESTIVE SYSTEM. extensive and thickest over the solid viscera, as the uterus, liver and spleen. The bands of adhesion may bind down a portion of the intestine and cause fatal obstruction, or they may form tense cords underneath which a loop of intestine may be suddenly incarcerated. On the surface of the solid viscera the new tissue gradually becomes indurated, resembling cicatricial tissue. Sometimes the new connective-tissue bands are so slight that the peristaltic motion of the intestines causes them to disappear. Firmer adhe- sions may cause displacement of the viscera or twisting of the intestines, or the whole contents of the abdominal cavity maybe matted into one globular mass. Acute peritonitis may cause a general thickening of the peritoneum without adhesions, its tissue becoming dense, white and fibrous. In these cases the fibro-cellular developments are chiefly in the substance of the peritoneum—not on its surface. The changes in the intestines vary: at first, vascular lines are seen running around the circumference, and in very acute cases the whole surface is red- dened. Interstitial cell-growth of the sub-peritoneal coat, accompanied by inflammatory cedema, causes their peritoneal surface to present an opaque appearance. The muscular coat loses its contractile power, and they become distended with gas, so that when the abdomen is opened they protrude through the incision. The abdominal muscles and the surface of the vis- cera, especially the liver and spleen, are paler than normal. The intestinal mucous membrane is sometimes paler than normal, sometimes intensely hyperaemic. In non-adhesive or sero-fibrinous peritonitis, with the plastic exudation there is a more abundant effusion of fluid, containing flocculi of lymph and cells which are most abundant in the most dependent portions of the abdominal cavity. Its color varies from a delicate straw color to a grayish red. Underneath the fluid on the surface of the peritoneum there is a layer of exudation which in its anatomical arrangement is the same as that in adhesive peritonitis, and it undergoes similar changes. Displace* ments of the abdominal and thoracic organs often occur from the pressure of a large fluid effusion. The fluid effusion may undergo absorption, and, the two plastic layers coming in contact, adhesions will form as in the adhesive variety. Acute suppurative peritonitis may have for its product a fibro- or sero- purulent exudation. In this variety, the parietal and visceral layers of the peritoneum are partially or completely covered and infiltrated with a gray, opaque, soft, fibrous exudation, which is infiltrated with pus cells. The effusion varies in color and consistency; it may be thick, creamy, and viscid, or turbid, thin and watery. It collects in the de- pendent portions of the pelvic cavity. The purulent exudation may be spread out over the entire surface of the membrane, or it may be associated with adhesions when it occurs in distinct collections ; it is bounded by or- ganized septa, and appears as if there were numerous separate abscesses. An ulcerative process may be established, and the purulent accumulation may be discharged through the abdominal walls into the intestinal canal, blad- PERITONITIS. 345 der, vagina, or even into the thoracic cavity. The purulent accumulation may find exit, in rare instances, along the plane of the psoas muscle. In "puerperal peritonitis," the uterus and its appendages are thickly covered and infiltrated with pus. Sometimes the ovaries and the Fallopian tubes contain pus. In nearly every instance of acute suppurative peritonitis the surfaces of the viscera present evidences of lymphangitis, phlebitis, or super- ficial abscesses. If recovery takes place without a discharge of the purulent accumulation, a part of it is absorbed, and the remainder becomes cheesy and encysted. If acute local peritonitis is secondary to visceral inflammation, the in- flammatory process in the viscus reaches its surface and involves the peri- toneum covering it. These inflammations have received various names, as perihepatitis, perisplenitis, perimetritis, etc. ; the inflamed peritoneum in this variety is usually sharply defined. Adhesions are quickly formed, and encysted purulent effusions frequently result. By the establishment of local peritonitis, ulcers of the stomach or intestine and abscesses of the liver are prevented from penetrating the abdominal cavity and causing a rapidly fatal general peritonitis. General Chronic Peritonitis.—An acute general peritonitis may run a protracted course, become chronic, and cause sero-purulent collections, or it may be chronic from the onset. An extensive adhesive or sero- fibrinous peritonitis may become chronic, causing numerous adhesions and thickenings of the peritoneum, and a more or less abundant collection of fluid contained in the spaces formed by the adhe- sions. The fluid after a time usually becomes sero-purulent or puru- lent, and in the latter case may be converted into a cheesy mass. Coils of intestine are matted together, or very firm adhesions with organs or with the abdominal parietes occur. In all cases of chronic peritonitis there are extensive peritoneal ad hesions and thickenings. When a considerable quantity of pus is circumscribed by fibrous septa, either an external opening takes place or it becomes encapsulated. In some cases of chronic general perito- nitis, there is a gradual ascitic accumulation. In most cases, pigmented and hemorrhagic spots stud the thickened peritoneum. Local or circum- scribed chronic peritonitis may be developed over an enlarged spleen, or a cirrhotic liver, or in connection with chronic intestinal diseases. Its ana- tomical changes are similar to those of general chronic peritonitis. Inhemorrhagic sub-acute peritonitis, the new tissue formations are exceed- ingly vascular, and the thin walls of the vessels may rupture. The new mem- brane may consist of one thin layer, or of several strata with effused blood between them. Sometimes the new tissue is infiltrated, and the entire sur- face of the peritoneum may assume a dark brown color, the fluid in its cavity having a distinct chocolate hue. This form of peritonitis is especially liable to occur with hypertrophic cirrhosis. In tubercular peritonitis there may be only a few tubercular nodules on the surface of the peritoneum, or there may be a gran- ular infiltration of the entire membrane. In its milder form only a few gray, semi-transparent tubercles will be found in that portion 346 DISEASES OF THE DIGESTIVE SYSTEM. of the peritoneum which overlies intestinal ulcerations. In severe or extensive tubercular peritonitis, the surface of the peritoneum is studded with tubercular granulations, which are also disseminated through the new tissue formation, and in the subjacent peritoneal and subperitoneal tissue The mesentery and omentum are also studded with granules. The adhe- sions formed in tubercular peritonitis divide the cavity into compartments, which contain the effusion. The effusion may be sero-fibrinous or puru- lent ; in some instances it is hemorrhagic, and varies in color from a light pink to a deep chocolate. In very severe cases tubercular peritouitis is always hemorrhagic. Ecchymotic spots and petechias are frequently pres- ent in the new membrane. No form of diffuse peritonitis, except can- cerous, causes such extensive thickenings, adhesions, and distortions as tubercular. Cancerous Peritonitis.—Cancer of the peritoneum is rarely primary, but is propagated to the peritoneum from adjacent organs. When peritonitis is the result of cancer in the peritoneum, it commences with the primary cancer- \ ous developments, or is established when cancer of the abdominal or pelvic vis- cera reaches their surface and involves the peritoneum covering them. The cancerous developments may begin in the omentum and gradually involve the entire peritoneum. Cancerous peritonitis may begin as a diffused sup- purative peritonitis, in connection with rapid cancerous developments in some of the abdominal viscera, especially in the uterus. Sometimes, in cancerous peritonitis, the peritoneum may be distended with a serous, lemon- colored or whey-like fluid, accompanied by a more or less abundant plastic I exudation with hemorrhages into the exudation. The hemorrhage into the effusion colors it as well as the cancerous nodules on the surface of the per- I itoneum. Adhesions are formed as in the other varieties of peritonitis, and collections of fluid may thus become encapsulated. This variety of peri- tonitis is not only attended by the development of tough, leathery mem- branes, but entire organs may be enveloped by the new tissue formations; in these cases the mucous membrane of the intestinal tract is usually the seat of chronic enteritis. Etiology.—Peritonitis may occur at any age, in the strong and robust as well as in the weak and feeble. It is met with more frequently in females than in males ; certain localities predispose to it, and the tendency to it is greater in those suffering from chronic diseases. Rarely, if ever, is acute peritonitis of spontaneous origin. But the discovery of its cause during life is often very difficult, yet very important, for on the cause depends the prognosis and to some extent the treatment. The exciting causes of acute peritonitis are : first, intestinal obstruc- tions and perforations. Under this head may be included typhlitis and perityphlitis, with ulceration; rupture of hepatic and other abscesses; ulceration and rupture of the stomach, the gall or urinary bladder; rupture of hydatid and ovarian cysts; ulceration and per- foration of the intestines in typhoid fever, syphilitic or tubercular in- testinal ulcers; and the rupture of an abdominal aneurism. In rare instances, hydatids of the lung or purulent pleural accumulations open A PERITONITIS. 347 into the cavity of the abdomen and set up a diffuse peritonitis. Injections into the uterus may pass through the Fallopian tubes into the peritoneal cavity and cause peritonitis. Rupture of an organ from a blow or fall, and penetrating wounds of the abdomen, are causes of traumatic peritonitis. Abscesses of the abdominal parietes, of the vesiculae seminales, or psoas and lumbar abscesses from caries and necrosis of the spine, ribs or pelvic bones, may open into the peritoneal cavity and cause general peritonitis. Secondly, the extension to the peritoneum of inflammation of organs covered by peritoneum is a common cause of local peritonitis. In this class of cases the peritonitis is first local, and then it may become general. Inflammation of the stomach or intestines may, by extension, involve the peritoneum covering them. Peritonitis may result from extension of in- flammation from the uterus and its appendages, liver, spleen and kidneys. .In typhlitis, perityphlitis, proctitis, periproctitis and chronic ulcer of the rectum, peritonitis may occur by extension of inflammation without per- foration. Venous thrombi, especially lymphangitis and phlebitis of the uterus, or severe contusions of the abdomen may cause peritonitis by exten- sion. Intestinal intussusceptions, volvuli, hernias, etc., quickly induce per- itonitis even when no rupture has occurred. Gangrenous and inflammatory ^processes in the umbilical vessels often give rise to peritonitis in the new- born. In the very young, incomplete descent of the testicle may cause ,t. Diverticula from hernia of the mucous membrane of the lower bowel through the muscular coat, may become filled with faeces and excite peri- tonitis.1 Thirdly, in many instances acute general peritonitis is the immediate re- sult of infection ; pyaemia, septicaemia, and puerperal fever are the condi- tions in which infectious peritonitis is most likely to occur. Puerperal peri- tonitis may occur with or without pyaemia. Intra-uterine peritonitis can often be traced to a syphilitic taint, and to puerperal sepsis in the mother. Exposure to cold and wet rarely, if ever, directly causes peritonitis. Serous inflammations of a rheumatic character are very interesting in their com- binations ; we may find peritonitis with pericarditis and pleurisy, or with .pneumonia and dysentery. Erysipelas has been complicated by peritonitis. Chronic general peritonitis may result from acute diffuse, or from acute local peritonitis, or from tubercle and cancer. It may be caused by long- standing ascites, in connection with cirrhosis of the liver and chronic splenitis. Chronic local peritonitis follows inflammatory conditions in or- gans which have a serous covering, by simple contiguity of tissue, as in hepatitis, hobnailed liver, enlarged spleen, chronic dysenteric ulcers, mronic typhlitis, etc., etc. Tumors may excite local chronic peritonitis when they are in contact with the peritoneum, as ovarian tumors. Chronic peritonitis has occurred, according to Virchow, in intra-uterine life. Ex- tra-uterine pregnancy without rupture, when the foetus undergoes degen- sration, may lead to chronic peritonitis. Hemorrhagic peritonitis occurs nost frequently with tubercular and cancerous peritonitis. Tubercular peri- 1 American Clinical Lectures, page 231. 348 DISEASES OF THE DIGESTIVE SYSTEM. tonitis is met with most frequently in early life, and cancerous peritonitii between the ages of forty and sixty-five. Symptoms.—The symptoms of acute peritonitis vary with its extent severity, and the causes which produce it. If it is the result of intestinal perforation, its onset will be marked by excessive pain over the whole ab- domen. In infectious peritonitis, the first symptom will be a severe chill. Peritonitis resulting from the extension of an already existing visceral in- flammation begins with local and gradually increasing pain. All varieties of acute peritonitis from whatever cause are ushered in by pain as one of the earliest symptoms. The pain may be local or diffuse. In severe cases, if local at first, it becomes diffuse in a few hours. It is described as a cutting, burning pain, aggravated by pressure and by movements of the abdomen. The more sudden the onset, the more intense the pain. In some cases, the weight of the bedclothes cannot be borne. The pain causes the patient to remain motionless, he lies on his back, with the knees drawai up, the breathing is wholly thoracic, the respirations are rapid and super- ficial, and the face, by its pallid, drawn and anxious look, is almost' diagnostic of the disease. In most cases, the pain is at first paroxys- mal. If the peritonitis is general the abdomen soon becomes distended andtym- panitic, the tympanites increasing as the disease advances. At the onset of acute peritonitis, the abdominal muscles are rigid and contracted; after this tonic rigidity they relax and allow of abdominal distention. Some-k times the distention is so great that the diaphragm is pushed up as far as the third or fourth rib, the lungs are compressed, and the heart, liver and! spleen are displaced. In local acute peritonitis, the tympanites is usually), slight; in diffused it is excessive and increases the pain and causes dysp- noea, the respirations often being increased to forty or sixty per minute, (. As the intestines become distended with gas, percussion elicits a tympa-v nitic note over the whole abdominal cavity. If there is a rapid effusion of' serum, it will gravitate to the most dependent portion of the peritoneal I cavity and an abnormal area of dulness will mark its position, the line of which will change with a change in the position of the patient. If a large amount of coagulable lymph is poured out over that portion of the perito- neum which covers the liver or spleen, a distinct fremitus may be com- municated to the hand as it passes over the hepatic and splenic regions, accompanied by distinctly audible friction sounds. The temperature in acute peritonitis has no typical range; it may not' rise above the normal. In most cases it ranges from 102 to 103° F.; it is| of the remittent type, being lowest in the morning. If recovery tabs place, it gradually falls to normal. In fatal cases it may fall below the). normal during the period of collapse. The pulse is accelerated, often reach- j ing 140 per minute. For hours before a fatal issue it may beat 200 peri minute. It is small, hard and wiry in character, and when very rapid «! hardly perceptible at the wrist. In exceptional cases it is tolerably full and j strong, and does not rise to more than 90 beats per minute. Vomiting is a prominent symptom; if that portion of the peritoneum | PERITONITIS. 349 covering the stomach is first involved, it precedes all other symptoms. It usually comes on about the second day ; the vomited matters at first con- sist of the contents of the stomach, later they are a mucus mingled with a spinach-green material, which by some is regarded as characteristic. Whenever stercoraceous vomiting occurs in peritonitis, it is evidence of intestinal obstruction, such an obstruction being the cause or the result of the peritonitis. • Total paresis of the lower bowel in rare instances may cause stercoraceous vomiting when the muscular wall of the intestine above is still active. Sometimes there is constant nausea without vomit- ing; hiccough and gaseous eructations indicate that the diaphragmatic portion of the peritoneum is involved. The tongue is covered with a thick coating, and anorexia is present from the onset. Constipation due to paralysis of the muscular coat of the intestine is the rule, especially in the early stage of peritonitis. Yet diarrhoea may not only occur during the later stages of the disease, but it may exist throughout its entire course. In puerperal peritonitis there is usually watery diarrhoea, and diarrhoea is often present in the peritonitis of children. The urine is scanty and deposits urates; "scalding" frequently occurs, and if the peritoneal covering of the bladder is involved there may be retention of urine or painful micturition. The tendency to heart failure and to collapse is one of the most striking characteristics of acute peritonitis. In all varieties it must be remembered that the disease rarely runs a typical course; even pain may be absent. A sudden collapse attended by a soft, feeble pulse and brown tongue, quickly terminating in death, may be fol- lowed by an autopsy which shows the intestines matted together by recent inflammatory products. When peritonitis follows intestinal perforation, all the symptoms from the onset are severe. The face quickly becomes haggard, drawn, and dejected; the eyes are sunken and surrounded by dark purple rings; the nose and cheeks are pinched, the lips are blue, the upper one being lifted and tightly drawn across the teeth, the voice becomes feeble, or the patient speaks in a husky whisper, the extremities are cold and covered with a clammy perspiration, the radial pulse is hardly perceptible, the respirations assume the type known as " Cheyne-Stokes " respiration, general cyanosis supervenes and death is reached within forty-eight hours. Sometimes death occurs within three or four hours from the shock of the perforation. The mind is usually clear throughout the entire course of the disease ; in infectious peritonitis loss of consciousness, apathy, or delirium may precede death by a few hours. The pulse and the amount of cyanosis are measures of the heart failure. In cases where there is a large amount of fluid effusion the pain subsides with the occurrence of the effusion, and this sometimes leads to a mistake in prognosis on account of the supposed subsidence of the peri- tonitis. In suppurative peritonitis the pain is not infrequently absent, but typl Did symptoms are present from the onset, delirium is the rule rather than the exception, recurring rigors are common, the fever increases toward evening, and the pulse becomes very rapid. Occasionally in typhli- tis, gastric ulcer, and intestinal perforation, the shock of the perforation, 350 DISEASES OF THE DIGESTIVE SYSTEM. or the feeling as if something had suddenly burst, or been torn within the abdomen, is distinctly appreciated by the patient. Local or circumscribed peritonitis usually pursues a sub-acute rather than an acute course. Chronic peritonitis (non-tubercular and non-cancerous) I is usually the sequela of an acute attack. If convalescence is not established during the first week of an acute general peritonitis, the character of the inflammation changes and it becomes chronic. Rigors alternate with irregu- lar sweats, and a steady increase in the size of the abdomen marks the pas- sage from an acute to a chronic peritonitis. There is rapid loss of flesh and strength, and a marked diminution in the general vital powers. The face assumes the haggard, drawn look so often found with chronic abdominal disease. The intense pain of the acute attack subsides, and a "dull ache" ' with more or less tenderness remains. The pain assumes a colicky character and not infrequently is increased by taking food. The abdominal muscles remain rigid and tense. The temperature ranges from 99° to 104° F. The pulse continues rapid and feeble. There is anorexia and progressive ex-. haustion; diarrhoea alternates with constipation. Fluid accumulates in' the peritoneal cavity, sufficient in some cases to cause dyspnoea. The thickenings and adhesions which develop may so interfere with the ve- nous return that oedema, thrombosis and albuminuria may result. In latent general chronic peritonitis there may be large ascitic accumulations, accompanied by abdominal tenderness, loss of appetite and progressive' anaemia. The pulse is small and rapid, the vomiting is persistent, and with I the accompanying diarrhoea exhausts the patient. Recurring attacks of acute local peritonitis hasten the fatal issue. In tubercular peritonitis the pain is paroxysmal in character. Its onset | is often sudden, attended by fever and well-marked constitutional disturb- ance, the pulse is rapid and feeble, there is nausea, vomiting and diarrhoea. I The tongue is heavily coated, thirst is intense, and there is rapid loss of flesh j and strength. The skin becomes harsh and dry. Typhoid symptoms appear early, fluids gradually accumulate in the peritoneal cavity and the patient ' dies of asthenia. Redness and cedema about the umbilicus are regarded as j characteristic of tubercular peritonitis. In some cases the pain is so slight as to amount only to a sense of tension and fulness in the abdomen; and yet there may be a large effusion into the peritoneal cavity. The tongue becomes red and shining, the stomach is irritable; hectic fever is accom- panied by profuse sweats during sleep, and the abdomen has a doughy feel. Some cases are unattended by ascites, and knots of intestine embedded in firm hard masses are felt in the region of the umbilicus. Friction sounds may be heard over these masses. Tubercular peritonitis may have for its chief and only symptoms, ascites, anaemia, and the evidences of geneial tuberculosis ; its progress is interrupted, now there is marked improvement and cessation of all the abdominal symptoms, and then there follows a period when death seems imminent. As a rule, there is moderate fever and slight pain, with considerable ascites. The mesenteric glands are usually en- larged. Cancerous peritonitis is attended by the same local symptoms as tuber- J PERITONITIS. 351 cular. Sometimes a tumor may be felt, especially in the region of the omen. turn and mesentery. There is always ascites ; the fluid collects gradually, and often in very large quantities ; constipation is more frequent than diar- rhoea, and death is often the result of intestinal obstruction. In some cases the abdomen is very sensitive, and paroxysms of colicky pains are not in- frequent. The temperature rarely reaches 100° F. If the peritonitis has extended from the stomach, liver or intestine, the symptoms of the primary disease will have been well defined before the development of the peritoni- tis. At any period in the course of cancerous peritonitis all the symptoms ^ of acute general peritonitis are liable to be developed. The diagnosis rests on the presence of a gradually increasing tumor and the cancerous cachexia. , Differential Diagnosis.—Peritonitis may be mistaken for colic, intestinal ..obstruction (without peritonitis), enteritis, abdominal neuralgia, hysteria, rheumatism of the abdominal muscles, renal and biliary colics, and suppu- rative cellulitis of the abdominal walls. The ascites of chronic peritonitis may be mistaken for that of the last stages of cirrhosis of the liver. The differential diagnosis of colic, intestinal obstruction, and enteritis has al- ready been given. The pain in abdominal neuralgia simulates that produced by a tightly drawn cord about the abdomen, and follows the course of the genito-crural nerve. There is tenderness on pressure only at the point of exit of the nerve from the spine. There is no tympanites, no asci- tes, no rise of temperature, or acceleration of the pulse, and no signs of -collapse. The muscular rigidity of commencing peritonitis is absent. In hysteria, the patient is ready to complain of increased pain before the [hand touches the abdomen, yet the firmest pressure does not increase the pain if the attention of the patient is engaged. The pulse, temperature, and signs of collapse of peritonitis are absent, the countenance is not that of peri- tonitis, and there is present the globus hystericus, and the attack is followed by the passage of a large quantity of watery, straw-colored urine. In rheumatism of the abdominal muscles, the pain and tenderness are most intense at the origin and insertion of the muscles. There is no rise of temperature, no vomiting, and no signs of collapse; the pulse is normal, and there will be a history of acute or sub-acute articular rheumatism. In the passage of a gall-stone, and in renal colic, the patient throws him- self about in excruciating agony, and the pain is referred to the region of the common bile-duct, or to the course of the ureter. In the passage of a gall- stone, it is paroxysmal in character, and will shoot back from the margin of the ribs over the gall-bladder to the spinal column. If it continues twenty- four hours, the patient becomes jaundiced. In renal colic the pain radiates from the kidney along the ureter to the testicle, which is retracted. Both are accompanied by characteristic changes in the urine or faeces, neither is attended by rise of temperature or great acceleration of pulse, and there is no tympanites or tenderness on firm pressure in either. Suppuration of the abdominal parietes is at first difficult to distinguish from peritonitis, but after the first two days the superficial swelling and the absence of the constitutional symptoms of peritonitis establish the diagnosis. 352- DISEASES OF THE DIGESTIVE SYSTEM. Prognosis.—Acute general peritonitis is a very fatal disease. Its average duration is from four to eight days ; death may occur in a few hours, or be delayed two or three weeks. The prognosis in any case is to a great extent determined by its cause ; it is most unfavorable when it results from perfora. tion, intestinal obstruction, or sepsis. General puerperal peritonitis is almost always fatal. The presence of typhoid symptoms, a very rapid and feeble pulse, cold extremities,with the other symptoms of impending collapse, in- dicate an unfavorable termination. Peritonitis from rupture of an organ is al- ways fatal. The prognosis is favorable when the peritonitis is due to extension of inflammation from a viscus. When the pain and vomiting cease, the tym- panites subsides, the pulse diminishes in frequency, the temperature reaches the normal, and the patient is able to turn in bed, a favorable termination is to be expected. Chronic diffuse peritonitis in children, unless purulent, usually terminates in recovery. Tubercular peritonitis, after weeks and months of anaemia and exhaustion, terminates in death. The same is true' of carcinomatous peritonitis. Death in acute peritonitis may result from . shock, from asthenia with typhoid symptoms, and from exhaustion. Among 1 its sequelae are collections of pus, stenosis or complete obstruction of the intestine, pyaemia, and septicaemia. Permanent jaundice may result from narrowing of the bile duct by the contraction of new tissue formations in the transverse fissure. , Treatment.—Acute peritonitis is a severe, rapidly progressive, and dan-' gerous inflammation, and on this account has always been treated heroic- ally. Formerly patients with acute peritonitis were subjected to excessive bleedings, tartar emetic was administered in nauseating doses, and to prolong the effects of the bleeding, and as an adjunct to these calomel was given for its specific effect. At the same time many physicians of recog- nized authority were eager to obtain the purgative effects of cathartics, and ' for this purpose recommended and administered large doses of drastic pur- < gatives. Local bleeding by leeches is often of great service in local perito- nitis, but it should be resorted to only at the very onset of the attack in the I strong and robust. Tartar emetic and calomel, so highly regarded as anti- plastics, have fallen into disuse. While acute peritonitis is progressing the bowels cannot be moved, and no benefit would result if they were; so that under no circumstance should there be an attempt at purgation. The plan of treatment which I have followed for years—a plan which gains in favor with me with every new experience—is the opium plan. Prof. Alonzo Clark first developed this plan and brough't it to the notice of the profession. The details of it are as follows :—as soon as the unmistak- | able symptoms of peritonitis are developed, administer at one dose from i two to five grains of opium or one-half to one grain of morphine. The exact j quantity in each case is to be determined by the condition of the patient; the rule is to bring the patient as soon as possible fully under the influence of the drug. In the treatment of this disease, it will be observed how greatly pain and inflammation modify the effects of this powerful drug. I have adminis- tered to patients with peritonitis four grains of opium every two hours for twenty-four hours, and then have obtained only a moderate effect of the I PERITONITIS. drug. The point which must be reached in its administration is moderate uarcotism, in which state the patient must be kept, not only until all pain and tenderness have subsided, but until the pulse has reached its normal standard and the tympanites has entirely subsided. The question arises : what are the indications which are to govern the administration of each dose of opium ? One must be prepared at the commencement of the treat- ment of a case of peritonitis, according to this plan, to be present and de- cide upon the quantity of opium to be given at each dose, until the patient has fully convalesced. It cannot be trusted to attendants, however intelli- gent they maybe. As the patient is brought fully under the influence of the opiate, it will be noticed that the entire surface of the body becomes bathed in a profuse perspiration. In twenty-four hours a rash, due to the opium, will make its appearance on the surface and neck ; this is accompanied by an itching of the surface and a constant disposition to rub the nose. The pupils become contracted, the eyes suffused, the countenance assumes a dull expression, and there is a constant irresistible disposition to sleep. The pulse becomes lessened in frequency and force, and the respirations, which, before the administration of the opium, may have ranged from 40 to 60 in a minute, become less and less frequent as the patient comes fully under its influence, until they are only twelve in a minute. Now the greatest care is to be exercised in the administration of the opium ; the patient is in the condition in which it is desirable to keep him. By holding him in this state of semi-narcotism, all will be accomplished that can be by the opium plan of treatment, and with the respiration at twelve per minute the patient is perfectly safe. The amount of sleep is not to be taken into account, but the profoundness of the slumber is of great importance. If it is found dif- ficult to arouse the patient, the administration of the opium must be stopped until he can be easily aroused. If by mistake or negligence the patient be- comes fully narcotized, the respirations will sometimes diminish in fre- quency to seven or even five in a minute. In this extremity, if the admin- istration of opium be stopped, the patient will usually rally from its effects after a few hours; but avoid extremes, endeavor to keep the patient in a quiet sleep, not profound, but one from which he can be easily aroused. When the pulse begins to diminish in frequency and becomes fuller, one may be certain that he is controlling the peritonitis, and as it is controlled the patient will become more and more susceptible to the influence of the opium. Slowness of respiration and absence of pain cannot be relied on as sure indications that the opium is controlling the inflammatory action ; but a diminution in the frequency of the pulse, and a subsidence of the tympa- nites are sure indications that the peritonitis is arrested, and that ultimate recovery is probable. In most cases, if an acute peritonitis does not depend for its exciting cause upon the escape of intestinal gases into the peritoneal cavity, or upon complete intestinal obstruction, the inflammatory action can be controlled within forty-eight hours from the commencement of the attack by adopting, within twelve hours, this plan of treatment. It must, however, be continued four or five days longer, for there is still danger of i renewal of the inflammation. As the condition of the patient demands 23 * 354 DISEASES OF THE DIGESTIVE SYSTEM. less opium, the dose may be diminished, or the interval between the doseg lengthened. A safe rule by which to be guided is that, so long as any tympanites exists, the opium should be continued. When convalescence is fully established, one should not be too anxious to overcome the constipation which usually exists, for a free, spontaneous movement of the bowels generally follows a complete subsidence of the peritonitis. Wait at least a week for this result before administering a ca- thartic, and then, if necessary, employ one mild in its action, such as cas- tor-oil. Warm poultices over the abdomen are usually the only local appli- cation which I have employed. It is claimed by some that cold compresses have a much more beneficial effect than warm applications. My experience leads me to doubt the utility of the former, while the latter are far safer, and I believe equally efficacious. It has been stated that when the peritoni- tis becomes general, excessive gaseous distention of the intestines occurs, and this distention greatly increases the danger to the patient; under such circumstances I have recently resorted to minute puncturing of the dis- tended intestine with a hypodermic or a very small aspirating needle, and have thus relieved the intestinal distention by allowing the gas to escape. By so doing, not only is the tension of the peritoneum (which becomes an exciting cause of the peritonitis) relieved, but the principal obstruction to the respiration is removed, and thus cyanosis is diminished. Immediate and marked relief is afforded by such a procedure, and as thus far I have had no bad results follow, I am disposed to resort to it in all cases where the abdomen becomes excessively distended and tympanitic. I remember one case in which the gaseous distention was excessive, and the peritonitis was supposed to be due to strangulation of a portion of intestine from old peri- toneal adhesions, where the relief of the distended intestine by puncture was soon followed by a removal of the intestinal obstruction and the rapid recovery of the patient. From this circumstance I can readily understand how a portion of intestine that was'partially constricted by a band of ad- hesion might become completely obstructed at the point of stricture by a rapid gaseous distention of the intestine above the point of constriction, and the relief of the intestinal distention by puncture would very likely liberate the constricted portion and thus overcome the strangulation, and so, per- haps, save the life of the patient. The necessity of absolute quiet, and of the frequent administration of nour- ishment and sometimes of stimulants, in small quantities, to this class of patients, is apparent. Preceding and during the stage of plastic exudation, large doses of quinine are beneficial; but little nutriment should be admin- istered, and that only in a fluid and a highly condensed form. Cracked ice may be given to relieve the thirst, and, if there are signs of asthenia, iced champagne or brandy should be given in small doses. If hiccough is dis- tressing, it should be relieved temporarily by the inhalation of chloroform. Vomiting is sometimes allayed by carbonated water, cracked ice and cham pagne, or hydrocyanic acid. Turpentine, as an injection and employed It cally as an embrocation, will sometimes relieve the tympanitis. With th asthenic form of peritonitis, a stimulating plan of treatment should be em ASCITES. 355 ployed with the opium. In puerperal peritonitis, great attention should be paid to the condition of the uterus and its appendages. Chronic peritonitis is treated by local applications of iodine and mercury, and by the internal use of iodide of potassium. Its products may be removed by tapping. The nutrition of the patient must be carried to the highest point. Tubercular peritonitis demands small doses of opium, warm anodyne applications, and the administration of tonics, cod-liver oil especially. The treatment of can- cerous peritonitis is purely symptomatic ; nausea and attacks of diarrhoea and constipation must be promptly relieved. Narcotics may be given for the sleeplessness. Concerning the prophylactic and sanitary treatment of puerperal peritonitis, the reader is referred to obstetrical works. ASCITES. {Abdominal Dropsy.) Ascites is a local dropsy,—an accumulation of serum in the peritoneal cavity. It has also been called peritoneal dropsy, dropsy of the abdomen, and hydro-peritoneum. The circumstances under which it occurs are similar to those which allow of general dropsy—viz. : obstruction to the capillary or lymphatic circulation of the peritoneum, a diminished amount of albumen in the blood, and inflammations of the peritoneum. Those hydraemic conditions which accompany exhausting chronic diseases, espe- cially diseases of the kidneys, will induce it. One or several of these con- ditions may be present in the same case. Morbid Anatomy.—The amount of fluid present in ascites may vary from a few ounces to four or five gallons. In consistency it may be viscid or watery. It is usually of a light straw color, having a faint greenish opal- escent tint. It may be opaque and dark, from admixture of blood. With disease of the lymphatics it is milky and opalescent. Sometimes it does not differ in appearance from pure water. It is alkaline in reaction, and may contain albumen, blood, fibrin, fibrinogen, bile-pigments, kreatin, kreatin- in, lymph flocculi, and bile acids. Pus cells are present, though they vary in number in different cases. The endothelia of the peritoneum are turbid, thick, and in various stages of fatty degeneration. The sub-serous tissue is thickened, and the whole membrane has the look and feel of being water-logged. The blood changes that cause it consist chiefly in a diminu- tion of albumen and an increase of water. Compression, dislocation, and diminished function of the abdominal viscera are the results of the ascitic accumulation. Etiology.—Ascites may be a late symptom of general dropsy. In most other instances it results from damming back of the blood in the portal tributaries, from pressure on the portal vein—either from hepatic and abdominal tumors, or from a diseased condition of the liver substance— as in cirrhosis, waxy degeneration, abscess, hepatic atrophy, portal throm- bosis, enlarged lymphatics in the transverse fissure, and the constrictions due to perihepatitis. These all mechanically impede the blood current in 356 DISEASES OF THB DIGESTIVE SYSTEM. the portal vessels. Diseases of the heart or lungs which interfere with the normal flow of the blood from the cavae will induce it in connection with general dropsy ;—under this head are included tricuspid obstruction and insufficiency, chronic bronchitis and emphysema, fibrous phthisis, and cer- tain forms of mediastinal tumors. Anaemia, hydraemia, chlorosis, malarial cachexia, purpura, chronic arsenical poisoning, scurvy and chronic Bright's disease, producing hydraemia—and old age or great exhaustion without structural disease__lead to what is often called asthenic ascites or cachectic- dropsy. Peritoneal dropsy not infrequently accompanies extensive degen- eration of the peritoneum, such as tubercle and carcinoma. Finally, ascites may occur from unknown causes—from taking cold, after suppression of the menses, after the sudden disappearance of acute and chronic cutaneous eruptions and ulcers, and perhaps from atmospheric causes.1 It has been suggested that malignant disease of the ovaries and other pelvic organs, and of "the mesenteric and retro-peritoneal glands, obstructs the capillaries.and the lymphatic orifices, increasing the functional activity of the endothelia, and thus induces ascites.2 Symptoms.—The first sign of ascites is a gradual increase in the size of the abdomen. The enlargement in simple ascites takes place without pain, tenderness, or local subjective symptoms. There is a feeling of fulness. and the patient is rendered uncomfortable by pressure of the fluid. The respiratory movements are interfered with, and dyspnoea soon results. The functions of the stomach may be disturbed, and there may be vomit- ing, anorexia, and perhaps haematemesis. Flatulence and diarrhoea are frequently present, but when the accumulation of fluid is large it producer colicky pains, and often obstinate constipation. All these symptoms ar relieved as soon as the fluid is removed. Gradually the dyspnoea increases, the patient walks with difficulty, with the legs spread widely apart; tlu urinary secretion is diminished from the pressure on the kidneys and renal vessels. The recumbent posture greatly aggravates the dyspnoea. The skin and mucous membranes become dry ; the liver and pelvic viscera are displaced ; the heart and lungs are pushed upward, and the skin over the abdomen becomes tense and shining. The umbilicus is bulged out in the form of a globular tumor. The superficial veins are enlarged and tortuous. If" the inguinal canal is open, fluid may pass into the scrotum ; and ex- cessive ascites, by pressure on the vena cava, causes oedema of the feet and legs. In hepatic diseases the fluid is chiefly confined to the abdomen, bui in cardiac and pulmonary dropsies the fluid accumulates first about the feet and extends upward, and the abdominal dropsy is then a part of a general anasarca. In hepatic dropsies the extremities emaciate while the abdomen enlarges ; the skin has a muddy jaundiced hue, and the patient becomes exhausted and apathetic. Jaundice, uraemia, delirium, convulsions, coma, and cholaemia are prominent symptoms as death approaches. Physical Signs.—The physical examination of the abdomen is most im- portant in the diagnosis of ascites. Inspection.—The abdomen, if distended with fluid, presents the appear- i Wagner, Gen. Path., pp. 334-5. a Oppolzer. ASCITES. 357 ance of a globular or dome-like tumor, the false ribs are elevated and pressed out, and the superficial veins are visible arid prominent. The cir- cumferential measurement of the abdomen will often be three times as great as normal. If the effusion is moderate, the shape of the abdomen changes with a change of the position of the patient: it broadens when he lies on his back, and when he stands the enlargement will be confined to the lower portion. The fluid always gravitates to the most dependent portion. Palpation.—Fluctuation is obtained when the level of the fluid is above the pelvic brim. To obtain the wave most distinctly place the patient on his back, place the flat of the hand on one side of the broadened abdomen, and with the other hand give one smart tap at a point opposite ; the im- pulse of the blow will be felt by the palm of the hand. Percussion.—There will be flatness below the level of the fluid, and tympanitic resonance above. The line of dulness changes with the change of position, and accurately measures the amount of fluid. When only a small amount of fluid is present the physical signs of its presence are commonly obtained by placing the patient in the " knee-elbow " position. Differential Diagnosis.—Ascites may be mistaken for ovarian dropsy, dis- tended bladder, pregnancy, hydatid cysts of the liver, and enlargement of the spleen. It is important in making a differential diagnosis between ascites and ovarian dropsy to have a perfect history of the case. The ab- dominal enlargement in ascites is uniform, in ovarian dropsy it is irregu- lar. Ascites, however slight, begins at the most dependent portion of the abdomen, while ovarian dropsy begins in one of the iliac fossae and gradu- ally extends upwards toward the umbilicus. With every change of posi- tion, in ascites, the line of dulness changes ; a large ovarian cyst is to be recognized by its fixed position and non-gravitation of its fluid. In ascites there is fluctuation on palpation ; in ovarian dropsy, fluctuation is absent or localized. The abdomen is usually tympanitic above the level of the fluid and flat below in ascites, while in ovarian tumor there is often a tym- panitic percussion sound at the most dependent portion of the abdominal cavity. In ovarian dropsy the outline of the cyst is generally appreciable, except in very large tumors where the peculiar form of the cyst may be lost, but a rectal or vaginal exploration will generally at once remove all doubts. In ascites there will generally be a history of liver, heart, or kidney disease, and the uterine organs and functions will be normal. On tapping the abdomen a serous fluid will be withdrawn in ascites ; in ovarian tumors, it may be dark, highly albuminous, and contain Drysdale's corpus- cles, supposed to be characteristic. A distended and sacculated bladder may be mistaken for dropsy, but the introduction of the catheter will decide the question. Pregnancy will afford ballottement, placental bruit, the sounds of the foetal heart, and will be accompanied by distinct mammary changes. The uterine tumor can be distinctly mapped out, and a vaginal examination combined with external palpation will rarely fail to make a differential diagnosis between it and ascites. 358 DISEASES OF THE DIGESTIVE SYSTEM. An hydatid cyst of the liver produces flatness undeviating in area, which gradually extends from above downwards, and seldom reaches the pelvic brim. Hydatids produce hydatid fremitus on percussion, which is charac- teristic. Again, on withdrawal of the fluid, a miscroscopical examination will often discover the hooklets of the echinococci. Enlargement of the spleen is unsymmetrical; the tumor is fixed, there is no tympanites, no fluctuation, and the boundaries of the enlarged organ can be mapped out on palpation and percussion. Usually the notch at the anterior border of the spleen is so distinct that it at once indicates the gland. Prognosis.—The prognosis depends upon the conditions under which the ! ascites occurs ; if it is dependent upon organic disease of the liver, heart, ' or kidney, the prognosis is unfavorable, but when it is not dependent upon i structural visceral lesions, e.g., idiopathic and anaemic ascites, the prog- nosis is good. The ascitic accumulation may take place rapidly, or weeks < or months may elapse before the cavity of the abdomen is distended. The average duration of hepatic ascites is about six months. So long as the cause remains, the fluid will accumulate. Ascites may terminate in re- covery by the spontaneous or mechanical removal of the fluid, or by the removal of its cause, or it may terminate in death from complications, as peritonitis, albuminuria or heart-failure, or from pure slow asthenia. j Treatment.—The first and most important thing in the treatment of ' ascites is to discover the cause, and either to remove or palliate it. In most cases the treatment merges into the treatment, of the diseased condi- tions which produce it. In all cases the diet should be highly nutritious and concentrated ; as little fluid as possible should be taken. The contin- ued use of powerful diuretics and hydragogue cathartics usually does harm. They weaken the patient and often favor rather than retard the \ ascitic accumulation. Elaterium is the most efficient drastic cathartic, i the potash salts, nitre, squills and juniper are the most efficient diuretics. J Jaborandi has recently been much employed for the removal of dropsical J accumulations. In most cases these accumulations can he rapidly removed , by this drug, but my own experience leads me to the conclusion that it hastens rather than retards the fatal issue. Hot-air baths should never be , employed for the removal of ascitic accumulations. Paracentesis abdominis will have to be resorted to sooner or later in these j cases, but the rule is to postpone it as long as possible. I am, however, j in favor of tapping before the accumulated fluid has caused pressure J upon the viscera. I am convinced that whenever fluid accumulation takes | place in the peritoneal cavity, tapping should be promptly resorted to, unless the cause can be removed by mild cathartics or non-stimulating diuretics; and the number of recoveries and the prolongations of life which have followed this course in my experience cause me unequivocally to recommend it in preference to the prolonged use of those remedial measures which increase the discharges from the skin, kidneys and bowels, j In a large number of cases, improvement of the patient's general health by : tonics, of which quinine, iron and cod-liver oil are the best, is followed by j ACTIVE HYPEREMIA OF THE LIVER. 359 subsidence of the dropsy, and its return is also prevented for a long time after its removal by tapping. DISEASES OF THE LIVER. Diseases of the liver may be classified under the following heads : L Hyperaemia:— III. Degenerations :— a. Active or Fluxion. Amyloid or Lardaceou*. b. Passive or Congestion. Fatty. II. Inflammations :— Pigmentary. a. Interstitial Hepatitis or Atrophy. Cirrhosis. IV. New Growths :-- b. Circumscribed Hepatitis or Cancer. Abscess. Gummata. c. Diffused Hepatitis or AcuU Hydatids. Yellow Atrophy. Tubercle. Perihepatitis, Local or Gen- V. Jaundice, Hepatogenous and eral. Hematogenous. Pylephlebitis, Adhesive and Sup- VI. Diseases of the Gall Ducts purative. and Gall Bladder. VII. Functional Derangements. ACTIVE HYPERAEMIA OF THE LIVER. Active hyperaemia of the liver is an abnormal determination of blood to the organ. It may be acute or chronic. Morbid Anatomy.—A liver that is the seat of active hyperaemia is more or less enlarged in all directions. Its color varies from a light to a dark red. It has a firmer feel than normal, although its consistency is really dimin- ished. The organ is heavier and smoother than normal, its surface present- ing a peculiar shining appearance. On section, its substance shows a uniform red color, blood flows freely over its cut surface, from the arteries and capillaries which are dilated and sometimes tortuous. When the hyperaemia is intense, the glandular sub- stance of the organ is compressed and there may be evidences of sub-peri- toneal effusion. So intense may be the hyperaemia that hemorrhagic soften- ing and apoplectic extravasation result, and isolated clots or an unbroken layer of coagulated blood may be found under its serous covering. In chronic hijpertemia the liver is often' found in a state of partial fatty degeneration, somewhat softened, and of a light red or yellow color. In rare instances, chronic hyperaemia may lead to induration and incipient cirrhosis. In the severer types abscesses may be found, and the infiltration of a substance resembling albumen has in some cases advanced so far as to give distinct colloid degeneration. In syphilitic new-born children, active hepatic hyperaemia is sometimes found associated with a peculiar plastic 360 DISEASES OF THE DIGESTIVE SYSTEM. exudation. It is important to remember that the normal hepatic hyper- emia temporarily developed after hearty meals or the free use of stimulants may be mistaken for active hyperaemia. Both acute and chronic hyper- emia of the liver may be associated with catarrh of the bile ducts. Etiology.—There is a normal functional hyperaemia of the liver induced by an unusually large meal, or one very rich in hydrocarbons, or by the free use of wines : this hyperemia is due to increased blood pressure in the vena porte ; it becomes abnormal in those who daily indulge in eating to excess, especially if they lead sedentary lives. If the liver-tissue, which supports the walls of the capillary vessels, becomes relaxed, there will be an abnormal afflux of blood to the organ. This is the case in traumatic hyperemia, where a blow over the viscus causes a localized fluxion. Any inflammation or growth causing softening of the parenchyma will induce it, The action of drugs, spices and alcohol is best explained on this basis. In- tense hepatic hyperemia may be caused by miasmatic influences, malaria, and other blood-poisons. Under the latter head is included a peculiar active hyperemia which occurs in the livers of syphilitic children, and in secondary syphilis of adults. High temperature undoubtedly gives rise to active hepatic hyperaemia, especially when it is associated either with acute or chronic malarial infection, Vaso-motor disturbances may undoubtedly lead to active hepatic hyperaemia. It sometimes occurs during and after pregnancy from some unknown cause ; also before the establishment of the menses, and during the menopause. Capillary embolism may cause local- ized hepatic hyperaemia. Symptoms.—Active hyperemia of the liver is usually attended by a sense of weight and constriction in the right hypochondrium, with some tender- ness on pressure under the free border of the ribs. In active malarial hyperaemia, there is also gastro-intestinal catarrh, nausea, vomiting, diar- rhea, and slight jaundice. There is a bitter taste in the mouth, loss of appetite, coated tongue, drowsiness and apathy. Headache is frequent, and the patient complains of pain shooting up the right side to the right shoulder. This pain is due to pressure on the phrenic nerve, and is more intense after meals and when lying on the left side. A sense of dizziness comes on when the patient assumes any other position than on the back or right side. It is more or less increased by pressure upward against the liver. In severe cases of malarial hyperaemia, or when it is associated with extensive blood changes, such as scurvy, the symptoms are often masked by those of the condition with which it occurs. Physical Signs.—Inspection in severe cases may show bulging of the right hypochondrium, and loss of motion of the lower ribs on the right side. On palpation the liver is found enlarged and smooth, and its free border is felt below the ribs ; firm pressure against its under surface causes pain. Percussion.—The area of hepatic dulness is increased in every direction, but more vertically than laterally. Differential Diagnosis.—A severe active hyperemia may be mistaken for circumscribed hepatitis with abscess. In circumscribed hepatitis there is PASSIVE HYPEREMIA OF THE LIVER. 361 acceleration of the pulse, rigors followed by a slight rise of temperature, yud localized pain. Recurring chills and sweats indicate the formation of pus. In abscess the hepatic enlargement is irregular, while in active hyperaemia it is uniform. If the case is seen early, and the enlargement is carefully followed, in hyperemia it will be seen to take place rapidly, while in abscess it will be slow. The hepatic enlargement from active hyperaemia may be distinguished from displacement of the liver downwards, by the fact that, although its free border may extend far below the free border of the ribs, the normal area of hepatic dulness is not increased. Prognosis.—Active hyperemia generally subsides as rapidly as it occurs. The only danger is that the causes which produce it may be continued, and lead to some form of hepatic degeneration. Treatment—The main indication in the treatment of this condition is to remove its cause. When high living and alcoholic stimulants cause it, re- strict the diet and stop the alcohol. When it occurs from prolonged high temperature, or from malarial influences, a change of residence is the only remedy. An excess of blood in the liver may be temporarily removed by saline or mercurial purges, by taraxacum or podophyllum ; their action will be increased by the application of one or two leeches about the anus. In active malarial hyperaemia, the mercurial purges and leeches may be followed by full doses of quinine. Turpentine stupes may be applied over a very tender liver. When there is gastro-intestinal catarrh with diarrhea, chloride of ammonium and ipecacuanha will be found of service. In those who have a predisposition to active hepatic hyperemia, the daily use of mineral waters will be found of service. PASSIVE HYPERAEMIA OF THE LIVER. Passive or mechanical hepatic hyperaemia ("congestion of the liver") consists in an excess of blood, chiefly in the portal veins, with a slowed current. Morbid Anatomy.—A congested liver, in its early stage, is larger, heavier and darker in color than the normal liver, the extent of the increase in size corresponding to the degree of the congestion. The capsule may be stretched tightly over the enlarged organ, and present a shining appear- ance. The consistency of the organ is increased, frequently amounting to a stony hardness. On section, the cut surface appears mottled, rarely uniformly red in color ; the small dark spots seen upon its cut surface are the enlarged and thickened veins in the centre of the liver lobules, and as the return of blood by these veins is impeded, the surrounding cells undergo atrophy, and a granular pigment is deposited about the venae centrales. This change in color is made more apparent by a deposit of fat globules in the periphery of the lobules, which causes a dirty white ring around the dark central spot. Occasionally there are yellowish spots about the central vein due either to a catarrh in, or obstruction of the bile ducts, or to distention 362 DISEASES OF THE DIGESTIVE SYSTEM. of the minute ramifications of the portal vein. In the advanced stage ol hepatic congestion, the liver is diminish- ed in size and has a peculiar hard feel. On section, it presents the characteristic " nutmeg " appear- ance, which has been called the red granu- lar liver. The proc- esses which were es- tablished in the ear- lier stage of the con- gestion, and the new conn ective- tissue which has been de> veloped in the inter- lobular spaces, dimin- ish the parenchyma of the organ.1 The rootlets of the central vein become dilated and hypertrophied and crowd upon the liver cells ; thus the central spot spreads nearly to the periphery of the lobules. Atrophy of the cells grouped around the central vein occurs, and a soft pultaceous mass, in which appear new vessels, takes their place. The cells at the periphery are in a state of fatty infiltration, and connective-tissue passing inward from the interlobular spaces produces the contracted, stony hard liver. In connection with these changes in the liver, the mucous mem- brane of the stomach is usually the seat of chronic catarrh, and the spleen is enlarged. Etiology.—The causes of hepatic congestion are mainly included under the head of impeded venous return. Heart disease is the most fre- quent cause of such obstruction. The damming back of the blood in the hepatic veins is the necessary result of tricuspid insufficiencj', and of right heart failure. When right ventricular hypertrophy fails to compensate for valvular lesions in the left heart, or when disease of the lungs, as emphyse- ma and chronic pleurisy, obstructs the blood current in the pulmonary artery so that the right ventricle is unable to empty itself, engorgement of the hepatic veins necessarily follows. The absence of valves in these veins, and the fact that they cannot collapse, favor this result. In the same way enfeebled heart power, occurring in the course of exhausting diseases, causes congestion of the liver. Habitual constipation and a sedentary * <*&'* Fig. 65. Passive Hepatic Hyperemia. Section of liver showing a single lobule. A. Central vein of lobule. B. Area ofcongestion.— Vessels filled with blood, crowding the hepatic cells'. C. Atrophied liver cells. D. Commencing fatty infiltration of cells in peripheral zone, x 350. 1 Atrophy is chronic congestion with dilatation of the central vessels and their radicles. PASSIVE HYPEREMIA OF THE LIVER. 363 mode of life, either singly or combined, may produce it. The sudden suppression of long-continued hemorrhages, as monorrhagia, or bleed- ing hemorrhoids, may lead to passive hyperemia of the liver. A large mediastinal tumor, such as a thoracic aneurism, may also produce it by pressure on the cava. Symptoms.—As there is usually some derangement in the circulation of the thoracic organs, the early symptoms are very apt to be confounded with those of cardiac or pulmonary disease. But soon slight jaundice follows the headache, drowsiness and apathy, and it lacks the peculiar greenish hue of that which sometimes accompanies the cyanosis of long-standing heart disease. Gastric catarrh will usually attend these symptoms, marked by loss of appetite, nausea, and vomiting. In the "India Liver" there is anaemia, and soon a cachexia is developed. The skin is dry and harsh. Later, hemorrhoids appear, and after a paroxysm of dyspnea and cyanosis the hepatic dulness is markedly increased. In severe cases haematemesis may occur. If congestion has reached the stage of induration, the gastric symptoms become greatly aggravated, and tympanitis, gastric hemorrhage, and general dropsy occur. The bowels become constipated, and the faeces clay-colored. The urine is scanty, high-colored, and usually presents traces of albumen ; it is loaded with lithates. These patients finally become irrit- able, and are subject to fits of palpitation and irregularities of the pulse. Physical Signs.—Inspection may show slight bulging of the right hypo- chondrium and some restriction in the movements of the lower portion of the right thoracic walls. Palpation.—In its early stage, the free border of the liver is readily felt below the margin of the ribs ; it is smooth and tender. Later the organ is diminished in size, but its free margin can still be felt, and is hard and uneven. Percussion.—At its commencement the normal hepatic dulness is in- creased in every direction, and firm percussion elicits pain. In advanced cases the area of hepatic dulness is uniformly diminished. It is always important to subject the chest to a thorough physical examination to deter- mine the presence or absence of pulmonary or cardiac disease. Differential Diagnosis.—Congestion of the live/ may be so masked by the primary disease which produces it, that it will be overlooked, but it will rarely be confounded with any other form of hepatic disease. Prognosis.—The prognosis depends upon the condition which causes it. If constipation and a sedentary life cause it, the prognosis is favorable. In chronic pleurisy and emphysema it can only partially be relieved. When it is associated with extreme cardiac disease, recovery is impossible and re- lief is only temporary. Treatment.—When the symptoms which attend congestion of the liver are urgent, a mercurial purge or a brisk saline cathartic with the applica- tion of a few leeches about the anus will give relief. If the symptoms are not urgent, a mild laxative followed by a course of mineral waters will be beneficial. If the gastric symptoms are severe leeches may be applied over the stomach. The diet must be as free from carbo-hydrates as is 304 DISEASES OF THE DIGESTIVE SYSTEM. compatible with nutrition. Nitro-muriatic acid internally and externally is recommended by English and East Indian physicians. Chloride of ammonium and iodide of potassium are often advantageous, reducing the enlarged organs. In some cases of extensive cardiac disease, mineral waters are not well borne; and although digitalis will relieve the conges- tion, it is apt to interfere with digestion. Each case is peculiar and requires its special treatment, which at best is only palliative. INTERSTITIAL HEPATITIS. (Cirrhosis.) Interstitial hepatitis is an inflammation of the connective-tissue of the liver. It has been variously named sclerosis of the liver, cirrhosis, the "gin-drinker's" liver, the " hob-nailed " liver, granular, and gouty liver. Cirrhosis of the liver, the name most commonly used, was first applied by Laennec. It means yellow, referring to the color, and not to the consis- tence of the organ. Morbid Anatomy.—The anatomical changes in interstitial hepatitis begin in the connective-tissue covering the smaller twigs of the vena porte, and gradually extend to its larger branches. The hyperplastic process consists in the formation of a soft, red, pulpy or gelatinous mass, which makes its appearance first in the portal canals. This mass consists of an immense number of small round cells, which soon undergo fibrilization and form new connective-tissue. The new tissue contracts ; this contraction may be limited, or it may involve the whole organ. In the latter case, both stages—namely, the stage of enlargement due to the hyperplasia, and the stage of diminution in size, the result of connective-tissue contraction- may exist in the same liver at the same time. The new tissue, contract- ing, presses on the portal capillaries and liver-cells, and gradually en- croaches on the intra-lobular structures, causing atrophy and disappearance of the cells at the periphery of the lobules, while those at the centre un- dergo fatty change, the result of defective nutrition. Sometimes the cells at the periphery undergo fatty change before they atrophy. The bile-ducts and hepatic capillaries suffer from compression, and the cells around the central vein are bile-stained. In the first stage of cirrhosis, the liver is slightly enlarged, noticeably in the vertical direction ; it is resistant and hard to the feel, the edges are rounded and smooth, and the capsule becomes opaque and thickened. Upon the capsule are numerous small flattened projections, which are, however, not sufficiently prominent to destroy the smoothness. In the first stage the liver is uniformly enlarged and hyperemic. In the second stage it is smaller than normal, the left lobe usually being but a caudal-like append- age to the right, which is nearly globular in shape. The whole organ presents a hob-nailed appearance, and is hard, rough, leathery and granu- lar. The serous covering assumes a dull gray color, and fibrous bands bind the organ to the adjacent parts, especially to the diaphragm. In syphilitic cirrhosis these changes are in patches, which are large and well defined. INTERSTITIAL HEPATITIS. 365 On section the liver-tissue, during the first stage, is extremely hvper- gemic. The new cell growth around the branches of the portal vein and be- tween the lobules has a pulpy, fleshy look. In the second stage, the liver gives a cartilaginous feel to the knife, and the capsule is thickened and resistant. The cut surface presents a yellow, mottled appearance, the mottling being due to three changes: first, the non-vascular fibrinous bands, which are of a slate color ; second, the obstruc- tion of the bile ducts inter- fering with the outflow of bile, and the centres of the atrophied cells becoming pigmented ; third, the cells at the periphery of the lobes becoming the seat of fatty degeneration. The new- formed connective-tissue is filled with an abundance of round cells, formerly called nuclei; they are now known as lymphatic corpuscles, and are probably emigrated leu- cocytes. The smaller branches of the portal vein are shrunken and twisted, and in extreme cases new capillaries are developed, which communicate with both hepatic and portal vessels. Again, a whole lobule may have disappeared and its place be occupied by connective-tissue. The bile-ducts have their commencing rootlets destroyed and their mucous membrane tumefied. In cases of long-standing cirrhosis, the gall-bladder will be found bound to the adjacent parts by adhesions, and its walls are thick and tough ; while the spleen is enlarged, softened and congested. The gross appearance of the liver in cirrhosis may vary in different cases, but the anatomical lesions are the same in all. There is a form of this disease which has been called hypertrophic cirrhosis, because the liver is markedly increased in size, sometimes reach- ing six or seven pounds in weight ; but the fibroid change, the yellow staining, the atrophy of liver-cells, and the fatty change at the periphery of the lobule, are the same as in the ordinary variety, the only difference being i marked increase in the size of the liver. As a result of the compression and obliteration of the branches of the Fig. 66. Interstitial Hepatitis. Section of liver in advanced cirrhosis, as shoivn by low mag nifying power. A, A, A. Bands of connective-tissue. B, B, B. Branches of portal vein. V, C, C. Hepatic ducts. D, 1). Newly formed connective-tissue. E, E, E. Lobules, separated by the advancing cirrhosis. F, F. Lobules nearly obliterated, x 40. 366 DISEASES OF THE DIGESTIVE SYSTEM. A portal and hepatic vein from the new connective-tissue in the advanced stage of cirrhosis, a chronic venous congestion occurs in those viscera which empty their blood into the portal vein. The spleen, stomach and intestines consequently be- come the seat of chronic ve- nous congestion. The result of this is, that with cirrhosis of the liver we find an en- larged spleen, and a chronic gastric and intestinal catarrh. If the portal obstruction is very great, there will be trans- udation of serum from the vessels of the peritoneum into the peritoneal cavity, causing ascites. Etiology.—The chief cause of cirrhosis is the intemperate use of alcohol. Alcohol is most rapidly absorbed when the stomach is empty. AVhen it is taken in a concentrated form without food it acts as Interstitial Hepatitis. ,. , . . . . . , Same tissue as in last illustration, more highly magnified. ^ 0.11 ect irritant to tlie UCpatlC A, A, A. Connective-tissue of a portal canal, containing, B, B, circulation. If this irritation Hepatic ducts; C, C, Portal veins ; and D, D, Hepatic ar- . . . teries. is long continued interstitial E. A/roplii'd liyxt/ic cells in periphery of a lobule. , ... . ,-, .. ml F. Infill ratio,, of round cells—the commencement of the new con- hepatitis IS the result. InOSe nectice-tissue growth, x 300. i j. l i ^ i i i» i i who take alcohol before break- fast as well as through the day are almost certain to develop cirrhosis of the liver. Those who partake freely and daily of highly seasoned food, even though they may not use alcohol, are also liable to develop this disease, especially if they reside in hot climates. Syphilis, gout and rheu- matism cause it. Gout, especially starting from faulty liver digestion, is liable to develop cirrhosis. Malarial hyperemia, if long continued, may lead to it. Extension of inflammation from the capsule of Glisson may develop cirrhosis. It may also occur without any assignable cause. Symptoms.—The early symptoms of interstitial hepatitis are those of hepatic congestion. Following the dull pain and tenderness in the hepatic region, the dyspnoea, apathy, headache, nausea and furred tongue, there is loss of appetite, especially for meats. The individual has a desire for food, but after a few mouthfuls the sense of hunger gives place to loathing; this occurs most frequently at breakfast. Diarrhea alternates with con- stipation, and distressing attacks of retching, especially on waking in the morning, are followed by intestinal pain and flatulence. As the dyspeptic symptoms increase, slight jaundice appears, but it is never very marked, for although the bile secretion is diminished, there is no obstruction to its INTERSTITIAL HEPATITIS. 367 passage into the intestine. Hemorrhoids are early signs of obstructed portal circulation and are a very constant accompaniment of cirrhosis, and, with the gastric symptoms, are the earliest indications of obstruction to the portal circulation. If cirrhosis has been induced by the excessive use of alcohol, a craving for alcohol persists. Attacks of vertigo and occasional Blight elevations of temperature with emaciation and cachexia mark the end of its first stage. The dingy hue of the surface, which was early present, disappears, and the skin gradually assumes an earthy pallor, rarely tinged with yellow. The increase in the hepatic symptoms and the severe pain and tenderness over the hepatic region, which are sometimes present, are due to intercurrent attacks of perihepatitis. At the commencement of the second stage gastritis is established as a result of the mechanical obstruction to the capillary circulation of the mucous membrane of the stomach, and is marked by acidity, nausea, and often by vomiting after taking food, in consequence of which emaciation, weakness, and depression of spirits occur; venous stigmata may now appear on the cheeks. The obstruction of the vessels of the gastric mucous mem- brane is often so great that haematemesis occurs, and although the patient may experience temporary relief after the first bleeding, the hemorrhage will recur, and may be the direct cause of death. Intestinal hemorrhage occasionally occurs from the same cause. If there is persistent diarrhoea during this stage, it indicates that there is gastro-intestinal catarrh. Tym- panites, as well as intestinal catarrh, usually precedes the occurrence of ascites, which is slow and insidious in its advent, and so masked by the preceding tympanitic distention that it is often difficult to determine the exact time of its occurrence. It will usually be noticed that, before the appearance of the ascites, the abdominal veins, especially of the right side, are distended, sometimes enormously. Ascites is sometimes absent in advanced stages of cirrhosis. When this happens, any or all of the following conditions may exist to ac- count for its absence : first, during the contraction of the new connective- tissue, the branches of the vena portae sometimes remain patent. Second, the hemorrhoidal branches of the inferior mesenteric may inosculate with the internal iliac. Third, the veins of the colon and duodenum may anastomose with the left renal vein. Fourth, the phrenic vein may com- municate with some of the more superficial branches of the vena porte. Fifth, new vessels may be formed in the adhesions Avhich bind the liver to the adjacent parts, and thus relieve the obstructed portal circulation. Sixth, the portal and hepatic vessels may anastomose sufficiently within the liver to relieve the portal obstruction. Seventh, branches of the vena portae, which are distributed on the under surface of the diaphragm, and on the inner surface of the abdominal parietes, may anastomose with the internal mammary and epigastric veins, and thus assist in-returning the blood to the right auricle. When the internal mammary in its turn be- comes engorged, there is a dark bluish mass surrounding the umbilicus, due to distention of the cutaneous veins, and called the "caput Medusa) " 368 DISEASES OF THE DIGESTIVE SYSTEM. When ascites is once developed it progressively increases. By its pressure dyspnea and often pulmonary cedema are developed, and the gastric de- rangements are so increased that rapid emaciation quickly follows its accumulation. (Edema, beginning in the feet, gradually extends upward. Fluid drawn from the abdominal cavity is of a pale amber color, highly albuminous, and of a specific gravity varying from 1.010 to 1.020 ; it is not turbid, and contains no inflammatory products. Slight jaundice may ap- pear with the ascites, but if excessive is due to pressure on the ducts, either from connective-tissue indurations or from enlarged lymphatics in the trans- verse fissure, which obstruct the outflow from the bile ducts. The mind is usually clear to the last, but sometimes the patient will pass into a state of complete stupor, Avhich is preceded by delirium and active cerebral symptoms. At first, it seems plausible to ascribe the cerebral symptoms to cholemia, but I have found the jaundice in inverse proportion to the cerebral symptoms. Cholaemia may occur in cirrhosis, and then, of course, exhibits its peculiar train of symptoms ; but I think the more reasonable view is the one that ascribes the delirium, coma, and other cerebral symp- toms which come on late in this disease, to alcohol. The stools in cirrhosis are characteristic. They are clay-colored in the centre ; surrounding this there is a dull pinkish ring, and around this a slaty gray ring tinged with mucus. The urine is scanty and very dark colored; in one-third of the cases it contains albumen. Bile pigment is present in the urine when jaundice exists. The urine is rich in urates, and a pinkish sediment of lithates is very common. Physical Signs.—Inspection, in the early stage of cirrhosis, may show a slight loss of motion over the lower portion of the right side. In a few in- stances the faint outline of the liver margin is seen below the free border of the ribs. Palpation.—The surface of the liver is smooth, or finely granular; the edges are round ; on firm pressure there is a marked tenderness, and more or less resistance. Percussion.—The area of hepatic dulness is somewhat increased in the early stage (especially over the right lobe) in a vertical direction, and so, too, is the area of splenic dulness. Inspection, in the advanced stage, shows enlargement of the superficial veins of the abdomen, chiefly on the right side, and the caput Medusce is often visible. There is usually more or less ascites, and the face and sur- face of the body are clay-colored, often tinged with yellow. Palpation is best performed when the patient is lying on the left side, and if the surface of the liver can be felt, it will be uneven and hob-nailed, with sharp, firm edges. Percussion gives a diminished area of hepatic dulness, and the left lobe of the liver may be so small that the line of hepatic dulness will not extend to the left of the median line. Persistent tympanitic percussion is present above the line of the fluid, and flatness below. The spleen is markedly en- larged, and the splenic dulness extends below the free border of the ribs. INTERSTITIAL HEPATITIS. .'369 Differential Diagnosis.—The early stage of cirrhosis may be mistaken for fatty or waxy degeneration of the liver. In fatty liver, the enlargement begins without localized pain, and there is no sense of constriction or dys- pepsia, so constantly present in the early stage of cirrhosis. In fatty liver, the skin is of a light yellow color, is greasy, and has a velvety feel; in cirrhosis, it is of a dingy hue, wrinkled, and rough. There is a history of high living, and of a sedentary life, or of some phthisical com- plication with fatty liver ; while in cirrhosis, a history of excessive spirit- drinking, gout, rheumatism or syphilis is elicited. The liver is doughy and painless in fatty degeneration, while it is hard, resistant and tender in cir- rhosis. The tendency in fatty liver is to obesity, while emaciation is rarely absent in cirrhosis. Ascites is never an attendant of fatty liver. Waxy liver is accompanied by a history of syphilis, prolonged suppura- tion, or disease of bones ; the face is pale and puffy, the urine is increased in quantity and of low specific gravity. Pressure over the liver gives no pain, and the surface of the organ is smooth, and its free edges sharp and well defined. These symptoms readily distinguish it from cirrhosis. The advanced stage of cirrhosis may be confounded with chronic peri- tonitis, of a tubercular or cancerous origin, with gastric ulcer, with adhe- sive pylephlebitis, chronic or brown atrophy of the liver, multilocular hy- datids, gummata and cancer. Gastric symptoms are prominent in cirrhosis, and absent in peritonitis. The ascitic fluid of cirrhosis is albuminous, while in chronic peritonitis it contains inflammatory products. The countenance has a clay-colored or jaundiced hue in cirrhosis ; in peritonitis, it is pale and anxious. The liver is diminished and the spleen increased in size in cirrhosis. The abdo- men is excessively tender in chronic peritonitis, and the fluid accumulates more rapidly than in cirrhosis. A history of drinking, dyspepsia, hematemesis and emaciation may sug- gest ulcer of the stomach ; but if it is remembered that tympanitis, asci- tes, hemorrhoids, clay-colored feces, dark, scanty urine, a small and hob- nailed liver, and an enlarged spleen are present in cirrhosis, and absent in ulcer of the stomach, the differential diagnosis is readily made. In cancer of the liver, the nodules are very much larger than in cirrho- sis. Ascites and enlarged spleen, if present in cancer, occur late, when the large size of the liver leaves no doubt in the diagnosis. The liver is exces- sively painful and tender on pressure, and there are marked exacerbations of the pain. A cancerous cachexia, with an almost chlorotic hue, exists in cancer. These, with the history of the case, and perhaps the presence of cancer in other organs, are sufficient for its diagnosis. Hepatic phlebitis may give symptoms identical with those of cirrhosis. The most important diagnostic point is, that in hepatic phlebitis the as- citic fluid accumulates very rapidly, and after paracentesis returns more quickly than in cirrhosis. Jaundice occurs early and rapidly deepens, and the stools are dark-brown and semi-fluid in phlebitis. The points of dif- ferential diagnosis between the other diseases which have been named and cirrhosis, will be considered under the head of those diseases. U 370 DISEASES OF THE DIGESTIVE SYSTEM. Prognosis.—The prognosis will be determined by the stage of the cirrhosis. In its early stage its progress may be arrested, but when the stage of contrac- tion is reached, the disease is progressive, and the prognosis is exceedingly unfavorable. A fatal result occurs in all cases. Its course is a chronic one, and though death has occurred in three months from the time the liver be- gan to be diminished in size, I have usually found a year and a half to be its average duration. Complicating diseases influence the prognosis. Hem- orrhage from the intestine and from the hemorrhoidal veins may be so great as to exhaust the patient, and render him too feeble to resist the inroads of the disease. This class of patients are especially liable to develop the cir- rhotic form of Bright's disease. Delirium tremens, pleurisy, and pneumo- nia sometimes complicate it. Death may result from exhaustion due to faulty nutrition, from the large fluid accumulation, from repeated and pro- fuse hemorrhages, and from wasting diarrhoea. Intercurrent pulmonary or cardiac disease, peritonitis, or delirium tremens may be the direct cause of death. Those cirrhotic patients live the longest who have large dropsical accumulations, the dropsy disappearing and recurring. Treatment—Cirrhosis, in its early stages, should be treated in the same way as active hepatic hyperemia. In alcohol drinkers, all spirituous liquors must be abstained from, and the patients must be placed on a nutri- tious, though restricted diet, from which all irritating ingesta are excluded, and alkaline waters should be freely taken. If the hepatic congestion is intense, leeches to the anus, mercurial purges, and nitro-muriatic acid will be found of temporary service. The importance of a restricted diet, and the free use of saline waters in this stage of the disease cannot be over- estimated. Cod-liver oil is indicated in this stage. After the stage of contraction is reached, the treatment can only be palliative. The most important thing to be accomplished now, is to improve nutrition, and to relieve urgent and troublesome symptoms. Mineral acids combined with vegetable tonics, such as dilute nitric acid and calumbo assist stomach digestion ; creosote and sulphite of sodium are of service when acid fermen- tation is a distressing symptom. Mineral waters should be discontinued during this stage. If constipation exists, the bowels may be regulated with rhubarb combined with small doses of ipecacuanha. Cod-liver oil should be constantly taken by this class of patients. Care must be taken not to suddenly check diarrhea, or hemorrhages, but if they become exhausting opium may be cautiously given. Ascites and general dropsy are the most troublesome symptoms in this stage of cirrhosis. When it becomes imperative to remove the dropsy, it may be attempted through the skin, kidneys and intes- tines, or it may be removed by tapping. If the patient is too feeble to employ drastic purges and hydragogue cathartics, diuretics and di- aphoretics may be resorted to. The condition of the intestinal tract, as well as the strength of the patient, will determine whether elaterium, or any of the other drastic cathartics can be employed. It must be remem- bered that they may excite acute gastric and intestinal catarrh. Diuretics HYPERTROPHIC CIRRHOSIS OF THE LIVER. 371 (as squills and digitalis) are more efficient in this than in any other form of dropsy. If the kidneys and renal vessels are compressed by the fluid, diu- retics will have little effect. Its removal must not be delayed too long, for the strength of the patient may be so diminished that after the removal of a large quantity of fluid, fatal collapse may occur. When, however, reme- dial measures fail and dyspnoea becomes troublesome, paracentesis abdo- minis should always be resorted to. The mechanical removal of the fluid may be effected either by the aspirator or trochar. After its removal, the hob-nailed surface of the liver may cause peritonitis by the constant irrita- tion produced by the respiratory movements. There are few cases where tapping has been frequently performed, in which after death a moderate amount of chronic peritonitis is not found. The ascites will return sooner or later after paracentesis; but when tapping is only required at sufficiently long intervals for the patient to recuperate between the tappings, and the amount of fluid gradually diminishes or becomes stationary, the case will continue for years. HYPERTROPHIC CIRRHOSIS OF THE LIVER. Hepatic cirrhosis with hypertrophy of the organ appears in two forms. One is known as simple or biliary cirrhosis; the other as fatty hypertrophic cirrhosis. Morbid Anatomy.—In biliary cirrhosis the bile ducts and radicles become distended, and pigment is deposited in the hepatic cells and connective- tissue. Degenerative changes affect the parenchymatous elements coin- cidently with an abundant development of connective-tissue. The liver thus becomes enlarged, hard, and deeply pigmented brown or black. As the degenerative changes cause in many parts complete destruction of the liver cells, the increase of size in the organ depends largely upon the new connective-tissue. Although the organ becomes harder, the fibrous forma- tions do not contract as firmly as in simple cirrhosis, and the organ thus retains its smooth surface. In fatty hypertrophic cirrhosis, called by the French "hypertrophic cirrhosis with icterus,^ the fibrous formations are equally abundant, but show even a less tendency to extreme degrees of contraction, while the de- generative changes within the parenchyma are distinctly fatty. These fatty products are not absorbed, and tend to still further increase the size of the organ. Such a liver differs from a simple fatty liver in the presence of abundant new connective-tissue between and within the lobules. The new growth originates in the portal spaces, and the portal vessels and bile ducts become surrounded by compact fibrous tissue from which bands radiate along the central and sublobular veins, in such amounts at times as to cause their entire obliteration. The biliary passages are affected secon- darily and in less degree, the vascular apparatus being the parts particularly involved. This forms one of the prominent pathological points of differ- ence from biliary cirrhosis. 37'J DISEASES OF THE DIGESTIVE SYSTEM. The hypertrophy, which is often extensive, affects particularly the edges of the organ, so that it is like a cube. Sabourin dwells particu- larly upon this. There are no granulations upon the surface, and Glis- son's capsule, sometimes thickened from perihepatitis, is smooth and so transparent that through it can be seen opaline-looking new connective- tissue enclosing yellow fatty parenchyma. Upon section the hepatic parenchyma seems made up of fatty nodules, usually circular, smaller or larger than the normal hepatic lobules, and almost completely sur- rounded by new tissue. The latter has sometimes induced absorption of the proper glandular elements. With a low power under the microscope there is an appearance like subcutaneous adipose tissue, with cirrhotic bands enclosing collections of fat cells. These groups of fat cells, which are often simply large oil globules, represent the hepatic lobules. The granulo-fatty degeneration peculiar to typhoid jaundice is absent. The kidneys are usually the seat of simple or similar sclerotic changes. The spleen is enlarged, often more than in simple cirrhosis. Etiology.— Biliary sclerosis is probably dependent in almost every instance upon some form of obstruction in the larger hepatic ducts, from gall stone, cicatricial contractions, pressure from tumors, etc. The causes of fatty hypertrophic cirrhosis are obscure. It occurs in alcoholic subjects, but is by no means confined to them. It seems possible that it may follow biliary cirrhosis, or even start as a simple cirrhosis. Symptoms.—The clinical distinctions between biliary and fatty hypertro- phic cirrhosis are not clear. In the earlier stages the symptoms are all ob- scure and often overlooked. Fullness and oppression in the hypochondrium usually are the first to attract attention. Jaundice appears early and is per- sistent, being more marked, as a rule, in the biliary form. The enlargement of the liver may perhaps be recognized if attention is called to it. When the second stage sets in, there will be abdominal pain, nausea, vomiting, anorexia, attacks of vertigo, nocturnal delirium or hallucinations, hyperes- thesia of the limbs, and then fever. A diagnosis is possible in most cases with these symptoms. They are followed by oedema of the face and limbs, profuse sweats and often signs of subacute peritonitis. With the increas- ing persistent jaundice there may be tendency to hemorrhages. The symptoms are very apt to increase and then recede. Usually little flesh is lost, and patients may even grow fat. When the abdominal fat is not too abundant, physical examination shows a large, smooth, rounded liver, seldom very tender on pressure. Splenic enlargement can also be recog- nized. Ascites is seldom present; when developed, it is slight. The whole course of the disease is from one to two years, and the second stage may last four or five weeks, or be prolonged several months by deceptive intervale of apparent recovery. Differential Diagnosis.—This must be made from other hepatic disease! causing jaundice, by the presence of signs of extensive portal obstruction) associated with enlargement of the liver. An alcoholic history, or th( CIRCUMSCRIBED SUPPURATIVE HEPATITIS. 373 presence of tubercular complications, are important diagnostic points, when associated with enlarged liver, in favor of hypertrophic cirrhosis. Prognosis.—This is invariably bad. Treatment.—The treatment is purely palliative and expectant. None of the many theories advanced as to its cause have been accepted. Those measures employed in simple cirrhosis may relieve the symptoms, but are even more uncertain in their action in this condition. CIRCUMSCRIBED SUPPURATIVE HEPATITIS. Abscess of the liver is an acute circumscribed hepatitis which results in irregular areas of suppuration, the liver-tissue surrounding the points of suppuration remaining normal. Morbid Anatomy.—In a certain proportion of cases circumscribed hepatitis has its origin in an infarction. The emboli which produce these infarc- tions are, in most instances, stamped with pyaemic infection or are necro- tic ; they may vary in number from two or three to a dozen. Immedi- ately around the inflamed spots the liver substance is normal or in a state of intense congestion, and corresponding to them on the surface of the liver are found brownish-red elevated patches from an inch to an inch and a half in diameter, and of firm consistence. Their most frequent seat is the posterior portion of the right lobe. They may be single or multiple. Soon after the development of the infarction purulent inflammation is estab- lished. In the centre of the mass the liver cells undergo albuminoid infil- tration, become larger, degenerate, and pus is formed. As the process advances small cavities containing pus are developed. These may en- large into one large abscess or remain separate. If abscesses result from other causes than pyemia, the process does not follow the lobular course, but begins by small exudations of lymph and pus, which soon coalesce and become surrounded by a membraneous wall. The cavity of the abscess varies in size from that of a hazel-nut to one capable of containing two or three quarts. Their con- tents are usually pale yellow pus; but when the suppu- rating process has broken through the wall of some vessel, then the contents are rust colored and have a granular appearance. If the process involves the bile-ducts the pus has a greenish or ochre-color Ciicumscribed Suppurative Hepatitis. Sketch shmving the cut surface of a portion of the left lobe of the liver, the seat of multiple abscesses. The open mouths of the di- vided hepatic reins are also shown. 374 DISEASES OF THE DIGESTIVE SYSTEM. A variety of changes take place in these purulent collections ; as they grow older, their walls may become smooth, and the encysted pus gradually become absorbed, or undergo cheesy or calcareous degeneration. If absorp- tion takes place, a cicatrix deeply indented on the exterior of the liver marks the place where the abscess approached the surface, and within its substance cicatricial tissue indicates its exact seat. In other cases, no lining membrane is produced around the purulent collection. As the inflamma- tion extends, a necrotic process is established which extends to the surface of the liver, and the abscess opens externally. This process may pierce the peritoneum, causing a fatal peritonitis ; but this is of rare occurrence, for adhesions are formed which bind the diaphragm and adjacent organs to the liver ; or the abscesses may open into the pleural cavity, the right lung, or the stomach. In rare instances the two large venous trunks, the vena porte and inferior cava may be pierced. Frequently the abscess ruptures externally, through the adhesions formed between the surface of the liver and the abdominal walls. The intestines, the gall-bladder, or the pericardium may be perforated by the abscess. Again, the pus may burrow in the cellular tissue, and discharge itself at some point at the lower part of the trunk. At the autopsy the liver may be found irreg- ularly enlarged, often attaining an immense size. The capsule is opaque and thickened, and on its surface are elevated flat spots varying in color from dark red to yellow. Adhesions generally exist between it and the adjacent parts, and a layer of lymph frequently envelops the entire organ. The whole liver is hyperaemic. Evidences of perforation, in any of the directions which have been mentioned, may be present. On section, a dark fluid oozes from the congested surface, and the interior of the abscess may exhibit any of the changes above described. Near an abscess the coats of the veins, especially the portal, are thickened, and their interior is often filled with a shaggy, fibrinous deposit. Etiology.—Pyaemic infarction must be regarded as a frequent cause of hepatic abscess, especially when associated with injuries to the cranial bones. Phlebitis, with the formation of thrombi leading to suppurative inflammation, the result of operations on the intestines (as for prolapsus ani, hemorrhoids, and strangulated hernia) and any intestinal traumatism, may give rise to abscess of the liver. Hot climates and miasmatic influences favor, if they do not cause, suppurative hepatitis. In hot climates dysen- tery, particularly the epidemic form, is frequently accompanied or followed by hepatic abscess, so that dysentery has come to be regarded as one of the causes of abscess of the liver. Hepatic abscess sometimes accompanies ulceration of the stomach and of the intestine, especially of the colon. Ulceration of the gall-bladder and of the appendix vermiformis, perityphlitis, pyelitis, ulcerative endocarditis, and cancer of the stomach or of the parts near the liver are often associated with hepatic abscess. Worms, calculi, or other obstructions of the ductus communis, causing inflammation of the hepatic ducts, sometimes lead to ulceration, and this ulcerative process is often followed by abscess. The prevailing tendency of modern pathology CIRCUMSCRIBED SUPPURATIVE HEPATITIS. 375 is to ascribe hepatic abscess to an infective embolus, from a preceding phlebitis, and the attempt has been made to trace back all the causes above named to such a primary cause, though, in many, direct proof is impossi- ble. Abscess of the liver may also be the result of inflammation of the bile- ducts and of the veins of the liver; and, finally, it may be developed without any recognizable cause. Symptoms.—An abscess of the liver of considerable size may exist with- out there being local or constitutional symptoms to point to its existence. A patient may have fever, gradually become emaciated, and finally die from exhaustion, without a single objective symptom of abscess, and yet a post-mortem examination will reveal a large central hepatic abscess. Again, symptoms of intermittent fever, associated with gastric and intestinal catarrh, may be all that, with the greatest care, can be elicited, when, in fact, a large abscess is developing in the liver. When abscess is associated with dysentery the difficulty is often increased ; for chills and rigors, enlargement of the liver, and pain may all be attendants of dysentery with- out abscess. Again, in pyaemia, when metastatic abscesses in the liver are especially liable to develop, the recurring chills, the sweats, the pyrexia, and the jaundice, are all part of the history of the pyaemia, so that in many cases we are compelled to rely almost exclusively on the physical signs for a diagnosis of abscess of the liver. Such cases of hepatic abscess are fre- quently overlooked. Usually the development of hepatic abscess is indicated by well-de- fined symptoms. A slight feeling of chilliness, sometimes a distinct chill, is followed by dull pain and weight in the right hypochondrium, the pain often radiating to the tip of the right shoulder ; the chilly sensations recur, and resemble those of a slight attack of ague. The pain increases, and is aggravated by position and pressure. The tongue is brown and furred, there is loss of appetite, slight nausea, and often vomiting, which is bilious in character. The bowels are at one time constipated, at an- other there is a bilious diarrhea. The respirations are hurried and shortened, either because of slight lo- calized pleurisy, which so often accompanies hepatic abscess, or because a long inspiration increases the pressure on the liver, and thus causes pain. With the dyspnea there is a short dry cough resembling that of pleurisy ; the skin rarely changes color. With the formation of the abscess there is a distinct exacerbation of symptoms : hectic, rigors, and recurring night sweats occur ; the gastric symptoms become urgent, and there is persistent and profuse vomiting. The pain becomes sharp, lancinating and localized, and indicates the direction of the future perforation. The temperature rises to 103° or 104° F., sometimes reaching 106° F. The pulse is accel- erated, generally keeping pace with the temperature. Exhaustion and emaciation are rapidly developed, and as the disease advances, typhoid symptoms may supervene. If the situation of the abscess is such that portal obstruction results, hemorrhoids, ascites and edema of the extremi- ties occur, though peritonitis may be suspected in those cases where there 376 DISEASES OF THE DIGESTIVE SYSTEM. is ascites. As the abscess advances toward the surface of the liver, attacks of perihepatitis are apt to cause severe exacerbations of pain, and the hepatic tenderness becomes excessive. Toward the end delirium, jactitation, som- nolence, and coma may develop. The urine is scanty, high-colored, and contains an abnormal amount of urates, often causing a considerable pink- ish deposit. Hepatic abscesses may be discharged (as has been stated) in a variety of ways. When an external opening is to occur, the skin becomes tense, red, shining, and edematous at some point over the hepatic region ; fluc- tuation can be detected, and becomes more and more marked as the ab- scess advances toward the surface. In some cases the heart impulse is transmitted to the abdominal walls by the intervening tumor. When the cavity of the peritoneum is perforated, signs of local or general peritonitis are developed, marked by rapidly developed tympanites, intense and sud- den collapse. When an opening occurs into the stomach, severe gastric symptoms are developed, accompanied by purulent vomiting and purulent stools. A sudden diminution in the size of the hepatic tumor, the sub- sidence of the pain and of the urgent symptoms, indicate that the intes- tine or biliary passage has suffered perforation. Symptoms of localized pneumonic inflammation in the right lower lobe precede the opening of an hepatic abscess into a bronchus. The expectoration suddenly becomes purulent and mixed with blood, serum, and shreds of disintegrated lung- tissue ; the breath becomes offensive, there is cessation of pain, and sub- sidence of the hepatic enlargement. Recovery in such cases is rare unless the abscess is a small one, the patient usually dying of exhaustion from long- continued suppuration. When the pleural cavity communicates with the abscess, the symptoms of pleuritic effusion and empyema are well defined, and when, in this case, an external opening is to occur, the evidences of it are the same as those of empyema. Almost immediate death follows per- foration of the pericardial sac by an hepatic abscess. Absorption of the fluid contents of an hepatic abscess, and the development of cicatricial tis- sue, followed by gradual diminution in the size of the liver, are of rare occurrence. Physical Signs.—Inspection. If the abscess is large, inspection will show a bulging of the right hypochondriac region, reaching nearly to the um- bilicus. The respiratory movements on the right side are restricted, and the respirations are accelerated. If the abscess is to open externally, there is a flattened, defined bulging near the free border of the ribs, between the intercostal spaces. Palpation.—The liver is enlarged and has an uneven feel, especially when the abscesses are multiple and superficial. The pain, localized in the case of a single abscess, is increased and diffused in multiple abscesses by pressure. Fluctuation is a valuable sign, but cannot always be de- tected. When it can be, a ring of abnormal hardness surrounds the spot. Palpation should be made from before backward ; if a single large abscess exists, its outline may be well defined. CIRCUMSCRIBED SUPPURATIVE HEPATITIS. 377 Percussion.—The area of hepatic dulness is always more or less in- creased. If the abscesses are multiple, it may be increased in all direc- tions ; but if there is only one large abscess, the area of dulness will correspond to the direction of enlargement, which may be upward or downward; by its direction we are able to determine the probable mode of the termination of the abscess. Differential Diagnosis.—The readiness with which the diagnosis of ab- scess of the liver may be made will depend upon its size and situation; small abscesses can only be suspected. Abscess of the liver may be mis- taken for hydatids of the liver, cancer, localized pleurisy, intercostal neu- ralgia, abscess of the abdominal walls, enlarged gall-bladder, perihepatitis, suppurative pylephlebitis, and active hyperaemia of the liver. Hydatids occur most frequently in those living in northern climates, and abscesses most in those who live, or have lived, in hot climates. Hyda- tid tumors run a chronic course, and are slow in growth ; while abscess is usually a rapid and acute disease. Accompanying hydatids there is no pain, rigors, hectic, or sweats ; but these are important symptoms in abscess. Gastric disturbances and a rapidly developing cachexia are prominent in abscess, and absent in hydatids. In some cases of hydatid tumor the hyda- tid " thrill" or fremitus can be detected ; it is never present in abscess. With the exploring trochar the liquid in the one will be found to be pus, in the other a clear saline fluid containing hooklets of the echinococci. Cancer of the liver is generally associated with cancer of the stomach, breast, or some other organ, primary cancer of the liver being very rare. In cancer, the hepatic enlargement is slower than in abscess, and there is usually a more or less marked cancerous cachexia. Suppurative fever, chills, hectic, and sweating are present in abscess, and absent in cancer. The temper- ature in cancer is normal or sub-normal, and jaundice, if present, is persist- ent. Ascites is common in cancer, and rarely present in abscess. In can- cer, palpation discovers scattered nodular masses, which rarely fluctuate; while in abscess a large fluctuating tumor can usually be mado out. The exploring needle withdraws pus from an abscess, while blood follows the puncture of a cancer nodule. Pleurisy on the right side can usually be readily distinguished from ab- scess of the liver by the physical signs alone. The grazing friction sound accompanies loss of vocal fremitus ; the dulness on percussion, the feeble respiratory murmur, and the crepitant friction sound decide the question. Intercostal neuralgia occurs most frequently in women with a neurotic history. The pain is located in the region of the sixth, seventh, and eighth intercostal spaces, and the three points of tenderness are almost diagnostic. When the pain of abscess becomes as excruciating as that of neuralgia, in- spection, palpation, and percussion will all reveal well-marked enlargement of the liver. Gastric disturbances, chills and profuse sweats are prominent signs of abscess, and are absent in intercostal neuralgia. In abscess of the abdominal walls, there is no history of pyemia, dysentery, or internal ulceration, which so often precede an hepatic abscess. In he- 378 DISEASES OF THE DIGESTIVE SYSTEM. patic abscess the line of dulness is well marked, and corresponds in outline to the hepatic area ; while in abscess of the abdominal walls the line of dulness is ill defined, and does not follow the hepatic outline. A tense, shining, edem- atous skin, and superficial tenderness and hardness appear early in abscess of the abdominal walls. The signs of pus formation are early in abscess oi the abdominal wall, and very late in abscess of the liver, if they appear at all. The respiratory movements cause an upward and downward motion in the tumor of an hepatic abscess ; while an abscess of the abdominal wall will remain stationary during the respiratory acts. An enlarged gall-bladder will usually be accompanied by a history of bil- , iary colic. The presence of a pear-shaped, movable, fluctuating tumor, oc- < cupying the normal position of the gall-bladder, a history of jaundice, and , the absence of constitutional symptoms indicate enlarged gall-bladder; while the tumor in abscess of the liver is broader, less movable, less globu- lar in shape, and is attended by chills and sweats. Prognosis.—The majority of abscesses of the liver terminate fatally. Py- aemic abscesses are generally multiple; their average duration is three ( months ; I have known death to occur within three weeks after the com- mencement, and I have known them to be prolonged over a period of two years. In abscess from other causes than pyemia, the prognosis is favora- ble whenever there are no indications of an opening into the pericardium, . peritoneum, or pleural cavity. When an hepatic abscess complicates a severe attack of dysentery, the prognosis is unfavorable. Their duration is shorter, ( and the prognosis is better when they open externally; their next most favorable termination is when they open into a bronchus, or into the intes- , tinal canal. Pyaemia and dysentery often cause death when the accompany- ^ ing abscess is too recent to have induced it. Exhaustion from suppuration may cause death, especially when accompanied by intestinal catarrh. Peri- tonitis, pericarditis, pneumonia, and empyema sometimes cause the fatal result. Treatment.—When multiple abscesses occur, antiseptics have been pro- posed, but there is no evidence that they arrest the progress, or diminish the severity of the suppurative process. When suppurative hepatitis can be recognized early, it should be treated according to the rules which have been given for the management of acute hepatic hyperemia. Local blood- < letting by leeches may be employed when the symptoms are localized and well defined ; and mercurial purges may be given at the onset, in combina- tion with large doses of quinine, but they should be discontinued when sup puration is established. We rarely have an opportunity to carry out the preventive treatment, for the abscess is formed before the patient seeks medical advice. When pus has formed, and the locality of the abscess can be determined, aspiration should be performed. If the withdrawal of the pus is followed by decided signs of improvement, the aspiration may be repeated at intervals indicated by the amount and effects of the purulent accumulation. Few cases, however, will be permanently benefited by aspira- tion. I question very much if those cases reported cured by one or two DIFFUSE PARENCHYMATOUS HEPATITIS. 379 gpirations were true hepatic abscesses. The dysentery and the gastro- atestinal catarrh, which are so often attendants of hepatic abscess, are est treated with large doses of ipecacuanha; a fuller description of this lethod of treatment will be found under the head of dysentery. The question of operative interference is one which it is often difficult a decide. Strong opinions have beeu given for and against it. On the ne hand, it is claimed that if a free opening is not made, death may result rom exhaustion produced by large purulent accumulations, or the abscess lay open into the peritoneal cavity, pericardial sac, or pleura, and thus ause death. The process is a progressive one, and each day more and more f hepatic tissue will be involved, and thus diminish the chances of recov- ry. On the other hand, those who oppose opening the abscess say that eritonitis and the entrance of air may result from it, that the ribs are more able to become eroded, and the surrounding tissue to become gangrenous, hen an opening is made. Some regard it as highly dangerous to pass an istrument into the liver, claiming that it may excite a suppurative process 1 healthy liver-tissue. All these objections are removed if antiseptic lethods are employed. If no adhesions have formed between the liver and re abdominal walls, they should be established by caustics, and then the ic may be opened ; if it is very large, all of the pus should not be allowed to scape at once. It is always safest to open the sac by means of caustics, sing the knife to divide the superficial tissues. The abscess should be pened as soon as possible. When hepatic abscesses open into the bronchi, ilon, or gall-bladder, absolute rest must be insisted upon. In all cases, uring convalescence, absolute rest and a careful regimen must be main- lined for months. The diet throughout the whole course of the disease muld be the most nutritious, and stimulants should be freely given. 'he importance of sustaining the patient in every possible way is ap- arent. DIFFUSE PARENCHYMATOUS HEPATITIS. This disease, also called acute yellow atrophy and malignant jaundice, as been regarded as a " passive degeneration," the metamorphosis being lore rapid than in any other gland structure in the body. Some think it ue to bilious liquefication or polycholia, and that it is a general disease— ke typhoid fever or cerebro-spinal meningitis—with a local lesion. The lore recent views are that acute yellow atrophy is a diffuse inflammation E the whole hepatic structure, where the inflammatory changes are so ipid as to lead to disintegration and complete destruction of the liver dls and subsequent atrophy. Whether it is an exudative process, or one in hich there first occurs albuminoid infiltration of the hepatic cells, and len molecular change, is still a disputed question, but the more reason- )le view is that it comes from albuminoid infiltration, irregular cloudy veiling of the cells, and subsequent softening of the hepatic tissue. Morbid Anatomy.—It is seldom that one sees a liver that is the seat of 380 DISEASES OF THE DIGESTIVE SYSTEM. Dells, etc., from an hepatic lobule in Acute Yellow Atrophy. A, A. Hepatic cells filled with granular detritus, with obscuration of nuclei and cell walls. B. A group of atrophied cells. C. Cells with fatty infiltration. P, E. Pigment granules, with blood and ty- rosin crystals, x 300. diffuse hepatitis until after the process is completed, but the few that have ■» been studied present the evidences of having been the seat of an intense congestive and exudative process. The liver lobules have a dark gray muddy ring at the periphery, due to granular degeneration or albuminoid swelling of the peripheral cells, while the liver structure immediately sur- rounding the central vein is normal. The latter is, however, soon involved and in place of liver cells there are fat and pigment granules, with traces of leucin and tyrosin. All outline of lobular structure disappears, the capillaries are' intensely engorged, and the bile-ducts become more or less completely closed, owing to the compression which thej| suffer from peripheral exudation. Thm, the bile formed between the central vein and the exterior of the lobule has no- mode of escape, except through the cen- tral vein. The liver is diminished in size, sometimes to two-thirds of its normal size; in the early stage the organ is supposed to be very slightly enlarged. The diminu. tion is most marked in the right lobe. It is so soft that it folds upon itself, and takes any shape and position from the pressure of the adjacent organs. At the post-mortem, the body will be emaciated|. the skin very much discolored, and ecchymotic spots will often be found scattered over the surface. The capsule is loose, freely movable, very much wrinkled, and opaque or| yellowish in appearance. The parenchyma is soft, flabby, and brittle, and, varies in color from a bright yellow to a yellow-red. On section, when the disease is far advanced, the color of the cutsur- lace is of a rhubarb red, the outlines of the lobules are lost, and only ai detritus of granular matter is left. The blood is darker and thicker than normal and coagulates imperfectly. It may contain leucin and traces of urea. If the organ be set aside for a while it becomes covered with crys- tals of leucin and tyrosin. The heart is jaundiced, fatty and pultaceous. The spleen is enlarged and softened, and leucin is found in it. The gall- bladder is empty, or contains a small amount of pale bile or mucus. The kidneys are slightly enlarged, and in most cases are in a state ol acute fatty degeneration. Hemorrhages from the surface of the mucoul membrane of the stomach and intestines are common. Occasionally there is softening of the central portion of the cerebral substance, and staining of the meninges. The serous cavities contain fluid, often bloody, and in rare instances nearly every organ in the body is blood stained and has leucin and tyrosin in its tissues. DIFFUSE PARENCHYMATOUS HEPATITIS. 38] Etiology.—Acute yellow atrophy is a rare form of disease. Its causes are regarded by some as constitutional, by others as due to a peculiar miasm. Two-thirds of the cases occur in pregnant females, between the ages of twenty and thirty. The supposed predisposing causes are sex, pregnancy, chronic alcoholism, syphilis, malaria, sexual excess, and a prolonged course of mercurials. But with our present knowledge, it is difficult to say whether these are really predisposing causes, or that the acute yellow atrophy is an intercurrent accident. Among the exciting causes may be 'named mental emotion, great grief, or fear. It is doubtful if obstruction if the bile-ducts alone can excite acute yellow atrophy ; some are inclined ;o regard malaria as an exciting cause, rather than a predisposing one. While its etiology is still so obscure, the history of its development leads to he conclusion that a malarial poisoning is present in a large proportion of jases. Symptoms.—The symptoms of the early stage of acute yellow atrophy lsually pass unnoticed, for they are not in themselves distinctive. When ;he disease is slow in its advent, loss of appetite, occasional vomiting, a lurred tongue, slight headache, and a sense of fulness in the right hypo- jhondrium may be the only symptoms for the first week. Jaundice may orecede it for a week or two. In cases where its advent is sudden, it will )e ushered in by constant vomiting and great prostration. In either case luring its early stage the temperature will be raised only a degree or two, md the pulse but slightly accelerated. A condition of despondency is often oresent, there are wandering pains simulating rheumatism, and a sense of ^reat depression. Delirium and convulsions may be the only ushering-in symptoms. After from three to five days, the characteristic symptoms of he disease are developed ; of these jaundice is the earliest and most con- stant, it is progressive and never very intense, first affecting the upper half >f the body. The rise in temperature and increased pulse-rate which narked its premonitory stage disappear, and now even a retarded pulse md sub-normal temperature may exist. In a few instances, after the first vventy-four hours, the temperature ranges from 100° to 101° F. during the vhole course of the disease. The vomited material consists of mucus inged with bile ; later it assumes the nature of black vomit, similar to that n yellow fever, the color being due to gastric capillary hemorrhage. There 3 intense pain in the epigastric and right hypochondriac regions, which is ncreased by firm pressure over the liver. In the stage of coma, the hepatic enderness is so great that pressing the liver up against the diaphragm may ouse the patient. At first the cerebral symptoms are those of mental de- iression and slight headache, which rapidly increases in severity ; this, ater, gives place to wild delirium, jactitation, and convulsions. Twitch- ngs of the voluntary muscles of the head and neck (trismus) mark the onvulsive stage of the disease. These spasms usually follow the vomiting, >ut in cases where the disease runs a rapid course, typhoid symptoms nake their appearance, sordes collect on the teeth, while low muttering lelirium, subsultus, muscular tremors, and partial stupor precede the 382 DISEASES OF THE DIGESTIVE SYSTEM. convulsions. The convulsions are epileptiform, and are sometimes ushered in by a peculiar shrill cry. During the period of nervous excitement, the pufae undergoes remark- able changes. It may rapidly rise to 120, 130, or even 140 beats in | minute, falling in moments of calm to 80 or 90. the temperature remain- ing unchanged. The breathing during the convulsions is interrupted or stertorous, and a peculiar groaning noise is heard with each inspira- tion ; the expirations are prolonged and puffing. Whether the convulsions have been preceded by typhoid symptoms or not, the patient gradually bj comes more and more tranquil, passes into stupor, and finally into deep! coma, from which he cannot be aroused. The discharges from thej bowels and bladder are either passed involuntarily or retained. The' pupils are normal or slightly dilated, and respond to light slowly. Thef breathing becomes sighing, the pulse reaches 140 to 150, and grows shorter and shorter until death occurs. The skin during the progress of the disease has become more or less deeply jaundiced, ecchymotic and petechial spots sometimes appear on the surface, and there may be hemorrhages from the stomach, nose, intestine, uterus, and kidneys. In pregnant females abor- tion is likely to occur before death. The faeces are firm, clay-colored, and often blood-stained. The urine is acid and dark in color, is not quite up to the normal amount, and often contains albumen and blood; urea: and uric acid have totally disappeared, the sulphates and phosphates are diminished in quantity, and leucin and tyrosin are found in their place,|: The duration of the disease varies from one to three weeks. Physical Signs.—Palpation elicits extreme tenderness over the epigas- trium and right hypochondrium. Percussion.—The area of hepatic dulness rapidly diminishes from day* to day, and as the liver decreases in size it is displaced backward, so thatl there is no well-defined area of hepatic dulness in front. As the liver) diminishes in size the spleen enlarges. Differential Diagnosis.—Diffuse parenchymatous hepatitis may be mis- taken for yellow fever, pyaemia, typhoid fever, and the bilious remittent 3 variety of pernicious fever. In acute yellow atrophy, the liver is diminishing in size from day tol day, while in yellow fever it is steadily increasing. The spleen is increaseii: in size in acute yellow atrophy, and is unchanged in yellow fever. The) urine in yellow atrophy is acid throughout, and contains leucin and tyro- sin ; while as soon as jaundice appears in yellow fever the urine becomes^ alkaline. Yellow fever is ushered in by a distinct chill, while yellow atrophy of the liver rarely begins with a chill. The pulse, in severe fonw' of yellow fever, is gaseous in character and is rarely over 110, while in acute atrophy the pulse may reach 140 or 150 per minute. The stools aw dark and fluid in yellow fever, and firm and clay-colored in acute atrophy. > Pyaemia is ushered in by distinct chills. The chills in pyemia aw ■ followed by irregular rigors and exhausting sweats, which do not occur in acute atrophy. In pyemia there is diarrhea, and in acute yellow atrophf DIFFUSE PARENCHYMATOUS HEPATITIS. 38'! the stools are firm and clay-colored. In pyaemia there is a peculiar sweet sickish breath, which is absent in acute atrophy. Evidences of multiple abscesses, especially in the lungs, soon follow the sweats of pyaemia ; these do not occur in acute atrophy. The presence of leucin and tyrosin and the absence of urea, with the other urinary symptoms of acute atrophv, are in marked contrast with the normal urine of pyemia. Physical (hepatic) signs are negative in pyaemia, while a daily diminishing area of hepatic dulness is usually present in acute yellow atrophy. Typhoid fever has nearly the same premonitory symptoms as acute yellow atrophy, hut the steady rise in temperature with the typical morn- ing and evening exacerbations and remissions during the first week, are in marked contrast with the continual low temperature of acute atrophy. The delirium is wandering in typhoid, and wild in acute yellow atrophy. The characteristic " rose rash " appears about the seventh day of typhoid fever. Diarrhea is the rule in typhoid fever, while constipation and clay- colored feces are the rule in acute atrophy. In typhoid, the urine is simply diminished in amount, and the urea is increased, while in acute yellow atrophy the urea is greatly diminished in quantity, and often com- pletely absent, and the other (mentioned) urinary changes are present. In typhoid fever the liver is slightly enlarged, while in acute yellow atrophy it is markedly diminished in size. The " bilious remittent" form of pernicious fever very closely re- sembles in its symptoms acute atrophy of the liver. The severe sudden mill, rapid rise in temperature to 105° or 107°, the sweating, and the re- mission in pernicious fever are all, however, absent in acute atrophy. Free pigment exists in the blood in bilious fever, and is absent in. atrophy. Jaundice is a late symptom of pernicious fever, but occurs early in acute itrophy. The liver is markedly enlarged in pernicious fever, and as markedly diminished in size in acute yellow atrophy. Poisoning from mosphorus can only be diagnosticated from acute yellow atrophy when we mow the drug has been taken. Prognosis.—This is exceedingly unfavorable, and those cases where a cure las been reported are in the doubtful list. The average duration is one veek, the extreme limits being twelve hours and four weeks. Cholaemia md uraemia, by inducing the cerebral symptoms which have been referred o, may be the direct cause of death. Peritonitis and hemorrhages from he stomach and bowels are also frequent causes of death. Treatment.—All plans of treatment have thus far failed either to arrest he progress, or to diminish the fatal tendency of this disease. It has >een preferred, in the early stages, to administer drastic purges, and apply eeches over the region of the liver and about the anus, and in the robust ^^M Fig. 74. Fatty degeneration. Section showing part of a Lobule in,a case of poisoning by phosphorus. A. Hepatic cells showing the granular change of true fatty degeneration. x 350. B. Capillaries. 398 DISEASES OF THE DIGESTIVE SYSTEM. however, attended with pain. The slightest indiscretion causes an attack of gastric catarrh and diarrhea, which persists long after the removal of the cause. The patient is anemic and moody, and there is a general loss of muscular power, with a disposition to sleep. The blood is hydraemia The skin is sometimes shining, always "velvety" to the feel, and often pasty and smooth, like that of a wax figure. The integument all over the body feels smooth, velvety, and flabby. Dyspnea results as much from the weakness and anaemia, as from pressure of the enlarged liver. When symp- toms of acholia, due to the altered state of the blood, are attended by absence of bile in the intestinal tract, rapid anemia, exhaustion, delirium and col- lapse occur, and extensive fatty metamorphosis is then usually associated with some other hepatic degeneration. The feces are usually normal in color and the bowels are irregular and constipated ; in the highest grades of fatty metamorphosis they are pale and clay-colored, and attacks of diarrhoea are frequent. The urine is pale, non-albuminous, and of a low specific gravity. Physical Signs.—Palpation. The rounded smooth edges of a uniformly enlarged liver are readily felt below the border of the ribs ; the organ has a doughy, soft feel. When fatty degeneration occurs with waxy or colloid disease, the liver is diminished or is of normal size and smooth. Percussion.—The area of hepatic dulness is increased in all directions, the increase being mainly downward and forward. Differential Diagnosis.—Fatty and waxy degeneration are frequently mistaken for each other. In waxy liver a history of syphilis, prolonged suppuration, or disease of bones will be elicited ; in fatty liver there is a history of alcoholism, prolonged wasting disease, or one of high living and sedentary habits. In waxy liver, the skin is pale, dry, and has a peculiar odor resembling that of indigo ; in fatty liver the skin shines with fat, and has a velvety feel. The blood is hydremic in fatty liver, and is leu- kaemic in waxy liver. The urinary symptoms in both are distinct: in waxy liver the urine is often increased in amount, is albuminous, and con- tains casts ; in fatty liver it is normal. In waxy liver the feces are early deficient in bile and pale in color ; in fatty liver they are normal until an advanced stage of the disease is reached. A waxy liver is hard ; a fatty liver is soft and flabby. A waxy liver may become much larger than a fatty liver, and its edges are sharply defined ; while in fatty liver they are smooth and rounded. With a waxy liver the spleen is enlarged, but with fatty liver it is normal in size. Prognosis.—Fatty infiltration of the liver is not a grave form of disease. There is danger only when fatty degeneration of liver-tissue occurs, Death may result from fatty heart, pulmonary edema, acholia, apo- plexy, the exhausting diarrhoea, and from the complications already re- ferred to. Treatment.—When the diet, mode of life, or climate is the main element in its causation, the indications for treatment are simple. A restricted diet, with no fat or sugar, and with regular daily exercise in the open air will, in most cases, increase the patient's strength and lessen the size of the liver. Care must be taken not to stop alcoholic stimulants too suddenly. PIGMENT DEGENERATION. 399 for fatty heart may co-exist. They must be decreased gradually. In all cases, a residence in an elevated temperate region, free from marshes, is im- portant. The vegetable bitters combined with alkalies will aid in restor- ing the appetite when it is lost. Iron should be administered in the form of the carbonates and lactates. Ehubarb and aloes will best relieve the constipation, and vegetable astringents control the diarrhea. In syphilis, iodide of potassium is of service. In the fatty liver of phthisis, nothing can be expected from treatment so long as the phthisis is progressive. PIGMENT DEGENERATION. The pigment or melanotic liver is that form of hepatic degeneration in which there is an abnormal deposit in the liver of pigment derived from the coloring matter of the blood. In pigmentation there must be prima- rily a fault in the circulation or in the blood-vessels ; usually it is the re- sult of slowing of the blood current. The red corpuscles either pass through the walls entire, or liberate the hemoglobin, which then transudes the capillary vessels. The blood from the spleen, loaded with pigment, passes into the portal vein, is carried through the interlobular veins, then into the veins just within the periph- ery of the lobule. Haemoglobin re- maining in the portal capillaries soon breaks up into hematoidin and, ac- cording to some, into melanin, though we are inclined to-day to regard me- lanin as altered haematoidin. This haematoidin is first yellowish, later it consists either of brownish-black granules or crystals of an intensely black color. Both hematoidin and melanin remain unaltered when once formed. Pigmentation of the liver is Confined to the Vascular SVStem. B- Longitudinal'section of a small hepatic duct. _ . . . . C Vessels containing small pigment granules in intensive CapillarV Stagnation with great numbers. The pigmentation in this case . r • was pretty general throughout the intralobular- a large amount of pigment matter oc- capillaries, x 250. eluding the vessels gives rise to atrophy of the cellular structure. Morbid Anatomy.—The liver is at first enlarged from congestion and the capsule is smooth and tense ; afterward the organ becomes smaller than normal and atrophies, its color being much deeper than in the ear- lier stage and its edges sharply defined. On section, in the first stage, dark blood flows from the congested paren- chyma. If the cut surface presents a mottled appearance there is a steel- gray or black ring around, and slightly encroaching on, each lobule, shad- ing off toward the central vein, In congestion of the liver pigmentation Fig. 75. Pigmentary Degeneration. Section of an Hepatic Lobule from a case of per nicious fever. A. Centred 'vein of the lobule. 400 DISEASES OF THE DIGESTIVE SYSTEM. commences about the central vein, and gradually diminishes toward the periphery of the lobule. If the surface is uniform it presents a color which resembles "graphite," a blackened gray color having a slight lustre, and the pigment deposit is seen to have reached the central vein. Occasionally spots of extravasation are found scattered throughout the organ. On sec- tion of an atrophied " pigment liver " the whole cut surface is black, and all trace of the lobules is frequently lost. A microscopical examination shows the capillaries, not only portal but hepatic, filled with granules or crystals, either throughout their entire extent or in isolated patches. The hepatic cells contain no pigment, but are filled with oily or amyloid material, or some- times with dark-colored bile. Leucin has often been found in the parenchy. ma of a pigmented liver. In an "atrophied" liver, the lobules and cells are shrunken, and the capillary svstem is a mass of pigment. The ■n'V " V^slJj ^ sPleen is softened and usually enlarged, ^/l^i^^tSP^ never smaller than normal, and is c Fig. 76. Pigment Degeneration. Section of the same tissue as preceding cut, show- ing the centre of a lobule more highly magnified. A. Central vein of the lobule. B, B. Strongly pigmented capillaries. C, C. Hepatic cells infiltrated with fat. x 450. more extensively pigmented than the liver. In some cases of pigment liver, there are evidences of hemorrhages into the various serous cavities. In connection with pigment degeneration of the liver, pigmentation may occur in all the organs of the body. Etiology.—Malarial infection is the only known cause of melanotic liver, but whether a large amount or peculiar kind of malarial poison is necessary for its development has not as yet been determined. Symptoms.—Frequently those who have had extensive pigment deposits in all the organs of the body, have given during life no symptoms to indi- cate their presence. The first effect of extensive pigmentation of the liver is an abnormal secretion of bile. The liver is enlarged and tender to press- ure. The skin in the milder forms is ash-colored, and in severer forms it is of a dark-bronze hue. There may be slight jaundice. There is gastro- intestinal catarrh with nausea, loss of appetite, flatulence, painful tympa- nitis, vomiting, and diarrhea which may pass into dysentery. In severe cases, hemorrhage from the gastro-intestinal mucous membrane and from the kidney occurs, attended by exacerbations and remissions correspond- ing to febrile exacerbations and remissions. There is rapid emaciation and extreme exhaustion with giddiness, headache, and ringing in the ears. Occasionally the vertigo comes on so suddenly that the patient falls to the ground without the least warning. Active delirium is often followed by profound coma. The urine and faeces are passed involuntarily during the period of stupor. Coma is the most frequent termination of the cerebral' CANCER OF THE LIVER. 401 variety of pigment liver. In severe cases which terminate in recovery there is often temporary loss of memory. Physical Signs.—Inspection shows the ashy-gray, jaundiced, or brown colored skin. Palpation.—The surface of the liver is smooth, and in the first stage the organ is larger, softer, and more tender than normal. In the second stage it is small and hard. Percussion.—In the early stage the area of hepatic dulness is increased; in the later stage it is uniformly diminished. Differential Diagnosis.—The liability of confounding pigment degenera- tion with other diseases of the liver is not so great as is the difficulty of recognizing its existence. If, in intense malarial infection, cerebral or urinary symptoms come on suddenly with hemorrhages from the mucous surfaces, a bronzed hue of the skin, and the physical changes in the size of the liver already referred to, pigmentation of the liver may be suspected ; and if, in addition to these, pigment matter is found in the blood, the diagnosis will be established. Prognosis.—The prognosis is favorable if the patient can be removed from the source of malarial infection. The elements which render the prognosis unfavorable are severe cerebral and renal symptoms combined with signs of extensive portal obstruction. Death may occur from exhaus- iion due to the diarrhea, dysentery, or intestinal hemorrhage. Treatment.—The preventive treatment corresponds to the preventive a-eatment of malarial fever. When the disease is once established, the mief indication is to administer large doses of quinine. The symptoms in ill varieties of the disease remit as soon as the individual is brought fully under the influence of this drug. Purges act unfavorably. If the cere- aral symptoms are urgent," ammonia may be combined with quinine. Preparations of iron and a change of residence to a non-malarial district we essential to its successful management. The diet should be of the most nutritious character and non-stimulating. CANCER OF THE LIVER. Cancer of the liver may be either primary or secondary. It is secondary ;o cancer of the stomach in one-half of the cases. It has been estimated 'hat one out of every one hundred persons has cancer of the liver. The varieties of cancer met with in the liver are scirrhus, medullary, melanotic, ^colloid cancer. Infiltrated cancer without any change whatever in the ormof the organ has been found. Scirrhus is usually primary, while medullary is almost always second- ary. Scirrhus makes its appearance first as rounded masses. These masses ncrease rapidly and soon attain their full size, which varies from that of a pea *> that of an orange ; they then remain stationary for a time until the fibrous assue contracts. The number of these nodules varies inversely with their nze. Scirrhus developments usually commence in the interlobular spaces md gradually extend toward the centre of the lobule. As the liver-cells 26 402 DISEASES OF THE DIGESTIVE SYSTEM. are being crowded upon, the portal capillaries disappear, while the hepatic vessels enlarge and ramify in the cancerous mass as a new and peculiar vascular net-work. The neighboring lymphatic glands may also become infiltrated with cancer, and often exert sufficient pressure upon the bile- ducts to obstruct the outflow of the bile. The cancerous growth sometimes involves the walls of the portal vein, and, extending in the direction of the capillary terminations, fills up their channel. The bile-ducts also may be obstructed, distended, or ruptured. With these changes, the centre of the cancer-nodule becomes harder and harder ; or by shutting off its own nutrition, the interior of the nodule becomes fatty, while the periphery is soft and vascular. The obliteration of the capillaries at the exterior of the mass shuts off the nutrition of the adjacent liver-cells, and this induce* fatty degeneration. The theory of the development of medullary cancer (the implantation theory, as it is called) is that cancer-cells pass through the lymphatics, or blood-vessels, and reaching the interlobular spaces become the starting points of the cancer development. This theory has received much attention, and experiments seem to warrant our adopting it as one method, at least, in which cancer may develop. Medullary cancer is simply a modification of scirrhus. Eapidity of de- velopment is the distinguishing pathological difference,—the line between the two forms often being arbitrarily drawn, for scirrhus may pass into, medullary, and vice versd. Melanotic cancer of the liver is also of rapid growth. The nodules, though very numerous, are small in size. The cancer-cells have a deposit at their centre of yellow, brown or blackish pigment, the "granite" loot] ing spot shading off toward the periphery. Its course is the same as in other varieties of hepatic cancer. Colloid cancer is of rare occurrence in the liver, appearing only as si degenerated form of scirrhus or medullary cancer. If either of these fonni undergoes mucoid or colloid degeneration, a gelatinous, gray, tenacious fluid takes the place of the cancer-juice, while the fibrous framework be- comes more distinctly alveolar. Melanotic sarcoma has been found; it often pursues as malignant a course as true carcinoma. Morbid Anatomy.—In nodular scirrhus cancer the liver is irregularly increased in size, the right lobe being usually most affected. With medul- lary cancer it is often so much enlarged as to fill the abdominal cavity. In color it is darker than normal, and it is increased in weight, sometimes reaching twenty pounds. Upon its surface are nodules, hard, elastic, rarely fluctuating, and umbilicated at their centres. Occasionally, there are no nodules on the surface, the cancerous developments being confinedj to the interior of the organ. The capsule of the liver is thickened and) sometimes the seat of cancerous development. Adhesions connecting ill to the adjacent parts are the result of intercurrent local peritonitis. On section, if the degeneration is advanced, the liver cuts hard, and creaks like cartilage under the knife. The cut surface is seen studded witk nodules, the diameters of which vary from one-eighth of an inch to four inches. Between the nodules the liver-tissue is sometimes congested, and! CANCER OF THE LIYER. 403 of a dark red color, or it is atrophied. The nodules increase in density from their centre outward, or have a central cavity filled with fatty granules. : On pressing them, more or less cancer-juice exudes according to the density of the tumor. The color of the tumor varies from a glistening dirty white to a deep red, according as the vascular net-work is meagre or abundant. If there has been obstruction to the bile ducts the parenchyma will be of a bright yellow color. Evidences of extravasation from distended vessels may be found throughout the liver-tissue and often in the interior of the can- cerous growth. Under the microscope, a cancer nodule will be found to consist of a fibrous framework or " stroma " in which are cancer-cells and cancer-juice. In Fig. 77. Cancer of the Liver. Section showing part of a cancerous nodule with the contiguous hepatic tissue. A. Connective-tissue of a portal canal in which the nodule was developed. B. Hepatic duct in longitudinal section. C. Hepatic artery. D. Stroma of cancer. E. Alveoli of the same filled with " cancer cells. " F. Empty alveoli. G. Peripliery of an hepatic lobule bordering on the cancer, infiltrated at HH. I. Infiltration of connective-tissue with same, x 300. eirrhus the fibrous stroma is greatly in excess of the other elements. The sancer-juice contains a large amount of fine granular matter, nucleated sells and distinct free nuclei. The cells are of large size and irregular, md the nuclei and nucleoli are often multiple and very distinct. The vails of the capillary vessels in the tumor are thin, and their calibre large. ^ ring of liver cells at the margin of the cancer-nodule exhibits well- narked degeneration. 404 DISEASES OF THE DIGESTIVE SYSTEM. Medullary Cancer.—The gross appearances of the liver are the same as in scirrhus, except that the nodules are fewer and larger. They are very soft and fluctuating, and frequently the more advanced tumors have ruptured through the peritoneal envelope of the liver. In this variety the cancer nodules are often lobulated. Those which occupy the surface of the liver project as large irregular tumors. On section large nodular masses of curdy-white homogeneous matter re- sembling fetal brain-substance are found scattered throughout the liver- tissue. Between the cancer nodules the liver substance is more or less in- tensely congested. Dark red hemorrhagic spots are seen scattered over its cut surface. On a microscopic examination a small amount of fibrous stroma is found containing a very large number of cells. The cells are much larger than in scirrhus, though the same in kind, and they are the seat of more fatty degeneration. Melanotic Cancer.—In common with the morbid appearance of all can- cerous developments, we find, besides, that the liver is nodular and very dark. On section the surface presents a peculiar mottled appearance resembling granite, and there are numerous small nodules studding the whole gland. On pressure a dark fluid flows from the cancerous mass, varying in color from a gray-brown to a deep black. A microscopical examination shows a stroma varying in amount and color. Sometimes it is colorless, sometimes very dark. The degree ot vascularity has wide ranges; the cells at certain spots in the liver often dis appear and only a peculiar pigment color remains. Colloid Degeneration.—The surface of the liver in this form of cancel differs from the other varieties in that it is smooth with large lobulations Under the microscope the cancerous mass is made up of large and spherical alveoli with thin walls. The alveoli contain mucoid or colloid matter, with fatty material and a few epithelial cells. Etiology.—The causation of primary hepatic cancer is unknown; in most instances there exists an hereditary predisposition. It is a disease of middle life, occurring oftenest between the ages of forty and sixty-five. Medullary cancer of the liver, especially when secondary, is sometimes met with in early life, even as early as the fourth year. It occurs equally among males and females. Some have dated its development fiom some great mental emotion or strain, others from the receipt of a blow upon the right hypochondrium. Cancer of the liver is often secondary to cancer of the stomach, mamma, ovary, uterus, pancreas, brain, or portal vein. Clinical experience indicates that extirpation of external cancerous masses is very apt to be followed by cancer of the liver. Symptoms.—The early symptoms of hepatic cancer are obscure. The more superficial its development, the more marked are the symptoms and the easier the diagnosis. It will be noticed that the individual is gradually losing flesh and strength, he complains of a sense of weight and fullness in the right hypochondrium, he is anaemic, and the surface assumes a doughy CANCER OF THE LIVER. 405 hue; with these there may be pain localized over the hepatic region, or shooting up toward the right shoulder, and sometimes to the back. The pain soon becomes lancinating in character, and is localized at some point over the liver which is tender to pressure. There is loss of appetite, flatu- lence, nausea, vomiting, and constipation alternating with diarrhea. The vomiting is often profuse and persistent. There is progressive emaciation, and the skin assumes an earthy pallor. Jaundice is present in one-half of the cases, and is due either to compression of the bile ducts or to intercur- rent catarrh of the ducts, and when once developed it is permanent. Asci- tes occurs more frequently than jaundice ; the accumulation at first is in- considerable in amount and increases slowly. It is due to compression of the portal vein by the cancerous tumor or by enlarged glands in the trans- verse fissure, or to chronic peritonitis. 03dema of the feet comes on late. The temperature is normal or sub-normal. Dyspnea may become an urgent symptom in the advanced stage of hepatic cancer. The cervical and inguinal glands may be enlarged. Hemorrhages from the stomach, intestines, mouth, and vagina, with petechial and ecchymotic spots, are sometimes accompaniments of hepatic cancer. It is to be remembered that hepatic cancer may run its entire course without pain, without jaundice. and without ascites. In medullary cancer, loss of flesh and the peculiar cancer countenance may not appear until the end of the case. The faeces are normal at first, later they are firm and clay-colored. The fluid stools of cancer diarrhea contain no bile. The urine is scanty and high-colored. Deposits of lithates and of bile pigment are rarely absent. Physical Signs.—Inspection. There may be a perceptible bulging in the right hypochondrium and the outlines of large nodules may be visible. Palpation discloses an enlarged and irregularly shaped liver, tender to pressure. Hard, smooth nodules are felt over its surface, which rarely fluctuate. If the nodules are um- bilicated it establishes the diagnosis of cancer. In colloid cancer of the liver, and when the cancerous devel- opment is central, no nodules will be felt. Percussion.—The area of hepatic dulness is irregularly increased and marked by an irregular line of flatness below the free border of the ribs. Auscultation.—A friction sound, caused by the rubbing of the rough- ened peritoneal surfaces, is sometimes heard. Differential Diagnosis —Cancer of the liver may be mistaken for hydatias Fig. 78. Diagram showing enlargemeids of the Liver as determined by percussion. A, A. Line of diaphragm. B, B. Lower border of costal cartilages. C. Dotted line erdargement upward. D. Shaded area indicating successive and in- creasing enlargements. E. Lower edge of Liver in Cancer, Leukmmia and Adenoma. 406 DISEASES OF THE DIGESTIVE SYSTEM. of the liver, abscess of the liver, toaxy degeneration with gummata, cancer of the stomach, and an enlarged gall-bladder. It hydatids there are no gastric or severe constitutional symptoms, Cancer of the liver is rapid in its development, rarely exceeding one year in duration, while hydatids are of slow growth, lasting from four to eight years. Gastro-intestinal hemorrhages are common in cancer, and do not occur in hydatids. Pain is a prominent symptom in cancer; hydatid tumors are painless. In cancer the nodules are hard, tender, and firm; hydatid tumors are large, soft, smooth and elastic, and can be freely manip- ulated without pain. The peculiar hydatid fremitus is sometimes obtained by percussing a hydatid tumor. In hydatids (with an exploring trochar) a saline fluid containing the hooklets of the echinococci may be withdrawn, which will decide the diagnosis. In waxy degeneration of the liver, there is a history of syphilis, pro- longed suppuration, or disease of bone ; and in cancer an hereditary cancerous history, or the evidences of carcinoma elsewhere. The progress of waxy liver is slow ; that of cancer is rapid. A waxy liver is painless, while pain in cancer is constant. In waxy liver the spleen is markedly enlarged; in cancer it is normal in size, unless it is the seat of cancer infiltration. Jaundice and ascites are rare in waxy degeneration, and frequent in cancer. In cancer of the stomach gastric symptoms are urgent and appear much earlier than in cancer of the liver. In cancer of the stomach there is usually coffee-ground vomiting and cancer-cells in the ejected matter. In cancer of the stomach the pain and gastric symptoms are aggravated after ingestion of food, while in hepatic cancer the pain and gastric symp- toms are constant. In cancer of the liver in thin subjects, immovable nodulated tumors may be felt by pressing up under the ribs; while in gastric cancer a single tumor which is movable, and changes its posi- tion as the stomach is full or empty, is usually felt. In hepatic cancer there is absolute dulness over the tumor; while in cancer of the stomach the percussion note has a peculiar tympanitic quality. Cancer of the right kidney, impaction of faeces, and various alterations in the size of the healthy liver will not long confuse one if the symptoms and physical signs are carefully analyzed. Prognosis.—Cancer of the liver is a fatal disease. The average duration is about one year. Medullary cancer runs its course in from two weeks to four months. The duration of all varieties will be influenced by the pres- ence or absence of complications. Death may result from exhaustion, from the cancerous cachexia, dropsy, diarrhoea, dysentery and hemorrhages, or from peritonitis, pneumonia or pulmonary oedema. Treatment.—All varieties of cancer of the liver are incurable, hence the absurdity of all the so called curative measures. The diet should be nu- tritious, and care should be exercised not to overfeed this class of patients. Easily assimilated preparations of iron are often of service. Diarrhea, if present, may be checked by such remedies as gallic acid, lead, and opium. The operation of paracentesis should be delayed as long as possible. In the advanced stage of the disease alcoholic stimulants are often necessary GUMMY TUMOR OF THE LIVER. 407 md beneficial. In the great majority of cases the principal office of th* physician is to relieve pain, and morphia is our most reliable remedy for this purpose ; it should be given in sufficient quantities to keep the patient comfortable. GUMMY TUMOR OF THE LIVER. This form of new growth is perhaps the most characteristic lesion of con- stitutional syphilis. Some writers group these tumors under the head of syphilitic disease of the liver. Those forms of perihepatitis, cirrhosis, and amyloid degeneration which are of evident syphilitic origin, I have preferred to describe in connection with the other corresponding forms, giving at the same time the few differences due to the syphilitic causation. Morbid Anatomy.—The syphilitic nodules, gummy tumors, or "gum- mata" appear first as small masses of reddish-gray, pulpy, vascular tissue, scattered throughout the liver. Their point of origin I believe to be the wall of the capillaries,—the cells and nuclei of the " syphiloma" being due to the growth of the nuclei of the capillaries. The mass is composed of highly organized granulation-tissue, and is usually spherical in shape. The liver may be enlarged, or may retain its normal size, according to the ex- tent of the waxy change which usually accompanies the development of the gummata. Diminution of its size is due to perihepatitis causing re- traction. Under these circumstances the organ is lobulated, and deep, whitish furrows indent it, the result of cicatricial contractions. Fibroid nodules occasionally lie in these cicatrices. The bulgings are soft and smooth to the touch. The capsule is firm and opaque, and the seat of fibroid thick- ening, and is frequently bound to surrounding parts by adhesions. On section there will be found scattered through the liver rounded masses varying in size from a pea to an orange, yellowish-white in color, either surrounded by congested parenchyma, or as isolated spots in the midst of an infiltrated homogeneous grayish-red mass. They may be en- capsulated, a layer of translucent fibrous-tissue surrounding them and shading off imperceptibly into the surrounding liver-tissue. Brown spots in the tumors correspond to obstructed bile-ducts. The liver parenchyma, between the nodules, undergoes various changes : at one time it is con- gested and hypertrophied, at another it is atrophied and undergoes fatty degeneration. In well-marked cases there are two zones, an outer, red and fleshy, and an inner, dry, grayish and firm. Again, nothing may remain of a previous gumma but a shrivelled cicatrix. A microscopical examination of a fully developed gummy tumor reveals three processes -.—first, at the periphery, there is a vascular mass of gran- ulation-tissue, embedded in which are cells bearing a striking resem- blance to white blood globules, and some larger nucleated ones. Sec- ondly, just beneath this zone is found a fibro-nucleated mass, the fibril- lations being very dense and cicatricial. Thirdly, in the centre of the mass we found fat-granules and broken-down cells, with occasional traces of cholesterin, and sometimes faint evidences of fibrillar tissue. Cheesy and calcareous masses are also sometimes found in the centre of the gumma. 408 DISEASES OF THE DIGESTIVE SYSTEM. Etiology.—As has been stated, gummata are the most characteristic of the lesions of internal syphilis. They are met with under no other condi- tions. Symptoms.—The subjective symptoms of hepatic gummata are few and inconstant. At a post-mortem, a liver may be found studded with gummy tumors, when no symptoms referable to the liver were present during life. There is generally a history of increasing debility, and a feeling of press- are, tightness, and dull pain in the region of the liver. Sometimes the pain is severe and localized, at other times it is dull and diffused over the whole hepatic region. The pain in one case is constant, in another intermittent. If jaundice exists, it is due to the pressure either of the gummata or of an enlarged lymphatic. The temperature is normal, and the pulse-rate is but slightly increased. Ascites may result from pressure on the portal vein, or from chronic peritonitis, which often complicates its development. Both jaundice and ascites are not present until the liver has become very much enlarged. The symptoms which are present in the advanced stage of this disease, such as diarrhea, loss of appetite, vomiting, hemorrhoids, gastric and intestinal hemorrhage, are due rather to the accompanying hepatic de- generation than to the gummata. Physical Signs.—Palpation may show the liver to be enlarged or normal in size ; a moderate increase in size is the rule. The organ has smooth lobules upon its surface between which run deep fissures. The lobulations are soft and elastic, never fluctuating. Percussion.—The area of dulness is increased and its outline is irregular below the free border of the ribs. The area of spleen-dulness in the ma- jority of cases is slightly increased. Differential Diagnosis.—Gummata of the liver may be mistaken for can- cer, and if the liver is diminished in size, for syphilitic cirrhosis. The' differential diagnosis of both has been considered. Prognosis.—Gummata of the liver rarely directly destroy life. The prog- nosis is unfavorable when ascites, gastro-intestinal hemorrhage, persist- ent diarrhea, or a marked cachexia exists. Complicating diseases also influ- ence the prognosis ; amyloid degeneration of the spleen and kidneys is a bad complication. The most frequent intercurrent lung diseases are pleurisy, pneumonia, pulmonary oedema, and chronic bronchitis. Death occurs from exhaustion due to the syphilitic marasmus, from diarrhoea, dysentery, and dropsy. Pneumonia and pulmonary oedema often cause it, and sometimes cholemia, with its peculiar symptoms, ends in coma and death. Treatment.—The treatment of this affection resolves itself into the treat- ment of syphilis. As it is a tertiary symptom, our main reliance is on large doses of the iodide of potassium combined with mercurial inunctions. With these iron and cod-liver oil should be constantly taken, and the patient should be placed under the best hygiene. The diet should be nutrition* and non-stimulating. Opium combined with nitric acid will always con trol the diarrhea if it becomes exhausting. HYDATIDS OF THE LIVER. 409 HYDATIDS OF THE LIVER. Hydatid tumors are cysts due to the development in the liver of the em- bryos of the tmnia echinococcus ; these embryos are called " echinococci," their development "hydatids" ; they are usually single, and for more than two or three to be present in the same liver is a phenomenal event. Morbid Anatomy.—An ovum of tenia echinococcus, either during masti- cation or from the action of the digestive juices, has the envelope containing the echinococcus removed, and then by its hooklets it bores its way from the stomach or intestine into the liver. It there becomes encysted: the cyst consists of an external laminated cuticular layer and an internal par- enchymatous lining. From the internal layer'numerous little heads bud forth in the form of vesicles, and these, the "daughter vesicles," in turn bear a second crop, the " grand-daugh- ter cells," the mother-sac meanwhile enlarging, partly from the increase in the number of the vesicles, and partly from itsown secretion, which is clear and wa- tery. As these successive generations of vesicles appear, broods of immature te- nia ("scolices") in the form of a gray- ish granular layer, are developed first upon the internal surface of the mother sac and then upon that of the other cysts, in the order of age. While the younger vesicles cling to the parent- walls, the larger and older ones become fig. 79. detached, and float in the interior of Multilocular Hydatid Cysts of the Omentum. the continually enlarging parent-sac. {After Bright.) Proliferation of connective-tissue upon the exterior of the sac resulting from the inflammatory process excited by the pressure of a foreign body, develops a fibrous capsule closely connected with the adjacent liver par- enchyma ; this is supplied with blood by the hepatic and portal capilla- ries. During its enlargement the hydatid tumor loses its spherical shape and becomes indented. As it increases in size, the fibrous capsule becomes thickened, rough and cartilaginous ; sometimes it undergoes ossification. The echinococci may be destroyed by the bile which enters the cysts when the bile-ducts are opened, or by the inflammation which is established be- tween the connective tissue capsule and the wall of the true sac, causing a grayish oily material of variable consistence to be developed. The clear fluid in the cavity of the hydatid becomes cloudy, then opaque, while all traces of the vesicles disappear, and at last only a few hooklets of the echi- nococci remain. This is a process of fatty degeneration. Sometimes the formation of vesicles is so rapid that their number is beyond all pro- portion to the fluid, and then they die and collapse, undergoing no degen- 410 DISEASES OF THE DIGESTIVE SYSTEM. erative process ; again, when neither of these terminations is reached, the hydatid tumor may continue to increase in size until finally it bursts into the adjacent cavities. The most frequent rupture is into the right pleural cavity. The hyda- tid tumor, by its pressure upon the diaphragm, causes it to become thin, and to rise upward, sometimes as high as the second rib. Finally the diaphragm ruptures and the sac is discharged into the pleural cavity, or when the pleural surfaces become adherent the tumor ruptures into the lung-tissue or bronchi. These tumors sometimes rupture into the perito- neal cavity, and peritonitis results, or the stomach or intestinal canal may communicate by a small aperture with the hydatid sac. A communication is sometimes established between the bile-ducts and the hydatid tumor, and the ducts become filled with the contents of the hydatid mass ; the ductus communis may become obstructed by a large hydatid vesicle. Another mode of termination is by an intense inflammatory action, causing sup- puration of the liver-tissue in the vicinity of a ruptured hydatid tumor, which consequently is filled with coagulated blood and pus ; more rarely a gangrenous process may be established in it. The liver is irregularly enlarged and displaced. The increase in size varies with that of the projecting cysts, which are sometimes large enough to fill the abdominal, and a portion of the thoracic, cavity. The bulging is globular if the cyst is simple and is situated in the right lobe of the liver. The tumor is elastic and often fluctuating. A uniform enlarge- ment of the liver results from a centrally located hydatid. The capsule covering the cyst is thickened, and adhesions often bind the liver to the surrounding parts. On section, the liver-tissue in the vicinity of the tumor is found com- pressed and atrophied, or congested and hypertrophied. The mother-sac is commonly the size of afetal head. The true cyst wall is a gelatinous, whitish, semi-transparent membrane, containing the hydatid fluid, floating in which are vesicles from the size of a millet-seed to that of an egg, and varying in number from hundreds to thousands. On the inner walls of the larger ones, and on that of the parent-sac, are younger vesicles about the size of a pin's head. On the inner side of the sac are also found patches of white granular matter. The cysts may be found filled with atrophied and shriv- elled vesicles embedded in a debris consisting of fat-granules, cholesterin, hemaglobin, and bile. Its consistency varies : sometimes it is liquid and watery, then semi-fluid, gelatinous, or like a thick paste; at other times only a few hooklets remain in this gray, putty-like mass. The cyst may contain blood or pus. A microscopical examination shows the sac of the hydatid to be a gela- tinous mass made up of concentric hyaline lamellae. The scolices are from 1-75 to 1-225 of an inch in length ; the head is furnished with four suckers and a proboscis, about which are sickle-shaped hooklets in number from twenty-five to fifty. The body is striped longitudinally and transversely, and has a groove between it and the head, which latter, being usually re- tracted into the body, causes the animal to look somewhat like an in- HYDATIDS OF THE LIVER. 411 dented rubber ball, the hooks fringing the depression. The fluid is clear or slightly opalescent, it has a specific gravity of 1010 to 1015, is usually neutral in reaction, and is non-albuminous. It is chiefly water containing chloride of sodium. Multilocular Hydatids.—This form of hydatid disease differs from the or- dinary hydatid cyst in that is con- sists of a tumor composed of numer- ous small vesicles, each the size of a pea or larger, and surrounded by a fibrous capsule. Hence on section the tumor has a trabeculated or honeycombed appearance. Each ves- icle has a parenchymatous lining capable of producing brood-capsules though they are usually sterile, that is without scolices. This peculiar ar- rangement IS supposed to result Hydatids of the Liver. from the development of daughter- •<*• Head of echinococcus from an hydatid tumor.—B. * ° Discs.—C. Hooklets.—D. Pedicle. CVSts On the Outside OI the parent- E. Fragment of capsule of hydatid tumor, showing J , . , its lamella.—F. Germs. x 200. cyst, as is known to occur some- times in animals, and their growth into pre-existing spaces, as lympathics or blood-vessels. The liver is enlarged, and as a rule uniformly. Etiology.—The essential cause of the development of hydatids is the en- trance into the stomach, or intestines, of the tenia echinococcus. If they remain in the intestine they become tapeworms; when they pass into the liver they develop hydatids. Hydatids are chiefly met with between the ages of thirty and fifty. They are rare in childhood and old age. They are most common among the poor and filthy, and in cold climates. It is estimated that one out of every six of the inhabitants of Iceland has hy- datids of the liver. Dogs, sheep, pigs, cats, and rats are subject to tape- worms, and as the ova of these parasites are discharged in the excrements of these animals, they can only gain entrance into the human stomach through polluted drinking-water, or the most filthy practices. Symptoms.—If an hydatid tumor is deeply seated and of small size, it gives ri^e to no symptoms and cannot be recognized. A large hydatid tumor will cause sufficient functional disturbance by its pressure to be easily reoognized. The patient may first see or feel a tumor in the region of the liver, and have a sense of weight and dragging in the right hypo- chondrium. Symptoms of pressure of the tumor on adjacent organs are the first, and often the only ones which attract attention. Dyspnoea, a dry hacking cough, and bronchial catarrh may result from the upward pressure of the tumor. When the heart is displaced by the tumor, there is palpitation; and when the stomach is encroached upon there is vomit- ing, dyspeptic symptoms and emaciation. When the portal vein or vena cava is pressed upon by the hydatid tumor, ascites, jaundice and hemor- rhoids may result. When the hydatid compresses the bile-duct, or when there is intercurrent catarrh of the ducts, or when they have become 412 DISEASES OF THE DIGESTIVE SYSTEM. obstructed by the hydatid vesicles, jaundice sets in and absence of bile in the faeces is noted. A large vesicle may, in passing the duct, give every symptom of gall-stone colic, and thus be confounded with it. When the pleura is perforated, the symptoms of acute pleurisy are devel- oped, and in most cases the cavity is rapidly filled with pus containing hydatid vesicles. Peritonitis may result from spontaneous or traumatic rupture of an hydatid cyst. The opening into the stomach or intestines being usually very small, it is rarely attended either by peritonitis or sec- ondary abscess; when a cyst is evacuated in this way the case usually ter- minates in recovery. When shreds of hydatid vesicles and echinococci are found in the urine, it indicates that the rupture has taken place into the urinary passages. When the hydatid tumor is to discharge itself through the abdominal parietes, redness of the skin, tenderness, pain, and fluctua- tion will precede its discharge. If, in a patient who is known to have hydatids of the liver, there is pain, elevation of pulse and temperature, extreme sensitiveness over the hepatic region with a peculiar friction sound on auscultation, it may be suspected that inflammation in and around the sac has occurred. In such case abscess may be excluded by the absence of rigors and sweats. Finally, the growth of an hydatid of the liver is in rare cases attended with pain caused by its pressure. The faeces are normal unless jaundice exists, in which case they are firm and clay-colored. The urine is generally ' normal, but if pus or albumen is found in it, pyelitis exists as a result of the pressure of the tumor on the renal vein. Physical Signs.—Inspection may show a distinct bulging in the right hypochondrium, which has the appearance of a globular elevation over the right or left lobe of the liver. The ribs often project, and respiratory j movements on the right side are interfered with. Palpation discovers an enlarged liver, elastic to the touch when the tumor is deeply seated ; when it is superficial, fluctuation may be detected. The tumor is smooth, but if two, three or more cysts exist, the liver will have a lobulated outline below the free border of the ribs. Percussion.—The normal area of hepatic dulness is increased in some one direction. When the tumor is superficial, the hydatid thrill or "fre- mitus " is elicited by firm percussion. This sign, peculiar to hydatids of the liver, is elicited in the following manner : place three fingers, slightly separated, firmly over the most prominent part of the tumor ; give a sharp blow upon the middle one, and a vibration or fremitus will be communicated to the other two. Differential Diagnosis.—Hydatids of the liver may be mistaken for cancer, abscess, abdominal aneurism, enlarged gall-bladder, pleurisy, rarely multi- locular hydatids, and a cyst of the right kidney. In abdominal aneurism there will be severe and constant pain in the back ; the tumor is soft, doughy, and compressible, has an "expansive" pulsation and is immov- able, while an hydatid tumor moves up and down with the respiratory movements and fluctuates. A "bruit" synchronous with the heart and often double will be heard over an aneurism, while neither of these is ! HYDATIDS OF THE LIVER. 413 ever present in hydatids. The femoral pulse will be altered in an abdom- inal aneurism, but normal in hydatids of the liver. When a pendulous hydatid cyst is attached to the liver by a pedicle, we may readily mistake it for an enlarged gall-bladder. An enlarged gall- bladder is usually preceded by jaundice, biliary colic, or symptoms oi catarrh of the ducts, while an hydatid has no such previous history. On palpation it will be found that an hydatid does not correspond exactly to the position of the gall-bladder. The gall-bladder is pear-shaped and evades manipulation or pressure, while an hydatid tumor is globular and readily manipulated. When hydatids extend into the pleural cavity so as to be mistaken for •pleurisy, the heart will be displaced much more than ever occurs in pleu- risy. Percussion in pleurisy marks out a line of dulness which is trans- verse when the patient is erect, and which changes with his position, while in hydatids the upper limit of dulness is irregular and stationary, being lower near the median line of the body than toward the axilla. This is an important point. In hydatids the lower edge of the liver is below the free border of the ribs and rises and falls with the respiration ; in pleurisy the liver occupies nearly its normal position and is station- ary. In a cyst of the right kidney, there is the history of a growth from below upward, while in hydatids the tumor grows from above downward. In cystic kidney the colon lies in front of the tumor, while in hydatids of the liver the colon is behind the tumor. An hydatid of the liver rises and falls with respiration, while a cyst of the kidney is motionless. In hydatids of the liver, an exploring needle will withdraw a non-albuminous, salty fluid, containing hooklets of the echinococci, while from a cyst of the kidney it will withdraw an albuminous fluid with chlorides and perhaps pus. Prognosis.—Hydatids are dangerous in proportion to their size and the direction of their growth ; if they cease to enlarge, they may be regarded as harmless. Their average duration is about four years. They have been known to exist twenty-five years. If they rupture into the pleura, lung, peritoneum, pericardium, or through the abdominal walls, the prognosis is unfavorable. When the discharge takes place into the intestines, stomach, or bronchi, the prognosis is favorable. Death occurs from exhaustion caused by the pressure of a very large hydatid, rarely from that caused by ascites through pressure on the vena cava. Suppuration of the cyst, or an abscess developed secondarily to phlebitis may induce fatal exhaustion. Any one of the pulmonary complications referred to may cause death. A fatal result has, in some few cases, followed hemorrhage from the sac through an ex- ternal opening. Peritonitis, pericarditis, and uremia are infrequent causes of death, and when the pulmonary artery is plugged, when the vena cava is opened, or when a large vesicle is lodged in a bronchus, asphyxia is the immediate cause of death. Treatment.—Prophylactic measures consist in preventing the drinking- water from being contaminated by the evacuations of animals, and in not al- lowing dogs to feed upon the offal of sheep. Chloride of sodium and iodide 414 DISEASES OF THE DIGESTIVE SYSTEM. of potassium have been proposed as internal remedies to destroy the echino. cocci. The chief solid ingredient of hydatid fluid is chloride of sodium, but no trace of iodide of potassium has ever been found in the fluid after the administration has been continued for months. If the tumor is of large size, and is still increasing in size, operative inter- ference is necessary. Select the point where the hydatid tumor is most prominent, and puncture with a fine aspirating needle. The dangers whick have been feared in this procedure are peritonitis, and the entrance of ait into the peritoneal cavity. Peritonitis maybe avoided by pressing the parts Sbout the puncture firmly against the tumor as the aspirating needle ii Withdrawn, so that no fluid can escape into the peritoneal cavity. All dan- ger of the entrance of air is obviated if a small aspirating needle is used; all of the fluid should not be withdrawn from the cyst at the first aspiration. It is important to enjoin absolute rest after the operation for two or three days ; febrile symptoms and pain will follow the withdrawal of the fluid, and the tumor will decrease in size ; usually a second puncture will be re- quired. It is not essential to wait for adhesions to form between the tumor and abdominal wall, though it is much safer if they exist. Where simple puncture is not sufficient to destroy the echinococci, iodine or bile may be injected into the cavity of the sac. When the fluid with- drawn is pus, or when the symptoms are indicative of a suppurating cavity, it is best to establish adhesions by caustics. Vienna paste is to be preferred for this purpose, and the same precautions are to be exercised as in the opening of an hepatic abscess. Puncture of the cyst by insulated needles,-*i electrolysis,—has been claimed to be very successful in those cases where it j has been resorted to, but it seems to me that it is the puncture, rather than the electric influence, which produced the favorable result claimed for it. Never hesitate to aspirate an hydatid tumor when it is well developed and elevated above the level of the abdominal walls ; the nearer the cyst is to , 'rhe surface, the better the result of the aspiration. TUBERCULOSIS OF THE LIVER. Tubercle of the liver is always secondary to tubercle elsewhere. It is probably more common than is usually supposed, from the fact that hepatic tubercle is always microscopic. Morbid Anatomy.—The liver is slightly but uniformly enlarged in size. On close inspection the surface is seen to be irregularly elevated and de- pressed, and looks and feels, in this respect, like the surface of an orange. On section the liver cuts hard, the parenchyma being tense and tough. The tissue is pale and yellow, resembling a fatty liver. The bile-ducts at points are expanded, the walls being thinned. They contain a turbid fluid mainly composed of mucus and bile. There are also small cavities filled with pus and bile. When the tubercle has undergone retrograde metamorphosis, small gray masses the size of a pin's head are seen, " yel- low tubercle," or larger yellow masses the size of a pea ; these changes are usually best marked just beneath the capsule. A microscopic examination shows miliary tubercles scattered between the JAUNDICE. 415 lobules. When, as a result of obliteration of blood-vessels, tubercles under- go fatty degeneration, the so-called " yellow tubercle " is the product. Etiology.—Hepatic tubercle occurs as part of acute miliary tuberculosis, and is secondary to tubercle in the lungs, peritoneum, spleen, and lym- phatics. Symptoms.—There are no symptoms indicative of hepatic tuberculosis, i independent of those of general tuberculosis.1 JAUNDICE. Jaundice is a yellow discoloration of the skin, due to the presence of bile or blood pigment. There are two varieties, hepatogenous or obstructive jaundice, and hematogenous or non-obstructive. Hepatogenous jaundice is the more common variety, and is caused by the absorption of bile, its passage into the ductus communis or intestine being prevented by some mechanical obstruction. Hematogenous jaundice results, probably, from a change in the blood, whereby its coloring matter is set free in excess. Morbid Anatomy of hepatogenous jaundice. In a normal state, the liver- cells are constantly manufacturing bile, which flows along the bile-ducts into the ductus communis. The cause of its outward flow is the vis a tergo,— the secretion of the bile in the hepatic cells,—for there are no muscular fibres except in the larger bile-ducts; the respiratory movements also assist slightly in its outward flow. When from any causes the bile cannot enter he common duct or the duodenum, the small hepatic ducts and radi- ces become overfull and distended. In consequence of this increased pressure, bile passes through the wall of the smaller ducts into the blood- vessels and lymph channels. If the normal tension of the capillary system in the liver is diminished, then the passage of bile through the walls of the vessels is favored and jaundice results. Bile pigment with serum exudes and stains the tissues, even the bones, the teeth and pathological new forma- tions. In both hepatogenous and hematogenous jaundice, the staining occurs in the same way. Hematogenous Jaundice.—In health the bile pigment is formed within the liver, by transformation of the coloring matter of the blood, and after it has been poured into the intestine, it is partly absorbed by the blood and appears, after another change, as one of the coloring matters of the urine. Under abnormal conditions, and as the result of processes that are not fully understood, coloring matter is either set free in excess or is not excreted with the bile, and is then deposited in the tissues producing jaundice. As this variety of jaundice is thought to have its origin in morbid conditions of the blood, it is called hematogenous. The anatomical lesions which are associated with hematogenous jaundice have already been considered in connection with the history of the different hepatic affections in which it occurs. 1 Lymphatic formations, simple cysts, dermoid cysts, erectile cavernous tumors, and benign fibrous growths occur in the liver, but are only of pathological interest. 416 DISEASES OF THE DIGESTIVE SYSTEM. Etiology.—The causes of hepatogenous jaundice may be included undei three heads : I. Those which obstruct the larger hepatic ducts. II. Those which obstruct the hepatic radicles. III. Those which diminish capillary tension. Those obstructions of the larger hepatic duct which have their seat within the duct are : (1) Inflammations of, or inflammatory exudations from, the lining mem- brane of the duct, that which accompanies duodenal catarrh being the most frequent. (2) Biliary calculi. (3) Inspissated bile and mucus. (4) Hydatid vesicles. (5) Distomata. (6) Foreign bodies from the intestinal canal, such as stones of fruits and round worms. (7) Congenital occlusion, or plugging of the duct. (8) Cicatrices from ulcers on the mucous membrane of the duct. (9) Carcinomatous growths from the lining membrane of the ducts. The causes which obstruct the duct by external pressure, are • (1) Contraction from perihepatitis, or from inflammation of thehepatico- duodenal ligament. (2) Tumors of the pyloric extremity of the stomach, of the head of the pancreas, and of the kidney. (3) Pressure from a preg- nant uterus, from ovarian and fibroid tumors, from omental tumors, and from large impaction of feces. (4) Enlarged lymphatic glands in the trans- verse fissure from waxy, cancerous, or tubercular change, abdominal aneu- rism, and the new tissue in hypertrophic cirrhosis of the liver. Slight hepatogenous jaundice may be caused by compression or oblitera- tion of the hepatic radicles, such as occurs in cirrhosis and the other atro- phies of the liver, in active and passive hyperaemia, in hydatid tumors and multilocular hydatids, in cancerous and syphilitic tumors, in abscess of the liver, in adhesive pylephlebitis, and perhaps in acute yellow atrophy. Finally,the bile may be prevented from entering the intestine in its normal amount when capillary tension is diminished. This may occur in severe right diaphragmatic pleurisy, in perihepatitis, in thrombosis of the trunk or of the larger branches of the vena porte, and in exhausting hemorrhage from the radicles of the portal vein. The causes of hematogenous jaundice are fevers, especially yellow, typhus, typhoid, and the malarial fevers. It is often an attendant of pyaemia, puer- peral fever, septicaemia, and suppurative pylephlebitis. The poison of snake-bites, p'losphorus, mercury, copper, antimony, and the excessive use of ether and chloroform may cause it. Pneumonia, probably by its action on respiration, and ulcerative endocarditis induce it; it.may follow a fright, a fit of anger, great anxiety, or cerebral concussion. A long con- tinued hepatogenous jaundice may lead to a hematogenous jaundice; and it is yet undecided whether the icterus in yellow atrophy belongs to the first or second named group. Differential Diagnosis.—Hematogenous jaundice accompanies acute in- fectious fevers and other conditions of blood poison, while hepatogenous jaundice can be traced to some mechanical interference with the outflow of the bile. The yellow staining is slight in hematogenous jaundice; while the discolorization in hepatogenous jaundice is more intense and mat CATARRH OF THE BILE-DUCTS. 41^ ppear suddenly without constitutional disturbances. A feeble and irreg- llar heart-action, a small pulse, and a tendency to hemorrhages attend hematogenous jaundice; while an unimpaired heart-action, a slow pulse, and i, low temperature mark the'development of hepatogenous jaundice. There j great itching of the surface in hepatogenous jaundice which is absent in he hematogenous variety. The faeces are dark in hematogenous jaundice, 1 ad white or clay-colored in hepatogenous. The urine is albuminous, con- tains a small amount of bile pigment, and deposits a sediment of uric acid in the hematogenous variety, while it is rarely albuminous in hepatogenous jaundice and contains bile-pigment in considerable amount, the quantity varying with the intensity of the jaundice. DISEASES OF THE GALL-BLADDER AND GALL-DUCTS will be considered under the following heads : 1, Catarrhal Inflammation of the III. Cancer of the Gall-Bladder. Biliary Passages. IV. Enlargement of the Gall-Blad- II. Exudative Inflammation of the der. Biliarg Passages {croupous V. Gall Stones, or diphtheritic). CATARRH OF THE BILE-DUCTS. Morbid Anatomy.—Catarrhal inflammation of the mucous membrane of tbe larger bile-ducts, the ductus communis, and the gall-bladder is similar to tliat of other mucous surfaces. There is hyperemia followed by an ab- normal secretion of mucus and muco-pus which more or less obstructs the outflow of bile. The catarrhal process usually begins in the duodenum and extends inward, and in severe cases may be so rapid that pus will be the pvoduct of the inflammation, in which case the deeper tissues are in- volved and numerous little ulcers may form, and when the duct is perfo- rated by them, cavities of varying sizes, resembling small abscesses, result. When the catarrh becomes chronic the deeper tissues are infiltrated, caus- ing thickening and induration of the ducts from the consequent obstruction to the exit of the bile. Dilatations occur at points along the bile ducts ; these dilatations often become very large and occasionally form cysts ; at other times the alternate dilatations and constrictions give the appearance of a string of beads. The lymphatics often become involved, and their en- largement gives a nodular appearance to the mucous membrane. Ulcera- tive processes are more frequent in chronic catarrh of the bile passages than in acute. The liver is uniformly enlarged and its margins are firm md sharp. On section, its substance presents a mottled appearance, resembling a nutmeg, and varies in color from a deep yellow to an olive green. The color is deeper at the centre of a lobule and shades off toward its periphery. The gall-ducts commonly have their mucous membrane pale and covered tfith a thick, purulent mucus; and plugs of mucus and epithelial debris 1 I 418 DISEASES OF THE DIGESTIVE SYSTEM. are found in them, most frequently near or at the opening of the duct into the duodenum. The gall-bladder is enlarged, and the cystic and common ducts often attain immense size ; in one case this diameter reached an inch and a half. In chronic catarrh the liver is normal or diminished in size, and is soft,' flabby and shrivelled. On section it is greenish-black in color, the hepatic ducts are dilated,! forming cysts, and little points of ulceration are formed on the mucouji surface of the duct, often extending into the adjacent parenchyma which is atrophied. The ramifications of the vena portae are compressed by the ducts, and thickened bile may cause these ducts to present the appearance of a dark brown tube. The gall-bladder is enlarged in size, and sometimes: there are spots of ulceration upon its walls which may also undergo cal- careous changes. Etiology.—The most frequent cause of biliary catarrh is extension of a: gastro-duodenal catarrh. Most of the structural diseases of the liver mav > lead to or be attended by catarrhal inflammation of the bile ducts. Thoracic disease where the venous return is impeded (as in cardiac valvular lesions and emphysema) may cause catarrh of the biliary passages. General blood diseases, syphilis and pyemia prominently, and mineral poisons, phos- phorus, and perhaps arsenic, cause it. A gouty diathesis causes or pre- disposes to a catarrh of the biliary passages, just as it does to catarrhal inflammations of the mucous membranes elsewhere in the body—bronchitis,, for instance. Foreign bodies, as calculi and parasites, in the bile passages may cause biliary catarrh. Exposure to cold and an altered condition oi, the bile may induce it. \ Symptoms.—The subjective symptoms of biliary catarrh are at first obscure. - It is usually preceded by the symptoms of gastro-duodenal catarrh, and hence for a few days there will be loss of appetite, furred tongue, flatulence, nausea and vomiting. There is also some pain and tenderness in the epi-. gastrium, and in most cases the temperature will be slightly raised, and the pulse accelerated. The bowels are constipated, unless it is accompanied by extensive intestinal catarrh, when diarrhoea will be present. The faecal discharges are of a light clay color and contain no bile. The urine is of a dark green color, and contains bile pigment. The liver is enlarged and tender, especially over the region of the gall-bladder. The absence of bile from the intestine favors gaseous distention of the bowel. The sclerotic becomes yellow, and gradually the entire surface assumes a yellow - hue. The temperature falls to normal and the pulse is slowed. As the jaundice deepens, there is a noticeable loss of strength, the patient becomes apathetic and disposed to sleep during the day. There is headache, vertigo, and great depression of spirits ; itching of the surface becomes exceedingly troublesome. All these symptoms remit, the appetite returns, and the feces and urine return to their normal color ; or the catarrh becomes chronic and continues\ for months, the jaundice deepening, exhaustion and emaciation becoming extreme. Then gastric and intestinal hemorrhages frequently occur, and * CATARRH OF THE BILE DUCTS. 410 ascites may be followed by general anasarca ; coma closes the scene. The last stage of chronic catarrh is accompanied by evidences of atrophy of the liver. Physical Signs.—Inspection reveals a jaundiced condition of the skin and conjunctivae, and perhaps a bulging in the right hypochondrium. Palpation discovers an enlarged, smooth and tender liver. The gall- bladder is enlarged, and sometimes there is a pear-shaped fluctuating tumor at its anterior margin. The gall-bladder is tender on firm pressure. Late in chronic catarrh the liver is diminished in size. Percussion shows a uniform increase in the area of hepatic dulness, which, however, in chronic disease may be normal or diminished. Differential Diagnosis.—This condition may be mistaken for suppurative pylephlebitis and exudative inflammations of the ducts. The former has already been considered, the latter will be considered under exudative in- flammations. Prognosis.—This is good ; catarrh of the bile ducts is not a dangerous disease. The jaundice usually continues from three to five weeks, but sometimes it continues for months. The prognosis is rendered unfavorable when oft-repeated biliary catarrhs lead to permanent closure of the ducts and atrophy of the liver. Catarrh of the bile-ducts may be complicated by peritonitis, pleurisy, pneumonia, dysentery, suppurative hepatitis, or acholia. Death then results from exhaustion, from faulty nutrition, or dropsy, from intercurrent diseases, rupture of the ducts, or with brain symptoms—" acholia." Treatment.—It should be remembered that the jaundice is only a symp- tom, and requires no treatment. The treatment of this catarrh is mostly symptomatic ; it is usually self-limiting and will subside without remedial measures. If the hepatic pain is severe, leeches followed by an anodyne poultice over the points of greatest tenderness will usually relieve it. When the bowels are constipated, " blue-pill," or a saline purgative is first de- manded, after which old cider or tamarinds will regulate the bowels for the remainder of the attack ; nitro-muriatic acid acts favorably in most cases. If there is diarrhea, ipecacuanha or Dover's powder will readily control it. When the urinary secretion is much diminished the salts of potash in com- bination with diaphoretics may be administered. The diet throughout should contain no carbo-hydrates ; the food should consist principally of lean or prepared meats, vegetables, and skimmed milk. When there is a gouty diathesis, colchicum and iodide of potassium are often of service. In a syphilitic diathesis, chloride of ammonium and the bi-chloride of mercury are indicated. Emetics rather aggravate the gastric intestinal catarrh than cause the expulsion of a hypothetical plug in the common duct, and should not be administered. Finally, if the hepatic parenchyma become involved, a tonic and diuretic plan, similar to that adopted in cirrhosis, may be adopted. The use of mineral waters must be determined by the influence which they exert on each patient; in some cases iu creased appetite results, while in others they seem to hasten the wasting process. 4;i0 DISEASES OF THE DIGESTIVE SYSTEM. EXUDATIVE INFLAMMATION OF BILIARY PASSAGES. Under the head of exudative inflammation of the biliary passages I in- clude both a croupous and a diphtheritic process. Both are rare and seldom recognizable during life. Morbid Anatomy.—The commencement of croupous inflammation is the same as catarrh ; but the inflammatory product is fibrinous. In diphtheritic inflammation, the deeper tissues of the walls of the gall- bladder and bile-ducts are involved, and large gray sloughs, more firmly adherent than in croupous inflammation, are formed upon their walls. The liver is usually enlarged. On section the ducts within the liver are seen clogged with inspissated bile, and occasionally there are abscesses. When constriction and occlu- sion of the ducts exist, they become dilated behind the narrowed portion, and resemble cysts, containing a pale yellow fluid with loose coagula floating in it. The gall-bladder is sometimes filled with a gray-white liquid, neutral, albuminous, and sometimes containing leucin ; at other times the liquid is purulent, or thick and dark like tar. On the mucous membrane of the gall-bladder and common duct is a yellowish-white fibrinous layer, varying in thickness and tenacity, having all the anatomical characteristics of a diphtheritic exudation. The walls of the gall-bladder and larger ducts are thickened and sometimes ulcerated. The ulceration may lead to perfora- tion and fistulous openings. Adhesions sometimes bind the gall-bladder to the surrounding parts. If the diphtheritic process extends to the venous coats pylephlebitis may result; sometimes the bile-ducts open into branches i of the vena portae. I Etiology.—These inflammations occur with typhus and typhoid fevers, cholera, diphtheria, pyaemia, septicaemia, bilious fever, and from the irritation produced by biliary calculi. Symptoms.—The first symptom of exudative inflammation of the biliary passages is a sense of constriction in the right hypochondrium. This is soon followed by pain, increased by pressure in the region of the gall-bladder, and vomiting. There are active febrile symptoms, but these are usually not marked. If ulceration of the ducts or implication of the branches of the portal vein occurs, then chills, sweats, and the other symptoms of pyaemic abscesses of the liver result, or the symptoms of pylephlebitis are developed. When an opening into the peritoneal cavity occurs, rapidly; fatal peritonitis is the result. If there is no obstruction to the outflow of bile, neither jaundice nor alteration in the color of the stools will be present. Physical Signs.—Inspection may show a slight elevation of the free border j of the ribs. Palpation discovers a pear-shaped, tender, movable tumor at the nor-; mal site of the gall-bladder. Slight pressure over it gives pain. Percussion.—The area of liver dulness is normal or slightly increased;! over the enlarged gall-bladder the percussion note is dull and somewhat tympanitic in character. CANCER OF THE GALL-BLADDER. 421 Differential Diagnosis.—Exudative inflammation of the bile-ducts may be mistaken for simple biliary catarrh. The points which will aid in a di- agnosis are the occurrence of intense pain, active febrile symptoms, and a careful study of the etiology of each case. Prognosis.—This is determined by the disease which it accompanies. It usually terminates in death. Treatment.—Absolute rest is important. To relieve the pain leeches may be applied over the tumor, followed by poultices and, later, by counter- irritation. The diet and saline purgatives should be the same as in sim- ple catarrh, unless the primary disease contraindicates their use. If symp- toms of pus formation are present, quinine may be given in large doses and tonics are indicated. If the tumor becomes large, so that there is danger of its rupture, it may be aspirated, the same rules being observed as in hydatids and abscess. CANCER OF THE GALL-BLADDER. Cancer of the gall-bladder is usually associated with cancer of the liver substance, and is often the primary seat of the development of scirrhus or medullary cancer of the liver. Morbid Anatomy.—The gall-bladder is enlarged, nodular and adher- ent to the surrounding parts ; sometimes there are spots of ulceration on its surface, and there may be fistule from the gall-bladder to the intestine. . On section its wall is found thickened, and the cavity sometimes filled with a cancerous mass in which are embedded numerous concretions. Etiology.—This is the same as that of cancer of the liver. It is often secondary to cancer of the stomach. Concretions are so often found that some have ascribed its development to gall-stones. Symptoms.—The subjective symptoms are few : none are constant except ihe gastric derangement and the paroxysms of lancinating pain ; vomiting l s common and severe, because of the pressure of the tumor on the py- lorus. Jaundice may be present when the common duct is involved. While the tumors often increase very rapidly, the cancerous cachexia and imaciation are slow in their development. In some cases the symptoms indergo marked exacerbations and remissions. Swelling of the glands in he inguinal and axillary regions may occur. Physical Signs.—Palpation will discover over the site of the gall-bladder ,1 hard, nodular and immovable tumor. It is tender, and sometimes fluctu- ites at the centre. Percussion shows an increase in the area of hepatic dulness below the free uorder of the ribs. ENLARGED GALL-BLADDER. t Dropsy of the gall-bladder is a term used to include those cases where, it:)n account of some obstruction, bile is prevented from entering the nat- ural reservoir, and an increased secretion from its mucous surface leads to its distention. 422 DISEASES OF THE DIGESTIVE SYSTEM. Morbid Anatomy.—The gall-bladder is found enlarged, sometimes reach. ing the size of a cocoa-nut. The walls are thickened, at some parts more than at others, and occasionally sacculations render its outlines uneven. The cystic wall is often tense, and now and then plates of calcareous matter are found upon it. On opening it there may be a discharge of gas from its interior, but more commonly a curdy white fluid fills its cavity. This fluid contains whitish flakes of albuminous matter resembling synovial fluid; it may contain bile, and then it is dark and viscid. On close examination the mucous surface resembles a serous membrane, and the muscular fibres of its wall are attenuated and wide apart. Later on, the fluid contents of the cavity may disappear, and only a mass of pultaceous matter remains. When the obstruction has been near the opening into the duodenum, the ductus communis and the cystic duct are dilated and their walls thick- ened. Etiology.—Hydrops cystidis felloe, as it is sometimes called, may be caused by a catarrhal, croupous, or diphtheritic inflammation of the cystic duct,, which obstructs the passage of bile into the intestine. Plugging of the common or cystic duct, or of the neck of the gall-bladder, by a calculus, may cause dropsy of the gall-bladder. Multilocular hydatids or hydatid cysts may plug the cystic duct and induce it. Pressure by tumors outside of the duct, as enlarged glands in chronic peritonitis, aneurisms, impacted feces, and cancerous growths of the adjacent parts, occasionally leads to it. Symptoms.—When the cystic duct alone is pressed upon or in some way plugged, there are few subjective symptoms. The patient may notice a bulging in the hepatic region, which steadily increases, and is accompanied by pain, nausea, vomiting, loss of appetite, and constipation. But the colon of the skin, urine, and feces exhibits no change. If a calculus is the cause of the obstruction, there is usually a history of "bilious colic," and if abdominal tumors press upon the cystic duct there will be the physical evidences of their existence. Physical Signs.—Inspection may reveal a globular tumor near the rectus muscle, at the free border of the ribs. Palpation discovers at the normal site of the gall-bladder a pear-shaped, extremely movable tumor, which is elastic and rarely fluctuating. When the ductus communis is obstructed, jaundice is a prominent symptom, and the other symptoms which have been described under "catarrh of the bile-ducts" are present. Occasionally the tumor suddenly disappears, the stools become dark, and the skin regains its normal color. This denotes that the obstruction, which is then com- monly a calculus, has been temporarily removed. When external openings are formed, or rupture into the peritoneal cavity occurs, there are, in the latter oase, evidences of a rapidly developed peritonitis, and, in the former, a remission of symptoms with a biliary fistula discharging externally. Differential Diagnosis.—Dropsy of the gall-bladder may be mistaken foi abscess, hydatids, and medullary cancer of the liver. In medullary cancer, there is, in nine-tenths of the cases, an hereditary predisposition or a his-' tory of cancer of the stomach or heart; while in dropsy of the gall-bladdel we get a history of previous biliary catarrh, or of the passage of gall-stonefl GALL-STONES. 423 In cancer, the constitutional symptoms and cachexia are marked, while persistent gastric symptoms, ascites and hemorrhages from mucous surfaces are absent in enlarged gall-bladder. Cancer growths are slow, and precede jaundice if it exists, while a gall-bladder enlarges rapidly, and follows jaun- dice. Palpation, in cancer, discovers a nodular, uneven, immovable mass be- low the free border of the ribs. An enlarged gall-bladder gives rise to a smooth, pear-shaped, elastic, or fluctuating tumor, which is movable and projects below the free border of the ribs in the direction of the gall-bladder. Prognosis.—This varies with the cause. When inflammatory products or gall-stones induce the dilatation, it is better than when it is due to external pressure ; it is always attended with more or less danger. Treatment.—The treatment, when it is the result of catarrhal inflamma- tion of the ducts, has already been considered. When it is due to the pres- ence of gall-stones, the treatment appropriate to such conditions is indica- ted. If the enlargement is very great and shows no indications of becoming stationary or diminishing in size, aspiration should be practised. GALL-STONES. When bile is retained in the gall-bladder for a long time it decomposes, and the cholate of soda and other bile salts, with cholesterin, globules of bile-resin, and granules are precipitated. These materials combine to form concretions, which are called biliary calculi. Catarrh of the gall-bladder always accompanies this retention and decomposition of bile. Morbid Anatomy.—The number of gall- stones varies : single calculi are rare ; eight thousand were found in one case. Their usual number is about thirty. Their size varies from that of a pin's head to that of a goose egg. In shape they are originally spherical, ovoid, or pear-shaped ; but when there are many and they lie in contact with one another for a long time, they have numerous facets developed on their surface; six, or even twelve are some- times found on a single calculus. Warty or "mulberry" calculi are occasionally met with ; solid or hollow casts of the larger bile ducts, and those which resemble rhomboidal crystals, and the star-like cal- culi with blunt points are rare forms of gall-stones. These calculi are commonly of a light-brown or greenish-yellow color ; thev mav be white o-rPPn blue red ov SMch of a gall-bladder filled with biliary iulv mdy oe wmte, gieeu, ume, leu, ui calculi This bladder contained 260 black. The specific qravitii of fresh calculi gall-stones. At b are single calculi r J v •' showing facets. is about 1.02, and it may reach 1 09, so that they will not float in water. In most cases a fresh biliary calculus can be Fig. 81. 424 DISEASES OF THE DIGESTIVE SYSTEM. crushed between the fingers. Gall-stones may form in the smallest radiclo of the hepatic duct. On section a biliary calculus will rarely be found homogeneous through- out. Its substance, if it breaks down like clay, consists of cholesterin and lime. If it has a saponaceous fracture, it consists of bile-resin and choles- terin. The ingredients of biliary calculi are cholesterin, the coloring matter of the bile, bile resin, lime salts, mucus, epithelium, biliary acids, margarin and traces of iron. A Fig. 82. Section of a large Gall-stone, showing successive layers. A. External crust.—B. Intermediate portion.—C. Nu- cleus. Natural size. gall-stone usually has a nucleus, an external crust, and an intermediate portion. The nucleus may be formed of crystals of cholesterin, cholate of lime, mucus, a distoma, blood-clot, round worm or foreign body. Most nuclei are formed of casts of the hepatic ducts. Some- times small calculi form the nu- clei of larger ones, and in very rare instances multiple nuclei are ob- served. The external crust varies in thickness at different points, and is distinguished from the interme- diate portion by its color; it is commonly composed of cholesterin, and its color is due to a mixture of cholesterin and biliary pigment; carbonate of lime gives a rough, whitish crtist. The intermediate structure usually consists of crystalline radia- tions of cholesterin, which substance forms about eighty per cent, of all gall-stones. In this radiation can be seen evi- dences of a lamellar deposit, and sometimes, when there is no radiation, the layers are concen- tric, like those of an onion. Again, light layers of cholesterin alternate with deeper ones of pig- ment ; gall-stones are rarely found to undergo a process of erosion or disintegration. The gall-bladder may be normal, or enlarged and sacculated, and is often adherent to the in- testine, abdominal wall, and adjacent organs. Its walls are thickened, and there are evidences of a crystals of cholesterin from gaB. local or general catarrh ; late in the disease there JgS; tS^ESTSK may be fibroid contraction and calcareous degen- x S00, eration in the cystic walls. Ulceration of the walls is frequently found in a bladder distended with calculi. When a gall-stone becomes impacted near the entrance of the ductus communis into the duodenum, the duct may become enormously dilated, and have its walls thickened, hyper- trophied, or calcareously degenerated. When the ulcerative process extends through the walls of the gall-blad- der or Of the larger ducts, we may have openings externally through the abdominal walls, usually about the umbilicus, called " biliary fistulae.'' Fig. 83. GALL-STONES. 425 These fistulous openings may lead from the gall-bladder or ductus com- munis to the duodenum, stomach, colon, right ureter, trunk of vena portse, pleura, or vagina. When calculi are found in the smaller ducts, they may excite abscess of the liver, local fatty degeneration, inflammation of the ducts or pylephlebitis. Either by rupture into the cavity, or by extension of inflammation, peritonitis may be caused by the presence of gall-stones. They may also excite ulceration and gangrene of the intestines, and there are rare cases where gall-stones, having escaped into the intestines, have caused death by intestinal obstruction. Etiology.—Gall-stones may be formed at any period of life, but are most frequent after thirty-five. A sedentary, physically inactive life is a great factor in their etiology, and I regard the greater prevalence of calculi in women than in men as due to their less active mode of life. Those who have to pass the greater part of their lives in bed, and prisoners who are confined in cells for a long time, are especially liable to the formation of gall-stones. A diet over-rich in fats, animal food, or alcoholic beverages, predisposes to the formation of biliary calculi. Cancerous growths in the liver and gall-bladder, catarrh of the gall-bladder, and in fact any morbid condition interfering with the excretion of bile and favoring its retention in the gall-bladder, predispose to the development of calculi. I have been able in a few cases to make out an hereditary predisposition to the forma- tion of gall-stones. The menstrual epoch seems to have some peculiar influence upon their formation. Symptoms.—Small gall-stones,—"gravel,"—in the hepatic ducts may cause hepatic congestion, but without enlargement of the liver, and give rise to dull pain, a sense of weight and constriction in the right hypochondrium, with nausea and the other symptoms of gastric disturbance. Jaundice in these cases is of rare occurrence. When the hepatic and larger ducts are occluded, the liver becomes enlarged, and there is jaundice, sharp pains, colic, and sometimes rigors and sweats. If the hepatic duct is closed, tlie gall-bladder is normal in size. Fatal rupture of the ductus hepaticus sometimes, though rarely, is the result of the impaction of a calculus in it. When small calculi are formed within the gall-bladder, they often cause no inconvenience ; when they reach a large size they excite inflammation, which may ultimately cause closure of the neck of the gall-bladder. When the gall-bladder contains a large number of calculi, violent physical exer- tion causes pain, which disappears during rest. Sometimes the patient may actually " feel something rolling around " in the vicinity of the gall-blad- der, which on a physical examination is found enlarged, more or less tender, hard, and nodulated, and by a stethoscope examination gives to the ear the impression of a number of pebbles being grated together in water. If biliary calculi in this situation cause perforation of the gall-bladder. a fatal peritonitis follows, or a biliary fistula may be formed between the gall-bladder and the stomach, which will be attended by sudden intense pain, with obstinate vomiting ; sometimes one or more calculi are found in the vomited matter. The vomiting of a gall-stone cannot be accounted tx 426 DISEASES OF THE DIGESTIVE SYSTEM. on the ground of reversed peristaltic action after the stone has passed the ductus communis into the duodenum. Again, when calculi are formed in the gall-bladder, a fistulous opening into the duodenum may occur, followed by vomiting and signs of a local peritonitis, or of intestinal hemorrhage and haematemesis. An opening from the bladder into the colon is exceed- ingly rare, for the colon is very movable. The symptoms which attend such a perforation are obscure. The gall-bladder may open into the pelvis of the right kidney, and then biliary concretions will be voided in the urine. There is an instance on record where, during pregnancy, a com- munication was made between the gall-bladder and the uterus, the discharge of the calculi taking place at the birth of the infant. If an opening from the gall-bladder into the vena porte occurs, symptoms of pyaemia will de- velop very rapidly. If perforation of the left pleural cavity occurs, fatal pleurisy will result. A single, rarely a double, fistulous canal may connect the gall-bladder with the external surface ; the opening is usually near the umbilicus, and may discharge for months. It may cicatrize, and form a mass of fibrous induration ; or abscesses may form when a large calculus plugs the fistula formed by previous perforation. If perforation occurs, recovery is most frequent when an external opening is established. When a gall-stone has by any means entered the intestinal canal, it may be voided per anum or it may lead to an intestinal obstruction, ulceration, or gangrene of the intestine. Obstruction in the common duct maybe temporary or permanent. If temporary there is no jaundice ; if the obstruction is complete and is continued for twenty-four hours, jaundice is added to the other symptoms ; this jaundice increases and is persistent When the obstruction is permanent. Biliary colic, or the passage of gall-stones, is the name applied to the pe- culiar and severely painful symptoms produced by the passage of one or more calculi along some one of the larger biliary ducts. Usually after a hearty meal, or after some jolting exercise, as horseback riding, the patient is suddenly seized with a severe pain in the epigastrium, which is increased by change of position or pressure. Sometimes slight rigors, nausea, eruc- tations, and attacks of yawning precede the colic. The pain is paroxysmal, and has its seat at a point where a line from the right nipple to the anterior superior spinous process of the left ilium crosses the free margin of the ribs. It radiates backward and upward, often as far back as the right shoulder, and may extend over both hypochondriac regions. It has been described by patients as boring, tearing, piercing, or lancinating. It is often so agonizing that patients will roll about the floor or bed, double themselves up, and groan with the pain. The face is pale and covered with cold sweat, and the pulse is very small. The abdominal muscles are rigid, and pressure greatly augments the pain. Vomiting, hiccough, a distended and tympanitic abdomen are often present during an attack, and a weak or feeble subject may faint, or pass into convulsions, which are epileptiform in character. Fatal syncope has occurred during an attack of gall-stone colic. After a few hours, sometimes a day, of exhausting and intense pain, the patient experiences sudden relief, and the pain entirely disappears; GALL-STONES. 427 often the pain remits, but does not cease until the calculus enters the du- odenum ; an exacerbation occurs at the moment the calculus enters the in- testinal canal. Jaundice is often present, but not until the attack has con- tinued for twenty-four hours. During the colic, the gall-bladder is very sensitive to pressure ; during and after the attack, the patient is very much exhausted, and shows great lassitude. When jaundice is present the faeces are clay-colored, and the bowels are apt to be constipated. After the at- tack, gall-stones may be found in the feces. It is to be remembered that fresh gall-stones are slightly heavier than water. The urine, if jaundice exists, contains bile-pigment and is mahogany in color; after the colic, it deposits urates. Differential Diagnosis.—Gall-stone colic may be mistaken for cardialgia, intestinal and renal colic. Cardialgia may be mistaken for biliary colic when there is no jaundice present. In cardialgia, pain comes on immedi- ately after eating; gall-stone colic has no necessary connection with taking food. In cardialgia, the symptoms are referred to the epigastrium alone, while in biliary colic the pain shoots to the right shoulder and back. In cardialgia, the pain gradually diminishes; in biliary colic it suddenly ceases. In gall-stone colic, the presence of a gall-stone in the feces is pathognomonic. In intestinal colic, the pain begins at the umbilicus, and radiates over the abdomen; in gall-stone colic it has its seat at the free border of the ribs, and shoots to the back and upward to the right shoulder. In in- testinal colic, pressure relieves the pain ; in gall-stone colic it aggravates it. In intestinal colic, the pain is intermittent; in gall-stone colic it is con- stant, though paroxysmal. In intestinal colic, jaundice is never present, while it may exist in biliary colic. Intestinal colic accompanies or is fol- lowed by diarrhoea ; in gall-stone colic, the faeces are firm and may be clay- colored. With renal colic, the pain shoots from the region of the affected kidney to the inner part of the thigh and end of the penis, and the testicle is retracted; in gall-stone colic, the direction of the pain is upward and back- ward. In renal colic there is a constant desire to micturate. There is no urinary disturbance in biliary colic. In renal colic, after the cessation of pain, pus, blood and epithelium are found in the urine; after gall-stone colic, bile-pigment is found in the urine. Jaundice and clay-colored stools frequently containing gall-stones may be present in biliary colic ; they are all absent in renal colic. The gall-bladder is very tender after biliary colic ; while there may be dull pains in the region of the loins after the passage of a renal calculus. Cancer of the head of the pancreas may readily be mistaken for gall-stones in the common duct. Prognosis. —The sudden and unexpected terminations and varied conse- quences due to the formation of a gall-stone, render it impossible to give any rule for the prognosis. A\rhen a large stone, without facets, has been voided, in any manner, from the bile passages, the prognosis is tetter than when small facetted calculi are found. Oft-repeated at- 428 DISEASES OF THE DIGESTIVE SYSTEM. tacks of biliary colic are bad. Catarrhal and exudative inflammations of the bile passages are frequent accompaniments of gall-stones ; and pul- monary gangrene, empyema, and pneumonia may sometimes complicate. Though it is not necessarily a fatal disease, death may result from peri- tonitis, ulceration, gangrene or obstruction of the intestines, pyemia, pylephlebitis, abscess of the liver, from exhaustion, or from the escape of bile through an external opening. Death may occur during an attack of colic, from unexplained causes. Treatment.—An attack of biliary colic demands that attention be given, first, to the pain : this is best relieved by morphine, which should be given hypodermically, but never in such amounts as would be toxic were the pa- tient free from pain. Inhalations of chloroform or ether may be employed to relieve the severity of the spasm. The application of two or three leeches over the gall-bladder is often followed by relief, and diminishes the chances of inflammation of the bile-ducts. Large draughts of warm water, con- taining bicarbonate of soda, often relieve the pain at the onset of the attack. At the same time put the patient in a tepid bath, or wrap warm cloths about the abdomen. In mild cases, and when opium is contra- indicated, belladonna will be sufficient, in connection with anodyne fomen- tations over the region of the gall-bladder. If the patient shows signs of collapse, stimulants, ammonia and brandy should be administered. A patient who has passed gall-stones must be put on a restricted diet; wines or fats should be prohibited ; exercise in the open air, and an entire change in the mode of life, are important. Mineral waters, whether by giving an alkaline bile or by an increase in the amount secreted, cause the number of gall-stones to diminish, and also allow them to be passed with less pain. A prolonged course of alkaline mineral water has been found the best remedy against the formation of gall-stones. Ether, turpentine, chloroform and hydrate of chloral have been proposed as specifics, it being thought that they have the power of dissolving the gall-stones. FUNCTIONAL DERANGEMENTS OF THE LIVER. The terms biliousness and torpid liver were more frequently used twenty years ago than now. Many, indeed, have denied that any such con- ditions exist, but there is undoubtedly a variety of symptoms (such as constipation, yellow and itching skin, dark urine, headache, lassitude, furred tongue, bitter taste in the mouth, etc.), which can properly be classed as dependent upon functional derangement of the liver. Writers describe ten varieties; I shall only briefly consider those which are the most common. In these functional hepatic derangements there are no morbid appearances in the organ itself to account for the symptoms. Etiology.—Functional derangement of the liver may be due to structu- ral diseases (e. g., cirrhosis, abscess, and acute yellow atrophy), to dyspep- sia, both gastric and intestinal, to atony of the bowels, to obstructive diseases of the heart and lungs, to the specific fevers, malaria especi- ally, to faulty diet, the food being too rich, to the daily use of alcoholic FUNCTIONAL DERANGEMENTS OF THE LIVER. 429 beverages, especially ales and sweet wines and liquors (not from whiskev brandy or gin, unless in the form of a hot toddy or sweet punch) to badlv ventilated, hot, and moist apartments, sedentary habits, a deficient supplv of oxygen, a warm climate (India, for instance), and finally to anxiety and prolonged mental labor. In many cases the tendency to " liver complaint" is inherited ; the children of the diabetic or gouty are very prone to func- tional derangements of the liver. Symptoms -Few cases are exactly alike. The prominent symptoms which usually first attract the patient's attention are anorexia, a bitter taste in the mouth (due to taurocholic acid in the blood) flatulency -acidity" and pyrosis.' The tongue is large, pale, and flabby,'with inden- tations of the teeth along its edges. It may be white, showing elongated papillae-like villi. The feces are pale, unless they have remained long in the large bowel, when they are blackish. Constipation and diarrhea may alternate. When bile is in excess the feces are semi-fluid and contain more bile than normal. It is a question whether melaena ever occurs as a sole result of hepatic derangement, but hemorrhoids are very common There is often a sense of weight, fulness, tightness, burning, or even actual pain over the liver. Those who suffer from functional derangement of the liver may become very fat, or they may emaciate rapidly. Emaciation results either from deficient production of bile or from derangement of the glyco- genic function of the liver. Bile may saturate the texture of the body for months, and yet no symptoms of blood poisoning occur so long as the eliminating function of the kidneys is not impaired. A deficient elimination of cholesterin may give rise to " biliousness " and thus be a part of functional derangement of the liver.8 " Cholester- aemia " is said to be associated with obstinate constipation, and Dr. Murchi- son regards this as "torpor of the liver," or at least one, and a frequent, form of it. Urates and pigments deposited in the urine should al- ways be regarded as signs of functional derangement of the liver arising from causes sometimes temporary and sometimes permanent. Murchison says "lithuria, like glycosuria, must be classed as a functional derangement of the liver," and he calls the antecedent morbid blood state lithcemia. In many, who by heredity are predisposed to "liver troubles," the liver is capable of performing its healthy functions only under the most favorable circumstances, and functional derangement is at once induced by articles of diet which most persons can easily digest. "Gouty dyspepsia," "latent gout," suppressed, anomalous or irregular gout, are terms which in many instances should be dismissed, and "func- tional derangement of the liver " substituted for them, for the symptoms which have been ascribed to them occur in those who neither inherit nor matIhreHllrCti°r0f Hh?]V "J6"""6' firsU ^"^''fication ; second, the re-combination of albuminous rZl a v ■, 1 °d a"d tlS8UeS ; mrd> the formatl°n °f "rea and lithic acid, both of which are 1,™ 'lm"lated bf the kidneys ? •«*»■«.the 8e"etion of bile, most of which is reabsorbed ; fifth, the E! ," /T5 the m°St con,ltant results 0{ functional hepatic derangement is imperfect K? h """S eV'denCJe