"WC^to ^tz> (Enlumbta Initi^rfitty in t\\s (Etty of Nrm lork ij&^tUvtntt ICtbrary Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/textbookofpracti01eich A TEXT-BOOK OF THE Practice of Medicine BY DR. HERMANN EJCHHORST Professor of Special Pathology and Therapeutics and Director of the Medical Clinic in the University of Zurich AUTHORIZED TRANSLATION FROM THE GERMAN EDITED BY AUGUSTUS A. ESHNER, M.D. Professor of Clinical Medicine in the Philadelphia Polyclinic ; Physician to the Philadelphia Hospital ; Assistant Physician to the Orthopedic Hospital and Infirmary for Nervous Diseases Mitb 84 irilustrations VOLUME I PHILADELPHIA AND LONDON W. B. SAUNDERS & COMPANY I90J GIFT Copyright, 1901, by W. B. SAUNDERS & COMPANY, Registered at Stationers' Hall, London, England. ELECTROTVPEO BY WESTCOTT & THOMSON, PHILADA. PRESS OF W. B. SAUNDERS Sc COMPANY. EDITOR'S NOTE. For those who read German no introduction to Eichhorst^s Practice of Medicine will be necessary ; and it is hoped that this translation may prove not less useful than the original, and as popular. The text will be found at once concise and compre- hensive, but additions and annotations have been made where it seemed they might be serviceable. The book differs somewhat from most other works on the practice of medicine in containing, among other things, appropriate sections devoted to a considera- tion of Diseases of the Skin, the Venereal Diseases, Impo- tence and Sterility in the Male, and Spermatorrhea. A number of illustrations have been added, in part replacing, in part sup- plementing, those in the original. The book has been written especially to meet the needs of tlie student, but it should prove useful also to the busy practitioner. For convenience of manipu- lation it has been^ deemed wise to present the work in two volumes. AUGUSTUS A. ESHNER. Philadelphia, March, 1901. PREFACE The impulse to write a short Text-book of Special Pathology and Therapeutics has not emanated from myself, but from my pupils. For a number of years the latter have repeatedly impor- tuned me, and all references to existing text-books written by me were in vain. Recently the demand has been made also from distant quarters, and I have therefore finally accepted it as a duty to respond to a request pressed with such persistence. The governing principle in the preparation of this work was to provide the student with a book that should afford him a ready and reliable source of information with regard to the principal, and especially to the most important, manifestations for the recog- nition of diseases. As the essential aim of the physician will ever be the cure of disease, earnest consideration has been given to the subject of treatment. Naturally, this text-book can deal only with the established facts of the practice of medicine. A certain degree of conciseness in expression and in description also was demanded, and especially in this connection considerable difficulty was encountered in the effort rigorously to separate the essential from the unessential. In how far I have been successful in this must be left to the decision of the reader. Those who are better acquainted with the manifestations of clinical medicine will find the necessary elaboration in my Hand- book of Special Pathology and Therapeutics.- I shall be gratified to know that the present volume will real- ize the expectations of those for whom primarily it was written. HERMANN EICHHOEST. 7 CONTENTS OF VOLUME I. PART I.— DISEASES OF THE CIRCULATORY ORGANS. PAGE I. Diseases of the Myocardium 17 "Weakness of the Myocardium 17 Dilatation of the Heart ' 24 Hypertrophy of the Heart 28 Fat Heart (Cor Adiposum) 29 Inflammation of the Heart-muscle 31 Tumors of the Myocardium 33 Echinococcus of the Heart 34 Dextrocardia 34 Cardiorhexis 34 II. Diseases of the Endocardium 35 Acquired Valvular Disease of the Heart 35 Congenital Heart-disease 45 Inflammation of the Endocardium 47 Ulcerative Endocarditis 47 Verrucose Endocarditis 49 Thromhosis of the Heart 51 III. Diseases of the Pericardium 52 Inflammation of the Pericardium 52 Pneumopericardium 58 Dropsy of the Pericardium 59 Hemopericardium 60 Chylopericardium 60 Tumors of the Pericardium 60 IV. Cardiac Neuroses 61 Paroxysmal Tachycardia 61 Paroxysmal Bradycardia 63 Cardiac Intermittency 63 Xervous Heart-pain 68 V. Diseases of the Aorta 65 Aneurysm of the Aorta . - 65 Constriction and Occlusion of the Isthmus of the Aorta 71 Embolism of the Aorta 72 PART II.— DISEASES OF THE RESPIRATORY ORGANS. I. Diseases of the Nose 73 ]Srasal Catarrh 73 Fibrinous Inflammation of the Xasal Mucous Membrane .... 77 Hay-fever 77 Mycosis Xasi 79 9 10 CONTENTS OF VOLUME I. PAGE 11. Diseases of the Larynx v . . . 79 Catarrh of the Larynx 79 Edema of the Glottis 85 Inflammation of the Perichondrium of the Larynx 87 Paralysis of the Muscles of the Larynx 89 Spasm of the Glottis 93 Phonatory Spasm of the Glottis 94 Sensory Disorders of the Laryngeal Mucous Membrane . . . . 95 Laryngeal Cough 95 Mycosis of the Larynx 96 III. Diseases of the Trachea 96 IV. Diseases of the Bronchi 96 Bronchial Catarrh 96 Fibrinous Bronchitis 103 Bronchial Dilatation 106 Bronchial Constriction Ill Bronchial Asthma 113 V. Diseases of the Lungs 117 Alveolar Emphysema of the Lungs 117 Interstitial Emphysema of the Lungs 120 Atelectasis of the Lungs 121 Hypostasis of the Lungs 122 Edema of the Lungs 123 Catarrhal Inflammation of the Lungs 125 Fibrinous Inflammation of the Lungs 128 Interstitial Pneumonia 139 Suppuration of the Lung . 142 Gangrene of the Lung . . . . • 144 New-growths of the Lung 149 Echinococcus of the Lung 151 Aneurysm of the Pulmonary Artery 152 VI. Diseases of the Pleura 152 Inflammation of the Pleura 152 Pneumothorax 162 Dropsy of the Pleura 169 Hemothorax 170 Chylothorax 170 Carcinoma of the Pleura 170 Echinococcus of the Pleura 171 VII. Diseases of the Mediastinum 171 Mediastinal Tumors 171 Inflammation of the Mediastinum 173 Interstitial Mediastinal Emphysema 174 PART III.— DISEASES OF THE DIGESTIVE ORGANS. I. Diseases of the Mouth 175 Catarrhal Stomatitis 175 Ulcerative Stomatitis 177 Aphthous Stomatitis 178 Thrush 179 Leukoplakia Oris 181 Ptyalism 182 II. Diseases of the Pharynx and the Soft Palate 184 Catarrh of the Pharynxand the Soft Palate 184 Mycosis Pharyngis Leptothricia 190 CONTENTS OF VOLUME I. 11 PAGE III. Diseases of the Esophagus 191 Carcinoma of the Esophagus 191 Diverticula of the Esophagus 197 Dilatation of the Esophagus 199 Catarrhal Esophagitis 200 Phlegmonous Esophagitis 201 Peptic Ulcer of the Esophagus 201 Spontaneous Rupture of the Esophagus 202 Softening of the Esophagus 202 Thrush of the Esophagus 203 Paralj'sis of the Esophagus 203 Spasm of the Esophagus 204 IV. Diseases of the Stomach 205 Preliminary^ Considerations 205 Acute Gastric Catarrh 210 Chronic Gastric Catarrh 212 Suppurative Inflammation of the Stomach 216 Round Ulcer of the Stomach 217 Carcinoma of the Stomach 222 Dilatation of the Stomach 227 Displacements of the Stomach 233 Gastric Neuroses 234 Motor Gastric Neuroses 234 Nervous Vomiting 234 Nervous Eructation 235 Nervous Regurgitation 235 Peristaltic Unrest of the Stomach 236 Hypermotility of the Stomach 236 Tonic Spasm of the Musculature of the Stomach . . . 236 InsufBciency or Incontinence of the Pylorus 237 Rumination 237 Atony of the Stomach 238 Sensory Neuroses of the Stomach 238 Nervous Gastralgia 238 Disorders of the Sense of Hunger and of Satiety .... 240 Secretory Neuroses of the Stomach 240 Hyperchlorhydria 240 Anachlorhydria and Hypochlorhydria 240 Hypersecretion of the Gastric Juice 241 Mixed Neuroses of the Stomach 241 Nervous Dyspepsia 241 V. Diseases of the Intestines 242 Acute Intestinal Catarrh 242 Acute Gastro-intestinal Catarrh in Infants 247 Chronic Intestinal Catarrh 252 Inflammation of the Cecum and the Vermiform Appendix and the Surrounding Tissues 257 Round Ulcer of the Duodenum 266 Carcinoma of the Intestine 267 Invagination or Intussusception of the Bowel 271 Stenosis and Obstruction of the Bowel 275 Hemorrhoids 284 Melena of the Newborn 288 Enteroptosis 288 Intestinal Neuroses 289 Motor Intestinal Neuroses 289 Atony of the Intestine 289 Nervous Diarrhea 290 Peristaltic Intestinal Unrest 290 12 CONTENTS OF VOLUME I. . PAGE Sensory Intestinal Xeuroses T . . . 290 Xervous Spasm of the Intestine 290 Nervous Enteralgia 291 Animal Parasites of the Intestine 292 Protozoa in the Intestine 292 "Worms in the Intestine 293 Flat Worms 293 Tapeworms 293 Sucking Worms 301 Eound Worms 301 Spool Worm ; 301 Seat-worm 303 Whip-worm . 30-i Trichina Spiralis 305 Ankylostomum Duodenale 311 Anguillula Intestinalis and Anguillula Stercoralis . . . 315 VI. Diseases of the Liver 315 Jaundice .......' 315 Hypostatic Liver 323 Inflammation of the Serous Coat of the Liver 325 Suppurative Hepatitis 327 Chronic Interstitial Hepatitis 331 Acute Yellow Atrophy of the Liver 338 Fatty or Adipose Liver 342 Amyloid Liver 343 Carcinoma of the Liver 345 Echinococcus of the Liver 350 Displacements of the Liver 355 Constricted or Fissured Liver 356 Diseases of the Biliary Passages 357 Catarrh of the Biliary Passages 357 Purulent Inflammation of the Biliary Passages 359 Dropsy of the Gall-bladder 360 Carcinoma of the Biliary Passages 361 Parasites in the Biliarv Passages 361 Gall-stones ' 362 Diseases of the Blood-vessels of the Liver 368 Thrombosis of the Portal Vein 368 Purulent Inflammation of the Portal Vein 370 Aneurysm of the Hepatic Artery 370 VII. Diseases of the Pancreas 371 VIII. Diseases of the Peritoneum 372 Inflammation of the Peritoneum 372 Abdominal Dropsy ' 382 Carcinoma of the Peritoneum 386 Echinococcus of the Peritoneum 386 PART IV.-DISEASES OF THE GENITO=URINARY ORGANS. I. Diseases of the Kidneys 387 Diagnostic Preliminary Considerations 387 Albuminuria 387 Hematuria 392 Uremia 396 Hypostatic Kidney • 401 DiflFuse Nephritis 402 Acute Diftuse Nephritis 402 Chronic Parenchymatous Nephritis 409 Chronic Interstitial Nephritis 411 CONTENTS OF VOLUME I. 13 PAGE Purulent Nephritis 416 Embolic Infarction of the Kidney 420 Amyloid Kidney 421 Carcinoma of the Kidney 423 Cystic Kidney 425 Echinococcus of the Kidney 427 Movable Kidney 428 Horseshoe Kidney 432 Absence of the Kidney 432 Inflammation of the Pararenal Connective Tissue 432 Aneurysm of the Kenal Artery 434 II. Diseases of the Pelvis of the Kidney and of the Ureter . . . 435 Dilatation of the Pelvis of the Kidney 435 Inflammation of the Pelvis of the Kidney 438 Kenal Calculi 441 Carcinoma of the Pelvis of the Kidney and the Ureter 447 Parasites of the Pelvis of the Kidney 448 III. Diseases of the Urinary Bladder 448 Inflammation of the Urinary Bladder 448 Carcinoma of the Urinary Bladder 455 Parasites of the Urinary Bladder 457 Foreign Bodies in the Urinary Bladder 457 Neuroses of the Urinary Bladder 458 Nocturnal Enuresis 458 Hyperesthesia of the Urinary Bladder 460 Spasm of the Urinary Bladder 460 Paralysis of the Urinary Bladder 461 IV. Diseases of the Male Sexual Organs 463 Impotence in the Male 463 Sterility in the Male 464 Involuntary Discharge of Seminal Fluid 465 True Spermatorrhea 466 Prostatorrhea .• 468 V. Diseases of the Adrenal Bodies 468 Addison's Disease 468 PART v.— DISEASES OF THE NERVOUS SYSTEM. I. Diseases of the Peripheral Nerves 472 Peripheral Paralysis 472 Preliminary Considerations 472 Motor Paralysis of the Trigeminal Nerve 476 Paralysis of the Facial Nerve 477 Paralysis of the Spinal Accessory Nerve 488 Paralysis of the Hypoglossal Nerve 489 Multiple or Combined Paralysis of Cerebral Nerves .... 490 Paralysis of the Phrenic Nerve 490 Paralysis of the Radial Nerve 492 Paralysis of the Median Nerve 495 Paralysis of the Ulnar Nerve 497 Paralysis of the Mu.«culocutaneous Nerve 498 Paralysis of the Axillary Nerve 498 Combined Parahsisof the Nervesof the Arm and the Brachial Plexus . '. 498 14 CONTENTS OF VOLUME I. PAGE Peripheral Paralysis of the Scapular Muscles ... .^ ... ' 500 Paralysis of the Serrate Muscle 500 Paralysis of the G-reater and Lesser Pectoral Muscles . . 503 Paralysis of the Ehomboid and the Elevator of the Angle of the Scapula 503 Paralysis of the Broad Dorsal Muscle 503 Paralysis of the Internal Rotators of the Arm 503 Paralysis of the External Eotators of the Arm . . . . 504 Peripheral Paralysis of the Muscles of the Back ....... 504 Peripheral Paralysis of the Abdominal Muscles ...... 504 Peripheral Paralysis of the Crural Xerve . . 505 Peripheral Paralysis of the Obturator !Nerve 505 Peripheral Paralysis of the Gluteal Xerves 506 Peripheral Paralysis of the Sciatic Xerve • . . 506 Periodic Paralysis 507 Spasmodic Disorders of Motor Xerves 507 Motor Trigeminal Spasm . 507 Spasm of the Muscles of the Face 508 Spinal Accessory Spasm 510 Hypoglossal Spasm . 510 Spasm of the Cervical and Scapular Muscles . ....... 511 Spasm of the Diaphragm .... 511 Spasm of the Abdominal Muscles 512 Muscular Spasm in the Upper and the Lower Extremities . . 513 Cramps 513 Neuralgia . 513 Preliminary Considerations 513 Trigeminal Neuralgia 516 Cervico-occipital Neuralgia 519 Phrenic Neuralgia ' 520 Cervicobrachial Neuralgia 520 Dorso-intercostal Neuralgia 520 Lumbo-abdominal Neuralgia 521 Crural Neuralgia 521 Obturator Neuralgia 522 Neuralgia of the External Cutaneous Nerves of the Thigh . . 522 Sciatic Neuralgia 522 Spermatic Neuralgia 524 Coccygodynia 524 Articular Neuralgia .,.,.,,, 525 Anesthesia 525 Trigeminal Anesthesia ... 528 Peripheral Disease of the Nerves of Special Sense 529 Disease of the Olfactory Nerve . 529 Disease of the Gustatory Nerve 530 Inflammatory and Degenerative Disorders of the Peripheral N erves . 531 Preliminary Considerations 531 Multiple Neuritis . . .' . 534 Toxic Neuritis 536 Saturnine Paralysis 536 Arsenical Paralysis 538 ' Alcoholic Paralysis 539 II. Diseases of the Spinal Cord 540 Preliminary Diagnostic Considerations . . 540 Atypical or Asystematic Diseases of the Spinal Cord 547 Anemia of the Spinal Cord - 547 Hyperemia of the Spinal Cord 548 Hemorrhage into the Spinal Cord 548 Acute Inflammation of the Spinal Cord 552 Chronic Inflammation of the Spinal Cord 558 CONTENTS OF VOLUME I. 15 PAGE Multiple Cerebrospinal Sclerosis 500 Tumors of the Spinal Cord 5fi4 Cavities in the Spinal Curd 564 Spinal Compression-paralysis 5f>7 Unilateral Lesions of the Spinal Cord 571 System-diseases of the Spinal Cord 572 Single System-diseases 572 Tabes Dorsalis 572 Spastic Spinal Paralysis 581 Diseases of the Ganglion-cells of the Anterior Horns .... 582 Acute Spinal Paralysis of Childhood 583 Acute, Subacute, and Chronic Inflammation of the Gan- glion-cells of the Anterior Horns in Adults 586 Spinal Progressive Muscular Atrophy 588 Combined System-diseases of the Spinal Cord 592 Hereditary Ataxia 592 Amyotrophic Lateral Sclerosis 593 Functional Disorders of the Spinal Cord or Xeuroses of the Spinal Cord 599 Acute Ascending Spinal Paralvsis 599 Reflex Paralysis ' 600 Psychic Paralysis 601 Diseases of the Spinal Meninges 601 Inflammation of the Spinal Dura Mater 601 External Spinal Pachymeningitis 601 Internal Spinal Pachymeningitis 602 Inflammation of the Soft Membranes of the Spinal Cord .... 603 Acute Inflammation of the Soft Membranes of the Spinal Cord 603 Chronic Inflammation of tbe Soft Membranes of the Spinal Cord 606 Hemorrhage into the Spinal Membranes 607 Neoplasms of the Spinal Meninges 609 Index to Volume 1 613 CONTENTS OF VOLUME II. Part V.— DISEASES OF THE NERVOUS SYSTEM ( ConimMec/). Part VI.— DISEASES OF THE MUSCLES. Part VIL— DISEASES OF THE SKIK Part VIIL— DISEASES OF THE SPEEN AND THE BLOOD. Part IX.— DISORDERS OF METABOLISM. Part X.— INFECTIOUS DISEASES. PART I. DISEASES OF THE CIRCULATORY ORGANS. I. DISEASES OF THE MYOCARDIUM. The termination in cases of heart-disease of all kinds depends in the majority upon the functional capability of the myocardium, and death occurs in most cases amid manifestations of overwhelm- ing weakness of the heart-muscle. Easy as it is to diagnose con- ditions of weakness or insufficiency of the myocardium, it is equally impossible, as a rule, to recognize during life the anatomic alterations that have taken place in the heart-muscle itself in every individual case. The anatomic diagnosis of disease of the myocardium will not reach beyond a certain degree of probability even under favor- able conditions ; and unfortunately often this degree is not obtained even by experienced, observant, and careful diagnosticians. The diagnostic scope of diseases of the myocardium is thus most circumscribed, and virtually includes only three conditions : First, that of weakness or insufficiency of the myocardium, already mentioned; second, enlargement or dilatation of the heart; and third, increase in volume, or hypertrophy, of the myocardium. WEAKNESS OF THE MYOCARDIUM (CARDIAC INSUFFICIENCY). Symptoms and Diagnosis. — The symptoms of enfeeble- ment of the myocardium are partly local, partly general, or in many instances of mixed character. The local, or strictly cardiac, manifestations usually attend the onset. The action of the heart is generally accelerated inordinately, and at the same time it is usually irregular. While at first these disturbances perhaps ovAy follow physical and mental exertion, large meals, or the use of stimulants, later they appear also during complete rest and a careful mode of life, lose their paroxysmal char- acter, and remain permanent. The patient often complains of a sense of distressing palpitation of the heart, at times also of a feel- 2 17 18 CIRCULATORY ORGANS ing of tension and pressure, less eonimonly of" a painful sensation in the region of the heart, suffers from shortness of breath, and speaks interrujitedly and at short intervals — staccato speech. The apcx-bcat of the heart appears feel)le or is not palpable. The .sounds of the lieart are faint, and often the first (systolic) sound is suggestive of a murmur. Not rarely f/a// op-rhythm is present, the systolic sound of the heart being preceded by a beat, the accentuation, however, falling upon the first sound itself. As a rule, increase in the area of cardiac percnssion-dulneHS to the right iuid left, in consequence of dilatation of the heart, is demonstrable. The disturbances of cardiac action can l)e admiral )ly studied in the radial pulse. This attains unusually great frequency, ex- hibits very unequal waves, and is irregular and frequently also intermittent, in consequence of which some pulse-beats become inappreciable, because the foi^ce of the heart is not sufficient to send a palpable wave of blood into the radial artery with every con- traction of the heart-muscle. As can be understood, the features of a frequent, irregular, unequal, and intermittent pulse will appear also in the sphygmographic tracing (Fig. 1). Fig. 1.— Sphyjnnographic tracing of a frequent, irregular, unequal, and intermittent ptulse attending" cardiac weakness In consequence of a valvular lesion (personal observa- tion, Zurich clinic). Only rarely are the consequences of weakness of the heart- muscle confined to the local or cardiac alterations described, and, as a rule, general disturbances or manifestations of stasis appear at the same time or more frequently somewhat later. If the functional activity of the right ventricle is impaired to such a degree that it is no longer capable of sending all of its blood into the pulmonary artery M'ith each systole, and a certain amount of blood will thus remain in the ventricle after each sys- tole, the flow of blood from the right auricle will first be inter- fered with, and at the same time also that from the superior and inferior vense cava? to the heart, and the condition of general venous stasis becomes estal)lished. This will be appreciable earlier and in greater degree in the territory drained by the inferior vena cava, as here the blood must be propelled against the force of gravity. H with weakness of the heart-muscle the left ventricle is espe- cially involved, tlie ultimate result is nevertheless the same as that described. At first blood-sta.-is occurs only in the left ventricle and in the left auricle, but from these it extends to the pulmonary WEAKNESS OF THE .MYOCARDIUM 19 veins, the pulmonary capillaries, the pulmonary arteries, and from these in turn to the right ventricle, the right auricle, and the vense cavse, so that the consequences of conditions of enfeeblement of the right and of the left heart are the same. Among the earliest indications of general venous stasis is edema of the skin. At first this appears on the inner aspect of the thigh and aboxit the ankles. At this time, also, it frequently recedes during the night, thus in the horizontal position of the body. Later, however, the cutaneous edema becomes persistent, increas- ing in extent, and advancing with progressive stasis to the geni- talia, to the posterior, lateral, and inferior portions of the anterior aspect of the abdominal wall, to the posterior and lateral aspect of the chest, to the arms, and even to the face. In patients accus- tomed to lie especially on one side of the body, the edema of the skin is also more marked upon that side. If edema of the skin has existed for a long time or if it recur persist- ently, a thickening of the cutis takes place, especially in the legs, and elephantiasis of greater or less degree develops. In addition to edema, general venous stasis gives rise to cyano- sis of the shin and mucous membranes. This is due to the fact that with retardation of the blood-current the blood gives off an un- usually large amount of oxygen to the tissues, and at the same time becomes overladen with carbon dioxid from them. Lips, cheeks, tip of the nose, ears, elbows, dorsa of the hands, knees, and dorsa of the feet are the parts in which cyanosis of the skin appears earliest and most distinctly, for in these places the skin is thin and at the same time rich in blood-vessels. On the cheeks and the nose dilatation of cutaneous veins frequently takes place, to which ultimately chronic inflammatory hyperplasia of the skin may gradually be superadded, so-called acne rosacea. On palpation reduction of the temperature of the skin, is generally apparent, and this may be explained by the fact that with retar- dation of the blood-current unusually active cooling of the blood can take place. Obstruction to the flow of blood from the renal veins into the inferior vena cava gives rise to manifestations of hypostatic (cyanotic) kidney and the urine of stasis. The urine is voided in diminished amount (less than 1500 c.c), and is characterized by its dark-red (high, saturated) color and high specific gravity (above 1017); it exhibits an acid reaction, frequently contains small amounts of albumin and hyaline tube-casts, and often on cooling- deposits a red, brick-dust-like (lateritious) sediment, which consists principally of acid urates, and mainly of acid sodium urate. On microscopic examination this appears in the form of irregularly distributed granules. Increase and diminution in venous stasis are accurately reflected in the state of the urine. 20 CIRCULATORY ORGANS Naturally stasis of the blood in the inferior vena cava will also interfere with the discharge of blood from the hepatic veins, and will consequently give rise to the Jn/pos(atlc (cj/anofic) liver. Under such conditions the liver increases in size, so that its lower border may reach to the level of the umbilicus or still lower. The organ is sensitive on palpation and unusually hard. The patients also eoniplain frequently of a sense of tension or pressure, or even of pain, as well as of constriction in the region of the liver. Xot rarely hypostatic catarrh of the biliary passages develops, with the appearance of jaundice (icterus), which is frequently confined to the ocular conjunctivae, but at times involves also the general cuta- neous integument. If cyanosis be present in addition to icterus, the skin frequently acquires a slight greenish tint, icterus viridis. Venous stasis generally extends from the area of the hepatic veins to that of the portal ' vein, and accordingly symptoms of stasis referable to the stomach, the intestine, the spleen, and the pentoneum will appear. Stomach and bowel become the seat of hypostatic catarrh, characterized by loss of appetite, eructation, vomiting, flatulent distention in the epigastrium, and irregularity in evacuation of the bowels. Dilatation of the hemorrhoidal veins also not rarely takes place, and hemorrhoids form. The spleen becomes increased in size, and in still greater degree in consistency, and very considerable amounts of transudate often collect in the abdominal cavity (ascites). The thoracic viscera, also, l^ecome involved in the manifesta- tions of stasis. The patients often suiFer from obstinate hypostatic catarrh of the bronchi. Xot rarely expectoration of blood (hemopty- sis) takes place, in consequence at times of rupture, at other times of embolic occlusion, of blood-vessels. On microscopic examina- tion of the sputum cells diffusely stained with hemoglobin, or containing hemoglobin in the form of granules, needles, and even plates or tables, are frequently found. These are improperly designated heart-failure cells, although they occur also in associa- tion with other diseases, for instance fibrinous pneumonia, and they are believed to be in part alveolar epithelium and in part round cells. The pleural cavities l)ecome filled with transudate (hydrothorax). Similar changes take place in the pericardium, and hyd roper icardiuni is frequently observed. Evidences of venous stasis are found also in the distribution of the jugular veins. These veins themselves are conspicuous on either side of the neck by reason of their unusual fulness and dilatation. The patients suffer from hypostatic catarrh of the pharync/eal and nasal mucous membrane, and at times from fre- quent epistaxis. Some complain of tinnitus aurium and impair- ment of hearing. At times the eyes protrude markedly, and in consequence of over-distention of the retrobulbar veins slight exophthalmos becomes appreciable. The blood-vessels of the WEAKNESS OF THE MYOCARDIUM 21 conjunctiva appear dilated and tortuous, and often excessive lac- rimal secretion accumulates in the conjunctival sacs. Many patients complain of vertigo, introspectiveness, cerebral . pressure, disturbed sleep, and the like, which are related to venous hyperemia of the brain. The duration and the course of weakness of the heart-muscle depend in every instance upon the operative causes. If these can be quickly removed, the manifestations of myocardial weakness likewise frequently recede within a short time. Naturally the condition must not have progressed too far, for then the danger will be great that to heart-weakness will be added paralysis of the heart Frequently the causes can only be temporarily removed or diminished, and accordingly the signs of myocardial weakness recur again and again. Many patients die in consequence of excessive hi/postatic jjhenoviena, for when accumulations of con- siderable amounts of transudate have taken place in the peritoneal, pleural, and pericardial cavities there is danger that heart and lungs will be impeded in their movement to so high a degree that the maintenance of life is impossible. Only rarely does death take place in consequence of unrestvainable pidmonary hemorrhage. Excessive edema of the skin also is attended with danger to life, as the skin may rupture at various points, and thus permit of the escape of edematous fluid. Infection with bacteria from the air may then readily take place, and give rise to an erythematous or erysipelatous inflammation of the skin, and general septicemia may lead to a fatal termination. In some cases intercurrent accidents take place, and pneumonia especially not seldom occurs. Chronic states of heart-weakness are among the most distress- ing conditions, and they may compel the patient to remain in bed for a long time and may engender a large number of complaints. Ktiologfy. — Weakness of the myocardium develops most fre- quently when unusually large demands are made upon the functional activity of the heart-muscle, and with which the heart cannot per- manently comply. Among such causative conditions are valvular lesions of the heart, chronic diseases of the respiratory organs, constrictions and dilatations (aneurysms) of the aorta or the pul- monary artery, arteriosclerosis, and chronic diseases of the kidney. Bodily over-exertion, for which of late excessive athletic exer- cises (mountain-climbing, bicycling, rowing) especially atford abundant opportunity, and the ingestion of excessive amounts of fluids (immoderate use of beer) may also give rise to insufficiency of the heart-muscle. Diseases of the myocardium itself (myocarditis, fat heart, tumors, echinococci) also may readily be associated with weakness of the heart-muscle, because, in the development of these condi- tions, muscular structure of the heart, therefore functionally capable tissue, is destroyed. At times the myocardium is involved through 22 CIRCULATORY ORGANS extension of disease from adjacent structures, as, for instance, pericarditis, obliteration of the pericardium, and endocarditis. Among the toxic varieties of myocardial weakness may be in- chided those that arise after excessive use of alcohol, coffee, tobacco, and tea. In this group })erhaps may be included also some infectious diseases, in which the toxins impair the integrity of the myocardium. At times general loss of bodily fluid gives rise to Meakncss of the myocardium, as, for instance, in pulmonary tuberculosis, carci- noma, chronic diarrhea, and suppuration. Occasionally weakness of the myocardium is dependent upon alterations in the blood, and it occurs in connection with chlorosis, leukemia, pseudoleukemia, pernicious anemia, or after the loss of considerable amounts of blood. From the nature of the. causative factors, weakness of the myocardium occurs but seldom in childhood. Conversely, a natural predisposition is present in advanced life — senile iceahiess of the myoc(nrUiim. Anatomic Alterations. — Weakness of the heart-muscle may cause death without any change in the myocardium whatever being discoverable, macroscopically or microscopically, at autopsy. In the majority of cases, it is true, the myocardium is marked at least by great flaccidity and dilatation, and often still other alterations in it will be found, such as have been suggested in the discussion of the etiology. The anatomic appearances of the hypostatic alterations are read- ily recognizable. The edema of the skin remains demonstrable also in the cadaver. From the serous cavities (pleura, pericardium, peritoneum) large amounts of clear greenish-yellow transudate may often be evacuated. The cavities of the heart, especially the right ventricle and auricle, are greatly distended with blood and blood- clots, and on incision of the ven^e cavfe such an abundance of blood escapes as to suggest the possibility of an increase in the amount having taken place. The lungs in long-standing cases present a brownish-red color, which, as microscopic examination proves, is caused by an abundant accumulation of blood-pigment. The lungs appear also remarkably dense, in consequence of increase in the interalveolar connective tissue, and the condition is therefore spoken of as brown induration of the htncjs. The mucous membrane of the bronchi is conspicuous for its marked redness and swelling, and is covered with secretion. The spleen is usually enlarged in but slight degree, but by reason of an increase in its connective tissue it generally feels remarkably firm. The Mclneys are in- creased in size, and usually present a bluish-red, almost blackish- red, color, which stands out sharply upon section, especially in the medullary portion. The condition is designated cyanosis of the kidneys, or, when the connective tissue has undergone hyperplasia WEAKNESS OF THE MYOCARDIUM 23 after long-continued stasis and the kidneys have acquired a firmer texture, ci/anotic induration of the kidneys. The liver also has in- creased in size and it contains an excessive amount of blood. On section, in consequence of marked dilatation and distention of the central veins with blood, a peculiar appearance is noted, suggest- ing the form of an oak-leaf or a nutmeg, whence the name cyanotic nutmeg-liver. If hyperplasia and contraction of connective tissue take place, the liver becomes harder and nodular upon its surface, and the condition is then described as cyanotic induration of the liver. The serosa of the stomach and intestine is often marked by unusually active distention of the finer venous blood-vessels, and upon the mucous membrane swelling, brownish-red discoloration, and active secretion of mucus are striking. The 'pancreas also exhibits venous distention, and frequently also unusual density in consequence of connective-tissue hyperplasia. Marked swelling and venous hyperemia of the mucous membrane are usually pres- ent in the urinary passages. The sinuses of the dura mater are, as a rule, distended with blood. The cerebrosjnnal fluid is incre'dsed, and upon the surface of tlie l^rain and in the cortex the marked distention of the veins is striking. Xot rarely edema of the brain and slight dilatation of the cerebral ventricles have developed. Prognosis. — The prognosis in a case of weakness of the myocardium depends upon the causes and the severity of the dis- order. Recovery can naturally be looked for only when the causes are removable; but even then death may occur wlien the degree of weakness of the cardiac muscle is so great that the heart is no longer capable of recuperating. Treatment. — In all conditions of weakness of the myocar- dium the first indication is the removal of the cause — causal treat- ment. In addition the following symptomatic treatment should be followed : The patients should permanently occupy as nearly a horizontal position in bed as possible, and confine themselves prin- cipally to a milk-diet. Frequently all of the symptoms will dis- appear after the institution of these measures alone. If marked palpitation of the heart be present, an ice-bag should be placed continuously over the heart, and finally resort is had to cardiac tonics or stimulants. Among heart-tonics digitalis-leaves alone are worthy of confidence, while their substitutes (tincture of stro- phanthus, caifein and sodium benzoate, caifein and sodium salicy- late, adonis vernalis, convallaria raajalis, spartein sulphate, and others) are quite unreliable agents. We prescribe digitalis-leaves principally in the form of powder, and, if diuresis be deficient, in combination with diuretin (theobromin and sodium salicylate) : R Powdered digitalis-leaves, 0.1 (1^ grains) ; Diuretin, 1.0 (15 " ).— M. Make 10 such starch-capsules. Dose : 1 every two hours. 24 CIRCULATORY ORGANS In the use of all preparations of digitalis certain precautionary meas- ures should be ol)served. At times (oxlc manifestations (vomiting, slowness of pulse, irregularity of pulse, diplopia, delirium) apj)ear, which necessitate the withholding of the remedy. The cumulative action of digitalis must also be b(jrne in mind. Some persons bear digitalis badly, and under such con- ditions enemata of infusion of digitalis have been employed. After too pro- tracted use of digitalis the heart becomes accustomed to the remedy, and the activity of the drug is lessened. Patients taking digitalis should remain under the constant observation of the physician, in order that the remedy may be withdrawn at the proper time. Stimulants may be prescribed with advantage when transient conditions of myocardial weakness are present, or when the myo- cardium has undergone such a degree of degeneration that digitalis is incapable of exerting its effect. A maintained influence is not to be expected under the latter conditions. Among agents of this class employed are especially camphor internally, or camphorated oil externally, ether, valerian-root, and ethereal tincture of valerian. At times it is necessary to treat specially certain threatening symptoms ; for instance, excessive cutaneous edema. Diaphoresis by means of pilocarpin hydrochlorate or sweat-chambers is usually not well borne, so that multiple incisions of the skin or puncture by means of Southey cannulas are preferably to be recommended. DILATATION OF THE HEART, Ktiology. — Dilatation of the heart may involve the right or the left side, or the entire organ. At times it is acute, at other times chronic in nature. The conditions favoring dilatation of the heart are always pro- vided when the /Tswtance of the myocardium is diminished or when the blood-pressure is increased in excessive degree. Under the con- ditions first mentioned simple dilatation takes place, whereas under the second to the dilatation hypertrophy of the heart-muscle is, as a rule, superadded (so-called eccentric cardiac hypertrophy). Diminished resistance of the heart-muscle and cardiac dilatation are observed in association with infectious diseases, loss of blood and of bodili/ fluids^ chlorosis, pernicious anemia, leukemia, pseudo- leukemia, and allied conditions. Frequently it involves only the right ventricle, which by reason of the greater thinness of its muscular wall appears of itself the more predisposed to dilatation. At times dilatation of the heart follows poisoning with mineral acids, alkalies, phosphorus, and arsenic. Diseases of the myocar- dium itself (cicatrices, fat heart) also give rise to dilatation of the heart. In some instances congenital deficiency of resistance on the part of the myocardium ajipears to bo h(Mvditarv. Dilatation (and hypertrophy) of the left ventricle in consequence of increased blood-pressure is observed especially in association with insufficiency of the aortic valve, stenosis of the aortic orifice, DILATATION OF THE HEART 25 insufficiency of the mitral valve, aneurysm of the aorta, constric- tion of the aorta, arteriosclerosis, and contracted kidney. Dilata- tion (and hypertrophy) of the right ventricle develops in association with insufficiency of the mitral valve, mitral stenosis, insufficiency of the pulmonary valve, stenosis of the pulmonary orifice, insuffi- ciency of the tricuspid valve, aneurysm and constriction of the pulmonary artery, pulmonary emphysema, chronic bronchial catarrh, chronic pleurisy, kyphoscoliosis, and the like. At times to dilatation of the one ventricle is gradually superadded a similar state of the other. The same condition arises especially in con- FiG. 2.— Increased area of cardiac dulness with dilatation of the right ventricle (mitral stenosis) ; from a photograph (personal observation, Zurich clinic). junction with valvular disease of the heart when derangement of compensation occurs. Acute dilatation of the heart in consequence of increased blood- pressure is at times induced by bodily over-exertion ; for instance, in military service, mountain-climbing, and excessive athletics. Dilatation of the heart is most frequently encountered in men and at advanced age, which is readily comprehensible from a con- bideration of the etiology. Symptoms and Diagnosis. — Dilatation of the heart may be readily recognized from tlie change in the area of cardiac dulness. With dilatation of the ridit ventricle the rioht border of the 2G CIRCULA TOR Y OIKiA XS (relatively) largo area of cardiac percussion-dulness extends beyond the right sternal margin to the right (Fig. 2), while with dilatation of the left ventricle the left border of the heart extends beyond the left niainniillary line to the left, in consequence of which the area of percussion-dulness at the same time acquires an oval outline (Fig. 3). In the presence of dilatation of the left ventricle the apex-beat of the heart attains unusual extent, being situated outside the left mammillary line and usually also lower than the fifth intercostal space on the left. When both ventricles participate in the dilatation the area of cardiac dulness exceeds its Fig. 3.— Increased area of cardiac dulness with dilatation of the left ventricle (insuflB- ciency of the aortic valve) ; from a photograph (personal observation, Zurich clinic). natural limits both to the left and to the right, and its outline becomes rather rectangular (Fig. 4). If in addition to dilatation of the heart hypertrophy also exists, this, if left-sided, will be attended with a heaving: apex-beat, accentuation of the aortic second sound, and a hard radial pulse; while if right-sided, there will be accentuation of the pulmonary second sound, and frequently also unusually active systolic vibration over the sternum. Individuals with dilatation of the heart may be entirely free from discomfort. This is especially so in cases in which, in addition to the dilatation, hypertrophy of the heart-muscle also exists, because both conditions tend to neutralize any possible DILATATION OF THE HEART 27 increase in blood-pressure. If this do not occur, then the clinical picture of cardiac insufficiency makes its appearance, with all of its sequels and dangers, and this takes place the more readily when only dilatation of the heart without hypertrophy is present. Anatomic Alterations. — Dilated chambers of the heart are conspicuous for their unusual size. If the left ventricle is con- siderably dilated, the right at times forms only a sort of small appendage. With dilatation of both ventricles the heart often attains such considerable proportions that it has been designated Fig. 4.— Increased area of cardiac dulness with dilatation of both sides of the heart (insufficiency of the mitral valves) ; from a photograph (personal observation, Zurich clinic). an ox-heart, hucardia (cor bovinum, enormitas cordis). In a healthy person the size of the heart should not exceed that of the closed fist. Changes in the shape of the heart also take place in consequence of dilatation, and if the left ventricle be involved this assumes an oval shape, and if the right ventricle this assumes a rectangular shape ; if both sides are involved, the appearance of the heart has been compared with a hunting-bag. Prognosis. — The prognosis in case of dilatation of the heart depends upon the fact whether conditions of cardiac weakness exist whose removal is possible. 28 CIRCULATORY ORGANS Treatment. — Treatment of dilatation of the heart is indi- cated only when manifestations of myocardial weakness appear, and is then to be conducted npon the lines laid down npon pages 23 and 24. HYPERTROPHY OF THE HEART. Anatomic Alterations. — Hypertrojihy of the heart may, in the same way as dilatation, involve individual portions or the entire heart. As a rule, it is combined with dilatation of the heart — eccentric hypertrophy of the heart. Concerning liypertrophy of the heart without alteration in the size of its cavities {simple hijperfrophy of tlie heart), and even concerning such hyper- trophy with diminution in size of the cavities [concentric hypertrophu of the heart), little of a certain nature is known. In many such instances the con- dition is probably one of contraction of an unaltered heart-muscle with the occurrence of death. The hypertrophied segments of the heart-muscle are conspicuous for the greater thickness of the wall, and usually also for their greater firmness. At the same time the weight of the heart (in a healthy individual 300 grams) increases. Further, not only the walls of the heart, but also the papillary muscles, frequently take part in the hypertrophy, the latter becoming converted into thick, plump columns. HistoIogicaUy it can be shown that the hypertrophy of the heart-muscle is brought about partly through increase in the muscle-fibers (hyperplasia) and partly through increase in the size of individual muscle-fibers (pure hypertrophy). The intermuscular connective tissue may also be increased in amount. Htiology. — Only increase in blood-pressure is with certainty known as a cause for hypertrophy (and dilatation) of the heart, and accordinglv as this involves the aortic system or the distribution of the pulmonary artery, or both, will the left or the right ventricle or the entire heart be involved in the hypertrophy. In detail all of those conditions must be taken into consideration that have been mentioned on pages 24 and 25 as causes for dilatation of the heart. Primary, idiopathic, or essential hypertropJiy of the heart has also been variously spoken of. The designation is inappropriate, and should l)e re])laccd by fvnrtionaJ JiypertropjJiy of the heart- muscle, for idiopathic hypertrophy of the heart occurs in persons who, it is true, exhibit no anatomic alterations in their circulatory organs, but who have been compelled to perform unusually severe bodily work, or have made unusually large demands upon the heart-muscle through the ingestion of excessive amounts of fluid (Munich beor-heart). Such functional hypertrojihy of the heart occurs especially in blacksmiths, locksmiths, seamen, wine-growers, mountain-climbers, and soldiers. Whether long-contimted palpitation of the heart and excessive eatinf/ gWe rise to hypertrophy appears not to have been demonstrated with certainty. FAT HEART 29 With regard also to toxic forms of cardiac hypertrophy, resulting from exces- sive use of coffee, tea, alcohol, tobacco, little that is reliable is known. Symptoms and Diagnosis. — Hypertrophy of the left ven- tricle may be recognized by the heaving apex-beat, the accentuation of the aortic second sound, and the hard radial pulse, conditions that are readily explained by the increased functional activity of the left ventricle. If the thorax be sufficiently yielding, an unusually marked prominence appears in the cardiac region, so-called pre- cordial bulging (voussure) takes place. Hypertrophy of the right ventricle is attended with accentuation of the pulmonary second sound (valvular), for the greater the force with which during the systole the blood is driven by the hyper- trophied ventricle into the pulmonary artery, the greater will be the violence with which it rebounds against the pulmonary valve and causes this to unfold with the succeeding diastole. Less regu- larly there is unusually active vibration of the sternum, beneath which the right ventricle lies. Hypertrophy of the heart is a desirable outcome in the pres- ence of circulatory disturbances, and through its agency existing obstacles can be overcome. There is great danger when the hypertrophied heart fails in strength, for then there develops the clinical picture of myocardial weakness, which has already been described. In the presence o£ idiopathic, or functional, hypertrophy also there is danger of cardiac weakness ; and it is pathetic to wit- ness the misery of a robust, well-developed man, with an immense heart, suffering from and eventually succumbing to the symptoms of cardiac weakness. Prognosis. — The prognosis in cases of hypertrophy of the heart depends upon the functional capahility of the heart-muscle. Every hypertrophied heart has a tendency to undergo connective- tissue and fatty degeneration, and to lead up to increasing and incurable cardiac weakness. At times such conditions occur as transient manifestations when extraordinary demands are made upon the myocardium in consequence of physical or mental excite- ment, alcoholic and venereal excesses, and the like. Under these conditions the prognosis is more favorable, providing the over- exertion of the heart has not exceeded a certain degree. Treatment. — Treatment for hypertrophy of the heart is only indicated when signs of cardiac weakness appear, and is then car- ried out in the manner indicated upon pages 23 and 24. FAT HEART (COR ADIPOSUM). Anatomic Alterations. — By fat heart in the clinical sense is understood a morbid increase in the fatty tissue that is present also in a slight degree beneath the epicardium of a normal heart. 30 CIRCULATORY ORGANS This tissue may in the presence of fat heart increase until it forms a fatty capsule more than one centimeter thick, whicli comjiletely envelops the heart-muscle. Often the fatty tissue has penetrated into the actual muscular substance, in which by pressure it has in places induced atrophy. The heart is conspicuous usually for its great fllaccidity, and as a rule it is increased in size. Ktiology. — Fat heart occurs most frequently as a manifesta- tion of plethora or of over-eating in obese individuals, and also in those who, as a rule, eat innucderately and drink alcohol freely, and take little physical exercise and perform little \sork. Of more sub- ordinate sitrnificance is the anemic or cachectic fat heart, which is observed in connection with anemic states (chlorosis, leukemia, pseudoleukemia, progressive pernicious anemia, following loss of blood and Avasting discharges, suppuration, chronic diarrhea). Fat heart is usually a disease of' adult.s, and it attacks men more com- monlv than women. Symptoms and Diagnosis. — The symptoms of fat heart are dependent essentially upon the fact that the movements of the heart-muscle are interfered with, and that signs of cardiac weakness gradually appear in progressively increasing degree. The patients, as a rule, complain at first of a sense of constriction, of pressure, of oppression, in the precordium, with palpitation of the heart and dyspnea on slight exertion, and finally are awakened from sleep and harassed by attacks of dyspnea at night — so-called car- diac asthma. The area of cardiac dulness is noteworthy by reason of its intensity and its increase in extent, especially toward the right. Xot rarely the action of the heart is irregular and acceler- ated. The latter symptom is, as a rule, to be looked upon as the first sign of beginning cardiac weabiess, upon which, sooner or later, manifestations of general venous stasis are prone to follow. At times fat heart is attended with attacks of bradycardia, Cheyne-Stokes breathing, and pseudo-apoplectic attacks, which are attril)utable to an(!mia of the medulla oblongata and the cerebral cortex. Obviously, the functional activity of the heart is then impaired in so marked a degree that it is no longer capable of adequately supplying the central nervous system with blood. This triad of symptoms is, as may be understood, not distinctive for fat heart, appearing also when the central nervous system is deprived of blood from other causes. Most patients with fat heart die in consequence of gradually/ increasing cardiac ireaJcness. Less commonly death results from excessive dilatation of the heart and cardiac ])aralysis. Some patients die within a short time from rupture of the heart. The diagnosis of fat heart is by no means easy, and is really never more than a probability, for the condition will be suspected when signs of disturbed cardiac activity or weakness of the heart appear in an obese individual. Specific svmptoms of fat heart are INFLAMMATION OF THE HEART-MUSCLE 31 unknown, and even in an obese person there may at times be other causes for cardiac Aveakness than fat heart. Prognosis. — Fat heart demands a cautious, though usually a serious, prognosis, for obese subjects are prone to be contrite, though but rarely reforming, offenders. The further, however, the development of fat heart progresses and the greater the amount of heart-muscle destroyed by pressure-atrophy, the more likely is incura1)le myocardial weakness to develop. Treatment. — If in a case of fat heart conditions of cardiac weakness have appeared, efforts should be directed to their removal according to the principles laid down on page 23 and 24, by means of heart-tonics, especially digitalis, or by means of stimulants. A r^'duction in the amoiuit of cardiac fat can, as a rule, be considered to have taken place only when the heart is again working with sufficient strength. AA^hen the condition arises from over-eating, food and drink should be restricted, and the patient should be enjoined to careful and progressively increasing indulgence in phys- ical exercise. Besides, the use of potassium iodid may be recom- mended, which, in addition to its fat-reducing qualities, possesses also those of a gentle heart-tonic : R Solution of potassium iodid, 5 : 200 (75 grains to 63 fluidounces). Dose : 1 tablespoonful thrice daily an hour after eating. Courses of treatment by baths at Marienbad, Homburg, Kis- singen, Tarasp, etc., will afford only temporary relief if on re- turning home at their conclusion the patient resumes his former habits. In cases of anemic and cachectic fat heart a nutritious diet and preparations of iron are to be prescribed. Among health-resorts iron-baths should be considered. INFLAMMATION OF THE HEART-MUSCLE MYOCARDITIS). Anatomic Alterations. — Among the various forms of in- flammation of the myocardium only those have thus far received clinical consideration that give rise to the development of con- nective-tissue foci or plates in the heart-muscle, so-called myo- carditic cicatrices. Whether these are from the outset strictly inflammatory in nature aj^pears doubtful from recent investiga- tions. Endarteritic alterations in the coronary arteries are believed to give rise to their development most frequently, by the formation of thrombi at the narrowed portions of the arteries, thus cutting off the blood-supply to the smaller branches of the coronary arteries. The related anemic areas of myocardium undergo necrotic soften- ing — myomalacia cordis ; the focus of softening is gradually 32 CIRCULATORY ORGANS absorbed, and in its place there appears a connective-tissue cardiac cicatrix. Tlie number and size of" such in(hirati(»ns and cicatrices are very variable, and it is especially noteworthy that isolated, small foci of connective-tissue proliferation have given rise to the most distressing symptoms, Avliile in other cases most extensive con- nective-tissue deposits have been unattended with symptoms. Often the heart-muscle undergoes hypertropliy. The detection of myocarditlc alterations requires the making of horizontal sections through the heart-muscle. Sucli changes are found with especial frequency in the neighborhood of the apex of the heart. Ktiology. — As the later years of life (l)eyond the age of forty) are frequently attended with endarteritic changes in the coronary arteries, it will be understood that the same period of life is also characterized by a tendency to the formation of connective-tissue cardiac cicatrices. At times, however, especially through the agency of certain toxic influences, presenile endarteritis and cica- trix-formation in the heart-muscle take place earlier in life, and excessive use of tea, coifee, alcohol, and tol^acco, as well as gout, diabetes, contracted kidney, and chronic lead-poisoning, are not without reason mentioned as causes. Closely related to the toxic varieties of myocarditis are the infectious varieties, which have been observed in the sequence of syphilis, malaria, articular and muscular rheumatism. In some cases myocarditic cicatrices have developed in the sequence of previous pericarditis or endocarditis through extension of the inflammatory process to the heart-muscle. Injuries of the precordium or of the heart-muscle itself are less common causes of myocarditic cicatrix-formation. With regard to the influence of expostire to cold nothing definite is known. That myocarditis is most common in men of advanced years should not excite surprise in view of the etiology. Symptoms. — Myocarditic cicatrices give rise to symptoms only when they interfere with the action and the functional capa- bility of the heart-muscle. Palpitation, irregularity of the action of the heart, and a sense of oppression and of fear are usually among the earliest symptoms, and are followed by manifestations of progres- sively increasing and graduallv insurmoimtable cardiac weakness and general stasis. The condition may persist for many months and years, and hence has also been designated chronic myocarditis. Overwhelming stasis is the most common cause of death. At times death fakes place suddenly in consequence of a variety of causative factors ; sometimes it may result from over-distention of the heart and cardiac paralysis. In the presence of marked narrowing of the coronary arteries in consequence of endarteritis, sudden occlu- sion by thrombi or, as it appears, also at times by abnormal angulation of the vessel, will under some conditions cause sudden death in consequence of anemia of the heart-muscle. Much less TUMORS OF THE MYOCARDIUM 33 commonly a sudden fatal termination occurs from rupture of the heart or cerebral embolmn, the latter originating from thrombi in the heart. Chronic aneurysm of the heart may be mentioned as on the whole an uncommon sequel of chronic myocarditis. It results in consequence of saccular dilatation of a connective-tissue cicatrix, and may exceed the size of the heart. The condition is scarcely susceptible of positive diagnosis. An area of cardiac dulness of unusual exient and irregular shape, anomalous pulsations in the precordium, and mimmirs in the same situation are the principal, but not unequivocal, symj^toms. Death may result from rupture- of the aneurysm, or from embolism arising from thrombi in the aneurysm. Diagnosis. — Chronic myocarditis can never be diagnosed with certainty. Only existing disturbances of cardiac activity and vigor can be recognized with certainty ; but that these are due to cicatrix-formation in the heart-muscle can under the most favor- able conditions be correctly interpreted only when there is reason to believe that all other causes for the manifestations named can be excluded. Prognosis. — The prognosis in cases of chronic myocarditis is unfavorable, for no remedy is capable of causing disappearance of the cicatrices. On the contrary, there is danger of the formation of new cicatrices, with steadily increasing cardiac weakness. Treatment. — Prophylactic treatment is applicable to the toxic varieties of myocarditis, and should be directed to the correction of gout, syphilis, lead-poisoning, and the use of alcohol, tobacco, coffee, and tea. Causative treatment is indicated when arterio- "sclerosis or syphilis is present. Under both of these conditions potassium iodid should be prescribed (5.0 to 200 — 75 grains to 6-1- fluidounces ; a tablespoonful thrice daily). Naturally, prophy- lactic and causative treatment overlap, as a rule, without sharp limitations. Symptomatic treatment aims principally at the cor- rection of existing derangement of cardiac action, and of diminu- tion in heart-strength, and can be carried out in accordance with the suggestions made on page 23 and 24. TUMORS OF THE MYOCARDIUM (NEW-GROWTHS OF THE HEART). Tumor-formations in the heart-muscle (carcinoma, sarcoma, myxoma, lipoma, fibroma, myoma) occur rarely, and can never be diagnosed with certainty. Small tumors are unattended with symptoms, while larger, by dis- placement of the heart-muscle, give rise to disturbed action of the heart and to weakness of the heart-muscle or to emboli, when fragments of the new-growth are broken off and are carried with the blood-current into peripheral arteries. At times symptoms of a valvular lesion appear from the projection of the tumor toward a valve, whose activity is thus interfered with. Under such conditions a probable diagnosis may be possible when tumors are demonstrable in peripheral organs. If the tumor of the myo- cardium has given rise to an increase in the area of cardiac dulness, there is danger of confusion with pericarditis. 3 34 CIRCULATORY OIKIANS Treatment is futile, and should be confined to the relief of individual symptoms. The j)rognosis is therefore invariably unfavorable. ECHINOCOCCUS OF THE HEART. Ec'hinococcus of the myocardium is an extremely rare affection, which experience has shown to involve the right ventricle most frequently. At times the cysts rupture, and accordingly as the discharge takes place into the right or the left ventricle they give rise to emboli in the distribution of the pulmonary artery or the aorta. Sudden occlusion of an orifice of the heart may lead to sudden death. Treatment is hopeless. DEXTROCARDIA. In some persons the heart is not situated on the left but on the right side of the thorax, so that the cardiac apex likewise is directed toward the right axillary region and the arch of the aorta winds around the right bronchus. The condition is an indiffereitf congeniiul one, and it may be present in the most healthy and most robust individual. The remaining organs may also participate in the displacement, so that the left lung has three lobes, the liver is situated beneath the left half of the diaphragm, the spleen beneath the right, the cardia of the stomach to the right of the ver- tebral column, the pylorus to the left, etc. Such a condition i.s known as situs viscerum j^ervcrms s. inversus. Care must be taken not to coni'ound dextrocardia with displacement of the heart in consequence of left-sided pleurisi/ wiih effusion. It may also happen that after absori)tion of a left- sided pleural effusion has taken place the heart is bound in its abnormal situation by adhesions ; but under such conditions the left side of the chest becomes retracted. Marked contraction of the right lung also may give rise to displacement of the heart in the right half of the chest ; but then the right side of the thorax becomes retracted. CARDIORHEXIS (RUPTURE OF THE HEART). Etiology. — Rupture of the heart, apart from injiirij of the heart, ]>rob- ably occurs only when the integrity of the heart-muscle has been impaired by previous disease. Among such causative conditions are especially fat heart, myocarditis, tumor-formation and echinococcus of the heart, aneurysm and abscess of the heart-muscle, and softening resulting from occlusion of the branches of the coronary arteries. At times aneurysm of a coronary artery leads to attenuation and rupture of the myocardium. As may be under- stood, rupture will readily take jilace when the blood-pressure has undergone increase. In accordance with this fact, rupture of the heart has not rarely been observed in connection with congenital narrmring of the isthmus of the aorta, and the condition has arisen frequently after psychic and physical exertion. The causes named explain why rupture of the heart is most com- mon in men of advanced years. Anatomic Alterations. — When rupture of the heart occurs blood is usually poureil out in large amount into the pericardial sac, so that this presents the appearance of an intensely distended bladder of a bluish-black color. The site of laceration is most f'requent in the left ventricle, close to the apex of the heart, and the opening as a rule is occluded by blood-clots. The tear usually takes place in the longitudinal axis of the fibers of the heart-muscle, frequently exhibits a sinuous course so that the epicardial and endocardial oi)onings are not in apposition, and at times presents ramifica- tions in its course. ACQUIRED VALVULAR DISEASE OF THE HEART 35 Symptoms and Diagnosis. — Eupture of the heart may cause sudden death. At other times the victim cries out that something has ruptured in the precordiuin ; he is seized with an indescribable fear and a premonition of death, presents pale and distorted features, and exhibits the signs of internal hemorrhage, with rapidly increasing enlargement of the area of cardiac dulness in consequence of the effusion of blood into the pericardial cavity. Under such conditions also death usually takes place within a short time, partly in consequence of the hemorrhage, partly in consequence of interference with the action of the heart, at times also as the result of shock. Prognosis and Treatment. — The prognosis is unfavorable, for scarcely any good can be hoped for from the application of an ice-bag to the ^jre- cordium and the administration of stimulants and styptics. II. DISEASES OF THE ENDOCARDIUM. ACQUIRED VALVULAR DISEASE OF THE HEART. iEtiolog'y. — Acqtiired valvular disease of the heart is one of the most common diseases of the heart and diseases in general. At times the condition is one of defect in closure or insujJicienGy of a valve, at other times one of constriction or stenosis of a valvular orifice. Often, however, both conditions are present together in one and the same valvular apparatus, and possibly only one may preponderate. If several valvular apparatus are simultaneously diseased, the condition is designated combined valvular disease of the heart. In the majority of cases valvular disease of the heart is de- pendent upon anatomic alterations. Much less commonly the valvular apparatus is itself healthy, but is insufficient to effect closure on account of morbid dilatation or distention of the val- vular orifice. Such a condition is designated relative vcdvular insufficiency. Acquired valvular disease of the heart aft'ects almost exclu- sively the valves of the left side, especially the mitral, Avliich most frequently is the seat of imperfect closure. Eight-sided valvular disease of the heart is, as a rule, congenital. An exception is con- stituted by relative tricuspid insufficiency, which develops not rarely in the sequence of mitral disease, and Avith especial fre- (juency after mitral stenosis. The most frequent cause of acquired valvular disease is endo- carditis. This usually develops after infectious diseases, and among these, acute articular rheumatism is most prominent. Acute artic- ular rheumatism is thus the most common cause of acquired vcdvu- lar disease of the heart. In childhood scarlet fever is an important cause. At times valvular disease of the heart does not develop till late 3G CIRCULATORY ORGANS in life, wlien tlio aorta and tlic aortic valves, less commonly the mitral valve, are attacked by arteriosclerosis, which leads to thick- ening;, calcification, and contraction of the valvular tissue. These alterations are frequently looked upon as constituting; rhroiiic endo- cardlfix. Oulv rarelv are valvular lesions of the heart induced by aneu- rysms of valves, neoplasms upon the valves or in their proximity, or by laceration of valves. Laceration may occur also in healthy valves in consequence of excessive physical exertion, and has been observed in all the valves of the heart, with the exception of the pulmonarv. Excessive distention of the heart is considered the cause for relative valvular insufticiency. As has been mentioned, relative tricuspid insufiieiency not rarely develops in association with mitral disease. In individuals eng'ao:ed in heavy physical exertion over- distention of the left ventricle develops at times, with mitral insufficiency, and which may recede Avith care. Acquired valvular disease of the heart occurs more frequently in adu/fs than in children, because articular rheumatism occurs but rarely in the latter. Clinical statistics are almost unanimous in indicating that valvular heart-disease is more common in women than in men. In certain regions at the seaside, and in damp and foggy places, valvular lesions of the heart are encountered with especial frequency. Anatomic Alterations. — The anatomic alterations attending acquired valvular heart-disease consist mainly in deposits, thicken- ings, even calcification, contraction, adhesions, or detachment of valvular tissue. Anatomic alterations are wanting only in cases of relative valvular insufficiency. In addition to the endocardium, the heart-muscle itself is almost always found dilated and hy]X'r- trophied in certain segments. The situation of the parts thus affected depends upon the nature of the valvular lesion. As most patients with valvular heart-disease die in consequence of weak- ness of the heart-muscle, the internal viscera, as a rule, exhibit the appearances of venous stasis, such as have been described on page 18. It is by no means always easy to decide at autopsy as to the nature of a valvular lesion of the heart. To demonstrate the existence of insufficiency of the aortic or pulmonary valve a strontr stream of water is permitted to fall from a considerable beisrht into tlie trunk of the arteries named. If the valve be incompetent, the water quickly flows into the ventricle, while if it be competent the water will be supported. In the presence of narrowinff of the aortic or pulmonary orifice sejitum-like adhesions of the valves with one another or cicatrix-like contractions of the orifice are frequently encoun- tered. In decidiuir as to the existence of incompetency or stenosis of the mitral or tricuspid valve or orifice the knowledire that in he.Tlthy adults the auriculoventricular orifices are permeable by the middle and index fingers will serve as a suide. ACQUIRED VALVULAR DISEASE OF THE HEART 37 Symptoms. — For the recognition of acquired valvular disease of the heart the local cardiac afterations furnish the indication. Frequently general disturbances of the circulation have also devel- ojjed, and these are most frequently manifested as general venous stasis, and much less commonly by emboli. We shall consider these three groups of symptoms successively. Local Cardiac Manifestations associated with Acquired Valvular Disease of the Heart. — 1. Ao>iic Insafficiency ; Aortic Iier/v.)rjita- fion. — The principal symptoms of aortic valvular insufficiency consist in an aortic diastolic nmrmiir, in dilatation and hyper- trophy of the left ventricle, and in an accelerated, full, hard radial pidse. If the aortic valves are incompetent, a portion of the aortic blood, during the diastole of the left ventricle, flows back into this chamber. As this cavity, in comparison with the lumen of the aorta, represents a sudden dila- tation of the blood-stream, there result eddies or whirls, which give rise acoustically to a diastolic murviur. This is frequently louder over the middle of the sternum than over the area of auscultation for the aorta (right second intercostal space), because the left ventricle is in closer proximity to the middle of the sternum. The murmur may also be transmitted with dimin- ishing intensity to the other valvular areas, to the carotid, and for consider- able distances upon the thorax. Only rarely is it appreciable at some distance from the patient, and more frequently it is palpable as a diastolic purring tremor (fremissement cataire). It is clear that if the left ventricle shall receive the blood regurgitated from the aorta in addition to that sent to it from the auricle, dilatation of the ventricle must take place, and this adjusts itself to the- degree of insuffi- ciency. This is recognized by the appearance of the apex-beat outside the left inammillary line and below the left fifth intercostal space, and the presence of an increased area of cardiac dulness extending beyond the left mammil- lary line (page 26, Fig. 3). As, however, the heart-muscle will be compelled during the systole to send more blood into the aorta than under normal con- ditions, and thus to perform a greater amount of work, hyjiertroplni of the left ventricle will be a further necessary sequel. This is recognized by the heaving apex-beat. The radial pulse exhibits the qualities of a large, hard, and quick pulse, because all of the arteries are filled with an abnormally large amount of blood under unusually high pressure, and during the dias- tole of the heart the blood flowing back against the semilunar valves is not Fig. 5.— Sphygmographic tracing from the radial artery in a ease of aortic valvular insuffi- ciency (personal observation, Zurich clinic). again sent on into the arteries, but is taken up by the left ventricle. A sphygmographic tracing exhibits the peculiarities of the pulse in a distinc- tive manner (Fig. 5). In addition to the manifestations described, secondary conditions are present as a rule in cases of aortic valvular insufiiciency, which, while they 38 CIIiCrLATOIlY (JlKJANS complete the clinical picture, are of subordinate importance with regard to the diagnosis. Amon<. — In the presence of con- striction of the aortic orifice there first occurs a systolic murmur as soon as the blood, during tlie systole of the left ventricle, has passed the narrowed aortic opening and has entered the wide first part of the aorta, as sudden enlargement of the current-bed leads to the formation of blood-whirls. The murmur is often marked by es]iecial intensity, so that it is transmitted from the right sec- ond intercostal space, the point of auscultation for the aorta, to the remaining valves and still fartlier, and it is not rarely palpable as a systolic purring tremor. An obstruction to the blood-stream at the beginning of the aorta must necessarily lead to hypertrophy and dilatation of the left ventricle, in order that the obstruction may be overcome. The dilatation will, however, be but slight in comparison with that which develops in association with aortic valvular insufficiency, because regurgitation of blood into the ventricle does not take i)lace. The condition of tlio radial |)ulse is important, exhibiting on palpation and in a sjihygmographic tracing the characters of an infre- quent, small, and retarded pulse (page 39, Fig. 6). Smallness and retardation of the pulse may be ex])lained by the slow entrance of the blood into the aorta, while the slow pulse may be referred to insufficient distention of the coronarv arteries of the heart. ACQUIRED VALVULAR DISEASE OF THE HEART 39 Persons with aortic stenosis usually exhibit a pallid appearance in consequence of imperfect filling of the arterial system with blood, and they not rarely suffer from attacks of syncope when cerebral anemia is excessive. 3. 3Iitral Lvmffi^ciency ; llitral Regurgitation. — Incompetency of the mitral valve gives rise to a systolic murmur, which is usu- FiG. 6. — Sphygmographic tracing of a radial pulse from a case of stenosis of the aortic orifice (personal observation, Zurich clinic). ally loudest at the apex of the heart, less commonly over the pulmonary orifice, and to dilatation and hypertrophy of both ventricles. When tlie mitral valve is incompetent the blood during the systole of the left ventricle is propelled not only into the aorta, but in part back again into the left auricle. In consequence, the left auricle is compelled to receive an unusually large amount of blood ; namely, that from the pulmonary veins plus that regurgitated from the ventricle. This is possible only if dilatation of the left auricle takes place, although this first physical consequence of mitral valvular insufficiency is without clinical significance. As the left auricle, in comparison with the contracting left ventricle, represents a sud- den expansion of the blood-stream, and, besides, as two currents of blood are poured into the auricle at the same time, blood-whirls must be gener- ated, which are appreciable acoustically as a systolic murmur, and if of sufficient intensity are also palpable as a sijstolic pur ring tremor. The blood passing from the pulmonary veins into the left auricle finds this cavity par- tially filled with blood regurgitated from the left ventricle, and stasis must therefore result. This blood-stasis extends from the area of the pulmonary veins to that of the pulmonary capillaries and the pulmonary artery, and finally to the right ventricle. In order that the latter may overcome the stasis dilatation and hypertrophy of the right ventricle must take place. This dilatation is manifested by enlargement of the area of cardiac dulness beyond the right sternal margin, while the hypertrophy leads to accentuation of the pulmonary second sound, and not rarely also to unusually active vibration of the sternum. In the presence of mitral valvular insufficiency increased functional demands are made not only upon the right, but also upon the left ventricle, for with each systole a greater amount of blood (normal amount of auric- ular blood plus the regurgitated blood) must be sent not only into the tube of exit (aorta), but into two cavities (aorta and left auricle). In order to acconnnodate the greater amount of blood dilatation of the left ventricle will develop, and in order to propel the blood hypertrophy of the left ventricle will be superadded. In accordance with the dilatation of the ventricles the area of cardiac dulness becomes enlarged both to the right and to the left (page 27, Fig. 4). The apex-beat of the heart is then generally extensive, being displaced outward beyond the left mammillary line and often also downward, and heaving, the last in consequence of hypertrophy of the left side of the heart. 40 CIRCULATORY ORGANS 4, 3fifrnl Ohsfnirfiou ; Jflfrfil e- quently a presi/stolic purring tremor is also palpable. Not rarely t\\e presystolic vmrmur appearit loudest at tite fjeginni/ig and at the close of the diastole, for at the beginning the left ventricle is still empty, and the formation of the blood-whirls therefore very active; and toward the end of the diastole the left auricle undergoes contraction, and thus gives rise to renewed activity in the formation of Ijlood-whirls. iJilatation and hyjjertrojjhji of the right venfricle are a natural consequence of the obstruction that the blood of the left auricle encounters at the con- stricted mitral orifice and of the resulting stasi-^, which extends through the pulmonary veins, the jjulmonary capillaries, and the pulmonary arteries to the right ventricle. ' At times the diastolic sound over the aorta and the pulmonary artery appears duplicated. This is explained by the fact that the pressure in tlie aorta and the pulmonary artery has undergone such pronounced alteration in conse- quence of the mitral stenosis that the semilunar valves of the aorta close earlier than those of the pulmonary artery. The systolic sound at the apex of the heart frequently is unusually clear and loud, perhaps in consequence of the fact that the difference in tension of the mitral valvular leaflets during the systole and diastole of the left ventricle in cases of mitral stenosis is unusually great. 5. Tricuspid luHvfficiency ; Tricuspid Ber/urr/itnfion. — In addi- tion to a systolic munnur over the tricuspid valve and dilatation and hypertrophy of the right ventncle, a positive venous pulse especially is indicative of incompetency of the tricnspid valve, and from the presence of which the valvular lesion can often be at once sus- pected. In cases of incompetency of the tricuspid valve a ]>ortion of the ventric- ular blood will flow back into the right auricle during the systole of the right ventricle. As, however, the right auricle n\ust also receive the blood from both veiuie cavts, it must undergo increase in capacity. Dilatation of the right auricle, therefore, takes place, but this plays clinically oidy a subor- dinate role. As soon as the blood, during the systole, is thrown back from the right ventricle into the right auricle blood-whirls ensue in the latter, and are ai)preciable acoustically as a systolic murmur, for the still empty auricle, as compared with the contracting right ventricle, represents ji sudden expansion of the blood-stream, and, in addition, it is distended by two cur- rents of blood (regurgitated blood from the ventricle and blood from the vena? cavse). Dilatation of the right ventricle \\'\\\, therefore, develop, because the right ventricle, during the systole, must receive, in addition to the normal auricular blood, also that forced back into the right auricle during the ]ireceding systole. As, however, the right ventricle, during the systole, must again jn-opel this large amount of l)lood. and must pump into two orifices of exit (pulmonary artery and right ventricle), it must perform a greater amount of work, and accordingly hypjertrnj>hy of the right ventricle takes place. The blood forced back from the right ventricle into the right auricle during the systole, presupposing sufficient power on the part of the heart- muscle, is driven into the superior and inferior vena? cavse, and thus gives rise to a positive venous pulse. In the distribution of the superior vena cava ACQUIRED VALVULAR DISEASE OF THE HEART 41 a positive venous pulse first appears in the neck, and earliest in the external jugular vein. The blood surging upward encounters resistance within the internal jugular vein at the point where the semilunar valves of the bulb of this vein are situated, and in consequence, between the inferior points of origin of the sternomastoid muscle just above the sternoclavicular articu- lation, a rhythmic cardiac-systolic vibration is visible, the bulbar pulse. This can also be felt as a short blow ; and on auscultation a short sound can be heard, the bulbar valvular sound. Soon, however, the orifice of the bulb becomes so greatly distended that its valves are no longer capable of effecting closure, and relative insufficiency of the bulbar valve takes place. The blood regurgitated from the right ventricle into the superior vena cava can now be forced into the internal jugular vein itself, and there results a venous pulse in this vessel. Above the bulb of the jugular vein a cardiac-systolic bulbar murmur is then not rarely audible, and at times a systolic bulbar thrill is also palpable. If, however, the jugular vein is greatly distended by the ujjward-surging blood-stream, a cardiac-systolic venous murmur results. A positive venous pulse may also be visible in the smaller branches of the superior vena cava, especially in the large veins of the arm and the face. An hepatic venous pulse results when the blood from the right ventricle is forced into the right auricle and the inferior vena cava with every systole, and rhythmically fills the distribution of the hepatic veins with blood. The pulsation can be seen and still more frequently felt with the hand when both hands are placed upon the anterior and jDOsterior aspects or upon the right and left sides of the liver. In some cases the blood- wave finds its way into the femoral artery, where it gives rise (just below Poupart's ligament), in the same manner as in the internal jugular vein, to a femoral bulbar pulse, a venous valvular mur- mur, relative valvular insufficiency, a femoral venous pulse, and even a saphenous pulse, to bulbar murmurs and a femoral venous murmur. Often a venous pulse appears only temporarily, disappearing when the vigor of the heart has grown so slight that regurgitation of a visible and palpable ])ulse-wave does not occur; and it will not appear in the internal jugular vein and the femoral vein as long as the bulbar valves close, or with diminishing stasis become again competent. The following condition may be mistaken for the cervical venous pulse: 1. Respiratory movements in the veins of the neck. These cease when respira- tion is suspended ; 2. Pulsatile movements imparted by the carotid artery. Pressure upon the artery mterrupts the pulsation in the carotid and at the same time also that in the veins of the neck; 3. Negative venous pulse. During the systole of the right auricle, and the diastole of the right ven- tricle, the blood stagnates in the superior vena cava and gives rise to a rhythmic pronounced distention of the cervical veins ; but in the first place this distention does not occur, like that of the positive venous pulse, at the time of the systole, but during the diastole of the heart, so that a negative venous and a carotid pulse are not synchronous but alternating ; and besides, when the vessel is compressed the negative venous pulse necessarily dis- appears below the point of compression, while the positive venous pulse is uninfluenced by this manipulation, and frequently becomes even more distinct. Hepatic venous pulse might be confounded with pulsation imparted to the liver from the abdominal aorta, but under such circumstances there would be only simple elevation and depression of the organ, while in the presence of a positive hepatic venous pulse a general cardiac-systolic enlarge- ment of the liver takes place. 6. Tricuspid Obstruction; Tricuspid Stenosis. — Tricuspid steno- sis is an uncommonly rare valvular lesion of the heart which gives rise to a presystolic murmur over the tricuspid orifice and to dilata- 42 CIRCULATORY ORfLiXS Hon and hypertrophy of the rir/ht auricle. The latter leads to increase in the area of cardiac dulness toward the right. 7. Pulmonary Ins-ajfictency ; Pulmonary Per/nrf/ifafion. — Insuf- ficiency of the pulmonary valve is recognized by a diastolic mur- mur over the pulmonary orifice (left second intercostal space close to the left sternal border) and by dilatation and hypertrophy of the rifjht ventricle. The development of these alterations is exactly tlie same as that of the corresponding manifestations attending insufficiency of the aortic valve, but referable to the right instead of the left heart. This form of valvular lesion also is rarely observed. 8. Pulmonary Obstruction ; Pulmonary Stenosis. — Constriction of the pulmonary orifice is usually a congenital and but seldom an acquired valrular lesion of the heart. A systolic murmur over the pulmonary orifice, frequently a systolic purring tremor, and dilata- tion and hypjertropjhy of the right ventricle are the distinctive mani- festations. These arise in the same manner as the corresponding alterations associated with aortic stenosis, but with reference to the circulation tlirough the pulmonary artery and the right ventricle. General Venous Stasis attending Valvular Lesions of the Heart, Weakness of the Heart-muscle, or Derangement of Compensation. — The circulatory disturbances to which a valvuhir lesion of the heart gives rise can only be neutralized to a certain degree by dilatation and hypertrophy of certain portions of tlie heart, which thus compensate for the valvular lesion. As soon as the vigor of the heart-muscle becomes impaired the condition arises tliat is designated derangement of compensation, and there develops the clinical picture of general venous stasis, as described on page 18. Such a derangement of compensation may be transitory and the result of disturbance of innervation or of over-distention of the heart. It occurs also in the sequence of mental and physical ex- ertion, of alcoholic and venereal excess, injudicious use of tea, coffee, tobacco, and the like. Many persons suffer repeatedly from attacks of derangement of compensation, which again subside under proper ]>recautions. Xevertheless, in spite of all care, derange- ment of compensation will become more and more marked, because an hypertrophied lieart-muscle manifests a tendency to fatty and connective-tissue degeneration, with increasing cardiac weakness. Such conditions are usually incurable and progressive, and eventu- ally cause death. Embolic Alterations attending Valvular Lesions of the Heart. — In addition to derangements of compensation, patients suffering from valvular lesions of the heart are especially exposed to danger from emboli. These result from the detachment of deposits upon the valves, which enter the blood-current and are with it carried to the arteries of remote organs, in tiie smaller branches of which thev finallv lodo;e as emboli. Emboli occur most frequently in ACQUIRED VALVULAR DISEASE OF THE HEART 43 the arteries of the spleen, the kidney, the extremities, and the brain, wliile they are much less common in the hepatic arteries, the mesenteric arteries, and the retinal artery. The sudden onset of the symptoms and the usually sudden pain are among the dis- tinctive features of embolism. Embolism of the splenic artery is characterized by the appearance of sudden pain in the splenic region, acute enlargement of the spleen, tender- ness of the organ on pressure, and at times by audible and palpable peri- splenitic friction-murmurs. With the occurrence of the embolism vomiting, chill, and fever may be present. Embolism of the renal artery may likewise be attended with vomiting, chill, fever, and sudden pain in the renal region. In addition the urine contains blood — hematuria. Embolism of the hepatic artery is very rare, and gives rise to marked jaundice and rapid diminution in the size of the liver, thus to the clinical picture of acute yellow atrophy of the liver. Embolism of the mesenteric artery causes sudden pain in the abdomen, peritonitis, and bloody stools. Embolism of the artery of an ex- tremity is attended with loss of pulsation and with coldness of the affected member below the point of occlusion, and if an adequate collateral circula- tion fails to be established gangrene sets in. Embolism of the cerebral arteries is m(jst common in the distribution of the left carotid, which represents the continuation of the aorta, and thus leads to occlusion of the left Sylvian artery. The patients are usually rendered unconscious with the occurrence of the embolism, and suffer a stroke or attack of apoplexy. When con- sciousness returns right-sided palsy will be observed, hemiplegia dextra, and frequently also aphasia. Embolism of the retinal artery causes sudden blind- ness. On examination with the ophthalmoscope the macula lutea presents the appearance of a cherry-red spot in the anemic retina. Diagnosis. — The diagnosis of a valvular lesion of the heart can be made only when endocardial murmurs are demonstrable on auscultation. At times the blood-pressure is so low as not to gen- erate audible blood-whirls, and when a valvular lesion is suspected an attempt may be made to increase artificially the blood-pressure by rapid walking or by movement of the body to and fro. It is also advisable to auscultate the heart in both the upright and the horizontal position of the body, at the end of inspiration and of expiration, and to note the presence of possible murmurs. While diastolic murmurs scarcely occur except in association with valvular lesions, systolic murmurs may also be present in association with febrile and anemic states as accidental murmurs. A diagnosis of valvular lesion of the heart may therefore be made from the presence of such murmurs only when some portions of the heart can be shown to be dilated and hypertrophied. Dilata- tion alone is not sufficient, as it may be the result also of the fever or the anemia. Besides, it should be borne in mind that accidental murmurs almost never give rise to purring tremor. For myself an additional important adjunct in differential diagnosis, which, as a rule, is not present in association with valvular lesions, is the fact that the pulse is least frequent in the recumbent posture, more frequent in the sitting posture, and most frequent in the standing posture. For the correct localization of heart-murmurs the rule should 44 CIRVULATORY ORGANS be rio^idly observed that iminmirs are generated at those valves over wliich they are heard with greatest intensity. As has been mentioned, exeeptions oeeiir at times in tiie ease of insntficieney of" the aortie and the mitral valve. If there be doubt whether a murmur is aortic or pulmonary, it should be noted whether it per- sists as the stethoscope is moved toward the right or the left. In the first instance it is generated in the aorta. If, h(jwever, it dis- appears as the stethoscope is moved toward the right, while it per- sists with the movement of the instrument toward the left, it is ])ulmonary in origin. The same principles apply to the differentia- tion between mitral and tricuspid mtn'murs. Combined valvular lesions of the heart may be readily recognized Avhen tlic one lesion gives rise to a systolic and the other to a dias- tolic murmur. If, however, murmurs occur at the same time, these may be transmitted from one valve to another, and the differenti- ation would depend upon the' fact whether the murmurs exhibited different acoustic characters at different situations, and whether the dilatation and the hypertrophic alterations in the heart-muscle indicated a combined valvular lesion. In order to diagnose an associated aortic stenosis together with the existence of aortic insufficiency from the presence of a systolic murmur, the fact should be taken into consideration, as has been mentioned, whether the radial pulse is retarded or not. The combination of a valvular lesion with tricuspid insufficiency is indicated by a positive venous pulse. The anatomic alterations are, as a rule, not susceptible of diagnosis. .Vs the clinieal diagnosis relates only to the functional disturbance of the diseased valve, it not rarely occurs that at the autopsy the impression is created of an existing stenosis nither than of the diagnosed insufficiency, and vice versa. Prognosis. — Valvular lesions of the heart are insusceptible of cure l)y the administration of drugs, and tiie prognosis is corre- spomlingiy unfavorable. In rare instances spontaneous recovery takes place, perhaps because of the gradual disappearance of deposits upon valves, or the stretching of healthy valves, or the retraction of dilated orifices. With the necessary rest of body and mind, and an (ij,j)i()pri((fe mode of /if e,yi.\\yu\av lesions of the heart may be survived for decades. \\] frhri/r disetisrs and in women pver/- nfdiri/ readily iniluce cardiac weakness and derangeuKMit of com- pensation. Valvular lesions of the heart acquired in childhood are attended with the danger of derangement of compensation at the period of puberty. Sufferers from valvular heart-disease are but rarely attacked by puhnondrii fiihercidosis.^ An exception is con- ' Tliis statement would seem to require iiioditication. While piilmonarv tuberculosis may be less common in association with valvular disease of the heart than with other conditions, it can scarcely be said to be rare. The subject woidd appear to be worthy of further investigation. — A. A. E. CONGENITAL HEART-DISEASE 45 stitiited by pnlinonarv stenosis, in connection ^vith which pulmonarv tubercidosis occurs frequently, probably in consequence of im- paired nutrition and diminished resistance on the part of the lungs. Treatment. — There is no remedy Jor valndnr disease of the heart. Of late saline baths have been much employed, especially those of Xauheim ; but recovery, even under these conditions, occurs only exceptionally. The greatest importance in the treat- ment of a patient suti'ering from valvular disease should be placed upon a quiet physical and psychic mode of life, and upon a light and yet nutritious diet, especially a judicious milk-diet. Medicaments should be prescribed only when threatening symptoms ariise. Most frequently weakness of the heart-muscle and derangements of compensation must be corrected, in accordance with the rules laid down upon page 23 and 24. Digitalis is the most trustworthy agent. CONGENITAL HEART-DISEASE. Anatomic Alterations. — Congenital lesions of the heart are rare forms of cardiac disease. The condition most commonly found is congenital stenosis of the pulmonary orifice. Lesions of the tri- cuspid, but es23ecially those of the valves of the left side of the heart, are unusually rare occurrences. Congenital heart-lesions, however, not only involve the valves and orifices of the heart, but also at times give rise to patency of the foramen ovale, to deficiency of the interauricular and the interventricular septum, to patency, absence, or aneurysmal dilatation of the duct of Eotal, or to transpo- sition of the great vessels, the aorta arising from the right and the pulmonary artery from the left ventricle. Frequently several con-- r/enital lesions of the heart exist in association ; especially with pul- monary stenosis the foramen ovale and the duct of Botal not rarely remain patulous, so that the l)lood may pass from the right into the left auricle and from the aorta through the duct of Botal into the pulmonary artery. Naturally, such persistence of fetal circulatory paths is unnecessar}' even when the pulmonary orifice is not merely constricted, l)ut entirely closed. !^tiology. — Xothing definite is knoM'u as to the causes of con- genital lesions of the heart. Among some that have been men- tioned are psychic disturbances and injuries during pregnancy, articular rheumatism during pregnancy, syphilis, and consanguinity in the parents. At times several children in the same family have been born with congenital lesions of the heart. Experience has shown that hoys suffer more commonly than girls. Most frequently the condition appears to be a defect in the development of the heart, to Avhieh this organ, by reason of the numerous changes in shape through which it passes during fetal life, appears to be particularly exposed. At times other developmental defects have been observed 46 CIRCULATORY ORGANS in association with congenital lesions of the heart ; for instance, liarelij), club-foot, congenital deaf-mntisin. In otlier instances the condition may be the consequence of fetal endocarditis, to which the right heart is the more predisposed during uterine life, because it receives the blood arteriaiized in the placenta, and to a certain degree assumes the functions later taken up by the left ventricle. Symptoms and Diagnosis. — Congenital lesions of the heart may hv unattended with symptoms — latent concjenital heiirt-disease. Among the a})])reeiab]e man- ifestations are congenital cya- nosis and local cardiac altera- tions. Congenital cyanosis is char- acterized by a bluish-red, at times almost blackish-blue, discoloration of the skin and mucous membranes, so that the condition has been named morbus coeruleus. Obviously the appearance is the result of delicient oxidation of the blood ; possibly, however, the unusually large number of red blood-corpuscles and the large amount of hemoglobin also may contribute to the result. Not rarely children with congenital lesions of the heart are apparently dead at birth. If resuscitation take place, the peculiar color of the skin is often conspicuous from the begin- ning. In other instances the cyanosis appears only on crying, on exposure to cold, and after physical exertion. The lips and the nose appear swollen and the eyeballs frequently project mark- edly forward. The terminal phalanges of the fingers and toes exhibit peculiar alterations, being expanded like drum-sticks — drum-stick fingers (Fig. 7). At the same time there is a tendency to frost-bite and inflammation of the terminal phalanges. The skin feels cool, and the patients suffer readily from cold and prefer the neighborhood of the stove. They avoid play with those of their own age, as they suffer from palpitation of the heart and shortness of breath, and they appear quiet, retiring, introspective, and mentally unresponsive. The local cardiac alferafions depend upon the nature of the congenital heart-lesion. In the presence of congenital ])ulmonary stenosis a systolic murmur is audible over the pulmonary orifice, and dilatation and hypertrophy of the right ventricle take place. Patulousness of the foramen ovale and deficiencv of the inter- Fio. 7.— Drura-stick fingers of congenital pul- monary stenosis ; from a photograph (personal observation, Zurich clinic). INFLAMMATION OF THE ENDOCARDIUM 47 auricular or the interventricular septum can never be recognized with certainty. At times extended presystolic or systolic mur- murs are audible over the lieart. Changes in the duct of Botal have hitherto been insusceptible of diagnosis. The principal dangers from congenital lesions of the heart con- sist in weakness of the myocardium and stasis, and in the case of congenital pulmonary stenosis in pulmonary tubei^Gulosis. Most subjects of congenital heart-disease do not survive the fourteenth year of life. Prognosis. — The prognosis is unfavorable in accordance with what has been said. Recovery is out of the question. Treatment. — The treatment is the same as that of acquired lesions of the heart. INFLAMMATION OF THE ENDOCARDIUM (ENDOCARDITIS). Several forms of endocarditis have been distinguished, and they have been designated ulcerative, verrucose, and contracting. Ulcerative and verrucose endocarditis are due to the activity of bacteria, and the same microorganisms may give rise to the one or the other variety. Transitional and mixed forms are also observed both anatomically and clinically. Contracting endocarditis leads to thickening, contracition, and frequently also to calcification of the endocardium, and is often the sequel of a preexisting verru- cose endocarditis. In other instances it develops independently as a manifestation of senility, and often in association with arterio- sclerosis. Excessive physical activity, excessive use of alcohol, chronic disease of the kidneys, gout, and diabetes also are causes. In contradistinction from ulcerative and verrucose endocarditis, the contracting variety pursues a chronic course, so that it has been designated also chronic endocarditis. It constitutes the most com- mon anatomic cause for valvular ledons of the heart, and it exhibits a great tendency to become again acute, when it is designated recurrent contracting endocarditis. ULCERATIVE ENDOCARDITIS. Ktiology. — Ulcerative endocarditis is most commonly the sequel of a preexisting wound-infection. Then, it is not rare in the sequence of infectious diseases. At times a causative factor is not elicitable, and under such conditions the designation crypto- genetic endocarditis has been employed. In this category prob- ably belong also the instances in which exposure to cold, excessive physical activity, and psychic disturbances have been assigned as etiologic factors. Among wonnd-infections it should especially be mentioned that ulcer- ative endocarditis not rarely develops in association with puerperal fever. 48 CIRCULATOR V OnCANS P'urther, the smallest wound is sufficient to afford entrance for bacteria into the blood and to the endocardium. In this connection, not only external, but also internal, wounds must be taken into consideration ; for instance, those of the mucous membrane of the digestive apparatus. Among iii/ec- tious (liseasen acute articular rheuuiatisni especially is a fiequent cause of ulcerative endocarditis. Among the acute exanthemata, xcarlet fever is of especial importance. Of late ulcerative endocarditis has been observed a number of times in the sequence of gonorrhea. In cases of cniptof/euetic ulcerative endocfirditis the tonsils may often be the portal of entry for the bacteria. Experience has shown that tcomen are more commonUj attacked by ulcerative endocarditis than men. The disease is rare in chihl- hood. It occurs most commonly between the twentieth and the fortieth year of life. Anatomic Alterations. — The first changes in ulcerative en- docarditis consist in a deposit ujion the endocardium that is com- posed principally of masses of bacteria. If this be detached, a loss of tissue, usually sharply circumscribed, becomes apparent. Fre- quently fibrinous masses are deposited at these points (endocarditic vegetations), which, as a rule, are less abundant than in cases of vcrrucose endocarditis. The lesion of the endocardium may lead to perforation and destruction of the valve-structure ; or it may give rise to an acute aneurysm of the valve if only one layer of the valve is destroyed. The ulcerative process may also extend to the myocardium and give rise to an acute myocardial ulcer. Should saccular dilatation of the myocardium take place at such a point, an acute aneurysm of the heart will result. Ulcerative endocarditis most frocpiently attacks the valves of the heart, especially those of the left side, and the alterations involve the lines of closure of the valves. It attacks the tendinous cords, the papillary muscles, and the mural endocardium much less commonly. At times several valves are involved sinuiltancously, both ujion the right and u])on the left side. The most frequent exciting agent of ulcerative endocarditis is the staphylococcus pyogenes aureus and the streptococcus pyogenes, although a number of other bacteria have been isolated from the endocarditic inflammatory areas, at times specific bacteria, such as gono(!occi and typhoid-bacilli. Ulcerative endocarditis is characterized by a great tendency to the development of bacterial embolism. Small masses of bacteria become detached from the inflamed endocardium, and are carried through the arterial blood-current into the most diverse organs, where they become lodged in the smaller blood-vessels, forming at first a grayish or grayish-white center, surrounded by a zone of hyperemia. Soon, however, inflammation and sup})uration are superadded. Frequently the individual organs contain numerous emboli and fi)ci of suppuration, and only few viscera escape this complication. INFLAMMATION OF THE ENDOCARDIUM 49 Symptoms and Diagnosis. — Ulcerative endocarditis is only susceptible of diagnosis when in addition to a septic general condi- tion signs of a valvular lesion of the heart are also present. As long as the cardiac valve remains functionally competent only the general septicemia can be recognized. This at times pursues a course sug- gestive of typhoid fever (continued fever, dry, coated tongue, dis- tended abdomen, roseola, splenic enlargement, diarrhea) ; at other times, chills followed by elevation of temperature, lasting for several hours, and recurring with a certain degree of regularity, and splenic enlargement, raise a suspicion of intermittent fever ; or iinally suppurative inflammation occurs in one or more organs, which, together with possible chills, are due to bacterial emboli. In doubtful cases it is especially important to look for emholie alterations in the skin, the mucous membranes (of the mouth, the conjunctiva), and the retina. In these structures hemorrhages may be frequently observed, in which the bacterial plug may be recog- nized as a white center. Further, roseolous, scarlatiniforra, and pustular eruptions also occur upon the skin. In a case of doubtful diagnosis a physician trained in bacteriologic methods would examine the stools, the urine, and the blood of the rose-spots for the presence of typhoid-bacilli, or the blood for malarial plasmodia. In cases of ulcerative endocarditis, on the other hand, it is not uncommonly possible to obtain pyogenic cocci from the blood. Such valvular alterations as may be present will manifest them- selves by endocardial murmurs, which are mostly systolic and less commonly diastolic in occurrence. To these dilatation of the heart may be superadded. The disease usually pursues too rapid a course for hypertrophy to develop. Death may take place within three days. At times, however, the disease is protracted for months. Recovery is scarcely to be hoped for. Life is terminated either with progressive failure of strength, or in consequence of secondary suppuration, or of embo- lism of an important cerebral vessel. Prognosis. — The prognosis is almost unexceptionably un- favorable. Treatment. — A nutritious liquid diet should be prescribed (milk, bouillon with egg, coffee, tea, wine), an ice-bag is kept ap- plied continuously to the precordium, and digitalis is prescribed to strengthen and slow the action of the heart ; the last may be com- bined with benzoic acid and camphor when asthma is present. Mercuric chlorid and quinin have also been employed for the pur- pose of destroying the bacteria upon the endocardium. VERRUCOSE ENDOCARDITIS. iJ^tiology. — Verrucose endocarditis is caused by the same bac- teria as the ulcerative variety. Why in the one instance the disease assumes the verrucose type and in the other the ulcerative type is 4 50 CIRCULATORY ORGANS not definitely known. Infectious diseases of all kinds are the most common cause of the disorder. Ainonir the most conspicuous of these are acute articular rheumatism and in childhood ncarlet fever. Debilitating diseases (carcinoma, })ulmoiiarv tuberculosis, chronic nephritis) also favor infection and iuHannnatiou of the endtjcar- dium. Exposure to cold and injury further act as etiologic factors, although these must be consitlered only as contributory causes favor- ing infection of the endocardium. Experience has shown that verru- cose endocarditis occurs more commonly in men than in women, and especially hefu-ren the fu-rntleth and the fortieth year of life. Anatomic Alterations. — The characteristic alterations of verrueose endocarditis consist in throml)otic deposits, endocarditic vegetations, upon the iuHamed areas of the endocardium, which not rarely in appearance resemble an extensive cock's comb, cauli- flower, or condyloma. As a rule, the endocarditis involves the valves, the vegetations being situated at the lines of closure. The mitral valve is attacked with especial frequency. Inflammation of the pulmonary and tricuspid valves is uncommon. As may be understood, the vegetations are capable of interfering with the function of the affected valves and inducing the manifestations of a valvular lesion of the heart. In the further course of the morbid process organization of the vegetations takes place. Thickenings occur, even calcification of the valve, with contraction and adhe- sions, and the valvular lesion becomes a permanent one. Bacteria can frequently be demonstrated in the vegetations only by cul- ture-methods. When the vegetations have existed for some time bacteria are no longer present. A frequent complication of verrueose endocarditis is constituted by emboli, which result from the disintegration of endocarditic vegetations. These do not, as a rule, excite inflammation in the affected organ, because they do not contain bacteria or contain them in too small number, but they give rise to the manifesta- tions of an emljolic infarct. Symptoms and Diagnosis. — Verrueose endocarditis can be recognized only ihmi the development, in the course of days or weeks, of the symptoms of a valvular lesion of the heart, most fre- quently those of mitral insufficiency. In the condition last named a systolic murmur first apjunirs. Gradually dilatation of the right side of the heart is superadded, and finally the jMilmonarv second sound becomes acc(Mitnated anpears reddened. The fibrinous membrane gradually becomes thicker, more opaque, more deeply yellow, and in consequence of the movements of the layers of the pericardium upcm one another the surface acquires an irregular, rough, and papillary appearance, by reason of which the terms villous heart, INFLAMMATION OF THE PERICARDIUM 53 for hirsutiim (cor villosum s. tomentosum) have been employed. The appearance of such a heart has also been compared with that of a sponge, of a honeycomb, of the fourth stomach of ruminants, or of two surfaces of buttered bread that have been separated. As a rule, fibrinous pericarditis involves simultaneously both peri- cardium and epicardium. Only rarely is one of the layers of the pericardium alone inflamed. In accordance with the extent of the inflammation a circumscribed (local) and a diffuse (total) peri- carditis are distinguished. Pericarditis humida (pericarditis with effusion) usually develops from a fibrinous pericarditis, the formation of a fluid exudate being superadded to the deposition of fibrinous coagula. If the inflam- matory fluid is deficient in cells and still to a certain degree trans- parent, the condition is described as serous pericarditis or, more accurately, serofibrinous pericarditis. Under other conditions the exudate resembles the pus of an ordinary abscess — purulent peri- carditis or pyopericardium. Finally, the effusion may be bloody — hemorrhagic pericarditis. At times, in consequence of the presence of putrefactive bacteria, putrid decomposition takes place in a purulent effusion — putrid pericarditis. This occurs especially as a result of septic influences ; for instance, puerperal fever. The amount of fluid exudate may exceed three liters, so that the peri- cardium appears tensely distended, and when punctured the fluid is ejected in a stream. It is worthy of note that the heart-muscle, by reason of its weight, sinks in the exudate, and that especially the portions contiguous to the pericardium exhibit inflammatory softening. Microscopically such portions are found to participate in the inflammatory process. Pericarditis but rarely undergoes recovery without leaving alterations in the pericardium. Of subordinate importance are tendinous thickenings of the epicardium — tendinous spots, maculce tendine/e s. albidce, also designated insulse. Frequently connective- tissue adhesions take place between the two layers of pericardium (pericardial synechice or adhesions). These sometimes cause com- plete obliteration of the pericardial cavity — obliteratio s. concretio pericardii. At times the synechise contain inspissated, cheesy, or calcareous remnants of the fluid exudate. In rare cases almost the entire heart appears to be enclosed in a calcareous capsule. At times the inflammation extends from the pericardial cavity to the outer surface of the pericardium — external pericarditis. Under such conditions also connective-tissue adhesions may form in the course of time, and these may surround the large arteries and the venous trunks of the heart, and possibly bind the pericar- dium to the sternum and to the vertebral column. Such altera- tions have been designated indurative or fibrous media stinoperi- carditis. Symptoms. — Pericarditis can be recognized only from the 54 CIRCULATORY ORGANS 'phynical alterations in the heart. Constitutional symptoms are wanting: or are only of indefinite nature. FibrinoiL.^ pericarditis is disclosed by the occurrence of a peri- carditic friction-mumiur. This is characterized by its superficial, rasping character, by not being confined strictly to the cardiac phases, and by usually exhibiting numerous interruptions which are dependent upon the movements of the auricles and the ven- tricles. It is at tin)es so loud that it can be felt with the hand as pericardial friction or aff'rictus pericardiacus, and that the patient may himself be conscious of its presence in the thorax as Fig. 8.— Area of cardiac percussion-dulness in a case of pericarditis witli efFiision : X, situation of the apex-beat. From a photograph (personal observation, Znrich clinic). a rubbing. Pericardial friction-murmurs are usually confined to the area of cardiac duhiess, or they are diffused in any event for but a short distance l)eyond. They are intensified l)y the pressure of tiie stethoscope. Their intensity varies also with the position of the body, and is increased as a rule by over-inclination for- ward. Frequently ])ericardial friction-murmurs are audible for days and -weeks ; at times, however, for only a few hours, because the inflammation is sometimes of but short duration. Pericarditis with Jin id e fusion first leads to increase in size and INFLAMMATION OF THE PERICARDIUM 55 change in shape of the area of cardiac dulness. This is induced by distention of the pericardium by the fluid. The area of car- diac dulness is increased both to the right and the left, and from above downward, and at the same time it assumes the shape of a trapezoid (Fig. 8). In the diagnosis it is important that frequently the area of cardiac dulness extends to the left beyond the apex-beat, because the fluid in the pericardial cavity is distributed to the right and the left beyond the borders of the heart. G-radual disappearance of the apex-beat in the course of the disease is likewise a valuable sign because layers of exudate gradually increasing in thickness are deposited upon the anterior surface of tlie heart, and the heart- muscle becomes the more deeply submerged. In consequence diminution in the intensity of the heart-sounds also takes place. Among symptoms of more subordinate significance may be mentioned marked bulging of the precordium in consequence of pressure exerted by the pericardial exudate and inflammatory paresis of the intercostal mus- cles, and cutaneous edema in the precordium, the latter resulting from the collateral edema. In the majority of cases pericardial friction-murmurs are en- countered in addition to signs of accumulation of fluid in the pericardium, as usually besides fluid effusion fibrinous inflammatory products are present. Friction-murmurs are absent only when copious fluid effusions have been poured out, because then a rubbing upon each other of the layers of the pericardium is impossible. Such murmurs appear only when a portion of the fluid exudate has undergone absorption. Constitutional symptoms may be entirely wanting in cases of inflammation of the pericardium. Frequently irregular febrile movement is present. Not rarely the patients complain of a sense of constriction, of pressure, and even of pain in the precordium. The action of the heart appears accelerated and irregular, and the radial pulse is conspicuous for its slight tension. The duration of inflammation of the pericardium may extend over several months. One of the most frequent and most serious complications is myocardial weahiess, with symptoms of stasis, and a considerable number of patients die in consequence of increasing edema. Sudden paralysis of the heart, for instance from carelessness in assuming the sitting or the erect posture, is less common. At times manifestations due to pressure of the pericardial exudate upon neighboring organs occur. Thus, there may be unilateral or even bilateral paralysis of the recurrent laryngeal nerve, con- striction of the esophagus, obstinate singultus, and vomiting. Frequently the lower lobe of the left lung is compressed until all of its air is expelled, with the development of dulness on percussion, increased vocal fremitus, and bronchial breathing. At 56 CIRCULATORY ORGANS times tlie inflammation of the pericardium extends to the pleura, and then pleurisy is superadded, usually left-sided. Not rarely attacks of accelerated heart-action and di/spnea occur which may be excited by physical or mental exertion, but which appear also during states of profound rest. Rupture of a pericardial effusion, with the formation of an external or an internal pericardial fistula, may be mentioned as an unusually rare complication. When pericarditis terminates in recovery a morbid hyperirri- tability of the myocardium often persists for a considerable time, and which is manifested in a marked tendency to accelerated and irregular cardiac action. Among the residua of pericarditis ten- dinous spots are unattended with symptoms ; in only one instance have I been able to detect friction-murmurs over an especially dense and thick tendinous spot. Pericardial adhesions also are unattended with symptoms so long as they do not affect the cir- culation in the coronary arteries of the heart and the movements of the heart-muscle. If the coronary arteries are constricted by adhesions, the nutrition of the myocardium must suffer, and signs of cardiac iveakness and stasis appear, to which the patient finally succumbs. Adhesions that interfere with the systolic movement of the heart downward give rise to systolic retraction in the region of the apex-beat with the systolic shortening of the heart. This becomes especially marked, and involves also the contiguous tho- racic wall, w^hen the apex of the heart is adherent to the inner aspect of the chest, and is capable of exerting direct traction on the chest-wall. Indurcdive mcdiastinopericarditis is indicated by an intermittent inspiratory or paradoxic pulse and inspiratory dis- tention of the cervical veins. Naturally, these are not unequivocal symptoms, for similar manifestations are sometimes observed also in association with pericarditis, pleurisy, and aneurysm of the aorta. Both the diminution in size and even the disappearance of the pulse during inspiration and the synchronous increased dis- tention of the cervical veins may be explained by the fact that the aorta and the vena cava are surrounded by adhesions, and their lumen becomes constricted by traction during inspiration. Diagnosis. — Vi^henever pericard ial friction-mnrmnrs arc heard fibrinous jicricarditis may be diagnosed, for it is extremely rare for heniorrhages, excessive dryness (in cases of Asiatic cholera) or tendinous patches of the pericardium, to give rise to such murmurs. Pericardial murmurs may be confounded with endocardial and pleuropericardial (external pericardial) murmurs. In coiitradi>t pericardial murmurs apjiear more superficial and rasping-, and are, as a rule, not audible beyond the limits of cardiac percussion-dulness. They are not strictly confined to the cardiac phases, and usually permit the recognition of a number of inter- ruptions. During inspiration they do not, like endocardial murmurs, INFLAMMATION OF THE PERICARDIUM 57 become fainter, but louder, because the dilating lung exerts pressure ujion the layers of the pericardium and favors their rubbing upon each other. They may also be increased by pressure with the stethoscope, and they vary greatly in intensity with the posture of the body. Pleuropericardial friction-murmurs occur with an intact pericardium when fibrinous pleurisy has developed in close proximity to the pericar- dium, so that the movements of the heart give rise to pleural friction- murmurs. The dependence of doubtful murmurs upon respiration may, however, usually be demonstrated by deep inspirations. If the breath be held after deep inspiration, the pericardial influences are suspended, and in general they do not appear when the breath is held. In the presence of pericarditis with effusion there is a possi- bility of confounding the enlarged area of cardiac percussion-dul- ness with dilatation of the heart. It is then important to determine whether the area of cardiac dulness extends to the left beyond the apex-beat, which is indicative of the presence of fluid in the peri- cardium, and whether the apex-beat gradually disappears in the course of the disease. When pericarditis with effusion is present the heart-sounds become faint and the action of the heart is scarcely, if at all, visible. Gerhardt has further called attention to the displacement upward of the upper limit of cardiac dulness in the sitting posture in cases of pericarditis. Sacculated pleuritic effusions and infiltration of the median borders of the lungs may give rise to increase in the area of cardiac dulness and to errors in diagnosis; but the dulness then usually assumes an irregular shape, and when infiltration of the lung is present bronchial breathing is audible. The character of the effusion can be determined with certainty only by exploratory puncture of the pericardium; otherwise de- pendence must be placed upon the results of clinical experience, which show that acute articular rheumatism is usually attended with serofibrinous, septic processes with purulent, and scorbutus, tuberculosis, sarcoma, and often also nephritis, with hemorrhagic effusions. Prognosis. — Pericarditis Is under all circumstances a serious disease. Even the cases that at first appear to be mild may with insufficient care acquire a grave character. Of great importance with relation to the prognosis is the etiology. Wliile pericarditis in the sequence of acute articular rheumatism is usually followed by recovery, the prognosis wlien septic factors are operative is materially more serious, and in the presence of new-formations it is invariably unfavorable. Treatment. — All varieties of pericarditis require the same general treatment (rest in bed, easily digestible diet, especially milk and soups). Further than this the treatment will vary with the character of the exudate. In cases of fibrinous pericarditis an ice-bag should be applied continuously to the precordium, and if severe pain or marked dyspnea be present an injection of morphin should be s^iven : 58 CIRCULATORY ORGANS R Morphin hydrochlorate 0.3 (4i grains) ; Glycerin, Distilled water, each 5.0 (75 minims). — M. Dose: 0.5 c.c. (8 minims) subcutaneously. If tlie action of the heart be accelerated, enfeebled, and irreg- ular, digitalis should be prescribed : li Powdered digitalis-leaves, 0.1 (1 J grains) ; Diuretin, 1.0 (15 grains); Sugar, 0.5 (7^ grains). — M. Make ten such powders. Dose : 1 powder every three hours. In cases of serous 2i^r{carditis also a similar course of treat- ment may be recommended. From sorbefacients (potassium iodid internally, potassium-iodid ointment or iodoform-ointment by inunction, and tincture of iodin applied locally) no great measure of success is to be expected. At times repeated applica- tion of an ordinary cantharidal plaster will hasten the absorption of the effusion. If absorption fails to take place after the lapse of weeks, or if perhaps after the fourth week the amount of effusion increases, or if it is from the outset so extensive that death is threatened through interference with the action of the heart, artilicial evacuation of the effusion by puncture of the pericardium may be recommended. Purulent pericardial effusions should be evacuated immediately by opening the pericardium with a knife, because experience has taught that absorption cannot be effected by any means, and if delay be too much prolonged irremediable cardiac weakness will develop. The same statement applies to putrid p>ericarditis. Hemorrhagic pericarditis has been observed to assume such enor- mous proportions in cases of scorbutus that puncture of the peri- cardium was necessitated. PNEUMOPERICARDIUM, Anatomic Alterations, — Pneumopericardium signifies an accumulation of gas in tite ppricanUal cavihf. If the amount of gas be considerable, the pericardium is tensely distended, and when punctured the gas escapes with a hissing sound. As a rule, pure pneumopericardium is not encountered, but a liiidrojtneiimnpericardinm ; that is, in addition to gas fluid also is present in the ])ericardial cavity. Accordingly as this fluid is serum, pus, or blood, a distinction is made between sernpncvrnopcricardium, pyopneumopericardinm, and hetnnpneiimnpfricardium. The pericardium at the same time presents evidences of inflammation. Etiology. — Pneumopericardium is a rare disease. It develops when the pericardia/ carifij commynirafes vifli air-confaininq vis^cera or through the thoracic wall directly with the external air. Such occurrences have been observed in cases of ruptured pulmonary cavities, carcinoma of the esoph- agus, gastric ulceration, carcinoma of tiie stomach, rupture of purulent w pericardial eff'usions into air-containing viscera, or externally, injuries of ' the chest-wall, and the like. It has been maintained that a pyopneumopericardium may be developed DROPSY OF THE PERICARDIUM 59 from a pyopericardium bij decomposition of the pus. This possibility must be conceded, as gas-generating bacteria are known to exist. Symptoms and Diagnosis. — The si/7npioms of pneumopericardium consist in disappearance of the area of cardiac dulness in the dorsal decubitus, and the presence instead of signs of a smooth-walled cavity : a metallic percussion- note, which is brought out with especial distinctness when auscultatory per- cussion is practised with the aid of a plexor and plexinieter. 'n\Q heart- sounds in consequence of the resonance also seem to possess a metallic char- acter, like a bell. If the air-fistula be patulous, percussion further will yield a cracked-pot sound. In the sitting posture, and on bending forward, the heart will become again applied to the chest-wall, and can then be demonstrated by the dulness on percussion. A pericardial splashing-sound is distinctive of hydropneumopericardium {water-wheel murmur). This is developed by the movement to and fro of the fluid contents of the pericardium through the action of the heart. At times it may be heard at some distance from the patient. In addition changes in the percussion-phenomena take place in accordance with the position of the body. These are dependent upon the fact that the fluid always seeks the lowest level, and over it dulness exists, while the gas-generating cavity yields a metallic note on percussion. Patients with pneumopericardium and hydropneumopericardium com- plain mostly of a sense of constriction and even of pain in the precordiuni, while the action of the heart is accelerated and often irregular; they suffer from dyspnea and threatening weakness of the heart, because the free move- ment of the organ is prevented. Weakness of the heart-muscle 2ind paralysis of the heart are the principal dangers of the disease. Prognosis. — The prognosis is unfevorable because of the serious nature of the primary disorder, independently of the dangers that attend pneumo- pericardium and hydropneumopericardium themselves. Treatment. — In cases of pneumopericardium and hydropneumopericar- dium efforts should first be made to allay fear and dyspnea by means of a subcutaneous injection of morphin. Should the collection of gas be consider- able, the pericardium may be punctured by means of a hollow needle, whose free extremity is covered with a rubber tube, the other end of which is placed beneath the surface of a solution of carbolic acid (5 : 100). In cases of pyopneumopericardium the pericardium should be opened by incision, while in cases of seropneumopericardium and hemopneumopericardium puncture of the pericardium, with subsequent treatment as in cases of serous and hemorrhagic pericarditis will suffice. DROPSY OF THE PERICARDIUM (HYDROPERICARDIUM) . Anatomic Alterations. — The accumulation of a serous transudate in the pericardial cavity is known as hydropericardium. The pericardium always contains a certain amount of serous fluid, so that hydropericardium is only spoken of when the pericardial cavity contains more than 100 c.c. of clear, amber-yellow fluid. The amount, however, may reach several liters. Xot rarely the pericardial tissue api)ears edematous, and the myocardium pale and saturated with fluid. Hydropericardium is distinguished from a serous exudate by the absence of flocculi and the clear appearance of the fluid. Etiology. — Transudation into the pericardial cavity results from causes similar to those that bring about transudation into other serous cavities and into the subcutaneous connective tissue, with which it is thus usually found in association. The condition present, therefore, is usually one of cachexia or of increase of pressure in the venotis system. It is observed quite frequently in association with diseases of long standing, such as pulmonary 60 CIRCULATORY ORGANS tuberculosis, carcinoma, suppuration, nephritis, respiratory and cardiac dis- ease. Rarely, local causes of stasis are present in the coronary veins, in consequence of adhesions or tumors of the pericardium. Symptoms and Diagnosis. — Dropsy of the pericardium gives rise to the same local cardiac alterations as a collection of pericardial fluid exudate, except that a pericardial friction-murmur is wanting. The area of cardiac duliiess is increased in extent, and projects beyond the apex-beat outward toward the left, tiie apex-beat becomes feebler and finally disappears, and the heart-sounds are faint. In addition there are signs of v:eakness of the heart, which is induced in part by the primary disorder, and in part by interference with the action of the heart. Usually there is complaint of marked dyspnea and a sense of constriction, because the movement of the lungs and of the diaphragm is embarrassed by coexisting hydrothorax and ascites. Death in consequence of jjaralysis of the heart is the most frequent termination. Prognosis. — Dropsy of the pericardium is not unjustly in evil repute among the laity, for frequently it is associated with incurable conditions, and, besides, the disorder itself is attended with the danger of cardiac weak- ness and paralysis of the heart. Eecovery is, however, possible if the cause can be removed. Treatment. — Treatment should in the first place be caiisal. Symptom- atically resort will often be had especially to heart-tonics, and particularly to digitalis and diuretin. Extensive transudates require puncture of the pericardium. HEMOPERICARDIUIVL Accumulations of blood in the pericardial cavity occur especially in association with injuries and rupture of the heart and of aneurysms of the a/)rta, 2^iil>'ionary artery, or coronary arteries. Their recognition depends upon the fact that the area of cardiac percussion-dulness increases rapidly in consequence of the increasing accumulation of blood, while the apex-beat disappears and the sounds of the heart become fainter, and at the same time manifestations of internal hemorrhaye appear. Death may result from hem- orrhage or in consequence of parali/sis of the heart. The prognosis is, there- fore, always serious. Therapeutically stimula7its may be recommended; for instance, camphorated oil (a syringeful subcutaneously every two to four hours). Not much will be accomplished by the use of hemostatics (ice- bag, subcutaneous injection of extract of ergot, fluid extract of hydrastis, twenty-five drops thrice daily, etc.). I have averted death in one case by puncture of the pericardial cavity and aspiration of the blood. CHYLOPERICARDIUM. In rare instances lacteal vessels rupture and an accumulation of chyle takes place in the pericardial cavity, which, if in sufficient amount, may give rise to an increase in the area of cardiac percussion-dulness. TUMORS OF THE PERICARDIUM Systolic murmurs are usually audible over aneurysms of the aorta, for the sudden dilatation of the lilood- stream gives rise to blood-whirls within the aneurysm. Murmurs will be wanting only when the aneurysm is so thoroughly filled with thromtii that dilatation of the blood-channel is no longer present. Not rarely a systolic and a diastolic murmur are audible over aortic aneurysms. The diastolic murmur is either generated within the aneurysm itself, when the diastolic reflux of the blood takes place with such energy that audible blood-whirls occur within the aneurysm, or transmitted from the aortic valve (which has frequently at the same time become incompe- tent in consequence of arteriosclerosis) to the aneurysm. Under the latter condition the acoustic character of the diastolic murmur over the aortic valve and over the aneurysm is the same. Aneurysms of the ascending aorta and of the arch of the aorta usually give rise to displacement of the heart downward and out- ward, so that the apex-beat is found outside the left mammillary line and lower than the left fifth intercostal space. Generally there is hypertrophy of the left ventricle (heaving apex-beat) ; which some observers, however, attribute to the aortic valvular insuf- ficiency as a rule present at the same time. In cases of pure aortic aneurysm atrophy of the heart is said to take place in con- sequence of deficient nutrition of the lienrt-muscle. The character of the pulse is further worthy of consideration in cases of aortic aneurysm ; it varies in accordance with the seat of the aneurysm. In cases of aneurysm of the ascending aorta all of the peripheral pulses appear belated, as compared with the apex-beat of the heart, because the blood is restrained within the aneurysm. Aneurysms of the arcli of the aorta permit the pulse to appear synchronously in the right radial and the carotid with the apex-beat, while the pulse in the left carotid, the left radial, and the femoral arteries is belated when the aneurysm is situated between the point of origin of the innominate and the left carotid. ANEURYSM OF THE AORTA 69 If, however, the aneurysm is situated between the left carotid and the left subclavian, the right radial pulse and the two carotid pulses occur synchronously with the apex-beat, while the left radial and the femoral, on the other hand, appear later. In cases of aneurysm of the descending aorta, finally the pulse in the neck and in the arms is palpable synchronously with the apex-beat^ while it occurs later in the femoral arteries. Eetardatiou of the pulse can take place in cases of aortic aneurysm only in consequence of constriction and distortion of the orifices of vessels arising close to the aneurysm ; but under such conditions the retarded pulse is further characterized by deficient fulness. Subjective discomfort may be wanting throughout the whole course of the disease ; but, as a rule, the patients complain of dis- tressing beating, a sense of constricton and pain in the chest. Attacks of palpitation of the heart and dyspnea also not rarely occur. Every aneurysm has a tendency to increase in size, and this may be a source of two dangers, namely, excessive pressure upon adjacent organs and rupture of the aneurysm. The pressure- phenomena vary in accordance with the seat and the direction of growth of the aneurysm. Aneurysms of the ascending aorta and of the aortic arch frequently give rise to unilateral or bilateral paralysis of the recurrent laryngeal nerve. Obstinate and severe eervicobracMal neuralgia is also not rarely observed. If motor nerves suffer in consequence of the pressure, pareses and paralyses appear in the arm (principally the left). Aneurysms of the descending aorta often give rise to the most distressing intercostal lumbo-abdominal neuralgia. They also frequently cause a pain- ful sense of stiffness in the vertebral column, so that patients are capable of moving about only with difficulty in a position bent forward. At times a bronchus is compressed. Math the develop- ment of the clinical picture of bronchostenosis (usually left-sided); or pressure on the esophagus gives rise to stenosis of that tube, with the danger of death from starvation. Even the bones are unable to resist the advance of an aneurysm. By erosion of the bony portion of the chest-wall the aneurysm may come to lie beneath the external integument. In other instances articular attachments are severed. Even the vertebral column is at times perforated by an aneurysm, with resulting compression of the spinal cord and spinal paralysis ; or the aneurysm ruptures and discharges its bloody contents into the vertebral canal. Rupture of an aneurysm is favored by excessive physical and mental activity, which increase the blood-pressure ; but it may occur also during complete rest and during sleep. At times rup- ture takes place outward through the skin. Sometimes, after pre- vious discoloration, the skin ruptures at several points, the blood at first trickling but slowly, so that at the beginning it may be 70 CIRCULATORY ORGANS possible to control the hemorrhage ; but at other times a great tear suddenly takes place in the skin, through Avhich the patient" bleeds to death witiiin a few seconds. Bnpture info tJte pericardial cavity not rarely takes place, the pericardium rapidly filling with blood, and sudden death occurs in consequence of cardiac paralysis. Rupture into one of the pleural cavities takes place still more fre- quently, and with especial frequency into the left pleural cavity. Rupiture into the esophagus, the bronchi, and the trachea has als(» been observed. Less conmionly rupture takes place into the cavi- ties of the heart or into the vence cava'. Aneurysms of the descend- ing aorta at times give rise to undermining and detachment of the pleura or the peritoneum through the extravasated blood. The duration of an aneu7'ysm does not, as a rule, extend beyond a year and a half, although observations are on record covering a period of more than twenty years. The termination is usually fatal, death occurring from rupture of the aneurysm or in consequence of pressure-disturbances (steno- sis of the esophagus, spinal paralysis), or from progressive maras- mus, or at times also from embolism derived from detached thrombi. It should be mentioned that pidmonary tubercidosis is not rare in association with aortic aneurysm. Diagnosis. — The recognition of aneurysm of the aorta is not rarely attended with considerable difficulty, even in cases in which the symptoms are not exclusively suspicious. In the presence of pulsating tumors care should be taken to avoid confusion with solid tumors situated upon the aorta, and receiving transmitted move- ment from it. Under the latter conditions, however, only eleva- tion and depression take jilace, but not expansile pulsation of the swelling. The location of an aneurysm will be indicated by the situation of the dulness, the tumor and the pulsation that may be present, and the character of the pulse as previously pointed out. Prognosis. — The cure of an aneurysm through abundant thrombus-formation and obliteration of the sac can scarcely be hoped for, and almost without exception death from rupture or exhaustion, or one of the complications already mentioned, is to be feared within a short time. The prognosis is thus unfavorable. Treatment. — Individuals suffering from aneurysms of the aorta must ol)serve permanently bodily and mental rest, and avoid all irritating articles of diet (strong coffee, tea, alcohol). A daily movement of the bowels should be secured, as expulsive efforts may cause rupture of the aneurysm. Fasting has properly been abandoned as a means of treatment, because it hastens the loss of strength already taking place. Rest in bed for months, the constant ajiplication of an ice-bag, daily applications of iodoform-collodion, and the internal adminis- tration of potassium iodid can be warmlv recommended : CONSTRICTION AND OCCLUSION OF THE AORTA 71 K Iodoform, 1.0 (15 grains) ; Collodion, 10.0 (2^ fluidrams).— M. Apply topically. R Solution of potassium iodid, { ^^ gi^fluidluncesr ' Dose : 1 tablespoonful thrice daily. Not much can be expected from astringents (plumbic acetate, tannic acid, ergot, solution of ferric chlorid). Surgical treatment has been variously recommended for aortic aneurysm, especially the introduction of gold needles connected with the positive pole of a galvanic current, so called electro- puncture, or the introduction of foreign bodies (watch-spring, horsehair, silk thread ^), in order to induce coagulation within the sac. Injections of solution of fei'ric chlorid are probably not free from danger of embolism. Subcutaneous injections of 100 or 200 c.c. of physiologic salt- solution containing one or two per cent, of white gelatin have also been employed with advantage. — A. A. E. Ligation of the right subclavian and carotid has been proposed in the treatment of aneurysm of the arch of the aorta. Among individual conspicuous symptoms severe neuralgia especially re- quires often the frequent employment of morphin subcutaneously. CONSTRICTION AND OCCLUSION OF THE ISTHMUS OF THE AORTA (ISTHMUS AORTAE PERSISTENS). The junction of the arch of the aorta with the descending aorta, where the duct of Botal enters into the aorta, is known as the isthmus of the aorta. In newborn children a constriction of the lumen of the aorta exists at this point, and which gradually disappears. Under some conditions the constriction may persist, or the aorta may even become closed. The distribution of blood to and the nutrition of the lower half of the body can then be effected only through the collateral paths that arise from the aorta above the isthmus, and anastomose with arteries that arise from the aorta below the isthmus. These collateral channels, which are scarcely ever seen in healthy persons, become tortuous, pul- sating, and vibrating vessels distended to the size of a finger, and over which, frequently, also cardiac-systolic murmurs can be heard. This is an important and distinctive diagnostic phenom- enon. The following principal collateral paths may be men- tioned : 1. Subclavian artery, internal mammary artery, anterior inter- costal arteries and superior intercostal artery, posterior intercostal arteries, thoracic aorta. ^ Success has also attended the introduction of long coils of gold wire through which a galvanic current is passed. — A. A. E. 72 CIRCULATORY ORGANS 2. Subclavian artery, transverse artery of the neck, dorsal artery of the scapula, posterior intercostal arteries, thoracic aorta. 3. Subclavian artery, transverse scapular artery, subscapular arteries, posterior intercostal arteries, thoracic aorta. 4. Subclavian artery, internal mammary artery, superior epi- gastric artery, inferior epigastric artery, iliac artery. The character of the femoral j)ulse is noteworthy, being greatly retarded in comparison with the apex-beat of the heart, and being further characterized by its slight fulness. The left ventricle undergoes dilatation and hypertrophy in consequence of the re- duction in the aortic blood-current, and frequently death has been observed to take place from rupture of the heart or cerebral hem- orrhage. In other instances paralysis of the heart takes place gradually, with weakness of the myocardium and general venous stasis. Patients may, hoAvever, attain great age. Nothing is known as to the causes of the condition. About one hundred cases have thus far been reported. The treatment is confined to the relief of prominent symptoms. EMBOLISM OF THE AORTA. Emboli in the aorta are mostly derived from detached thrombi and vegetations on the aortic or mitral valves, less commonly from cardiac thrombi in the left ventricle or from perforating tumors or echinococcus-cysts of the heart. Thrombi in aneu- rysms or upon arteriosclerotic lesions in the aorta may also become detached and be swept into the aorta as emboli. If the orifice of the aorta be occluded by an embolus, sudden death occurs, because the supply of blood to the heart-muscle and to the brain ceases. Frequently emboli reach the point of bifurcation of the aorta, upon which they ride, sending branches into both common iliac arteries. The patients then complain mostly of sudden pain in the lower extremity with the lodgment of the embolus. The femoral pulse is wanting, and the extremities appear pale and feel cold like those of a corpse. The function of the sensory and motor nerves is abolished, with the development of anesthesia and motor palsy in the e.vtremities. If an adequate collateral circula- tion do not develop promptly, gangrene of the extremities takes place, and the patients die in consequence of septicemia. From a therapeutic point of view the physician is powerless in the face of such conditions. PART II. DISEASES OF THE RESPIRATORY ORGANS. I. DISEASES OF THE NOSE. NASAL CATARRH (CATARRHAL RHINITIS), Ktiology. — Catarrhal inflammation of the nasal mucous membrane, also designated coryza, is a most ividespread disease. Although every person is probably attacked by coryza more than once during his life, it appears that the tendency to suffer from this disorder is a variable one. Delicate, pale, and slightly built persons are attacked by coryza with especial frequency and readi- ness. Scrofulous persons, also, are in marked degree susceptible to the disorder, and likewise persons who are exposed to the inhalation of dust and irritating gases. Among the causative factors infectious, toxic, and traumcdic (mechaniccU) influences may be especially mentioned ; to these may be added extension of con- tiguous inflammcdion. Infectious rhinitis may occur either as an independent and 'primary disease, or as a secondary disorder in the sequence of other infectious diseases, such as influenza, measles, typhoid fever. Primary infectious rhinitis is often attributed to exposure to cold ; but even though it be conceded that coryza may quickly follow such exposure, this, in all probability, acts only as a contributing influence, lowering the resistance of the tissues and affording better opportunity for the invasion and propagation of lower forms of organisms capable of exciting inflammation (bacteria) by inducing changes in the circulation in the nasal mucous mem- brane. It is true that nothing positive is yet known as to the nature of these bacteria. Bacteriologic examinations have dis- closed the presence of bacteria in the nasal secretion, but as a matter of course nothing is thereby demonstrated, as bacteria can also be found in the nasal mucus of healthy persons, being taken up from the inspired air by the moist mucous membrane. There seems scarcely any doubt that coryza possesses a considerable 73 74 REsriUATony organs degree of contagiousnesH, and among careful laymen it is, there- fore, a rule not to kiss any one suffering from the disorder. Toxic rhiiiiti.^ may l)e induced by agents taken internally, thus through the l)lood, or by the inhahition of irritating gases. It is well known tliat coryza may result from the ingestion of potas- sium iodid or potassium bromid. It may likew'ise follow inhala- tion of tiie vapors of hydrochloric acid, nitric acid, chlorin-gas, and the like. TrauiiKiiic (niechanicd/) rhinitis is at times a result of the inha- lation of dust, and therefore occurs frequently as an occupation nasal catarrh. Foreign bodies that have penetrated the nares also frequently give rise to rhinitis. Those who indulge in snuff often suffer from catarrhal rhinitis, this substance, irritating the nasal mucous memljrane in part mechanically, in part chemically. At times catarrhal rhinitis arises by extension from adjacent disease, and it may occur, for instance, in association with ab- scesses of the gums. Symptoms, Diagnosis, Anatomic Alterations, and Prognosis. — A distinction is made between acute and chronic catarrhal rhinitis in accordance with the duration and the course of an attack of coryza. In many cases acute coryza begins like and pursues the course of an acute infectious disease. The patients frequently at first feel languid for hours, and even for days, as if worn out, and they not rarely fear the onset of some serious dis- order. Chilliness and febrile movement give added justification for anxiety. Soon, however, local alterations in the nose make their appearance. A burning and prickling sensation becomes appreciable in one nasal passage, or in both. The nares become impassable to the current of air, and speech acquires a nasal quality. In a short time a tendency to frequent sneezing becomes manifest, and finally an unusually active secretion takes place from the nasal mucous membrane, so that in the course of a day a large number of handkerchiefs are soiled. The nasal secretion is at first thin, like water, colorless, and of a salty taste ; after a while it becomes less abundant, more viscid, and greenish and purulent, because round cells in large number have become added to the secretion originally deficient in cellular elements. If the upper lip is moistened by the nasal secretion, slight redness and swelling of the skin develop. In the course of a few days the manifestations described usually begin to disappear, and in some a feeling of almost remarkable freshness sets in. The anatomic alterations can be best followed with the aid of a nasal mirror during life. ^Marked redness and swelling of the nasal mucous membrau(\ accumulations of mucus and pus, and here and there also small hemorrhages can be ol>served. Complications occur especially through extension of the inflam- mation to adjacent mucous membranes. Pain on either side of the NASAL CATARRH 75 root of the nose, often severe and distressing, is dependent upon niflammation of the mucous membrane of the frontal sinuses. Painful sensations in the upper jaw indicate involvement of the antrum of Highmore. Marked lacrimation and active redness and swelling of the conjunctiva indicate that the inflammation has attacked the lacrimal duct and the conjunctiva. Catarrh of the mucous membrane of the Eustachian tube (tinnitus aurinm, impairment of hearing), and especially inflammation of the middle ear, constitute unpleasant accidents. Catarrh of the mucous mem- brane of the pharynx, larynx, trachea, and bronchi is not rarely superadded to that of the nasal mucous membrane. Chronic catarrh of the nasal mucous membrane frequently de- velops from repeated attacks of acute nasal catarrh, especially if recurrence takes place before the preceding attack has been cured. In other instances, however, chronic coryza appears in its chronic form from the outset. The result depends in part upon the causa- tive factors. Patients with chronic coryza suffer from impermea- bility of the nares, so that they are compelled to breathe with the mouth open. As a result the facial expression acquires a stupid appearance, and the deficient warming of the inspired air predis- poses to inflammatory afiPections of the upper air-passages. The sense of smell, and, in connection therewith, the sense of taste appear impaired. Speech becomes nasal. Usually purulent se- cretion i^s formed in excessive amount, which in part dries upon the mucous membrane as grayish-green crusts and mussel-like deposits, and often can be expelled only with great difficulty by blowing the nose. At times the inflamed nasal mucous membrane secretes an abundance of thin fluid, and this condition has been designated rhinorrhea. On rhinoscopic examination it is found that a distinction must be made between hypertrophic and atrophic chronic nasal catarrh. In the presence of chronic hypertrophic catarrhal rhinitis the nasal mucous membrane appears thrown into folds and thickened, so that the nasal passages are constricted. The mucous membrane is grayish or brownish-red in color, and widely dilated and tortuous blood-vessels are often visible upon it. In addition there are pres- ent considerable deposits of mucus and pus and desiccated grayish- green crusts. Chronic atrophic catarrhal rhinitis may develop from the hypertrophic variety, but appears to occur also as an inde- pendent affection. The nasal mucous membrane is characterized by pallor and attenuation, so that the nasal cavity is noteworthy for its unusual roominess. Microscopic examination of the nasal mucous membrane discloses absence of erectile tissue, collection of round cells in the subepithelial layer of the mucous membrane, and transformation of the ciliated epithelium into squamous epi- thelium, whicli in part is cornified. Experience has shown that chronic atrophic rhinitis develops especially in persons with 76 RESPIRATORY ORGANS broad, depressed nasal bridges, and that in some families it is hereditary. Chronic coryza may be attended with various complications, of which ozena is especially annoying. Often this is a sequel of atrophic rhinitis, while in other instances ulcers have formed upon the nasal mucous membrane, and have extended from this to the bony substructure, and thus maintain an offensive nasal discharge. It is, therefore, customary to make a distinction between simple ozena and ulcerative ozena. Xot rarely the inflamed nasal mucous membrane undergoes hyperplasia and nasal polypi develop. At times reflex neuroses arise, and these have been observed with especial frequency in association with hypertrophic catarrh. Among such reflex neuroses bronchial asthma, ocular diseases, psychic dis- turbances, even deformities of the thorax, scoliosis, and a tendency to abortion have been described, although some of the statements must be received with a certain amount of skepticism. Unpleasant complications may arise from extension of the chronic i njlarnmatary process from the nose to contiguous mucous membranes. Among these may be mentioned chronic inflammation of the frontal sinuses, the antra of Highmore, the ear, and the pharynx. Although chronic coryza is a disorder scarcely dangerous to life, it is never- theless a most obstinate and a trying disease. Treatment. — Prophylactic measures may be employed in the case of delicate persons and those exposed to the inhalation of dust and irritant gases. In an attack of acute febrile coryza recumbency in bed should be recommended, with the ingestion of hot infusions (pectoral species, elder-flowers, linden-flowers — a tablespoonful to two cups of hot water). In addition, inhala- tions of hot steam afford great relief. Attempts have been made to abort acute coryza, and for this purpose the following formula of Hagen-Brandt has a certain reputation : R Carbolic acid, 5.0 (75 grains); Alcohol, 15.0 (.} fluidounce) ; "Water of ammonia, 6.0 (75 minims); Distilled water, 16.0 (4 fluidrams).— M. Keep in a dark bottle with a glass stopper. Dose : A few drops poured upon three or four sheets of thick bibulous paper, and inhaled every two hours, with the eyes closed, so long as an odor is appreciable. Severe frontal pain is best relieved by means of salicylic acid, sodium salicylate, or phenacetin (1.0 — 15 grains — thrice daily). In the treatment of chronic coryza various snuffs and irrigations (nasal douche) have been employed. Astringents and disinfectants have been recommended for the latter purpose. I prescribe irrigation of the nares, morning and evening, with carbolic acid (2.0 : 200) or solution of aluminum acetate (2.0 : 200), and then insuflflation into the nose of a small amount of the following powder : HA Y-FEVER 77 R Mercurous chlorid, 3.0 (45 grains) ; Alum, 5.0 (75 " ).— M. Use as a snufF. In the treatment of hypertrophic rhinitis the galvanocautery is used a good deal. Crusts can be removed by repeated injec- tions of hikewarm solution of sodium chlorid (1.5 : 200). In the treatment of ozena I have observed the best results from the use of iodoform as a snuff, while internally potassium iodid (5.0 : 200 — a tablespoonful thrice daily) may be employed. Ulcers should be cauterized with silver nitrate. Change of residence not rarely exerts a favorable influence in cases of chronic coryza ; for instance, a sojourn by the sea. FIBRINOUS INFLAMMATION OF THE NASAL MUCOUS MEMBRANE (FIBRINOUS RHINITIS) ♦ Fibrinous inflammation of the nasal mucous membrane is rare. It is attended with the formation of fibrinous membranes upon the surface of the nasal mucous membrane, and which can be detached without loss of substance. Among the causative factors are especially chemic and infectious agencies. The disorder may thus occur at times in consequence of cauterization of the nasal mucous membrane. In some instances it is excited by diphtheria- hacilli, which usually find lodgment upon the nasal mucous membrane in the sequence of pharyngeal diphtheria, and rarely independently, and give rise to nasal diphtheria. It is probable, however, that a number of other as yet but little known bacteria are capable of" giving rise to fibrinous inflammation of the nasal mucous membrane. This is true especially of those cases in which the condition develops in conjimction with other infectious diseases (measles, scarlet fever, typhoid fever, fibrinous pneumonia). The symptoms consist in obstruction of the nares and in nasal discharge, which may acquire a putrid character. The diagnosis is easy when fibrinous membranes are extruded or are visible on rhinoscopic examination. The treatment consists in irrigation of the nose with carbolic acid (from 1.0 to 4.0 : 100), mercuric chlorid (1.0 : 100), or lime- water. HAY- FEVER (AUTUMNAL CATARRH). il^tiology. — Hay-fever is known also as Bostock's catarrh, because it was first thoroughly described by Bostock in 1819. It occurs either as a severe catarrh of the nasal mucous membrane, or as asthma, or as a mixed form. It is attributed to inhalation of the pollen of the G-ramineae, as pollen-grains have been found in the nasal and lacrimal secretions of patients. In support of the etiologic significance of the pollen of plants is the fact that the 78 RESPIRATORY ORGANS manifestations of hay-fever appear just at the time when grasses and irniins are in bloom, and that many are only attacked in pass- inu' a l)l()()niing- meadow or a Lrraiii-tield. Nevertiieless a certain predisposition to the disease exists, ■which is to he sought for in an acquired or conoccnital, or even inherited, neuropathic state. Accordinjilv, individuals in the higher walks of life are attacked (cultured persons, menrhants) most frequently. The disease is especially prevalent in America, where the neuropathic state is quite common. Within a few years it has appeared to me that the disease is gradually l^eeomiug more common among us. Symptoms and Diagnosis. — Xot rarely the symptoms of hay-fever develop immediately in the sequence of preceding injury, and some are attacked by the disease whenever they inadvertently come into proximity with a blooming meadow, or perhaps in going about are compelled to pass a hay-Avagon. Uay-cori/za is mani- fested by a sense of prickling, of burning, and of a foreign body in the nose. The patients sneeze frequently, and are unable to obtain air through the nose. Speech becomes nasal. In a short while an abundant, watery, salty nasal discharge sets in. Exten- sion of the nasal catarrh to the lacrimal canal and the conjunctiva is attended with profuse secretion of tears, and with redness and swelling of the conjunctiva. At times the tegumentary covering of the nose becomes deeply reddened. Many patients suffer from .severe frontal headache in consequence of catarrh of the frontal sinuses, and are as a result incapacitated from work. At times chilliness and slight febrile movement are present. The disorder may persist for weeks, during the entire period that the Graminese are in bloom, and it is further characterized by the unpleasant fact that it habitually recurs whenever opportunity is afforded for the inhalation of pollen. Hay-asthmfi entirely resembles ordinary bronchial asthma, and accordingly manifests itself in attacks of shortness of breath, attended with expiratory dyspnea especially, and loud snoring and whistling rales. Pollen has been found in the sputum, in addition to asthma-crystals. In the mixed forms of hay-fever the disease most frequently begins as a corvza, with which asthma subsequently becomes associated. Prognosis. — Hay-fever, although not dangerous to life, is a most obstinate disease, and not rarely renders its victims incap- able of pursuing their vocation for weeks. Treatment. — The treatment should in the first place be pro- phylactic. An existing neurotic state should be attacked by the ]irescription of a sensible mode of life, by means of cold-water treatment, residence at the seaside, and nervines. Hay-fever has frequently been found in association with al)normal distensibility of the nasal mucous membrane, and cauterization of this mem- brane has, therefore, been recommended. In addition, the patients must avoid exposure to inhalation of pollen, and often for this CATARRH OF THE LARYNX 79 reason they must change their residence. I have observed good results in the treatment of hay-coryza from the use of a snuff of calomel and alum : JR Calomel, Alum, each 3.0 (45 grains) ; Morphin hydrochlorate, 0.3 (4i " ).— M. Use thrice daily as a snufl'. Irrigation of the nose with a solution of quinin has also been praised (1.0 : 740). Hay-asthma may be most certainly relieved by means of narcotics ; for instance, by a subcutaneous injection of morphin. MYCOSIS NASL In isolated cases molds {Aspergillus), filamentous fungi {Botrytis Bassiana), and budding fungi [O'idium albicans, thrush fungus) have been found upon the nasal mucous membrane, and yellowish-gray or greenish fungous masses in the nasal discharge. In treatment irrigation Avith carbolic acid (from 1.0 to 5.0 : 200), mercuric chlorid (1.0 : 1000) and insufflation of boric acid may be practised. II. DISEASES OF THE LARYNX. CATARRH OF THE LARYNX (CATARRHAL LARYNGITIS), Ktiology. — Catarrh of the laryngeal mucous membrane is one of the most widespread diseases. Delicate, anemic, and debili- tated individuals are especially predisposed to the affection. The causes are almost the same as those responsible for nasal and bron- chial catarrh. A distinction must be made here also between infectious, chemic, thermic, and traumatic (mechanical) causes, to Avhich may be added laryngeal catarrh by extension from adjacent disease, and hypostaiic catarrh. Infectious catarrh of the larynx may be primary or secondary. Secondary catarrh develops in the sequence of other preceding disease ; for instance, whooping-cough, measles, influenza, pulmo- nary tuberculosis, syphilis. Primary infectious catarrh of the larynx is also variously known as rheumatic or refrigeratory, as formerly it Avas attributed to the influence of cold (rheuma). While this influence in the development of laryngeal catarrh cannot be denied, and although this is observed to occur with especial frequency in northern and rugged regions, and in the spring and autumn at the time of variations in the weather, the influence of cold appears to be confined to the circumstance that 80 RESPIRATORY ORGANS the lower teraperatufe provides favorable conditions for the inva- sion of certain bacteria, through altered blood-distribution and diminished powers of resistance, whereas the actual excitants of the disease are bacteria with their toxins. Accurate information as to the nature of these Ijacteria is, it is true, as yet wanting. In harmony with the infectious nature of the catarrhal conditions of the larynx under consideration is the fact that the disease, like many other infectious diseases, not rarely occurs in epidemic dis- tribution. Infectious laryngeal catarrh must further be included amono^ those infectious diseases that leave a marked tendencv to repeated attacks. Laryngeal catarrh due to cheniic injiuences may result from in- halation of irritating gases (vapors of hydrochloric or nitric acid or of chlorin) or develop after the ingestion of certain substances, among which potassium iodic! and potassium bromid are the best known. In the latter event the substances are eliminated from the blood through the laryngeal mucous membrane, in which they excite inflammation. Laryngeal catarrh is a common manifesta- tion in alcoholics. Perhaps cheraic influences are operative in the production of the laryngeal catarrh of patients sufiering from renal disease. Among the thermic causes of laryngeal catarrh is inhalation of hot vapors. Laryngeal catarrh due to traumatic {mechanical) injiuences is frequently au occupation-catarrh, and accordingly of chronic nature. Prolonged speaking, singing, or commanding is a common cause of chronic catarrh of the larynx in teachers, ministers, actors, public speakers, singers, and officers. In other individuals catarrh of the larynx results from the inhalation of dust and smoke (mil- lers, glovers, stone-cutters, smokers). Ilypostatic catarrh of the larynx develops in conjunction with chronic disease of the heart and of the respiratory organs, when the flow of blood from the vente cava; to the right auricle is inter- fered with, because the action of the right ventricle is thereby impaired and all of the blood is not sent into the pulmonary artery with each systole. Laryngeal catarrh by extension from adjacent disease is at times secondary to similar disease of the nose or of the pharynx above, or of the bronchi and the trachea below. Symptoms, Anatomic Alterations, and Diagnosis. — The symptoms of catarrh of the larynx require especial consid- eration, accordingly as the condition is acute or chronic. Acute catarrh of the larynx not rarely pursues the course of a febrile, infectious disease, with initial chill and fever. In other instances elevation of temperature is wanting. In diagnosis the local alter- ations are naturally the most significant. The patients usually complain first of a sense of tickling and of irritation in the larynx. CATARRH OF THE LARYNX 81 The congli is often especially annoying toward evening and during the night, and thus disturbs sleep. At first a small amount of viscid, transparent mucus is expectorated with difficulty (sputum crudiuii). Only after some time does the expectoration become more abundant and looser — that is, more readily ejected — opaque, and greenish-yellow (sputum coccum). If the vocal bands are involved in the catarrhal process, the voice is changed, becom- ing veiled, impure, and in marked cases completely toneless. The reason for this resides most frequently in the fact that the inflamed and thickened vocal bands are no longer capable of coming in accurate approximation during speech. The anatomic alterations attending acute catarrh of the larynx may be most accurately studied with the aid of the laryngoscope^ much more accurately than on the cadaver, because after death the alterations (hyperemia, swelling) may have receded to a con- siderable degree. The inflamed parts are characterized by exces- sive distention with blood, and correspondingly appear abnormally reddened. Here and there an isolated tortuous and distended blood-vessel can be recognized. Besides, the inflamed areas are swollen. The secretion of the mucous membrane is also greatly increased, and raucous and purulent deposits are often seen upon the surface of the mucous membrane. IVot rarely these have formed between the vocal bands, so that long strands of mucus and pus are visible in this situation in phonation. At times the distention of the mucous membrane with blood is so great that vessels rupture and the interior of the larynx is covered with free blood. If this be removed with a camel's-hair brush, under the guidance of the laryngoscope, it rapidly reaccuraulates at times. The expectoration is at the same time bloody, and the patients are thrown into a great state of alarm by the fear of pulmonary tuber- culosis, of which they consider the expectoration of blood a certain precursor. This variety of laryngeal catarrh has been designated hemorrhagic laryngitis. At times the epithelial layer of the laryn- geal mucous membrane is exfoliated in places, with the develop- ment of catarrhal erosions and ulcers. In some cases the inflammatory exudation extends to the laryngeal muscles, with the development of paralysis of individual muscles. Most frequently the arytenoid and the internal thvro- arytenoid are affected (gaping of the posterior third of the chink of the glottis — cartilaginous glottis — in the first, and of the anterior two-thirds — ligamentous glottis — in the latter case in phonation. In children signs of laryngeal stenosis appear suddenly at times, and disappear within a short time. As the symptoms resemble those of laryngeal diphtheria or of croup, the con- dition has been designated pseudocroup. The children often are awakened during the night with a cry that they are suffocating. 82 RESPIRATORY ORGANS Respiration is labored ; inspiration is stridulous ; the face presents an expression of fear and is cyanotic ; inspiratory retraction of tlie intercostal spaces is visible ; and the signs of embarrassed brcatiiin«: are evident. In tiie course of a few hoars the threaten- ing numifestations usually subside, but they may be repeated on succeeding nights. The condition is distinguished from laryngeal diphtheria by the absence on laryngoscopic examination of diph- theric deposits in the larynx, disappearance spontaneously as a rule of the danger of suffocation, and the possible repetition of the paroxysm a number of times. The symptoms of pseudocroup may be induced by various diseases, especially by marked SM'elling of individual laryngeal structures (false vocal bands, interarytenoid fold, mucous membrane below the true vocal bands), paresis of individual laryngeal muscles, or accumulation of mucus above the true vocal bands, with adhesion of these structures. Pseudocroup is rare in adults because, as compared with children, the larynx is much more commodious. Acute laryngeal catarrh usually terminates within a few days, and but rarely lasts longer than two weeks. CJironie catarrh of the larynx either occurs as an independent affection or it develops in the sequence of a preceding acute catarrh, when this has recurred a number of times, particularly if the recurrences set in before the previous acute attack has ended. Certain causes (occupational influences, stasis, pulmonary tubercu- losis, nephritis) are especially calculated to give rise to chronic catarrh of the larynx. Chronic laryngeal catarrh is luiattended Avith febrile movement unless an acute exacerbation of a chronic inflammatory condition takes place. A sense of irritation, of tick- ling, and of the presence of a foreign body in the region of the larynx, and a rough and hoarse voice are the principal symptoms. Examination with the laryngoscope discloses not a bright-red or rose-red appearance, but rather a brownish-red color of the laryn- geal mucous membrane. The thickening of the mucous memlirane depends less upon infiltration with fluid than u])on an inflammatory hyperplasia of the mucosa and submucosa. In addition there is increased secretion of mucus. In cases of chronic laryngeal catarrh also catarrhal erosions and ulcers may form. At times there develop, especially on the true vocal bands, proliferations and thickenings of the epithelium in the form of warts. A similar condition is observed especially in persons compelled to strain the laryngeal structures (singers, speakers), and it has been designated pacht/dcrmia of the larynx. In singers and speakers nodules form also at the free margin of the vocal bands, in consequence of connective-tissue hyperplasia, so-called singers' vocJes. Active hyperplasia of the follicles of the mucous membrane causes the interior of the larynx to present a gramdar surface — r/ranular laryngitis. If the true vocal bands especially are nodular, the CATARRH OF THE LARYNX 83 condition is designated tuberous cliorditis. Circumscribed hyper- plasia of the laryngeal mucous membrane leads to the formation of pendulous tumors, laryngeal polypi and papillomata. At times the mucous membrane of the inferior surface of the true vocal bands is involved in active hyperplasia {chorditis vocalis hyper- trophlca inferior), and the mucous membrane beneath the vocal bands can be seen to project toward the median line like a fish- bladder, and constrict the chink of the glottis. Should the hyper- plasia become excessive, suffocation may result from stenosis of the chink of the glottis. Some clinicians consider syphilis as the cause of these alterations. Paralysis of the laryngeal muscles also not rarely takes place in conjunction with chronic catarrh of the larynx. Chronic laryngeal catarrh is a troublesome affection, which sometimes never disappears. It interferes with the pursuit of one's vocation, and may compel the adoption of another. Prognosis. — The prognosis of acute catarrh of the larynx is almost always favorable. Chronic catarrh of the larynx also rarely endangers life, but recovery can only be hoped for when the causes of the disorder can be permanently removed. Occu- pational catarrhs are frequently attended with insurmountable difficulties. Treatment. — Certain prophylactic measures should not be overlooked by the careful clinician. These include intelligent hardening and the avoidance of inhalation of dust and vapors and of excessively loud and long-continued speaking and singing. In cases of acute catarrh of the larynx rest in bed is to be advised when fever is present. In addition hot infusions may be adminis- tered (pectoral species, elder-flowers, linden-flowers, one table- spoonful to two cups of hot water) and a narcotic prescribed for the laryngeal irritation ; for instance : R Bitter-almond water, 10.0 (2J fluidrams) ; Morphin hydrochlorate, 0.1 (li grains). — M. Dose : 10 drops for laryngeal irritation. Or, R Morphin hydrochlorate, 0.003 (-^ grain) ; Sugar, 0.3 (4J grains).— M. Make 10 such powders. Dose : 1 powder for laryngeal irritation. Or, R Powder of ipecacuanha and opium, Sugar, each 0.3 (4| grains).— M, Make 10 such powders. Dose: 1 powder for laryngeal irritation. Or, R Potassium bromid, 1.0 ( 15 grains); Morphin hydrochlorate, 0.02 (^ grain). — M. Sugar and tragacanth sufficient to make 10 troches. Dose : 1 troche every hour or two. 84 RESPIRATORY ORGANS As long as the inflamed laryngeal nmcous membrane secretes viscid mneiis inhalations of alkalies by means of Siegle's appa- ratus (sodimn chlorid, from 1.0 to 5.0:100; sodium bicarbon- ate, from 1.0 to 5.0:100; sodium carbonate, from 1.0 to 5.0: 100; potassium bromid, from 1.0 to 3.0:100) may be recom- mended at intervals of two hours. AVhen the secretion subse- quently becomes more abundant and more diffluent, the alkalies should be replaced bv astringents (argentic nitrate, from 0.1 to 1.0:100; tannic acid, from 1.0 to 3.0:100; alum, from 1.0 to 3.0:100; solution of aluminum acetate, from 0.3 to 1.0: lOOj. In cases of hemorrhagic laryngitis inhalations of solution of ferric chlorid (from 0.1 to 0.3 : 100) should be employed. When symptoms of pseudocroup arise the fears of the patient should be allayed by gentle encouragement. In addition deriva- tives should be applied to the skin of the neck (alcoholic frictions, sponges dipped in warm water). Should the shortness of breath increase in a noteworthy degree an emetic should be administered (solution of copper sulphate, 1.0 : 100 — a dessertspoonful every ten minutes until vomiting is induced ; or solution of apomorphin hydrochlorate, 0.2 : 10.0 — one-quarter of a hypodermic syringe- ful subcutaneously). Only rarely will it be necessary to resort to intubation or tracheotomy. Chronic laryngeal catarrh is usually treated locally by means of inhalations, applications, or insufflations. In the employment of any of these measures the rule should be observed to change the medicament after the lapse of a few days, as the mucous mem- brane readily becomes accustomed to the remedy, and then no longer reacts thereto. In practising the procedures named, astrin- gents are employed, although it is advisable to use stronger solu- tions than in the treatment of acute laryngeal catarrh. For insufflation into the larynx tannic acid (0.1 — 1^ grains), plumbic acetate (0.05 — -| grain), or alum (0.1 — 1-t grains) is employed. At times it is necessary to institute causative treatment, and, for in- stance, in cases of syphilis to employ preparations of iodin and mercury, or in the presence of hypostatic catarrh digitalis and other heart-tonics. Those who can afford it will do well in the presence of obstinate chronic catarrh of the larynx to take a course of treatment during the summer at a bathing-resort. The alkaline- chlorin springs (Ems, Selters, Wiesbaden, Gleichenberg), saline baths (Soden, Reichenhall, Baden-Baden, Ischl), sulphur-springs (Neundorf, Weilbach, Stachelberg, Baden near Vienna, Baden in Switzerland. Schinznach, Mehadia, Eaux Bonnes), and earthy springs (Lippspringe, Weissenburg), deserve especial consideration in this connection. Ulcers of the larynx should be cauterized with the stick of silver nitrate, while laryngeal polypi and pajjillomata should be removed by operative measures. In cases of chorditis vocalis EDEMA OF THE GLOTTIS 85 hypertrophica inferior an endeavor should be made to cause the disappearance of the hyperplasia by means of potassium iodid (5.0 : 200, a tablespoonful thrice daily), and when the dyspnea attains threatening proportions intubation or tracheotomy should be practised. Dilatation of the chink of the glottis l)y means of sounds also has been attempted. I have effected a cure in a number of cases of obstinate chronic laryngeal catarrh in the treatment of which all possible remedies had previously been employed without result by means of inhalations of compressed air and faradization of the larynx. EDEMA OF THE GLOTTIS, Anatomic Alterations. — Edema of the glottis consists in infiltration of the submucous tissue of the larynx with transuda- tion or exudation. Accordingly, a distinction is made between hydropic and inflammatory edema of the glottis. In cases of in- flammatory edema of the glottis the fluid poured out into the submucosa may be serous, seropurulent, purulent, and in rare cases even bloody. A circumscribed accumulation of pus is designated an abscess of the larynx. The diseased laryngeal structures are conspicuous for their great increase in volume, and if they be punctured fluid usually escapes, when the mucous mem- brane covering the previously swollen structures becomes wrin- kled and collapsed. Further, the swelling has not rarely sub- sided in the cadaver. In cases of hydropic edema of the glottis the mucous membrane often presents an exceedingly anemic hue, while in cases of inflammatory edema, on the other hand, the mucous membrane may be deeply reddened, although here also a paler hue is present when the accumulated fluid has made the blood-vessels of the mucous membrane empty through pressure. Edema of the glottis is usually best developed upon the epiglottis and the aryepiglottic folds, because in these situations the sub- mucosa is looser and provided with a more abundant network. The structures named are often converted into distorted swellings as thick as a finger, which obstruct the entrance into the larynx. Accordingly, the false vocal bands and the region of the aryte- noid cartilages are with especial frequency the seat of edematous swelling. ^l^tiologfy. — Hydropic edema, of the glottis develops with espe- cial frequency in the course of cachectic diseases and of conditions . of stasis, of which nephritis, pulmonary tuberculosis, carcinoma, and chronic diseases of the heart and lungs may be mentiohed as examples. At times local causes of stasis are present in the veins of the laryngeal mucous membrane (goiter, enlargement of lymph- atic glands, mediastinal tumors, aortic aneurysm), and under such conditions the edema of the glottis may be unilateral and circum- S6 RESPIRATORY ORGANS scribed. Inflammatory edema of the r/lottis occurs most frequently in association with disease of the larynx, as, for instance, after inrtanunation, ulceration, in association witli larvngeal perichon- dritis, after inhahition of hot vapors, irritating gases, dust, after injuries of the larvnx, and after the inspiration of foreign bodies. At times tlie disorder develops in the sequence of infectious dis- eases, among which typhoid fever, pneumonia, and erysipelas may be mentioned. It occurs at times as a collateral edema in cases of parotiditis, angina, and angina Ludovici. Rarely edema of the glottis is of angioneurotic origin, developing in conjunction with angioneurotic edema of the skin and of the jiharyux. Occasionally edema of the glottis has been observed to occur without demonstrable cause — >lace, the peculiarly deep tym- panitic percussion-note, which has been designated by Biermer as the box-note, and also the displacement of the margins of the lungs. Both of these depend upon the fact that the inspired air still enters the pulmonary alveoli with comparative facility, but is unable to escape completely during expiration. As a result BRONCHIAL ASTHMA 115 overfilling of the lungs with air must take place, and acute pulmonary distention thus occurs. Only after termination of the asthmatic paroxysm does gradual escape of air from the lungs take place, so that now the boundaries of the liver, which were displaced downward, and the semilunar space have risen to their usual situation, and the area of cardiac dulness, diminished during the attack, resumes its ordinary extent. The respiratory murmur is not audible, as a rule, during the attack, among other reasons because it is suppressed by the loud sonorous and sibilant rales. The individual attack lasts, as a rule, for several hours, and terminates sometimes rapidly, sometimes gradually. Some patients will be exempt from attacks for months, while in others they may be repeated daily. With the termination of an attack mucopurulent expectoration takes place. Often, but by no means regularly, the asthma-crystals and spirals discovered by v. >^.>.. Fig. 20.— Asthma-crystals from the expectoration in a case of bronchial asthma ; magni- fied 275 times (personal observation, Zurich clinic). Leyden can be found. Asthma-crystals are pointed double pyra- mids that often lie in groups in small opaque plugs of sputum. Further, they do not occur in bronchial asthma alone, but they are encountered also in bronchial croup and in the expectoration in cases of echinococcus of the lungs. I have found them also in pleural exudates. They have been found in the blood, the bone- marrow, the juice of the spleen, and in other organs in cases of leukemia. In contradistinction from the sperm- crystals that resemble tliem, asthma- crystals are not four-sided, but six-sided, on transverse section. The spirals also have been found not alone in association with 116 RESPIRATORY ORGANS bronchial asthma, but also in cases of fibrinous pneumonia and of bronchial catarrh. They represent coiled, often also fibrillar, filaments, which on microscopic examination not rarely display a bright central thread in their axis, around which at times bright threads yet wind (Fig. 21). In all probability asthma-spirals result from the expression of bronchial secretion through narrow orifices. Fig. 21. — Asthma-spirals from the sputum in a case of bronchia] asthma; magnified 275 times (personal observation, Zurich clinic). Crystals of calcium oxalate (octahedra, envelop-shaped) and of acid cal- cium 'phosphate are rarely found. Prognosis. — Although bronchial asthma is a distressing dis- order, often persisting throughout life, it scarcely ever causes death, for, when the cyanosis becomes excessive, the spasm of the bronchial muscles relaxes or the acute swelling of the bronchi sub- sides, in consequence of carbon-dioxid narcosis, and the attack comes to an end. Treatment. — An attackofastlima can be most speedily relieved by subcutaneous injection of morphin : R Morphin hydrochlorate, 0.3 (42- grains) ; Glycerin, Distilled water, each 5.0 (75 minims). — M. Dose: from 0.2o to 0.5 (4 to 8 minims) subcutaneously. However, the asthmatic patient should never be entrusted witli a syringe and a solution of morphin, as the danger of morphinism is too great. This danger renders it necessary for the physician to make use of morj)hin only in the excessively severe attacks, and when these do not occur too frequently. At times, however, the patients have themselves accidentally (liseovered certain means of amelioration ; for instance, the illumination of dark rooms. A large number of remedies have been recommended for the relief of this distressing affection, among which sometimes the one, at ALVEOLAR EMPHYSEMA OF THE LUNGS 117 other times another, will prove efficacious. Thus, many patients are relieved when paper that has been dipped in a solution of potassium nitrate is burned in the room. Others use instead of such paper so-called asthma-cigarets, which generally contain stramonium and belladonna. Great stress should be placed in treatment on preventing recurrence of the attacks. This indica- tion is met by prophylactic and causal treatment. Thus, the patient should carefully avoid such odors and articles of food as experi- ence has shown to be capable of readily inducing an asthmatic attack. Existing diseases of the nose, the pharynx, etc., should be carefully treated. In the presence of chronic bronchial catarrh the employment of compressed or rarefied air should be recom- mended (apparatus of Waldenburg, Geigel, and Mayer, pneumatic cabinets). Pasty and arthritic patients should undergo courses of treatment at Carlsbad, Marienbad, Tarasp, Vichy, or at similar springs. At times it is an advantage to attack existing nervous- ness by means of a strict diet and an appropriate mode of life. In this connection change of residence is not rarely of great service. Some patients are free from asthma at mountainous elevations. Among internal remedies potassium iodid and bromids may be espe- cially recommended. In some cases, also, I have found arsenic to be of much good : Or, R Solution of sodium bromid, 15.0 : 200 ; Potassium iodid, 5.0 (75 grains). — M. Dose: 1 tablespoonful thrice daily after eating. R Solution of potassium arsenite, Bitter-almond water, each 5.0 (75 minims). — M. Dose : 10 drops thrice daily after eating. V. DISEASES OF THE LUNGS. ALVEOLAR EMPHYSEMA OF THE LUNGS. Anatomic Alterations. — Alveolar emphysema of the lungs gives rise in the first place to dilatation of the alveolar and infun- dibular spaces. In addition there occurs atrophy of the alveolar septa, so that adjacent alveoli coalesce. Adjacent infundibula also enter into communication with one another, and as a result unusuallv large air-spaces form in the lungs. As may be under- stood, destruction of elastic tissue and of pulmonary capillaries is an associated phenomenon. Accordingly, alveolar emphysema of the lungs gives rise to diminution in the elasticity of the lungs, and to increase of blood-pressure in the pulmonary artery. 118 RESPIRATORY ORGANS On microscopic examination an accumulation of fatty granules is found around the alveolar epithelium, with atrophy of the elastic fibrous net^'ork, and fatty degeneration of the pulmonary capillaries. The last form a loose network, and are remarkably straight, and in places occluded or interrupted. A di.stinction can be made between local, unilateral, and bilat- eral alveolar emphysema of the lungs. The emphysematous por- tions are conspicuous for their defi(;iency in blood and in pigment, their light-rose color, an absence of crepitation and a downy con- sistence on palpation, and the presence of large air-sacs, which at times project beneath the pulmonary pleura as thin transparent bladders up to the size of an apple. The median anterior and the lower margins of the lungs are especially predisposed to emphy- sematous alterations. In cases of bilateral alveolar em/jJii/sema of the lungs the thorax is often remarkable for its barrel-like shape. On opening the chest the lungs do not collapse. The lungs cover the heart with their median bonders, and upon both sides have pushed the diaphragm markedly downward. Their margins appear swollen and rounded, and even with the unaided eye large air-spaces can be made out in them. Usually chronic bron- chial catarrh exists in addition to alveolar emphysema of the lungs. The heart exhibits dilatation and hypertrophy of the right ventricle, and frequently signs of venous stasis are present. Ktiology. — Alveolar emphysema of the lungs may be induced by respiratory disturbances of most varied kind, provided these give rise to permanent increase in the intra-alveolar air-pressure. Most frequently such disturbances are effective during expiration, less commonly during inspiration. Alveolar emphysema of the lungs developed durinr/ inspiration is observed in cases of catarrh of the finer bronchi (bronchiolitis), when, with swelling of the bron- chial mucous membrane, the power of the muscles of inspiration is yet sufficient to aspirate air into the pulmonary alveoli, although expiration is too feeble to force the air out again through the constricted bronchial tubes. Exactly these conditions are present 2C'hen spasm of the bronchial muscles takes place, such as has been observed in some cases of bronchial asthma, and in the presence of foreign bodies in the bronchi. Under all such circumstances the pulmonary emphysema is preceded by acute distention of the lungs, which may even undergo involution when the causes are removed. Expiratory alveolar emphysema of the lungs may de- velop in connection with all chronic diseases attended irilh cough. For this reason chronic bronchial catarrh is one of the commonest causes of the disorder. In efforts at cough the air in the lungs is exposed to excessive pressure because the thorax and the dia- phragm are contracted in expiration, while the chink of the glottis is at the same time closed. The same conditions attend all ex- pidsive efforts, and it is, therefore, not surprising that pulmonary emphysema is observed in those who play wind-instruments, in ALVEOLAR EMPHYSEMA OF THE LUNGS 119 Singers, speakers, and such persons as are compelled to carry heavy weights. Mountain-climbers also not rarely suffer from emphysema of the lungs. A special form of alveolar empliysema of the lungs is known as vicarious or compensatory alveolar eiaphy- sema of the kings, which develops when some portions of the lungs are prevented from taking part in the respiratory process, so that other portions are compelled to assume the functions of the inac- tive lung. Vicarious alveolar emphysema is not rarely unilateral if the respiratory disturbance involves the opposite lung. Pul- monary emphysema occurs most commonly in men and after the period of puberty, which is readily comprehensible from the nature of the causative factors. Symptoms and Diagnosis. — In cases of bilateral alveolar emphysema of the lungs the shape of the chest is often conspic- uous, the thorax being barrel-shaped, dilated, in a permanent inspiratory position, and emphysematous. The respiratory move- ments of the chest are restricted, and on pressure upon the thorax increased resistance is generally found, which is dependent upon premature ossification of the costal cartilages. Percussion yields a deep, slightly tympanitic percussion-note (box-note), as the tension of the pulmonary tissue has been diminished. The expiratory diminution in respiratory pressure may be demonstrated directly by means of the pneumatometer (the normal expiratory pressure = from 30 to 60 mm. of mercury).. The vital capacity of the lungs also, which the spirometer shows to be between 2000 and 4000 c.c. in healthy persons, is reduced in cases of pulmonary emphysema. On auscultation the diminished intensity of vesicular breathing is striking. The area of cardiac dulness is unusually small, or it has completely disappeared, if the median borders of the lungs completely overlie the anterior surface of the peri- cardium. The heart-sounds are remarkably faint, as tlie lung over- lying the anterior aspect of the heart intercepts their trans- mission. Tlie upper limit of hepatic dulness is unusually low (in healthy persons in the right mammillarv line between the sixth and seventh ribs) and upon the left the semilunar space is much re- duced. It is noteworthy, further, that the respiratory displace- ment of the lower maro-ins of the luno^s is exceedins^lv slio^ht. At times the heart is pushed so far down that not only is its pul- sation visible in the epigastrium, but also its right border can be felt. In the presence of unilateral alveolar emphysema of the lungs, the manifestations described are confined to the side of the chest containing the emphysematous structures. Alveolar emphysema of the lungs is not rarely attended with complications. Almost constantly bronchial catarrh is present, and it may seriously aggravate the existing respiratorv disturbances. At times a subpleural empliysematous vesicle ruptures, and pneumothorax develops. Not rarely the vigor of the right ven- 120 RESPIRATORY ORGANS tricle gradually fails, and signs of venous stasis appear (cutaneous edema, hypostatic urine, ascites, hypostatic liver, hypostatic catarrh of the stomach and intestines, hydrothorax, hyperemia of the brain, cyanosis, etc.). A large proportion of emphysematous patients die as a result o^ excessive stasis and of suffocation, after perhaps it had been possible at first to overcome the manifesta- tions of stasis. Prognosis. — The prognosis of alveolar emphysema of the lungs is unfavorable, inasmuch as recovery is impossible. On the other hand, however, vicarious pulmonary emphysema must be looked upon as a favorable development. The tendency of emphysematous patients to chronic bronchial catarrh and to myo- cardial insufficiency is particularly troublesome. Life may, never- theless, be prolonged for many years. Treatment. — Prophylactic measures should be directed to the avoidance of persistent increase in the inspiratory and expiratory alveolar air-pressure, or the removal of such as may be present. Recovery from or improvement in pulmonary emphysema by means of internal remedies is impossible. At times some relief is obtained through pneumato therapy. To this end the apparatus of ^yaldenburg or of Geigel and Mayer, or pneumatic bells, may be employed. As in cases of pulmonary emphysema the act of expiration is especially disturbed, the patients should be made to expire into rarefied air. Gerhardt suggested, further, rhythmic compression of the thorax during expiration. INTERSTITIAL EMPHYSEMA OF THE LUNGS. Ktiology. — Interstitial emphysema of the lungs is a rare disease Avhich results from the escape of air from the pulmonary alveoli into the interalveolar and interlobular connective tissue of the lungs. Often the air passes in the connective tissue accompanying the bronchi to the hilus of the lung and into the mediastinal connective tissue, whence it finds its way into the sub- cutaneous connective tissue of the neck, and even beneath the skin of the trunk and of the extremities. The air may also find its ^vav beneatli the pulmonary pleura, which it may raise in the form of air-containing vesicles, and these may at times be arranged at the boundary between adjoining lobules like a string of pearls. Should subpleural air-vesicles rupture, pneumothorax will develop. Among the causes of this disorder are severe efforts at cough- ing and expulsive efforts, extreme dyspnea, ulcerative disease of the lungs and bronchi, contusions of the tliorax and the lungs, too vigorous insufflation of air into the larynx for asphyxia of the newborn. The diagnosis of interstitial jmhnonarii cmphiffpearance — serous expectoration — so that it has been compared with white of es:g that has been beaten into snow and subsequently liquefied, and with soapsuds. Its color is usually light yellowish or reddish, from admixture with blood. If pulmonary edema be superadded to fibrinous pneumonia, the expectoration acquires the appearance of prune- juice. The presence of considerable quantities of fluid in the air-passages frequently gives rise to loud bulibling rales over the chest, and the plienomenon has also lieen designated as boiling in the chest. If expectoration be interfered with and fluid accumu- late in the trachea, the tracheal rales so much and justly feared CATARRHAL INFLAMMATION OF THE LUNGS 125 develop, and which so frequently appear in the death-struggle. The patient suffering from pulmonary edema exhibits signs of objective dyspnea, which are manifested in accelerated breathing, inspiratory retraction of the intercostal spaces, participation of the auxiliary muscles of respiration, cyanosis, and, in consequence of increasing accumulation of carbon dioxid in the blood, in progres- sive stupor. Pulmonary edema may cause death within a short time from suffocation. In other instances it persists for days, or appears and disappears repeatedly, so that a distinction must be made between acute, chronic, and recurrent pulmonary edema. Prognosis. — The prognosis of pulmonary edema is serious on all occasions, as the condition is often dependent upon incurable disorders ; and besides, whenever the edema is extensive, there is danger of death from suffocation. Treatment. — In cases of pulmonary edema venesection is indicated as an important measure should the pulse be strong. Bandaging of fh'e extremities (by means of rubber tubing or compresses), in order to diminish the flow of venous blood to the right heart, is a less reliable procedure. In addition, stimulants and expectorants should be employed to increase the force of the heart and to clear the air-passages through increased expectoration ; for instance : R Powdered digitalis-leaves, 0.1 (Ij grains) ; Benzoic acid. 0.3 (42- grains) ; Camphor, 0.05 ( f grain) ; Sugar, 0.5 (7+ grains). - -M. Make 10 such powders. Dose : 1 powder every two hours. The administration of strong wine can be warmly recommended. If the patients are unable to swallow, camphorated oil may be in- jected subcutaneously (15 minims from every two to four hours), and dry cups and mustard-plasters or alcoholic frictions to th« chest should be prescribed. CATARRHAL INFLAMMATION OF THE LUNGS (CATARRHAL PNEUMONIA) » Htiology. — Catarrhal pneumonia is always a secondary dis- order, developing in the sequence of preceding inflammation of the smaller bronchi — bronchiolitis. The disease is, therefore, also designated bronchopneumonia. In some instances the inflammatory process extends directly from the bronchial mucous membrane to the pulmonary alveoli, while in others exciting agents of inflammation are aspirated from the bronchial tubes into the pulmonary alveoli, where they give rise to secondary inflammation. Bacteria are looked upon as the exciting agents of inflammation, although vari- ous kinds must be taken into consideration. Frankel's pneumonia- 12() CIRCULATORY ORGANS cocci, which act also as the causative agents of fibrinous |3neu- raonia, are found with especial frequency. The Streptococcus pyogenes and the Staphylococcus pyogenes aureus and albus are next in frequency as exciting factors. Friedliinder's pneumococci have also been described as causative agents. The bacteria named are frequently found in the inflammatory foci in pure culture. Occasionally other specific bacteria are found accidentally; as, for instance, diphtheria-bacilli. A(/e has an important influence upon the development of catarrhal pneumonia, for the disease, as a rule, attacks cJi'ddren or the (if/ed. Diminislied powers of resistance on the part of the pulmonary tissue, smallness of caliber of the bron- chial tubes in children, and deficient activity of respiratory move- ment in the aged may be responsible factors. Delicate, anemic, rachitic, and scrofulous children are attacked with especial fre- quency, as well as those compelled to live in over-crowded, dusty rooms with an insufficiency of light and of air. Catarrhal pneu- monia occurs with especial frequency in connection witli infectious diseases, particularly in children with measles, whooping-cough, and di])htheria. It occurs not seldom in the form of a foreign- body pneumonia or an aspiration-pneumonia, when saliva, food, or fluid gains entrance into the air-passages and reaches the alveoli of the lung. Similar conditions are observed in those profoundly ill (typhoid fever), in the debilitated (carcinoma, pulmonary tuber- culosis), in those suffering from paralysis of the muscles of deglu- tition (bulbar paralysis, pharyngeal diphtheria), and in C(mnection with frequent vomiting and regurgitation ("carcinoma of the esoph- agus). Inhalation of irritating gases must also be considered a cause of catarrhal pneumonia. Anatomic Alterations. — Areas of catarrhal pneumonia are almost always situated at the surface of the lung, where they are conspicuous for their dark-red color and dense, airless consistency. On section no air can be expressed, but in contradistinction from atelectatic areas, which are not rarely found side by side, the pneumonic areas cannot be filled with air from the bronchus, and when placed in water they sink to the bottom. Usually numerous small foci of inflammation are found, which exhibit a lobular arrangement ; hence the name lobular or insular pneumonia. These are usually especially numerous in the posterior and infe- rior portions of the lungs. At times they coalesce and involve the larger portion of a pulmonary lobe. With comparative frequency they form airless bands, which begin at the side of the vertebral column at the base of the lung and extend upward, growing grad- ually smaller and smaller. Generally the inflammatory areas are situated in both lungs. The lung on section is usually smooth, although granular areas of inflammation occur which to a certain degree represent a transition to fibrinous pneumonia. Such a transition may be observed also microscopically. Although the CATARRHAL INFLAMMATION OF THE LUNGS 127 majority of the pulmonary alveoli are filled with a fluid exudate consisting of blood-plasma, desquamated and swollen alveolar epithelial and round cells, fibrinous coagula can be detected in others. In addition to atelectasis, vicarious pulmonary emphysema is not rarely found in association with catarrhal pneumonia. Hyperemia, hemorrhage, and fibrinous deposits upon the pleura are also common. The bronchial glands are usually enlarged and hyperemic. Symptoms and Diagnosis. — It is often extremely difficult to detect the presence of areas of catarrhal inflammation in the lungs, because, by reason of their small size, they are not acces- sible to the methods of physical examination and are often con- cealed behind the manifestations of bronchial catarrh. Suspicion of bronchopneumonia should always be aroused when, in addition to signs of bronchial catarrh, high fever (above 39° C. — 102.2° F.) persists for a number of days. In the diagnosis auscultation is of especial value, frequently disclosing the presence of bronchial breathing and ringing rales over even small bronchopneumonic areas. Duluess on percussion can be expected only when inflam- matory areas have coalesced and attain a circumference of five centimeters and a thickness of two centimeters. Even then light percussion is necessary. The impaired percussion-note is likely to be at the same time tympanitic, as the tension of the pulmonary tissue is diminished. Usually signs of disturbed interchange of gases in the lungs are conspicuous, as manifested by accelerated and frequently gasping and moaning respiration, by inspiratory retrac- tion of the intercostal spaces, participation of the auxiliary muscles of respiration, and cyanosis. Often there is distressing cough; but both children and the aged are given to swallowing the sputum, so that this is rarely submitted for inspection. It is then found to be mucopurulent and free from peculiarity. On coughing and on deep inspiration pain in the chest is frequent in conse- quence of over-stretching of the thoracic muscles. The course of catarrhal ])neumonia may be acute, subacute, or chronic, and extend over a period of from two to eight weeks and more. Not rarely improvement and aggravation alternate with each other. Death results as a rule in consequence of asthenia or of suffoca- tion. Not rarely progressive stupor develops toward the close of life in consequence of excessive accumulation of carbon dioxid in the blood (carbon-dioxid narcosis). There may also be twitchings in some muscles and Cheyne-Stokes breathing. Should the dis- ease terminate in recovery, this takes place but slowly ; a crisis does not occur. Further, the symptoms of bronchial catarrh fre- quently persist for a long time after those of the pneumonia have subsided. Among complicaUons pleurisy, pericarditis, endocarditis, and nephritis may be mentioned. At times miliary tuberculosis develops and leads to a fatal termination. 128 RESriRArORY onaANS Prognosis. — Catarrlial ])neuni<)nia is always a serious affec- tion. In sonic epidemics of measles and whooping-cough the largest proportion of children attacked by bronchopneumonia die. The more extensive the inflammatory process, and the higher the fever, the greater is the danger to life. Treatment. — Individuals with catarrhal pneumonia should be placed ill a bright and airy room, which can be ventilated directly in the summer, and in the winter through an adjacent room. The air of the room should be kept moist by placing a solution of sodium chlorid (0.7 per cent.) or of carbolic acid (2 per cent.), or creosote or oil of turpentine (15 drops on the surface of water), in a vessel upon a stove during the winter, or by diffusing one of these three or four times a day by means of a suital)le spray- apparatus during the summer. In addition a bath at a tempera- ture of from 26° to 28° R. (90.5° to 95° F.) and of from fifteen to thirty minutes' duration should be given at nine o'clock in the morning and at four o'clock in the afternoon. If the fever be persistently high, an effort should be made to reduce it by means of a cold pack or phenacetin (from 0.3 to 0.5 — 4|- to 7^ grains). Expectorants should be prescribed to remove the secre- tion from the air-passages ; for instance : R Infusion of ipecacuanha-root, 0.3 : 100.0 (4V grains to 3} fluidounces). Simple sirup, 20.0 (5 fluidrams). — M. Dose : 5 c.c. (1 teaspoonful) every two hours. Should, nevertheless, excessive accumulation of carbon dioxid in the blood or of secretion in the bronchial tubes take place, a warm bath should be prescribed, while cold water is poured from a considerable height upon the chest. The resulting deep respira- tory movements will then help to clear the air-passages. It may also be useful in the warm bath to direct a stream of cold water against the upper portion of the cervical spine, in order to stimu- late the respiratory center to greater activity. After recovery from the disease a sojourn in the country or in the woods should be urgently recommended. FIBRINOUS INFLAMMATION OF THE LUNGS (FIBRINOUS PNEUMONIA). Ktiolog'y. — Fibrinous pneumonia, often designated also croupous pn(>unionia, is an exceedingly common infeciiov.s. disease, by which almost 4 per cent, of the community are attacked annually. The pneumoniacoccus of Friinkel acts as the carrier of the infection, although it has been maintained that in a small number of insUuices other bacteria also induce the disease. The pneumoniacocci of Frankel are somewhat long structures, in shape resembling a candle-flame, which are surrounded by a bright capsule and FIBRINOUS INFLAMBIATION OF THE LUNGS 129 are arranged usually in pairs, but frequently also in groups of several within a common capsule'(Fig. 22). They have, therefore, also been designated diplococcus jmeumo/iice s. lanceolatus. They occur also in the saliva of healthy individuals, and cause death in rabbits, with septic manifestations, so that they have also been designated sputum-cocci or cocci of sputum- FiG. 22.— Pneumoniacocci of Frankel from pneumonic sputum. Gentian-violet stain; oil-immersion ; magnified 1000 times (personal observation, Zurich clinic). septicemia. It is noteworthy that, in contradistinction from the pneumonia- cocci of Friedlander, which resemble them, and which for a time were erroneously considered as the exciting agents of fibrinous pneumonia, they can be stained by Gram's method. Although infection with the pneumoniacocci of Frankel is essential for the development of fibrinous pneumonia, there are certain conditions that favor infection of the lungs — so-called con- tributory causes of the infection. Among these exposure to cold occupies the most conspicuous place, while traumatism and pre- ceding infectious disease are less commonly operative. In over- crowded barracks, prisons, and reformatories, extensive epidemics of pneumonia have at times occurred, obviously because the air was contaminated and filled with pneumoniacocci. Transmission of the disease from one person to another or through the intermedia- tion of a third person has also been observed. Frequently, how- ever, no contributory cause can be elicited, and the condition is then designated a genuine or pjrimary fibrinous pneumonia. Like most infectious diseases, fibrinous pneumonia also occurs sporadic- ally and epidemically. Epidemics occur especially in the spring months, from March to May. Experience has shown that men are attacked more commonly than women. Individuals debilitated by disease, advanced age, or alcoholism exhibit a more marked predisposition to the disease than others. The disorder spares no 9 130 RESriRATORY ORGANS period of life, and not rarely attacks chiklron. There is an undeniable tendency to repeated rdtachs, so that some persons pass through more than twenty attacks of fil)rinous pneumonia in the course of their lives. Anatomic Alterations. — The inflammatory alterations of fibrinous pneumDuia do not occur in numerous lobular areas like those of catarrhal pneumonia, but, as a rule, involve the entire lobe of a lung, or still more, whence the designation lobar pneu- monia. It is customary to distinguish several stages of the in- flammatory process, and to designate these congestion, hepatization, and resolution. In the stage of inflammatory congestion the pulmonary capillaries are dilated and tortuous. Blood-plasma is thrown out into the pulmonary alveoli ; at the same time round cells and also red blood-corpuscles accumulate in the alveoli, while the alveolar epi- thelial cells become detached and are in part desquamated. In. the stage of hepatization the lung presents a characteristic appearance. On removal of the organs it is noteworthy that in the area of inflammation the impression of the ribs upon the surface of the lungs is visible, because the lungs have obviously increased in volume. The pleura probably is unexceptionally clouded, and covered with fibrinous membrane, if, as is the rule, the inflammation has extended to the surface of the lungs. The condition is thus usually one of fibrinous pleuropneumonia. On palpation the lung yields the impression of an airless, solid struct- ure. On section its granular surface is striking, suggesting the appearance of a section of liver, whence the name hepatization. The granular condition is due to coagulation of the primarily fluid alveolar exudate. For this reason the hepatized portions of lung present in the aged and in emphysematous patients with large pulmonary alveoli a coarsely granular, and in children Avith small pulmonary alveoli a finely granular, appearance. The mucous membrane of the supplying bronchial tubes is reddened and swollen, and the fibrinous inflammation has not rarely ex- tended to the smaller bronchial tubes, so that they contain bron- chial casts or fibrinous coagula. Less commonly the larger bron- chial tubes also are filled with fibrinous casts, and the condition is then designated ntassive pneumonia. At the outset the hepa- tized pulmonary tissue exhibits a red color — stage of red hepati- zation. The more, however, the over-distention of the pulmonary blood-vessels subsides the more does the tissue present a grayish color — star/e of gray hep(di~ation, which ultimately gives place to a yellow color — stage of yellou- hepatization, as soon as active fatty degeneration takes place in the inflammatory products. As a rule, the inflammation develops in diflerent portions of the lungs at different times, so that generally various stages of hepatization are present side by side. In consequence the lung acquires a FIBRINOUS INFLAMMATION OF THE LUNGS 131 mottled appearance, which has not inappropriately been desig- nated as marbled or granite-like. This appearance is especially marked when the diseased lung contains a good deal of melanin. In the stage of resolution liquefaction of the coagulated alveolar exudate takes place in conjunction with mucoid and fatty degen- eration, perhaps also in consequence of digestion by bacteria, the liquefied masses are expectorated or absorbed, the pulmonary alveoli again receive air, and gradually the lung resumes ita normal appearance. On microscopic examination of the lungs during tlie stage of hepatizatiorr the pulmonary alveoli will be found filled with a fibrinous network, in the' midst of which lie round cells, red blood- corpuscles, and alveolar epithelial cells. The fibrinous network is especially dense at the periphery of the pulmonary alveoli, while the cells are more numerous toward the center of the alveoli. Pneumoniacocci are present, partly free, partly enclosed in cells. In the stage of resolution the fibrinous network undergoes disinte- gration into small granules, and active fatty degeneration takes place in the round cells and the alveolar epithelium. Fibrinous pneumonia occurs most frequently in the lower lobe, particularly on the right side, and least commonly in the right middle lobe. At times inflammatory foci are present in both lungs — pneumonia jibrinosa dwplex. If under such conditions corresponding lobes are not involved on both sides, for instance, the right lower and the left upper lobe, the condition is designated pneumonia jibrinosa cruciata. If all the lobes of one lung are involved, the condition is known as pneumonia totalis. The situation of pneumonia most commonly in the lower lobe of the right lung is explained by the fact that foreign bodies (pneumoniacocci) more readily enter this lung through its larger bronchus, and on account of its greater aspirating force, and that these by reason of their weight readily find their way into the lower lobe. Persons dead of fibrinous pneumonia usually exhibit signs of suffocation and of constitutional infection. The right heart and the veins are generally filled with blood, the heart with ham-fat clot and masses of coagula, while the left heart contains no blood. The muscles of the trunk and the extremities appear dry and of the color of ham, and exhibit, on microscopic examination, gran- ular turbidity, fatty and vitreous degeneration of the muscle-fibers. Similar histologic alterations are present in the fibers of the heart- muscle. The liver-cells, the parenchymatous cells of the gastric and intestinal glands, the epithelial cells of the uriniferous tub- ules, and the parenchymatous cells of the pancreas exhibit gran- ular cloudiness and fatty degeneration. Swelling and hyperemia of the bronchial glands are constant manifestations of fibrinous pneumonia, and result from absorption of the inflammatory agents from the diseased lung. The spleen is frequently but not con- stantly enlarged, and of diminished consistency (acute infection- spleen). 132 EESPrn. 1 TOR Y OR a A NS Symptoms. — Fil)rin()ns pncuimonia belongs to the class of cijclic acute j'c/ji-i/e iiijcctioim diseases, as it pursues a typical course, and terminates usually within two weeks, with manifestations of a crisis. Two groups of plionomona must be distinguished : In the first place, the local manifestations, and in the second tiie feb- rile constitutional manifestations. The hitter are probably due to the entrance into the circulation of toxins generated by the pneu- moniacocci. The period of incubation — that is, the interval be- tween the occurrence of infection and the development of the first symptoms of the disease — apj^ears in many instances to be only a few hours, although it may be from two to four days, and at times Fig. 23.— Typical tciiipLTatnre-curvo n of the lung occurs at times in the sequence of suppuration, ulceration, and inflammation, in the distribution of the inferior vena cava, thus in conjunction with jmerperal ])rocesses, interstitial ulceration, etc. Ulcerative endocarditis involving the right side of the heart also affords opportunity for the development of embolic pulmonary abscesses. At times suppuration in the lungs is excited by rupture of suppurative processes in adjacent organs, as, for instance, pleural SUPPURATION OF THE LUNG 143 empyema, pyopericardium, abscess of the liver and of the spleen, and burrowing abscess of the vertebral column. Suppuration of the lung is not a common disorder, and is only exceptionally observed in childhood. Anatomic Alterations. — In accordance with the number of foci present a distinction must be made between single and mul- tiple abscess of the lung. Multiple abscesses of the lung occur especially as a result of hematogenous influences and of the aspi- ration of food. Pulmonary abscesses vary greatly in size. At times they are barely visible (^miliary abscess of the lung), while in other instances they involve the largest part of a pulmonary lobe. Accordingly as the pus lies free in the pulmonary tissue, or is sur- rounded by a membrane resulting from interstitial pneumonia, the condition is designated a. free or an encapsulated pulmonary abscess. The former is distinguished by an irregular villous wall, the latter by a smooth wall. It may further happen that the encapsulation is incomplete. The a,mount of pus varies, and in addition to the size of the purulent focus, it depends especially upon the fact whether copious expectoration has taken place shortly before death. Symptoms and Diagnosis. — The most important phenom- enon for the recognition of an abscess of the lung is the peculiar expectoration. This is purulent, diffluent, and abundant, so that it may be as much as 500 c.c. in the course of a day. It usually gives off an acid, buttermilk-like odor. Of especial significance is the occurrence of shreds of pulmonary tissue, which on micro- scopic examination exhibit a gray or a blackish color, as well as the alveolar structure of the pulmonary tissue. They may attain the size of a phalanx of the thumb. At times hematoidin-crystals are found in the sputum, and if the disease pursue a chronic course cholesterin-plates also may be present. Frequently, expectoration in niouthfuls is noteworthy. The patients expectorate but seldom, although on each occasion such large amounts of pus are expelled as to be frequently discharged from the mouth and the nose, and, if they in part reenter the esophagus and the larynx, to give rise to vomiting and renewed cough. Of importance also is the attitude of the patient, who usually lies constantly upon the affected side, in order that the secretion may collect for a long time before it reaches the mouth of the entering bronchus and excites cough ; in the presence of centrally situated purulent foci in the lungs the expectoration may be the only means by which it is possible to recognize the affec- tion, while from the attitude of the patient the lung in which the lesion is situated may be suspected. The local conditions found in the lung vary accordingly as the abscess-cavity is filled with pus or contains air, between manifestations of airlessness and those 144 RESPIRATORY ORGANS of ciivity-formation. The course of suppuration of the lung is usu- ally acute. Generally there is fever, which often exhibits a hectic character. The patients attract attention on account of pallor, a tendency to sweating, anorexia, in short, on account of septic mani- festations. Death may result from increasing asthenia, or from complications, such as gangrene of the lung and pyopneumothorax. At times a focus of suppuration in the lung ruptures externally, and gives rise to extensive burrowing beneath the skin. Complete recovery may, however, take place, leaving only circumscribed retraction of the chest and dulness on percussion. Prognosis. — Although the prognosis of suppuration of the lung is always serious, recovery not rarely occurs. Treatment. — Tn the first place, an effort should be made to sustain the bodily strength by means of a nutritious diet. In addition balsamics and disinfectants should be employed to prevent sujjpuration and decomposition of the pus ; for instance : R Oil of turpentine, 10.0 (2^ fluidrams). Dose: 10 drops in milk thrice daily. Oi R Creosote, 0.15 (2i minims). Make 100 such gelatin-capsules. Dose : 1 capsule every two or three hours. Abscesses of the lungs have in a niuuber of instances been sub- jected to operative intervention, Mhich has resulted in recovery in about 60 per cent, of the cases. GANGRENE OF THE LUNG. Ktiology. — Gangrene of the lung is characterized by the occurrence first of moiiification and then of putrid decomposition of the necrotic pulmonary tissue. The first alteration results from an enormous invasion by pyogenic cocci, especially the various forms of Staphylococcus pyogenes, while the putrefaction is induced by the putrefactive bacteria (Leptothrix pulmoiialis, oidium, Bacte- rium coli commune, etc.). Pulmonary gangrene is not a common disorder, and experience has shown that it occurs most frequently in men between the sixteenth and the fortieth year of life. It may be of bronchogenic, alveolar, or hematogenous origin. At times putrid bronchitis extends to the pulmonary tissue, and gives rise to gangrene of the lung. Aspirated foreir/n bodies and particles of food also not rarely cause pulmonary gangrene. Sometimes this condition has been observed in the sequence of carcinoma of the lips and of the tongue, and of operations upon the oropharyngeal cavity, when ]>utrid masses of degenerated a)id disintegrcded material have gained entrance into the larynx, and thence more deeply into the bronchial tubes and alveoli, and have excited inflammation and GANGRENE OF THE LUNG 145 putrefaction in the lungs. At times the exciting agents of disease gain entrance only after preceding rupture into the bronchial tubes, as, for instance, in the sequence of carcinoma of the esophagus, burrowing abscesses attending tuberculosis of the vertebrse, sup- puration of the bronchial glands, new-growths and suppuration in the mediastinum, carcinoma of the stomach, gastric ulcer, etc. Among the alveolar causes fibrinous and less commonly catarrhal pneumonia should be mentioned first. Drunkards and debilitated persons are especially exposed to the danger that pneumonia may be transformed into gangrene of the lung. Abscess of the lungy pulmonary tuberculosis, carcinoma of the lunr/, and echinococcus of the lung, may also give rise to gangrene of the lung. Occasionally pulmonary gangrene occurs in the sequence of injuries to the lung. Among such factors are not alone gunshot wounds, stab-wounds, and punctured wounds, but also blunt injuries, such as contusions of the thorax, and a long time may elapse before the gangrene supervenes upon the injury. Hematogenous gangrene of the lung may be due to pulmonary embolism. This occurs especially when emboli are derived from putrid foci, as, for instance, in cases of septicemia, caries of the mastoid process, abscess of the liver or of the brain, gangrene and diphtheria of the skin. Certain con- tributory causes may favor the occurrence of gangrene of the lung. Among these may be mentioned alcoholism, asthenia, over-crowd- ing, and deficient ventilation of living-rooms. Pulmonary gangrene has occasionally been observed to occur endemically under such con- ditions. Gangrene of the 1 ung occurs not rarely in cases of diabetes. Anatomic Alterations. — It is customary to make a distinc- tion between circumscribed and diffuse gangrene of the lung, accord- ingly as the gangrenous area is sharply demarcated from the healthy pulmonary tissue, or gradually passes into healthy tissue without sharp limitation. The diseased pulmonary tissue at first appears as a friable, brownish, and putrid or offensive-smelling mass, which suggests the appearance of an erosion effected with potassium hydroxid. The tissue gradually undergoes softening, and its products usually find exit externally through a bronchus. If expectorated, it is replaced by a gangrenous pulmonary cavity, which at first exhibits a ragged and villous inner surface. This cavity may be gradually encapsulated by connective tissue, which forms in consequence of interstitial pneumonia, and the formation of granulations upon the inner surface may eventually lead to oblit- eration of the cavity. The number and the size of the gangrenous areas in the lungs are subject to wide variation. At times a single area may occupy an entire lobe, or even an entire lung. Usually the gangrenous foci are situated at the surface of the lung, and this is especially true of embolic foci. The bronchi generally exhibit signs of inflammation, and their mucous membrane may also suffer loss of structure. 10 146 RESPIRATORY ORGANS Symptoms, Diagnosis, and Prognosis. — In the recoirni- tion of gaugrcne of the hmg the churaeter of the expectoration is decisive. In the first place, the sputum often diffuses an un- bearablij offensive odor, which is penetrating and has been com- pared with that of horse-radish. Often the air of the room is contaminated within the shortest period of time by the fetid odor. In some cases the expectoration loses its offensive odor when exposed to the air, but this becomes again unmistakably apparent as soon as the sputum is vigorously agitated in a vessel. The amount of expectoration not rarely reaches 500 c.c. and more per day, and its consistency is diffluent. In accordance with its prin- ■cipal constituents the sputum is mucopurulent, the purulent masses forming grayish-green opaque globules. The tendency of the ex- pectoration to form layers is noteworthy. On standing for some time four layers can be distinguished in the sputum. The upper- most is a frothy layer ; the next, one of purulent masses ; then follows a grayish-green, thin serous layer ; and the lowermost is a crumbling layer of sediment. The expectoration may acquire a reddish-yellow or clay-colored appearance, in consequence of the presence of disintegrated hemoglobin. In contradistinction from putrid bronchitis the presence of shreds of pulmonary tissue in the expectoration is decisive in diagnosis, and these may usually be readily recognized from their smoky-gray color. They may be larger than the extremity of the thumb, and consist merely of exfoliated pulmonary tissue. Their number varies widely. On microscopic examination the alveolar structure of the lungs can be detected. The contained elastic fibers have not rarely undergone destruction, probably in conse- quence of a digestive process, as ferments resembling trypsin have been obtained from the sputum. Frequently yellowish or even brownish particles, so-called Dittrich or mycotic bronchial plugs, are found in the sediment-layer of the sputum, and which, as has been disclosed on post-mortem examination, form in the bronchial tubes that enter the gangrenous area. If these plugs are compressed, they diffuse a peculiarly dis- agreeable odor. On microscopic examination they are found to consist mainly of bacteria, partly bacilli, and partly cocci. On addition of tincture of iodin the l^acteria largely acquire a violet or bluish color, like the leptothrix-fi laments in the mouth, whence the name Leptothrix pulmonalis. Further, only the interior of the leptothrix is stained violet or bluish, while the peripheral mem- brane appears bright yellow. At times thicker structures are found, with eel-like movement, and also spirilla. Infusoria have also been observed, monas lens and cercomonas. The former appears as a roundish glolnde with an oscillating flagellum, while the latter is of oblong shape with a tail-like process posteriorly, and one or two fla^ella anteriorlv. In addition to bacteria and GANGRENE OF THE LUNG 147 infusoria, needles of fatty acids, fat-globules, flakes of pigment, and hematoidin-crystals are also found in the bronchial plugs. At times expectoration is wanting in cases of pulmonary gan- grene, and only the offensive odor of the expired air is noted. The condition is to be distinguished from simple fetor of the breath originating in the mouth from the fact that the latter is not appreciable at a short distance from the patient, while the putrid odor of the expired air persists. Not rarely patients have them- selves first noticed this odor, which may create an aversion to food and drink. I have seen patients die of pulmonary gangrene who presented no other morbid manifestation than the horribly offensive odor of the expired air. Individuals with pulmonary gangrene unconsciously prefer the lateral decubitus upon the affected side of the body, in order that the fluid secretion may collect in the gangrenous cavity for as long a time as possible before reaching the mucous membrane of the afferent bronchus, and thus induce cough. When the gangrenous area is situated centrally the aifected side may be recognized from the attitude of the patient. The condition just described explains why the patients expectorate but seldom, though in great amounts — so-called expectoration in mouthfuh. The local pulmonary alterations consist either in signs of infil- tration (dulness on percussion, bronchial breathing, ringing rales, increased vocal fremitus and bronchophony) or in signs of a cavity (dull-tympanitic and even metallic percussion-note, bronchial or metallic-bronchial breathing, metallic-ringing rales, increased vocal fremitus and bronchophony, variation in the percussion-note be- tween dull and tympanitic accordingly as the gangrenous cavity contains secretion or after previous expectoration air). Patients with pulmonary gangrene usually attract attention by reason of their ashen-gray complexion, and they rapidly lose strength. Generally the temperature is elevated, and the fever may be of hectic type. The appetite is, as a rule, impaired, and diarrhea readily occurs in those who swallow their expectoration, in consequence of decomposition of the ingested food. The course of the disease may be acute, subacute, or chronic. At times death takes place from progressive asthenia within a few days. Nevertheless, the disease may terminate in recovery, and the signs of a cavity may recede in consequence of cicatrization, which is indicated by retraction of the chest and dulness on per- cussion. Not rarely improvement and aggravation of the disorder frequently alternate with each other. Complications are common. Among these one of the most serious is pulmonary hemorrhage. The danger of this accident resides especially in the fact that the blood (perhaps in conse- quence of the presence of ferments in the sputum) undergoes coagulation with difficulty, so that death may result from hemor- 148 RESPIRATORY ORGANS rhage. At times j)leurisy is superadded to gangrene of the lung. The fluid exudate may be serous, puruk'ut, or putrid, and in the presence of putrid pk'ural effusions that apparently occur without appreciable cause suspicion should always be aroused that they may liave been excited by a concealed focus of gangrene in the lung. Rupture of the pulmonary pleura will be followed by pneumotJwra.r, usually by liydropneumothorax. Strangely, the exudate under the conditions last named may be serous. At times rupture of the gangrenous process may take place externally, and long fistulous passages may form. Rupture into the mediastinum, into the pericardial cavity, into the esophagus, and through the diaphragm, has also been observed. In some cases metastases in distant organs take place through dissemination of pyogenic micro- organisms ; for instance, abscess of the brain or of the liver. I have also observed multiple painful swelling of the joints. Among the secondary condit'ions observed is the formation of drmnstick- finrfers, when pulmonary gangrene pursues a chronic course. Treatment. — ^^'ith reference to prophylactic measures, atten- tion may be directed especially to the importance of carefully feeding by means of the stomach-tube persons suffering from diffi- culty in deglutition. The treatment of pulmonary gangrene is based upon similar lines to those that govern that of suppuration of the lungs. A nutritious diet is prescribed, and the use of alcohol should be permitted for the purpose of sterilizing sputum that may have lieen swallowed. If possible the patient should be placed in a spacious room, which he should occupy alone, because contamina- tion of the air is injurious and the offensive odor of the expectora- tion and of the exjjired air would be extremely disagreeable to other occupants. The offensive odor of the expectoration can to a certain extent be neutralized by the introduction of J .0 or 2.0 (15 to 30 grains;) of naphthalin into the sputiun-cup, and covering this with a tightly closing lid. The room must be frequently and thoroughly ventilated. On fine days the patient should be exposed to the open air. Among internal remedies balsamics and disin- fectants may be recommended to restrict the secretion and decom- position ; for instance : R Oil of turpentine, 10.0 (21 ffuidrams). Dose: 10 drops thrice daily in milk. Or, Or, R Myrtol 0.15 (2J minims). ]\Iake 30 such gelatin-cajisules. Dose : 1 or 2 capsules every two or three hours. R Creosote, 0.15 {2h minims), ^lake 30 such gelatin-capsules. Dose: 1 capsule every two or three hours. It is advisable to place in the room three or four times daily vessels containing hot water to which 10 drops of oil of turpentine NEW-GROWTHS OF THE LUNG 149 or of creosote have been added, or in winter upon the stove or in the stovepipe, in order that the patient may inhale the vapor. The employment of inhalation-apparatus and inhalation-masks is less convenient to the patient, and in my experience does not yield better results. Operative treatment of pulmonary gangrene has also been attempted (incision and drainage or thermocautery), and recovery has followed in about 50 per cent, of the cases. NEW-GROWTHS OF THE LUNG. Ktiologfy. — Among tumors of the lungs only carcinomata and sarcomata are of clinical significance. Both varieties of new- growth usually develop secondarily. The organ primarily involved is at times remote from the lungs, at times in close proximity, so that under the latter conditions the new-growth extends directly into the lung, as, for instance, from carcinoma of the esophagus, the vertebral column, or the mammary gland. Primary carcinoma and sarcoma of the lungs are exceedingly uncommon. At times traumatism is assigned as the cause. Primary carcinoma of the lung has been observed frequently in miners in the cobalt-mines of Schneeberg, and has been attributed to the inhalation of dust containing arsenic. Both carcinomata and sarcomata of the lunges occur more commonly in men than in women, and they develop principally after the fortieth year of life. Sarcomata are considerably less common than carcinomata. Anatomic Alterations. — Carcinoma of the lung appears in two forms, either as an infiltrating growth, whose limits are not sharply circumscribed with relation to the healthy tissue, or as a nodular growth. The nodules vary in size. At times the lung is filled with innumerable small carcinomatous nodules, which sug- gest the appearance of miliary tubercles, whence also the designa- tion miliary carcinosis of the lung ; while in other instances a single carcinomatous nodule occupies almost an entire pulmonary lobe. jSTot rarely the nodules project from the surface of the lung as hemispherical tumors, whose centers exhibit a slight depression (carcinomatous umbilication). The number of carcinomatous nodules is, like their size, also susceptible of wide variation. All varieties of carcinoma have been observed in the lungs — the hard scirrhus, the juicy and soft medullary carcinoma, the alveolar car- cinoma, and the epithelial carcinoma. Primary carcinoma of the luug arises at times from the epithelium of the bronchial mucous membrane or of the bronchial glands, at other times from the alveolar epithelium. In cases of secondary carcinoma of the lung the elements of the disease gain entrance into the lungs partly through the lymphatics and partly through the blood-vessels. The neoplasm extends by preference from the hilus into the lungs, where it follows the ramifications of the bronchial tubes, advancing 150 RESPIRATORY ORGANS especially within the lymphatics of the peribronchial connective tissue. Experience has shown that primary carcinoma of the. lung involves most commonly the right upper lobe, while pulmonary sarcoma is more common in the left Iniig. Symptoms, Diagnosis, and Prognosis. — The most cer- tain symptom of carcinoma and sarcoma of tlie lung is the appear- ance of tumor-particles in the expectoration, although this occurs but seldom. At times such particles are demonstrable only micro- scopically, although in one case of sarcoma of the lung I have found in the expectoration pieces of new-growth as large as the end of the thumb. As may be understood, the expectoration of particles of new-growth can only take place if the tumor has pre- viously undergone softening, and the softened masses have ruptured into a bronchus. Not rarely hemorrhage takes place into sarco- mata and carcinomata of the lungs. There may thus at times be repeated hemoptysis, which becomes serious by reason of its pro- fuseness ; or if the blood is retained for some time in the air-passages, in consequence of transformation of the hemoglobin, a raspberry- jelly-like or currant-jelly-like, reddish or brownish-black, or even a greenish material, is expectorated, which is, to a certain degree, distinctive of the aifection, though it is also observed at times in cases of pulmonary tuberculosis. The local phenomena referable to the chest are variable. In the first place, neoplasms of the lung may conceal themselves behind a plcnrisij. Under such conditions bloody, fat-containing, and colloid exudates especially are suspi- cious. On microscopic examination of the fluid obtained by puncture, the presence of fatty granule-cells and of cells with numerous nuclei should be looked for. Miliary carcinosis of the lungs at times strongly suggests the clinical picture of miliary tuberculosis of the lungs. The patients attract attention espe- cially on account of extreme dyspnea and cyanosis, and death results from suifocation. Tumors of considerable size may be recognized from the presence of percussion-dulness of irregular outline. If the entire lung is involved in the new-formation, flat- ness is obtained everywhere upon the affected side of the chest, and generally increased resistance also is appreciable. If the bronchi are not occluded by carcinomatous masses, bronchial brecdhing will be audible. Under such conditions vocal fremitus and resonance ai'c increased. The chest is frequently enlarged. Adjacent organs (heart, liver) are displaced. By compression or by extension of the \\e\\-irYO\\\\\ prexsure-manifestations are not rarely induced in adjacent organs, among which may be mentioned brachial and intercostal neuralgia, constriction of the esophagus, tracheal and bronchial stenosis, pressure upon the veins of the neck with resulting cyanosis and tumefaction of the skin, and paralysis of the vocal bands. At times the supraclavicular -^nd the axillary lymph- glands are enlarged and degenerated. The patients suffer mostly ECHINOCOCCUS OF THE LUNG 151 from dyspnea, and alarming attacks of threatening suffocation often occur. The disease terminates almost unexceptionally in the course of a few months in death, which results in consequence of pro- gressive dyspnea or of marasmus, less commonly from uncon- trollable hemorrhage. At times pulmonary gangrene has been superadded to carcinoma of the lung. In rare cases rupture ex- ternally has also been observed. Treatment. — Treatment can be directed only to the amelio- ration of distressing symptoms. Subcutaneous injection of mor- phin especially will frequently be required. Kronlein in one case removed successfully a sarcoma of the lung by operative means. ECHINOCOCCUS OF THE LUNG. Echinococcus of the lung is a rare disease that is acquired by aspiration of the ova of the Taenia echinococcus of the dog. The echinococcus-cyst may have developed priinarily in the lung, or have invaded the lung secondarily from other organs, as, for in- stance, in the presence of echinococcus of the heart, by embolism, or of echinococcus of the liver following rupture through the dia- phragm. The echinococcus-cyst is almost always monolocular. The condition consists in the development of a vesicle with milk- glass-like walls, containing clear fluid, and frequently also daugh- ter-cysts. At times suppuration occurs in an echinococcus-cyst, and in consequence of inspissation a putty-like mass forms. Most frequently echinococcus-cysts have developed in the right lower lobe. In size they may become as large as a man's head. Multi- locidar echinococcus of the lung has been observed in only a few iustances. The individual vesicles were developed either in the distribution of the pulmonary artery, or in that of the pulmonary veins. Echinococci of the lungs can scarcely be diagnosed with cer- tainty unless echinococcus-cysts or echinococcus-hooklets are found in the sputum. The membranes may be readily recognized from their laminated structure, and no difficulty is encountered in recog- nizing echinococcus-hooklets. When echinococcus-membranes are expectorated they may be replaced by gangrene of the lung. At times echinococcus of the lung is attended with frequent hemoptysis, concerning whose origin doubt still exists. When echinococcus-cysts are seated at the surface of the lung their presence is disclosed by duhiess on percussion of irregular outline and over which the respiratory murmur, vocal fremitus, and bronchophony are wanting. Frequently the patients complain of dyspnea and of stabbing pain in the side. Echinococcus-cysts have a tendency to grow and to rupture into adjacent cavities. Rupture into the bronchial tubes has already been mentioned. Ru])ture may take place also into the pleural cavity, to which 152 RESPIRATORY ORGANS pleurisy, pneumothorax, or hydropneuniothorax will b.e super- added. Rnj)turc may even take place througli the chest- wall. The prognosis of cchinococeus of the lung is serious. Among otlier conditions sudden rupture or exploratory puncture may be followed by the entrance of echinococcus-fluid into the air-pass- ages, and death from suffocation. The treatment can only be surgical, the cyst being removed by means of the knife or the thermocautery. ANEURYSM OF THE PULMONARY ARTERY. Aneurysm of the pulmonary artery is rare, but it may occur even in early life. It gives rise to a diffuse (expansile) pulsating tumor in the left second intercostal space, to cardiac-systolic murmurs, and to dilatation and hypertrophy of the right ventri- cle. This last condition distinguishes it from aneurysm of the aorta. The patients are usually cyanotic and dyspneie, and suffer a good deal from hemoptysis. The principal danger consists in rupture and fatal hemorrhage. The treatment is like that of aneurysm of the aorta (pages 70 and 71). VI. DISEASES OF THE PLEURA. INFLAMMATION OF THE PLEURA (PLEURISY). Ktiologfy. — Inflammation of the pleura arises tlirough the agency of bacteria. Whether such inflammation may occur as a result solely of chemic irritants has not yet been demonstrated. Various bacteria may give rise to inflammation of the pleura, though it is by no means invariable to detect bacteria in the pleural exudate. In addition to the widespread exciting agents of inflammation and suppuration (Streptococcus and Staphylo- coccus pyogenes) specific bacteria have been found in the pleural exudate, among which may be mentioned Frjinkel's pneumococci, tubercle-bacilli, typhoid-bacilli, and gonococci. The Bacterium coli commiuie has also been found in the pleural exudate in numerous instances. All of those influences that were formerly considered as causes of inflammation of the pleura are now looked upon as merely contributory causes for the infection. These in- clude exposure fo cold, traumatis-m, preceding infectious disease, pre- ceding disease of the pleura itself (titbcrcidosis, carcinoma), and de- bilitating diseases (carcinoma, tuberculosis, suppuration , chronic disease of the kidneys, chroiuc disease of the heart, sj/philitic ca- chexia, scorbutus, etc.). At times inflammation of the pleura INFLAMMATION OF THE PLEURA 153 arises by extension from adjacent disease, as, for instance, pneu- monia, pulmonary tuberculosis, gangrene or abscess of the lung, pericarditis, inflammation of the ribs, peritonitis, etc. In some cases no cause for the inflammation of the pleura can be deter- mined {cryptogenetiG plearisy). Under such conditions the pleu- risy is usually tuberculous, and frequently secondary to preexist- ing tuberculosis of the tracheobronchial lymphatic glands. Pleu- risy occurs at all periods of life, but most commonly between the fifteenth and the fortieth year. 3Ien are attacked more commonly than women. Anatomic Alterations. — In like manner, as in the case of pericarditis, a distinction is made between dry and moist pleurisy. Dry pleurisy is also known as fibrinous pleurisy, because it is attended with the formation of fibrinous deposits upon the pleura. At first these are thin and transparent, so that the smooth and glistening surface of the healthy pleura appears as if clouded with vapor. Later, they increase in thickness, and collect in consider- able amount, especially in the interlobular fissures of the lung. If recovery takes place, the fibrinous exudate may undergo com- plete absorption. Often, however, it undergoes organization into connective tissue, and p)hural adhesions form, uniting the pul- monary and the costal pleura by connective-tissue bands or mem- branes. At times the adhesions are so extensive as completely to obliterate the pleural cavity. Moist pleurisy is characterized by the accumulation of a fluid exudate in the pleural cavity. This may be serous, purulent, or hemorrhagic in nature. Accordingly, a distinction' is made be- tween serous j^leurisy, purulent pleurisy (pyothorax, empyema), and hemorrhagiG pleurisy. Should 2:)utrid decomposition take place in the pus through the agency of putrefactive bacteria, putrid pleurisy develops. The inflammatory alterations in a case of moist pleurisy usually begin with the symptoms of a fibrinous pleurisy, and these persist also at the time of fluid effusion. This fact is expressed by the designation serofibrinous pleurisy. The amount of the exudate may reach ten liters and more, and it is therefore not surprising that the lung should be compressed until it is airless, while adjacent organs (heart, diaphragm, liver, spleen) undergo more or less marked displacement. Symptoms. — Fibrinous pleurisy can be recognized with cer- tainty only in the presence of a pleuritic friction-murmur. This may be of varying intensity and extent and of variable duration. At times it is appreciable only on most careful auscultation as a faint rubbing, Avhile in other instances it gives rise to a loud, creaking murmur, which has been designated as the creaking of new leather, as it has been compared with the sounds generated by the bending of the sole of a leather shoe. It also resembles the crackling of a firmly compressed snow-ball. Murmurs of con- 154 RESPIRATORY ORCIANS siderablc intensity can be felt as pleural fremitus. At times the patient is conscious of rubbing movements in his chest. The mur- mur may also be propagated for a slight distance from the patient. At times pleuritic friction-murmurs are audible only within circum- scribed areas, not exceeding one or two centimeters in diameter. In other instances they can be heard over almost the entire half of the chest. At times pleuritic friction-murmurs persist for only a few hours. On the other hand, however, they may continue for many weeks and months. Not rarely they disappear after repeated deep inspiratory efforts, because under such conditions the layers of the pleura move smoothly upon one another. After a short time, however, they generally reappear. Fibrinous pleurisy is usually associated with pleural pain, and it is important to determine its extent by means of palpation in order to obtain an approximate idea of the inflammatory area. The pain is augmented considerably on cough and on deep breath- ing, in consequence of increased rubbing of the inflamed layers of the pleura. In some instances fibrinous pleurisy discloses itself only by pleural pain, and the diagnosis of the disease under such conditions is exceedingly difficult. The pleural pain is responsible for certain respiratory disturbances. The respiratory movements are often belated upon the affected side of the chest, are only superficial, and follow at intervals. In harmony with this fact the respiratory murmur is faint and frequently also interrupted (jerky). At times there is marked dyspnea, because the respiratory movements cannot take place with sufficient freedom. The pleural pain causes the patient, as a rule, to assume a passive attitude upon the healthy side of the body. Patients with fibrinous pleurisy are often harassed by dis- tressing irritation of the air-passages and cough. They expectorate little or none at all, and suffer from so-called dry cough. Pressure in an intercostal space is usually followed by cough. Apart from pain and disturbed sleep tlie general condition may remain un- changed. At times, however, febrile movement occurs, but this is usually moderate. Among the sequclce of fibrinous pleurisy pleuritic adhesions are especially to be named. These may cause obliteration of the complementary pleural spaces, indicated by respiratory immobility of the lower and median borders of the lungs ; or they may cause complete obliteration of the pleural cavity, to which dilatation and hypertrophy of the heart may be superadded in consequence of the impaired aspirating power of the lungs upon the blood-stream. All forms of moist pleurisy agree with regard to tlieir physical alterations. From a diagnostic point of view dulness on percussion and diminution in vocal fremitus are especially distinctive. We shall now consider in detail the individual methods of examination. On inspection it will frequently be observed that the patients prefer INFLAMMATION OF THE PLEURA 155 to lie upon the diseased side of the body, obviously in order that respiratory movement of tlie free, healthy side of the chest directed upward may be as extensive as possible. The diseased side of the chest participates but little, if at all, in the respiratory movement, because the pressure of tlie pleural effusion prevents distention of the thorax and of the lung. The circumference of the chest u])on the diseased side is increased, and not rarely the apex-beat of the heart is displaced toward the healthy side, and the liver is displaced downward. The type of bi^eathing is characterized by active participation of the abdominal muscles. Palpation yields important diagnostic information, disclosing enfeeblement or dis- appearance of vocal fremitus. The fluid that has insinuated itself between the surface of the lung and the chest-wall is quite capable of preventing conduction of the voice- waves from the bronchial tree to the chest-wall. If the examination for vocal fremitus be made with the border of the hand, it is possible to determine accurately the level at which the exudate begins, from the diminu- tion in the vocal fremitus. The same information can also be gained by direct palpation of the thorax, because the sense of resistance is increased at the limits of the exudation. On percus- sion, dulness is detected within the limits of the exudate, and becomes the greater as the lower portions of the thorax are approached, that is, as the layer of exudate becomes the thicker. In the majority of cases the upper limit of dulness is highest at the side of the vertebral column, gradually declining toward the side and the front of the chest. This manifestation can be ex- plained by the fact that in the dorsal decubitus a horizontal section passes through the vertebral column at a higher level than through the anterior aspect of the chest, and that the surface of a pleural exudate tends to occupy a horizontal position in the thorax. Pleural adhesions naturally may prevent this arrange- ment. Probably wavy elevations and depressions in the limits of dulness upon the side of the chest frequently depend upon such adhesions (Damoiseau's curves). Percussion of the upper intercostal spaces upon the anterior aspect of the chest discloses upon the diseased side frequently a deep-tympanitic note, because the pulmonary tissue here is relaxed. If the pleural effusion is large, the percussion-note in this situation is not rarely dull-tympanitic, and this varies as the mouth is opened and closed — Williams' tracheal note — in consequence of vibrations of air in the bronchus. Auscultation not rarely discloses a pleuritic friction-murmur at the upper level of a pleural exudate. In other instances this may be heard only when absorption of the exudate has begun, and the pleural layers covered with fibrinous deposit again come in con- tact. The respiratory murmur may be vesicular, bronchial, or abolished. It retains its vesicular character as long as the lung is not compressed sufficiently to expel all of the air. In the latter 156 RESPIRATORY ORGANS event bronchial breathing sets in. Over exceedingly thick exu- dates no respiratory nuirinur at all is audible. On auscultation of the voice either diminished bronchophony, (jr egophony, is appre- ciable. The latter is observed especially over small exudates or at the upper level, and beside the vertebral column when larger exudates are present. It depends upon the fact that superficial bronchial tubes are readily compressed, so that the voice-waves for the time being pass beyond the points of compression and reach the surface of the chest. The influence of pleural exudates upon adjacent organs is noteworthy. In the presence of right- sided pleurisy the heart is at times displaced so far to the left that its apex-beat may be present in the midaxillary line, while in the presence of left-sided pleurisy the heart may be displaced to the right beyond the right mammillary line. At the same time it should be emphasized that the heart is always so displaced to the right tliat its apex is directed to the left and outward, so that the pulsating part furthermost to the right corresponds to the right border of the heart. In addition to the heart, the liver also is frequently dis})laced by pleural effusions. Right-sided pleural effusions dis- place the lower margin of the liver at times below the level of the umbilicus. In the presence of left-sided pleurisy the left lobe of the liver is at times deflected downward at the round ligament. Left-sided pleural effusions, as a rule, cause diminution in size or obliteration of the semilunar space, lying below the heart and cor- responding to the fundus of the stomach, by their weight push- ing the diaphragm and the stomach downward. In the same Avay the spleen, not enlarged, but displaced, may be accessible to the fingers. The general condition at times suffers surprisingly little in spite of an extensive effusion, and some persons continue their M^ork uninterruptedly, although the entire pleural cavity may be filled with exudate. Others complain of dyspnea, stitches in the side, and cough. In persons with a ]iurulcnt exudate pallor and ano- rexia often develop rapidly. Not rarely distention of the veins of the neck and marked cyanosis appear. Usually there is febrile movement of varying degree, although the disease sometimes pur- sues an afebrile course. The elimination of urine is generally di- minished. In accordance with the duration of the disease a distinction is made l)etween acute, subacute, and chronic pleurisy, as the disease is protracted for as long as four weeks or eight weeks or more. The designation pleuritis acutissima has been applied to cases in which the attack has set in with a chill, followed by high fever, delirium, meteorism, and enlargement of the spleen, and has ter- minated fatally, often within a few days. After absorption of a pleural exudate has taken place complete recovery may ensue. Often areas of dulness remain, because considerable thickening — INFLAMMATION OF THE PLEURA 157 pleuritic cicatrices — have formed. Under such conditions uni- lateral retraction of the chest readily takes place, especially when the lung has been compressed by the exudate for a long time, so that complete distention of the atelectatic areas in the lung is pre- vented by adhesions. At the same time displacement of the heart and the liver frequently takes place. The heart is pushed unusually deep into the diseased chest, while the liver often occupies an uncommonly high position. Such conditions fail to develop only when the organs named become fixed by adhesions in the positions to which they were displaced at the time of the exudate. Patients who have recovered from an attack of pleurisy suffer for a long time from stitches in the diseased side of the chest, and from shortness of breath, conditions that probably depend essentially upon pleuritic adhesions. The complications of pleurisy with eflfiision depend upon the amount and the nature of the exudate. Large accumulations of fluid in the pleural cavity may by marked compression of the lungs and the heart give rise to danger of suffocation. At times fatal syncope of sudden onset has been observed, occurring espe- cially on assuming the vertical posture. Various conditions may be responsible for such accidents, especially cardiac weakness and cerebral anemia, and embolism of the pulmonary artery, the emboli being derived from cardiac thrombi in the right ventricle. Much less commonly sudden distortion of the inferior vena cava takes place in consequence of a pleural effusion. In the presence of purulent pleural effusions rupture of the pus may take place externally, or into internal organs. Rupture of pus externally is preceded by bulging of the skin, with fluctuation, the protrusion diminishing in size during inspiration, while it increases in size during expiration, and is capable of extinction on careful pressure. The skin gradually becomes reddened, and finally it may rupture, with escape of the pus, sometimes in a strong stream. The rupture of pus externally is designated empyema 'pleurae necessitatis. If the condition is left to itself, and this would be a grave mis- take, the discharge of pus may cease after a time from closure of the fistula. Renewed accumulation of pus in the pleural cavity may then take place, and rupture again occurs. The patient eventually dies from exhaustion or amyloid degeneration. Em- pyema necessitatis usually develops in the lateral inferior aspects of the chest, although extensive burrowing at times occurs. Rupture of purulent pleural effusions into internal organs takes place most frequently through the lungs. This occurrence will be recognized by the sudden expectoration of large amounts of pus (in mouthfuls), while the exudate in the pleural cavity dimin- ishes. At times the air-passages are so greatly filled with pus that there is danger of suffocation, particularly if the accident occurs during the night. Not rarely the pus within the air- 158 RESPIRATORY ORGANS passages acquires a putrid odor, although it may have been odor- less in the pleural cavity. The expectoration of considerable amounts of pus may be repeated for a varying length of time, and in varying amount, but, as a rule, the pus constantly reaccumu- lates in the pleural cavity, and also here threatens to cause death by exhaustion or amyloid disease. In rare cases the discharge of pus does not take place through a pul- monary fistula of considerable size, but the pus is taken up by the pulmo- nary tissue as by a sponge and is gradually expectorated in the form of purulent sputum. Rupture of a purulent pleural effusion into the pericardium, the mediastinum, the trachea, the esophagus, the stomach, the intestine, etc., takes place but rarely. Among the complications of pleurisy pericarditis may yet be mentioned, and this, experi- ence has shown, occurs most commonly in association with left- sided pleurisy. Diaphraginatic pleurisy is a special variety of the disease, which, as its name indicates, involves the diapliragmatic pleura. The patients complain of severe pain in the lower portion of the chest, and there is usually marked tenderness upon pressure at the lower border of the chest. The irritation of the air-passages may be considerable. Often there is painful eructation, and the act of swallowing may be attended with severe pain as soon as the ingesta pass the esophageal foramen. At times frequent vomiting takes place. Jaundice has been observed in cases of right-sided dia- phragmatic pleurisy, and it has been attributed to the deficiency in the respiratory movement of the diaphragm, which is thus no longer capable of causing expulsion of the bile from the biliary passages in the liver. Dulness over the thorax may be wanting because fluid may accumulate between the base of the lung and the diaphragm without coming in contact with the chest-wall. The designation interlobular pleurisy is applied to cases in which fluid exudate has collected in the interlobular fissures. The exudate is usually purulent, gives rise to an area of girdle-like dulness around the thorax, and frequently ruptures into the lung. Muliilocular pleurisy is characterized by the presence of a number of encapsulated foci of exudate. Usually the exudate is of similar character in all of the foci, but it may be that in some the fluid is serous, in others ])urulent. Pulsating pleurisy is characterized by pulsation of the diseased side of the chest, transmitted from the heart to the exudate and the chest- wall. It is almost always asso- ciated ^vith a left-sided purulent exudate, though I have observed right-sided pulsating serothorax in a boy. Pulsating pleurisy may be confounded with aneurysm of the aorta, but it is unattended with vascular murmurs. Diagnosis. — The recognition of a fibrinous jyleurisy is, as a rule, easy if a pleuritic friction-murmur can be heard. This might INFLAMMATION OF THE PLEURA 159 at best be confounded with snoring or sonorous rdles, but these are largely dependent upon eiforts at cough, which may cause their disappearance or material alteration in them. The cJiJferentiation between pleuritic and pericarditic murmurs is discussed on page 57. Should it be necessary to make a diagnosis of fibrinous pleurisy from the pleuritic pain alone, care would be demanded to avoid confusion with muscular rheumatism and intercostal neuralgia. In cases of muscular rheumatism pain occurs especially when the affected muscles are grasped between the fingers, and in cases of intercostal neuralgia the pain is accurately limited to the course of an intercostal nerve. The diagnosis of a fluid exudate in the pleural cavity is based principally upon dulness on percussion, diminution in vocal fremitus, and displacement of adjacent organs. Massive pneumonia and new-growths of the lung also give rise to dulness and diminution in vocal fremitus, but they are unattended with displacement of the heart and of the liver. The differentiation between pleurisy with effusion and new-groicths of the pleura may be impossible, but the latter are rare. There is but one certain and harmless mode of determining the nature of an effusion into the pleural cavity, namely, exploratory puncture, which should be made in as low an intercostal space as possible, by means of a sterile syringe specially designed for this purpose. Encapsulated pleurisy at times gives rise to error in diagnosis, for if it be situ- ated near the heart, the spleen, or the liver, it might be mistaken for an enlargement of one of the organs named. In the differen- tial diagnosis especial consideration should be given to the fact that in encapsulated pleurisy the outline of the area of dulness is irreg- ular. Difficulties may further arise in the differential diagnosis between encapsulated empyema, and subphrenic abscess. The diag- nosis of an accumulation of pus beneath the diaphragm is based upon the previous existence of disease of the abdominal organs, the unusually high level upon the anterior aspect of the chest of the dulness corresponding to the accumulation of pus, the fecal odor of the pus obtained on exploratory puncture, and the exist- ence in the abscess-cavity of positive pressure in inspiration and of negative pressure in expiration as disclosed by a manometer con- ' nected with the cannula of a trocar. Empyema pleurce necessitatis finally may give rise to confusion with cutaneous or muscular abscesses, bone-abscesses of the ribs, and burrowing abscesses of the vertebral column, but under all of these conditions respira- tory variations in the external extent of the abscess are wanting. Prognosis. — ^Nlost cases of pleurisy terminate in recovery, and the prognosis is therefore favorable. Unfortunately, however, almost two-thirds of the cases are tuberculous in nature, and in this fact resides the danger that after a time infection and tubercu- losis will make their appearance in other organs, most frequently in the lungs. At times exudates are, by reason of their great size, 160 RESPIRATORY ORGANS attended with danger of suffocation. In rare cases the general condition may also be seriously affected. Treatment. — The treatment of pleurisy depends upon the nature of the infammafiou. Patients suffering from fibrinous jjJ (u- r/sj/ should remain in bed and warm cataplasms should l)e applied to the inflamed area. If severe pain be present, a subcutaneous injection of morphin will be required. Dry or wet cups also often quickly relieve pain. In obstinate cases derivatives are employed, as, for instance, mustard-plasters, cantharidal plaster, and api)liea- tions of tincture of iodiu. >Serou,s pleuri.^ij requires scarcely more than expectant treatment. 3Ioist warm applications to the thorax and the internal administration of potassium nitrate, salicylic acid, or sodium salicylate — measures that increase the excretion of urine, and thus favor absorption of the pleural exudate — are usually sufficient : Or, R Solution of potas- sium nitrate, 10.0 : 200 {2i drams : 6\ fluidounces). Dose : 1 tablespoonful every two hours. B Salicylic acid, Make 10 such starch-capsules. Dose : 1 powder every three hours. R Sodium salicylate. Make 10 such starch-capsules. Dose : 1 capsule every three hours. 1.0 (15 grains). 1.0 (15 grains). I have not observed any specific influence of salicylic acid and its sodium-combination upon serous pleurisy. Extensive experi- ence has convinced me that no better and speedier results are obtained from the use of dcrivatices (cups, leeches, mustard-plasters), 6W- befacients (potassium iodid, applica- tions of tincture of iodin or of oint- ment of potassium iodid or of iodo- form), diapihorctics (pilocarpin, hot- air baths), diuretics (digitalis, din re- tin), and laxatives. Operative treat- ment for serous pleurisy is indicated only when the effusion is so exten- sive from the outset that death from suffocation is threatened in conse- quence of displacement of the lungs and the heart, or when no diminu- tion in the effusion can be recognized after the lapse of four weeks, or when even an increase in the effu- sion has taken place in the fourth week of the disease. For punc- ture of the pleural cavity I employ an inexpensive and simple Fig. 24. — Apparatus for puncture of the pleural cavity. INFLAMMATION OF THE PLEURA 161 apparatus consisting of a hollow needle, a rubber tube, which is interrupted at its middle by a glass tube in order that the flow of fluid may be the better observed, and a glass funnel and a clamp (Fig. 24). The apparatus is filled with sterile water and the clamp is closed. After the skin has been thoroughly washed with soap, alcohol, ether, and carbolic-acid solution (5.0 : 100), the needle is introduced into an intercostal space, when the funnel is depressed and immersed beneath the surface of a solution of carbolic acid in a glass vessel one-quarter filled, aud then the clamp is released. The pleural exudate will flow into the glass- receptacle, while entrance of air into the pleural cavity is impos- sible. I permit the escape of fluid to continue until the patient begins to cough actively or complains of pain, or the flow ceases spontaneously. Naturally the flow will stop when the pressure in the pleural cavity equals that of the external atmosphere. It is impossible for negative pressure to develop in the pleural cavity. Rarely in cases of pleurisy negative pressure exists in the pleural cavity before puncture is undertaken. Under such conditions the apparatus de- scribed would fail to secure evacuation of the pleural contents, and aspirating instruments would be required, among which maybe mentioned the syringe of Dieulafoy, the apparatus of Potain, and the jar of Fiirbringer. Operative intervention is the only appropriate treatment for all cases oi 'purulent pleurisy, and I should recommend resection of ribs and incision. After puncture is performed fluid usually reaccumu- lates. Siphon-drainage by the method of Biilau has often been employed. With the aid of a trocar a rubber tube is introduced into the pleural cavity, while the other extremity of the tube is immersed beneath the surface of a carbolic-acid solution (5.0 : 100) contained in a suitable vessel. In this way provision is afforded for constant discharge of the pus. Often, however, the formation of pus continues for weeks, and resort must eventually be had to rib- resection and incision. Putrid pleurisy requires the same treatment as purulent pleurisy, except that after opening of the thorax and discharge of the pus disinfectant and deodorant irrigation should be practised. In this connection carbolic acid and mercuric chlorid should be avoided, as fatal intoxication may result from rapid absorption of these substances, and zinc chlorid (from 3.0 to 6.0 : 100), aluminum acetate (from 1.0 to 2.0 : 100), or boric acid (2.0 : 100) should preferably be employed. Hemorrhagic pleurisy will require puncture only when life is threatened by the large amount of blood present. After recovery from pleurisy has taken place it is often desirable to restore the distensibility of the previ- ously compressed lungs by means of pulmonary gymnastics. A succession of deep inspirations while one arm is raised, and re- peated several times daily, will suffice. The arm corresponding to the diseased side of the chest should be raised, Pneumatotherapy also should be recommended, particularly if the pleurisy is tuber- 11 162 RESPIRATORY ORGANS culous in nature. Under such conditions the patients should avoid inlmlation of dust and employment in closed rooms. PNEUMOTHORAX. Anatomic Alterations. — Any accumulation of gas in the pleural caviti) is designated pneumothorax. As a rule, fluid also is present in addition to the gas — thus a hydrojjueumothorax. The fluid may be serous, purulent, putrid, or hemorrhagic (seropneumo- ihorax, pyopjncuniothorax, heiaopyiieumothorax). Accordingly as gas and fluid are freely movable in the pleural cavity or are encap- sulated by pleimtic adhesions, the condition is spoken of as either a Jree or an encapsulated pneumothorax or hydrojmeurnothorax. In the cadaver also the existence of pneumothorax and hydropneumo- thorax is often characterized by unusual dilatation of the diseased side of the chest (ectasis), which' on percussion yields a deeply resonant note like an empty barrel. On opening the abdominal cavity the diaphragm is usually found pushed downward, wdth its convexity projecting into this cavity, and the liver or the stomach and the spleen in consequence occupying an unduly low position. On jjunc- ture of the thorax gas generally escapes with a hissing sound, and often diffuses a disagreeable odor of hydrogen sulphid. The lung is, as a rule, compressed and airless, being pushed upward and backward at the side of the vertebral column. At times an opening in the pulmonarv pleura can be readily demonstrated, through which the air has entered the pleural cavity. In other instances, however, the opening has closed or is concealed beneath flbrinous deposits. Under such circumstances a tube may be introduced into the main bronchus, the lung submerged in water and filled with air through the bronchus, notice being taken of the point at which air-bubbles appear. Displacement of adjacent organs (mediastinum, heart, dia- phragm, liver, stomach, and spleen) is, further, distinctive of pneumothorax and hydropneumothorax. It results from the same causes as are operative in pleurisy, but generally attains a more marked degree. Ktiology. — The conditions for the development of pneumo- thorax are ]*rovided when the pleural cavity communicates directly with air- containing organs or with the external air. This occurs most commonly in connection with ulcerative destruction in the pul- monary tissues, especially pulmonary tuberculosis, gangrene, and abscess of the lung, and less commonly echinococcus, tumors, and embolic infarction of the lung. It is noteworthy that at times the lung contains only a few small tuberculous-caseous foci just beneath the pulmonary pleura, which may escape diagnosis, and when they rupture into the pleural cavity the impression may be created that the pneumothorax was of spontaneous development. The same statements apply to pneumothorax associated icith alve- PNEUMOTHORAX 163 olar pulmonary emphysema, in which at times emphysematous vesicles immediately ])eneath the pulmonary pleura rupture in consequence of insignificant physical exertion or spontaneously during sleep. At times pneumothorax develops in consequence of injuries of the lungs. Among these, punctured wounds are less common than excessive expulsive efforts, physical over-exertion, extreme dyspnea, severe cough and the like — conditions attended with such increase in the intrapulmonary air-pressure that rupture of the pulmonary and pleural tissues takes place. Pneumothorax may be caused also by fracture of the ribs, if the extremities of the fractured bone have penetrated the lung. At times pneumo- thorax is dependent upon destructive processes in the esophagus, such as are observed in association with carcinoma, abscess, soften- ing, and unskilful sounding. Suppuration of the bronchial glands also may give rise to ])neuraothorax, if rupture of the pus takes place simultaneously into the air-passages and the pleural cavity. Destructive processes in the stomach and intestines (ulceration, abscess, carcinoma) are among the less common causes of pneumo- thorax. Injuries of the chest-wall also (stab-wounds, gunshot- wounds, and the like) are not common causes of pneumothorax, because the margins of the wound usually become closely applied to the cutting instrument, Pneumothorax is at times associated with disease in the pleural cavity itself. Thus it may develop in connection with rupture of an empyema of the pleura through the lungs or the chest-wall. Xaturally the fistula is generally so con- stituted that while it permits escape of the pus, it does not permit the entrance of air into the pleural cavity. It is further maintained that gas may develop spontaneously in puru- lent pleural exudates. The possibility must be conceded, as there are bacilli with gas-generating properties. V. Ziemssen observed transitory pneumo- thorax develop after puncture of a pleural effusion, and he attributed the condition to evaporation of gases from the exudate. Symptoms. — When pneumothorax develops in the presence of healthy lungs the patient is seized with intense dyspnea and a sense of suffocation. Breathing is difficult and gasping, the face exhibits an expression of fear, cyanosis develops, and an appear- ance of suffocation is presented. If, however, the lungs were previously diseased — for instance, in a case of pulmonary tuber- culosis — the pneumothorax may develop so insidiously that the condition will be recognized only upon careful investigation. In cases of pulmonary tuberculosis persistent occupation of the same lateral decubitus should arouse suspicion. In addition to dilata- tion of the chest and displacement of adjacent organs, the metallic quality of the physical phenomena on percussion and auscultation are especially distinctive of pneumothorax, while in the presence of hydropneumothorax movable dulness and splashing sounds are superadded. Pursuing the several methods of physical ex- 164 RESPIRATORY ORGANS aniination in detail, it is first observed upon inspection that dila- tation of the chest (tiioraxectasis) is present on the side on wiiieh the pneiunotliorax is situated, because the negative pressure of the luniks has disappeared ; and that the diseased side participates but little if at all in the respiratory rnoveineut. Breathing- is vis- ibly embarrassed, and takes place with the aid of the auxiliary muscles of respiration. Often marked displacement of the heart toward the opposite side and unusual depression of the liver are also appreciable to tiie eye. The patients lie upon the diseased side of the chest in order that the other lung may be as unre- stricted as possible in its fimction. Vocal fremitus is diminished or abolished in the area of the air-accumulation, and, in cases of hydropneumothorax also in that of the fluid accumulation. Only in places where pleural adhesions with the chest-wall exist may it be maintained or even increased. If the pleural cavity con- tains gas and fluid, increased resistance will be readily appreciable at the upper level of the exudate upon immediate palpation of the chest. Measurement of the circumference of the chest will disclose a difference between the two sides of as much as 10 cm. and more. Tracings of a trans- verse section of the chest, which can be readily obtained with the aid of a piece of pliable lead wire, applied to both sides of the chest exactly at the same level, and then recording the outlines upon paper with a lead-pencil, will disclose distinctly the differences between the two sides. The percussion-note upon the diseased side is unusually deep and loud, the chest-wall being but rarely so greatly distended by the gas that has escaped as to yield a dull percussion-note. As pneumothorax is attended with the presence of gas in a large cavity with smooth walls, metallic percussion-phenomena will be present. As a rule, their development requires special devices — namely, percussion with plexor and pjleximetcr, and auscultatory percussion. In the former a metallic plexor or the handle of the plexor is used instead of one of rubber, because percussion by means of hard substances will elicit by consonance the high over- tones that give rise to the metallic note. These can be heard with especial distinctness when the stethoscope is applied to the chest while percussion is practised, and in this way auscultatory percussion is employed. Further, the metallic phenomena can be developed distinctly cmly at certain points. It will be observed on percussion of a free pneumothorax that the boundaries of adja- cent organs (heart, liver) are greatly displaced. As long as the opening through which gas has entered the pleural cavity remains unclosed percussion will yield a cracked-pot sound. The percus- sion-note also may vary in ]iitch accordingly as the mouth is open or closed, becoming higher under the former condition — so-called AVintrich's change in pitch — if the opening is in imme- diate communication with a bronchus of considerable size. If the PNEUMOTHORAX 165 opening is situated in the chest-wall, the cracked-pot sound will naturally be no longer heard on closure -with the finger, and at the same time the percussion-note will become deeper. In cases of hydropneumotkorax the percussion-phenomena described will be present in the upper portions of the chest corresponding to the accumulation of gas, while in the lower, in which fluid has accu- mulated, dulness will be present. While in the dorsal decubitus the upper limits of dulness are higher posteriorly than anteriorly, they assume a horizontal level in the sitting posture, and it is especially characteristic of hydropneumothorax that the limits of dulness vary in accordance with the position of the body. The cracked-pot sound and Wintrich's change in pitch may also be present in cases of hydropneumothorax as long as the air-fistula remains open, and is situated above the level of the fluid. If by change of position and displacement of the fluid the fistula is temporarily closed, both the cracked-pot sound and Wintrich's change in pitch disappear, and in this way is provided a means of determining the position of an air-fistula. Biermer has called attention to the fact that in cases of hydropneumo- thorax the pitch of the percussion-note varies in accordance with the posi- tion of the body — so-called Biermer's change in ipitch. Usually the percus- sion-note is increased in pitch in the erect posture because the exudate, by reason of its weight, depresses the diaphragm, and the diameter of the air- cavity is thus increased. The auscultatory phenomena elicited in a case of pure pneumo- thorax vary. At times no respiratory murmur at all is heard, and it has, not without reason, been maintained that unilateral dilatation of the thorax, with a deep, loud percussion-note and an absence of respiratory murmur, is indicative of pneumothorax. In other instances metallic bronchial breathing is audible. This is especially distinct, and sometimes is present exclusively during expiration. Bronchial breathing occurs when the lung is com- pressed to the degree of airlessness, and within tlie pleural cavity filled with gas it acquires metallic properties through consonance. Should rales develop within the air-passages, they also acquire a metallic character. Even bronchophony, which is diminished in cases of pneumothorax, also exhibits a metallic character. Hydropneumothorax is distinguished by the occurrence of a pleural splashing sound (succussion-sound, Hippocratic succus- sion), which is generated on movement of the body by the impact of the pleural fluid against the chest-wall. Vigorous agitation of the patient, change in position from one side of the body to the other, rapid assumption of the vertical posture, jumping upon the feet, and the like, are capable of generating the sound in question. At times the sound of the falling drop, gutta cadens — meiaJlic tinJding — may be heard. Tliis results at times on change of posture, as, for instance, in sitting erect, from the dropping of fluid that has accumulated upon the roughened surface of the pleura. 1(36 RESPIRATORY ORGANS As long, in a case of hydropneumothorax, as the air-fistula in the pulnionarv pleura remains patulous, expectoration of purulent material in mouthfuls may take j)laee. The patients do not ex- pectorate often in the course of the day, but then the sputum is ejected in large amounts, and is not rarely expelled from both mouth and nose, and in part may enter the larynx and excite vomiting. Expectoration takes place only when sufficient exu- date has accumulated in the pleural cavity to reach the level of the air-fistula, and discharge into the bronchi has taken place. The same effect may be induced also by certain positions of the body. As a rule, the patients persistently occupy the same lateral decubitus, in order to breathe with the least possible restriction with the free lung placed above. At times, however, the patient assumes quite extraordinary attitudes in order to prevent for as long as possible the entrance of pleural fluid into the air-fistula and the air-passages. The duration of pneumothorax and hydropneumothorax is most variable. At times death from suffocation results within a few hours after the development of the disease, while in other instances the affection may persist for years. Under the latter conditions the patients may at times be out of bed and indulge in various physical activities. In a case of pneumothorax gradual absorption of the gas, and thus recovery, may take place. Hydropneumo- thorax is not rarely converted into a simple pleurisy, the gas dis- appearing and the pleural effusion remaining. In the presence of a purulent or a putrid hydropneumothorax, not treated by operative measures, death may take place from progressive asthenia and septicemia. Diagnosis. — The recognition of pneumothorax and hydro- pneumothorax is usually easy. Often dyspnea and threatened suffocation of sudden onset will attract attention, and in addition tliore will be found dilatation of the chest, absence of vocal fremi- tus, metallic phenomena on percussion and auscultation, and in cases of hydropneumothorax also pleural splashing sound. To decide the nature of the pleural effusion in a case of hydropneumothorax ex- ploratory puncture will be necessary. The persistence of an air- fistula in the puhnouary pleura may be recognized from the pres- ence of the cracked-pot sound, and of Wintricli's change in pitch, and the occurrence of expectoration in mouthfuls. At times a valvular fistula may be temporarily closed by the excessive pres- sure of the gas in the pleural cavity. If, in addition to the accumulation of gas, fluid also is present in the pleural cavity, and if the fistula is situated below the level of tlie fluid, gurgling murmurs will be audible if gas be removed from the jileural cavity by means of an aspirator. The sounds generated have been designated puhnonary-jidula, or bubbling murmurs. These result from the entrance of air through the again patulous fistula PNEUMOTHORAX 167 into the pleural cavity and its passage upward through the effusion. Naturally, the same manifestation may be observed in the pres- ence of an open hydro])neumothorax when the air-fistula is situated beneath the level of the pleural effusion. lu accordance with the character of the air-fistula four varie- ties of pneumothorax may be distinguished, namely the open, the closed, the valvular, and the transitional. Open pneumothorax is provided with a single opening through which air enters the pleural cavity without obstruction, and can again make its exit. The pressure of the gas does not exceed that of the atmosphere, and the displacement of adjaceut organs is, therefore, usually not excessive. The means for recognizing an open air-fistula have already been described. Closed 'pneumothorax is attended with a closed air-fistula. In accordance with the amount of gas present the pressure in the pleural cavity may equal that of the atmo- sphere, or be less or greater than this. If air be permitted to escape from the pleural cavity, the intrapleural pressure is dimin- ished and remains permanently unchanged, as additional gas cannot enter. The conditions are different in the presence of valvular pneumothorax. Here the pleural cavity continues to be filled with gas until the latter by excess of pressure causes closure of the valvular fistula. The displacement of adjacent organs is usually quite considerable. If gas be evacuated from the pleural cavity by puncture, the fistula reopens, and the conditions become the same as before the puncture. An example of the transitional variety of pneumothorax is furnished by valvular pneumothorax, which in the presence of a great excess in the pressure of the gas in the pleural cavity acquires the character of a closed, and with a diminution in the pressure presents those of an open, pneumo- thorax. Free hydropneumothorax may be confounded with subphrenic hydropneumothorax, and with the stomach distended with gas and fluid. Subphrenic hydropneumothorax consists of a cavity filled with pus and gas situated beneath the diaphragm and between this and the liver or the spleen. It is noteworthy that the devel- opment of this disorder has been preceded by disease of the abdominal organs (stomach, intestines), that the purulent masses obtained on puncture possess a fecal odor, and that, if the respir- atory variations in the pressure of the gases be studied with the aid of a manometer, it will be found that the pressure is increased during inspiration, to be diminished during expiration, whereas in cases of hydropneumothorax the reverse conditions prevail. If the stomach he greatly distended, ivith gas, and fluid be simultane- ously present, the resonance of the stomach may give rise to metallic phenomena in the lower portion of the left half of the thorax on percussion and auscultation, and on agitation of the body splashing sounds may appear ; but these phenomena are at once 168 RESPIRATORY ORGANS modified when a tube is introduced into the sttjmacli and the gases are evacuated. Encapsulated hjidropneumothorax gives rise in part to the same manifestations as puhnonary cavities, but over the latter the inter- costal spaces are usually retracted, while the vocal fremitus is increased, and succussion-sounds are but rarely appreciable. Prognosis. — The prognosis in cases of pncuniothorax and liydropneumotliorax depends upon the amount of gas that has escaped into the pleural cavity and the cause of the disorder. Quite considerable accumulations of gas in the pleural cavity at times cause death by suffocation in the shortest possible time. Under certain conditions pneumothorax and liydropneumotliorax must even be considered as fortunate occurrences, for it is main- tained, not without reason, that such events in cases of pulmonary tuberculosis check the progress of the disease. Treatment. — In cases of simple pneumothorax an expectant attitude should be assumed for a time. If serious dyspnea be present, alleviation may be sought by means of subcutaneous injec- tion of morphin : R Morpliin hydrochlorate, 0.3 (4j grains) ; Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose : 0.5 (8 minims) subcutaneously. In cases in which the action of morphin fails, the air in the pleural cavity should be evacuated by puncture, a hollow needle and a rubber tube being employed for the purpose. One end of the rubber tube is connected with the needle, while the other is submerged in a vessel containing a solution of carbolic acid (5.0 : 100). In cases of open pneumothorax puncture Avould be useless, as the air at once enters the pleural cavity through the fistula. In cases of valvular pneumothorax also there is a possi- bility of renewed accumulation of gas, so that permanent success can be expected only in cases of closed pneuiiKithorax. In cases of hydropneumothorax, rib-resection and incision into the pleural cavity should be practised when the pleural effusion is purulent or ])utrid. Tuberculosis of the lungs is not a contraindication of operation. In cases of putrid hydropneumothorax great care must be observed in irrigating the pleural cavify us lonjr as the air-fistula in the lung remains open, as the irrigating fluid may fill the air-passages and cause death by suffocation. Seropneumothorax requires puncture of the pleural cavity when danger of suffocation is imminent ; but otherwise an expectant attitude should be assumed. Internal remedies exert no influence upon the disease. DROPSY OF THE PLEURA 169 DROPSY OF THE PLEURA (HYDROTHORAX) , i^tiology. — Hydrothorax is characterized by tlie accumula- tion of a serous transudate in tlie pleural cavity, and usually is bilateral. Among the causes are increased blood-pressure in the venous system (^hypostatic edema) and anemic and cachectic states (cachectic edema). Hypostatic edema of the pleural cavity depends, as a rule, upon weakness of the right ventricle, such as occurs especially in conjunction with valvular disease of the heart, myo- cardial disease, disease of the pericardium, of the lungs, and of the pleura. Local hypostatic edema occurs but rarely in the pleural cavity when the azygos vein or hemiazygos vein is obstructed by pressure or by thrombosis. Cachectic edema develops in cases of nephritis, carcinoma, suppuration of all kinds, profound anemia, and allied conditions. Anatomic Alterations. — Hydrothorax occurs generally in association with edema of the skin and accumulation of transudate in other serous cavities. The amount of fluid in the pleural cav- ity may reach several liters, and under such conditions it is con- siderably greater in one pleural cavity than in the other in cases in which the patient persistently occupies the same lateral decu- bitus. The fluid is amber-yellow or greenish-yellow in color, and transparent, and contains at most a few flocculi, Avhich consist of desquamated and swollen endothelial cells or of soft fibrin. At times the fluid presents a bloody appearance and in some cases of jaundice an icteric hue. The lungs are rendered airless in greater or lesser degree in consequence of pressure. Symptoms and Diagnosis. — Hydrothorax may develop quite insidiously. Increasing compression of the lungs gives rise to progressive dyspnea. When the latter becomes excessive, suffo- cation results. The diagnosis depends upon the demonstration of an accumulation of fluid in the pleural cavity (dulness, enfeeble- raent of vocal fremitus and of the respiratory murmur). Inflam- matory manifestations, such as stitch-like pain in the side and fever, are usually wanting. To distinguish a pleural exudate and a pleural transudate from each other the specific gravity of the fluid should be noted. A figure below 1015 is indicative of a transudate and a figure above 1018 is indicative of an exudate. Prognosis. — The prognosis depends upon the nature of the primary disorder. If, for instance, it is possible to increase the vigor of the heart, the hydrothorax likewise may be made com- pletely to disappear. Treatment. — The treatment should in the first place be directed to the correction of the primary disorder. If the hydro- thorax has attained dangerous prf)portions, it should be relieved by puncture, which may be repeated if necessary. 170 RESPIRATORY ORGANS HEMOTHORAX Collections of blood in the pleural cavity may be of traumatic origin or result from rupture of aneurysms of the aorta or the pulmonary artery, from ulceration of the aorta, tlie ])uhiionary artery, or the pulmonary vein, in consequence of tuberculous or gangrenous destructive processes in the lungs. The blood in the pleural cavity retains its fluidity for a long time, and occasionally it induces secondary pleurisy. The diagnosis depends upon the signs of an effusion of fluid into the pleural cavity, together with symptoms of internal hemor- rhage. Besides, respiratory disturbances become manifest when the lungs are greatly compressed. The prognosis depends upon the amount of the hemorrhage, and its susceptibility of control. Treatment should be directed to the control of the hemor- rhage by means of hemostatics and to the prevention of asthenia by the use of stimulants. Under certain conditions it will be necessary to remove the blood from the pleural cavity as quickly as possible by means of puncture. CHYLOTHORAX, The accumulation of chyle in the pleural cavity is an exceed- ingly rare occurrence. The fluid that collects presents a milky appearance, yields an alkaline reaction, contains sugar and a sugar- generating ferment, and microscopic examination discloses the presence of isolated lymph-corpuscles. Care must be taken to avoid confusion with pleural exudates containing fat, such as occur especially in association with carcinoma of the lung. Exudates containing fat present an abundance of fatty granule-cells. The diagnosis of chylothorax can be made only by puncture and chemic examination of fluid found in the pleural cavity. The fluid is derived from the ruptured thoracic duct. CARQNOMA OF THE PLEURA. Carcinoma of the pleura is usually secondary, and develops at times in consequence of direct extension from adjacent structures (lungs, mammary gland, mediastinum) and at other times by metas- tasis from remote organs. While in some cases innumerable miliary carcinomatous nodules are found upon the pleura, in others tumor-masses larger than a fist are present. Often a fluid effusion is present, at times serous, at other times purulent or hemorrhagic, and at still other times colloid or fatty. The diagnosis of earcinoma of the pleura is difficult. Miliary carcinosis is not rarely attended with intense dyspnea and uncon- MEDIASTINAL TUMORS 111 trollable cough. At times carcinoma of the pleura is concealed behind the signs of a pleurisy with effusion. Under such condi- tions the presence in the fluid obtained on exploratory puncture of many fatty granular cells, and especially numerous multinucle- ated cells, is significant. Tumor-masses of considerable size cause dilatation of the heart, displacement of adjacent organs, and diminu- tion of vocal fremitus and of the respiratory murmur, just as does pleurisy with effusion, but the former is distinguished from the latter by the irregular outline of the area of percussion-dulness. At times pulsation is imparted to new-growths from subjacent arteries, so that the presence of an aneurysm is suggested, but the diffuse expansile pulsation of an aneurysm is wanting. Numerous complications may be superadded in consequence of pressure upon and constriction of the esophagus and adjacent vessels. The prognosis is unfavorable. The treatment consists in the relief of the most prominent symptoms. ECHINOCOCCUS OF THE PLEURA, Echinococcus-cysts occur but rarely in the pleural cavity. They may rupture into the pleural cavity from the lungs or the liver, or, less commonly, they may develop primarily in the pleural cavity. At times they give rise to pleurisy especially purulent in character. They occasion dulness on percussion, with enfeebled vocal fremitus and respiratory murmur, the dulness being charac- terized by its irregular limits. At times they cause protrusion externally, and finally they rupture in the same direction. If puncture be deemed necessary, it would be important to examine the fluid obtained — which will be found free from albumin — for the presence of echinococcus-scolices, booklets, and laminated mem- brane. The patients often complain of stitch-like pain in the side and dyspnea. The condition is only susceptible of treatment by operative measures. VII. DISEASES OF THE MEDIASTINUM. MEDIASTINAL TUMORS. Anatomic Alterations. — Mediastinal tumors include new- growths of all kinds in the mediastinum. These are most com- monly situated in the anterior mediastinum. They are associated with especial frequency with diseases of the lymjDhatiG glands (lymphoma, sarcoma, carcinoma). Much less commonly they arise from the mediastinal connective tissue (fibroma, lipoma). At 172 RESPIRATORY ORGANS times they are dependent upon disease of the thymus gland (sar- coma). Sometimes osteomata arise from the sternum. Substernal struma also is inchided among' mediastinal tumors. In rare instances dermoid cysts and echinococci have been observed in the medias- tinal space. At times new-urowths extend from adjacent structures — as, for instance, the pericardium — to the mediastinum, where they attain considerable and conspicuous proportions during life. Ktiology. — In many instances no cause whatever for the development of mediastinal tumors can be elicited. In other instances traumatism is assigned as the cause. At times enormous enlargement of lymphatic glands takes place in the sequence of scrofufosis, leukemia, pseudoleukemia, and syphilis. Experience has shown that mediastinal tumors occur more commonly in men than in women. They appear mostly between the twentieth and the thirtieth year of life. Symptoms and Diagnosis. — Mediastinal tumors are at- tended principally Avith two groups of symptoms — in the first place with abnormal areas of dulness, and in addition with pressure upon and displacement of adjacent organs. Both groups of symptoms may be present together, or one alone may be encountered. Abnormal areas of dulness occur most commonly over the manubrium sterni, and it appears noteworthy in this connection that on percussion, in contradistinction from the normal conditions, the manubrium sterni yields a duller note than the body of the sternum. In the presence of mediastinal tumors of considerable size the area of dulness extends fir beyond the borders of the sternum, and if the new- growth has invaded the lungs throughout a large extent, the greater portion of the anterior aspect of the chest may yield dulness on percussion. Further, the marked resistance on percussion is often conspicuous. Tumors in the posterior mediastinum give rise to abnormal areas of dulness at the side of the vertebral column. In this situation also the dulness may attain a considerable extent. Pressure-phenomena and displacement involve especially the circu- latory and respiratory organs and the nerves. At times, however, the chest itself may be distorted in consequence of pressure, and particularly tlie manubrium sterni may undergo marked protrusion forward. At times the bony portions of the thorax may be eroded, and the new-growth may l)e situated directly beneath the skin. At the same time it may be the seat of pulsation transmitted from sub- jacent arteries, but the movement ahvays consists only in simple elevation and depression, and never, in contradistinction from an aneurysm, in expansile pulsation. The heart is often displaced down- ward and outward l)v mediastinal tumors, so that the apex-beat may be situated below the left fifth intercostal sjiace, and outside the left mam miliary line. Xot rarely the increased extent of the apex- beat is noteworthy, resulting from the greater application of the heart to the anterior wall of the chest. Often marked fulness and INFLAMMATION OF THE MEDIASTINUM 173 tortuosity of some cutaneous veins are noticeable if pressure has been exerted upon the veins. At times such vessels are apparent beneath the skin of the chest, at other times upon one side of the neck and face, at still other times upon one arm. Usually cyanosis is associ- ated, and frequently also circumscribed edema of the skin. Pres- sure upon arteries may give rise to retardation and reduction in the size of the pulse upon one side of the body. Cardiac-systolic mur- murs due to pressure may also be present. At times signs of uni- lateral or bilateral bronchostenosis appear. Cyanosis and intense dyspnea are occasionally due to pressure upon the lungs or to extension of the new-growth to the pulmonary tissue. Not rarely attacks of increased^ dyspnea occur, without the development of demonstrable alteration in the objective conditions. Large medias- tinal tumors may cause displacement of the liver and the spleen. Obstruction of the esophagus also may result from pressure. Fre- quently p«ra7y.sts of the recun'ent laryngeal nerve is caused by pres- sure. This is at times unilateral, at other times bilateral, or it may be at first unilateral and subsequently become bilateral. Pressure upon the cervical symjiathetic gives rise to pupillary changes. Uni- lateral irritation of the sympathetic causes dilatation, paralysis, and contraction of the pupil. Symptoms o^ paralysis of the vagus also occur, and are manifested by unusual slowness of action of the heart (irritation of the vagus) or, in the presence of paralysis of the vagus, by acceleration of the action of the heart. Attacks of spasm of the esophagus, eructation, and vomiting have also been attributed to irritation of the vagus. Irritation of peripheral nerves may give rise to severe neuralgia. The course of mediastinal tumors is generally chronic and fatal. Death results most com- monly from suffocation, though at times from progressive asthenia. Prognosis. — Mediastinal tumors require a serious prognosis in all instances, although in rare cases the possibility of recovery cannot be excluded, as, for instance, in those of syphilis. Treatment. — Causal treatment is probably applicable only in cases of syphilis, and then consists in the external and internal employment of preparations of iodin and of mercury. Opportu- nity for operative intervention will be but rarely afforded. Accord- ingly, symptomatic treatment alone will usually be available. It often becomes necessary to relieve the suflFerings of the patient as much as possible by means of narcotics, especially subcutaneous injections of morphin. INFLAMMATION OF THE MEDIASTINUM (MEDIASTINITIS). Inflammation of the mediastinum is one of the rarest of dis- eases. It occurs either as a chronic mediasfinitis, with cicatricial thickening of the mediastinal connective tissue, or as an acute medi- 1 74 RESl'IRA TOR Y One A y.s adiiiifis, Avhieli mav g-ivo rise to a circumscribed mediadinal abscess. Among causative factors traumatisrn, exposure to cold, infectious diseases, and injiainmation of adjacent organs are mentioned. Acute hicdiastinitis is attended witli .sejjfic manifestations (chiWsy fever). The patients frequently complain of a sense of pressure and pain beneatii the sternum, and not rarely also of difficulty in swallowing. The skin over the sternum exhibits redness and inflammatory collateral edema. Should a mediastinal abscess develop, dulness over the manubrium sterni appears if the accu- mulation of pus is situated in the anterior mediastinal space. Kupture of the pus may take place internally or externally, and in the latter event the pus may find its way beneath the skin of the neck or to some remote point in conseqiience of burrowing. At times large blood-vessels are eroded by the suppurative pro- cess, and fatal hemorrhage results. The diagnosis often remains doubtful during life. In the first place, antiphlogistics (ice-bag, leeches, inunctions of mercu- rial ointment) will be employed, and if the pus be not too deeply situated incision may be practised. The dangers of chronic mediastinitis consist principally in in- volvement, distortion, and angulation of large vessels or the esophagus or bronchial tubes. At times they give rise to paral- ysis of the recurrent laryngeal nerve. Treatment is futile. INTERSTITIAL MEDIASTINAL EMPHYSEMA, Accumulation of r/as in the connective tis.w.e of the rncdiastincd space may result from rupture of air-containing organs (lung, eso})hagus, stomach, intestine) into the mediastinum. It occurs frequently in association with interstitial emphysema of the lungs, and is then dependent upon the same causes. The principal manifestations include a clear percussion-note over the sternum, displacement of the heart outward toward the left, and of tiie liver downward, and crepitating and clacking rales with the movements of the heart. There may be dyspnea and a sense of oppression. The treatment is purely symptomatic. PART III. DISEASES OF THE DIGESTIVE ORGANS. DISEASES OF THE MOUTH. CATARRHAL STOMATITIS. Htiology. — Like most catarrhal conditions of mucons mem- branes, catarrh of the mucous membrane of the mouth may be due to mechanical, thermic, toxic, or infectious causes. It may, in addition, result from the extension of adjacent inflammation. Among mechanical etiologic factors the sharp edges of teeth may be especially mentioned. Thermic injurious agencies include burns due to hot articles of food. Toxic stomatitis occurs not only in the sequence of ingestion of corrosive acids, alkalies, and other poisons, but also in drinkers and smokers from the irritation caused by alcohol and tobacco. Catarrhal stomatitis occurs in infants if the mouth is not cleansed or is but imperfectly cleansed of remnants of milk, the fermentation of which then gives rise to irritation of the mucous membrane ; or if the cleansing of the month is effected by means of coarse cloths and with too much vigor. Under the conditions last named mechanical irritation of the mucous membrane of the mouth also takes place. At times catarrhal stomatitis arises after the internal or external employ- ment of certain medicaments, as, for instance, potassium iodid or bromid, arsenic, and mercury. Infectious catarrhal stomatitis is frequently of secondary origin, and develops in the course of other infectious diseases (typhoid fever, measles, scarlet fever, small-pox, syphilis). Little is known with regard to primary infectious catarrhal stomatitis. It may arise, for instance, by inoculation of gonococci upon the mucous membrane of the mouth. tStomatitis arising by extension from adjacent disease occurs ^vith especial frequency in the sequence of diseases of the teeth. In infants it accompanies the irruption of the teeth. Catarrhal conditions of the nares, the pharynx, and especially 175 176 DIGESTIVE onaAxs the stomach, frequently give rise to secondary catarrh of the mucf)ns nieinhrano of th(! mouth. Symptoms, Anatomic Alterations, Diagnosis, and Prognosis. — In accordance with the course of the disease a distinction shouhl be made between acute and chronic catarrhal stornatitiii. Tiie hitter occurs especially in drinkers and smokers. At times the condition is clrcumscribefJ, at other times (Uffasc. Acute catarrhal stoniatiiis is characterized by redness, swelling, and increased heat of the diseased parts. At times the lymph- follicles of the mucous membrane are greatly swollen, and supcr- iicial loss of tissue may take place. The patients complain prin- cipally of a sense of burning and even of pain in the mouth, and infants frecpiently dig their fingers into the mouth. The latter also not rarely cease nursing in the midst of the act, or they refuse nourishment altogether on account of the pain. The secretion of saliva is increased in consequence of reflex irritation. In children the saliva usually pours out of the mouth, often irritating the external integument and giving rise to linear redness correspond- ing to the course followed by the secretion. In adults, on the other hand, there is increased frequency in the act of swallowing. The tongue, as a rule, presents a grayish or yellowish, even a brownish coating, consisting of remnants of food, desquamated and fattily degenerated epithelial cells, bacteria, especially lepto- thrix-threads, but containing at times also cholesterin-plates and lime-crystals. At the margins of the tongue and also upon the mucous membrane of the cheeks the impressions of the teeth are visible in the form of grooved depressions. Often a disagreeable, fetid odor emanates from the mouth. Frequently complaint is made also of a disagreeable and pasty taste. At times there is increased thirst. Elevation of temperature occurs now and then in infants. The disease often terminates within a few days, and is unattended with serious sequelse. In cases of chronic catarrhal stomatitis also the mucous mem- brane presents an altered, and usually a brownish-red color. Often the epithelium is thickened and turbid, so that grayish- white spots form. At times painful fissures occur in the mucous membrane, but apart from these a sense of burning and of sore- ness in the mouth is often cotnplained of. Alcoholics and smokers not rarely suffer from chronic catarrhal stomatitis throughout life, but the disorder is quite a harmless one. Treatment. — The first indication is the removal of the causa- tive factors, causal treatment, and in addition the mouth should be rinsed after each meal with potassium chlorate (5.0 : 200). In infants the mouth should be carefully cleansed after each meal with the solution named by means of a bit of linen. Applica- tions of mercuric chlorid (0.5 : 50) or argentic nitrate (1.0 : 50) have been recommended for chronic catarrhal stomatitis. ULCERATIVE STOMATITIS 177 ULCERATIVE STOMATITIS, Symptoms, Anatomic Alterations, Diagnosis, and Prognosis. — Ulcerative stomatitis is characterized by gangren- ous destruction of the mucous membrane of the mouth, especially that of the gums. The disease begins as a rule with marked red- ness and swelling of the gums. Most frequently the gums of the lower jaw, especially around the left incisor tooth, are first affected. The gums are unusually soft, and bleed readily on the slightest touch. Eventually they are transformed into a necrotic brownish or blackish mass, which on microscopic examination is found to contain round cells, red blood-corpuscles, at times algae and infu- soria, but especially innumerable bacteria. At times the gum& are so completely destroyed that the teeth are loosened, and can be removed with the fingers without difficulty and without pain. The disease of the gums appears only in such situations where there are teeth. If any teeth are absent, the gums in those situa- tions escape. Edentulous infants are not attacked by ulcerative stomatitis. The patients complain of pain in the mouth, which is increased especially on the ingestion of food. The secretion of saliva is increased by reflex irritation. The saliva flows from the mouth, is often streaked with blood, and gives off" a disagreeable odor. The skin of the chin is frequently reddened in streaks by the saliva and slightly inflamed. The sleep is often disturbed in con- sequence of the excessive flow of saliva, which may enter the larynx or be discharged upon the pillow. Patients usually exhale a horribly offensive odor from the mouth, which permeates the air of the room within a short time, and becomes evident even to the patient, causing a distaste for food and drink. Usually adjacent lymph- glands, particularly the submaxillary, undergo inflammatory swelling. The patients not rarely acquire within a remarkably short time a grayish, almost cachectic appearance, and they suffer from unusual languor. The bodily temperature generally remains unaltered. The disease almost always terminates in recovery, although a patient under my observation died in consequence of septicemia. A distinction has been made between acute and chronic ulcerative stomatitis, accordingly as the disease terminates within one or two weeks or after the lapse of several months. In the absence of sufficient care in treatment adhesions may form between opposed ulcerated surfaces — as, for instance, between the mucous membrane of the cheek and the border of the tongue — and which often can be removed only with difficulty by operative means. At times the necrosis extends to the lower jaw. i^tiology. — A distinction should be made between infectious and toxic ulcerative stomatitis. The infectious variety often occurs 12 178 DIGESTIVE ORGANS endcmically, as, for instance, in l)arraeks, jails, orphan-asylums, boarding-sciiools. Over-crowded, poorly ventilated, and damp dwellings favor its development, as do likewise deficiency of food and neglect in the care of the mouth. The conditions named render it explicable that the disease has been encountered almost exclusively among the poorer classes. Ulcerative stomatitis is observed most commonly in children. Anemic, rachitic, scrofu- lous, and otherwise debilitated children display a marked predis- position to the disease. The disorder occurs most commonly in the summer months. Specific bacteria are as yet unknown in the etiology of ulcerative stoma- titis. The Staphylococcus pyogenes aureus has been obtained from the necrotic tissue. Toxic ulcerative stomatitis may be induced by mercurial prepa- rations, either because these have been employed in excessive doses or because the individuals are unduly susceptible to the action of mercury. Treatment. — Causal treatment will require the withdrawal of mercurial preparations, the provision of healthy dwellings, and food sufficient in amount and variety. Symptomatically, irrigation of the mouth after each meal with potassium chlorate (5.0 : 200) may be recommended. The food should consist especially of milk, weak wine, beer, broth, cocoa, coffee with milk and eggs. Hot and solid articles of food should be avoided on account of the pain in the mouth. APHTHOUS STOMATITIS. Sjrmptoms, Anatomic Alterations, Diagnosis, and Prognosis. — Aphtha? appear as yellowish or whitish deposits upon the mucous membrane of the mouth, which are surrounded by a red hyperemic zone, and in contradistinction from masses of casein or of thrush cannot be detached with the finger. They occur with especial constancy njwn the anterior aspect of the tongue, and upon the line of reflection from the gums to the mucous membrane of the lips. Their average size is between that of a lentil and that of a pea. They are at times roundish in shape, but by coalescence they may acquire an irregular shape. Their number is subject to wide variations. The patients complain of a sense of burning, and even of pain in the mouth. Infants, therefore, often suddenly cease nursing, or altogether refuse nourishment. There is usually increased secre- tion of saliva from reflex irritation. The general condition, as a rule, exhibits no alteration. In the course of a few days the spots disappear, becoming smaller and smaller by absorption or by curl- ing up at the margins, then becoming detached and exfoliated, and leaving a shallow ulcer, which within a short time becomes covered THRUSH 179 with epithelium, and heals without loss of structure. The disorder usually lasts from one to two weeks ; at times, in consequence of repeated relapses, somewhat longer. It is unattended with danger. At times there may be retention of saliva in the salivary glands if aphthae develop at the orifice of a salivary duct and cause obstruc- tion. Exceptionally acute nephritis has been observed in the sequence of aphthous stomatitis. Microscopic examination of the spots discloses the j^resence of fibrin admixed with a small number of round cells and bacteria (Staphylococcus pyogenes albus and aureus, the pneumococcus of Friedlander, the diplo- coccus of Stooss). It is assumed tliat aphthous stomatitis is an infectious disease, and that bacteria cause coagulation-necrosis of the epithelial cells of the buccal mucous membrane, so that fibrinous coagulation can take place in the exudate. The deeper layers of the mucous membrane are not involved in the inflammatory process. Ktiology. — Like most varieties of inflammation of the mouth, aphthous stomatitis occurs with especial frequency in children, par- ticularly anemic, rachitic, and scrofulous children. Any irritation of the buccal mucous membrane may be followed by the develop- ment of aphthous stomatitis. In infants it is observed in associa- tion with the irruption of the teeth, with uncleanliness of the mouth, and with irritation of the buccal mucous membrane from improper cleansing of the mouth. Aphthous stomatitis may be associated with the most varied diseases of the mouth (catarrhal stomatitis, ulcerative stomatitis, thrush). It may result also from the irrita- tion excited by sharp projections of teeth. In women the disease sometimes appears at the menstrual period or during pregnancy or lactation. At times it appears in the course of infectious diseases (typhoid fever, pneumonia, pulmonary tuberculosis, diphtheria). Occasionally aphthous stomatitis occurs epidemically, particularly in the summer months, and instances of contagion may also be observed. Treatment. — In the first place, all obvious causes should be removed — causal treatment. In addition the mouth should be rinsed after each meal with potassium chlorate (5.0 : 200) or, in the case of small children, brushed or carefully swabbed. THRUSH (STOMATITIS OIDICA), Symptoms, Anatomic Alterations, Diagnosis, and Prognosis. — Thrush is attended with the formation of whitish or yellowish deposits upon the mucous membrane of the mouth, which can be readily detached with the finger or a hard object. Micro- scopic examination discloses the presence of a readily recognized bacterium. The thrush-fungus, O'idium albicans, belonging to the budding fungi, forms in part septate thallus-filaments, in part roundish or elongated spores (Fig. 25). The tip and margins of the tongue are as a rule attacked first, although the proliferation 180 DIGESTIVE ORGANS may extend to the mucous membrane of the pharynx, the esoph- agus, and the kirynx, and cause varied disturbances in these structures. Microscopic examination has shown that the thrush-fungi ])enetrate between the cement-rsubstance of the uppermost layer of epitheUal cells, and then extend especially in the middle layer of epithelium, in which they cause atrophy by pressure. At times the fungous masses proliferate down to the submucosa, where they grow into the blood-vessels and the lymphatics. From this point fragmentation and embolic dissemination into the vessels of the brain have been observed. Patients suffering from thrush complain principally of a sense of burning and pain in the mouth, while the buccal mucous mem- brane appears reddened and inflamed, and the secretion of saliva is increased. The saliva yields an acid reaction, as in most varie- FlG. 25. — Thrush-fungus (O'ldium albicans) from the mouth of a child, nine mouths old (personal observation). ties of stomatitis, and it may contain no ptyalin. With careful attention the disease can be usually cured within one or two weeks, although in the case of a woman the duration was more than one and a half years. As a rule, the disorder is itself free from danger. In newborn children thrush is attended with diarrhea, which may threaten life. This is attributed to decomposition by the swal- lowed thrush-fungi of the ingested milk in the gastro-intestinal tract. ISIarkod proliferation in the esophagus may render swal- lowing im]i()ssible in infants, with danger of starvation. Ktiolog"y. — The conditions for the development of thrush are always provided whenever the mouth is not kept sufficiently- clean. The disease is, therefore, observed in the newborn and in LEUKOPLAKIA ORIS 181 infants whose mouths are not freed from residua of milk after each meal, or whose mothers or nurses do not regularly cleanse the nipple, or who are given inadequately cleansed nipples and nursing- bottles. In adults thrush develops in the buccal cavity in the sequence of long-continued and debilitating disease, such as diabetes, pulmonary tuberculosis, typhoid fever, leukemia, and carcinoma. Thrush-fungi gain entrance into the buccal cavity in part through inhalation from the air, in which the fungi have been demonstrated, and in part they are conveyed by solid substances to which the fungi have become attached. Thus, the thrush-fungi have been found upon both human and artificial nipples that were not properly cleansed. It should, therefore, not occasion surprise that epidemics of thrush have been observed in hospitals and materni- ties, particularly in the past. Thrush occurs with especial fre- quency in the summer months, because heat favors the develop- ment of fungi. Treatment. — Prophylactic and causal treatment furnish the same indications. Attention should be directed to careful cleans- ing of the mouth and of nipples and bottles. In addition irriga- tion or rinsing of the mouth with borax may be recommended : R Solution of sodium biborate, 5.0 : 200. For irrigation of the mouth after each meal. Grayish-white, frost-like deposits similar to those of thrush occur as a result of proliferation of sarcince in the mouth [stomatomycosis sarcinica), although microscopic examination will under such conditions disclose square fungi grouped together in fours side by side and also upon another. Sar- cinse may be readily confounded with the Micrococcus tetragenus, but it should be noted that with the latter the fungi lie enclosed in a common sheath in fours. LEUKOPLAKIA ORIS. This disease leads to the development of grayish-white, yel- lowish or brownish spots, which appear most commonly upon the tongue, but may occur also upon other portions of the buccal mucous membrane, and even upon the uvula, the arch of the palate, and the tonsils. At times a large portion of the buccal mucous membrane is covered with confluent spots. These are frequently raised above the adjacent surface, especially at the margins, and at times they appear cornified. Microscopic ex- amination discloses hyperplasia of the epithelial cells, with detach- ment and swelling in the superficial layers, flattening of the papillse, dilatation of the blood-vessels, and accumulation of round cells in the subepithelial tissues — in brief, signs of chronic inflam- mation. Among causative factors may be mentioned irritation of the buccal mucous membrane, such as often occurs in heavy smokers, in alcoholics, in consequence of carious teeth, in syphilitics, and 182 DIGESTIVE ORGANS in those with gastric disorders. Men are most commonly attacked, as may be readily understood from the nature of the causative factors. Often the disorder gives rise to no symptoms and is dis- covered purely by accident ; in other instances complaint is made of soreness, burning, or pain in the mouth and of impairment of taste. Frequently the patients exhibit a hypochondriacal tendency, and are harassed by a fear that they are suffering from an incurable disease of the stomach or from syphilis. The prognosis, however, should be cautious, as epithelioma has not rarely been observed to arise from leukoplakia. The treatment consists, first, in the removal of causative influences. In cases of syphilis iodin should be administered internally and applied topically. Suiferers from gastric disease at times obtain relief, and are even cured, by courses of treatment at Carlsbad or Yicliy. Among medicaments arsenic has been employed : R Solution of potassium arsenite, Bitter-almond water, each, 5.0 (75 minims). — M. Dose : 10 drops thrice daily after meals. In addition cauterization with lactic acid or chromic acid, topical applications of mercuric chlorid, argentic nitrate, tincture of iodin, or papayotin, and the galvanocautery have been recom- mended. 1. Geographical tongue is the name that has been given to an irregu- larly shaped collection of often confluent red spots upon the tongue lying below the level of the unchanged adjacent surface. Microscopic examination dis- closes in these situations desquamation of the uppermost layer of epithelial cells, round-cell accumulation among the remaining epithelial cells and in the papillary body, and a coagulated albuminous exudate in place of the desquamated epithelium. The disease either has been unattended with symptoms or has caused a sense of burning in the mouth. It has proved most obstinate and chronic, although the spots varied in shape from day to day. The disease attacks children most commonly, particularly anemic, scrofulous, and rachitic children. 2. Black, hairy tongue is characterized by a blackish discoloration of the tongue. Frequently the tongue presents also a felt-like roughness and multiple nodules. The condition is dependent especially upon hyperkera- tosis of the epithelial cells of the filiform papillse, the epithelial cells con- taining black and brownish pigment-granules. Such fungous formations as may be found are accidental contaminations that have nothing to do witli the black pigmentations. The condition, which is often unattended with symptoms, or at most gives rise to a sense of burning in the mouth, occurs especially in nervous, debilitated patients and those suffering from gastric disorders, and it can only be corrected by mechanical removal and cauteriza- tion of the hyperplastic epithelial structures. PTYALISM (SALIVATION), Symptoms, Diagnosis, and Prognosis. — Ptyalism con- sists in increased secretion of saliva, so that either the patients are compelled to swallow the saliva frequently or the mouth is kept PTYALISM 183 open and the saliva escapes, and must be received into a pocket- handkerchief or a receptacle of some kind. Often the integument of the chin is irritated by the discharge, and it is actively red- dened, and slightly inflamed. It should be noted that the escape of saliva is not a result of paralysis of sivalloiving (bulbar palsy). Earlier physicians designated this condition false ptyalism. The collected saliva usually appears turbid, as it contains epi- thelial cells and remnants of food. Occasionally it yields an acid reaction, and at times potassium rhodanate and ptyalin are absent. The patients suifer most from the distress dne to efforts at swal- lowing or in consequence of disturbed sleep. Some complain of a drawing sensation in the region of the parotid glands, and even of increased warmth and tension in the same situation. The amount of urine may be diminished. In ptyalism of parox- ysmal occurrence I have observed the amounts of urine and saliva to vary reciprocally. The duration of the disease is variable. At times ptyalism is a disorder of a few hours or wrecks, while at other times it may extend over years. In cases of chronic ptyal- ism progressive pallor and emaciation develop, because the large amounts of saliva swallowed interfere with gastric digestion. Ptyalism cannot be considered a disease directly dangerous to life, but the likelihood of cure depends upon the curability of the causative disorder. Ktiology. — Salivation results most frequently from reflex irri- tation of the salivary nerves ; much less commonly there is irrita- tion of the salivary centers of the cerebrum or the medulla oblongata, as, for instance, in consequence of central hemorrhage, softening, or new-growth. Ptyalism occurs also in the insane and the hys- terical. The influence of the cerebrum upon the secretion of saliva is recognizable from the fact that the thought or the seeing of food causes an accumulation of water in the mouth, thus an increased secretion of saliva. In consequence of reflex irritation ptyalism occurs in association with most diseases of the mouth and teeth. The irruption of the teeth also is usually attended with increase in the secretion of saliva. Ptyalism often occurs in con- nection with diseases of the stomach and bowel, as, for instance, chronic gastric catarrh and the presence of tapeworm in the intestine. Diseases of the liver, kidneys, and pancreas also are not rarely attended with ptyalism. Frequently the reflex irritation emanates from the sexual organs. It is well known that ptyalism not rarely occurs during pregnancy. In some persons an excessive secretion of saliva occurs before and during coitus. Sensory irrita- tion is at times attended with ptyalism, as, for instance, tickling of the skin or the hearing of shrill notes. Occasionally inflam- mation of the salivary glands themselves may be followed by ptyalism, but the opposite condition may likewise occur. At 184 DIGESTIVE ORGANS times it is impossible to elicit any cause for the ptyalism, and under such circumstances the condition has been designated idio- pathic or pr'unurij ptyalism. Salivation may be excited intentionally by means of various medica- ments, particularly Jaborandi- leaves and their alkaloid, pilocarpin hydro- chlorate. Treatment. — In order to suppress systematically an increased secretion of saliva there is but one trustworthy remedy, namely, atropin sulphate, which may be injected subcutaneously or be administered internally : R Atropin sulphate, 0.01 (J^ grain) ; Distilled water, 10.0 (2.} fluidrams).— M. Dose : From 0.25 to 0.5 (4 to 8 minimsj, subcutaneously once or twice daily. Or, B: Atropin sulphate, 0.005 {-^tj grain) ; Powdered althea-root, sufficient to make 10 pills. Dose : From 1 to 3 pills daily. In addition causal treatment should be pursued, and the causes of the salivation should be removed. An uncommon disease \» fibrinous sialodochitis. This alFection is attended with the formation of a fibrinous exudate and of coagula in the excretory ducts of a number of salivary glands, so that the discharge of saliva is pre- vented, and a sense of tension and swelling in the neighborhood of the affected glands develop. At times the disease occurs paroxysmally. Cure can be effected only by mechanical means, attempts being made to expel the coagula by pressure. II. DISEASES OF THE PHARYNX AND THE SOFT PALATE. CATARRH OF THE PHARYNX AND THE SOFT PAL- ATE (CATARRHAL PHARYNGITIS AND ANGINA). Ktiology. — Inflammatory processes in the soft palate are designated angina, because in swallowing a sense of constriction is felt at the site of inflammation. A distinction should be made between acute and chronic inflammation of the pharipix and soft palate. Among causative factors, adjacent infectious, chemic, thermic, and traumatic (mechanical) irritation, stasis, and inflamma- tion may be mentioned. lufectious inflammation usually pursues an acute coiwfie, and is at times primary and at other times secondary. When primary it develops as an independent infectious disease, and Avhen secondary it occurs in the sequence of other infectious diseases, among which CATARRH OF THE PHARYNX AND THE SOFT PALATE 185 may be mentioned scarlet fever, measles, syphilis, typhoid fever, erysipelas, and small-pox. Primary infectious inflammation of the pharynx and the soft palate was formerly attributed to exposure to cold, and it was therefore designated, rheumatic (refrigeratory), but at present the tendency is correctly to believe that the inflammation is not excited by the cold alone, but that this, by causing changes in the circulation, diminishes the resistance of the tissues to the invasion of low forms of organisms, and thereby favors infection. Recent bacterioloffic iuvestio:ations have shown that various bacteria are capable of exciting inflammation of the soft palate ; for instance, the Streptococcus pyogenes, the Staphylococcus pyogenes, the pneu- moniacocci of Friinkel, the pneumoeocci of Friedlander, and others. Experience has shown that the tendency to infectious angina is most irregularly distributed. Anemic, debilitated, and delicate persons as well as rachitic and scrofulous individuals, are attacked by infectious angina with especial frequency. Chronic hypertrophy of the tonsils likewise favors the development of the disease. The affection occurs most frequently in childhood, and it is recognized that those who have recovered from an attack of in- fectious angina often suffer several times during the remainder of life from the same disease. Not rarely it occurs in epidemic dis- tribution, or in institutions witli many inmates endemics appear from time to time. Meteorologic influences are of importance in this connection, as the disease occurs ^\'ith especial frequency and is widely distributed with sudden changes in the weather. The chemic irritants that give rise to angina include, in addition to actual caustics (acids, alkalies, mercuric chlorid, argentic nitrate), also indulgence in alcohol and tobacco. Alcoholics and smokers of tobacco suffer mostly from chronic angina and pharyngitis, because in them the injurious influences are constantly operative. Certain medicaments taken internally also may give rise to inflam- mation of the soft palate and the pharynx, particularly potassium iodid and mercury. Among thermic irritants hot articles of food are especially to be mentioned. Inhalation of hot vapors occurs much less commonly. In consequence of traumatic or mechanical irritation angina and pharyngitis occur with especial frequency in conjunction with in- halation of dust, and it should therefore not excite surprise that those engaged in certain occupations (millers, furriers, stonecutters, hatmakers, bakers, etc.) frequently suffer from chronic angina and pharyngitis. Continued and loud speaking also is capable of ex- citing the disease, and it is therefore frequently encountered in speakers, singers, actors, teachers, officers, and w^aiters. Hypostatic catarrh of the soft palate and thepjharynx usually pur- sues a chronic course, and occurs most commonly in the sequence of chronic disease of the heart or of the respiratory organs. Catarrlial pharyngitis and angina caused by extension from adja- 186 DIGESTIVE ORGANS cent disease develops in conjunction with inflammation of the nasal, larvngcal, and gastric nmcous membrane. Symptoms, Anatomic Alterations, Diagnosis, and ProgtlOSis. — i he sym})t()ni.s of acute catarrh of the .saft pa/atc and t/ic jj/tari/iix occur in purest form in cases of primary infection. The patients either are suddenly seized with fever, which may have been preceded by a chill or slight shivering, or general malaise and languor may occur for several liours or days as prodromes. The fever may subside suddenly within twenty-four hours, often Avith perspiration, but it not rarely persists for several days. The pa- tients at times present no other symptoms, and the affection may be recognized accidentally on inspection of the oropharyngeal cav- ity, resort to which may possibly be had because no explanation for the fever is ol)vious. Such conditions occur with especial fre- quency in children, in whom so-called ephemeral fever is often nothing more than the mauifestatiun of an acute angina. Labial herpes often appears. I have also not seldom observed enlargement of the spleen. As a rule, the subjective symptoms naturally direct attention to the diseased parts. The patients coniplain of severe pain in swal- lowing and in speaking at the junction of the buccal and pharyn- geal cavities, where also a sense of constriction is appreciable. This is induced in part by the inflammatory swelling of the dis- eased structures, partly also by the increased sensitiveness of the inflamed tissues. The pain is all the more noteworthy because the patients are compelled to swallow frequently in consequence of increased secretion of mucus. Yawning also induces pain, as the inflamed tissues are stretched in consequence of this act. Often the nasal speech is conspicuous, and it appears when the tonsils are greatly swollen and obstruct the nasopharyngeal space. Under such circumstances the mouth is generally kept open, in order that air may enter the larynx — mouth-breathing. The patients often hold the head stiffly, and avoid rotatory and nodding movements, because pain in the inframaxillary region and in that of the soft palate is thereby induced. On palpation of the inframaxillary region painful, hard, roundish structures are found on one or both sides in the neigliborhood of the angle of the jaw — inflamed and enlarged submaxillary lymphatic glands — representing tlie conse- quences of secondary infection. If the mouth be opened widely and the dorsimi of the tongue is depressed with a broad, hard body — for instance, the handle of a firm spoon — the changes in the inflamed structures can be well studied, and with greater accuracy than on the cadaver. These appear in three forms, which may be designated superficial, lacunar, and parenchymatous inflammation. In cases of superficial inflammation the aft'ected areas are charac- terized by vivid redness and swelling and increased secretion of mucus. At times follicles of the mucous membrane appear as CATARRH OF THE PHARYNX AND THE SOFT PALATE 187 small, enlarged, almost transparent nodules, partly because they contain retained secretion and partly because inflammatory cellular hyperplasia has taken place in them. In consequence of rupture superflcial follicular ulcers may develop. Here and there, also, superficial ulceration of the mucous membrane may occur in places where the epithelium has been desquamated. The altera- tions may be confined to circumscribed areas or they may involve the entire mucous membrane of the soft palate and the pharynx, sO that a distinction must be made between circumscribed and diffuse angina and pharyngitis. Lacunar angina is attended with the formation of yellowish or yellowish-gray deposits in the lacunse of the tonsils, so that the latter are often strewn with nodules averaging about the size of a pin-head. Often each nodule is surrounded by a red hyperemic zone. Not rarely the deposits extend gradually beyond the limits of the individual lacunse and coalesce, so that yellowish or grayish- green smeary deposits are visible upon the tonsils and, not rarely, also upon the uvula and the arch of the palate. On microscopic examination these are found to consist of round cells, fat-globules, needles of fatty acids, and cholesterin-plates, but especially of bac- teria (leptothrix-fi laments, Streptococcus pyogenes, Staphylococcus pyogenes, pneumoniacocci, etc.). The same anatomic alterations that occur in superficial and lacunar catarrh occur also in 'pharyn- geal diphtheria. The differential diagnosis can be made only by means of bacteriologic examination, for in all diphtheric diseases diphtheria-bacilli are found in the inflammatory products. Parenchymatous inflammation, also designated phlegmonous angina, is characterized by the formation of a circumscribed col- lection of pus, thus an abscess. It is usually attended with intense pain. The inflamed area is conspicuous for its great redness and prominence. The abscess often ruptures into the oropharyngeal cavity in the course of a few days, w4ien the pain at once dimin- ishes and the swelling is reduced in size. Often the inflammation disappears in the course of a few days. Most frequently the accumulation of pus takes place in the periglandular connective tissue about the tonsil — so-called tonsillar abscess. Disagreeable complications arise at times in consequence of rupture of the abscess and entrance of the pus into the larynx during sleep, with cough and danger of suffocation ; or in consequence of rupture of the abscess externally, with dangerous erosions of large blood- vessels in the neck, or burrowing downward of the pus, or rupture through the skin of the neck. Most cases of acute angina and pharyngitis terminate favorably within a few days. Among complications may be mentioned albu- minuria, which often disappears from one day to another, acide nephritis, jjaralysis of the muiicles of the palate, and septic cdtera- tions {multiple, painful articular sicelUng and endocarditis). The 188 DIGESTIVE ORGANS couviction has but recently been arrived at that the tonsils fre- quently constitute the portal of entry for bacteria into the body, even when those structures themselves remain unchancred. Chronic infiammation of the soft palate and the pharynx is unat- tended with fever, elevation of temperature taking place only when acute exacerbations occur. Superficial, lacunar, and parenchyma- tous forms of chronic inflammation also may be distinguished. In superficial chronic angina and pharyngitis the inflamed parts are notable for their brownish-red or grayish-red color and the abundant secretion of viscid mucus. Frequently a number of the vessels of the mucous membrane are tortuous and exhibit varicose dilatation. Bleeding may take place from these and give rise to hemorrhagic expectoration, so that many persons suft'ering from chronic pharyngitis believe themselves to be suffering from pul- monary tuberculosis. Owing to the presence of abundant secre- tion the mucous membrane frequently appears glazed. At times the mucus dries during the night into grayish-green mussel-like crusts, which in the morning occasion a feeling as if a foreign body were present, and often can be expelled only with difficulty after protracted hawking and struggling. Often the lymph-follicles of the mucous membrane undergo hypertrophy, and also new lymph- follicles form, so that the posterior wall of the pharynx especially is strewn with small gray nodules — granular pharyngitis. The patients complain of a feeling as from the presence of a foreign body, even of pain and soreness in the pharyngeal cavity, while an abundance of viscid mucus gives rise to increased frequency in the act of swallowing, and often to retching and nausea. The symp- toms mentioned usually become apparent in speaking and singing, particularly also in the morning if during the night there has been opportunity for the mucus to collect and become adherent in the pharyngeal cavity, and it is a common observation that such patients begin the day with a rather protracted period of hawking and retching, which subside only with the completion of the toilet of the pharynx. Impairment of hearing and tinnitus aurium occur not rarely as complications, either because the buccal orifice of the Eustachian tube becomes occluded by swelling of the mucous mem- brane of the pharynx or because the catarrhal condition itself has extended to the mucous membrane of the tube, and at times even to the tympanic cavity. Although the aflection is not a fatal one, it is nevertheless an extremely obstinate and troublesome one, as it often renders the pursuit of the patient's occupation most diffi- cult, and at times even impossible. In chronic lacunar angina, as in the acute form, yellowish or gravish smeary masses accumulate in individual lacunae of the tonsils, consisting princijially of bacteria, and especially of lepto- thrix-filamcnts. ^V.hcn crushed these plugs emit a most offensive odor. The patients complain principally of a sense of tickling. CATARRH OF THE PHARYNX AND THE SOFT PALATE 189 or of the presence of a foreign body, and from time to time hawk up the accumulated plugs. At times these undergo calcification, and form tonsillar calculi, and are from time to time expelled by hawking. They may possibly be mistaken by the patient for calcified tubercles from the lungs. The disagreeable odor may be a source of distress to the patient. Parenchymatous angina and pharyngitis are attended with in- flammatory hypertrophy of the diseased structures. If the tonsils are involved in the inflammation, they may attain double their normal size, and they not rarely project into the entrance of the pharynx to such a degree as to come in contact in the middle line. In consequence speech suffers and acquires a nasal character ; be- sides, the patients are consequently compelled to breathe through the mouth, and they snore during sleep. Finally the orifice of the Eustachian tube becomes obstructed, and impairment of hear- ing and tinnitus aurium result. It should not be forgotten that inflamed and hypertrophied tonsils manifest a tendency to acute inflammation, and frequently are the seat of acute recurrent dis- ease. In some cases the uvula undergoes hypertrophy, and its tip may come to lie upon the dorsum of the tongue. The patients then complain frequently of retching and nausea. At times chronically inflamed jjharyngeal mucous membrane presents a pale, atrophic, and attenuated appearance — chronic atrophic pharyngitis. Frequently similar alterations are at the same time present upon the nasal mucous membrane. Of the chronic inflammatory conditions of the soft palate and the pharynx it may be said that none is dangerous to life, while all are distressing affections, curable with difiiculty, particularly as they are often dependent upon the occupation or upon bad habits (smoking, alcohol), which the patients are unwilling to give up. Not rarely chronic angina and pharyngitis predispose to the occur- rence of chronic catarrhal conditions of the nasal, laryngeal, tra- cheal, and bronchial mucous membrane. At times nervous com- plications also arise through reflex influences, as, for instance, bronchial asthma, and even epilepsy. Treatment. — Patients suffering from acute angina and phar- yngitis should remain in bed, and partake only of a liquid diet, preferably milk, and inhale every two or three hours a solution of potassium chlorate through the apparatus of Siegle. Gargles are less worthy of recommendation on account of the unavoidable irritation of the inflamed structures : R Potassium chlorate, 5.0 : 200. For inhalation (or gargling) every two or three hours. If the mucous membrane is the seat of severe pain and great swelling, bits of ice may be sucked. The application about the neck of a long rubber bag filled w^ith ice may also be recom- mended — a so-called ice-collar. If parenchymatous inflammation 190 DIGESTIVE ORGANS is complicated by the formation of an abscess, escape of the pus externally must be provided for by incision. Chronic auf/ina and pharyngitis demand, in the first place, thorough considera- tion of the causative influences, causal treatment, and, for instance, excessive indulgence in alcohol and t()l)acco must be as rigidly as possible enjoined, and the patient should be advised to avoid loud and continuous speaking and the inhalation of dust. Sjrmptom- atic treatment consists principally in the local employment of gargles, topical ap])lications, insufflations, cauterization, inhala- tions, and a sojourn at certain springs. At times surgical inter- vention becomes necessary.- For gargling solutions of potassium chlorate, alum, sodium chlorid, sodium bicarbonate, and ammo- nium chlorid have been recommended — all in the proportion of 5.0 : 200. The therapeutic agent must be varied from time to time, as the mucous membrane readily becomes accustomed to the same remedy, and is then no longer susceptilile to its influ- ence. For topical application dilute tincture of iodin especially may be recommended, but it is to be Avithheld if a more acute inflammation results in consequence of the application. Imme- diately after the application the patient should gargle with water : B Tincture of iodin, Tincture of galls, each, 5.0 (75 minims). — M. Use daily as an application with a brush. Insufflations are made Avith either a glass tube or a quill, and tannic acid, alum, or iodoform may be employed for the purpose. Caustics (silver nitrate, copper sulphate, chromic acid, the gal- vanocautery) are especially applicable to granular pharyngitis. InJtalations may be practised with the aid of Siegle's apparatus, and the same medicaments are employed as have been named for gargling. Courses of treatment at springs often yield good results because the patient is for a time removed from the exciting causes. Especial repute in this connection is enjoyed by sulphur-springs (Aachen, Baden, Heustrich, Nenndorf, Schinznach, Stachelberg, Weilbach), chlorin-springs (Eras, Homburg, Kissingen, Reichen- hall, Soden, Wiesbaden), and ioclin-springs (Salzbrunn, Tcilz, Adelheid Springs). Hypertrophied tonsils and elongated uvulas should be removed by surgical means. In order to avoid recur- rences of inflammation of the soft palate and the pharynx certain prophylactic measures should be observed. These will vary in accordance with the nature of the exciting cause, and consist in part in intelligent hardening of the body and in part in protec- tion against inhalation of dust and the like. MYCOSIS PHARYNGIS LEPTOTHRIOA, This disorder is attended with the formation of yelloicish spots, often apparently cornified, which lie especially in the lacunae of the CARCINOMA OF THE ESOPHAGUS 191 tonsils, and on microscopic examination are found to consist prin- cipally of leptothrix-filaments. The disease either is unattended with symptoms, and is discovered accidentally, or it gives rise to the feeling of a foreign body and to efforts at retching. At times the fungous granulation extends to the dorsum of the tongue, espe- cially to the circumvallate papillee, and to the mucous membrane of the larynx and even of the trachea. The affection, which is in itself free from danger, is usually most obstinate. At times it has been observed to disappear spontaneously ; at other times it seems to be dissipated by smoking. In addition, gargling ivith mercHi'iG chlorid (1.0 : 2000), and mechanical, removal of the deposit and its destruction by means of the galvanocautery , have been employed. III. DISEASES OF THE ESOPHAGUS. CARONOMA OF THE ESOPHAGUS. * Anatomic Alterations. — Carcinoma of the esophagus is almost exclusively of primary origin. Only a few instances of secondary carcinoma, arising from dissemination of the germs of the disease from other organs previously the seat of carcinoma, are known. Most frequently carcinoma of the esophagus is situ- afed just above the cardia, but somewhat less commonly it devel- ops at the level of the bifurcation of the trachea, and least commonly it occurs at the beginning or in any other portion of the esophagus. It is rare for isolated carcinomata to be present in several portions of the esophagus. The new-growth begins as a small insular formation, and then forms upon a more or less extensive portion of the mucous membrane a roundish nodule pro- jecting into the lumen of the esophagus. As a rule, it is gradu- ally transformed into a girdle-shaped or annular carcinoma, as it encircles the entire circumference of the esophagus like a ring. The mucous membrane in the diseased area is thickened to the extent of several centimeters, and consists here of a whitish, medullary, friable tissue. This may be observed also in the muscular layer of the esophagus, in which extension within the connective-tissue septa takes place. The muscular layer under- goes thickening, and even the external surrounding connective tissue. Histologically, carcinoma of the esophagus is always of the pavement epithelial variety. The morbidly proliferated, squamous epithelial cells are derived from the epithelial cells of the mucous membrane, but in part also from those of the glands of the mucous membrane. 192 DIGESTIVE ORGANS As may be understood, stenosis of the esophagus occurs at the situation of the new-growth. Above the point of constriction dikitation of the esophagus takes place at times, but by no means constantly, while, below, the eso})hagus may be unusually narrow. The tracheobronchial glands adjacent to the esophagus are usually enlarged and the seat of carcinomatous infiltration. Less com- monly similar alterations are present also in the cervical lymphatic glands. Like carcinoma elsewhere, that of the esophagus also exhibits a tendency to consfant r/roirfh and to dmntegration. The first quality is responsible for the fact that in the course of the disease the constriction of the esophagus increases, and that at times adjacent organs are compresseil and impaired in function, as, for instance, the recurrent laryngeal nerve. As a result of disintegration of the carcinomatous tissue ulceration takes place, leaving an eroded and villous, and at times an offensively smell- ing, surface. The destruction may become so extensive that scarcely any carcinomatous tissue is visible, and the nuiscular layer of the esophagus is exposed as if dissected free. Formerly it was even erroneously supposed that the ulcer under\\ent cica- trization, and that the carcinoma was as a result capable of being entirely healed. The disintegration of the carcinomatous tissue further is attended with the danger that adjacent organs may be attacked, and rupture of the esophagus take place into them (pleura, lungs, trachea, mediastinum, aorta, pericardium). Persons dying of carcinoma of the esophagus present extreme emaciation, brown atro])hy of the myocardium, and almost emptv intestines. Ktiologfy. — Clinical observation has shown that carcinoma of the esophagus, like carcinoma of other organs, occurs late in life (after the fortieth year), and in men with twice the frequency that it occurs in women. Immediate causes are, as a rule, not elicit- able, although I have observed the disease in numerous instances in drinkers and smokers, so that I would ascril)e some etiologic influence to the irritation of the mucous membrane of the esoph- agus by alcohol and swallowed tobacco-juice. Some patients attribute the disorder to the entrance into the larynx of hot articles of food or foreign bodies. In a few instances carcinoma has been observed to doveloji from ulcers of the esojihagus. Symptoms. — The most constant, and frequently also the first, symptom of carcinoma of the csoj)hagus consists in spontaneously developed and progressively increasing stenosis of the esophagus. In other instances other suspicious symptoms have appeared, first among which particularly pain and paralysis of the recurrent laryngeal nerve are to be mentioned. I have at times observed pain to precede by months the earliest difticulty in swallowing. The pain always remained confined to the same situation, and was at times referred to the vertebral column, and at other times behind the sternum. It frequently increased in intensity during the night CARCINOMA OF THE ESOPHAGUS 193 and disturbed sleep. No resistance was found on introducing a bougie into the esophagus, but the same point in the esophagus remained constantly sensitive on contact with the instrument. Paralysis of the recurrent laryngeal nerve as a result of carcinoma of the esophagus is due either to pressure or to proliferation of the new-growth in the trunk of the nerve. Usually it is the left recurrent nerve that is affected, but less commonly both are in- volved in the paralysis. Unilateral paralysis of the recurrent laryngeal nerve can be recognized only by laryngoscopic examina- tion (cadaveric position of the paralyzed vocal band, page 91, Fig. 17) ; when both vocal bands are paralyzed disorders of speech, in cough, and in expulsion are also present. In some cases my atten- tion was attracted entirely by secondary carcinoma in other organs (liver, cranium), and the carcinoma of the esophagus was over- looked because the patients failed to complain of either difficulty in swallowing or pain in the esophagus. Progressive difficulty in swallowing, in consequence of increasing stenosis of the esophagus, begins as a rule gradually. Exceptionally, however, I have observed it to set in suddenly, and further after great mental and physical exertion and strain. The patients gener- ally note at first that customary boluses of food will not pass beyond a given point in the esophagus, but threaten to remain impacted. The endeavor is made to avoid this circumstance by the swallowing of smaller boluses, but these after a time also encounter obstruction. Other expedients are attempted, such as more thorough chewing of the food and more complete insalivation of the food, together with rotatory movements of the head and neck, but these also fail after a time. Finally, the only resource left is to restrict the diet to fluids, because all solid substances are regurgitated in a macerated state shortly after ingestion, and excessive distention of the esoph- agus with solid material gives rise, by pressure partly upon the trachea and partly upon the adjacent vagus, to shortness of breath, a sense of anxiety, and palpitation of the heart. The ingestion of liquids, also, is attended with increased resistance, and thus the patient passes gradually into a state in which no food can be intro- duced into the stomach and the bowel through the mouth, and death from starvation cannot be long deferred. It is distinctive of the food regurgitated that, in contradistinction from the acid con- tents of the stomach, it yields a neutral reaction and not rarely has a fetid odor. Amylacea are partially transformed into sugar in the esophagus by the saliva, and the patients therefore often state that the regurgitated matters possess a sweetish taste. Further, repeated variations in the degree of stenosis of the esophagus occur in the course of the disease, partly because portions of the new- growth are broken off, and the lumen of the eso])hagus is thus increased, partly because at times ingested materials become im- pacted above the constriction. 13 194 DIGESTIVE ORGANS The patients uiulorgo progressive emaciation, and tlie skin acquires a grayish-yellow or earthy hue and a leathery and wrinkled aj)pearance. Owing to their asthenia the patients are compelled to remain in bed, and f"re(piently on assuming the erect posture they suffer, in consequence of cerebral anemia, from tinnitus aurium, obscurity of vision, palpitation of the heart, and syncope. At times delirium due to inanition occurs. The abdo- men is generally scaphoid on account of the empty state of the intestines, and tlie bowels are obstinately constipated. The urine is voided in small amounts and contains much indican. The bodily temperature is often subnormal. Progressive apathy sets in, and finally gradual dissolution takes place. The duration of the disease is usually more than six and less than twenty- four months. Naturally, when carcinoma of the esophagus is suspected investigation for ol)jective evidence of the presence of stenosis of the esophagus should never be omitted, and the only certain way of doing this consists in the introduction of a bougie into the esophagus. The most serviceable bougies are the Enf/lish red bougies with lateral fenestra. If it be desired to determine the degree of stenosis, bougies of varying size should be employed. It is important to examine microscopic- ally with care the substances caught in the fenestra, as these sometimes consist of carcinomatous tissue, considei'ation being given especially to the abundant presence of ])avement epithelial cells, with numerous nuclei, and to spherical laminated epithelial cells (carcinoma-nests or carcinoma-pearls). If these structures be not found, the examination with the bougie will dis- close only the presence of stenosis of the esophagus, and the carcinomatous character of the affection must be determined from other circumstances. In order to learn the seat of the disease the simplest method consists in applying the bougie externally alone the mouth aud the vertebral column, and noting the position of the tip of the instrument. The observation can be made more precisely by measuring the bougie with a centimeter-measure and comparing the result with the average measurements of the esophagus. The following are the dimensions of the esophofjus : Entire length of the esophagus, 2o cm. (9.8 inches). The distance from the edge of the teeth to the beginning of the esoph- agus, 15 cm. (5.9 inches). Length of the cervical portion of the esophagus, 5 cm. (1.9 inches). Length of the dorsal portion, 17 cm. (G.7 inches). Length of the abdominal portion, 3 cm. (1.2 inches). The point of intersection between the esophagus and the left bronchus cross is : From the beginning of the esophagus, 8 cm. (3.1 inches). From the edge of the teeth, 15 — 8 = 23 cm. (9 inches). Should a bougie not be at hand, tentative observations should be made by auscultation of the esophagus. The stethosco]ie is applied along the left side of the vertebral column from the seventh cervical to the eleventh dorsal vertebra. If the ])atient swallows water when directed, there is heard in healthy persons throughout the entire course of the esophagus a peculiar sound like that which every one may hear when the ears are closed with the fingers and the act of swallowing is practised. In persons suftering from stenosis of the esophagus this swallowing sound is audible only down to the point of constriction, while below this it is wanting. The stoallowing sounds of the stomach also are altered in the presence of constriction of the CARCINOMA OF THE ESOPHAGUS 195 esophagus. In order to detect these the stethoscope is placed in the angle between the ensiform cartilage and the left costal margin while water is swallowed. In healthy persons two murmurs will be audible in from five to ten seconds, the first of which is designated the injection-sound and the second the expression-sound. These sounds are explained by the fact that the ingested fluid is usually forced through the esophagus into the stomach by the contraction of the muscles of the oropharyngeal cavity, and that then the remainder is forced into the stomach by contraction of the muscu- lature of the esophagus. When the esophagus is constricted the injection- sound occurs after an unusually long interval, and often appears gurgling and prolonged, while the second sound is often wanting. For the detection of alterations in the esophagus, examination with mirrors — esophagoscopy — has been proposed, but this has not yet received general application, prin- cijially because the instruments thus far constructed are not sufficiently mauipulable on the part of both physician and patient. Carcinoma of the esophagus is not rarely attended with com- IjlicaUons, which may give rise to serious consequences. Paral- ysis of the recurrent laryngeal nerve has already been considered. Bilateral recurrent paralysis renders easily possible the entrance of foreign bodies into the air-passages, with the development of aspiration-pneumonia, abscess, and gangrene of the lungs. Similar alterations in the lungs occur not rarely also Avithout recurrent paralysis, because in the act of regurgitation individual masses of food readily enter the larynx and the deeper air-passages. In some instances I have observed symptoms of paralysis of the sympathetic nerve (contracted pupils, narrowing of the palpebral fissure, recession of the eyeball). Occasionally serious hemor- rhage takes place, at times soon after the introduction of a bougie into the esophagus, and at other times spontaneously. In the latter event the bleeding may be due to disintegration of carcino- matous tissue and perforation of blood-vessels, or to erosion of adjacent large blood-vessels, as, for instance, the aorta. Under such circumstances death may take place rapidly from hemor- rhage. Often rupture of the esophagus into adjacent organs takes place, most frequently into the left bronchus. The patients are then seized with severe cough after the ingestion of food, and expectorate portions thereof. Further, aspiration-pneumonia and abscess and gangrene of the lung soon develop, because a portion of the food enters the deeper air-passages. In other instances rupture takes place into the larynx, directly into the lungs, into the pleural cavity, or into the mediastinum. If air enters the mediastinal connective tissue from the esophagus, it generally extends upward beneath the connective tissue of the jugular fossa, with the development of subcutaneous emphysema (projec- tion of the skin, crepitation on manipulation). I have frequently observed rupture of the esophagus preceded for several days by inexplicable febrile movement. At times carcinoma of the esoph- agus extends to the vertebral column, destroying the vertebrae, and giving rise to spinal pressure-paralysis. The complications 196 DIGESTIVE OliGANS include further secondary or metastatic carcinoma in other organs, as, for instance, in the liver, and these may dominate the clinical picture to such a degree that the primary growth in the esophagus will be overlooked. Diagnosis. — The diagnosis of carcinoma of the esophagus is usually indirect. In a person at a susceptible age constriction of the esophagus is found, and its carcinomatous nature is decided upon because of its develoj)ment without demonstrable cause, its gradual increase, its advance Avith progressive asthenia, and its continuance without appreciable alteration in organs contiguous to the esophagus. It is rare that portions of the new-growth are caught in the fenestra of the bougie that on microscopic ex- amination can be definitely recognized as carcinomatous, or that portions of the growth are found in the regurgitated matters. Especial care should be taken to determine that the stenosis of the esophagus is not dug to an aneurysm of the aorta, and in no instance should a bougie be introduced into the esophagus until aneurysm of the aorta has been excluded by the absence of ab- normal duluess, vascular murmurs, and alteration in pulse. If this precaution be neglected, it may happen that an aneurysm of the aorta compressing the esophagus may be perforated by the tip of the bougie, and death result rapidly from hemorrhage. With regard to othe?' varieties of stenosis of the esophagus a few remarks of etiologic significance may be apjjropriate at this jjlace. The symptoms and the treatment agree essentially with those of the stenosis due to carci- noma. In accordance with the seat of the constriction a distinction is made between intra-esophageal, parietal, and extra-esophagcat stawsis of the esopjh- agtis. Intra-esophageal stenosis may be due to the lodgment of articUs of food and foreign bodies and proliferated thrush-masses. Parietal stenosU< of the esophagus may result from cicatrices in the sequence of burns, corrosion, tuberculous, diphtheric, peptic, and syphilitic ulcers, and variola. It occurs in association with nev-groirths (carcinoma, polyps, gummatous nodules) and abscesses. Pulsion-diverticula Avhen filled give rise to constriction of the esophagus. Among other causes for constriction of the esophagus that have been mentioned are congenital stenosis, hypertrophg, and spas7n of the rmisculatiire of the esophagus. Extra-esophageal stenosis may also be desig- nated compression-stenosis of the esophagus. The following examples may be mentioned : Aneurysm of the aorta, pericarditis, pleurisy, ne\v-growths of the lung, the mediastinum, the pleura, the pericardium, the vertebral col- umn, the thyroid gland (struma), ossification and thickening of the cricoid cartilage, burrowing abscesses of the vertebral column, luxation of the hyoid bone. Prognosis. — The prognosis of carcinoma of the esophagus, as of carcinoma elsewhere, is unfavorable, and a fatal issue is unavoidable. Treatment. — Internal remedies for the cure of carcinoma are not known, and the only reliable method of treatment con- sists in removal of the growth with the knife. As a matter of fact, resection of the carcinomatous portion of the esophagus has been attempted, but the operation naturally can only be undertaken DIVERTICULA OF THE ESOPHAGUS 197 when the carcinoma is sitnated in the cervical portion of the esophagus and is thus accessible to the knife — and this is un- common. In the majority of cases symptomatic treatment alone is possible, and the indications are by means of nutritious food to maintain the strength and to prolong life as well as possible, and to preserve the permeability of the esophagus. The most suitable diet consists in liquids and soft food. Among these may be mentioned milk with somatose, broths, milk with tea, milk with chocolate, milk with cocoa, eggs, wine, beer, rice, oatmeal- gruel prepared with milk, beef-tea, scraped ham or tenderloin, tender meat-sausage, and chopped meat. Food should be taken every hour, but slowly and not too much at a time. In order to main- tain the patulousness of the esophagus for as long a time as pos- sible systematic employment of the bougie should be practised daily or at intervals of several days in accordance with existing con- ditions. Even if the sound cannot be passed through the con- stricted portion of the esophagus, deglutition will be rendered materially easier or again possible. Attempts have been made to introduce permanent catheters through the constricted portion of the esophagus and permit them to remain, but objection has been raised to this procedure from various sources that it favors disin- tegration of the tumor. If the stricture of the esophagus has become impassable, two methods only remain of introducing food into the body — either gastrostomy or nutrient enemata. Ga,stros- tomy has heretofore not been attended with brilliant results, per- haps because it has generally been undertaken too late ; nor can life be prolonged for any considerable length of time by means of nutrieait enemata, because it is impossible to secure absorption of a sufficient amount of nutrient material from the mucous mem- brane of the large intestine. The following formula may be recommended as a nutrient enema : 150 c.c. of lukewarm milk, 150 c.c. of lukewarm, slightly salted meat-broth, two eggs, 3 teaspoonfuls of somatose, 2 tablespoonfuls of starch-flour, 1 tea- spoonful of sugar, and 10 drops of tincture of opium. By means of a Hegar funnel a mixture of this sort at the temperature of the body is permitted to flow into the rectum thrice daily — in the morning three hours after having evacu- ated the contents of the rectum by means of cold water. Great difficulty arises from the circumstance that the patients, by reason of their weakness, are unable to retain the enemata, or that, in spite of all care, the mucous membrane of the rectum soon becomes irritable, and in consequence reten- tion of the enemata is impossible. DIVERTICULA OF THE ESOPHAGUS, A diverticulum of the esophagus consists in cii-cumscribed dilatation of this tube. A distinction is made between pulsion- diverticula and traction-diverticida, accordingly as the dilating force is applied from within outward or traction is exercised from without. 198 DIGESTIVE ORGANS Pulsion-diverticula arc almost always situated at the jnnetion of the pharynx w itli the esophagus, and are rather a part of" tiie former. Most commonly they arise in the middle line, bulging outward from this situation in one or both directions. Under such conditions they may attain the size of a child's head. On anatomic examination they are frecfuently found to be unsupplied with a muscular layer, so that it has been correctly assumed that the tendency to the development of a pulsion-diverticulum is con- genital, and is attributable to deficient development of the muscular layer, and therefore to diminished resistance on the part of the wall of the esophagus. Other observers are of the opinion that pulsion-diverticula result from incomplete internal cervical fistulse in the region of the first branchial cleft. Persons with pulsion- diverticula of the esophagus frequently state that, after eating, a swelling forms on the left side of the neck, which gradually increases in size with the further ingestion of food. Pressure and manipulation may cause disappearance of the swelling, ^vhile the patients are conscious of the entrance of food into the esophagus. At the same time loud gurgling murmurs are not rarely generated. The diverticulum has a tendency to intercept swallowed articles of food, and during the process of eating to have its orifice directed more and more into the lumen of the esophagus. Often regurgitation of the food takes place some time after its ingestion. The ejected matters appear macerated, and often emit a fetid odor. On introducing a bougie into the esophagus it will be observed that at times the instrument passes readily into the esophagus, while at other times it is obstructed if its extremity enters the divertic- ulum. It may also happen that if two bougies are introduced into the esophagus the one will enter the diverticulum, while the other passes into the stomach without obstruction. By distention with the aid of a teaspoonful each of sodium bicarbonate and tartaric acid, given separately in a wineglassful of water, it may be pos- sible to induce a prominence in the neck, which on percussion yields a tympanitic note. A pulsion-diverticulum is attended with the danger of progressive emaciation and of sfarration, for in addi- tion to the interception of food a distended pulsion-diverticulum, by projecting into the esophagus, prevents the passage of food to the stomach. Pulsion-diverticula have recently been excised suc- cessfully ; otherw^ise the only remedy would consist in systematic nutrition by means of the stomach-tube. Pulsion-diverticula occur mo,'it comuionlji in men. The earliest symptoms usually do not appear until the fortieth year of life, and they are often attributed to swallowed foreign bodies, injuries of the cervical region, and constrictina: articles of clothins:. Ossification and thickening of the cricoid cartilage occurring late in life appear also to be of causative influence. Traction- diverticula of tlie esophagus are not recognizable during DILATATION OF THE ESOPHAGUS. 199 life on account of their smallness. They are most frequently situ- ated at the level of the bifurcation of the trachea, for they are principally dependent upon inflammatory alterations in the tracheo- bronchial lymph-glands. In consequence of periadenitis adhe- sions readily form between the lymphatic glands and the esophagus, and if subsequently contraction and diminution in size take place in the inflamed lymphatic glands the wall of the esophagus is drawn outward in the form of a small, acute funnel. Often the glandular structure will be visible at the apex of the funnel as a dark body. The danger from traction-diverticula resides in their tendency to rupture, aiKl this may occur spontaneously or be caused by incarcerated, hard particles of food. Rupture may take place into the air-passages, when the entrance of food gives rise, in addition to distressing irritative cough, also to inflammation, sup- puration, and gangrene of the lungs ; or into the mediastinal con- nective tissue, where it gives rise to putrefaction or to accumulation of air, or to both ; or into the pleura, the pericardium, or the aorta, with the development respectively of pleurisy or pericarditis, or the occurrence of death from hemorrhage within a short time. DILATATION OF THE ESOPHAGUS, Dilatation of the entire esophagus may be congenital or acquired, and in the latter event some of the causes mentioned include fre- quent vomiting, excessive ingestion of hot water, impaction of hot food, chronic catarrh of the esophagus, a blow upon the chest, and the carrying of heavy weights. The dilatation of the esoph- agus is at times spindle-shaped and at other times more uniform. In the first instance, the greatest degree of dilatation usually cor- responds with the mid-dorsal region. The dilated esophagus is at times capable of enclosing a man's arm, but it is also considerably increased in length, and at times makes numerous lateral turns in its course. Dilatation of the esophagus may be recognized from the fact that considerable lateral movement can be made with a sound that has been introduced. If, on the other hand, the esoph- agus makes lateral turns, the introduction of the bougie may be attended with considerable difficulty. Under such conditions the patients also complain of, difficulty in swallowing and often regur- gitate ingested matter, and they may slowly undergo great emaci- ation and die in consequence of inanition. Experience has shown that difficulty in swallowing generally does not occur until after the twentieth year of life. Partial congenital dilatation of the esophagus constitutes the so-called ante-stomach, which consists in a dilatation of the ]3or- tion of the esophagus that is situated below the diaphragm. The condition is without significance, and has nothing to do with rumi- nation, as was formerly supposed. 200 DIGESTIVE ORGANS Secondary dilatation of the esophagus takes place above con- strictions of the esophagus, but it is by no means a necessary consequence of such conditions. The dilatation becomes the ijreater the o;reater the amoimt of food ing;ested and the lony-er it remains above the constriction. CATARRHAL ESOPHAGITIS, Ktiology. — Catarrh of the esophagus is of only subordinate clinical importance. It develops, like catarrhal conditions of otlu'r mucous membranes, in consequence of the action of mecliaiii- cal (hard articles of food, swallowed foreign bodies, careless intro- duction of the sound), toxic (the swallowing of acids, alkalies, and other corrosive substances), and thermic irritants (hot articles of food, abuse of alcohol and of tobacco). Infectious influences prob- ably play a part in the inflammatory processes that develop in the course of certain infectious diseases (small-pox, measles, scarlet fever, typhoid fever, erysipelas). At times inflammation of the mucous membrane of the esophagus arises by extension from catar- rhal conditions of the stomach, the pharynx, the larynx, the bron- chi, from mediastinitis, pericarditis, and pleurisy. A special variety is constituted by the hifpostatie catarrh that is observed in connection with chronic cardiac and respiratory diseases. In accordance with the course of the disease a distinction has been made between acute and chronic, and, in accordance with its dis- tribution, between diffuse and circumscribed catarrh of the esoph- agus. Anatomic Alterations. — Acute catarrh of the esophagus is characterized less bv unusual eno;oro;ement with blood and redness of the mucous membrane, than by marked detachment and des- quamation of the epithelium. The follicles of the mucous mem- brane, in consequence of accumulation of secretion, often appear as small, clear and transparent nodules, which not rarely are arranged upon the summit of the folds of mucous membrane like strings of pearls. If follicles rupture, superficial follicular ulcers result. In addition, if excessive desquamation of epithelial cells takes place epithelial ulcers form. Chronic catarrh of the esopJiagus is attended with brownish- red discoloration of the mucous membrane and thickening of the epithelium. The muscular layer, also, may undergo inflammatory tiiickeuing. At times dilatation of th(> esophagus takes place. The abundant formation and accumulation of mucus further con- stitute a striking feature. Symptoms, Diagnosis, and Prognosis. — The morbid manifestations are in part indefinite in character, including deep- seated pain in the course of the vertebral column, or between the scapulae, pain in swallowing — odynphagia, at times dificulty in PEPTIC ULCER OF THE ESOPHAGUS 201 swallowing, and even regurgitation. In cases of acute catarrh it has frequently been observed that phigs of desquamated epithelial cells from the mucous membrane were ejected. The introduction of a bougie into the esophagus should if possible be avoided, in order that no irritation be excited. It is noteworthy that an abundance of mucus, at times blood-tinged, frequently adheres to the sound. The duration of the disease and the prognosis depend upon the fact whether the cause can be removed or not. Treatment. — In cases of acute catarrh of the esophagus only cool liquid nourishment should be permitted. If severe pain be present, bits of ice may be sucked and subcutaneous injections of morphin given. Chronic catarrh of the esophagus has been treated by means of astringent ointments (argentic nitrate, 0.5 — 7| grains ; wool-fat and lard, each, 5.0 — 75 grains), which are applied by means of a sponge-bougie. It is important to direct attention to causal treatment (withdrawal of alcohol and tobacco). PHLEGMONOUS ESOPHAGITIS. Phlegmonous esophagitis is attended with suppuration in the submucosa of the esophagus. The purulent infiltration may also extend to the muscular layer. The pus often ruptures through several openings into the lumen of the esophagus. The disease is difficult of recognition. The most important manifestation con- sists in sudden disappearance of the signs of constriction of the esophagus after regurgitation of the pus. jS'aturally the possibility will always be present that an abscess in the neighborhood of the esophagus — for instance, a burrowing abscess of the vertebral column — has ruptured into the esophagus. Among the causes of this uncommon disorder are impacted foreign bodies, intense corrosion, infectious diseases, extension of inflammatory processes (phlegmonous pharyngitis, phlegmonous gastritis), and suppuration in the neighborhood of the esophagus. At times it is not possible to elicit any cause. The treatment is purely symptomatic. PEPTIC ULCER OF THE ESOPHAGUS. Peptic or round ulcer of the esophagus is a rare disorder. The ulcer is situated near the cardia, where it develops in consequence of digestion of the mucous membrane in places by active gastric juice left with food after the act of vomiting. The ulcer is usually round, with sharp margins. It is scarcely recognizable during life. Its dangers consist in hemorrhage, perforation, cica- trization with stenosis of the esophagus, and carcinomatous degen- eration. 202 DIGESTIVE ORGANS SPONTANEOUS RUPTURE OF THE ESOPHAGUS. A few instances are on record in ^\•lnch ruptnre of the esoph- agus has taken ph\ce in the midst of perfect health, at times after preceding efforts at vomiting or expulsion, with the occurrence of death within a short time. The jjatients were usually men ad- dicted to excessive indulgence in alcohol, and probably the wall of the esophagus had been previously softened. As a rule, a longi- tudinal tear up to five centimeters was present, beginning at the cardia and extending to the lower extremity of the thoracic por- tion of the esophagus ; less commonly two longitudinal tears were present or a single circular tear. As a result the contents of the stomach had entered the mediastinum, and hence the pleural cavity, and the surface of the lung was brownish and softened. The patients, as a rule, have cried out at the onset of the accident that something had ruptured within their body, and have com- plained of agonizing pain in the course of the vertebral colunm, with a sense of annihilation and a fear of death, with coldness and pallor of the skin and an imperceptible pulse. Signs of pneumo- thorax and of subcutaneous emphysema appeared, because air passed from the esophagus into the pleural cavity and into the mediastinal connective tissue, and thence into the subcutaneous connective tissue. There Mere also nausea, retching, and inability to swallow. Death usually resulted within twenty-four hours, with increasing asthenia. The prognosis is unfavorable. The treatment consists in subcutaneous injections of morphin and camphor in order to relieve the pain and sustain the strength. SOFTENING OF THE ESOPHAGUS (ESOPHAGO- MALACIA). Softening of the esophagus takes place especially in patients in Avhom the agonal period is protracted (tuberculous meningitis, dis- eases of the brain). The wall of the esophagus is swollen and so friable that it tears on the slightest manipulation. Often it is found perforated in the dead subject, and the contents of the stomach have escaped into the abdominal or the pleural cavity. In accordance with the color of the softened tissue, a distinction is made between gray, white, and brown softening. White and gray softening have probably developed only after death, from the entrance of the contents of the stomach into the esophagus, with digestion of its wall. Brown softening may also have occurred during the agonal period, with failure of the circulation, when the acid gastric juice is no longer neutrali/ed by the circulating blood and thereby rendered innocuous. The condition can scarcely be diagnosed during life. PARALYSIS OF THE ESOPHAGUS 20-3 THRUSH OF THE ESOPHAGUS (OESOPHAGOMYCOSIS OIDICA), Thrush of the esophagus probably occurs always in association with thrush of the oropharyngeal cavity, and is attended with the presence upon the mucous membrane of the esophagus of yellowish or grayish-yellow deposits, in which on microscopic examination the readily recognized thrush-fungus, Oidium albicans (page 180, Fig. 25), can be found. The deposits, which usually develop abun- dantly in the upper and lower portions of the esophagus particu- larly, and do not extend to the mucous membrane of the stomach, are at times punctate, at other times striate, and occasionally they assume the form of hollow or solid casts of the esophagus. As a result they may give rise to difficulty in swallowing. At times, also, plugs of thrush-fungi have been ejected. The mucous membrane of the esophagus is unchanged, or beneath the thrush- deposit there may be observed hyperemia, rarely loss of tissue, purulent infiltration of the submucosa, penetration of the fungi into the blood-vessels, and embolic dissemination to the brain, together with corresponding cerebral manifestations. The aifec- tion develops usually in association with thrush of the mouth in debilitated individuals who neglect to keep the buccal cavity clean, and particularly in children with diarrhea and in patients suffering from pulmonary tuberculosis, carcinoma, and diabetes. Should difficulty in swallowing arise, emetics may be administered for the purpose of removing the thrush-masses mechanically. Under some conditions introduction of the sound will be necessary. In addition, the internal employment of borax may be recommended : R Solution of sodium biborate, 5.0 : 200. Dose : from 5 to 15 c.c. (from 1 teaspoonful to 1 table- spoonful) every two hours. PARALYSIS OF THE ESOPHAGUS. Paralysis of the esophagus occurs in association with disease of the brain and the cervical cord (hemorrhage, abscess, softening, new-growth, echinococcus, tabes dorsalis, multiple cerebrospinal sclerosis, progressive paralysis of the insane, bulbar paralysis). At times it occurs in conjunction with hysteria. It has also been observed in consequence of pressure on the cervical vagus by en- larged lymphatic glands. The cases in which the disorder develops in the sequence of diphtheria, syphilis, alcoholism, lead-poisoning, and mercurial poisoning are probably attributable to neuritic alter- ations. At times the affection has appeared after exposure to cold, the ingestion of hot food, and psychic distu7'bances. The disorder is characterized by difficulty in sivalloiving — paralytic dysphagia. Especial difficulty usually attends the swallowing of fluids and of 204 DIGESTIVE ORGANS small particles of food. The act of swallowing is often attended with a p'ecidiar gurgling sound — dysphagia sonora. If the patients are careless in the ingestion of food, over-distention of the esoph- agus therewith may give rise to a sense of fear, danger of suffoca- tion, and 2^f(^p^f'^if^on of the heart. A sound introduced into the esophagus can be moved to and fro with undue readiness and free- dom. The prognosis depends upon whetlier the causative condi- tions can be removed or not. Nourishment should be introduced by means of a tube, the paralyzed musculature should be stimu- lated daily by means of a suitable sound-electrode connected with a faradic current of not too great strength and introduced into the esophagus, and the fundamental disorder should be attacked, as, for instance, syphilis with mercury and iodin, diphtheria with injec- tions of strychnin, lead-poisoning with potassium iodid. SPASM OF THE ESOPHAGUS (ESOPHAGISM) , Spasm of the musculature of the esophagus is observed in some central neuroses (chorea, epilepsy, tetanus, hydrophobia, hysteria, hypochondriasis). The disorder may also occur in association with anatomic diseases of the central nervous system. At times it is induced by local irritation of the esophagus (introduction of the sound, hard articles of food). Those cases in which the condition arises after the employment of belladonna, stramonium, or spoiled meat may be considered as instances of a toxic variety. Esoph- agism occurs through reflex influences in association with enlarge- ment of the tonsils, chronic pharyngeal catarrh, chronic esophagitis, carcinoma of the esophagus and of the stomach, the presence of worms in the intestine, and diseases of the sexual organs. Occa- sionally it occurs as a result of emotional disturbances, as, for instance, in persons ^^■ho incorrectly believe that they have been bitten by a rabid dog. The principal symptom consists in dijfi- culty in surdloicing — spastic dysphagia. Liquids can be better swallowed than solids. The act of deglutition is attended with a disagreeable sense of constriction internally, which at times sets in in the presence or the tli ought of food. The introduction of a sound is attended with resistance, or the instrument is suddenly grasped spasmodically and cannot be pushed onward. A dis- tinctive feature is the fact that if the sound is permitted to remain quietly the spasm frequently relaxes, and the passage of the in- strument into the stomach can take place without obstruction. The condition may occur parox3'sraally or continuously, and, in accordance wnth the causative condition, it may persist for hours, days, or months. Should the nutritive disturbance become pro- found, nourishment must be administered by means of the tube or of nidrient enemcda. In addition narcotics (subcutaneous injec- tions of morphin) and local galvanization with currents of not too DISEASES OF THE STOMACH 205 great strength may be employed. Of particular importance is the treatment of the primary disorder. IV. DISEASES OF THE STOMACH. PRELIMINARY CONSIDERATIONS, Until within a few years it was considered sufficient to apply also to the study of the diseases of the stomach the physical methods of examination alone of inspection, palpation, percussion, and auscultation. However valuable the diagnostic results yielded even yet by these methods, they still leave the investigator com- pletely in the dark as to the functions of the stomach, and the fact is therefore to be welcomed that within recent times a study of the functions of the stomach has been added to the physical methods of examination. Three conditions especially must be taken into consideration, namely, the absorptive power of the stomach, the motor activity of the stomach, and the constitution of the gastric juice. 1. To determine the absorptive power of the stomach a small gelatin-capsule, containing 0.2 (3 grains) of. potassium iodid, is employed. This is swallowed by the patient in the morning when the stomach is empty, and the saliva is then examined every five minutes for the presence of iodin. For this purpose starch-paper (bibulous paper that has been dipped in a paste of starch and water and then dried in the air) and fuming nitric acid are used. By touching the mucous membrane of the cheek the paper is moistened with saliva, and then, by means of a glass rod, a drop of fuming nitric acid is applied to the moistened spot. If iodin has been absorbed and has made its appearance in the saliva, the starch-paper is stained reddish or bluish at the exposed spot. In performing this test care should be taken that the gelatin-capsule is wholly swallowed and is not possibly crushed in the mouth, in order that the potassium iodid be not admixed with the saliva already in the mouth. It is absolutely necessary that the test be made when the stomach is empty, because, after food has been taken, the absorptive activity of the stomach is exceedingly variable, even in healthy persons. In a healthy person ten or fifteen minutes will elapse before the first traces of iodin can be demonstrated in the saliva. In the presence of disease of the stomach there is fre- quently a prolongation of the period of absorption. This period is prolonged with especial regularity in cases of carcinoma of the stomach, not rarely for more than sixty minutes. The same con- dition may, however, be present also in cases of acute and chronic 206 DIGESTIVE ORGANS gastric catarrh, gastric ulcer, and gastric dilatation. The absorp- tive activity of the stomach is impaired, further, in anemic, cachectic, and febrile states. Little is known with regard to acceleration of gastric absorption. It ia believed to have been observed in cases of recent ulcer of the stomach, without cicatrization. 2. The motor activity of the stomach is studied l^y having the patient take a test-meal, and determining after an interval of six hours, with the aid of a soft tube introduced into the stomach, whether remains of the food are still present or not. If the motor activity of the stomach is unimpaired, the viscus will have pro- pelled its contents into the intestine within six hours. A test-meal consists of a plate of soup made with water or with ilour, a tender beefsteak with an eg^, and a wheat roll. An ordinary rubber gas- tube may be employed as a stomach-tube, the sharp edges being cut away with the aid of scissors, or a soft stomach-tube with lateral fenestra, which is virtually nothing more than an unusually long and thick Xelaton catheter. Both varieties of tube can be readily introduced into the stomach with swallowing move- ments. In order to obtain the gastric contents the expression- method may be employed. After the tube has been introduced into the stomach down to the lower curvature the patient begins to make active expulsive efforts. If the stomach contains chyme, this M'ill be expelled, and it can be received into a vessel held beneath the free opening of the tube. Should unexpectedly nothing appear, a glass funnel must be introduced into the free opening of the stomach-tube, and through this lukewarm water should be introduced into the stomach. As soon as the flow ceases the introduction is suspended, the tube is pinched between the fingers, the glass funnel is inverted into a suitable vessel, and the pressure of the fingers is released, when the water and the gastric contents will escape. Diminution in the motor activity of the stomach may be recognized from the fiict that the viscus still contains considerable amounts six hours after the ingestion of food. The condition occurs especially in association with carcinoma, dilatation, and atony of the stomach, but it may also attend other diseases of the stomach, as, for instance, gastric catarrh. Little is known with regard to morbid increase in the motor activity of the stomach, although a number of observations are on record in which the stomach was empty two hours after the ingestion of food, and the patient constantly complained of hunger. It should further be noted whether the gastric contents obtained exhibit evidence of insufficient mastication of the food — a common fault and a frequent cause of diseases of the stomach of varied kind. 3. The digestive power of the gastric juice depends upon the fact whether free hydrochloric acid, pepsin, and lab-ferment are present, and attention should be directed to all of these in cases DISEASES OF THE STOMACH 207 of disease of the stomach. In order to obtain gastric juice for examination a test-meal or a test-breakfast is given. A test-meal may be constituted of the ingredients previously named, viz., a plate of soup made with water or with flour, a tender beef- steak with an egg, and a wheat roll. The test-breakfast consists of a large cup (250 c.c.) of tea without sugar and of a wheat roll (35 gm.). The gastric contents are obtained by expression with the aid of a soft stomach-tube four hours after, and a test-meal one hour after, a test-breakfast. The periods named have been shown by experience to be the most favorable for the examina- tion. Personally, I prefer the test-breakfast to the test-meal, because the manipulations are cleaner and the examination can be more quickly terminated without aifecting its reliability. The contents of the stomach obtained are naturally not pure gastric juice, but chyme mixed therewith ; experience has, however, shown that under normal conditions this somewhat dilute gastric juice possesses quite definite and constant properties. In the first place, the materials obtained are carefully inspected with the unaided eye for the presence of foreign admixture (blood, mucus, shreds of tissue), and with regard to the condition of the food ingested. Then the reaction of the gastric juice is tested by means of litmus-jmper. This will be found almost unexcep- tionally acid, so tliat blue litmus-paper is stained red. The pres- ence of an acid reaction by no means indicates that the gastric contents contain free acid, for it may be due also to acid salts in solution, especially phosphates. Next, Congo paper (bibulous paper stained with a solution of Congo red) is used to determine whether the gastric contents contain free acid. In this event the Congo paper is stained blue. The Congo reaction yields no in- formation as to the nature of the free acid, and whether it be due to hydrochloric acid or to organic acids (acetic, lactic, butyric). To demonstrate the presence of free hydrochloric acid the 'phloroglucin-vanilUn solution of Giinzburg (phloroglucin, 2.0 ; va- nillin, 1.0; alcohol, 30.0) is employed. Of this reagent about 5 drops are placed upon a porcelain dish, and an equal amount of filtered gastric contents is added. The mixture is then carefully heated over a flame until dried. If the gastric juice contain free hydrochloric acid, a beautiful carmine-red color appears on evapo- ration. Complete investigation of tlie ga.stric juice requires further also quantitative determination of the hydrochloric acid. It is necessary to understand that two kinds of hydrochloric acid must be distinguished in the gastric contents, the combined and the free hydrochloric acid. The proteids of the gastric con- tents immediately enter into combination with a portion of the hydrochloric acid of the gastric juice, and only when tliis combi- nation has been completely saturated does hydrochloric acid remain uncombined, therefore, as free hydrochloric acid. In the 208 DIGESTIVE ORGANS further digestion of proteids this free hydrochloric acid only is of ijnportance, and this fact will explain why attention has been directed especially, and often even exclusively, to the free hydro- chloric acid. Experience has shown that in a healthy person after ingestion of the test-meal previously mentioned the pro- portion of free hydrochloric acid in the gastric juice is from 0.15 to 0.25 per cent. The cheraic methods for determining the total hydrochloric acid, the combined and the free hydrochloric acid in the gas- tric juice, are too complicated for the general practitioner, apart from the fact that they cannot even be considered as accurate, and often it will suffice for the physician to estimate the total acidity of the gastric juice, which can be done without much trouble or the consumption of much time. In doing this not only the hydrochloric acid must be considered, but everything in solution in the gastric contents that yields an acid reaction, as, for instance, phosphates, and under some conditions lactic and acetic and butyric acids. To determine the total acidity of the gastric contents a 1 : 10 normal sodium-hydroxid solution is employed, of which 1 c.c. neutralizes 0.00365 gm. of hydrochloric acid. The test is made in the following manner : 10 c.c. of filtered gastric contents are introduced into a glass by means of a pipet, and 5 drops of an alcoholic solution of phenolphthalein are added. The gastric contents remain unchanged ; at most a slight and entirely insignificant cloudiness forms. From a graduated buret normal sodium-hydroxid solution is permitted to drop until a coloration appears, and persists in spite of constant shaking. By this means evidence is furnished that the first drop of normal sodium-hydroxid solution is in excess, and that all of the acid of the gastric con- tents is neutralized, for a phenolphthalein solution that remains colorless in an acid solution at once assumes a red hue with the slightest excess of alkali. The estimation is made as follows : If 4 c.c. of normal sodium-hydroxid solution are employed, 1 " sodium hydroxid = 0.00365 of hydrochloric acid, 4 " " '" =0.01460 '" " and 10 " gastric contents contain 0.0146 " " and 100 " " " " 0.146 " " = 0.146 per cent. If, continuing the illustration, 4 c.c. of sodium-hydroxid solu- tion have been required to neutralize 10 c.c. of gastric contents, and therefore 40 c.c. of sodium hydroxid to neutralize 100 c.c. of gastric contents, the total acidity of the gastric juice is for brevity's sake designated simply as 40. The gastric contents of a healthy individual should have a total acidity of from 30 to 60. If the total acidity be less than 30, the condition is designated hypacidity, and if more than 60, hyperacidity. Hypacidity is inconceivable without deficiency of free hydro- chloric acid in the gastric juice, so that the demonstration of total DISEASES OF THE STOMACH 209 hypaoidity indicates also hypochlorhydria. Hyperacidity of the gastric juice can, however, be induced also by increase in the organic acids. Under such circumstances the free hydrochloric acid and the organic acids must be determined quantitatively. For this purpose the filtered gastric contents are shaken vigor- ously with an equal amount of ether in a separatory funnel, and the gastric contents are then poured back into a glass vessel. The ether will take up the organic acids. Then normal sodium- hydroxid solution is added to 10 c.c. of gastric contents until the first drop of gastric contents heated upon a porcelain dish with a drop of phloroglucin-vanillin solution no longer yields a red color. In this way demonstration would be aiforded that all free hydro- chloric acid has been neutralized by the normal sodium-hydroxid solution. The amount of hydrochloric acid can be readily esti- mated from the amount of sodium-hydroxid solution employed. If it be further desired to estimate the amount of organic acids, it would be necessary to evaporate the ether, to dissolve the residue in water, and to determine the acidity of the aqueous solution by means of normal sodium hydroxid and phenolphthalein in the manner previously described. Organic acids are generated in the stomach by the fermentation of carbohydrates. Lactic acid is almost constantly present in the gastric contents. It can be readily demonstrated with the aid of Uffelmann's reagent (solution of ferric chlorid, 1 drop; carbolic acid, 0.4; distilled water, 30.0). If filtered gastric juice be added to Uffelmann's reagent, a canary -yellow color appears in the amethyst-blue solution in the presence of lactic acid. Hydrochloric, acetic, and butyric acids likewise induce discoloration, but the color is smoky gray and not yellow. For the recognition of acetic and butyric acids dependence will generally be placed upon the sense of smell. A penetrating sour odor is indicative of the presence of acetic acid, and a rancid odor of that of butyric acid. The determination of the hydrochloric acid in the gastric juice is naturally of great significance in treatment. Originally it was thought that the knowledge was of great diagnostic importance, but this has not been confirmed by more extensive experience. Anachlorhydria occurs frequently, but not constantly, in associa- tion with carcinoma of the stomach. It is also observed in con- nection with acute and chronic gastric catarrh, extensive cicatri- zation of the gastric mucous membrane after the action of corrosive agents, amyloid degeneration of the gastric mucous membrane, and anemic, cachectic, and febrile states. Hyperchlorhydria has been observed in connection with round ulcer of the stomach, and it also occurs as an independent gastric neurosis. Among organic acids the abundant and persistent appearance of lactic acid has erroneously been given diagnostic significance with regard to the presence of carcinoma of the stomach. Organic acids may be abundantly present in connection with all fermentative processes of the gastric con- tents, and with especial constancy with gastric dilatation. Pepsin occurs almost always in sufficient amount in the gastric juice. It is only wanting, together with hydrochloric acid, when the 14 210 DIGESTIVE ORGANS glmuls of the gastric mucous nicnibranc luivc undcrgono atrophy — so-called gastric anadcnia. In order to form an opinion as to the sufficiency of the pepsin in the gastric contents the so-called Jour- (/lasH test is made. Into each of four test-tubes are introduced 5 c.c. of filtered gastric contents. The first tube is left unchanged, to the second are added 0.5 of })epsin, to the third 2 drops of dilute hydrochloric acid, and to the fourth 0.5 of pepsin and 2 drops of dilute hydrochloric acid. Then a disc of albumin of uniform size, best obtained by means of a cork-cutter, or flakes of fibrin of equal amount, are introduced into each tube. The fibrin should be thoroughly washed and freed from blood, and it can then be ke])t in glycerin. The four tubes are placed in the thermostat at the tem- perature of the body, and the digestive process during the suc- ceeding hours is observed. If satisfactory digestion takes place in the first tube, the result indicates that the gastric juice contains sufficient free hydrochloric acid and pepsin. If digestion takes place in the second test-tube and not in the first, this indicates a deficiency of pepsin ; if in the third test-tube and not in the first or second, a deficiency of hydrochloric acid ; and if only in the fourth tube, a deficiency of both pepsin and hydrochloric acid. The gastric juice almost always contains lah-ferment also in suf- ficient amount. This is absent only in gastric adenia. To demon- strate its presence, to 10 c.c. of unboiled milk 5 drops of filtered gastric contents are added, and the mixture is jilaced in a thermo- stat at the temperature of the body. The presence of lab-ferment is indicated by the occurrence of coagulation in the milk within from fifteen to thirty minutes. ACUTE GASTRIC CATARRH. Ktiology. — Acute gastric catarrh is an exceedingly common disorder, and in the majority of cases it is dependent upon errors in diet. These may at times consist in the ingestion of too full a meal, at other times in the ingestion of food that is too hot or too cold or insufficiently masticated, and therefore generally eaten too hastily, and at still other times finally in the ingestion of spoiled food or drink. Infants are frequently attacked by acute gastric catarrh, l)ecause milk is readily decom])osed and frequently ■contains fermentative bacteria. All other causative factors are much less commonly effi'ctive. Gastric catarrh is, however, most likely to be of toxic origin, less commonly from the ingestion of chemic poisons than from indulgence in alcohol in too great con- centration or in too great amount. Traumatic gastric catarrh, resulting from injury in the epigastrium, and rheumatic or refrige- ratorii gastric catarrh, resulting from the local or general influence of cold, are of rare occurrence. Acute infectious and debilitating diseases generally are more frequently accompanied by acute gastric ACUTE GASTRIC CATARRH 211 catarrh. Gastric catarrh may arise by extension from adjacent disease, as, for instance, in connection with intestinal catarrh or peritonitis. Anatomic Alterations. — Little is definitely known with regard to the anatomic alterations of acute gastric catarrh in human beings, because opportunity is seldom afforded for post- mortem examination. The principal alterations usually involve the pyloric region, and consist in redness and swelling of the mucous membrane and increased secretion of mucus. Microscop- ically granular cloudiness of the main cells, the glands, hyperemia of the blood-vessels, and proliferation of round cells in the gastric raucous membrane will be apparent. Symptoms and Diagnosis. — Among the symptoms of acute gastric catarrh the most constant is loss of appetite — anorexia. In some cases there is a desire for piquant and highly salted or acid articles of food particularly. Thirst is usually increased. Not only the sight, but also the thought, of food excites disgust and nausea. Often vomiting occurs, the food not rarely being expelled in a state of fermentation and decomposition. When vomiting is repeated the ejected matters not rarely acquire a greenish color from admixture with biliary coloring-matter. Often the patients complain that the vomited matters possess a bitter taste, which may be due not alone to the biliary coloring-matter, but also to the peptone present. In less severe cases, or in connection with previous vomiting, there occurs frequently eructation — singultus.^ Often acid or rancid gases are thus expelled, which at times dif- fuse an odor of hydrogen sulphid. Acid gastric contents also are sometimes brought up, leaving in the epigastrium or in the lower segment of the esophagus a burning, boring sensation, which is known as heartburn — pyrosis. Local examination of the stomach usually discloses extensive tenderness on pressure in the epigastrium, M'hich is at times dis- tended with gas like an air-cushion. The patients also often complain of a sense of tension, of pressure, or of pain in the epigastric region. The functions of the stomach are altered in so far as the secretion of hydrochloric acid ceases, while mucus is produced in increased amount. The motor activity of the stomach is diminished, and the food therefore remains in the stomach for an unduly long time. The tongue is usually coated, and a dis- agreeable odor often emanates from the mouth. The patient fre- quently complains of a pasty taste. Frequently tlie bowels are irregular, sometimes constipation, sometimes diarrhea, existing. The urine is not rarely voided in small amount, presenting a deep-red, highly concentrated or saturated color, and frequently depositing a brick-dust sediment of urates. The disorder is at times attended ^ In English, eructation is synonymous with belching, and singultus with hiccup. — A. A. E. 212 DIGESTIVE ORGANS ^\•ith slii2:ht fever — gastric fever. It is noteworthy that the gen- eral condition may be greatly disturbed. Vertigo, mental eoiii'u- siun, and headaclie are frequently recurring symptoms, and are perlia2)s to be attributed to tlie action upon the central nervous system of toxins formed in the stomach. The frequent occur- rence of facial herpes, especially labial herpes, is perhaps also due to toxic effects upon peripheral nerves. The duration of acute r/astric catarrh varies between days and one or two weeks. Relapses are extremely common in the presence of recurring in- jurious influences, and these readily lead finally to the develop- ment of chronic gastric catarrh. Prognosis. — Acute gastric catarrh is not a fatal disease, and the prognosis is therefore favorable. With the cooperation of the patient relapses can be generally avoided. Treatment. — In the treatment of diseases of the stomach in general and particularly in that of acute gastric catarrh the great- est importance should be attached not to the administration of numerous medicaments, but to appropriate dietetic regulations. Solid food should be entirely prohibited, and only weak tea, broths, milk-soup, and mucilaginous soups permitted. Abstinence from food is the best treatment. Causal indications are present when the stomach has been overloaded. The viscus should tlien be emptied by means of an emetic, most serviceably by apo- morphin hydrochlorate (0.2 : 10 ; 8 minims subcutaneously). If the sense of pressure and of pain be excessive, a hot cataplasm should be applied to ihe epigastrium. Symptomatically, (Jidde hydrochloric acid (10 drops in a wine-glassful of tepid water half an hour after meals) may be prescribed. For the relief of heartburn alkalies, as, for instance, sodium bicarbonate (from 10 to 20 grains) or lime-water (1 tablespoonful) or mineral waters, may be given. Vertigo and headache may be relieved by antipyrin or phenacetin (1.0 — 15 grains — thrice daily). CHRONIC GASTRIC CATARRH. Ktiology. — Errors in diet are also the most common cause of chronic gastric catarrh. Irregularity and nndue haste in eating are especially important, so that tlie food is not sufficiently masti- cated. Those engaged in certain pursuits (merchants, lawyers, physicians) suffer from this disorder with esjiecial frequency, because the influences named are particularly operative among them. Defective teeth are also responsible for the entrance of the food into the stomach in an imperfectly prepared state, Xot rarely acute gastric catarrh if frequently repeated gradually passes into the chronic f)rui. An unfortunately common variety of chronic gastric catarrh is that known as drunkards^ catarrh, from Avhich tliose who indulge in alcoholic excess frequently suffer. Heavy CHRONIC GASTRIC CATARRH 213 smokers also are not rarely the victims of chronic gastric catarrh. Under both of the last-named conditions toxic influences are oper- ative. Hypostatic gastric catarrh occurs especially in association Avith chronic diseases of the respiratory and circulatory organs, and with diseases of the liver, especially cirrhosis. Cachectic and anemic gastric catarrh develop in the course of chronic disease attended with impoverishment of the blood and Avasting discharges. At times chronic gastric catarrh occurs in conjunction with other diseases of the stomach, as, for instance, carcinoma. From the nature of the causative factors chronic gastric catarrh is most com- mon in men, and it occurs almost exclusively in adults. Anatomic Alterations. — The anatomic alterations of chronic gastric catarrh involve the pyloric region by preference. The mucous membrane is usually covered with an abundance of mucus, which in places is turbid and pus-like, and may even be bloody or brownish in color. In addition the mucous membrane presents a brownish- red appearance, and it exhibits here and there dilated vessels and extravasations of blood. At the same time the nuicous membrane is notably swollen and thickened. On microscopic examination the superficial epithelium of the gastric mucous membrane will be found involved in marked mucoid degeneration. The glandular cells exhibit granular turbidity, are in part shrunken and uniform, so that the differentiation between the parietal cells and the chief cells is lost. Accumulation of round cells in greater or lesser number has taken place between the gland-tubules. The blood-vessels are dilated and greatly distended. Xot rarely remains of blood-pigment are present, indi- cating preceding hemorrhage. . Chronic gastric catarrh readily gives rise to inflammatory hyperplasia of the submucosa, and even of the muscularis and the serosa, and under such conditions the designation hypertrophic gas- tric catarrh may be employed. In consequence of excessive hyperplasia of the submucosa in places the mucous membrane sometimes presents numerous wart-like elevations, and there results the condition described as etat mamelonne. At times the hyperplastic tissue undergoes cicatricial contraction, and the stomach undergoes the change known as cirrhosis. If circum- scribed hyperplasia of the mucous membrane take place, there form under some conditions numerous pendulous tumors, or gastric polypi — so-called chronic poh/pous gastritis. Excessive prolifera- tion of round cells between the glands may cause atrophy of the latter by pressure, and, if at the same time, in consequence of pre- ceding hemorrhage, much gray or blackish pigment be present in the mucous membrane, the condition is designated atrophic pig- mentary induration of the gastric mucous membrane. At times almost the whole of the glandular structure is destroyed, so that the mucous membrane resembles granulation-tissue, and the con- dition is then known as chronic atrophic gastritis, or j)fiihisis 214 DIGESTIVE ORGANS ventrlcuU, or gastric anadenia. Finally, it may be that some glands, after occlusion of the excretory duct, are transformed into cystic cavities — so-called chronic ci/dic (jadritis. Symptoms and Diagnosis. — The symptoms of chronic gastric catarrh rcscailjlc in many respects those of acute gastritis, but tlie peculiarities of an acute disorder are wanting. Alterations in appetite are among the most constant symptoms. Usually there is anorexia, but at times there may be bulimia, and especially a desire for piquant articles of food. Thirst is often, but not always, increased. Generally the tongue presents a grayish or brownish deposit, and the patient often complains of an unpleasant and pasty taste. Not rarely a disagreeable odor emanates from the mouth. At times tiiere is increased secretion of saliva. Frequently there is troublesome eructation — singultus, ^^■hich often is followed by heartburn — pyrosis. The gases brought up by eructation not rarely taste and smell rancid or acid. Vomiting occurs less commonly with chronic than with acute gastric catarrh. The vomited mat- ters often consist of rancid or acid fermenting gastric contents, in which microscopic examination discloses the presence of yeast- fungi and sarcin?e. Drunkards frequently suffer in the morning, when the stomach is empty, from distressing retching and vomiting of masses resembling saliva, and which consist of saliva swal- lowed during the night, and less commonly of carbohydrates that have undergone mucoid fermentation. This manifestation is known as the morning vomiting of chnmkards. The epigastrium is not rarely tender upon pressure throughout an extensive area. The functions of the stomach are variously altered. The motor function of the stomach is impaired with especial constancy, so that the food is retained in the stomach for an unduly long time and readily undergoes decomposition. Absorption on the part of the gastric mucous membrane also is almost always delayed. In the less severe cases (simple chronic gastric catarrh) the secretion of hydro- chloric acid is diminished, M'hile in the more severe cases (chronic mucous gastric catarrh) free hydrochloric acid is wanting in the gastric contents. When anadenia exists, not only is hydro- chloric acid wanting, but also pepsin and lab-ferment. The bowels are usually constipated and irregular. Urine is generally voided in small amounts; often on cooling a red granular, brick-dust sediment of urates is precipitated. Frequently mental manifestations are associated with chronic gastric catarrh. The patients become hypochondriacal, prefer to be alone, are disinclined to mental and physical activity, and oppress themselves with the most dismal reflections as to their future. Imperative conceptions and fear of places — agoraphobia — also occur. Often com])laint is made of mental confusion, a sense of beating in the head, or headache. Vertigo occurs with especial frequency — so-called gastric vertigo — which usually is particularly CHRONIC GASTRIC CATARRH 215 noticeable in the morning. Some patients complain of palpitation of the Jteart and of irregularity in the action of the heart. Asth- matic conditions arise also in connection with marked distention of the stomach with gas — dyspeptic asthma. Chronic gastric catarrh is unattended with fever. At times emaciation and earthy pallor become so pronounced that latent gastric carcinoma is rather suspected. Anemia of high grade with its sequels develops in conjunction with gastric anadenia, and the clinical picture may then entirely resemble that of progressive pernicious anemia. The duration of the disease is extremely variable. Some patients suffer for years, and even throughout life, from chronic gastric catarrh. Among the sequels dilatation of the stomach — gastrectasis — may be mentioned particularly, but carcinoma of the stomach also is by no means rarely a sequel of chronic gastric catarrh. Prognosis. — The prognosis depends not rarely upon the cooperation of the patient, and upon his willingness to forego excesses in eating and in the use of alcohol and tobacco. In- curable causative factors naturally render the prognosis unfavor- able. Treatment. — The treatment should be in the first place causal and at the same time prophylactic. The patient should be advised to eat slowly and with regularity, taking care to masticate the food thoroughly and to keep the teeth in good condition. Drunk- ards must give up the use of alcohol, and smokers be restricted in that of tobacco. The symptomatic treatment depends upon the nature of the gastric disturbances. If the gastric contents are free from hydrochloric acid, dilute hydrochloric acid, (10 drops in a wine-glassful of tepid water half an hour after meals) should be prescribed. To the hydrochloric acid from o to 10 grains of j^epsin should be added, if this also be absent from the gastric juice. If active fermentation take place in the gastric contents, systematic irrigation of the stomach by means of a siphon-arrangement should be practised. Only rarely will it be possible to correct gastric fer- mentation by the internal administration of antizymotics, as, for instance : R Salicylic acid, 0.5 (7 J grains); Saccharin, 0.02 ( ^ grain). — M. Make 10 such starch-capsules. l3ose : 1 capsule thrice daily half an hour before eating. R Resorcin, 0.1 (1} grains) ; Saccharin, 0.02 ( | grain). — M. Make 10 such powders. Dose : 1 powder thrice daily half an hour before eating. Prolonged stasis of food in the stomach may at times be overcome by administration of bitters, which improve the tone of the gastric musculature, as, for instance : 21 G DIGESTIVE ORGANS Or, R Strychnin nitrate, 0.1 (lo grains) ; Powdered altliea-root, sufficient to make 15 pills. Dose : 1 pill tiirice daily. \i Wine of condurango, 200.0. Dose : 1 tablespoont'ul thrice daily. Water-cures are much employed, and those that can be carried out at batliing-resorts, where the diet is strictly regidated, are especially commendable. Carlsbad serves as au example. In general, alkaline mineral springs (Neuenahr, Yichy, Bilin, Giess- hiibel, Fachingen), alkaliue-chlorin springs (Ems, Selters, Gleich- enberg), alkaline-saline sjmngs (Carlsbad, Marienbad, Franzensbad, Tarasp), and sodium-chlorid springs (Wiesbaden, Homburg, Kis- singen) are worthy of consideration. Residence in the mountains and pedestrian tours in the mountains also may be recommended, and they frequently exert a useful influence upon the mental state. SUPPURATIVE INFLAMMATION OF THE STOMACH (PURULENT OR PHLEGMONOUS GASTRITIS). Purulent gastritis is an extremely rare disease. It is attended Avith suppuration in the submucosa, the pus either infiltrating the tissues in a diffuse manner or collecting in a circumscribed manner into an abscess. At times the pus has been partially evacuated into the cavitv of the stomach or into the peritoneal cavity, and perforation may take place through numerous cribriform openings. Often purulent peritonitis develops. Signs of general septicemia, especially enlargement and softening of the spleen, are frequently observed. The causes are either of infectious or of toxic nature. Thus, phlegmonous gastritis is at times observed to develop in the sequence of infectious diseases. At other times it is associated with other disease^ of the stomach — as, for instance, carcinoma — or the inflammatory j^rocess has extended from the pharynx or the esophagus to the submucosa of the stomach. Poisoning with cor- rosive acids and alkalies, and excessive indulgence in alcohol may also be mentioned as causes. Recognition of the disease is scarcely possible. It is often concealed behind the clinical picture of r/ener(d septicemia or peritonitis. Fever, epigastric pain, and vomiting are particularly constant manifestations. The disorder would be most readily recognized if a tumor in the epigastrium becomes smaller or disappears after the vomiting of pus. Death usually occurs within a few days amid signs of ]irogressive asthneia. Recovery with cicatrization ^irobably takes place but rarely. The treatment consists in the administration of stimulants, the swallowing of bits of ice, and the application of an ice-bag to the epigastrium. ROUND ULCER OF THE STOMACH 217 ROUND ULCER OF THE STOMACH. Htiology. — Round ulcer of the st'omach is a common disorder that in some regions attacks more than 5 per cent, of the popula- tion. Childhood is usually exempt from the disease, while the age between the fifteenth and the thirtieth year of life suffers especially. Women are attacked more than twice as commonly as men. The disorder develops with striking frequency in the sequence of chlorosis, in consequence, it is thought, of anemic fatty degeneration of the blood-vessels of the stomach, and throm- bosis in the diseased areas. At times the ingestion of hot articles of food is followed by the formation of a round ulcer of the stom- ach. The disease is, therefore, observed with unusual frequency in cooks. Traumatism in the epigastric region, as, for instance, a severe blow, may act as a cause of the disorder. In this group of etiologic factors may be included also violent efforts at vomit- ing, which may give rise to hemorrhage and to hemorrhagic ero- sion of the gastric mucous membrane, and secondarily to gastric ulceration. Certain infectious diseases, particularly pulmonary tuberculosis and syphilis, have been made responsible for the development of round ulcer of the stomach, but this supposition still requires confirmatory evidence. At times round ulcer of the stomach, like ulceration of the duodenal mucous membrane, has been observed to develop after extensive burns of the skin, perhaps in consequence of thrombosis of gastric vessels by blood-plates. Further, the predisposition to round ulcer of the stomach may be augmented by certain injurious influences acting upon the stom- ach, among which may be named the ingestion of starchy food and of alcohol in excessive amounts. Anatomic Alterations. — The round ulcer of the stomach acquires its name from its shape. It is generally round, and if it is confined to the gastric mucous membrane it presents an appear- ance as if the mucous membrane in the diseased situation had been cut out with a punch. It is, therefore, characterized by its sharp borders, which usually are but little elevated, and on micro- scopic examination exhibit slight alterations (round-cell infiltra- tion). The muscular layer of the stomach is not rarely exposed in the floor of the ulcer, as if it had been artificially dissected out with a knife. The ulcer varies in size. At times it is so small that it may be readily overlooked, while at other times it may attain the size of the palm of the hand. It is most frequently situcded in the neighborhood of the pylorus and upon the posterior w^all of the stomach, and least commonly at the cardia. Usually but a single ulcer is present. If there are several, they may be in various stages of development. At times contiguous ulcers coa- lesce, and as a result irregular excavated losses of tissue take place. Not rarely the ulcerative process extends from the 218 DIGESTIVE ORGANS iiuK'oiis membrane to the muscular layer, and even to the serosa. Such a condition is attended with danger of rupture of the Htom- fU'h, and this accident occurs with such frequency that the round ulcer of the stomach has also been designated perforating ulcer of the stomach. Fortunately, free rupture of the stomach into the peritoneal cavity is frequently averted by the formation of adhesions between the stomach and adjacent organs, as with the liver, the pancreas, or the spleen, as a result of previous circum- scribed peritonitis. At the same time the destructive process may also extend to these organs, and give rise to alarming hemor- rhage by perforation of large blood-vessels. The borders of deep ulcers are sometimes terrace-like, and usually steeper upon one side than upon the other. The ulcer is sometimes funnel-shaped, with its broad base directed toward the gastric muccnis membrane. The apex of the funnel, however, is not situated vertically over the center of the base, but eccentrically. The entire shape of the ulcer is suo-gestive of the mode of division of the 2:astric vessels, and the impression is created as if the distribution of a gastric artery had been involved in the ulcerative process. If a gastric ulcer undergoes cicatrization, the mucous membrane in the vicinity of the margin of the ulcer is often thrown into radiatino; folds. Gastric cicatrices at the pylorus not rarely are followed by ste- nosis at this orifice and dilatation of the stomach. By contrac- tion cicatrices may give rise to deformities of the stomach. At times cicatrices at the middle of the stomach may cause the stom- ach to assume tlie shape of an hour-glass. Symptoms and Diagnosis. — Occasionally gastric ulcer is wholly unattended with symptoms, and is accidentally discovered on post-mortem examination — latent gastric ulcer. In other in- stances the development of a gastric ulcer is insidious, but hemor- rhage or perforation takes place suddenly, and may cause death within a short time. Among all the symptoms of round ulcer of the stomach, hemorrliage from the stomach — gastrorrhagia — is the most reliable in diagnosis. In its al)sencc the diagnosis will only be more or less probable. Hemorrhage from the stomach takes place, however, in but one-third of the cases, and its occur- rence depends upon whether vessels of considerable size are per- forated by the ulcerative process before thrombosis has taken place. Most frequently hemorrhage from the stomach gives rise to the vomiting of blood — hematemesis. The vomited blood appears as dark-red. partly coagulated masses, is often admixed with particles of food, and usually yields an acid reaction. The loss of blood mav be so consideral)le as to render death imminent. The patients present a cadaveric jiallor, with a soft, small, and dicrotic pulse, feeble heart-sounds, often systolic heart-murmurs, and dilatation of the right ventricle. Not rarely albuminuria develops, with slight edema about the ankles, and even edema ROUND ULCER OF THE STOMACH ' 219 of the face. In consequence of cerebral anemia attacks of syn- cope occur, especially upon assuming the upright posture, with roaring in the ears, impairment of hearing, blurring of vision, palpitation of the heart, and shortness of breath. Death takes place amid chronic convulsions. At times blindness follows recovery from gastric hemorrhage. Much less commonly hemorrhage from the stomach is attended with coffee-ground, ink-like, or soot-like vomiting, which, on the other hand, is common with gastric carcinoma. It occurs with gastric ulcer when but small hemorrhages have taken place, and the blood remains in the stomach for a considerable time, in consequence of which the hemoglobin is con- verted into hematin by the hydrochloric acid of the gastric juice. Far less commonly hemorrhage from the stomach is unat- tended with hematemesis, but discharge of blood takes place from the bowel, as manifested by the appearance of black, tarry stools. This occurrence must always be thought of when patients suddenly lose consciousness at stool and become pale. Not rarely slight febrile movement occurs, probably in consequence of absorp- tion of decomposed blood from the intestine into the circulation. It is rare for hemorrhage from the stomach always to be mani- fested by bloody stools alone. More frequently bloody vomiting occurs in conjunction with bloody stools. Epigastric pain — gastralgia — is an exceedingly common symp- tom of gastric ulcer, but it is of varied significance. Pain in the epigastrium appears usually a short time after the ingestion of food, and is readily induced by inappropriate food. Palpation of the stomach also induces pain, and especial consideration should be given to the fact that this pain is confined to a circumscribed area. At times pain in the stomach appears in certain postures, as, for instance, the lateral decubitus. The functions of the stomach exhibit no peculiarity. The period of absorption is generally pro- longed, rarely shortened. The hydrochloric acid of the gastric juice is often, but by no means constantly, increased (more than 0.25 per cent.). The motor functions of the stomach exhibit no alteration. The patients often complain of frequent and persistent vomiting. Some scarcely retain food for weeks and months, and alarming emaciation may result. Eructation and pyrosis are not uncommon symptoms. The appetite is usually wanting, while thirst is increased. In patients in whom vomiting is frequent the tongue often presents a vivid-red color and a clean appearance, probably in consequence of irritation due to the marked acidity of the vomited matters. Individuals with round ulcer of the stomach, as a rule, emaciate rapidly and acquire a pallid appear- ance. Often they become extremely nervous and sleepless. Even when cicatrization of the ulcer takes place, they must frequently be careful in eating and drinking throughout life. The duration of the disease usually extends over several months. 220 DIGESTIVE ORGANS whence the name chronic gastric ulcer. Besides, there is a great tendency to recurrence, so that some patients, in spite of all care, are annoyed and alarmed from time to time by renewed symptoms of gastric ulceration. Among the compdcdtionii of round ulcer of the stomach the most frequent, and diagnostically tiie most impor- tant, has already been mentioned, namely, hemorrhage from the stomach. Another serious complication consists in peritonitis and perforative peritonitis. Simple ])eritonitis is generally confined to the immediate vicinity of the ulcer. Perforative peritonitis as a rule sets in abruptly, and gives rise to alarming collapse. The abdomen becomes distended, tense, and universally tender on pressure, hepatic and splenic dulness have disappeared, and death results often within a short time. Perforation of the ulcer takes place less commonly into the bowel, through the diaphragm into the pleural or the pericardial cavity, and even into the lungs or into the heart, than into the abdominal cavit}'. A sub- phrenic abscess may also develop in consequence of perforation of a gastric ulcer. Among complications gastralgia and great sensitiveness of the stomach should be especially mentioned, and these may occasion- ally persist throughout life. Cicatrized ulcers at the pylorus may give rise to pyloric stenosis and dilatation of the stomach. Destruc- tion of the muscular ring of the pylorus is followed by jyyloric insujficiency. Especial significance should be attached to the fact that at times in advanced life carcinoma develops at the border of a gastric ulcer. Opinions are divided as to the pathogenesis of round ulcer of the stomach. In our opinion local disturbances in the circulation in the gastric mucous membrane constitute the first alteration. In favor of this view is the shape of the ulcer, which often reproduces the area of distribution of a blood- vessel of moderate size. At times thrombotic occlusion may have taken place, at other times rupture of a blood-vessel with hemorrhage. The por- tion of gastric mucous membrane cut off from its blood-supply may be digested by the gastric juice, a process that is prevented under normal cir- culatory conditions by the alkalinity of the blood. If in addition hyper- acidity of the gastric juice be present, digestion is favored in a still greater degree. The round ulcer of the stomach nuiy, therefore, be designated a peptic ulcer. Possibly bacteria also take some part in the destruction of the gastric mucous membrane. Prognosis. — The prognosis of round ulcer of the stomach is always grave, for of the most dangerous complications there is no small number, and these may occur unexpectedly in spite of all watchfulnoss over the patient. Treatment. — In the treatment of round ulcer of the stom- ach diet plays an important ])art. As long as the ulcer has not undergone cicatrization the patient should remain in bed and keep a hot cataplasm constantly applied to the epigastrium. Only liquid and unirritating food should be permitted. A milk-diet is the best. The milk, after thorough boiling, should be taken in small swallows ROUND ULCER OF THE STOMACH 221 every quarter of an hour to the amount of one or one and a half liters per day. For patients who have an aversion to milk, Aveak tea, coffee, or meat-broth may be added. Should milk not be well borne, it can be made into a thin soup with the aid of fine flour ; and should it undergo fermentation and acid decomposition readily in the stomach, a tablespoonful of lime-water may be added to each glass. Some persons bear buttermilk better, and it will then be advisable to prescribe a course of buttermilk-treatment. If the stomach is exceedingly sensitive to the ingestion of food, it may be necessary for a time to forbid all food by the mouth, and to confine the feeding to nutrient enemata. The simplest mixture for this purpose consists of equal parts of milk and slightly salted meat-broth, to which some sugar, 2 raw eggs, and 10 drops of tincture of opium may be added. This mass, at the temperature of the body, is permitted to flow slowly into the rectum thrice daily in amounts up to 300 c.c. by means of a Hegar funnel, after the rectum has previously been cleared of fecal matter by irriga- tion. The resumption of solid food should be effected slowly. There may then be administered soft-boiled eggs, meat-peptone, calves' brain, scraped beef, scraped ham, scraped sirloin, veal-cutlets, rice- pap, potato-pap. With regard to vegetables, fruits, and fatty articles of food, care must be taken for a long time, often through- out the remainder of life. Among medicaments we would espe- cially recommend artificial Carlsbad salt and bismuth salicylate. Of the salt, 1 or 2 teaspoonfuls should be dissolved in 500 c.c. of tepid water, and this should be drunk slowly every morning for four weeks while the stomach is empty. The object aimed at is to diminish the hyperacidity of the gastric juice, to remove from the gastric mucous membrane such mucus as may be present, and to induce evacuation of the bowels. The bismuth salicylate is intended to favor the process of granulation and cicatrization of the ulcer. It is preferably given an hour before meals, in order that it may readily reach the floor of the ulcer. If pain in the stomach is present, the bismuth may be combined with narcotics ; as, for instance : -M. Should hemorrhage from the stomach take place, the patient should at ouce be put to bed. Small bits of ice may be given and be swallowed, an ice-bag applied to the epigastrium, about 8 min- ims of fluid extract of ergot with an equal amount of sterile water injected beneath the skin twice or thrice daily, and lead acetate administered internallv ; for instance : R Bismuth salicylate, 0.5 (7^- grains) ; Morphin hydrochlorate, 0.005 ( xV grain) ; Extract of belladonna, 0.02 { i " ); Sugar, 0.03 ( ^ " ).- Make 10 sucli starch-capsules. Dose: 1 capsule thrice daily before meals. 222 DIGESTIVE ORGANS R Lead acetate, 0.05 ( f grain) ; Powdered camphor, 0.02 (J " ) ; Sugar, 0.5 (7^ grains). — M. Make 10 such powders. Dose : 1 powder thrice daily. It is advisable to administer no food by the mouth for several days, substituting nutrient enemata of the composition already described. In ease of peritonitis and perforative peritonitin rest, the application of an ice-bag to the abdomen, and administration of opium (0.03 — \ grain ; 1 powder every two hours) are neces- sary. Should collapse set in, 15 minims of camphorated oil should be injected beneath the skin every two or three hours. Surgical intervention has been practised successfully in a number of in- stances in the treatment of round ulcer of the stomach. Ulcers attended with uncontrollable and dangerous hemorrhage have been excised after exposure of the stomach, and in cases of perforative peritonitis the abdominal cavity has been opened, the pus removed as thoroughly as possible by sponging, and the rupture closed by suture. At times certain sequels of a round ulcer of the stomach necessitate operative intervention, as, for instance, cicatricial steno- sis of the pylorus and hour-glass contraction of the stomachy For the relief of these conditions pyloroplasty and gastro-enter- ostomy have been practised with good results. In the after-treat- ment patients of means should be advised courses of treatment at the springs. An especial reputation in this connection is borne particularly by the springs of Carlsbad. CARCINOMA OF THE STOMACH. Ktiology. — Carcinoma of the stomach, like carcinoma in general, is a disease of advanced life, usually developing after the fortieth year. Why this period of life is more predisposed to carcinoma is as yet unknown. Experience has shown that car- cinoma of the stomach is more common in men than in women. It is also observed more commonly in seme regions than in others, probably in consequence of local peculiarities in dietetic, injurious, and irritative influences acting upon the stomach. Without doubt preceding disease of the stomach has an influence upon the develop- ment of gastric carcinoma. Among such disorders are chronic gastric catarrh, round ulcer of the stomach, and irritation of the gastric mucous membrane by excessive indulgence in alcohol. Injuries in the epigastrium probably are not incorrectly looked upon as causes of carcinoma. The influence of heredity, however, is highly (loulitful. Anatomic Alterations. — Carcinoma of the stomach is almost always of primary nature; but few examples of secondary car- cinoma of the stomach are on record. The most common seat is the pylorus, and next in frequency are the cardia and the lesser CARCINOMA OF THE STOMACH 223 curvature. The fundus almost always escapes, even when the remainder of the stomach is involved in the new-growth. In some cases the tumor is circumscribed and attached to the gastric mucous membrane by a small base, and not rarely presenting a cup-shaped depression upon its surface. The shape of the tumor has under such conditions been compared with the appearance of a fungous growth, and on this account it has been designated a fungus of the stomach. In other instances diffuse carcinomatous infiltration takes place, which may attain a considerable extent, especially in the subjnucous connective tissue, and often sends medullary white strands of carcinomatous tissue into the connective-tissue septa of the muscular layer of the stomach, and even into the serosa. Tihe wall of the stomach is often increased in thickness to several centi- meters in the diseased area. In accordance with the appearance of the neoplastic tissue, several varieties of carcinoma of the stomach are distinguished. If, in consequence of marked development of connective tissue, the new-growth is dense and deficient in fluid, it is designated a fibrous carcinoma — scirrhus. It is designated medullary or alveolar car- cinoma when so-called " carcinoma-milk " can be scraped without difficulty from the carcinomatous tissue with a knife. Colloid or gelatinous carcinoma is attended Avith the presence of spaces filled with gelatinous contents resembling isinglass. On microscopic examination the carcinomatous tumor is found to be con- stituted of epithelioid cells, which lie close together in a nest-like arrangement, and in consequence of which the individual collections of carcinoma-cells are separated from one another by connective-tissue septa. The carcinoma- tous tissue is developed as a result of abnormal proliferation of the chief cells of the lab-glands, the proliferation rapidly advancing into the sub- mucous tissue, where it finds exceedingly favorable conditions for its further development. The portion of gastric raucous membrane involved in the new-growtb frequently exhibits signs of chronic interglandular catarrh and even atrophy of the lab-glands (anadenia). Carcinomatous tissue has a great tendency to undergo disinte- gration. Therefore the superficial layers of the new-growth are usually found destroyed, and thus the so-called carcinomatous ulcer is formed. In the process of disintegration hemorrhage from or perforation of the stomach may readily take place. The latter is often averted by the previous formation of adhesions between the stomach and adjacent organs in consequence of circum- scribed peritonitis. Generally the 'perigastric lympJwtic glands also undergo carcinomatous degeneration and are converted into hard, nodular tumors. Not rarely secondary carcinoma develops in other organs, most commonlv in the liver. Symptoms and Diagnosis. — The symptoms of carcinoma of the stomach are in part local, in part general. The latter con- sist in manifestations of carcinomatous marasmus, and these occur with especial readiness precisely in cases of carcinoma of the 224 DIGESTIVE ORGANS stomach, because, in addition to the injurious influences usually exerted by carcinoma upon the general nutrition, in cases of car- cinoma of the stomach the injurious effects of the disturbance of gastric digestion are superadded. As long as local symptoms are wanting the diagnosis will remain doubtful. Progressive emacia- tion, increasing pallor of the skin, and the occurrence of cachectic edema may, perliaps, arouse suspicion of latent internal car- cinoma, but its situation in the stomach will be suggested only when gastric disturbances are at the same time present. Further, most extensive carcinoma of the stomach may exist in the absence of local symptoms referable to the stomach. Among all of the local iiianifestations the demonstration of a tumor of the stomach is the most important from a diagnostic point of view. Usually this will be appreciable to the right of the median line just below the inferior margin of the liver, or it may extend from this situation toward the left in the course of the lesser curvature of the stomach. As, however, under normal conditions the pylorus, as well as the lesser curvature of the stomach, is concealed by the liver, it follows that tumors in the portions of the stomach named will become accessible only when they have attained considerable size and, by reason of their weight, are capable of dragging the stomach downward, so that as a result the pylorus and the lesser curvature of the stomach are directly applied to the abdominal wall. When the abdominal walls are thin and emaciated the gastric tumor is not rarely visible as a roundish and nodular mass. On palpation the growth will be felt to be of solid consistence and irregularly nodular. Almost always it is tender, even upon slight pressure. It is important that in contradistinction from new-growths of the liver and of the spleen displacement does not take place with the movements of respiration. Exceptions to this rule occur only when the tumor is adherent to the liver, and participates in its respiratory displacement; or, if the entire stomach is involved in carcinomatous degeneration, so that, by reason of the rigidity of its walls, it is no longer capable of yielding before the respiratory movement of the diaphragm. Further, care must be taken to avoid confounding the respiratory gliding of the abdominal walls over the tumor with the respiratory movement of the latter itself. Percussion over the gastric tumor yields a dull-tympanitic note. Carcinomafa of the cnrdia are never accessible to examination through the abdominal wall, but they can be detected only with the aid of the esophageal bougie, which encounters resistance 40 cm. (15f in.) from the edge of the teeth. The employment of the sound should never be omitted in any doubtfid case of marasmus. Auscultation of the stomach is also important. If a patient with carcinomatous stenosis of the cardia be made to swallow fluid, there are heard, if the stethoscope is placed in the angle between CARCINOMA OF THE STOMACH 225 the eiisiform process and the left costal margin, either after a con- siderable length of time an injection-murmur and an expression- murmur, or after an nnusually long interval but a single murmur. At the same time the murmurs are usually strikingly loud and long continued. In the presence of gastric carcinoma the functions of the stomach are not altered in any such characteristic manner as to permit the recognition of the disorder with certainty. Frequently, almost constantly, the period of absorption, as determined by the potas- sium-iodid test, is prolonged, occupying, instead of ten or fifteen minutes, as much as from thirty to sixty minutes, or even more. The motor activity of the stomach also will be found diminished, and foreign bodies — for instance, cherry-pits — may remain in the stomach at times for months. Hydrochloric acid is almost always wanting in the gastric contents. Boas has attached great diagnostic significance to the presence of lactic acid in the gastric contents, but without justification. Persons suflPering from gastric carcinoma complain principally of severe epigastric pain or gastralgia. This not rarely sets in toward night and disturbs sleep. Often there is singultus or vomiting. The regurgitated gases not rarely emit an offensive odor and that of hydrogen sulphid. The vomited matters often contain large numbers of sarcinse, and long, curved bacilli, which have been considered responsible for the lactic-acid fermentation of the gastric contents. Of diagnostic importance is the occur- rence of small masses of blood coloring-matter demonstrable micro- scopically. At times portions of carcinomatous tissue may be found in the vomited matters, but this is an uncommon occurrence. Most patients with carcinoma of the stomach complain of obstinate loss of appetite — anorexia. Thirst is not rarely in- creased. The tongue as a rule is coated. In diagnosis the pres- ence of carcinomatous induration, and enlargement of the supra- clavicular lymphatic glands upon the left side is significant. The inguinal lymphatic glands, also, not rarely exhibit induration and enlargement. The urine is generally passed in small amoiuits ; it is therefore usually deep red in color and concentrated, and as a rule contains much indican. The botvels are commonly consti- pated, although diarrhea may occur periodically. The general nutrition usually suffers early. The patients emaciate markedly within a short time, and acquire a pallid or waxy-yellow appear- ance. The latter is found on examination of the blood to be depend- ent upon diminution in the number of red blood-corpuscles and in the amount of hemoglobin. If the anemia be advanced, poikilocytosis may be present. There may also be hemorrhages into the retina, cutaneous edema, and small hemorrhages 15 226 DIGESTIVE ORGANS and foci of softening in the spinal cord, such as take place in pernicious anemia. Death occurs within a year, usually with progressive asthenia. Among the complications hemorrhage from the stomacli is the most conspicuous. This often gives rise to the vomiting of blood — hematemesis. Most frequently the vomited matters resemble coffee-grounds, or ink, or soot, Avhile less commonly fresh blood is present. These variations are to be explained by the fact that, as a rule, small blood-vessels are opened in the process of disintegra- tion of the carcinomatous tissue, so that the small amounts of blood extravasated remain for a considerable time in the stomach, while the hemoglobin undergoes alterations in consequence of the action of the' acids of the gastric juice. Although hemorrhage from the stomacli may be repeated frequently, it rarely causes death. Carcinoma at tlie pylorus frequently gives rise to dilatation of the stomach — gastrectasis. The pyloric ring may also be destroyed, and pyloric incontinence result. At times secondary carcinoma develops in other organs, and it may divert attention from the primarily involved stomach. In this connection secondary carci- noma of the liver especially should be mentioned. At times rupture of the stomach takes place, sometimes into the abdominal cavity, at other times, after previous adhesion of the stomach, into neighboring organs, rarely through the anterior abdominal wall. Carcinoma of the stomach is usually unattended Avith fever. At times, however, febrile movement occurs, and it may even be of intermittent type. Possibly it results from the absorption of toxic substances from the stomach. At times the patients unexpectedly become comatose, and die in coma. Such a result has been attrib- uted to the absorption of toxic substances from the stomach ; therefore an auto-intoxication. The urine frequently, though not constantly, exhibits a dark-red color on the addition of dilute solution of ferric chlorid — so-called ferric-chlorid reaction. Prognosis. — The prognosis of carcinoma of the stomach is invariably unfavorable, as death results at the latest in the course of a few months. Treatment. — No internal remedy is known that is capable of effecting a cure of carcinoma of the stomach. Attempts have been made to bring about this end by operative measures. Com- plete removal of the tumor by resection of the pylorus will be possi- ble only when the carcinoma is not too extensive and is not bound by adhesions to adjacent organs, and has not yet given rise to metastases in other viscera, particularly not in the adjacent lym- phatic glands. AVhen signs of pyloric stenosis are present and resection of the pylorus is not possible, gastro-enterostomy should be effected ; that is, the stomach should be sutured to a loop of small intestine, and at this point the lumen of the stomach and the bowel should be made continuous by means of an orifice of DILATATION OF THE STOMACH 227 communication. In cases of carcinoma of the cardia gastrostomy may be attempted if the cardia is no longer permeable for food and drink, but this operation has not yet yielded brilliant results. Internal treatment can only be purely symptomatic. The most important matter is that of diet. Such food should be prescribed as makes the smallest possible demands upon the digestive activity of the stomach ; as, for instance, milk, milk with coffee, milk with tea, beef-soup Avith addition of peptone, milk with soraatose, wine, old beer, rice-pap, mashed potatoes, etc. Wine of con- durango may be prescribed to stimulate the appetite : R Wine of condurango, 200.0 (6J fluidounces). Dose : 15 c.c. (1 tablespoonful) thrice daily. The use of dilute hydrochloric acid (10 drops in a wine-glassful of tepid water 30 minutes after the midday and the evening meal) may be recommended. Morphin hydrochlorate will be required for the severe pain, although this should be prescribed only when absolutely necessary, as experience has shown that the dose must be progressively increased, as a result of which certain dangers may arise. Great relief is often afforded by systematic irrigation of the stomach, and under such treatment the bodily weight is frequently observed to increase considerably within a short time. By this means the stomach is freed from the stagnating remnants of food and also from toxic substances. From a diagnostic point of view it is further important to examine the irrigation-fluid for the presence of flakes that, upon microscopic examination, may prove to be carcinomatous tissue. DILATATION OF THE STOMACH (GASTRECTASIS) . !]^tiology. — Dilatation of the stomach consists primarily in an acquired increase in the capacity of the stomach, although this is almost always invariably associated with stasis and fermentation of the gastric contents, so that the latter process must also be included in the clinical conception of gastrectasis. The most common cause for dilatation of the stomach is stenosis of the pylorus, and this is often due to cicatrized ulcers. Carcinoma of the pylorus may also give rise to stenosis of this orifice. Benign hypertrophy of the pyloric ring occurs less commonly, and obstruction of the pylorus by for- eign bodies or gastric polypi still less commonly. At times the pylorus is obstructed by pressure or traction from without, as, for instance, by new-growths of the intestine, the omentum, the liver, or the kidneys, by wandering kidney, and the like. It will be easily understood that stenosis of the pylorus may readily give rise to gastrectasis, for if the food stagnates in the stomach it causes stretching of this viscus by reason of its weight, and in addition there is the influence of fermentation of the gastric contents. 228 DIGESTIVE ORGANS Also, in the absence of pyloric stenosis long-continued over-filling of the stomach with food may give rise to gastric dilatation. This condition is observed in gourmands and in diabetics, in whom the appetite is morbidly increased. The filling of the stomach with indigestible articles is also dangerous. For this reason conjurers suffer from gastrectasis in consequence of the practice of swallow- ing stones and other indigestible articles for the purpose of sus- staining their supernatural powers. Finally, dilatation of the stomach is frequently a sequel of diseases of the wall of the stom- ach, as, for instance, chronic gastric catarrh. Gastrectasis has been observed also in connection with extensive ulceration of the stomach. At times nervous influences are operative by causing diminution in the tone of the gastric musculature. Anemic, nervous, and debili- tated individuals (as, for instance, tuberculous patients), therefore, not rarely suffer from gastrectasis. It is noteworthy that perigastric adhesions may give rise to dilatation of the stomach. Gastrectasis is a most common disorder, which may appear even in children. Naturally it is often diagnosed Avhen it does not exist, even by so-called " stomach-specialists," Avho do not deem it necessary to determine accurately the size of the stomach in every case. Anatomic Alterations. — Dilatation of the stomach is char- acterized principally by the increased size of the viscus, the enlarge- ment taking place in all directions. Upon opening the abdomen in advanced cases scarcely anything but the stomach comes into view, with its lesser curvature at the level of the ensiform carti- lage and its greater curvature projecting into the true pelvis. Usually the enlarged organ contains a large amount of jiuid — at times more than 20 liters ; and if the wall of the stomach be palpated, not rarely the fluid can be observed to fluctuate to and fro. The mucous membrane of the stomach usually exhibits signs of a chronic catarrhal condition. The walls of the stomach at times present great thickening, especially of the muscular layer, which is often traversed by broad bands of connective tissue ; at other times the walls of the stomach are unusually thin. Increased thickness of the walls of the stomach may be expected, particularly in association with stenosis of the pylorus, to a cer- tain degree in the nature of compensatory muscular hypertrophy, while thinning attends conditions of general debility. A distinc- tion has accordingly been made between hypertrophic and atrophic gastrectasis. Symptoms and Diagnosis. — In order to demonstrate dila- tation of the stomach the most convenient and most reliable method consists in distending the viscus artificially by means of carbon dioxid. For this purpose 1 or 2 teaspoonfuls of tartaric acid dissolved in a wine-glassful of water are swallowed, and immedi- ately afterward a like amount of water containing 1 or 2 teaspoon- fuls of sodium bicarbonate in solution. After the lapse of a few DILATATION OF THE STOMACH 229 seconds the outlines of the stomach often become visible beneath the abdominal walls. On percussion or palpation with flexed fingers a sense of resistance like that yielded by an air-cushion will be perceived, which disappears below the greater curvature of the stomach. On percussion over the stomach a deep-tympanitic note is yielded, and on auscultation not rarely small moist rales are audible in the course of the greater curvature, resulting from ebullition of the carbon clioxid. The distinctive feature of dilatation of the stomach consists in the uniform enlargement of the viscus. The greater curvature is not, as in health, situated above the umbilicus, but it is displaced for a greater or lesser distance below. Toward the left the stomach extends beyond the left anterior axillary line, and toward the right beyond the right parasternal line. Often the. lesser cur- vature of the stomach, which in health is concealed by the liver, is displaced unduly downward, and is distinctly appreciable to the eye. Displacement downward of the greater curvature of the stomach below the umbilicus, without displacement of the lateral boundaries of the stomach to the right and to the left, is not indicative of dilatation of the stomach, for such a condition may be due to displacement downward of the stomach as a whole — gastroptosis. Even a stomach enlarged in all directions is not neces- sarily to be considered as abnormally dilated, but the condition may be congenital — so-called megalogasfria. In contradistinction from dilatation of the stomach, the functional activity of the organ is unimpaired when megalogastria exists. In consequence of fermentative decomposition of the contents of the stomach the viscus is often so greatly distended with gas that its boundaries can be made out by inspection, palpation, and percussion, without artificial distention by means of carbon dioxid. If dilatation of the stomach be dependent upon pyloric constric- tion, active muscular waves may frequently be seen to pass from the cardia to the pylorus beneath the abdominal wall. At times bubbles of gas can be heard arising from the fermenting gastric contents. If the stomach be vigorously agitated, loud splashing sounds frequently occur, which some patients can induce by rapidly rising upon the feet, or by rapidly rolling from one side of the body to the other. These murmurs occur with especial frequency and loudness in association with dilatation of the stomach, but they appear also under all conditions in which the stomach contains at the same time both gas and liquid. At most it is distinctive of dilatation of the stomach that these sounds are appreciable when the abdominal wall below the umbilicus is suddenly jarred. With the physical alterations thus far described in cases of gas- tric dilatation manifestations indicative of deranged functional activity of the stomach are constantly associated. A peculiar variety of vomiting occurs with especial frequency. The patient may not vomit at all for several days in succession, but when 230 DIGESTIVE ORGANS vomiting occurs such enormous masses are expelled that the amount of vomited matter alone is indicative of dilatation of the stomach. The vomited mattei- is generally conspicuous for its markedly rancid or penetrating acid odor. If it be permitted to stand in a vessel in a warm room, it frequently continues to undergo fermentation, and eventually frothy matter may over- flow the margin of the receptacle. Microscopic examination dis- closes, in addition to particles of food and bacteria, especially oblong yeast-cells, and layers of sarcinse, at times also molds (Fig. 26). The vomitus is usually characterized by a highly acid reaction, although often it contains no free hydrochloric acid, "svhereas in consequence of fermentation of carbohydrates it con- tains an abundance of lactic, acetic, and butyric acids. The Fig. 26. — Yeast-cells and sarcinse from the vomitus in a case of gastric dilatation ; magni- fied 275 times (personal observation, Zurich clinic). patient often complains of an acid, almost burning, taste on the part of the vomited matter, and the teeth are set on edge. Patients are frequently annoyed by eructation — singultus. After both vomiting and also eructation a burning, boring sensation not rarely remains behind the sternum — heart-burn, jyyrosis. Eructation of combustible gases has been observed on a number of occa- sions, and is at times first noticed by patients on lighting a cigar. Analy- sis has shown that these gases consist, in addition to oxygen, nitrogen, hydrogen, and carbon dioxid, also of marsh-gas, carbon monoxid, oil-form- ing gas, and hydrogen siilphid. The functions of the stomach are greatly altered in cases of gastric dilatation. The period required for the absorption of potassium iodid is prolonged (more than fifteen minutes). The motor activity of the stomach also has suffered considerable im- pairment. Free hydrochloric acid is frequently wanting in the gastric contents. The appetite at times suffers, as, for instance, DILATATION OF THE STOMACH 231 in -cases of carcinomatous stenosis of the pylorus. In other in- stances, on the contrary, the appetite is excessive, because but little of the food ingested is absorbed. There is almost always marked increase in thirst, as fluids likewise are absorbed only with difficulty by a dilated stomach, and also are but inadequately propelled into the intestinal canal. The tongue is frequently marked by unusual redness and cleanness, because it is irritated and cleaned by the highly acid vomited matters. The urine is usually passed in small amount. After abundant acid vomiting it not rarely yields an alkaline reaction, and a peculiar sediment, which, in addition to coffin-lid crystals of amraonio-magnesium phosphate, consists of rhombic plates of magnesium phosphate. The boioels are generally constipated. The general nutrition suffers in marked degree. The patients undergo great emacia- tion ; their muscles become flabby, the skin thin like tissue-paper and deficient in fat, the face wrinkled, and the complexion ashy gray or grayish' yellow. Some patients present an almost desic- cated, mummy-like appearance. If the nutritive disturbance cannot be checked, death may result from progressive asthenia. In some cases dilatation of the stomach is attended with pecu- liar complications, which have been attributed to auto-intoxication, upon the assumption that certain putrefactive alkaloids or pto- mains have developed in the stomach, which exert an influence upon the nervous system especially. Under such conditions symptoms of tetany appear. This complication is not unattended with danger, and may be the immediate cause of death. The duration of dilatation of the stomach will depend upon the fact whether the patients observe strict dietetic precautions or not. If they will obey appropriate medical advice, the disease may exist for decades, and be tolerated without serious discomfort. The course of events is often sucli that periods of aggravation and of improvement alternate accordingly as the mode of life is careful or indifferent. Prognosis. — The prognosis of dilatation of the stomach depends, in the first place, upon the causative factors. It is from the outset unfavorable in cases of carcinomatous stenosis of the pylorus, for instance. If the condition is not dependent upon some disorder in itself dangerous to life, not only relief, but even cure, may be effected. Treatment. — Dilatation of the stomach requires both causal and dietetic treatment. If the condition is dependent upon ste- nosis of the pylorus, an attem])t should be made to correct this, and surgical measures will probably always be required for the purpose, as, for instance, resection of the pylorus — pyloroplasty, or bloodless dilatation of the pyloric ring. If the obstruction be irremediable, brilliant results are often attained by gastro-enter- ostomy ; that is, the establishment of an artificial communication 232 DIGESTIVE ORGANS between tlie stoniacli and tlic bowel, and tluis avoiding the pylorus. The sugi^estion of Jiireher, to eorreet dilatation of the stonuicli by making a fold in the viscus, appears as yet to have been acted upon in but few instances. Kspecially good results may be attained by systematic siphonage of the stomach, in order to free the viseus from its excessive contents, and to afford it opportunity gradually to contract to its natural size. Fig. 27. — Stomach-siphon of soft rubber. As a stomach-siplion a soft stomach-tube may be employed, and this is connected by a glass tube with a rubber tube 1 meter long. Into the free end of the rubber tube a glass funnel is introduced (Fig. 27). The stomach- tube is introduced as far as possible into the stomach, while the patient makes efforts at swallowing, and the warm water is permitted to flow into the funnel until the patient complains of a sense of fulness or no more water will enter. Tbe rubber tube is then compressed between the fingers and the funnel is inverted downward into a vessel. If the pressure upon the tube be now relaxed, the water that has been introduced, together with the contents of the stomach, will escape. This procedure is repeated until the irrigating fluid returns perfectly clear. At times the discharge is pre- vented by obstruction of the fenestra of the tube by coarse particles of food, as, for instance, pieces of meat. Usually the obstruction can be overcome by strong pressure with the hand upon the tube or by the introduction of water into the funnel. Otherwise the tube nuist be removed and the lumen made clear. If the patient complain of marked acidity, it is well at the conclusion of the procedure to wash the stomach with artificial Carlsbad salt (one teaspoonful to a quart of tepid water). In order to prevent fer- mentation of food in the stomach, irrigation with dkinfrofanis has also been practised. It is important to determine by means of graduates the amount of water introduced, and also that which escapes, for only if the latter be greater than the former can there be certainty that the contents of the stomach have been removed. Under the opposite conditions there is danger that the stomacii would be more greatly overloaded. At first the irrigations are practised daily, and we make them, not, as some have advised, DISPLACEMENTS OF THE STOMACH 233 in the evening, but in the morning. Gradually one, then two, and finally several days are permitted to intervene. Patients learn how to irrigate the stomach in a short time, as a rule, and intelligent patients may be permitted without concern to jn-actise the irrigation at home. Should signs of aggra- vation appear, the irrigation must again be practised with greater frequency. Most patients usually feel so much improved after the first irrigation that they can scarcely await the time for the next. The favorable influence of the procedure also becomes clearly appreciable in their appearance. The dull aspect again becomes fresher and animated. Bodily weight and vigor often increase with remarkable rai^idity, and the complexion acquires a healthy color. Disagreeable accidents but rarely occur in connection with irrigation of the stomach. At times tetany has been observed to follow directly upon the manipulation, probably in consequence of the mechanical irritation of the stomach. At the conclusion of the irrigation it is well for the patients to remain in bed for one or two hours, and to apply an ice-bag to the epigastrium in order to improve the tone of the musculature of the stomach. It may also be advantageous to practise massage of the epigastrium, or to apply the faradic current, or to inject strych- nin subcutaneously (0.1 : 10; 0.3 — 4 minims). Individuals in wliom dilatation of the stomach has developed in consequence of over- eating should be provided with a rigid diet-list, so as to avoid overloading of the stomach in the future. In cases in anemic and nervous individuals preparations of iron, courses of cold-water treatment, and the like, are indicated. Relax- ation of the abdominal walls requires the use of an abdominal binder. The dietetic regulations are the same in all varieties of dilatation of the stomach. Carbohydrates are to be avoided as strictly as possible, on account of the readiness with which they undergo decomposition. The ingestion of liquids should also be restricted. Patients should confine themselves especially to an animal diet, and the intervals between meals should not be too long. In order to relieve the stomach of catarrhal conditions of the mucous membrane that may be present, courses of treatment at springs are often of great utility, and particularly such as are fol- lowed at Carlsbad have yielded brilliant results. DISPLACEMENTS OF THE STOMACH (DYSTOPIA VENTRICULIj. Displacements of the stomach are either acquired or congenital. Congenital displacement of the stomach occurs in connection with transposition of the viscera, when other organs are likewise dis- placed, so that, for instance, the heart may be situated on the right side of the thorax, the liver in the left hypochondrium, the spleen in the right, etc. Under such circumstances the cardia will be found upon the right and the pylorus upon the left side. This condition is unattended Avith other disturbances. Acquired dis- placement of the stomach is also known as gastro^jtosis. Attention 234 DIGESTIVE ORGANS has only of late been directed to the frequency of this occurrence. The condition is with especial frequency characterized by an abnormal depression of the stomach, so that when the viscus is distended with carbon dioxid the greater curvature will be found below the level of the uml)ilicus, while the transverse area appears rather diminished. There is often besides a wandering kidney on the right side, and the impression is created that both conditioxis are dependent upon the same cause, which most frequently consists in the pressure of constricting clothing. In addition, derange- ment in the functional activity of the stomach occurs, and with especial frequency anacidity of the gastric juice and motor weak- ness. The patients often complain of a sense of pressure or of pain in the epigastrium, of loss of appetite, eructation, and even vom- iting. The wearing of constricting clothing should be interdicted and appropriate diet directed, and, in the presence of anacidity of the gastric juice, dilute hydrochloric acid prescribed. GASTRIC NEUROSES. Such disorders of gastric activity as are not attended with anatomic alterations in the wall of the stomach, but with morbid activity of the gastric nervous siqyply, are designated gastric neu- roses. A distinction is made between motor, sensory, secretory, and mixed gastric neuroses, accordingly as the one or the other nerve- path is involved. At times the functional activity of the nerves is morbidly increased, at times diminislied. MOTOR GASTRIC NEUROSES. NERVOUS VOMITING. Symptoms, Diagnosis, and Prognosis. — As the name of the disorder indicates, nervous vomiting is characterized by more or less frequent emesis. This may be so abundant and occur with such constancy after each meal that the nutrition of the patient may become impaired to an alarming degree, with the possibility of starvation. In other instances the vomiting occurs only at certain times and transitorily. In contradistinction from the vom- iting that occurs in connection with demonstrable anatomic disease of the stomach, it is peculiar to nervous vomiting that it usually takes place without preceding nausea, and that the matters ejected consist of the unaltered and unfermented contents of the stomach. The duration of the affection varies, and, together with the prog- nosis, is dependent upon whether the causative conditions can be removed or not. etiology. — Xervous vomiting is not rarely due to diseases of the brain and the spinal cord (concussion of the brain, cerebral tumor, abscess of the brain, cerebral hemorrhage, parasites, cere- GASTRIC NEUROSES 235 bral meningitis, tabes dorsalis, etc.). It has been observed also in association with central neuroses, and with especial frequency with hysteria. Often nervous vomiting is of reflex origin. The best-known instance of this kind is the vomiting of pregnancy. Frequently nervous vomiting attends biliary and renal calculi. Irritative conditions in the most diverse organs may, however, also give rise to nervous vomiting. Vomiting dependent upon toxic influences may likewise be considered of nervous origin. This may be induced intentionally by certain remedies (emetics, such as ipecacuanha-root, tartar emetic, copper sulphate, apomorphin hydrochl orate) ; or it may be due to certain poisons generated within the body itself as a result of metabolic processes (auto- intoxication), as, for instance, in uremia and cholemia. Nervous vomiting occurs most commonly, in icomen, because it is often dependent upon disease of the uterus and its appendages. It is less commonly encountered in children than in adults, as many of the causative conditions are observed only in the latter. Treatment. — Nervous vomiting requires, in the first place, causal treatment. Symptomatically, sulphuric ether (5 drops on sugar repeatedly), ethereal tincture of valerian (25 drops thrice daily), tincture of iodin (1.0 : 200 ; 15 c.c. — 1 tablespoonful — every two hours), and morphin hydrochlorate (subcutaneously) are indi- cated. The swallowing of small bits of ice is also advisable. NERVOUS ERUCTATION. J^ervous eructation occurs especially in cases of hysteria, neuras- thenia, and hypochondriasis. The patients suffer from eructation of gas that they have swallowed a short time previously and often expel with a loud, belching sound. At times the condition may persist for hours or even days, or it may occur in paroxysms in consequence of psychic disturbances. Sometimes an attack can be induced by pressure upon certain parts of the body. The dis- order is unattended with danger. The treatment should be partly psychic and in part directed against the primary affection. NERVOUS REGURGITATION. Regurgitation of food is a phenomenon that occurs also in healthy persons when the stomach is irritated by the ingestion of an excess of food or of food that is too cold or too hot, or by too rapid eating and insufficiently masticated food. The condition may be morbidly exaggerated in cases of hysteria, neurasthenia, and hypochondriasis. If fermentative processes in the stomach are superadded, the regurgitated matters may have an acid or a rancid taste. Regulation of the diet, the cooperation of the patient in an effort to suppress the regurgitation, and treatment of the primary disorder are capable of correcting the condition. 236 DIGESTIVE ORGANS PERISTALTIC UNREST OF THE STOMACH (NERVOUS TORMINA OF THE STOMACH). Nervous and neurasthenic individmils complain at times of a disagreeable feeling in the stomach and of restless movements in the epigastrium, which not rarely set in during the evening and even during the night, and disturb sleep. These manifestations are frequently associated with visible active contractions of the mus- culature of the stomach, and peristaltic movements may be ob- served passing slowly from the cardia to the pylorus. Care must be taken to avoid confounding the condition with the active movements of the stomach that occur in the presence of pyloric stenosis in the endeavor to overcome the obstruction to the passage of the chyme from the stomach into the duodenum. The absence of the causes and of the alterations of stenosis in the pyloric region, and the normal character of gastric digestion in other respects, are indicative of nervous unrest of the stomach. Treatment should be directed against the primary disorder. In addition, the diet should be regulated. Rest in bed and hot cataplasms should further be advised. HYPERMOTILITY OF THE STOMACH. Hypermotility of the stomach may be recognized from the fact that after a meal of meat the stomach is empty in a short while^ at times as early as an hour. The patients complain of excessive appetite. TONIC SPASM OF THE MUSCULATURE OF THE STOMACH. Spasm of the cardia — cardiospasm — prevents the unobstructed entrance of food into the stomach. The stomach-tube also en- coimters resistance at the cardia — thus at 40 cm. (lof inches) beyond the margin of the teeth ; but this frequently yields, in contradis- tinction from organic stenosis of the cardia, if the sound be per- mitted to remain quietly for a few seconds. The disorder occurs in nervous ])ersons, but may also be induced by reflex influences in connection with some diseases of the stomach, as, for instance, gastric ulcer. Spasm of the pylorus causes obstruction to the passage of food from the stomach into the intestine, and may be readily confounded with organic stenosis of the pylorus. At times there is spasm simultaneously at the pylorus and at the cardia. Under such con- ditions marked distention of the stomach with gas may take place, and this may give rise to disagreeable sensations in the epigastrium and to conditions of dyspnea — so-called dyspeptic asthma. The distinctive feature of pure nervous pyloric stenosis is the parox- ysmal ocrurrcnec of the phenonicua mentioned. Tonic spasm of the entire stomach occurs in connection with pyloric stenosis, and also as an independent neurosis. The stom- GASTRIC NEUROSES 237 ach appears contracted with board-like hardness. Often painful sensations in the epigastrium are appreciable during the spasmodic attack. All spasmodic conditions of the stomach should be treated by dietetic measures, hot cataplasms, bromids, or injections of morphin. Besides, the primary disorder should be relieved. INSUFFICIENCY OR INCONTINENCE OF THE PYLORUS. Insufficiency of the pylorus is characterized, on generation of carbon dioxid in the stomach, by failure of distention to take place or by its transitory occurrence ; whereas protrusion of the entire abdomen occurs because the gas has passed into the intestine from the stomach through the inefficient pylorus. The condition is encountered in cases of hysteria, neurasthenia, and spinal softening, and as a purely nervous disorder, although it may result in connection with severe gastric catarrh and destruc- tion of the pyloric sphincter by ulceration or carcinoma. Physio- logically incontinence of the pylorus is believed to be present when the stomach is empty. The treatment should be directed against the primary dis- order. RUMINATION (MERYCISM). Individuals who practise rumination return the food from the stomach into the mouth a sliort time after its ingestion, often re- chewing it with great satisfaction, and many experiencing a more agreeable sensation than when the food was originally ingested. Some patients repeat the practice after each meal ; others only when they eat hastily and do not masticate the food sufficiently. The nutrition may remain unchanged; and only when, in consequence of gastric catarrh or dilatation of the stomach, decomposition of the food takes place, and the patients, by reason of the disagreeable taste of the food, eject the regurgitated material, do emaciation and anemia occur. The functional activity of the stomach varies, and at times anacidity and at other times hyperacidity of the gastric juice have been observed. Rumination is a much more common disorder than is generally believed. I have quite accidentally detected a number of persons engaged in rumination who from a sense of shame were cleverly able to conceal the unpleasant prac- tice. Among the causative factors nervous diseases must be con- sidered, as, for instance, chorea, epilepsy, and idiocy. Individuals suffering from pulmonary tuberculosis not rarely practise rumina- tion. Imitation is an important etiologic factor. Dietetic errors are often operative, particularly too hurried eating and insufficient mastication of the food. At times rumination develops in the course of diseases of the stomach and the intestines (a blow upon the stomach, constipation). Patients frequently state that the disorder has begun with eructation, that subsequently they acquired the 238 DIGESTIVE ORGANS ability of inducing the eructation intentionally, and that finally they became ruminants, the contents of the stomach being forced into the mouth unconsciously. Many are able to suppress the practice voluntarily. Anatomic alterations of a distinctive char- acter are unknown. The presence of dilatation at the cardia, con- stituting a so-called fore-stomach, is an accidental and rare condi- tion. For the development of rumination weakness of the mus- culature at the cardia is probably necessary, as otherwise the food could not be returned. In the treatment the cooperation of the patient and his will- ingness to suppress the practice are the most important factors. Some persons, however, are unwilling to be deprived of the pleasure afforded by rumination. It is important, further, that the food should be eaten slowly, and be thoroughly masticated. At times rumination can be prevented by the swallowing of bits of ice. Besides, nervines, as, for instance, bromids, should be employed. ATONY OF THE STOMACH. Atony of the stomach consists in diminution in the tone of the gastric musculature and in motor weakness. The condition is thus attended with the danger that the food may remain stagnant in the stomach for a long time, and undergo decomposition, with the development of dilatation of the stomach. The patients com- plain principally of a sense of fulness and of pressure in the epi- gastrium. The condition is frequently encountered in anemic, del^ilitated, nervous, hysterical, and hypochondriacal individuals. The disorder is curable. A nutritious diet, consisting rather of solid than of liquid food, should be prescribed, and the general invigoration of the body promoted by cold frictions and massage. Besides, an effort should be made to correct the primary disorder* SENSORY NEUROSES OF THE STOMACH. NERVOUS GASTRALGIA. Symptoms and Diagnosis. — Nervous gastralgia is often attended with intense pain in the epigastrium, which appears at times when the stomach is empty, and at other times soon after the ingestion of food, in the latter event particularly Avhen food or drink is taken that is not well borne even in a condition of health. Not rarely an attack of gastralgia has been preceded by psychic disturbances, or in women it may occur at the menstrual period. The severity of the pain is frequently so great that, in consequence of reflex spasm of the cutaneous vessels, the skin becomes pale and cool, and covered with a clammy sweat. The pulse becomes small. The patients moan, and double themselves up. Syncope and clonic muscular contractions may occur. At times the dis- ease may terminate with a single attack of pain or after a small GASTRIC NEUROSES 239 number, while in other instances it may persist for mouths and years. In the latter event several attacks may occur in the course of a single day. Examination of the stomach yields little infor- mation, and it is often difficult to differentiate nervous gastralgia from that attendant upon anatomic disease of the stomach, as, for instance, round ulcer of the stomach. It is noteworthy that nervous gastralgia is at times relieved by firm pressure in the epigastrium, so that not rarely during the attack the patients make such pressure with their hands or press the epigastrium against some resistant body. If the ingestion of food is not observed to exert any influence upon the occurrence of an attack of pain, this is rather indicative of nervous gastralgia. It is further contended, also, that nervous gastralgia disappears upon galvanization of the epigastrium, with the positive pole (anode) applied. Prognosis. — Nervous gastralgia is a most distressing, but not a fatal disease. It, therefore, occasions no concern with regard to the continuance of life. ;^tiologfy. — The disorder occurs most commonly in associa- tion with certain central neuroses, particularly hysteria and neu- rasthenia. Anatomically demonstrable disease of the nervous sys- tem may also be attended with gastralgia, as, for instance, tabes dorsalis. The disorder is often dependent upon reflex influences. Women with disease of the uterus or the ovaries especially suffer not rarely from nervous gastralgia. In some families the disease is transmitted by heredity, probably because the morbid condition of the nervous system is inherited. Mental over-exertion, wasting discharges, excessive indulgence in alcohol, tea, and tobacco, and sexual excesses engender an undeniable predisposition to the dis- ease. Women are most commonly attacked because a large num- ber of the causative influences are operative among them. Chil- dren are attacked much less commonly than adults. Treatment. — In the treatment of nervous gastralgia two indications should be borne in mind : in the first place, the relief of the individual attack of pain, and in addition the prevention of recurrence — symptomatic and causal treatment. In the attack of pain hot cataplasms may be applied. If the pain be intense, a subcutaneous injection of morphin should be given, but the patient should never be entrusted with a solution of morphin and a syringe for use at his discretion, as the danger of abuse and of addiction to the drug is too great. Causal treatment should be directed against the primary disorder, and will be based upon the principles applicable to the individual diseases. 240 DIGESTIVE ORGANS DISORDERS OF THE SENSE OF HUNGER AND OF SATIETY (ACORIA ; BULIMIA; PICA). Disorders of the sense of hunger occur, like most other gastric neuroses, especially in cases of hyderia and neurasthenia, and they disappear, as a rule, when the primary disorder is cured. Acoria is a condition in which the sense of hunger is lost, so that the patients do not realize when they should take food. In other persons the sense of satiety is lost, and they are exposed to the danger of overloading the stomach. Bulimia or excessive hunger is characterized by a morbidly ravenous appetite, so that the patient can scarcely await the usual hour for meals, and often endeavors to suppress the sense of hunger by means of chocolate and other confections, which he constantly carries about with him. Pica is an unnatural desire for unusual and at times indigestible articles of food, as, for instance, ink, slate-pencils, vinegar, and the like. SECRETORY NEUROSES OF THE STOMACH, HYPERCHLORHYDRIA. Hyperchlorhydria, less accurately designated also hyperacidity or superacidity, indicates an increase in the hydrochloric acid of the gastric juice, so that the total acidity of the gastric contents after a trial-breakfast may exceed 70, and the percentage of free hvdrochloric acid may exceed 0.25. The patients complain prin- cipally of a disagreeable sense of pressure and of burning in the epigastrium. The condition at times accompanies a number of diseases of the stomach, as, for instance, round ulcer of the stom- ach ; and it occurs also as an independent neurosis, particularly in neurasthenics. In the latter event efforts should be directed to the relief of the primary disorder. In addition, systematic irri- gation of the stomach Avith Carlsbad salt (1 teaspoonful dissolved in 1 quart of tepid water) should be practised, and a generous animal diet, including but little amylacea, be permitted, as the digestion of starch is particularly interfered with by the excess of free hydrochloric acid. ANACHLORHYDRIA AND HYPOCHLORHYDRIA. Anachlorhydria and hypochlorhydria are known also as an- acidity and hypacidity or subacidity, and are characterized by either total absence of free hydrochloric acid from the gastric contents or its presence in amounts below 0.15 per cent. The total acidity may be below 30. These conditions occur in con- junction with certain diseases of the stomach (acute and chronic gastric catarrh, gastric carcinoma, amyloid degeneration of the gastric mucous membrane, excessive cicatrix-formation), but they may occur also as independent neuroses of the stomach. I have observed them with particular frequency in association with a GASTRIC NEUROSES 241 wandering right kidney and gastroptosis. They are encountered also, as a rule, in the presence of fever and of anemic states. The treatment consists in the administration of dilute hydro- chloric acid (10 drops in a wine-glassful of tepid water half an hour after meals), and in the correction of the primary disorder. HYPERSECRETION OF THE GASTRIC JUICE (GASTROSUCCORRHEA). Hypersecretion of the gastric juice, also known as gastro- succorrhea, is characterized by the presence in the stomach, even in the morning before food is taken, of as much as several hun- dred cubic centimeters of fluid, which, from the amount of free- hydrochloric acid that it contains, and its ability to digest albumin, is without doubt gastric juice. The disorder may be associated with hyperchlorhydria, and particularly under such conditions the patients usually complain during the night of a sense of boring and of burning in the epigastrium, and of increased thirst. The affection may be persistent or occur periodically, so that a distinc- tion must be made between continuous and paroxysmal gastrosuccor- rhea. Relief can be afforded by systematic irrigation of the stom- ach with a lukewarm solution of Carlsbad salt (1 teaspoonful to 1 quart of tepid water), and by the use of animal food, particularly at night. In addition, the nervousness usually present will require treatment. MIXED NEUROSES OF THE STOMACH. NERVOUS DYSPEPSIA. Symptoms, Diagnosis, and Prognosis. — Dyspepsia sig- nifies primarily only embarrassed gastric digestion. This mani- fests itself, in cases of nervous dyspepsia, particularly by the development of various discomforts after the ingestion of food. A sense of pressure in the epigastrium, abdominal distention, and frequent eructation are complained of with especial frequency. In addition there occur general nervous disturbances, particularly a sense of pressure in the head, mental confusion, vertigo, tinnitus aurium, a sense of fear, palpitation of the heart, redness of the skin, sweating, and the like. Examination of the functional activity of the stomach frequently discloses the existence of ana- chlorhydria or hypochlorhydria and diminution in the motor activity of the stomach, while, on the other hand, all signs indica- tive of anatomic alteration in the stomach are wanting. The patients are generally conspicuous on account of their pallid appearance, and frequently also by reason of their emaciation. In addition, they usually exhibit evidences of neurasthenia or hysteria. The disorder is troublesome and obstinate, but the prognosis is good, as it is scarcely capable of causing death. j^tiology. — Nervous dyspepsia is a common result of neuras- 16 242 DIGESTIVE ORGANS thenia, hysteria, and hypocliondriasis. As modern methods of living are highly conducive to the development of neurasthenia, it should not occasion surprise that nervous dyspepsia is a common disease <»f the stomach. Treatment. — Nervous dyspepsia will be most successfully treated if attention is directed primarily toward the general ner- vous condition. In addition, a nutritious but easily digestible diet should be prescribed. It is noteworthy that the patients, as a rule, l)ear badly courses of treatment at the springs, such as are fre- quently directed by physicians who have attributed the symptoms of nervous dyspepsia to anatomic alterations in the stomach. Under the name of periodic vomiting v. Leyden has described attacks of vomiting, associated with gastralgia, occurring in anemic and nervous individuals. Rossbach has designated as gristroxyims attacks of excessive secretion of hydrochloric and lactic acids in the stomach, giving rise to vomiting, headache, and vertigo. Xervous individuals and heavy smokers especially are attacked. The condition can be relieved by irrigation of the stomach. The attacks not rarely can be controlled by the ingestion of hot water. V. DISEASES OF THE INTESTINES. ACUTE INTESTINAL CATARRH. Ktiology. — Like acute gastric catarrh, acute intestinal catarrh also develops most commonly as a result of dietetic errors, and fre- quentlv both disorders exist together. Explanation is scarcely required for the fact that if the contents of the stomach are abnormally irritating the intestines also will be involved in the morbid process as soon as it has taken up the irritating gastric contents. The nature of the dietetic error may be most varied. Excess in food and drink may readily become injurious from the occurrence of fermentation in the ingested matters in the digestive tract, with irritation of the mucous membrane. Acute intestinal catarrh develops still more readily after the ingestion of decomposed food and drink, as, for instance, after the eating of unripe fruit or vegetables, fermented drinks, putrid water, etc. In this category belongs also the acute intestinal catarrh of children, which occurs with especial frequency in the hot months of summer, and is de- pendent upon fermentation of the milk ingested. Also, the inges- tion of food that is too hot or too cold, or is insufficiently masticated, or is indige.stible, is capable of inducing acute intestinal catarrh. Some persons exhibit an idiosyncrasy to certain kinds of food, as, for instance, cucuralu-rs, prunes ; that is, they develop symptoms of acute intestinal catarrh regularly after the ingestion of certain articles of food, even when these are taken in the smallest amounts. ACUTE INTESTINAL CATARRH 243 Aeute intestinal catarrh of toxic origin develops after the swal- lowing of certain irritant poisons (acids, alkalies, arsenic, mercuric chloric!), but this is not a common mode of origin. Acute intes- tinal catarrh may be caused also by excessive use of purgatives. There is no doubt that refrigeratory {rheumatic) intestinal catarrh resulting from exposure to cold occurs. Thus, a cold bath when the bodv is in a state of perspiration may give rise to acute intestinal catarrh ; sleeping upon damp ground has also at times been found to be a cause. I have in several instances observed acute intestinal catarrh to occur after the application of an ice-bag to the abdomen, so that it became 'necessary to withhold the appli- cation. Scarcely anything is known definitely with regard to trau- matic intestinal catarrh in so far as external injuries are concerned. On the other hand, acute intestinal catarrh may result from inter- nal injuries, as, for instance, in connection Avith constipation, in C(msequence of the irritation due to hardened scybalous masses, after the swallowing of bones or fruit-stones, and from the presence of biliary calculi in the bowel. Possibly some cases of acute intestinal catarrh associated with the presence of worms in the intestine should be included in this category. Epidemic acute intestinal catarrh occurs at times in the hot months of summer or atitumn as an independent disorder. It may be so severe as to suggest the clinical picture of Asiatic cholera, and it has then been designated also cholera nostras s. europaea. Secondary acute intes- tinal catarrh may either arise by extension from adjacent disease (peritonitis) or accompany other intestinal or constitutional disease (typhoid fever, dysentery, cholera, carcinoma of the intestine, in- vagination of the intestine, febrile infectious diseases, etc.). Acute intestinal catarrh occurs at all periods of life. It attains a wide distribution in infancy on account of the readiness with which milk undergoes fermentation, and annually many thousands of children die from acute gastro-enteritis — cholera infantum. Anatomic Alterations. — An inflamed intestinal mucous memljrane, like other inflamed mucous membranes, exhibits red- ness, swelling, and increased secretion. The redness, which results from distention of the vessels of the mucous membrane with blood, is usually most pronounced upon the summit of the villi and the prominences of the folds. Here and there, probably, some blood-vessels have ruptured and small hemorrhages have taken place. The swelling of the mucous membrane is appreciable in the increased thickness of the tissues and excessive infiltration with blood-plasma. The lymph-follicles are involved in the swell- ing with especial regularity. They are increased in size, and are usually surrounded by a zone of hyperemic vessels. At first the swelling of the lymph-follicles depends only upon serous infiltra- tion. They therefore resemble watery vesicles, and on puncture they give exit to a drop of clear fluid, while they collapse at the 244 DIGESTIVE ORGANS same time. Later, on the other hand, inflammatory hyperplasia of lymph-cells takes place in them, and they then acquire an opaque appearance and no longer collapse when punctured. The increased secretion of the mucous membrane is manifested by the accumulation upon the surface of the membrane of vitreous mucus, or mucus presenting a greenish-gray mottling in consequence of admixture with exfoliated epithelial cells or with pus. If the iuHammation of the mucous membrane be intense, it will extend to the serosa, which then appears markedly hy])eremic and of a rose tint. The contents of the intestine are usually thin and fluid. Not rarely they consist of a flocculent admixture of exfoliated epi- thelial cells from the intestinal mucous membrane. If the intestinal evacuations have been numerous and copious, the contents of the bowel may be gray and deficient in bile. In connection with severe intestinal catarrh the mesenteric lymphatic glands may also be involved and present swelling and redness. Acute intestinal catarrh may involve the entire bowel or only certain sections; and in the latter event, in accordance with the seat of the disease, a distinction has been made between acute duodenitis, jejunitis, ileitis, typhlitis (catarrh of the cecum), appendicitis (catarrh of the vermiform appendix), colitis, and proctitis (catarrh of the rectum). Ileocolitis is most commonly encountered. It is worthy of note that not rarely the most intense manifestations during life are attended with only slight alterations in the intestinal mucous membrane, obviously because a portion of the anatomic changes has disappeared in the cadaver. Among the comjjlications of acute intestinal catarrh superficial loss of tissue, erosions of the bowel., more profound ulceration of the mucous membrane, and destruction of the bjmph-foUicles of the intestine may be mentioned. Symptoms and Diagnosis. — The symptoms of acute intes- tinal (iatarrh vary in accordance with the extent of the disease and with the portion of the bowel involved. If the large intestine is the seat of the disease, diarrhea occurs, in consequence of the increased peristaltic activity ; the contents of the bowel are so rapidly sent through the large intestine that sufficient time is not allowed for inspissation to take place. Catarrhal conditions con- fined to the small intestine, on the other hand, are unattended with diarrhea, for the fecal matter acquires its usual consistency in the uninjured large intestine. In the most common variety of acute intestinal catarrh — Uco- colitis — there occur, at first, in many cases rumbling and noises in the abdomen — borborygmi — which result from unusually active and vigorous intestinal movement and the associated rapid propulsion of the intestinal contents. In consequence of decomposition of the intestinal contents there is active development of gas in the bowel, and the abdomen becomes distended — intestinal meteorism or tympanites. The gas seeks a means of exit downward, and fre- ACUTE INTESTINAL CATARRH 245 quently flatus occurs, and this is often attended with an offensive, ahiiost fetid odor. Often there is frequent desire for stool, and the stools themselves are thin, not rarely like water. The dejections are frequently marked by a decomposing or putrid odor, and they vary between brown, yellow, green, and gray in color. At times the stools contain unusually large amounts of undigested food (meat-fibers, tendon, portions of vegetables) — so-called lientery. Of especial significance in diagnosis is the presence of mucus in the stools. The appearance of blood is one of the less common phenomena. The reaction of the stools is usually acid. Fre- quently the evacuated matters are abundantly admixed with gas, and are frothy. Microscopic examination of the feces discloses, in addition to numerous remains of food, desquamated epithelial cells, round cells, and crystals of cholesterin, fat at times, also Charcot-Neumann crystals (pointed double pyramids), and, besides, numerous bacteria, although it has not yet been possible to isolate specific bacteria. Yeast-cells also are frequently found in the stools. The number of bowel-movements is subject to great variation (from two to twenty in twenty-four hours). At times the patients are scarcely able to leave the commode, from a fear that they will at once again be compelled to resort to it, and that they may fail to reach it in time. The desire for stool appears with especial frequency after the ingestion of food. It is fre- quently preceded by abdominal pain — tormina ; or there is escape of gas after pain has first appeared in the abdomen, and this like- wise changes its position with the onward movement of the gas. If gastric catarrh exist in addition to intestinal catarrh, there will be present nausea, vomiting, loss of appetite, and coated tongue. Often there is labial herpes. Acute intestinal catarrh may be unattended with alteration in the bodily temperature, while in other instances, on the contrary, febrile movement is observed. Many patients complain of gen- eral languor and malaise, and of drawing pains in the muscles and joints. Thirst is usually increased under all conditions, in consequence of the loss of fluid with the loose bowel-movements. The abdomen is frequently distended and tender to touch. The urine is usually voided in diminished amount. It is concentrated, and often deposits a sediment of urates. The amount of indican is frequently increased. Not rarely there is slight albuminuria, with cylindruria. Severe diarrhea causes a sense of weakness, and may even give rise to manifestations of collapse. As in Asiatic cholera, there may also be pains in the muscles, especially in those of the calves, and the voice may be high and hoarse. The duration of acute ileocolitis varies from a few days to between two and four weeks. In adults recovery is the rule. Acute catarrhal duodenitis can be recognized only when the choledoch duct also is involved in the morbid process. This may 246 DIGESTIVE ORG Ays result from obstruction at the orifice of this duct in consequence of tiie swelling of the duodenal mucous membrane ; or from the entrance of a plug of mucus from the intestinal mucous membrane into the duct and causing its occlusion ; or, finally, from thicken- ing of the mucous membrane of the duct in consequence of partici- pation in the inflammatory process. Under all of these condi- tions biliary stasis and icterus develop, and the condition has then been designated gastroduodenal icterus, or catarrhal jaundice. JeJiDiitis and ileitis cannot be diagnosed with certainty. Typhlitis and appendicitis will be considered in a special section. Proctitis is characterized by persistent desire for stool and pain when the bowels are moved — anal tenesmus. The anal sphincter is usually contracted spasmodically. Digital examination of the rectum causes severe pain. The mucous membrane of the rectum seems hot and unusually relaxed. Considerable mucus remains adherent to the finger, which at times is streaked and dotted with blood. After the condition has existed for some time paralysis of the anal sphincter sometimes develops, so that thin fecal matter escapes continuously from the rectum, moistens and irritates the skin in the anal region, and excites inflammatory reaction. There may also be prolapse of the bowel. Prognosis. — The prognosis of acute intestinal catarrh is favorable if the disease occurs in adults, and no serious primary disorder is present. In infants acute intestinal catarrh is quite a serious disease, and in the aged also there is danger that death may result from asthenia. Treatment. — Prophylactic measures may be extremely use- ful. Care in diet particularly should be observed. The treatment of acute intestinal catarrh depends upon the causative factors — causal therapy — and in part also upon the seat of the disease. In all varieties of the disease a febrile patient with frequent bowel-move- ments should remain in bed, keep a hot poultice applied constantly to the abdomen, and avoid solid food for several days. AVeak tea, coffee, Avater Mith red wine, mucilaginous soups, and almond- milk may be permitted. Should intestinal catarrh be dependent upon dietetic errors, it is often most advantageous to prescribe a purgative (castor-oil, 25 c.c. — 6 teaspoonfuls — in a cuj) of coffee ; or calomel, 0.5 — 7^ grains), in order to expel speedily tiie ferment- ing and irritating intestinal contents. OfttMi the symptoms disap- pear as soon as the bowels are emptied. Sliould the diarrhea per- sist, and frequent rumbling indicate abnormal increase in intestinal peristalsis, preparations of opium should be prescribed in order to keep the bowels quiet. R Powdered opium, 0.03 ( I grain ) ; Sugar, 0.5 (7^ grains). — M. Make 10 such powders. Dose : 1 powder every three hours. ACUTE GASTRO-INTESTINAL CATARRH IN INFANTS 247 R Powder of ipecacuanha and opium, 0.3 (4^ grains) ; Sugar, 0.5 (7^ " ).— M. Make 10 such powders. Dose : 1 powder every three hours. R Tincture of opium, Ethereal tincture of valerian, each, 10.0 (2^ fluidrams). — M. Dose : 20 drops thrice daily upon sugar. R Morphin hydrochlorate, 0.3 (4^ grains) ; Glycerin, Distilled water, each, 6.0 (75 minims). — M. Dose : From 0.25 to 0.5 (4 to 8 minims) subcutaneously. It is often useful to combine preparations of opium with astrin- gents (styptics) ; a combination of bismuth salicylate with opium is particularly reliable : R Bismuth salicylate, 0.5 (72 grains) ; Powdered opium, 0.03 (J grain) ; Bugar, 0.3 (4^ grains).— M. Make 10 such powders. Dose : 1 powder every three hours. Duodenitis and gastroduodenal catari'li should be treated accord- ing to the rules that have been laid down for the treatment of acute gastric catarrh. If jaundice be present, special care should be taken that all fatty substances are excluded from the diet. Acute injiammation of the rectum is readily accessible to local treat- ment, particularly with irrigation of the bowel (infusion) and suppositories. The latter, containing narcotics, may be employed especially when tenesmus is severe ; for instance : R Morphin hydrochlorate, 0.03 (J grain) ; Cocoa-butter, sufficient to make 3 suppositories. Dose : 1 suppository twice or thrice daily. ACUTE GASTRO-INTESTINAL CATARRH IN INFANTS. i^tiology. — Infants are in high degree predisposed to acute gastro-intestinal catarrh, and a large number of children succumb annually to this disease. In the first place, milk is a readily decom- posed article of food, and, besides, the gastro-intestinal mucous mem- brane of infants appears particularly sensitive. Experience has shown that infants ffiven mother's or wet-nurse's milk suffer much less commonly than those nourished with cow's milk or substitutes for milk. Milk undergoes decomposition the more readily the higher the external temperature, and in accordance with this fact acute gastro-intestinal catarrh occurs with especial frequency in the hot months of summer and autumn (from July to September). The con- dition has, therefore, also been designated summer diarrhea of infants. The greater the want of cleanliness in the dairies from which the milk is obtained, the greater is the danger of fermentative bac- 248 DIGESTIVE ORGANS teria gaining entrance into the milk, especially with small particles of excrement from the cow, so that the milk is contaminated from the ontset. It is important that the milk be thoroughly boiled, in order, so far as possible, to destroy fermentative bacteria ; that the receptacles for the milk be kept cold and covered ; that rem- nants of milk not drunk by the infant be thrown away or be used for other purposes ; and that the bottles and the nipples be kept scrupulously clean. Failure to observe these precautions may expose the infant to grave danger. At times error is committed in giving the infant milk in too large quantities or at irregular intervals. Experience has shown that infants bear poorly the milk of cows supplied with green fodder. Dentition undoulitedly pre- disposes to gastro-intestinal catarrh. It is not rarely observed that a perfectly healthy child is attacked by diarrhea, and in spite of the greatest care in feeding, only when a new tooth is in process of irruption — so-called dentition-diarrhea. The circum- stance that the connection between the two conditions is not recog- nized cannot justify doubt of the fact itself. Some infants are attacked by severe acute gastro-intestinal catarrh when the attempt is made to wean them from an exclusive milk-diet — diarrhoea ablactatorum ; and at times the disease cannot be controlled until the exclusive milk-diet is resumed. The sensitiveness of the infant's stomach and intestines with regard to a milk-diet may be recognized from the fact that some breast-fed infants are attacked by diarrhea when the mother or the nurse becomes angry, or suffers other psychic disturbance, or with the occurrence of menstruation. At times also a sort of idiosyncrasy is observed — one child not tolerating the milk of a given nurse, while another child may tlirive upon it. Children of the lower classes suffer most commonly from acute gastro-intestinal catarrh, because less atten- tion is devoted to their care. The poor also cannot always pro- vide proper milk on account of the expense. It is, therefore, not remarkable that the disease is particularly prevalent in large cities, niegitimate children perish in large number, because they are placed at board at the smallest possible cost, and in consequence are poorly nourished and cared for. Such foster-mothers are appropriately designated " angel-makers." Symptoms and Diagnosis. — The earliest symptoms of acute gastro-intestinal catarrh in infants often consist in frequent eructation and vomiting. The vomited matter at first contains lumps of casein ; but if the vomiting has persisted for some time the milk is returned uncoagulated, obviously because the gastric juice has become too deficient in acid to effect coagulation of the milk. Soon diarrhea sets in, and in some cases it may be the earliest symptom ; or, if the bowel principally be involved, it may be unattended with vomiting. The stools become thin, exhale a fetid and acid odor, and are either greenish in color or yellowish ACUTE G ASTRO-INTESTINAL CATARRH IN INFANTS 249 when evacuated, but when exposed to the air soon acquiring a greenish hue. If the bowels move with great frequency, the stools present a grayish color, and the condition is then designated cholera infantum. The abdomen frequently is greatly distended in consequence of excessive development of gas in the intestine. From time to time rumbling and gurgling sounds — borborygmi — are audible, indicating increased intestinal peristalsis and rapid pro- pulsion of the fluid intestinal contents. From time to time the little patient cries aloud, distorts the face in pain, and draws the legs upon the abdomen, in consequence of paroxysmal abdominal pain — tormina. Frequently escape of fetid gas follows, not rarely associated with fluid intestinal contents. When the diarrhea has existed for some time inflammatory redness of the skin about the anus and the buttocks develops, because soiling and irritation of the parts by fecal matter are unavoidable. The secretion of urine almost ceases entirely. The urine frequently contains albumin and tube-casts and considerable indican. In consequence of the copious loss of water in the stools thirst is greatly increased, and the mouth feels sticky and dry. The peripheral portions of the body are usually cool, while the covered portions of the trunk are unusually hot, in consequence of febrile elevation of the in- ternal temperature. Unfortunately, rapid and dangerous collapse often occurs in the course of the disease. The face becomes shrunken and presents a tired and aged appearance. The fon- tanels also become depressed, and the margins of the cranial bones can be slightly moved upon one another, the voice becomes faint and feeble, movement is painful and difficult, and the action of the heart is greatly accelerated. In consequence of progressive anemia of the brain cerebral manifestations appear that have been designated hydrocephaloid. At the same time the little patient becomes more and more apathetic, lying with its eyes half closed, and presenting tonic twitchings of the face or in the extremities ; finally, general clonic spasms may occur and death result. In rare instances the exposed cornea becomes desiccated and it may undergo rupture. Anatomic Alterations. — In the acute gastro-intestinal catarrh of infants the statement already emphasized in connec- tion with acute intestinal catarrh, that the most intense symptoms during life are often associated with only slight alterations in the intestinal mucous membrane, is frequently confirmed. In addi- tion to fluid intestinal contents, not rarely only slight swelling of the lymphatic follicles is found besides, and these are surrounded by a garland of dilated blood-vessels. In other instances the lesions of acute gastro-intestinal catarrh already described are found. Prognosis. — Acute gastro-intestinal catarrh in infants is a 250 DIGESTIVE ORGANS most serious disease, and the prognosis is grave. This depends especially upon the cooperation, the intelligence, and the care, in part upon the means, of those upon whom the nursing of the sick child devolves. Treatment. — Prophylactic measures first of all require thor- ough discussion and consideration. These apply to the nourish- ment of the infant. The most natural and the best food for an infant is the breast-milk of its mother or of a, wet-nurse. Unfortu- nately, however, it is a growing custom that mothers, from motives of convenience or from the unfounded fear that their beauty will suffer in consequence of nursing, do not nurse their children ; apart from those instances in which mothers are forljidden by physicians to nurse their children ; for instance, at an age below eighteen years, in the presence of profound anemia, pulmonary tuberculosis, inherited nervous disease (epilepsy, neurasthenia, psychopathy), and the like. The employment of a wet-nurse is expensive, and therefore accessible only to families of means. Further, certain precautions should be observed in nourishing infants with the breast-milk of the mother or of a wet-nurse. Infants readily develop gastro-intestinal catarrh when nursing women indulge in acid food, or become greatly excited, or permit coitus, or menstruate. It also happens occasionally that, from causes that elude scrutiny, the infant fails to thrive, although the nurse is apparently faultless, "while it bears admirably the milk of another nurse possibly not presenting so good an appearance. Under such circumstances a change should be made in good time. Should acute gastro-intestinal catarrh develop on weaning the infant, there is no other remedy but to restore the child to the breast and to repeat tlie attempt at weaning at a later period. In cases in which nourishment at the breast of the mother or of a wet-nurse is not practicable, /e^f/Z/ii^ icith animal milk is the next best method, and, as a rule, cow's milk is then employed. Goat's milk is less digestible on account of the greater amount of fat and albu- min that it contains, and mare's and ass's milk, which more closely resemble human milk in chemic constitution than does cow's milk, are not generally available. The use of cow's milk is attended with two dangers — namely, infection with tuberculosis and undue readiness of decomposition. Tuberculosis is common in cows, and it may readily happen that tubercle-bacilli gain entrance into the milk, especially when tuberculous nodules have developed in the udder, and the milk is thus infective. This danger cannot be averted with certainty, although it can be diminished if the cow whose milk is to be used is most carefully examined for the pres- ence of tuberculosis, and is no longer employed if even suspicious signs are present, and, besides, if the milk is always thoroughly boiled for a considerable length of time liefore it is used, in order to effect destruction of any tubercle-bacilli or their spores. The ACUTE GASTRO-INTESTINAL CATARRH IN INFANTS 251 suggestion appears worthy of consideration, to use the milk of several cows, in order to attenuate such tuberculous virus as may be present. In order to prevent, so far as possible, the decomposition of milk, cleanliness of the dairy and of the dairy-utensils should be observed, and cleansing the udder of adherent contamina- tions before milking, and of the fingers and the hands of the milker, practised. The milk should at once be covered and kept in a cool place. The cows should be supplied with dry fodder. In large cities establishments for the supply of infants' milk exist, which engage in the preparation of milk for infants in accordance with the principles outlined. Milk is also sterilized by many establisli- ments, and is sold in this condition. As may be understood, the greater labor expended in obtaining such milk entails a higher price for the product, and therefore the poor are scarcely able to purchase this specially prepared article. In this connection private philanthropy may render a great service by disj^ensing such milk under proper conditions. To sterilize milk in private dwellings, the use of the apparatus of Soxhlet may be especially recom- mended. Under all conditions milk for children should be thor- oughly boiled for a considerable length of time after its reception, and be introduced into a clean vessel, which is covered with a glass plate and is placed in a cool spot, and if possible preserved upon ice. The addition of a tal)lespoonful of lime-water to every quart of milk may also be advised in order to prevent fermentation. It should be borne in mind that cow's milk differs from mother's milk in containing a larger amount of solids, particularly casein ; W'hile, on the other hand, it contains less sugar. In order to make the former more closely resemi)le the latter it is necessary to add water and sugar to cow's milk. Even then the resemblance between the two is not complete, the casein of cow's milk coagu- lating in large masses, while that of mother's milk coagulates in fine flakes. In consequence, mother's milk is more readily acces- sible to the action of the gastric juice and is more digestible than cow's milk. By the addition of lime-water to cow's milk its casein will be precipitated in small flakes. Children in the first months of life should receive cow's milk and water in equal parts. Then, gradually, one-tenth less water is added, until from the fifth month the child will receive pure cow's milk. To each 250 c.c. of milk a pinch of sugar should be added. The use of sugar of milk is not necessary. For the preservation of the health of the infant it is further important to regulate the amount of food and the time of feeding. The stomach and the intestines should be protected from over- loading, In the first two months of life an infant should receive food every two, and thereafter every three, hours. The last meal should be given at ten o' clock at night and the first at six in the 252 DIGESTIVE ORGANS morning. It is further important to keep the feeding-bottles and the ni])plcs ck-an. The bottle is thoroughly cleansed with water and salt after each nursing, and is kept filled with water until the next jueal. Also, the nipples, in Avhich germs readily lodge, are thoroughly rubbed externally and internally with salt, and are kept in water. Care should further be taken to have the mouth of the infant cleansed after each nursing with a bit of soft, clean linen that has been dipped in water, as, otherwise, remnants of milk may readily undergo fermentation in the mouth, and if they be swal- lowed they may excite fermentative processes in the stomach. It is understood that the milk should be given not cold, but at the temperature of the body, being warmed in the bottle at each nursing by being placed in hot water. The feeding of an hfant icith Hubditute.H for milk — as, for instance, Liebig's, Nestle's, Kufeke's, Lofflund's foods, Biedert's cream- mixture, Gartner's fat-milk — is not worthy of commendation, because children thus nourished frequently become rachitic and also suffer readily from intestinal catarrh. If acute gastro-intes- tinal catarrh has developed in an infant, it is wise to withhold milk for from one to three days, and to replace it by pure water, to which a little red wine or Cognac has been added. Should the dis- ease be protracted, Nestle's food, beef-tea, or mucilaginous soups of oatmeal-gruel, sago, or arrow-root may be given instead of milk. Among medicaments calomel deserves first place : B Mercurous chlorid, 0.01 ( i grain) ; Sugar, 0.5 {7^ grains).— M. Make 10 such powders. Dose : 1 powder every two hours. Among styptics, colombo-root (infusion of colombo-root, 10.0 : 100 — 2^ drams : 3 fluidounces ; 5 c.c. — 1 teaspoonful — every two hours), cascarilla-bark (infusion of cascarilla-bark, 10.0 : 100 — 2^ drams : 3 fluidounces ; 5 c.c. — 1 teaspoonful — every two hours), and silver nitrate (solution of silver nitrate, 0.1 : 100 — 1^ grains : 3 fluidounces ; 5 c.c. — 1 teaspoonful — every two hours) may be mentioned. Preparations of opium should not be prescribed, because children readily develop alarming toxic symptoms from their use. Of late, disinfectants (lactic acid, carbolic acid, benzol, najjhthalin, thymol, resorcin, etc.) have been much used, but we fail to see any particular advantage in them over the remedies already recommended. If signs of cerebral anemia appear, strong Avinc in small doses should be administered, and the head should be lowered. CHRONIC INTESTINAL CATARRH. ^Etiology. — Chronic intestinal catarrh not rarely develops in the sequence of acute intestinal catarrh if this be frequently re- CHRONIC INTESTINAL CATARRH 253 peated, and especially if recurrence take place after incomplete recovery from the preceding attack. At other times it develops as an independent affection, and under such circumstances definite causes will be found to have been operative. HypostatiG catarrh exhibits a marked tendency to pursue a chronic course. It may be induced by the general stasis attending chronic disease of the heart or of the respiratory apparatus, or it may develop as a result of stasis in the portal circulation, and most commonly in associa- tion with cirrhosis of the liver. Chronic debilitating disease, as, for instance, pulmonary tuberculosis, carcinoma, leukemia, pro- tracted suppuration, often maintains chronic intestinal catarrh. Not rarely chronic intestinal diseases (carcinoma, hemorrhoids, tuberculous ulceration, parasites) are accompanied by chronic intestinal catarrh. Chronic constipation is often a cause of chronic intestinal catarrh. Anatomic Alterations. — Intestinal mucous membrane the seat of chronic inflammation is conspicuous for its color. It is brownish-red or grayish-red in appearance, especially on the villi and at the summit of its folds. At times the brownish hemo- globin has been transformed into black melanin, so that the mucous membrane presents a mottled appearance — so-called vil- lous melanosis. Besides, the presence of excessive secretion is conspicuous, the mucous membrane being covered with trans- parent or slightly turbid mucus. The lymph-follicles are often enlarged, and surrounded by a brownish or blackish zone of pig- ment. As a rule, the mucous membrane is thickened in conse- quence of inflammatory hyperplasia of the connective tissue, and often the muscularis and the mucosa also participate in the hyper- plasia and thickening. Under such circumstances the condition can be designated hypertrophic chronic gastric catarrh. In con- tradistinction from this, atrophic chronic gastric catarrh is attended with abnormal attenuation of the intestinal wall, together with atrophy of the glandular layer of the mucous membrane. Further, especial care should be taken in reaching a decision as to the ex- istence of chronic atrophic intestinal catarrh, as frequently the condition of intestinal atrophy is simulated by insignificant post- mortem alterations. Among the complications of chronic intes- tinal catarrh catan^hal ulceration of the bowel may be mentioned, which may have resulted from disintegration of lymph-follicles — follicular intestinal ulceration — or from destruction of the tissue of the mucosa itself — catarrhal ulceration of the mucous membrane. Among rarer occurrences polypoid hyperplasia of the mucous membrane and cystic degeneration of the glands of the intestinal mucous membrane may be mentioned. Symptoms and Diagnosis. — Alterations in the stools con- stitute the main symptom of chronic intestinal catarrh. As a 254 DIGESTIVE ORGANS rule, there is irregularity in the movement of the bowels, and often constipation and diarrhea alternate with each other. The abundant presence of mucus in the stools is distinctive. In the presence of catarrh of the large intestine the individual fecal masses are often enclosed in a layer of mucus. In the presence of catarrh of the small intestine, on the other hand, there is intimate admixture of fecal matter. Often the stools are stained yellow by biliary coloring-matter, and on addition of nitric acid they yield the reaction of biliary coloring-matter. At times peculiar, swollen and transparent, sago-like granules are present in the stools, which consist in part of swollen carbohydrates and in part of mucus. These were formerly considered erroneously as distinctive of follicular ulceration of the bowel. The stools at times contain a strikingly large amount of undigested food. If this be recognizable with the unaided eye, the condition has been designated lientery. Microscopic examination of the stools dis- closes, in addition to remnants of food and bacteria, isolated round cells and epithelial cells. The latter are often peculiarly swollen, and, in the presence of catarrh of the small intestine, bile-stained. Rumbling in the abdomen — borborygmi, distention of the abdo- men — intestinal meteorism, and abdominal pain — tormina — are fre- quently recurring symptoms, which at times become particularly severe. Chronic intestinal catarrh is usually unattended with fever. Nutrition may suffer in marked degree. The patients emaciate progressively, and acquire a grayish and sallow appear- ance. Psychic alterations occur with especial frequency, and they have not improperly been explained as the results of auto- intoxication, inasmuch as abnormal metabolic products are ab- sorbed from the intestine and derange the functions of the nervous system. The patients become hypochondriacal, believe themselves to be suffering from all possible serious diseases, develop a fear that they will become insane, are involved in doubts as to their mental and physical ability, and complain of all possible conditions of fear. They are often troubled by annoying vertigo — intestinal vertigo, which can at times be devel- oped voluntarily by pressure upon the bowel. Palpitation of the heart and asthmatic states also occur occasionally. The appetite is variable, and is impaired especially when the stomach is also involved in the inflammatory process. Thirst is usually increased. The urine is usually voided in small amount, is therefore gen- erally characterized by its dark-rod color, and frequently precipi- tates a reddish, granular sediment of urates. The duration of chronic intestincd catarrh is subject to Avide variations. In some individuals it persists throughout life. If ulceration of the intestinal mucous membrane has taken place, hemorrhage, rupture, and, after cicatrization of ulcers, stenosis of CHRONIC INTESTINAL CATARRH 255 the bowel may occur as complications, but these occurrences are rare. Most commonly chronic inflammation of the bowel in- volves the ileum and the colon, in correspondence with the like con- ditions that attend acute intestinal catarrh, and what has been said in the preceding refers principally to chronic catarrhal ileocolitis. Chronic catarrhal duodenitis is characterized by involvement of the choledoch duct and chronic catarrhal jaundice. Chronic inflammation of the rectum — chronic catarrhal proctitis — like acute proctitis, is attended witlv a persistent desire for stool — anal tenes- mus. The stools at times consist only of mucus or of mucus and pus. Sometimes the structures surrounding the rectum become involved in the inflammatory process — periproctitis; and if a col- lection of pus in this situation ruptures outward or inward, or in both directions simultaneously, an external or an internal or a complete rectal fistida will result. Prominence should be given to that form of colitis which has been designated membranous enteritis — mucous colic. This is characterized generally by the periodic evacuation of whitish membranes, tubes, and shreds, consisting of mucus, and less commonly of fibrin and all)uminoid material, and which have collected along the bands of the colon. The evacuations are usually preceded by disagreeable sensations in the abdomen, with distention, and the expulsion of the sometimes long casts is attended with severe pain and difficulty. Care should be taken, further, to avoid confounding such casts with tendinous struct- ures, the fibrous remains of asparagus, and the like, and this can readily be done by microscopic examination. The membranes and tubes exhibit under the microscope a swollen structure, which becomes striated on addition of acetic acid, and contains epithelial cells, isolated round cells, and crystals of triple phosphate and cholesterin. This condition occurs principally in nervous indi- viduals, particularly women, and while not dangerous is often very obstinate. Only in the minority of cases does the condition appear to be the sequel of chronic intestinal catarrh — true mem- branous enteritis ; while in the majority of cases it appears to be a secretory neurosis of the intestinal mucous membrane — mucous colic. The occurrence in children suffering from chronic intestinal catarrh of stools containing considerable fat has been described as fatty diarrhea, the absorption of fat being obviously much dimin- ished. The stools present a yellowish or grayish appearance, give off* an odor of fatty acids, when rubbed up with water and ex- amined microscopically exhibit an abundance of fat-globules, and on analysis are found to contain 67 per cent, instead of 20 per cent, of fat. The condition is observed especially in association with catarrh of the small intestine, and also when the pancreas is dis- eased and the discharge of bile into the intestine is interfered with. PrognosiS.^Although chronic intestinal catarrh is as a rule 256 ^ DIGESTIVE ORGANS not a dangerous disorder, it is often extremely obstinate and annoy- ing. At times the prognosis is unfavorable, because the causative conditions (carcinoma, tuberculosis) are incurable. Treatment. — In the treatment of chronic intestinal catarrh consideration should first be given to the causative conditions, and an elibrt made to relieve them — causal therapy. Symptomatic treatment will have to be directed most frequently to the relief of existing constipation. The mode of life and the diet will next require correction. The patients should take Avalks regularly, indulge in gymnastic exercises and physical activity, and never suppress the desire for stool, however slight this may be (a rule that must be especially impressed upon women), while a daily eifort to evacuate the bowel at the same time should be encour- aged, even in the absence of the normal desire, in order to accus- tom the bowel to habitual activity. The diet should include such articles of food as experience has shown to be capable of stimu- lating the bowels to increased activity. Among these may be mentioned Graham bread witli butter and honey in the morning, Graham bread with butter in the evening, fruit at noon and in the evening, and vegetables at noon. Often the patients have themselves discovered certain domestic remedies capable of induc- ing movement of the bowels, as, for instance, the ingestion of a glass of cold water when the stomach is empty, or the smoking of a cigar. Among medicaments, laxatives, mineral waters, and enemata may be mentioned. It should be pointed out that the intestine readily becomes accustomed to a given medicament or procedure, so that variation is necessary from time to time. Among laxatives, rhubarb-root, senna-leaves, aloes, jalap, and podophyllin particularly may be recommended ; as, for instance : R Aloes, Compound extract of rhubarb, each, 1.5 (22J grains) ; Powder and fluid extract of licorice, sufficient to make 30 pills. Dose: 1 or 2 pills at night. B Aloes, Compound extract of rhubarb, Powdered jalap, each, 1.0 (15 grains) ; Powder and fluid extract of licorice, sufficient to make 30 pills. Dose : From 1 to 3 pills at night. R Aloes, Compound extract of rhubarb, each, 1.5 (22.1 grains); Podophyllin, 0.3 ( 4.} " ) ; . Powder and fluid extract of licorice, sufficient to make 30 pills. Dose : 1 or 2 pills at night. R Compound licorice-powder, 100.0 (3 ounces). Dose: 1 or 2 teaspoonfuls in a wine-glassful of tepid water in the morning. R Electuary of senna, 50.0 (1^ ounces). Dose : 1 teaspoonful in the morning. INFLAMMATION OF CECUM AND VERMIFORM APPENDIX. 257 Among mineral waters may be mentioned the various bitter waters (Ofen, Pullna, Saidschutz, Friedrichshall, Birraenstorf, Baden), of which one or two wine-glassfids should be taken in the morning when the stomach is empty, to be followed in a short time by an equal quantity of cold water. Carlsbad salt (solution of artificial Carlsbad salt — 1 or 2 teaspoonfuls to a glass of water when the stomach is empty) is often employed with success. Enemata may be administered advantageously in the form of intestinal infusions. For this purpose either an irrigator with a tube and a rectal nozzle, or the funnel-apparatus of Hegar, con- sisting of a large glass funnel with a rubber tube and rectal nozzle,, is employed. The irrigating fluid should be water at room-tem- perature, and from 1 to 2 liters should be permitted to flow into the large intestine. The introduction is best effected with the pelvis elevated, and even more satisfactorily in the knee-elbow posture. Frequently the water will not flow because the rubber tube is filled with air. This can be removed readily by repeated and vigorous pressure with the fingers upon the tube. Russian physicians were the first to recommend large enemata of oil for the relief of obstinate constipation (from 400 to 500 c.c. of poppy- seed oil — about 1 pint — to each enema). Glycerin-enemata are also highly efficacious (2.0 — 30 minims — glycerin to each enema), while glycerin-suppositories are less reliable in action. Well-to- do patients may during the summer undertake courses of treat- ment at the springs. Among these, the springs of Carlsbad, Marienbad, Tarasp, Kissingen, Homburg, Ems, Wiesbaden, and Vichy especially should be mentioned. In cases of chronic duo- denitis loith jaundice all articles of food containing fat should be interdicted. Membranous enteritis is often resistant to all forms of treatment. In the first place, the nervous general condition should be taken into consideration, and in addition intestinal infu- sions of oil, water, and astringents should be employed. INFLAMMATION OF THE CECUM AND THE VER- MIFORM APPENDIX AND THE SURROUNDING TISSUES (TYPHLITIS; APPENDICITIS; PERITYPH- LITIS; PARATYPHLITIS)* Btiology and Anatomic Alterations. — Inflammatory processes not rarely occur in the right iliac fossa, which have certain important symptoms in common (usually sudden onset, pain, and acute tumor-formation). Inflammation of the cecum is known as typhlitis, while inflammation of the vermiform process is designated appendicitis. Circumscribed inflammation of the peritoneal covering of the cecum or the vermiform process is luiown 2ii^ perityphlitis. Inflammation of the retrocecal connective tissue, by which the vermiform appendix is attaclied to the iliac 17 258 DIGESTIVE ORGANS fossa, is known as paratyphlitk. Typhlitis and ap})enclicitis are almost always independent diseases, while perityphlitis and para- typhlitis are usually of secondary origin, and most commonly result from preceding appendicitis or typhlitis. Appendicitis and peril i/phlitis are the conditions most commonly encountered. In the majority of cases the process pursues the following course : Fecal matter becomes lodged in the vermiform appendix, and in consequence of desiccation becomes solidified into so-called false fecal concretions, which after a while cause mechanical irritation of the walls of the appendix, with secondary inflammation and necrosis. The inflammatory process readily extends to the adja- cent peritoneum, so that to appendicitis is superadded perityphlitis. The latter frequently occurs from perforation of the walls of the appendix by a fecal concretion, which may become lodged in the orifice of perforation or is expelled into the peritoneal cavity. At times the free extremity of the vermiform process is detached in its circumference, the stone occupying the mouth of the ap- pendix. Perityphlitis usually gives rise to the formation of an encapsulated, purulent exudate, which may acquire a fecal odor even if perforation of the bowel has not taken place. After peri- typhlitis has existed for a considerable length of time adhesions are usually so numerous that it is difficult to find the appendix at all, not to speak of the point of perforation and a fecal con- cretion. Clinical experience has shown that the tendency to the forma- tion of fecal calculi, and therefore also to appendicitis and peri- typhlitis, is unevenly distributed. In some families the disease occurs with such remarkable frequency that the causative factors have been looked for in some anatomic peculiarity of tlie vermiform appendix (excessive length, undue development of Gerlach's valve at the entrance to the vermiform appendix, unusual size). Without doubt the character of the food has an influence upon the forma- tion of fecal concretions, as these are observed most commonly in individuals who live excessively upon a vegetable diet. The swallowing of foreign bodies is also a dangerous practice in this connection. Thus, I have observed fecal concretions formed about swallowed hair from the beard and bristles from the tooth-brush. A sedentary mode of life predisposes in marked degree to the formation of fecal concretions and their consequences; so does also constipation. As several of the causative factors named are ojjerative in the individuals concerned throughout life, it can be readily understood that appendicitis and perityphlitis are frequently recurrent. Atten- tion has recently been called to the foct that inflammatory condi- tions (catarrhal j hemorrhagic, purulent, gangrenous) of the mucous membrane of the vermiform process are not uncommon, and that these also may be followed by the formation of fecal concretions, INFLAMMATION OF CECUM AND VERMIFORM APPENDIX. 259 appendicitis, and perityphlitis. True fecal concretions constitute much less commonly than false fecal concretions the starting-point for inflammation of the vermiform appendix and its vicinity. True fecal concretions consist of mineral deposits, whose princijial con- stituents are generally calcium phosphate, calcium carbonate, and ammonio-magnesium phosphate. At times swallowed foreign bodies give rise to appendicitis and perityphlitis. Thus, a railway-official under my care died with pyemic manifestations in the sequence of appendicitis and perityphlitis, w^ho attributed his disease to the sharp fragment of a tooth-pick that he had swallowed. It should not be forgotten that at times ulceration of the mucous membrane of the vermiform appendix (catarrhal, typhoid, tuber- culous, carcinomatous, actinomycotic) may be followed by appen- dicitis. Not rarely traumatism, exposure to cold, and, in my experience, with especial frequency, the ingestion of cold fluids (beer) are named as causes of the disease, but these influences probably play the rd/e rather of contributory factors, which fur- nish the final impulse for the outbreak of the disorder, long after the true germ had been present. Although appendicitis is the most common cause for perityphlitis, it is by no means the sole cause. Perityphlitis may, for instance, be dependent upon a preceding typhlitis. At times it originates from a perimetritis, a salpingitis, or an oophoritis, and it may happen that the exudate has already disappeared from the actual starting- point of the inflammation, and an apparently primary perityphlitis is encountered. In women it is, therefore, not uncommon for the manifestations of perityphlitis to appear in the sequence of menstrual disturbances. Constipation was formerly considered the cause of inflammation of the cecum (typhlitis), and the condition was, accord- ingly designated stercoral typhlitis. Stagnation of fecal matter may readily take place in the cecum, because here the intestinal con- tents become inspissated, and to a certain degree must be propelled against the force of gravity. A sedentary mode of life and ex- cessive use of vegetables, as well as swallowed foreign bodies, will favor fecal stagnation. Kecently attempts have been made to cast doubt upon the occurrence of stercoral typhlitis, but upon the basis of personal experience it appears to me that they have not succeeded. Ulcerative processes may induce inflammation in the cecum in the same manner as in the vermiform process. Trau- matism is at times followed by typhlitis. Paratyphlitis may arise by extension from typhlitis or peri- typlitis, or it may develop in the sequence of paranephritis, para- metritis, periproctitis, psoas-abscess, inflammation of the innominate bone or of the vertebral column, when the inflammatory process extends to the iliac fossa or gives rise to burrowing abscesses therein. As in perityplitis, so also in paratyphlitis it may happen that the exudate at the site of primary inflammation has been 260 DIGESTIVE ORGANS absorbed, leaving a paratyphlitis. At times paratyphlitis develops in the sequence of infectious diseases (typhoid fever, septicemia). Trauiiiafic paratt/pJtlitis may occur as an independent disorder, as after the lifting of lieavy weights, after over-exertion in the process of washing and tlie hanging up of linen, and in some persons it may be recurrent. The occurrence of refrigeratory {rheiimntic) paratyphlitis may properly be doubted. The inflammatory processes under consideration may develop at any period of life, though most commonly between the sixteenth and the twenty-fifth year, and the impression has been created that their frequency has become progressively greater witliin recent times. Men are attacked, experience has shown, more than twice as often as women. Symptoms. — Appendicitis and pcritypjhlitis frequently set in with sudden, sharp pain in the right iliac fossa, the intensity of which is often so great that the patients will not tolerate the slight- est pressure with the fingers, not even that of a light sheet. The abdomen is generally distended, obviously because a large amount of gas has accumulated in the small intestine. Often a con- siderable prominence is noticeable in the right iUac fossa. On pal- pation, which naturally should be practised with great care, only increased tension of the abdominal walls and increased resistance without sharp limitation, may at first be appreciated. In the course of a few days at most, a readily circumscribed tumor will have formed in the right iliac fossa. The most common variety of tumor begins below at about the middle of Poupart's ligament, forming a convex arch toward the median line of the al)domen and disappearing on the right side of the abdomen below the lower margin of the liver. The right lumbar region also is fre- quently distinctly resistant. Xot rarely the tumor is smaller in extent. Palpable exudates of band-like shape also occur. In addition to the local abdominal alterations there are usually disturbances of gastric and intestinal activity. Vomiting is an ex- ceedingly frequent manifestation. The vomited matters consist at first of gastric contents, but after emesis has persisted for some time they assume a bilious character, and present at times a yel- lowish, and at other times a greenish color. Eructation — singultus — is one of the common symptoms. Appetite is entirely M'anting, while thirst is greatly increased. The tongue is almost always coated. Often the breath is extremely offensive. The bowels are usually constipated, although at the beginning of the attack a few thin bowel-movements may be passed. The urine constantly con- tains an increased amount of indican in consequence of derange- ment of digestive activity in the small intestine and increased proteid decomposition in the bowel. The urine is at the same time passed in small amount, and consequently is generally dark red in color. Appendicitis and perityphlitis are almost always INFLAMMATION OF CECUM AND VERMIF0B3I APPENDIX 261 attended -svith fever; a perfectly afebrile course is exceptional. The elevation of teniperature may reach 39° C. (102.2° F.) or 40° C. (104° F.). The fever pursues no definite type, and declines gradually after a variable period of time. The patients usually occupy a peculiarly rigid posture, lying upon the back, as a rule somewhat inclined toward the right, and as much as possible avoiding all change in position on account of the resulting severe abdominal pain. The duration of an attack of appendicitis and jjeritypliUtis is extremely variable, and fluctuates between days, weeks, and months. In the natural course of the disease the fever disappears slowly, the pains beccmie less severe, the exudate becomes smaller, harder, and more sharply circumscribed. Painless residues of exudate and infiltrations in the right iliac fossa often persist for many months. Frequently it is remarkable how after a copious evacuation of the bowels the exudate becomes almost suddenly smaller, obviously because the accumulated fecal matter has arti- ficially increased the extent of the exudate. Often sharp pain and tenderness in the right iliac fossa persist for a long time. Dropsy of the vermiform process develops at times as a sequel of appen- dicitis, and it may be represented by a smooth and movable tumor as big as a fist. A similar condition may develop when ulcers, and subsequently cicatrices, form in the neighborhood of the entrance to the vermiform appendix, and these give rise to occlusion of the appendix. Mucoid masses then accumulate in the appendix with increasing distention. Among the complications, one of the most dangerous is diffuse acute peritonitis, which may be readily recognized from the exten- sive tenderness of -the abdominal walls, the increased distention of the abdomen, and the aggravation of the general condition. At times incautious bodily movement or dietetic error may be found to be a causative factor. Improper manipulation of the abdominal walls also may give rise to diffuse peritonitis, an encapsulated peritiphlytic exudate rupturing into the abdominal cavity. Con- stipation and expulsive efforts at stool may likewise give rise to general peritonitis. Pneumoperitonitis develops "when in addition to fecal matter air also enters the abdominal cavity through a perforation in the vermiform appendix. The principal distinctive features of this condition consist in marked abdominal distention, abdominal tenderness, absence of hepatic and splenic percussiori- dulness, and general collapse. At times symptoms of ileus appear (fecal vomiting, constipation, and absence of flatus) without a me- chanical obstruction of the intestine being demonstrable at autopsy. Under such circumstances the condition is probably one of dynamic or paralytic ileus resulting from partial paralysis of the muscular coat of the bowel. Some patients complain of dysuria, which is probably dependent upon perityphlitis, and it may be- come necessarv to remove the urine with the aid of a catheter. 2G2 DRiEHTIVE ORGANS I have observed the iwine to be alkaline for days with particular frequency whcu absorption of the exudate has set in. Pleurisy develops in about one-third of the cases. Most commonly it is right-sided, althougii it may be left-sided or bilateral. Usually it is serous in character. Often it is absorbed with marked rapid- ity. Among the complications rupture of the pus may yet be mentioned. This may take place into the intestine, and its occur- rence can be recognized from the presence of pus in the stools. I have on several occasions also observed a desire for stool and pain during evacuation of the bowels — tenesmus ani. In other instances the pus ruptures into the urinary ])assages (pelvis of the kidney, ureter, bladder), and pyuria and dysuria develop. Rup- ture into the uterus or the vagina is also conceivable. At times the pus burrows beneath the cutaneous integument. Redness and doughy induration of the skin, increasing prominence and fluctuation of progressively increasing distinctness are indicative of the advent of this condition. The point of rupture is at times in the neighborhood of the right iliac fossa itself, but at other times in consequence of burrowing it may be situated at a remote point, as, for instance, at the umbilicus, below Poupart's ligament, etc. Occasionally subphrenic pyothoj^ax, or pyopneumothwax — that is, an accumulation of pus or of pus and air between the diaphragm and the upper surface of tlie liver — has been observed to develop in the sequence of perityphlitis. At times appendicitis and peri- typhlitis give rise to septicopyemia, jiurulent thrombi foi'ming in the mesenteric veins, from which emboli may be detached and be swept into the circulation, giving rise especially to multiple abscess of the liver. In one case I observed such a condition develop seventeen years after an attack of acute appendicitis. Stercoral typhlitis usually occurs after preexisting constipation. The patient complains suddenly of pain in the right iliac fossa, and in this situation is found a painful tumor, which, in contradistinc- tion from a perityphlitic exudate, yields a dull, and not a dull- tym))anitic note upon percussion, and does not extend to the median line of the abdomen and upward to the lower margin of the liver, but which at times, when marked pressure is made with the finger, presents depressions due to indentations of the fecal fnatter. It is further distinctive that after a copious evacuation of tiie bowels the timior usually disajijicars, and at most slight indu- ration remains for a short time, which may possibly be dependent upon inflammatory swelling of the intestinal mucous membrane. The abdomen is intensely distended, in consequence of fecal stag- nation and abundant generation of gas. There is no increase in the amount of indiean in the urine, or this is but slight. Febrile move- ment also is wanting, or is not marked. As a rule, a rapid change for the better occurs when a copious bowel-movement lias been INFLAMMATION OF CECUM AND VERMIFORM APPENDIX 263 induced ; otherwise, naturally, serious dangers may arise, among which may be mentioned ileus, perityphlitis, peritonitiH, and rupture of the bowel. Paratyphlitis also is attended with pain and tumor-formation in the right iliac fossa, but the tumor is not so superficial as in the case of perityphlitis and typhlitis, and it is concealed by the tym- panitic percussion-note yielded by the cecum. The amount of indican in the urine is not increased. Fever is present, and the patient usually keeps the right thigh flexed, probably in conse- quence of involvement of the iliopsoas. At times unyielding muscular contractures develop. Occasionally pressure exerted by the exudate upon the nerves to the extremity passing through the pelvis gives rise to paresthesia, neuralgia, and paralytic conditions in the right leg. Pain in the right testicle and spasmodic elevation of this organ have been observed. Pressure of the exudate upon the veins of the extremities may give rise to edema in these parts. The disease is not unattended with dangers and other complica- tions. Thus, general septicopyemia may develop, or the pus may rupture into the intestine, the urinary pas-sages, the peritoneal cavity, or externally. In the last-named event extensive bur- rowing of the pus may take place, as, for example, down into the extremities, the perineum, the vagina. In one case I observed rupture of the pus upon the left side of the abdomen. It may also occur that the pus in the right iliac fossa has been absorbed, and that suppuration is present only at the most dependent point. In this way paratyphlitis may be transformed into paranephritis, parametritis, or periproctitis. Rupture of the pus into the peri- toneal cavity is particularly dangerous, as it is usually followed by fatal peritonitis. After rupture of the pus into the bladder or the bowel recovery not rarely takes place, because the fistula is so con- stituted that while it permits the escape of pus it prevents the access of urine or feces to the inflammatory focus, with the devel- opment in it of putrefaction. At times perityphlitis is superadded to paratyphlitis without preceding rupture of the pus. Paratyph- litis frequently pursues a chronic course, and the patient at times dies from progressive exhaustion. Diagnosis. — With regard to the diflerentiation between appendicitis, perityphlitis, paratyphlitis, and typhlitis the essen- tial facts have already been stated. Attention should, further, be directed to the circumstance that these diseases may at times be confounded with other disorders. Carcinoma of the cecum usually occurs in old persons, gives rise to the development of a nodular tumor, induces rapid marasmus, begins insidiously, and pursues a chronic and often afebrile course. Invagination of the bowel also gives rise to a palpable tumor and to constipation, although the latter is usually preceded by thin bloody and mucous stools. Fecal impac- tion — coprostasis — is unattended with inflammatory manifestations 264 DIGESTIVE ORGANS (pain, fever). Tuberculosis of the vertebral column or of the pelvic bones is at times atteiuled with acciiimikition of pus in the right iliac fossa, but each is usually associated with alterations in the vertebral column or the pelvic bones respectively. Psoitis is unat- tended with disturbance in intestinal activity. Carcinoma and tuberculosis of the mesenteric glands give rise to the formation of multinodular tumors. At times it is impossible to ditJ'erentiate appendicitis from salpingitis. Confusion with biliary or renal colic can be avoided if jaundice or alterations in the urine be present. Wandering kidney constitutes a smooth, bean-shaped, usually movable tumor, without tenderness on pressure. Prognosis. — Tiie prognosis of the inflammatory disorders under consideration is not unfavorable. It is the more favorable the more certain the diagnosis, and the more clearly the clinician constantly has in mind the therapeutic measures to be employed. Treatment. — Appendicitis and perityphlitis should be treated, like acute peritonitis, with rest in the recumbent posture, a liquid diet (milk, beef-broth with egg, coffee with milk, tea with milk, dilute wine), and opium : R Powdered opium, 0.03 ( h grain) ; Sugar, 0.3 (4 J grains).— M. Make 10 such powders. Dose : 1 powder every two hours. An ice-bag that is not too heavy should be applied over the right iliac fossa. When the acute inflammatory manifestations have subsided and the exudate has been well circumscribed, the ice-bag should be replaced by a hot cataplasm, which will better favor the absorption of the pus. Severe pain will frequently be relieved speedily by the application of from 6 to 10 leeches. Treatment with opium should be persisted in until all pain in the right iliac fossa has disappeared, even if many weeks should be required. Some persons, however, complain of nausea and in- creased pain after the administration of opium. Under such circumstances the opium should be replaced by subcutaneous injec- tions of morphin : R ]\Iorphin hydrochlorate, 0.3 (4J grains) ; Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose: 0.5 (8 minims) subcutaneously twice daily. Painless residua of exudate may be made to disappear by means of daily saline baths (5000 grams of salt to a full bath at a tem- perature of 28° R. — 95° F.), and by covering the skin in the right iliac fossa Mith a flannel cloth smeared with mercurial oint- ment or with potassium-iodid ointment, ctv with an ointment of iodoform or of ichthyol. ^lassage may also be practised cau- tiouslv. Especial consideration should be given to the question as to whether, and how often, existing constipation should be INFLAMMATION OF CECUM AND VERMIFORM APPENDIX 265 relieved. In the presence of acnte inflammatory manifestations the constipation should be permitted to continue, but also subse- quently it will be sufficient if the bowels are moved once every eight days. This end can be best attained by means of a glycerin- enema (2.0 — 30 minims — glycerin to the enema), whose action remains rather local. To avoid recurrences of the disease certain dietetic regulations must be observed (avoidance of an excess of vegetable food, daily exercise in the open air, care to secure a daily evacuation of the bowels, and the like). At times appen- dicitis and paratyphlitis will require surgical intervention, and this indication may arise either when an abscess has formed in the peritoneal cavity, or if rupture of pus into the abdominal cavity has taken place, or, finally, in cases of recu7Tence of the disease. The contention of some surgeons that appendicitis and perityphlitis are always surgical diseases is an error, as most cases pursue a favorable course with internal treatment.^ Incision of an encapsulated abscess in the peritoneal cavity becomes neces- sary in order to avoid rupture of the pus, although it is often difficult to elicit deep fluctuation with certainty through the tense abdominal wall. Although exploratory puncture is considered by some physicians as wholly free from danger, we can by no means coincide with this view, and fear not without reason the possibility of accidental puncture of the intestine, and fecal and putrid infection of the inflammatory products. The abdominal cavity has also been opened after rupture of the pus into the peritoneal cavity, and extensive perforative peritonitis, the fecal and purulent masses removed by sponging (toilet of the peritoneum), and when possible also the appen- dix excised. Repeatedly recurring perityphlitis has been treated by resec- tion or extirpation of the vermiform appendix. Most surgeons select for the performance of the operation a period when the inflammatory exacerbation has come to an end, while others operate at the time of the attack. In general, the first method mentioned is to be preferred, and the latter should be selected only when the attack itself demands surgical intervention. Stercoral typhlitis requires the administration of purgatives. Intestinal infusions of cold water by means of Hegar's funnel- apparatus may be recommended, because their action is rather restricted to the large intestine. It may happen that the first infusions will be unattended with the evacuation of any fecal matter, so that the water returns from the bowel almost unchanged. Under such conditions it is advisable to repeat the infusion every three hours, in order to soften the excessively inspissated fecal matters, and to facilitate their progress in the intestine. Even if copious evacuation of the bowels have taken place, the infusion should be repeated upon the following days in order to empty ^ With these views the consensus of clinical opinion is scarcely in accord. The results from the medicinal treatment of appendicitis are at least uncertain. The administration of an opiate is likely to mask the symptoms and induce a false sense of security. Should the bowels remain constipated despite the admin- istration of a laxative, and especially if vomiting be present, operation should be resorted to. — A. A. E. 266 DIGESTIVE ORGANS the bowel as thoroughly as possil)le. In addition, a hot cataplasm should he applied over the right iliac fossa for the contn^l of the inflammatory manifestations. The patient must thereafter secure regular evacuation of the bowels. Parafi/phlitis is rather a surgical disease. An effort should be made by means of hot cataplasms to induce aljsorption of the inflammatory products, but should fluctuation appear incision of the accumulation of pus should be undertaken. ROUND ULCER OF THE DUODENUM. Round ulcer of the duodenum is a rare disorder whose devel- opment, manifestations, and treatment coincide with those of round ulcer of the stomach. The condition is attended with a sharply circumscribed loss of tissue in the mucous membrane of the duodenum of circular outline, and resulting from the digestive activity of gastric juice that has entered the duodenum "svheneyer local stagnation has taken place in the blood-vessels of the mucous membrane. The lesion may thus be designated a diges- tive or a peptic ulcer. Duodenal ulcers are almost unexceptioually found above the point of entrance of the choledoch duct into the duodenum, most frequently in the upper horizontal segment, for below the entrance of the choledoch duct the gastric juice becomes inactive, because the bile causes precipitation of the pepsin, and the alkaline intestinal and pancreatic juices neutralize the hydro- chloric acid of the gastric juice. Nothing definite is known with regard to the causes of round ulcer of the duodenum. In numer- ous instances the condition has been observed to develop after burns of the ski)i. Experience has shown that, in contrast with round ulcer of the stomach, duodenal ulceration occurs more com- monly in men than in women. Pain in the right upper quadrant of the abdomen is quite a constant symptom, and in the differen- tiation from round ulcer of the stomach emphasis has been placed upon the fact that this pain does not succeed immediately upon the ingestion of food, but it appears only after tlie lapse of from two to four hours, when the gastric contents enter the duodenum. Often duodenal hemorrhage takes place. This most frequently gives rise to bloody stools, and much less commonly also to hemate- mesis. Perforation of the ulcer is a serious danger, and this may take place either free into the abdominal cavity, and then give rise to rapidly fatal perforative peritonitis, or into a previously encapsulated cavity. Two of my patients died at an advanced age o( carcinoma of the dxiodennm, which developed at the margins of a round ulcer of the duodenum. In one of the cases metastatic growths developed in the spinal cord, with pressure-paralysis, and in the other secondary carcinoma of the liver occurred. Should cicatrization of a duodenal ulcer take place cicatricial stenosis CARCINOMA OF THE INTESTINE 267. of the duodenum, and above the constriction dilatation of the duo- denum, of the stomach, and even of the esophagus, may result. The prognosis is grave under all conditions. At times ulcer of the duodenum develops insidiously, and causes death within a short time from uncontrollable hemorrhage or from perforative peritonitis. The treatment is the same as that for round ulcer of the stomach (pp. 220-222). CARCINOMA OF THE INTESTINE. Btiology and Anatomic Alterations. — Nothing definite is known with regard to the causes of carcinoma of the intestine, and the knowledge must suffice that carcinoma of this organ, like that of other organs, is a disease of advanced years. Only rarely does the disorder appear before the fortieth year of life. That in a small number of cases it may develop from an ulcer of the intes- tine has already been pointed out in the preceding section. Car- cinoma of the intestine occurs more commonly in men than in women. Almost always the netv-growth is primary. Secondary carci- noma of the intestine is rare. Most commonly the new-growth is seated in the large intestine, and particularly in the rectum. The flexures of the bowel are attacked with especial preference, perhaps because in these situations the mucous membrane is subjected to particularly active mechanical irritation by the advancing column of fecal matter. Accordingly, the sigmoid flexure, the hepatic flexure, and the splenic flexure of the colon and the cecum are the principal seats of carcinoma of the bowel. The most common form of carcinoma of the intestine is the annular variety, the entire circumference of the bowel being involved in the new-growth. Accordingly as the carcinomatous tissue is dense and deficient in fluid, of medullary consistency, or traversed by cavities with gelatinous contents, a distinction is made, as with carcinoma in other organs, between scirrhous, medullary, and alveolar carcinoma. Histologically the new-growth is a cylindrical-cell carcinoma, as its cellular elements result from abnormal proliferation of the epithelial cells of the glands of the intestinal mucous membrane. Disintegration of carcinomatous tissue gives rise to carcinomatous ulcers. Under such conditions the destruction of tissue may be so extensive that possibly remains of carcinomatous tissue are found only at the margins of the ulcer. This process is attended with two dangers, namely, hemorihiage from and perforation of the intestine. Should the ulcers undergo cicatrization, stenosis of the bowel results at times in consequence of contraction of the cica- tricial tissue. Dilatation of the intestine occurs not rarely above the position of the new-growth, because the lumen of the bowel 268 DIGESTIVE ORGANS is diniinislied by tlie carcinoma or the cicatrix. If, naturally, the carcinDmatous tissue has undergone extensive disintegration, the lumen of the bowel may be converted into a large cavity at the site of the ne\v-gr<)\\th. Symptoms and Diagnosis. — The diagnosis of carcinoma of the intestine can scarcely be made with certainty unless it has been possible to deliionstrate the presence of a nodular tumor of the bowel, which has undergone gradually progressive increase in size in a person of advanced years, and is attended with progressive asthenia and anemia. The tumor may be felt either through the abdominal wall or after introduction of the anointed finger into the vagina or tiie rectum. Carcinoma of the rectum may at times be accessible also to ocular inspection after the introduction of a rectal speculum. In addition there are also changes in intestinal activity. The patient usually suifers from constipation as long as the new- growth diminishes the lumen of the bowel, and as a result the abdomen may he tensely distended in consequence of stagnation of fecal matter and gas. At times the feces present a pecidiar shape, appearing as small, abbreviated columns, like the fecal matter of the sheep or the goat. It is true that the feces acquire a similar appearance also in cases of inanition and in connection Avith obstinate constipation, if the latter be due to spasmodic contrac- tion- of the musculature of the intestine. Should disintegration of the carcinomatous tissue take place subsequently, diarrhea fre- quently occurs. The thin intestinal evacuations not rarely are noteworthy for their putrid and fetid odor, and they contain blood and pus. The discovery in them of fragments of carcinomatous tissue that can be definitely recognized as such on microscopic examination is an exceedingly uncommon event. The patient often suffers from severe pain at the site of disease, and this fre- quently is especially severe at night ; the tumor is further exceed- inglv tender to touch. The urine is generally passed in diminished amount, and it contains an increased amount of indican. The inguinal lymphatic glands arc frequently enlarged and indurated. Although the appetite is impaired, thirst is generally increased. The bodily temperature is frequently elevated if the carcinomatous tissue is in process of disintegration and gangrene, and under such conditions septic symptoms — chills — are also observed. The diagnosis of nro])hisrn of the intestine must not be consid- ered as by any means easy. It is important, in the first place, to localize the new-growth correctly, in order not to confound it with neoplasms of the stomach, the liver, the kidneys, the omen- tum, the mesentery, and the abdominal lymphatic glands, and with enca]>sulated peritoneal exudates — perityphlitis. In the differential diagnosis the situation and the mobility of the tumor, and the existence of functional disturbances, should particularly be given consideration. It may be of diagnostic importance to fill the CARCINOMA OF THE INTESTINE 269 intestine alternately with air and water through the rectum, in order to determine the situation of the tumor and the variations in the percussion-note over it. If a neoplasm has been recognized as arising from the intestine, it next becomes necessary to decide whetlier it be carcinomatous or not. Insidiousness of development, advanced age, and progressive marasmus are suggestive of car- cinoma. Especial consideration in the differential diagnosis should be given to fecal tumors, which likewise give rise to nodular intestinal swellings. These, however, are unattended with pro- gressive marasmus, and they not rarely permit the production of depressions with the finger, and, above all, they disappear when purgatives are employed for a sufficiently long period. It should, however, be made a rule in the diagnosis of intestinal tumors to pursue a course of purgative treatment, even when the conditions appear clear, as the danger of error in diagnosis is considerable. The duration of carcinoma of the irdestine but rarely extends over more than a year, and many patients die in consequence of progressive asthenia, after marantic edema or venous thrombi have developed in the lower extremities, or amid septic manifestations. At times, in consequence of auto-infection, a comatose state de- velops rather suddenly, in which tiie patient dies — carcinomatous auto-intoxication or coma. At times, however, death results from complications, among which hemorrhage from the boioel, obstruction of the bowel, and rupture of the bowel particularly may be men- tioned. As may be readily understood, hemorrhage from the bowel may accelerate the loss of strength, especially if it be repeated frequently, and, if it be uncontrollable, death will result from hemorrhage. At times the symptoms of obstruction of the bowel or ileus appear suddenly, with insurmountable constipation, absence of flatus, and fecal vomiting. This danger is especially to be feared when the patient is indifferent with regard to regu- larity in the movement of the bowels or incautiously indulges in indigestible articles of food^leguminous plants or fruit with kernels. Rupture of the bowel may take place in various direc- tions, as, for instance, into the peritoneal cavity, when rapidly fatal peritonitis usually follows ; into adjacent loops of intestine, when a bimucous intestinal fistula forms; in cases of carcinoma of the cecum into retrocecal connective tissue, with gangrene thereof; into the stomach, the urinary passages, the vagina; or externally, through the skin, with the formation of a fecal fistula or preternatural anus. At times complications result from the situation of the new-growth in the intestine. Carcinoma of' the duodenum not rarely develops at the papilla of Vater, and by pressure upon the choledoch duct, which enters at this point, gives rise to chronic jaundice. If the tumor be situated, however, in the upper portion of the duodenimi, it will give rise to dilatation of the stomach. 270 DIGESTIVE ORGANS Frequently carcinoma of the rectum is recognized either not at all or so late that the proper time for operative intervention is per- mitted to escape. Pain in the sacnnn, often radiating to the pelvis and the thighs, inuc(j[)urulent and l)loody diarrhea, and the development of hemorrhoids in elderly persons should ahvavs demand digital examination of the rectum. Often paralysis of the sphincter ani muscle develops, so tiiat putrid fecal matter con- stantly escapes from the anus, and the patients must protect them- selves against the incontinence as best they can by means of linen cloths or paper. Carcinoma of the rectum sometimes pursues a most protracted course. One of my patients died only after the lapse of five years. It should further be mentioned that carcinoma of the intestine may be latent, not being recognized at all during life, or under favorable conditions only being suspected to the point of proba- bility from the presence of certain symptoms. Thus, in elderly persons intestinal hemorrhage or ileus is frequently associated \vith latent carcinoma of the bowel, as is also fecal fistula. At times carcinoma of the bowel is concealed behind a carcinomatous peri- tonitis. Prognosis. — The prognosis of intestinal carcinoma is unfavor- able, for even if an operation will prolong the life of the patient, recurrence or metastasis occurs as a rule, and life cannot be pro- longed for any considerable length of time. Treatment. — Carcinoma of the intestine can be cured only by operative measures through resection of the portion of intestine involved in the malignant disease. Naturally, certain limitations surround the employment of the knife. The area involved should especially not be too extensive in length, nor should metastases in other viscera be present. Fiu'ther, extensive adhesions may render operation not only exceedingly difficult, but even impossible. If resection of the carcinomatous bowel be impossible, the establish- ment of a preternatural anuf< above tlie new-growth, or entero- aiiadomosis, is yet available, but this will be indicated only when symptoms of stricture of the bowel appear. In cases of inoper- able carcinoma of the rectum curetting and destruction of the new- growth with the galvanocautery have been undertaken. Internal treatment will be confined to lessening the sufferings of the patient symptomatically and maintaining his strength as fully as possible by means of suitable diet (milk, meat-broth, eggs, wine). Among the remaining tumors of the intestine sarcomata and polypi are yet of clinical interest. Sarcomata of tlie intestine give rise to the same symp- toms as carcinomata, so that they are indistinguishable from the latter during life. They are much less common than carcinomata, and usually develop as primary neoplasms. Polypi of the intestine develop not rarely in children, and are often situated in the rectum. The patients suffer fre- quently from chronic nuicous or mucous and bloody diarrhea. Solid masses of fecal matter are sometimes conspicuous from the presence of a depression INVAGINATION OB INTUSSUSCEPTION OF THE BOWEL 271 resulting from the pressure exerted by a polyp. Deep-seated polypi may at times protrude from the anus. Sometimes polypi are detached by the pressure of the column of fecal matter and are found in the stools. If the anointed finger be introduced into the rectum, the soft, smooth tumors can often be felt. Removal can be effected only by operative measures. Polypi at a higher level in the bowel at times give rise to obstruction, or intussuscep- tion. INVAGINATION OR INTUSSUSCEPTION OF THE BOWEL. Anatomic Alterations. — Invagination of the bowel results from the inversion of one portion of the bowel into an adjacent portion, like the finger of a glove. The invaginated portion is known as the intussusceptum, while the external ensheathing por- tion of bowel is designated the sheath or intussuseipiens. A dis- tinction is made between the inner or entering, and the outer or departing, portion of intestine. The point of reflection from the sheath to the intussusceptum is known as the upper angle of reflec- tion, while the point of reflection between the outer and the inner portion of intestine of the intussusceptum is known as the lower angle of reflection. A distinction is further made between descend- ing and ascending invagination of the bowel, accordingly as an upper portion becomes inverted into a lower, or a lower into an upper. All varieties of intestinal invagination do not have clinical signifi- cance, and a clear distinction must be made between -yite/ and agonal intussusception. The latter is unattended with interest, and occurs with especial frequency in children that have passed through a protracted death-struggle or have suffered from diarrhea. Agonal invagination of the bowel may be recognized from the fact that it is frequently multiple and situated at different parts of the bowel, is often ascending, almost always involves the small intestine, is free from all inflam- matory alterations, and can therefore be reduced without difliculty by trac- tion on the bowel. Vital invagination of the boivel is almost unexceptionally descend- ing and single. Naturally, together with the bowel the related mesentery is also invaginated, in consequence of which traction is usually exerted upon the invaginated intestine, so that the intus- susceptum presents a concavity on its mesenteric aspect and a fissure-like constriction at its lower extremity. It can be readily understood that invagination of the intestine is attended with the danger of stricture or obstruction of the bowel. Another danger arises from the fact that nutritive disturbances may occur in the intussusceptum, in consequence of compression of the mesenteric vessels — either inflammatory adhesions and, distortions or gangrene of the bowel. Most commonly the ileum with the ileocecal valve in advance is inverted into the colon — ileocecal invagination. Under such conditions the invagination of the bowel has a ten- 079 DIGESTIVE ORGANS dency to increase gradually in size in consequence of the pressure exerted by the column of fecal matter, and in this way the flex- ures of the colon may be obliterated and be represented by a band passing transversely from one to the other iliac fossa. At times the invaginated portion of intestine may protrude a greater or lesser distance from the anus. In order to indicate by name the situation of an invagination of the bowel the following nomenclature has been adopted: Jejunal or iliac invagi- nation indicates that a portion of the jejunum or the ileum has become invaginated into another portion of bowel of the same name. Jejuno-iliac invagination indicates inversion of the jejunum into the ileum. An ileo- colic invagination is distinguished from an ileocecal invagination by the fact that in the former the ileum has found its way through the ileocecal valve into the colon, while in the ileocecal invagination the valve with the ileum is inverted. Individuals dead of invagination of the bowel usually exhibit evidences of peritonitis, or of rupture of the bowel, or of septico- pyemia. Ktiology. — Children are most commonly attacked i)y invagi- nation of the bowel, and boya more commonly than girls. The disorder develops with especial frequency bchceen the finrd and the twelfth month of life. Both constipation and diarrhea are named as causes. At times intestinal polypi induce invagination by exerting traction directly on the intestinal wall. Invagination has also been observed in connection with stricture of the bowel, as, for instance, from carcinoma. Injuries of the abdominal walls, as by a fall or a blow, have also been mentioned as causative factors. The mechanical occurrence of invagination of the bovel has been repeat- edly discussed and investigated experimentally. The conditions are clear- est in cases in which a tumor, by its weight, has gradually pulled the intestinal wall inward and downward. Under other conditions it seems most probable and most natural to explain the development of invagina- tion of the bowel by conceiving that a portion of intestine engaged in active movement slips into another portion of bowel situated beyond it, and at rest. The slipping of a lower segment of bowel over an upper is an unnat- ural process. The invagination of a loop of intestine will occur the more readily if the adjacent portion of bowel is paralyzed or constricted by mus- cular spasm, and accordingly a distinction has been made between parali/tie and sj)astic invagination of the bowel. The first variety is believed to be the more common. Symptoms and Diagnosis. — With the onset of invagina- tion of the bowel the patients are as a rule seized with abdominal pain so severe as to compel them to cry out. The pain occurs paroxysmally, and is colicky for the succeeding twenty-four or thirty-six hours. In most patients there is also repeated vomiting. Soon there apj^ear in addition alterations in the stools, whi<'h may be thin and contain mucus and blood. Often the anus is open in consequence of paralysis of the sj^hincter, and mucus and bloody fluid constantly trickle out. The anal orifice appears INVAGINATION OR INTUSSUSCEPTION OF THE BOWEL 273 retracted, and the skin in its vicinity is unusually smooth. Soon, however, the diarrhea ceases, and is replaced by obstinate con- stipation. The diagnosis of invagination of the bowel becomes the more certain if examination of the abdomen discloses the presence of a tumor, which is most frequently situated in the umbilical region or the right iliac fossa. This tumor is of oval shape, almost like that of a sausage, with a smooth surface, and at first of inconsiderable tenderness on pressure. It is, further, dis- tinctive that not rarely it gradually changes its position and increases in size, in accordance with the increase in the invagina- tion. At times it extends transversely from one iliac fossa to the other. In consequence of gaseous distention of the intestines and great tension of the abdominal walls, it may be exceedingly diffi- cult after the lapse of a few days to appreciate the presence of a tumor through the abdominal walls, even if all the aid of the usual devices is invoked — examination with warm hands, the knee- elbow position, conversation with the patient during the examina- tion, examination in a warm bath, chloroform-narcosis. Exami- nation of the rectum with the anointed finger should never be omitted, as it is possible at times to feel the invaginated portion of bowel in the rectum itself or in the vicinity. Little diagnostic aid will, as a rule, be yielded by the introduction of a sound into the rectum or by an infusion into the bowel. The influence exerted by the intestinal alterations upon the general condition is noteworthy. Symptoms of shock appear, as manifested by a cold skin, shrunken features, an anxious expres- sion, and a small, accelerated pulse. Under especially favorable conditions invagination of the bowel may undergo spontaneous reduction, or it may be reduced by artificial aid, and all of the morbid manifestations disappear. Much more commonly serious dangers arise, among which symptoms of ileus occupy first place. This mav be recognized from the presence of insurmountable constipation, the failure of gas to escape from the anus, and the occurrence of vomiting, with evacuation at first of the con- tents of the stomach, then of bilious intestinal contents, and finally of material of fecal odor and appearance — so-called fecal vomiting, miserere. Although this condition alone is indicative of serious menace to life, this becomes in marked degree greater from the development within a short time oi jperitoniti.'i, originat- ing at the point of intussusception, and soon extending to the entire peritoneum. Progressive distention of the abdomen, espe- cially severe pain on palpation of the abdomen, here and there developing dulness on percussion of the abdominal wall, in corre- spondence with disseminated accumulations of exudate between adherent loops of bowel, usually permit ready recognition of the process. At times rupture of the bowel takes place from lacera- 18 274 DIGESTIVE ORGANS tion of the gangrenous intestine. An already existing inflamma- tion of the jx'ritonciim l)ecomes in consequence transformed into a fecal and putrid peritonitis. At times natural recovery takes place from invagination of the bowel by gangrenous exfoliation of the invaginated portion of intes- tine, and evacuation with the stools, in consequence of which the previously oeeluded intestine becomes again patulous. INIost fre- quently spontaneous separation of the gangrenous bowel takes place between the eleventh and the twenty-tirst day. It is usually re- vealed by the occurrence of stools of extremely offensive odor and often of bloody character, in which black, necrotic shreds and at times also portions of bowel of considerable length are encountered. Further, the separation of the gangrenous portion of the bowel may be attended with serious dangers, among which uncontrollable hciiiorrhaye from and perforation of the bowel may be mentioned. At times also i^ejjticojn/emia is superadded in consequence of absorp- tion of gangrenous material, and as a result of which death takes place. Attention should be called here to an important sequel of invagination of the bowel. Should, subsequently, considerable contraction of the cicatricial tissue take place at the point of sepa- ration, stricture of the bowel and even occlusion of the bowel may result, and in consequence of which death may take place. The course and the duration of invagination of the bowel may be peracute, acute, subacute, or chronic, accordingly as a few hours, days, weeks, or months, or even years transpire. In the first event death results amid symptoms of shock. It is noteworthy, further, that intestinal invagination exhibits a great tendency to recurrence. It is often possible to relieve the invagination, but it recurs within a few hours. The cases are rare in which an invag- inated portion of bowel has protruded persistently from the rec- tum, and has required operative intervention for its removal. Prognosis. — Invagination of tlie bowel always demands a serious prognosis, but the probabilities of a favorable issue have become materially improved of late since it has been learned that some of the dangers can be averted by operation. Treatment. — It is an almost obvious indication that jiersons with invagination of the bowel should remain constantly in bed, and partake in small amount of exclusively liquid nourishment (milk, milk and coffee, meat-broth), a teaspoonful or tablespoonful at intervals of half an hour. Besides, a hot cataplasm should be applied to the abdomen, and opium be administered internally in order to relieve the ]iain, and to keep the bowel at rest, thereby avoiding the occurrence of inflammation and extension of the in- flammatory process. It should, however, be borne in mind that children, and especially infants, are exceedingly susceptible to the action of opium, so that even small doses may at times be followed by serious symptoms of intoxication. Instead of opium, morphin STENOSIS AND OBSTRUCTION OF THE BOWEL 275 may be employed subcutaneously. Then an attempt should be made to reduce the invagination by mechanical means. For this ])urpose intestinal infusions of cold water are to be preferred, and tliese, if necessary, may be repeated thrice or four times during the day. In order that the water introduced may reach as high a point in the bowel as possible, the patient should occupy the knee- elbow posture or the pelvis should be elevated. Rectal injections in chloroform -narcosis may also be practised. At times the invag- ination may be observed to correct itself with a distinctly audible murmur. The employment of injections of air or of carbon dioxid is less convenient and in my opinion less efficient than that of injections of water into the bowel. Injections of air are made most simply with the aid of a rectal tube^ connected with the bulb of a Richardson spray-apparatus. In cases in which the invagina- tion has advanced to the rectum an attempt may be made to eifect reduction by means of a long but not too rigid rectal bougie (sponge-bougie). If recurrences of the invagination take place, it may become necessary to permit the sound to remain in the rectum, fastening it externally. Attempts have also been made to reduce invagination of the bowel by means of abdominal massage, but this procedure cannot be considered as entirely free from danger. If all efforts have been unattended with success, surgical treat- ment becomes necessary. It is particularly important not to defer this too long, for if necrotic alterations have already taken place in the intestines, or if extensive peritonitis has developed, the results of operation may also be doubtful. The operative pro- cedure will depend upon the existing conditions. Opening of the abdomen (celiotomy), determination of the situation of the invagi- nation, and reduction by traction upon the bowel will first have to be considered. At times loops of bowel have been fastened by means of sutures in order to prevent recurrence. If, however, the invaginated portions of bowel have already become so adher- ent that separation is not possible, only two procedures remain feasible, namely, e'lthev resection of the invaginated portion of bovel or the establishment of an intestinal fistida above the point of in- vagination. In the latter event there would still be danger that gangrene might develop at the point of invagination, with its seri- ous consequences. STENOSIS AND OBSTRUCTION OF THE BOWEL (ENTEROSTENOSIS AND ILEUS), Ktiology. — The causes of stenosis or of obstruction of the bowel may be congenital or acquired. Congenital obstruction of the bowel is rare, and occurs when the anus is occluded or when in 276 DIGESTIVE ORGANS the upper portion of the bowel deficient development and closure in certain portions of the intestine have taken place. Death will occur soon after birth, unless in the presence of congenital atresia of the anus the lumen of the intestinal tube can be rendered patu- lous by means of an operation. Acquired stenosis and obstruction of the bowel are divided into intra-intestinal, extra-intestinal, and parietal varieties, in a(;cordance with the situation of the causative conditions. Among intra-intestinal caasatice conditions fecalaccuniu- lation — coprostasis — occupies first place. Such a condition may be induced by the presence o^ foreign bodies in the intestine. At times the foreign bodies may have been swallowed (bone, tendon, fibrous remains of asparagus, fruit-kernels, masses of shellac, etc.) ; at other times they may have been introduced into the rectum through the anus, as, for instance, bottles ; and at still other times they may consist of substances from viscera whose excretory ducts dis- charge into the intestine. The last category includes principally gall-stones, which either have become awkwardly impacted in the lumen of the bowel or cause obstruction by cohesion. There are on record a number of instances in which masses of spool-worms have obstructed the lumen of the bowel. Rarely intestinal concre- tions — enteroliths — act as the cause of obstruction of the bowel. Among the parietal causes of stenosis and obstruction of the bowel cicatrices and neoplasms may first be mentioned. Not all ulcerative and cicatricial processes lead with the same degree of frequency to stenosis of the bowel. Such a condition occurs but rarely in association with catarrhal and typhoid ulceration ; but somewhat more frequently in the case of tuberculous ulcers ; still more dangerous are dysenteric and syphilitic cicatrices. Among intestinal neoplasms carcinomata should first be mentioned ; there may also be sarcomata, polypi, at times also lipomata and ade- nomata. Stenosis of the bowel may be due to hemorrhoids. Rarely it occurs as a result of echinococcus of the intestinal wall. Displacements of the boicel often give rise to stenosis or obstruction. The importance of invagination of the bowel has already been dis- cussed in the preceding section. Incarcerated hernia deserves especial consideration by reason of the frequency of its occur- rence. The incarceration may involve an external or an internal hernia. In the latter event either loops of bowel enter abnormal fissures, such as are known to occur in the mesentery and the omentum, and also in the round ligament of the uterus ; or, in consequence of jirevious peritonitis, bands or adhesions have formed between the abdominal viscera and the abdominal wall, beneath which loops of bowel find their way and are incarcerated. There are besides a considerable numl)er of internal hernial open- ings, in which loops of bowel may be incarcerated. Among these varieties of hernia may be mentioned the duodenojejunal, intra- epiploic, cecal, intersigmoid, iliacosub fascial, anterior retroperito- STENOSIS AND OBSTRUCTION OF THE BOWEL 277 neal, hernia into the vaginal tunic of the testicle and the broad ligament of the uterus, and diaphragmatic hernia. The last may- be congenital or be acquired through traumatism. An especial variety of obstruction of the bowel results from twist- ing of the intestine (volvulus), axial rotation of the bowel, and the formation of a knot. The longer and the more mobile the mesen- tery of a portion of bowel the more readily, naturally, will twisting and axial rotation take place. Such conditions develop with especial frequency at the sigmoid flexure of the descending colon, as this part of the bowel turns upon the axis of its mesentery, which, while long, is narrow at its attachment. At times several loops of bowel surround others in the form of a knot, and thus obstruct the lumen of the latter. Most commonly the sigmoid flexure is twisted about dependent loops of ileum. A diverticulum of Meckel or the vermiform appendix may form a knot-like constriction around adjacent loops of bowel and render these impermeable. Natur- allv, it may happen that such a diverticulum or the vermiform appendix has become adherent with its free extremity to the abdominal wall or to other abdominal viscera, and that loops of intestine enter the interval and become obstructed. So-called paralytic ileus should also be mentioned here; its production is dependent upon the fact that the musculature of the intestine is paralvzed throughout a limited extent, and is therefore incapable of propelling the intestinal contents onward. This condition has been observed to occur in association with chronic diseases of the brain and the spinal cord, with peritonitis and perityphlitis, and after celiotomy and the replacement of incarcerated hernia. Among the extra-intestinal causes of stenosis and obstruction of the boivel may be included all 'constrictions due to pressure, and which are usually dependent upon diseases of the adjacent viscera. Naturally loops of intestine may, by reason of fecal accumulation or of the presence of a neoplasm, exert mutual press- ure on one another, and thus cause obstruction of the bowel. Tumors and displacements of the liver, spleen, or kidney, marked increase in the size of the pancreas, neoplasms of the omentum, the uterus, the ovaries, and the bladder, parametritic, perimetritic, and peritonitic exudates, the impregnated and retrodisplaced uterus, these all are capable of exerting pressure upon the intes- tine. At times stenosis of the bowel has been observed in cases of prostatic hypertrophy, and in consequence of the presence of uterine pessaries. The disorder occurs most commonly in men. It may develop at any time of life, although age has a certain influence upon the nature of the causative factors. Thus, invag- ination of the bowels occurs with especial frequency in childhood, and carcinoma of the intestine, on the other hand, in the aged. Anatomic Alterations. — The bodies of those dead from stenosis or obstruction of the bowel are characterized by unusual 278 DIGESTIVE ORGANS size of the abdomen. The intestines above the point of obstruc- tion are greatly distended with gas, and exhibit a tendency to escape through the opening made in the abdomen. Peritonitis often develops, giving rise to numerous adhesions between differ- ent portions of the intestine, and in conjunction with marked in- testinal nieteorism often rendering extremely difficult the deter- mination of the alterations present. In accordance with the marked accumulation of gas in the intestine the diaphragm is at quite a high level, and, in addition to the diaphragm, the liver, the stomach, the spleen, the lower border of the lung, and the heart, are greatly displaced upward into the thoracic cavity. The bodies of those dead from intestinal obstruction are generally greatly emaciated, and the face appears sunken and furrowed. The more deeply situated the obstruction the greater the extent of bowel involved in the changes described. The intestine just above the point of obstruction is greatly distended. Upon the mucous membrane more or less extensive losses of tissue are not rarely observed, and these are designated fecal or stercoral ulcers. They are probably caused less by the mechanical irritation of the feces, as is generally stated, than by chemic irritation, and espe- cially by the great multiplication of bacteria (Bacterium coli com- mune) capable of exciting inflammation, as I have observed them also in the presence of perfectly liquid intestinal contents. As early as the second week of stenosis of the bowel an increase in the thickness of the musculature of the bowel takes place, a kind of functional hypertrophy, which is due not to increase in the number of muscle-cells, but to their increase in size. The por- tion of bowel beyond the obstruction ajjpears narrow and collapsed. The constricted or obstructed portion of bowel itself frequently exhibits inflammatory and even necrotic alterations. Rupture of the bowel may take place at this point. At times, however, this accident occurs also above the point of obstruction, as a result of excessive distention of the bowel by gas and stagnating fecal matter. Symptoms and Diagnosis. — The si/mpfoms of ohsfruciion of the bowel are manifested as a rule in obstinate constipation. The longer it has persisted the more do the patients complain of distention of the abdomen and a sense of tension. Palpitation of the heart, dyspnea, a sense of fear, and fulness of the head idso readilv develop. Xot rarely the intesfiiia/ movements above the point of constriction are so active as not only to give rise to loud rumbling — borborygmi, but they may also be visible beneath the abdominal wall as alternately protruding and receding loops. Should liquid contents be forced through the constriction, sounds are sometimes heard resembling those produced when fluid is driven through a syringe. AVhen the large intestine is the seat of stenosis the fecal discharges frequently acquire a peculiar shape. Small, abbreviated cylindric masses occur, presenting the appear- STENOSIS AND OBSTRUCTION OF THE BOWEL 279 ance of coffee-beans, or the fecal discharges of the sheep or the goat. The same variety of feces occurs also in cases of inanition and of constipation when the latter is dependent upon spasm of the musculature of the bowel. The feces may also exhibit gutter- like depressions, as, for instance, when intestinal polypi are present. If the fecal matter be forced through the constricted area, most severe abdominal pain is often produced, which may cause syncope and general clonic muscular spasm. Although constipation is the rule in cases of constriction of the bowel, diarrhea is by no means rare. This may result from the maintenance by the stagnating fecal material of a chronic catarrh of the intestinal mucous mem- brane above the point of constriction. It is noteworthy that the thin stools often contain unusually hard masses of fecal matter. At times blood is found in the stools, and its appearance is to be explained by mechanical injuries inflicted by the fecal matter, and in other instances by tissue-disintegration. In order to determine the seat of constriction of the bowel con- sideration should be given to the degree of abdominal distention, for the more deeply situated the constriction the greater will be the abdominal distention. If intestinal movements are visible, the point at which these are especially active and regularly terminate is often of diagnostic importance. As a matter of course, an effort should be made by careful palpation through the abdominal ivalls, the vagina, and the rectum, to reach the obstruction directly. Ex- amination of the rectum with a sound, and an injection into the bowel, as well as the employment of a rectal speculum, will also yield valuable diagnostic information. A careful history and a knowledge of the mode of development of the disorder are also important. Thus, for instance, attention should be directed to preceding dysentery and syphilis, to tuberculous alterations, to the state of the bowels, to sudden or gradual development, and the like. In this way the exciting cause of the disorder, and from this not rarely also its seat, can be determined. The course of stenosis of the bowel may be terminated within a few hours, or it may be extended over years, in accordance with the nature of tlie causative factors and the care observed by the patient with regard to diet and to regularity in movement of the bowels. One of the most important dangers consists in the fact that the constriction may progress to occlusion of the bowel. This may develop gradually or occur suddenly, as, for instance, from the ingestion of indigestible articles of food, which may accumulate above the point of constriction like a valve, or from constipation. Naturally most cases of obstruction of the boicel or ileus begin suddenly. Not rarely heavy lifting, the ingestion of excessively cold or of indigestible food, a fall or a blow upon the abdomen, and the like are assigned as causes. At times the dis- order sets in with severe pain in the abdomen. 280 DIGESTIVE ORGANS The principal symptoms of obstruction of the bowel are reten- tion of fecal matter and of intedinal gases, and fecal vomiting — mis- erere. Naturally, it may happen at the beginning of the disease that repeated thin stools are voided, and these, in cases of invagina- tion of the bowel, may partake of a mucous and bloody character, but soon thereafter most obstinate constipation sets in. Like the feces, gas also may be unable to pass tlie obstructed portion of bowel, and the patient cannot discharge flatus. Naturally, if air is introduced into the bowel in addition to fluid in the process of making an intestinal infusion, it may happen that the air is ex- pelled in the form of flatus, a phenomenon without significance that should not be referred to a restoration of the permeability of the bowel. The vomited matters consist at first only of gastric contents, and accordingly their appearance varies with accidental conditions. After the stomach has been emptied the greenish bilious contents of the small intestine are voided in the act of vomiting. Finally, vomiting of fecal matter occurs. This is conspicuous, in the first place, from its marked fecal odor. Usu- ally it consists of a yellowish, thin mass, which often contains light-yellow or brownish-yellow fragments of fecal matter. The presence of formed fecal nodules is an exceptional occurrence. The deeper the situation of obstruction of the liowel, the more abundant and the more fecal does the vomited matter become, for the greater will be the contents of the intestine, and the fecal matter acquires its distinctive character in the deeper portions of the bowel. In the past various explanations were offered for the occurrence of fecal vomiting. At present it is assumed not that it is dependent upon anti- peristaltic intestinal movement, but that the intestinal contents endeavor to escape backward from the obstruction in consequence of the pressure resulting from the peristaltic intestinal movement. On examination distention of the abdomen, horborygmi, and active peristaltic intestinal movements are observed for the same reasons as in cases of intestinal constriction. Xot rarely cer- tain loops of intestine appear as unusually thick and tensely dis- tended structures lying one upon another. Careful palpation of the abdomen, particularly of all external hernial orifices, and thorough examination through the vagina and the rectum should never be omitted, in order to determine, if possible, the situation and possibly also the nature of the obstruction. The deleterious influence of intestinal obstruction upon the general condition is most striking. The features of the patient soon become sunken, and he often speaks in a faint and high-pitched voice, like a cholera-patient. The bodily temperature is frequently subnor- mal, and the pulse small and running. After severe vomiting the skin loses its turgor, remains ele,vated in folds, and feels moist and cold like that of an amphibious animal. The urine is dimin- STENOSIS AND OBSTRUCTION OF THE BOWEL 281 ished in amoimt and dark in color. Examination of the urine for indican is of importance, for if peritonitis be absent and carci- noma is not the cause of the obstruction, increased elimination of indican is indicative of obstruction of the small intestine. For the demonstration of indican the test of JafFe may be employed. To this end a test-tube is half-filled with urine, the remaining half with hydrochloric acid, and from 1 to 5 drops of fresh concentrated chlorinated lime are added. After the addition of each drop the opening of the tube should be closed with the thumb, and the tube inverted several times. The addition of chlorinated-lime solution is suspended when a deep-blue discoloration of the urine no longer takes place. Chlorinated lime in excess would cause a diminution in the intensity of the color. An increase in the amount of indican in the urine will be indicated by the fact that the urine acquires a violet-red, bluish, or deep blue-black color. Obstruction of the small intestine gives rise to an increase in the amount of indican in the urine in consequence of interference with intestinal digestion and in- creased fermentation of proteid bodies in the contents of the bowel. The substances of the indigo-group are derived from proteid decomposition in the intestinal contents. For the same reason the urine contains an abun- dance of phenol and ethereal sulphates. The duration of obstruction of the bowel may at times extend over only a few hours, death occurring amid manifestations of shock. In other instances the disorder persists for days, and even for more than a week. Death results in consequence of either progressive exhaustion or complications, of which peritonitis and rupture of the bowel with secondary perforative peritonitis are the most common. Not rarely inspiraiion-pneumonia develops, be- coming converted into pulmonary abscess and gangrene of the lung, and resulting from the aspiration of vomited matters. The condition is often unrecognized during life, for the reason that frequent raising of the patient to the erect posture for the examina- tion of the posterior portion of the lungs is avoided on account of weakness. In some cases rupture of the bowel takes place into an encapsulated cavity, and there forms a fecal abscess, with which septicopyemia may be associated. It may also happen that after previous adhesion of the intestine with the abdominal walls rupture takes place externally, with the formation of a fecal fistula. A sort of natural cure takes place in rare instances from the formation of adhesions between loops of intestine above and below the point of obstruction, with the establishment of communication through a fistula — so-called bimucous intestinal fistula. Relief from ileus may be recognized from the fact that flatus again escapes, bowel-movements are resumed, and the vomit- ing ceases. The escape of flatus is of especial importance, as the residue of fecal matter below the point of constriction might give rise to a bowel-movement. Some persons pass through several attacks of intestinal obstruction in the course of their lives. At times the causative factors are obvious (fecal accumulation, gall- 2ny of the bowel. The condition is therefore frequently observed in women who are in the habit of suppressing the desire for stool in order not to be interrupted in their work. The disorder is exceedingly common, as the modern mode of life favors its development in marked degree. It is not rarely riljservcd in pupils at school. Symptoms, Diagnosis, and Prognosis. — Atony of the bowel gives rise to constipation, so that the patients at times have a bowel-movement once or twice a week, or not at all without the emplovment of purgatives. At the same time it is characteristic that symptoms are wanting indicative of anatomic changes in the bowel. When the bowels are moved, excessive expulsive efforts must be made, and the feces are dry, hard, and black, as if charred or burned, and they readily cause severe pain in the rectum and the anus by mechanical iiTitation. Injuries of the mucous mem- brane and (generallv small) hemorrhages may also occur. The 19 290 DIGESTIVE ORGANS longer the interval between the bowel-movements the greater becomes the complaint of abdominal distention, disagreeable pressure, and even of" pain in the abdominal cavity, and the like. The constipation has, without doubt, an injurious influence upon the gcnei'dl nutrition, and many patients are extremely pallid, and become emaciated, depressed, and incapable of" mental activity. Possibly these may be consequences of" auto-intoxication, with evidences of increased intestinal putrefaction. The disorder is not dangerous to life, but is distressing and obstinate. Treatment. — The treatment is in part general and in part local. The f/eueral treatment should be directed to the correction of existing anemia, conditions of weakness, and neuroses. The local treatment should secure regular evacuation of the bowels, and the same remedies will be required that have already been mentioned in the treatment of constipation in consequence of chronic intestinal catarrh (pp. 256 and 257). NERVOUS DIARRHEA. The nervous system exerts an important influence upon in- testinal activity, as many persons are seized with a desire for stool and looseness of the bowels under the influence of fear ami embarrassment. In hysterical and neurasthenic individuals diar- rhea not rarely occurs for a considerable length of time, and with frequent relapses, but with an absence of all signs of anatomic changes in the bowel. Tchetic patients also are at times seized with attacks of nervous diarrhea. It is important to appreciate the disorder properly from its etiologic aspect, for the treatment of the general condition and the prescription of bromids are far more serviceable than the employment of styptics. Xervous diarrhea may be due to increased peristaltic activity of the intestine alone, although it is not impossible that at times increased secretion of intestinal juice also takes place. PERISTALTIC INTESTINAL UNREST (NERVOUS INTESTINAL TORMINA^. Like the stomach (p. 236), the intestine also may be the seat of abnormally excessive motility, which gives rise to a disagreeable feeling of rumbling and of unrest, and disturbs sleep at night. The causative factors and the treatment are identical with those of nervous unrest of the stomach. SENSORY INTESTINAL NEUROSES. NERVOUS SPASM OF THE INTESTINE. In hysterical and neurasthenic individuals spasm of the mus- cular layer of the intestine sometimes occurs Mithin certain ])or- tions of the bowel, and gives rise to circumscribed abdominal INTESTINAL NEUROSES 291 pain, and also to constipation. There are thus two varieties of constipation dae to intestinal neuroses, namely, the atonic and the spastic. The peculiar appearance of the feces is considered distinctive of the latter. As with stenosis of the bowel, the feces form small, abbreviated columns or they resemble coflPee-beans, or the feces of the sheep and the goat. The treatment should be directed to the cure of the funda- mental disorder. Locally narcotics may be advised, especially bromids, opium, and belladonna. NERVOUS ENTERALGIA. Ktiology. — Intestinal pain independent of anatomic alter- ations occurs especially in anemic, hysterical, and nervous individ- uals. It is well known that in cases of tabes dorsalis attacks of severe intestinal pain not rarely occur — so-called intestinal crises. At times toxic influences are operative, as a result of which the colic due to lead and copper is best known. Gouty patients also are not rarely seized with attacks of intestinal colic. Some persons suffer from intestinal pain after indulgence in certain kinds of food, without the occurrence of other derangement of intestinal activity. Intestinal worms also at times give rise to intestinal pain, as do likewise fecal accumulation and gaseous accumulation in the bowel. Intestinal pain of reflex origin at times attends diseases of the uterus, the kidneys, and the liver. Attacks of intense pain are sometimes excited by old peritonitic adhesions. Symptoms and Diagnosis. — The principal symptom of the disorder, which is also known as intestinal colic, is abdominal pain. This is most commonly referred to the umbilical region, but it may radiate thence for a considerable distance, and at times it changes its position. Its severity is susceptible of great varia- tion, and fluctuates between slight abdominal griping and cutting and stabbing pain of such intensity that the patient writhes in bed, while the skin becomes pale and cool (reflex vascular spasm), cold sweat appears, the face presents an expression of fear, the pulse is small and hard, and the heart-sounds faint. Syncope (cerebral anemia) and general clonic spasm may occur. At times palpitation of the heart, a sense of oppression, contraction of the cremasteric muscle, and the like, may be present. The duration of an attack of pain is susceptible of great variation, as is also the frequency of recurrence. At times an attack of colic terminates rather suddenly, after vomiting or the escape of gas from the intestine. The abdomen is often scaphoid and distended and of board-like hardness, as, for instance, in the presence of lead-colic, although abdominal distention may also result from fecal and gaseous accumulation. As distinctive, in contradis- tinction from intestinal pain dependent upon anatomic changes in 292 DIGESTIVE ORGANS the bowel, it is pointed out that strong pressure upon the abdom- inal walls does not increase, but usually mitigates the pain, and, as a matter of fact, the patients not rarely press their hands firmly upon the abdomen or apply the abdomen forcibly against some hard body. Prognosis. — Death scarcely ever occurs as the result of an attack of nervous intestinal pain, and if the fundamental disorder is curable the prospects are good for the prevention of a recur- rence of the attacks of jDain. Treatment. — Attacks of nervous intestinal pain are most speedily and most certainly relieved by a subcutaneous injection of morphin (0.3 : 10 — 4.5 grains : 2i fluidrams ; from 0.25 to 0.5 — (from 4 to 8 minims — subcutaneously), but this should be resorted to only when the pain has attained a marked degree of severity. Under no conditions should the patient be entrusted with the syringe, morphin, and the injection, because the danger of and the temptation to morphinism are too great. In less severe cases the abdomen should be covered with a hot cataplasm, and hot carminative infusions mfiy be drunk (peppermint-leaves, fennel, caraway — 1 tablespoonful to 3 cups of hot water for an infusion). Besides, consideration should be given to the causative factors — causal therapy — which coincides with the lyropliylaxis. ANIMAL PARASITES OF THE INTESTINE (INTES- TINAL HELMINTHIASIS). PROTOZOA IN THE INTESTINE. Protozoa in the intestine have been frequently discovered acci- dentally on microscopic examination of the stools. They liave been found especially in cases of chronic diarrhea, so that it is assumed not without reason that they are capable of inducing or maintaining chronic diarrhea. Many physicians consider these parasites as harmless bodies. Earnest consideration has been given in recent years to the presence of amebse in cases of tropical endemic dysentery, so that the designation amebic dysentery has been employed. Stools intended for examination for the presence of protozoa should be fresh, for on standing the protozoa are transformed into roundish, immo- bile structures, -which cannot be distinguished from the colorless blood- corpuscles. It is advisable to obtain the fecal matter directly from the rectum by means of blunt-edged glass tubes. Among the better known protozoa are the following: 1. Amceba coU. — This is a rhizopod, and appears in the form of round- ish granular bodies, with a nucleus and a nucleolus, which engage in move- ment by the extension and retraction of pseudopods (p. 293, Fig. 28). A distinction has further been made between Amceba coli, Amoeba coli mitis, Amoeba intestinalis vulgaris, and Amoeba coli felis. ANIMAL PARASITES OF THE INTESTINE 293 2. Cercomonas intestinalis (p. 294, Fig. 29) is a pear-shaped body, which possesses a long vibratile flagellum at its anterior extremity, and a caudal process posteriorly, which serves as a means of attachment. This body, like all of the following protozoa of the intestine, belongs to the Infusoria. 3. Cercomonas coli is provided with four vibratile flagella arising from the anterior portion of the body. A lateral border undulates (p. 294, Fig. 30). 4. Trichomonas intestinalis. — This parasite resembles an almond-kernel in shape. Cilia are present upon one side, while posteriorly there is a pointed process for purposes of attachment (p. 294, Fig. 31). 5. Megastomum entericum. — This parasite has been compared with the half of a pear. Anteriorly it is provided with six flagella, which in the dead parasite have disappeared (p. 294, Fig. 32). 6. Balantidium s. Paramoeciwn coli. — This parasite is egg-shaped and is surrounded by cilia. Anteriorly an oral orifice and posteriorly an anal orifice can be recognized. The interior of the body contains vacuoles and particles of food (p. 294, Fig. 33). It is well in all cases to cause the expulsion of protozoa from the intestine even when morbid manifestations are not present. Intestinal infusions of quinin (1.0 : 1000), of mercuric chlorid (0.3 : 1000), or of a solution of tannic acid (0.5 per cent.) are espe- cially to be recommended. WORMS IN THE INTESTINE. FLAT WORMS (PLATYHELMINTHES). TAPEWORMS (CESTODES). il^tiology. — Among the various kinds of tapeworm three are of practical significance on account of their frequent and wide- spread occurrence, namely, the unarmed tapeworm, Taenia medio- canellata s. saginata, the armed tapeworm, Taenia solium, and the Bothrioeephalus latus. Tapeworms are acquired only by the in- gestion of measly meat. In the stomach the capsule of the measle is digested, and its head or rather that of the tapeworm (scolex) is set free, and then develops within the intestine by the forma- tion of segments or proglottides into the mature parasite. From time to time the more distal (the oldest) segments are expelled. Animals that eat feces contaminated with proglottides digest the segments. In this way the contained ova are set free, and migrate from the intestine into the muscles, where they again develop into measles. The Tcenia saginata is acquired from the measle of beef, the Tcenia .solium from that of swine, the Cysticereus cellulosce and the Botliriocephahis latus from that of fish. As the use of beef is customary in all parts of the world, it may be readily understood that the Taenia saginata occurs most commonly and in all countries. The use of pork is avoided by many on account of its fat, and is forbidden Jews and Orientals on religious grounds, so that the Taenia solium is much less common. The occurrence of Bothrio- eephalus latus is confined to certain situations on the coast and on 294 DIGESTIVE ORGANS inland seas, among which may be mentioned the Russian provinces on the Baltic Sea, the coast of Eastern Prussia and Pomerania, Fig. 29.— Cercomonas intestinalis (after Lambl). Fig. 28. — Amceba coli (after Losch). Fig. 30. — Cercomonas coli (after Jlay). and the banks of the Lake of Geneva. Various fish may contain measles, such as salmon, eel-pout, pike, salmon-trout. Fig. 31. — Trichomonas intestinalis (after Zenker). Fig. 32. — Megastomum entericum : a, in the fresh, b, in the dead state (after Bizzozero and Grassi). Tapeworms occur in different countries with varying frequency. In tlie Orient persons free from tapeworms are almost the excep- tion. This may be explained in part by local customs — as, for instance, the use of raw meat favors the prevalence of tapeworm, as the measles are generally destroyed and rendered harmless by cooking ; and in part by want of cleanliness in the stables, and carelessness in the inspection and sale of meat. If domestic animals are not restrained from eating human fecal matter, if the sale of measly meat is not prohibited, if measly meat is sold in butcher- shops together with healthy meat, and if all meat is carved with the same knife, all of these conditions are factors that favor the infection of animals and human beings. Tapeworms occur with greatest frequency in adults. They have Fig. 33.— Balantidium s. paramoecium coli. ANIMAL PARASITES OF THE INTESTINE 295 been variously observed in children when raw shaved beef has been recommended in the presence of diarrhea. Symptoms, Diagnosis, and Anatomic Alterations. — The presence of a tapeworm in the intestine can be recognized with certainty only when proglottides or ova or tlie entire worm is voided with the stool. Proglottides or segments can be readily recognized, and may be properly compared wdth the appearance of flat noodles. Only on superficial examination would confusion with undigested elastic tissue or with the fibrous remains of aspar- agus be possible. Proglottides are passed singly from time to time, or in case of the Bothriocephalus latus in groups of several in the form of small chains, and facilitate a diagnosis as to the variety of tapeworm. In the fresh state they exhibit movement, inversion, and the like. Proglottides of the Taenia saginata are greater in length than in width, and exhibit upon one side at about the middle a knob-like process — the entrance to the genital canal — and in addition numerous ramifications (from 15 to 20) of the uterus. The latter can be seen with particular distinctness if a proglottis is compressed between two slides. The proglottides of the Taenia solium resemble entirely those of the Taenia saginata, with the exception that the divisions of the uterus are thicker and less numerous (from 5 to 12). The proglottides of the Bothrio- cephalus latus present an entirely different appt^arance. In the Tapeworm-proglottides ; natural size (from personal preparations) Fig. 34.— Of Taenia saginata. Fig. 35.— Of Taenia solium. Fig. 36.— Of Bothriocepha- lus latus. first place, their width is greater than their length, and, besides, the uterus is arranged in the shape of a roset in the middle (Figs. 34, 35, 36). The ova of tapeworms are too small to be seen with the unaided Tapeworm-ova; magnified 370 times (from original preparations). Fig. 37.— Of Ta;nia Fig. 38.— Of Taenia Fig. 39.— Of Bothriocephalus latus. saginata. solium. eye. They are at times discovered accidentally on microscopic examination of the stools. The differentiation between the ova of bothriocephalus and those of the tsenise is easy. The eggs of 296 DIGESTIVE ORGANS bothrioccphalus are oval, present at one extremity a cover, and are filled with a number of spherules. The ova of taeniae, on the other hand, possess a striated shell, i2:ranular contents, and six booklets in the latter. The differentiation between the ova of Taenia sagi- nata and those of Ta?nia solium is difficult, as they resemble each other, and differ only in size, those of Taenia solium being smaller (0.032 and 0.036 m'm.) than those of Taenia saginata (0.035 and 0.039 mm.) (Figs. 37, 38, 39). It is rare for tapeworms to be expelled entire with the stools. This has been observed in febrile patients, in cases of diarrhea, and during courses of treatment at the springs. In rare instances tapeworms pass from the intestine into the stomach, are in part vomited, and must be extracted with the fingers. The recognition of the variety of tapeworm naturally can be readily made from the appearance of the individual segments. These become shorter, smaller, and thinner as they approach the head, and the neck is almost filamentous. The head barely attains the size of a pin-head (p. 297, Figs. 40, 41). In the Bothriocephalus latus it has a flat and club-shaped appearance, in the Taenia saginata and the Taenia solium a roundish form. If the head be examined with high powers of the microscope, four suckers are observed ; in the Ttenia saginata, and in the Taenia solium in addition to four booklets also an anterior prominence or rostellum, which is sur- rounded by from 26 to 30 booklets, and finally in the bothriocephalus two longitudinal deep grooves like suckers (p. 299, Figs. 42, 43, 44). It may be incidentally mentioned that of all tapeworms the Taenia saginata attains the greatest length (up to 8 meters). It may consist of as many as 1300 seg- ments, of which about the six hundredth belaind the cervical portion begins to be mature sexually. The Taenia solium attains a length of 3^ meters, and is constituted of as many as 850 segments. The Bothriocephalus latus measures from 5 to 8 meters in length, and is composed of as many as 4000 segments. Tapeworms are found in the small intestine, to the mucous mem- brane of which they adhere by means of their suckers, while the remainder of the body is directed with numerous convolutions toward the anus. In the majority of instances but a single tapeworm is present in the bowel. Should several be present, they are generally of the same variety. In rare instances a number of tapewoi'm-heads have been observed in an entangled convolution, with their adjacent cervical portions. Injuries of the intes- tinal mucous membrane are not induced by the application of the suckers of the head of the tapeworm. Persons harboring tapeworms are often wholly free from sub- jective symptoms, and become cognizant of the presence of the parasite accidentally through the discovery of the proglottides in the stools. In others a train of symptoms develops ; but these are unreliable, and in some instances only a result of the fear of tape- worm. Among suspicious symptoms there have been mentioned irregularity in the action of the bowels, with at times extremely constipated, at other times loose stools, colic, borborygmi, a sense of distortion and twisting in the bowel, excessive secretion of saliva, a disagreeable odor from the mouth, eructation, vomiting, insatiable hunger, but also anorexia, emaciation, and pallor. Earlier physicians reported the occurrence of serious nervous dis- ANIMAL PARASITES OF THE INTESTINE 297 turbances, such as eclampsia and chorea. Vertigo is not rarely complained of. Inequality of the pupils is often present. The occurrence of Charcot-Neumann crystals in the stools in abundance is suspicious (p. 115, Fig. 20). Recently attention has been directed to profound anemic states in persons harboring Bothriocephalus latus. This bothriocephalus-anemia in its m im Tapeworms, natural size. (From personal preparations). Fig. 40.— Taenia saginata. Fig. 41.— Bothriocephalus latus. 298 DIGESTIVE ORGANS symptomatology completely resembles pernicious anemia, except tiiiit retinal hemorrhages and febrile movement are less eecomes difficult ; breathing becomes embarrassed and painful ; and also in the extremities stiffness and intolerable pain appear on any attempt at movement. In many instances muscular con- tractures and fixed positions of the extremities develop. Flexion at an acute angle takes place at the elbow-joints, and also in the hip-joints and the knee-joints ; the masseters are contracted with board-like hardness, and lock-jaw or trismus results. I have also observed stiffness in the muscles of the neck and the back, so that distinct opisthotonos developed, the vertebral column being greatly curved forward, and the patient resting only with the occiput and the sacrum upon the bed. To the distressing pains in the muscles there are thus superadded stiffness and immobility of the entire body, and the patient requires assistance for all movement. The occurrence of edema of the skin is, further, noteworthy. This is noticeable especially in the eyelids, but also in the extremities. Its cause is not definitely known. Symptoms of general infection further play an important part in the clinical picture of trichini- asis. These may perhaps be dependent upon the activity of toxic substances excreted by the trichinae, but perhaps they may be due to the absorption of products of abnormal metabolism developed in consequence of the extensive inflammation of the muscles. Trichiniasis is, as a rule, attended with fever, and the temper- ature may reach 39° C. (102.2° F.), 40° C. (104° F.), and even more. The temperature does not pursue a definite course, and periods of continued and remittent fever alternate with each other. Often the fever extends over several weeks. In corre- spondence with the elevation of bodily temperature thirst is increased, while the appetite suffers. Trichinous patients almost constantly suffer from copious sweating. The face and the trunk are usually covered with large drops of sweat, and often the skin in the portions of the body covered by clothing is raised by stag- nant sweat into innumerable, small, transparent, dewdrop-like vesi- cles — sudamina or miliaria. Frequently the patient complains of persistent sleeplessness — agrypnia. The abdomen is often greatly distended. The spleen can be demonstrated to be enlarged by percussion, and frequently also by palpation. The coated tongue and the persistent diarrhea, in conjunction with a por- tion of the symptoms described, often excite suspicion of typhoid fever, a suspicion that can readily be removed by showing that the blood-serum of the trichinous patient fails to cause clumping and loss of motility of typhoid-bacilli. The urine is usually passed in small amounts, although later polyuria may develop. Albuminuria is an uncommon symptom, and is usually of febrile origin. 310 DIGESTIVE ORGANS [Trichiniasis is attended with a marked increase in the number of white blood-corpuscles, and it is characteristic that the augmentation involves particularly the eosinophile cells. — A. A. E.] Trichiniasis generally pursues a subacute or a chronic course. Frequently the strength grows progressively less, pronounced marantic edema sets in, and the patients die from exhaustion after ■sveeks of misery. Occasionally death takes place from pneumonia amid manifestations of progressive respiratory dis- turbance. Among the complications septic manifestations are especially to be named, as, for instance, furunculosis and suppu- rative parotiditis. Should recovery from the disease take place, muscular and articular pains and stiffness, at times muscular in- duration and great irritability of the abdomen and the intestine, frequently persist for a long time. Diagnosis. — The recognition of trichiniasis is easy and cer- tain if small bits of muscle are excised and examined microscopi- cally for trichinse. The biceps of the arm is the muscle best suited for this purpose, as it contains trichina? with great constancy. It may also be important to examine the stools for trichinae. Inquiry should further be made to determine whether any of the meat partaken of can still be secured, and this also should be examined for trichinae. It is always susj^icious when a number of persons who have taken part in the same meal, or have obtained their supply of meat from the same butcher-shop, are attacked with the symptoms described. Formerly trichiniasis was most com- monly mistaken for typhoid fever, or for olistinate and serious varieties of muscular or articular rheumatism. A similar clinical picture is presented by acute pjolymyositis, but this disorder occurs independently, apart from the ingestion of meat, and only in iso- lated instances. Prognosis. — The prognosis of trichiniasis is exceedingly grave, as no remedy is known that is capable of preventing the migration of young trichinae from the intestine into the muscles and of destroying trichinae present in the muscles. In some epidemics of tricliiniasis death occurred in one-third of those attacked.^ Treatment. — If a number of persons have partaken of tri- chinous meat from the same animal, experience lias shoMu that the severity of the disease may be most variable. This will depend, in the first place, upon the fact whether one person has oaten more and another less of the meat, Avhether alcohol was used at the meal, and whether this was possibly followed by vom- iting and diarrhea. Under fiivorable conditions trichiniasis may not develop in one or another of those who have partaken of infected meat. It is rare for persons to observe soon after inges- tion tliat the meat partaken of was tricliinous. Under such cir- cumstances the contents of the stomach should be at once removed ^ The mortality among large numbers of cases is about 5 per cent. — A. A. E. ANIMAL PARASITES OF THE INTESTINE 311 by irrigation, and the intestinal contents evacuated as rapidly as possible by means of castor-oil (30.0 — 1 fluidounce). In addition the administration of glycerin internally has also been recom- mended (15 c.c. — 1 tablespoonful — every hour), as trichinae die rapidly in this substance. When trichiniasis has fully developed, onlv symptomatic treatment is available. Severe pains can be relieved by hot baths (from 28° R.— 95° F.— to 30° R.— 99.5° F.), and subcutaneous injections of morphin. The diet should be light yet nutritious. Profuse sweating is best relieved by means of atropin sulphate (0.0005 — yto g^'^'i" — o"ce or twice daily). Within the first eight days an effort should be made to expel any trichinae possibly present in the intestine, as, for instance, by : R Santonin, 0.05 (f graiuj ; Mercurous chlorid, Jalap, Sugar, each, 0.5 (TJ grains). — M. Make 5 such powders. Dose : 1 powder twice daily. Great importance is to be attached to the prophylaxis. As has been indicated in the consideration of the etiology, this includes cleanliness in the pig-pens, caution in the feeding of hogs with the meat of slaughtered animals, thorough meat-inspection, the destruc- tion of trichinous meat, and the avoidance of uncooked or insuffi- ciently cooked pork. Pickling and smoking of pork are not capable of removing with certainty all danger of infection. ANKYLOSTOMUM DUODENALE Btiolog'y. — Until within a few years it was believed that anhyhstomiasis occurred only in the Orient and in Italy. In the course of construction of the St. Gotthard tunnel it developed that the disease was introduced into Switzerland by Italian laborers. Foci of the disease were then observed in certain mines of France, Sardinia, Belgium, and Hungary, and in recent years the disorder has been encountered in brick-yards at Bonn, Cologne, Wiirz- burg, and Berlin. As the most prominent symptoms consist in progressive anemia, the disease has been given the designations tunnel-anemia, miners'' anemia, brichnakers^ anemia, in accordance with the conditions under which it occurs. In Egypt, where the disease has been known for some time, it has been named tropical chlorosis. It has been repeatedly demonstrated with certainty that the disease is spread by foreign wandering laborers, who come from localities in which ankylostomum occurs, and where they have themselves contracted ankylostomiasis. The danger of infection becomes the greater the more intimately the sick and the well live together and the less the degree of care observed in the dispo- sition of the fecal discharges in secure and closed receptacles, in ^ Uncinaria duodenalls. — A. A. E. 312 DIGESTIVE ORGANS order to prevent their entrance into the water used f(jr drinking and other domestic purposes. Infection usually takes place through water polluted with fecal matter containing ankylostomum-ova, or througii particles of earth containing larvte of ankylostomum and adherino: to the fino-ers, and which mav be readilv swallowed when food is ingested. Anatomic Alterations. — The Ankylostomum duodenale is a small cylindrical worm (Fig. 51) ; the females, of which there may be more than twice as many as of the males, are longer (up to 18 mm.) than the males (from 6 to 10 mm.). The number of the })arasites in the intestine may vary between 15 and 3000. Fig. 51. — Ankylostomum duodenale : the male to the left, the female to the right (natural sizei. Fig. 52. — Ova of ankylostomum. The eggs of ankylostomum are found in the stools in almost uniform distribution, and they may be readily recognized on microscopic examination. They are of oval shape, and possess a bright shell and granular contents, which are usually in a state of fission (Fig. 52). Ankylostoma are found much more constantly in the jcjunuDi. and the ileum than in the duodenum. They attach themselves by suction to the intestinal raucous mem- brane by means of their mouth, which is armed Avith six chitinous teeth, and thus extract blood from their host. The females appear to be especially bloodthirsty, and they suck much more blood than is necessary for their existence. They therefore present a brownish appearance, dependent upon the blood collected within their body. On post-mortem examination anl-cylostoma are found free in the intestinal contents or firmly attached to the intestinal mucous membrane. In the latter event they are often engaged in rolling movements. The intestinal mucous membrane exhibits in places recent as well as older extravasations of blood and hemor- rhagic suffusions that correspond to the points of attachment of the parasites. In addition, all of the viscera are conspicuous for their exceeding anemia and pallor. In consequence hemorrhage has taken place in various situations. These are found with espe- cial frequency upon the inner aspect of the cerebral dura mater, Avhere they are often converted into pachymeningitic membrane. Anemic fatty degeneration also generally develops, particularly in the myocardium, the cells of the liver, and the epithelial cells of the convoluted uriniferous tubules. The bone-marrow appears defi- ANIMAL PARASITES OF THE INTESTINE 313 cient in fat, and at times contains nucleated red blood-corpuscles in unusual number. Symptoms. — The symptoms of ankylostomiasis consist in gradually progressive anemia and its consequences, and are depen- dent upon abstraction of blood by the parasites. Whether, in addition, toxic influences are also operative has not yet been demonstrated. On the average anemic manifestations appear within five or six weeks after infection has taken place. The patients acquire a pallid appearance, which may attain such a marked degree as to create a cadaveric aspect. Examination of the blood discloses the fact that the number of red corpuscles may be diminished to one-fifth of the normal, and that also the hemo- globin-percentage is diminished correspondingly. At the same time the red blood-corpuscles are characterized by their variability in shape — poikilocytosis. They also vary greatly in size, and assume the appearance of a pear, a club, a figure of eight, and the like. At times nucleated red blood-corpuscles also are found. The greater the degree of anemia the more markedly do the func- tions of the body become impaired. The patient tires readily from work, suffers from dyspnea and palpitation of the heart, and is attacked by sweats. Finally, tlie weakness becomes so excessive that the patients are compelled to remain in bed constantly be- cause vertigo, tinnitus aurium, confusion of vision, and syncope may occur in the erect posture, — all signs of increasing cerebral anemia on assumption of the erect posture. The heart appears enlarged toward the right (anemic dilatation of the less resistant, because thin-walled, right ventricle), and over it anemic systolic murmurs may be audible. Over the bulb of the internal jugular vein a loud venous hum or "nun's murmur,'' sometimes palpable as a thrill, may be detected. A cardiac-systolic arterial sound is audible over the large peripheral arteries (brachial, radial). Not rarely cutaneous edema develops, because the blood-vessels, whose nutrition has been impaired, are excessively permeable to the blood-plasma. Accumulations of fluid (transudates) may take place also in the serous cavities (pleura, pericardium, peritoneum, meningeal spaces). Nutritive disturbances in the blood-vessels give rise also to the occurrence of hemorrhages, M'hich may take place into the external integument, the mucous membranes, and in isolated instances also the retina, and under circumstances may increase the anemia to a considerable degree. The appetite is, as a rule, impaired, while thirst is greatly in- creased. At times there may be paradoxic appetite — allotriophagy — for inedible and indigestible substances, as, for instance, earth (geophagy). The stools may then contain also sandy and earthy constituents. At times they contain blood. The occurrence of ankylostomum-ova is important, while ankylostoma themselves are but rarely encountered. Usually the stools contain a large 314 DIGESTIVE ORGANS number of Charcot-Neuniann crystals (p. 115, Fig. 20). The bowels are at times constipated, at times loose. Frequently there is complaint of a sense of pressure, of fulness, and of pain in the abdomen, which is distended from mcteurism. The urine is usu- ally' passed in large amounts, and contains a good deal (jf indican. The temperature of the body is often subnormal, although febrile movement may occur for periods of greater or lesser duration (anemic fever). Should no attempt be made to expel the para- sites, or should this be successful only after the anemia has become excessive, the patients may die like the victims of hemor- rhage. The l)odily weakness becomes excessive and conscious- ness obscured, and finally death takes place. The disorder is usually chronic in course. Improvements and exacerbations take place, the former after expulsive treatment, and the latter when the results of treatment are not entirely successful. Diagnosis. — Ankylostomum-anemia resembles perfectly pro- gressive pernicious anemia, and a differentiation can be made only from the fact that in cases of pernicious anemia the stools are free from ankylostoma and ankylostoma-ova. The latter circumstance likewise distinguishes ankylostomiasis from all other anemic states — in old persons, for instance, from carcinomatous cachexia. A positive opinion as to the absence of parasites and ova from the stools will naturally be possible only if the intestinal discharges remain unchanged after the administration of extract of filix mas. Prognosis. — The prognosis of ankylostomiasis is serious, because some patients are already in such an anemic and ex- hausted state when they first come under medical observation that death soon occurs in spite of expulsive treatment. The likelihood of recovery is further not rarely lessened by the fact that occasionally the patient declines thorough treatment because he does not have time to give up his work and submit to proper treatment in a hospital for a sufficiently long period. In cases in which the instructions of the physician will be followed and pro- fessional aid is not sought too late, recovery can be promised. Treatment. — Extract of filix mas has proved the most cer- tain remedy for ankylostomiasis, but it must be given in large doses (from 10.0 — 2i^fluidrams — to 20.0 — 5 fluidrams). The pre- paration for tapeworm mentioned on p. 300 may also be employed. Frequently ankylostoma remain in the intestine, and the males especially apjiear, by reason of their small size, to be able to con- ceal themselves readily behind folds of the intestinal mucous mem- brane, and thus to escape tiie action of the remedy. For this reason the stools must again be examined for ankylostoma-ova a short time after the treatment, and if eggs be found present the expulsive treatment should be repeated. The anemic conditions induced as a result of ankylostomiasis should be corrected by means of nutritious food, arsenic, and mild preparations of iron. JA UNDICE 315 The prophylaxis is important. This consists in excluding the car- rier of ankylostoma from work-places, enjoining the laborers to eat only with carefully cleansed hands, and exercising care to secure perfect closure of water-closets and of water- conduits. ANGUILLULA IXTESTINALIS GUILLULA STEECORALIS AND 1 AN- Anguillula intestinalis and Anguillula stercoralis have been found in the stools in some cases of tropical diarrhea, espe- cially Cochin- China diarrhea, although they have been found also in the laborers on the St. Gotthard tunnel in conjunction with the Ankylostomum duodenale. In all probability these are not two different varieties of worm, but the Anguillula stercoralis represents an earlier stage in the development of the Anguillula intes- tinalis. The latter occurs especially in the small intestine, and the Anguillula stercoralis throughout the entire large in- testine. On microscopic examination the Anguillula intestinalis is found to be a circular worm, with a conical caudal ex- tremity, within whose interior the diges- tive tube with two enlargements can be seen (Fig. 53). Thymol (1.0 — 15 grains — every hour) especially has been recom- mended for the expulsion of the para- sites. Fig. 53.— Anguillula intesti- nalis ; magnified 100 times (after Seifert). The larvse of flies have in a number of instances been found in the stools, having been swallowed with food. The patients have com- plained of pain in the abdomen, and have at times suffered from obstinate diarrhea. VI. DISEASES OF THE LIVER. JAUNDICE (ICTERUS), Htiology. — Jaundice is an exceedingly common symptom of disease of the liver and biliary passages. Among diseases of the liver fatty liver and amyloid liver alone are unattended with jaun- ^ Stronffvloide? intestinalis. 31() DIGESTIVE ORGANS dice in the absence of complications. Jaundice occurs most com- monly in consequence of obstruction of the biliary passages, whether this involves the larger ducts or those within the liver. The cases arc much less common in which in the presence of thrombosis of the portal vein the blood-pressure in the intrahepatic branches of this vessel becomes so slow that, contrary to the rule, the bile secreted by the liver-cells passes over, not into the biliary capilla- ries, but into the branches of the portal vein. In rare instances the bile stagnates in the intrahepatic biliary passages because the movements of the right half of the diaphragm are interfered with, and, as a result, the inspiratory pressure of the diaphragm upon the liver and the mechanical propulsion of the secreted bile toward the intestine are removed. For this reason jaundice is sometimes observed in association with right-sided diaphragmatic pleurisy. Occasionally the biliary passages become so greatly distended with bile that they are incapable of conveying all of this secretion to the intestine, and a portion thereof passes over into the blood- vessels and lymphatics. This condition has been described as jaundice due to polycholia or pleiochromia. Such conditions arise especially after the ingestion of certain poisons that cause dissolu- tion of the red blood-corpuscles. The hemoglobin set free in the blood-current is acted upon by the liver-cells, and converted into biliary coloring-matter, and pleiochromia results. Under all of the conditions thus far mentioned the jaundice re- sults from mechanical, hypostatic, or resorpAhe influences. In recent years attention has been directed to another variety of jaundice, which has been designated difusive or acatectic. Under normal conditions it is the function of the liver-cells not only to produce bile from blood coloring-matter, but also to convey the bile into the biliarv passages. Under morbid conditions the latter property may be lost, so that the bile produced by the liver-cells is not discharged into the biliary passages, but into the lymphatics and the blood-vessels. It has been assumed that such a diffusion- icterus may develop in consequence of the action of poisons, ptomains, and toxins. The theory of diffusion-icterus, however, still requires more convincing evidence, and it appears premature to attempt to explain almost all varieties of icterus as due to diffusion. Among all of the varieties of jaundice thus far mentioned that is the most common which develops in consequence of obstructit)n of the biliarv passages, and which has long been known as hepa- togenous, mechanical, resorptive, or hj/postatie icterus. Obstruction of the larger biliary passages occurs with especial frequency in con- nection with gastro-intestinal catarrh, either from constriction or occlusion of the mouth of the choledoch duct in consequence of swelling of the duodenal nuic<^us membrane, or from the entrance of a plug of mucus from the inflamed mucous membrane into the choledoch duct, or, finally, the mucous membrane of the choledoch JAUNDICE 317 duct has become involved in the inflammation of the intestinal mucous membrane, and the inflammatory swelling of the mucous membrane of the duct has given rise to obstruction of its lumen. The jaundice resulting from gastro-iutestinal catarrh is designated catarrhal or gastroduodenal. Not rarely the biliary passages are obstructed by foreign bodies. Most commonly these consist of r/all-stones, and only exceptionally of distomata or spool-worms, which have migrated from the duodenum into the choledoch duct, or fruit-kernels and foreign bodies from the food. Cicatricial and carcinomatous obstructions of the biliary passages are not common. The former usually result from gall-stones that have injured the mucous membrane of the biliary passages in their progress. At times the larger biliary passages are obstructed by pressure from toithout. The most common causes of this condition are tumors of the stomach, the intestine, the pancreas, the kidneys, wander- ing kidney, peritoneal exudates, bands, aneurysms of the hepatic artery, enlargement of the uterus or ovaries. Enlargement of the portal lymphatic glands may also be mentioned as a cause of obstruction of the biliary passages. Obstruction of the intra- hepatic biliary passages and the resulting jaundice are, as has been mentioned, frequent symptoms of the most varied diseases of the liver. It was formerly assumed that jaundice might be 'paralytic or spastic, the former depending upon paralysis, the latter upon spasm of the biliary pas- sages, and upon the secondary biliary stasis. This view is unfounded and improbable. Opinions are divided as to the causes of toxic jaundice, and probably various disturbances are operative in this connection. Thus, in cases of jaundice due to phosphorus-poisoning catarrh of the smallest biliary passages in the liver has been found. Other poisons (ether, chloroform, hydrogen arsenid) are destructive of the red blood-corpuscles, and give rise to jaundice in consequence of polycholia or pleiochromia. DifPusion-icterus appears to develop especially in consequence of the action of bacterial poisons — toxins. Jaundice is observed not at all rarely in the course of certain in- fectious diseases (typhoid fever, septicopyemia, diphtheria, relaps- ing fever, pneumonia, etc.), although other accidental influences, as, for instance, gastro-intestinal catarrh, may give rise to jaundice under such conditions, and this possibility must be carefully con- sidered in the individual case. Symptoms. — The most conspicuous symptom of jaundice is the yellowish discoloration of the skin, the urine, and the mucous membranes. This results from the presence of biliary coloring- matter in the blood. In part the blood takes up the biliary color- ing-matter directly from the liver, but in the presence of biliary stasis the lympliatic vessels play by far the more important part 318 DIGESTIVE ORGANS in the absorption of bile, which in turn they convey to the blood. Cutaneous jaundice is characterized by a yellowish discoloration of the skin, the intensity of which varies with the amount of biliary coloring-matter circulating in the blood from a light sul- phur-yellow to a coppery-brown or yellowish-gray. In the latter event the designation mel as Icterus has been employed. The yel- lowish discoloration becomes first apparent in places where the skin is thin and well supplied with vessels, therefore earliest in the face, and here especially in the temporal region, upon the fore- head, on the nasolabial folds, and upon the chin. Upon the fore- arms and the legs the. yellowish discoloration of the skin is often less pronounced because the epidermis is thick and in laborers is brown from exposure to the rays of the sun. AVhile at the outset cutaneous jaundice is dependent solely upon the yellowish dis- coloration of the blood-})lasma by the biliary coloring-matter, subsequently the cells of the epidermis become saturated with biliary coloring-matter, which crystallizes in the form of brownish granules in the epithelial cells. This fact explains the darker color of the skin when jaundice has existed for some time, as well as the experience that cutaneous jaundice may persist much longer than the remaining manifestations of jaundice, for it disappears only when the epidermic cells discolored by the biliary coloring- matter are desquamated. Icterus of the mucous membranes is most readily recognized in the conjunctivae. The sclerae appear more or less deeply yellow, instead of white. Usually this icterus of the conjunc- tivae is an early manifestation of jaundice, and in mild cases discoloration of the skin and of the urine may be absent, and only that of the conjunctiva be present. Upon other mucous membranes (lips, mouth, and pharynx, labia and vagina) the jaundice is concealed by the red color of the mucous mem- brane ; but if pressure be exerted and the blood-vessels are thus emptied the icteric discoloration of the mucous membrane becomes distinct. In the buccal cavity when the mouth is widely opened, two bands of yellowish mucous membrane, increasing in size posteriorly in the course of the middle line of the hard palate, are visible. Icteric urine is discolored brown, blackish brown, at times greenish brown, on agitation yields a yellowish foam, stains white paper, linen, and other materials yellow, and on standing retains its foam for an unusually long time. The presence of biliary coloring-matter in the urine may be best demonstrated by means of Gmelin's or jSIarechal's test. The presence of biliary acids can generally be demonstrated also by means of Pettenkofcr's test. Tube-casts occur constantly in the urine, most frequently hyaline, and often stained yellow by biliary coloring-matter. Slight all)mninuria also is not uncommon. Cylindruria and albuminuria result from the interference by the biliary acids cir- JAUNDICE 319 culating in the blood with the activity of the epithelial cells in the convoluted urinary tubules. GmelMs test for biliary coloring-matter is performed in the following manner: A test-tube is filled one-third with nitric acid containing some nitrous acid, and from another test-tube filled with urine this fluid is per- mitted to flow slowly upon the nitric acid, most conveniently by holding the two tubes obliquely in relation with each other at their mouths, so that the urine overlies the acid and forms a layer upon it. If the urine contain bilirubin, a play of colors takes place at the line of contact with the nitric acid, and from below upward rings of yellow, red, blue, and green will be seen to develop successively. The green ring alone is distinctive of biliary coloring-matter, as a brownish ring occurs also when the urine contains con- siderable indican. If the urine contain a small amount of bilirubin, it is advisable to pass the urine through filter-paper, in order to concentrate the bilirubin thereon, to spread the filter upon a porcelain dish, and then to apply a glass rod that has been dipped in impure nitric acid. At the point of contact the ring of color mentioned will appear, the red being innermost and the green outermost. MarichaV s test for biliary coloring -matter requires even less skill than Gmelin's. To urine with which a test-tube has been half filled several drops of tincture of iodin are added, or, still better, a solution of iodin and potassium iodid— so-called Lugol's solution, which consists of pure iodin, 0.5 (7^ grains) ; potassium iodid, 5.0 (75 grains) ; and water, 200 (60 fluidounces). The presence of bilirubin in the urine is disclosed by the development of a grass-green or an emerald-green color. Gmelin's and Marechal's tests are not always equally distinct with the same urine, and it is possible that only one or the other may yield a positive reaction. In my experience Marechal's test fails the less commonly. Pettenkofer^ s test for biliary acids depends upon the fact that these acids when gently heated with pure sulphuric acid and sugar give rise to a carmine color. As, however, it would be difficult for the practising physi- cian to obtain the biliary acids in pure form from the urine, Strassburger has proposed the following procedure, which in my experience has proved wholly practicable : A bit of sugar is dissolved in the urine, and then a piece of white filter-paper is dif)ped in the solution and permitted to dry. The filter-paper is then touched with a glass rod carrying a drop of pure, concentrated sulphuric acid. If the urine contain biliary acids, a carmine- red color appears at the point of contact, while, otherwise, a blackish-brown color at once appears in consequence of the action of the sulphuric acid. A number of other symptoms appear in the clinical picture of jaundice, but they are rather of subordinate importance in com- parison with the yellowish discoloration of the skin, the mucous membranes, and the urine. Alterations in the frequency of bowel- movement and in the stools are among the most common. If jaundice be the result of biliary stasis, the patient usually suffers from constipation, for if no bile enters the bowel the stimulating effect of the biliary acids upon the intestinal musculature will be wanting. At the same time the stools consist of large nodular masses. Usually they give oflF an offensive, putrid odor, because the antiseptic influence of the bile upon the intestinal contents has been withdrawn. The color of the stools is also striking, and, accordingly as the flow of bile to the intestine is restricted or abolished, it varies between that of clay and that of ash. At 320 DIGESTIVE ORGANS times the stools present almost a silvery luster. This is due to the large amount of fat present, and this in turn is dependent upon the faet that the biliary acids in the intestine aid in the absorption of the fat in the food, so that in the presence of biliary stasis and deficiency of bile in the intestine the absorption of fat is dimin- ished. If the stools be stirred in water, drops of fat collect upon the surface on standing, and if these be examined microscopically innumerable delicate needles of sodic or magnesic soaps will be found. The stools retain their bilious color in the presence of jaundice if the obstruction to the flow of bile through the intes- tine is not complete, or if the icterus be of pleiochromic or diffu- sive origin. Jaundiced persons are often annoyed by distressing itching of the skin — cutaneous pruritus — the existence of ^vhich may disclose itself to the eye by the presence of scratch-marks and crusts upon the skin. The itching frequently occurs at night, and deprives the patient of needed sleep. In all probability it depends upon the action of the biliary acids circulating in the blood upon the cutaneous vasomotor and sensory nerves, . as some patients maintain with positiveness that the sense of itching has been pre- ceded by a sensation of coldness in the skin. Less common cutaneous alterations in association witli jaundice are erythema, urticaria, xanthelasma. Not rarely jaundice is attended with slowing of the action of the heart and of the pulse — bradycardia and slow pulse. These like- "wise are attril)utable to irritation of the ganglion-cells of the myo- cardium by the biliary acids circulating in the blood. The pulse has been observed to be as low as 21 beats in the minute. Among less common phenomena are disorders of vision, as, for instance, yelloxo vision — xanthopsia — the development of which is attributed by some to nervous influences, while others explain its occurrence by infiltration of the optic structures of the eye with biliary coloring-matter. At times hemeralopia and nyctalopia are observed. Besides the blood and the urine, the biliary coloring-matter may appear also in the sweat and the milk, although it is not found in the saliva, the tears, and the seminal fluid. Jaundiced patients complain frequently of anorexia, a bitter taste, insomnia, and mental irritability. The tongue is usually coated. The duration of jaundice varies with the causes present in the individual case. Chronic jaundice is usually attended with progressive emaciation, because the nutrition is impaired and inter- fered with. Under the same conditions disMolution of the blood may occur, so that more or less extensive and numerous hemor- rhages may take place into the skin and the various mucous membranes, and also into the retina. Occasionally profound jaun- dice is attended with nervous manifestations, which have been designated cholemia. The patients become stupid and delirious, throw themselves restlessly about in bed, grind their teeth, and are seized with clonic muscular spasm in one or more extremities or JAUNDICE 321 throughout the entire body. Death occurs quite frequently under such conditions. The cause of cholemia was formerly thought to be an intoxication of the central nervous system with biliary con- stituents — according to some with biliary acids, according to others with cholesterin ; but at present the tendency is to adopt the view that cholemia depends upon auto-intoxication, and that the injurious substances consist in putrefactive alkaloids — ptomains — which are generated in the intestine in consequence of the deranged digestion. Diagnosis. — The recognition of jaundice is easy, although the clinician should never be satisfied with a diagnosis of jaundice, but in every instance he should determine the causes of this symp- tom. Under these circumstances considerable difficulty may arise, which can be overcome only by a careful consideration of the etiology and the alterations in individual organs. Icteric discol- oration of the skin can be readily recognized only by daylight, and not at all by the light of a lamp. It can be easily differentiated from the yellowish color of the skin in brunets, because in the latter the sclerse remain w^hite and the urine presents no change. The skin and the urine may present a yellow color after the use of picric acid or santonin, and the urine, as in jaundice, may yield a yellow foam, but the color of the urine is a light yellow, and the reaction for biliary coloring-matter is wanting. On the other hand, the urine acquires a reddish color on the addition of potas- sium hydroxid. Prognosis. — The prognosis in cases of jaundice depends upon the curability of the causative conditions. Anatomic Alterations. — In the bodies of those dead of jaundice the icteric color, not only of the skin and the mucous membranes, but also of almost all of the tissues and organs, is striking, the nervous tissues alone remaining unaffected. Serous effusions into the pleural cavity, the pericardium, the peritoneal cavity, and in the meningeal spaces present a yellowish, icteric hue. Chicken-fat clots in the cavities of the heart likewise present an icteric appearance. The endocardium and the intima of the blood-vessels are stained yellow. The kidneys are characterized especially by their icteric color. The epithelial cells in the con- voluted uriniferous tubules are in a state of more or less marked fatty degeneration, and are often stained yellow by biliary coloring- matter. When jaundice has existed for a long time the biliary coloring-matter is precipitated in the form of granules in the epi- thelial cells. Cylindric collections of biliary coloring-matter also occur in the uriniferous tubules. The liver is generally enlarged, and often presents a deep yellowish-black or greenish-yellow appear- ance. If the jaundice is dependent upon obstruction to the flow of bile by occlusion of the biliary passages, the bile-ducts appear dilated, and in places represent cystic enlargements distended with bile. Under such circumstances there may be connective- 21 322 • DIGESTIVE ORGANS tissue hyperplasia and cellular proliferation around the biliary passages. On microscopic exaniinatiou the liver-cells are found to be saturated -with biliary col(n*ing-matter. In eases of long standing the biliary coloring-matter is precipitated in the cells in the form of granules, and less commonly in that of needles or plates. Enlargement of the spleen is common. It is important to observe to what point the biliary passages are stained yellow, for the obstruction to the flow of bile must have been seated at the junction between the portion containing and the portion free from bile. This point is often not capable of demonstration in the dead body. At times microscopic examination of the liver furnishes for the first the explanation for the development of the jaundice. Thus, for instance, it has been demonstrated of the jaundice following phosphorus-poisoning that it is dependent upon a catarrhal condition of the smaller intrahepatic biliary ducts. Treatment. — Although the treatment of jaundice should always be directed to the removal of the causative factors, there are, however, certain rules to be observed in the presence of any variety of the condition. In connection with the food it should be a fixed rule to interdict the use of fat (butter, fat meat, fatty sauces, unskimmed milk, yolk of egg). AYeak coffee with milk, tea with milk, strained meat-l)roth, lean meat, good white wine, alkaline and carbonated waters, may be permitted. Daily evacua- tion of the bowels should be secured. Rectal injections of water at ordinary temperature are to be preferred. A single large dose of calomel (0.5 — 7^ grains) or of a preparation of rhubarb or senna mav prove useful. Patients of means with chronic jaundice mav be sent to bathing-resorts, among which especially Carlsbad, Marienbad, Homburg, Kissingen, and Tarasp may be recom- mended. Of medicaments, hydrochloric acid and nitric acid are much employed, and these in any event exert a favorable influence upon the stomach, whose function is generally affected : R Solution of dilute hydrochloric acid, 5.0 : 180.0 (75 minims : 6 fluidounces). Sirup of raspberry, 20.0 (5 fluidraras).— M. Dose: 15 c.c. (1 tablespoonful) every two hours after food. R Dilute hvdrochloric acid, Dilute nitric acid, each, 2.5 (40 minims); Sirup of raspberry, 20.0 (5 fluidrams) ; Distilled water sufficient to make 200 {^ fluidounces).— M. Dose : 15 c.c. (1 tablespoonful) every two hours. For the relief of the often intolerable itching of the sJcin warm baths may be employed (28° R.— ;3o° C— 95°' R), followed by the application of a carbolated ointment : R Carbolic acid, 5.0 (75 grains) ; Wool-fat. Lard, each, 25.0 (6 drams).— M. For inunction. HYPOSTATIC LIVER 323 Application to the skin of lemon-juice and the administration of potassium bromid internally (2.0 — 30 grains) have also been recommended. In order to accelerate the desquamation of the icteric shin after recovery from jaundice warm baths with soda (100.0 — 3 ounces) may be given. For the relief of cholernia stimulants should be employed, as, for instance, camjahorated oil (1.0 — 15 minims — subcutaneously thrice daily), and active diuresis should be induced by the generous administration of tea and milk in order to eliminate the injurious substances rapidly from the body. If the patients are unable to swallow on account of stupor, rectal injections of tepid milk or physiologic salt-solution (0.75 per cent.) should be given or subcutaneous infusions of saline solution. HYPOSTATIC LIVER (VENOUS HYPEREMIA OF THE LIVERj, Ktiology. — Hypostasis of the liver develops when the flow of venous blood of the liver from the hepatic veins into the infe- rior vena cava is obstructed. Such a condition occurs in asso- ciation with chronic diseases of the heart and of the respiratory- organs, and the mechanism generally consists in failure in the function of the right ventricle. As a result a certain amount of blood is left in the right ventricle after each systole of the heart. In consequence the right auricle next becomes imper- fectly emptied, then also the superior and the inferior vena cava, and thus are provided the conditions that lead to hypostasis of the liver. In rare instances hypostasis of the liver develops in consequence of stenosis of the hepatic, veins. This is dependent at times upon congenital septum-like obstruction, at other times upon acquired thickening and con- striction of the vessel-wall. Under such circumstances the stasis is con- fined exclusively to the liver and the portal circulation, while in the pres- ence of stasis of cardiac origin the entire distribution of the inferior vena cava is involved in the stasis. Anatomic Alterations. — Hypostasis of the liver is attended with increase in size and marked hyperemia, so that the organ often exhibits a reddish-black color. On section an oakleaf-like or nutmeg-like appearance is disclosed, the darker portions cor- responding to the dilated central veins in the individual lobules of the liver distended with blood. The organ is therefore also designated cyanotic nutmeg-liver. On microscopic examination also the dilatation of the central veins and the efferent intra- lobular capillaries, and their distention with blood, are conspicu- ous. If the condition has existed for some time, there may readily result, in consequence of the pressure exerted by the dilated blood- vessels, atrophy and disappearance of the liver-cells, and the atro- 324 DIGESTIVE ORGANS phic nutmeg-liver develops. Under such conditions also hyper- plasia of the connective tissue not rarely takes place around the dilated vessels. The consistence of the liver at the same time increases, and in consequence of cicatricial contraction of the connective tissue the liver may even undergo diminution in size, with the formation of nodules upon its surface — the so-called cir- rhotic- n utiiicr/-liv('i\ Symptoms and Diagnosis. — If, as in the majority of cases, hypostasis of the liver is dependent upon chronic disease of the heart or of the respiratory organs, the first manifestation of stasis is general cutaneous edema in the lower extremities, as the con- sequences of general stasis are observed earliest in the dependent portions of the body. Symptoms of hypostasis of the kidneys (diminution in the amount of urine, which has a high color and a high specific gravity, with a small amount of albumin) also often appear earlier than those of hypostasis of the liver. Patients with Itypostasis of the liver complain principally of a sense of weight, of pressure, of constriction, and even of slight pains in the region of the liver. On palpation and percussion the liver is found enlarged, and particularly Avitli its lower border projecting in greater or lesser degree beyond the right costal margin. At the same time the consistence of the organ appears increased, although its surface feels smooth. Manipulation of the liver is frequently attended -with tenderness. Xot rarely hypostatic catarrh of the biliary passages develops, with obstruction and hypostatic jaundice. The jaundice is commonly not pronounced, and is often confined to the conjunctivae. If at the same time tiiere is cyanosis of the skin in consequence of the stasis, the jaundiced integument at times acquires a slightly greenish hue — iderua viridis. Exami- nation of the liver is rendered difficult, and sometimes even im- possible, when marked ascites is present. An attempt should then be made to determine the limits and the consistency of the organ by shock-like palpation in the region of the liver. It is also advisable under such circumstances to examine the liver with the patient in the left lateral or in the supine decubitus. If the stasis can be relieved and the right ventricle can be strengthened, it is often remarkable in how short a time the enlargement of the liver subsides. If, however, the stasis has existed for a considerable time or has recurred frequently, complete involution will no longer take place, obviously on account of the hyperplasia of the con- nective tissue of the liver. The liver, therefore, remains hard and large. If ascites be present, it will also prove obstinate under such conditions. In the differentiation of hypostasis of the liver from other varieties of enlargement of tlie liver and from indura- tion of the liver the demonstration of causes of hypostasis is imjiortant. Prognosis. — The prognosis depends upon the possibility of INFLAMMATION OF THE SEROUS COAT OF THE LIVER. 325 renioviDg the causes of stasis. As a rule, this is possible at first ; but subsequently the heart becomes insusceptible to the influence of medicaments, and deatli results in consequence of excessive general stasis. Treatment. — The principal remedies consist in heart-tonics, particularly digitalis. In general, the treatment is that of weak- ness of the myocardium (pp. 23 and 24). In the presence of marked tension and pain in the region of the liver from 5 to 10 tcet cups should be applied. INFLAMMATION OF THE SEROUS COAT OF THE LIVER (PERIHEPATITIS). Anatomic Alterations and Btiology. — A distinction is made between acute and chronic perihepatitis. Acute perihepa- titis is attended with the presence of fibrinous deposits upon the serous covering of the liver; Accumulations of pus also may readily take place between the surface of the liver and the diaphragm, and often the pus is encapsulated in several cavities. At times the serosa of the liver is detached from the surface of the organ by small accumulations of pus. Acute perihepatitis occurs most commonly in association with diiFuse peritonitis. At times it attends diseases of the liver extending to the serous cov- ering, as, for instance, abscess, carcinoma, gumma, echinococcus. Injuries in the region of the liver are of less common occurrence. AVhether refrigeratory (rheumatic) perihepatitis occurs is at least doubtful. On the other hand, acute perihepatitis may result by extension from adjacent disease, and it may be superadded to pleurisy or pericarditis. Chronic perihejxttitis develops at times from an acute perihepatitis, while in other instances it occurs as an independent disorder. It is characterized by thickening of the serous covering of the liver and by band-like or extensive adhe- sions between the surfice of the liver and neighboring structures, particularly the diapliragm. At times the thickening may attain the extent of several millimeters, and appear white and opaque, and cut almost like cartilage. If the liver is entirely surrounded bv a serosa thus altered, an appearance is created as if the organ were enclosed within a layer of icing, whence the name mold or cast of the liver. In consequence of contraction of the thickened connective tissue, nodules not rarely form upon the surface, and distortion of the organ results. Frequently the liver assumes a globular shape. Further, the connective-tissue hyperplasia ex- tends here and there into the superficial interlobular spaces of the liver. Syphilis is not an uncommon cause for chronic perihepa- titis. Hereditary syphilis also at times causes extensive peri- hepatitic changes in children. At times the disorder develops in 326 DIGESTIVE ORGANS the course of clironle diseases of the liver, as, for instance, chronic interstitial hepatitis. Traumatic chronic perihepatitis occurs in association witli constricted liver in the course of the constriction and in the adjacent tissue. Chronic peritonitis also may give rise to chronic periiiepatitis. Symptoms and Diagnosis. — Acute periiiepatitis can l)e diagnosed with certainty only when a perihepatitic friction- sound is generated with the respiratory movements of the liver. This may be appreciable only with the stethoscope, or it may le felt with the hand as the creaking of new leather. It is encoun- tered most commonly over the lower portion of the right side of the chest, although it may be observed also upon the lateral and posterior aspects, or it may be present in these situations and ab- sent anteriorly. At times it can be induced artificially by sliding the abdominal walls upon the surface of the liver. Its duration is susceptible of great variation. At times it is observed for only a few minutes, in other instances for several weeks, now disap- pearing, but soon reappearing suddenly. Perihepatitic friction is distinguished from pleuritic friction-sounds by the fact that it ex- tends especially toward and may even pass beyond the lower bor- der of tlie chest. The patients complain principally of pain in the region of the liver, which is increased on deep inspiration and on pressure. On percussion it may often be demonstrated tliat the respiratory movements of the liver are restricted, because the ]Datients involuntarily avoid active respiratory movement on account of the pain. Consequently a slight degree of hypostatic jaundice devel- ops at times, as active respiratory movement of the liver favors the discharge of bile. Chronic perihepatitis also is frequently attended with palpable and audible friction-phenomena. Intimate adhesions to surrounding structures prevent the respiratory dis- placement of the liver. If the hepatic veins or the inferior vena cava be surrounded and constricted in consequence of connective- tissue thickening, ascites or general stasis in the veins of the extremities and of the abdomen develops. At times stenosis of the portal vein or of the large biliary ducts in the hilus of the liver results, and is followed by incurable ascites or persistent icterus. Prognosis. — The prognosis of acute perihepatitis is favorable if the causative conditions are not dangerous. The prognosis of chronic perihepatitis also is usually not unfavorable. Stenosis of the inferior vena cava and the hejiatic veins, of the portal vein, and the large biliary ducts naturally gives rise to conditions of incurable venous stasis or to chronic jaundice, which finally termi- nate fatally Avith progressive asthenia and interference with the movements of the diaphragm. Treatment. — If pain be severe, hot cataplasms over the liver and cups, and even subcutaneous injections of morphin may be ad- vised. Excessive ascites will require repeated puncture of the SUPPURATIVE HEPATITIS 327 abdomen. Chronic jaundice ^\•ill demand regulation of the diet and regularity of bowel-movement. SUPPURATIVE HEPATITIS. l^tiology. — Suppurative inflammation of the liver occurs only when bacteria capable of inducing inflammation gain access to the organ. The demonstration of bacteria will be possible only in recent accumulations of pus, as they undergo destruction in the older, so that the abscess becomes sterile. Streptococcus pyogenes, Staphylococcus pyogenes albus and aureus, and Bacterium coli commune have been found in abscesses of the liver. In abscesses of the liver secondary to dysentery the amebce. of dysentery have been observed repeatedly, although it is doubtful whether these are not rather accidental contaminations, the suppuration being really induced by pyogenic cocci. The same statement is applicable to an observation of flagellates in hepatic pus. Any of the vessels of the liver may be the portal of entry for bac- teria into the organ ; thus the hepatic artery, the portal vein, the hepatic veins, the biliary passages, and in the newborn the umbili- cal vein. The biliary passages and the portal vein are the most common channels. The portal vein is a frequent portal of entry for bacteria into the liver in connection with all pyemic abscesses of the liver. These develop when inflammatory ])rocesses occur in any organ connected with the distribution of the portal vein, and from which exciting agents of inflammation can enter the portal vein and its intrahepatic ramifications. Among primary inflammatory processes may be mentioned ulceration of the intes- tinal mucous membrane, in connection with which endemic tropi- cal dysentery particularly has an unfavorable reputation, opera- tions upon and inflammation of the rectum, the uterus, the ovaries, and the tubes, the testicles, ulceration of the vermiform appendix and the stomach, the spleen, the pancreas, etc. Suppurative pylephlebitis may also be responsible for secondary suppuration in the liver. Suppuration in the liver by way of the hilkiry pas- sages occurs especially in the sequence of gall-stones, in connection with which the Bacterium coli commune appears to be the exciting agent of the purulent process with especial frequency. Less com- mon] v parasites in the biliary passages may be the starting-point for suppuration in the liver. The hepat'iG artery is the medium for infection of the liver particularly in the presence of ulcerative endocarditis, and at times also in association with pulmonary gangrene and putrid bron- chitis, as the thrombi, containing bacteria, invade the distribution of the aorta, and then that of the hepatic artery, finally to be- come obstructed in the arterial capillaries of the liver, and from this point to excite inflammation of the liver. Bacteria can 32« DIGESTIVE ORGANS enter the liver through the Jiepafic vci)is only by passing in a direction contrary to that of the blood-stream. Experimental investigation has shown that corpuscular elements may pass down- ward in the inferior vena cava, in opposition to the blood-stream toward the heart, and enter the he])atie veins, and this phenomenon has been accepted in explanation of cases of su[)})uration of the liver in which hepatic abscesses have developed in the sequence of inflammation and suppuration of the cranium and at the periphery of the body. At the present day such an assumption is, in our opinion, no longer necessary, as bacteria can, without difficulty, if they have gained entrance through the superior vena cava to the right auricle, the right ventricle, and the pulmonary artery, migrate through the pulmonary capillaries, and pene- trate the pulmonary veins, the left side of the heart, the aorta, and the hepatic artery. Only if the question arose as to the dissem- ination of coarse, solid particles "would scarcely any other explana- tion be conceivable than the entrance from the superior into the inferior vena cava and thence into the hepatic veins and their rami- fications. In the newborn, infection of the liver sometimes occurs through the umbilical wound or through the intermediation of the umbilical vein. Infection of the umbilical wound, in case the mother be suffering from childbed-fever (puerperal septicemia), or infection of the umbilical wound from want of cleanliness in treatment, is the causative factor. It thus appears that suppurative inflamma- tion of the liver may occur at any period of life. At times abscess of the liver results from injuries to the organ, even of a blunt char- acter. In other instances it develops in the course of infectious diseases, as, for instance, malaria. It is especially widespread in tlie Orient, in consequence of the frequent occurrence of endemic dvsentery. There are, however, cases in which no cause can be demonstrated — so-called spontaneous abscess of tJic liver. An espe- cial group of cases of abscess of the liver is constituted by those varieties that develop in consequence of the svppvration of tuber- cles, carcinornata, or cchinococci of the liver. Abscess of the liver occurs most commonly in men. Anatomic Alterations. — A distinction must be made be- tween si)i(jlc and multiple absce.ss of the liver. INIultiple abscesses occur in the liver particularly in relation with pyemic influences. The size of a liver-abscess is susceptible of great variation. At times the collection of pus is scarcely visible, while at other times it may be so enormous as to occupy almost an entire lobe. In accordance with the situation of the accumulation of pus a dis- tinction can be made between superficial (peripheral) and deejy (central) abscesses. Accumulations of pus of some standing are usually surrounded by a connective-tissue capsule, whereas more recent accumulations are in direct contact with the tissue of the liver — encapsulated and non-encapsulated abscesses of the liver. The SUPPURATIVE HEPATITIS 329 pus in many instances resembles ordinary greenish and creamy pus, altliough at times it acquires a viscid consistency or, from being stained by bile, an appearance of wine-lees. At times, also, it possesses putrid qualities. The liver is as a rule enlarged, and almost always there is likewise enlargement of the spleen. If the abscesses of the liver are of pyemic origin, similar collections of pus may be present in numerous other organs. On microscopic examination necrosis of the liver-cells and the adjacent tissue will be found in the structures surrounding the pyogenic bacteria. Next there collect about these small necrotic areas round cells that have probably wandered principally out of the blood-vessels, but have resulted in part also by multiplication of the liver-cells and other cells. A sub- miliary or miliary abscess is thus formed. By the confluence of adjacent small abscesses larger collections of pus are formed. Even large abscesses not rarely coalesce with one another, as indicated by their multilocular form. Symptoms and Diagnosis. — In order to be recognized with certainty during life, abscesses of the liver must have attained a certain size and be situated at the surface of the organ. Deeply seated collections of pus are either entirely inaccessible to recog- nition or can at best be suspected with some degree of probability. The demonstration of a fluctuating prominence upon the surface of the liver is decisive in the diagnosis. Although unilocular echino- coccus and soft carcinomata or sarcomata of the liver are also attended with fluctuating prominences, septic constitutional mani- festations are wanting under these conditions. Naturally an abscess of the liver will be accessible to the palpating fingers only when it is in contact with the abdominal wall, and but rarely will it be possible to feel it in the intercostal spaces. If it has devel- oped at the summit of the convexity of the liver, it can be recog- nized only from the presence of dulness on percussion, which abruptly interrupts the course of the upper border of the liver and forms a convex prominence toward the pleural cavity. Under such conditions there may be danger of confounding an abscess of the liver with an encapsulated pleural empyema or with a sub- phrenic abscess or with an echinococcus-cyst. It will then be neces- sary to take into consideration the mode of development of the disorder (cough, pleural pain, previous gastric or intestinal disturb- ance), and to make exploratory puncture of the doubtful accumu- lation of pus. A fecal odor of the pus is suggestive of a subphrenic abscess, while in the presence of an echinococcus-cyst a clear fluid free from albumin would be expected. At times an abscess of the liver is so closely applied to the abdominal wall that it may be mistaken for an abscess of the abdominal wall. The important point in differential diagnosis would then be whether the accumu- lation of pus moves with the respiratory movement, and this is indicative of abscess of the liver. The development of an abscess of the liver is usually attended with 330 DIGESTIVE ORGANS raost indefinite symptoms. The patients complain frequently of pain in the liver, which at times extends to the right shoulder and tlie right arm; also, tiic liver is frequently tender on pressure, in part throughout an extensive area and in part to an especially marked degree in a circumscribed area corresponding to the situa- tion of the abscess. Enlargement of the liver then usually takes place progressively. Frequently jaundice develops, but this is by no means a constant symptom. Enlargement of the spleen is almost always demonstrable (infection-spleenj. In addition there are signs of general sepsis : irregular febgle movement, generally remitting or hectic fever, chills preceding the elevation of tem- perature, sweats, loss of appetite, progressive anemia, and exhaus- tion. Should permanent relief not be afforded, death may result from asthenia. At times, however, alarming coinjjlications may arise in consequence of rupture of a liver-abscess. Rupture into the peritoneal cavity is particularly dangerous, as this is generally soon followed by fatal perforative peritonitis. The abscess may, however, rupture also into any of the adjacent organs (pleural cavity, pericardium, lungs, stomach, intestines, urinary passages), and even through the external integument, and at times a natural cure of the abscess has then been observed to take place. A serious occurrence is rupture of the pus into the hepatic veins, the portal vein, or the interior vena cava, as fatal hemorrhage or general septicemia may result. The duration of an abscess of the litter may extend over a few weeks, several months, and a number of years (up to fifteen), so that a distinction is made bet^\ een acute, subacute, and chronic abscess of the liver. In addition to rupture, natural cure of an abscess of the liver may take place in consequence of inspissatiou and calcification, and in the case of small collections of pus, of cicatrization ; Ijut these occurrences are extremely rare. Small and deeply situated abscesses of the liver cannot be recognized during life. In some instances scarcely more than the clinical picture of sepiicopjiemia is devel- oped, without alterations in the liver itself. At times chills occur at such regular intervals that intermittent fever may be suspected, but malarial ])lasmodia cannot be found in the blood. Also, if jaundice should develop the diagnosis cannot be estalilished beyond the point of jirobability, as jaundice may occur in conjunction with pyemic conditions, even apart from su]ipuration of the liver. Progtiosis and Treatment. — The prognosis of abscess of the liver has been materially improved since time is no longer wasted with internal remedies, but as soon as the condition is discovered it is subjected to siu'gical treatment. Naturally, the prognosis depends besides upon the nature of the causative factors. The outlook for pyemic abscesses is grave, because they are often multiple, and are, therefore, less readily susceptible to surgical intervention, and, besides, because the pyemic constitutional state CHRONIC INTERSTITIAL HEPATITIS 331 is in itself a most serious condition. An abscess of the liver should be opened as soon as the diagnosis is made with certainty, in order to avoid the dangers of rupture. Internal remedies are incapable of causing absorption of pus in the liver. A nutritious diet and alcohol in generous quantities may be advised for the septico- pyemic general condition. CHRONIC INTERSTITIAL HEPATITIS (CIRRHOSIS OF THE LIVER), !]^tiology. — Chronic interstitial inflammation of the liver is also known as contracted liver and cirrhosis of the liver, but both of these designations are inadequate, because chronic interstitial in- flammation of the liver does not always give rise to diminution in the size or to contraction, and because, also, the diseased organ does not always present a light-yellow color, for xippo;; means yel- low. The causes for chronic interstitial inflammation of the liver consist in chemic poisons, bacterial poisons (toxins), or anomalous metabolic products. It has been known for a long time that excessive indulgence in alcohol is the most common cause for the disorder. Spirit-drinkers are particularly exposed to danger, and the condition has been spoken of as spir it-drinkers' or drunk- ards' liver, and the less dilute and the more abundantly spirit is drunk the more readily does the disease develop. Those who partake liberally of food in conjunction with indulgence in spirit may the longer escape the evil effects of their habits. Cirrhosis of the liver occurs much less commonly in those who indulge in wine and beer. Whether other irritating articles of food also are capable of inducing interstitial inflammation of the liver is not definitely known. It has been stated that such a result may be brought about by excessive use of curry. In animals hyperplasia of the interstitial connective tissue of the liver has been induced by long-continued administration of phosphorus. I have observed a similar condition in a girl after phosphorus-poisoning. Cirrhosis of the liver develops occasionally in the sequence of infectious disease, as, for instance, after hereditary or acquired syph- ilis, pulmonary tuberculosis, miliary tuberculosis, and malaria. At times the disease is associated with alterations in the biliary- passages (calculi, stenosis or occlusion), and under such circum- stances infectious factors must be taken into consideration. Pos- sibly the toxins of the colon-bacterium play an important part, as this organism, under the conditions named, is readily capable of gaining access to the biliary passages. Among the metabolic dis- orders that may give rise to chronic interstitial inflammation of the liver diabetes and c/out may be named. Some varieties of chronic interstitial hepatitis are dependent upon arteriosclerotiG alterations in the hepaiic artery and its intrahepatic ramifications, 332 DIGESTIVE ORGANS and in the same way as in the kidneys also senile contraction of the liver may be recognized. Among all of the causative factors excessive indulgence in alcohol is the most important, and this explains the fact that the disease is most common in ineu in the lower icalhs of life, and that it is more prevalent in some countries than in others. Experience, unfortunately, demonstrates that at times children also are encouraged by their parents to drink spirit, with the result that cirrhosis of the liver develops. Anatomic Alterations. — Chronic interstitial inflammation of the liver may appear in various anatomic forms, and accord- ingly several varieties of the disease have been distinguished. All, however, agree in the fact that the interlobular connective tissue throughout the entire liver has undergone diffuse and ab- normal hyperplasia. Accordingly that variety of circumscribed connective-tissue hyperplasia that takes place about abscesses, new-growths, and echinococci in the liver, and forms a capsule for these, does not belong in this category. Likewise the connective- tissue hyperplasia that develops in connection with conditions of chronic venous stasis and involves at first and principally the dilated intralobular blood-capillaries is not included. Probably every liver in which the connective tissue has undergone morbid hyperplasia appears at first enlarged. Subsequently cicatricial contraction of the connective tissue often takes place, and as a result the contracted liver or atrophic cirrhosis of the liver develops. If, on the contrary, the liver remains persistently enlarged, the condition is one of hypertrophic cirrhosis of the liver. The drunk- ard's liver is usually one of atrophic cirrhosis, but there are cases in which, although the disease has been of long duration, the liver remains enlarged. We shall first describe fully alcoholic cin'hosis of the liver. In the developed stage of the disease the liver is diminished in size, particularly its left lobe, and the designation contracted liver is therefore appropriate for this condition. The organ is light yellow or light yellowish-brown in color, whence the designation cirrhosis of the liver. The surface of the organ exhibits numerous irregularities and nodules, in consequence of which the disease has acquired the name of granular atrophi/ of the liver. The nodules vary in size between that of a poppy- seed and that of a cherry. The depressions are represented by a grayish, almost translucent, tissue, and they result from contraction of the newly formed connective tissue, while the projecting nodules consist of liver-tissue, which in places presents an almost ochre- vellow color from saturation of the liver-cells with biliary coloring- matter. The capsule of the liver often appears thickened in cir- cumscribed or in extensive areas, and it is at times adherent to adjacent organs, particularly the diaphragm. Also, on section of the organ the nodular appearance of the surface is conspicuous, and CHRONIC INTERSTITIAL HEPATITIS 333 likewise here, as upon the surface of the liver, grayish, depressed areas, consisting of newly formed connective tissue, are visible, and between which light-yellow or ochre-yellow colored liver-tissue projects. At times, owing to the dense hyperplastic connective tissue present, the liver has acquired such an indurated consistency that on section with a knife a creaking sound is audible, aud ac- cordingly the designation hardening or induration of the liver seems appropriate. In some cases thrombosis of the jwrtcd vein develops. The abdominal cavity almost always contains transudate. The spleen is generally enlarged and hard ; the mucous membrane of the stomach and intestines presents the appearances of chronic catarrh. On microscopic examination of the liver the increase in the interlobular connective tissue is conspicuous. Generally several lobules are surrounded by a broad band of connective tissue, and for this reason alcoholic cirrhosis has also been designated multilobular cirrhosis of the liver. The connective tissue often presents the appearance of cicatricial tissue deficient in cells, although in more recent areas an abundance of young cells are present, and these are particularly numerous close to the peripheral liver-cells. The intrahepatic branches of the pjortal vein are obstructed or occluded in numer- ous places in consequence of obliterative endophlebitis. It is assumed that the vascular changes are dependent upon the connective-tissue hyperjilasia, and for this reason alcoholic cirrhosis of the liver is designated hho portal cirrhosis. The liver-cells themselves are often in an advanced state of fatty degeneration, and this is probably due in part also to the action of the alcohol, while in other places they have undergone atrojjhy in consequence of the pressure exerted by the newly formed connective tissue. Often they are stained deeply yellow with biliary coloring-matter. The ascites that almost constantly attends alcoholic cirrhosis of the liver, the hypostatic catarrh of the gastro-intestinal membrane, and the enlargement of the spleen are considered as consequences of stasis in the portal circulation dependent upon obstruction of the intrahepatic branches of the portal vein. An hypertrophic biliary or monolobular cirrhosis of the liver has recently been distinguished from the alcoholic form of chronic interstitial inflammation of the liver first accurately described by Laennec, and therefore designated Laennec's cirrhosis of the liver. The former is characterized by aljnormal enlargement of the liver, with a smooth surface and a bilious and dark-green color. The bands of connective tissue may attain quite considerable pro- portions, and the liver may then be traversed by grayish bands, which at times may be confounded with neoplastic infiltration. The biliary passages frequently are abnormally dilated and exces- sively distended with bile. The weight of the liver may become twice or thrice the normal. On microscopic examination the hyperplastic connective tissue will be found generally surround- ing individual lobules of the liver (monolobular cirrhosis), and to be the seat of marked increase and ramification of the smaller biliary passages, from which the connective-tissue hyperplasia appears to have arisen {biliary cirrhosis of the liver). The newly 334 DIGESTIVE ORGANS formed connective tissue exhibits no tendency to undergo cica- tricial contraction, and therefore the liver does not become reduced in size. l^yphilitic cirrhosis of the liver has been designated also monocellular cirrhosis of the liver, because the connective-tissue hyperplasia occurs about individual liver-cells and causes their destruction by pressure. The liver is often greatly changed in shape, one or more portions of the organ becoming detached from the main body by bridges of connective tissue, and the liver is thus converted into a multilobulated organ — syphilitic- lobulated liver. Little is as yet kuo^Yn -with regard to senile or arteriosclerotic ciiThosis of the liver, which resembles the alcoholic variety of the disease and is attended Avith contraction after previous enlarge- ment. ]\Iicroseopically the extensive obliterative endarteritis in the intrahej^atic branches of the hepatic artery is a conspicuous feature. Symptoms and Diagnosis. — The several anatomic varie- ties of cirrhosis of the liver correspond also with various clinical pictures, and we shall describe these with the qualification that typical conditions will be considered. The distinctive symptoms of alcoholic cirrhosis of the liver are usually preceded by manifes- tations of chronic gastro-intestinal catarrh, which likewise is dependent upon excessive indulgence in alcohol. The patients become more and more emaciated, lose their appetite, and acquire a peculiar grayish-yellow color of the skin. The sclerse generally are distinctly jaundiced. ^Marked icteric discoloration of the skin and mucous membranes does not occur, as a rule. In some cases disagreeable sensations of tension, of pressure, and even of pain in the region of the liver occur, while in others attention is first attracted to the disease by increase in girth in consequence of accumulation of fluid in the abdominal cavity. If oppor- tunity be afforded to examine the liver at an early stage of the disease, it will be found to be enlarged, with its lower border at the level of the umbilicus, and even lower. At the same time the hardness of the organ is notable, and this may be distinctly recognized by palpation of the lower margin of the liver. Gradu- ally the liver undergoes progressive diminution in size, and its lower border Mill be found above the right costal margin. If the abdominal walls are thin and deficient in fat, the trained hand may succeed in detecting nodular irregularities upon the surface of the liver. The examination of the liver is sometimes attended with insurmountable difficulty from the accumulation of fluid in the abdominal cavity, causing distention of the abdominal walls and displacing the liver upward into the concavity of the diaphragm. At times the information desired can be gained through percussion and palpation to a certain degree by practis- CHRONIC INTERSTITIAL HEPATITIS 335 in^ shock-like palpation in the dorsal decubitus, or percussion and palpation with the patient occupying the left lateral decubitus or the prone position. Dropsy of the abdominal cavity — ascites — is quite a constant symptom of alcoholic cirrhosis of the liver, and is dependent upon stenosis and partial occlusion of intrahepatic branches of tlie portal vein, and the resulting increase of blood-pressure in the trunk of this vein. The abdominal walls are not rarely distended to the utmost, and the heart and the lower margins of the lungs, together with the diaphragm, may be greatly displaced upward. The umbilicus not rarely forms a marked projection forward, and in transmitted light appears translucent because the umbilical hernia contains serous fluid from the abdominal cavity. Not rarely points of rupture in the cutis are observed upon the lower half of the abdomen in the form of strige. Often excessively dis-. tended and markedly tortuous cutaneous veins in the abdominal wall attract attention. Usually the trunk of each inferior epigas- tric vein ascends from the middle of Poupart's ligament, and sends off various ramifications at the level of the umbilicus. These unite with branches of the superior epigastric veins, which generally disappear at the level of the nipple and in the direction of the axillary cavity. Obviously these conditions are dependent upon the venous collateral circulation that develops because the ascitic fluid rests upon and compresses the inferior vena cava. An uncommon variety of venous collateral circulation in cases of cir- rhosis of the liver is known as the caput Medusce — cirsomphalos. This con- sists in the presence of greatly dilated veins surrounding the umbilicus, and constituting a sort of cavernoma. The vessels are branches of the epi- gastric veins, which have entered into anastomosis with the patulous umbil- ical vein in the round ligament of the liver. In contradistinction from hypostatic ascites, it is distinctive of the ascites of alcoholic cirrhosis of the liver that the extrem- ities are free from cutaneous edema. Only when the ascites, by reason of its weight, causes considerable stenosis of the vena cava will hypostatic edema develop ; but this is characterized by the fact that it is slight as compared with that of marked ascites. At times cachectic edema of the skin, or edema of the extremities on one side, develops in consequence of marantic thrombosis of the femoral vein. The spleen is almost always enlarged, although excessive ascites often prevents recognition of this condition. Recently attention has been called to the fact that the old view, according to which the enlargement of the spleen is due to stasis in the portal vein, appears not to be correct, because enlargement of the spleen at times occurs so early that it is more probably correct that the enlargement of the spleen and that of the liver are dependent upon identical causes. If the excessive indulgence in alcohol has already given rise to chronic gastro-intestinal catarrh, 336 DIGESTIVE ORGANS this becomes materially aggravated in consequence of portal cir- rhosis of the liver, because tiie obstruction and occlusion of the intrahepatic branches of the portal vein give rise to stasis in the veins of the stomach and the intestine. At times hemorrhoids develop. If the stasis becomes excessive, there may be extensive hemorriiagcs in the mucous membrane of the stomach, and vomit- ing of blood — hematemesis. At times, however, blood that is vomited may come from varicose dilatations of the veins in the lotcer portion of the esophagus. Death from hemorrhage may take place within a short time from uncontrollable bleeding. The duration of alcoholic cirrhosis of the liver is, as a rule, more than a year (up to live years). But rarely is an acute course of a few weeks observed. The course of the disease is usually afeb- rile. At times, however, febrile movement occurs, the cause of which is unknown — hepatic fever. In some cases death results from aspjhyxia and cardiac parcdysis if the accumulation of fluid in the abdominal cavity has become so considerable that the lungs and the heart are unduly displaced upward. Other patients die amid signs of progressive asthenia. Under such conditions symp- toms of dissolution of the blood appear upon the skin and the mucous membranes. The occurrence of fatal hemorrhage from the dilated esophageal veins has already been mentioned. The diagnosis of alcoholic cirrhosis of the liver is easy if the three main symptoms — a small, hard, nodular liver, enlargement of the spleen, and ascites — are present, particularly if the patient is admittedly a spirit-drinker and presents a salloAV, slightly icteric tint of the skin. Should, however, marked ascites prevent examina- tion of the liver and the spleen, the condition may lie confounded with thrombosis of the portal vein, and tuberculous, carcinomatous, and chronic-serous peritonitis. Under .such conditions the most reliable procedure is to remove the ascites by puncture of the abdom- inal cavity, because subsequently the liver and the spleen become accessible often with surjirising distinctness immediately after the puncture, and are susceptible of examination. At times, natur- ally, the liver remains in the concavity of the diapliragm in spite of abdominal puncture, generally in consequence of perihepatitic adhesions to the diaphragm. It should then not be forgotten that thrombosis of the portal vein usually develops in the sequence of inflammatory and ulcerative processes in the stomach, intestine, and gcnito-urinary a])paratus ; that carcinomatous inflammation of the peritoneum occurs in advanced life, and is associated with cachexia ; and that tuberculous peritonitis is generally secondary to tuberculosis of the lungs, intestines, or mesenteric glands, and is usually associated with pain and febrile movement, but without icterus. At times pericardial adhesions, with myocardial weak- ness and stasis, particularly in the veins <>f the peritoneum, con- stitute a source of great diagnostic difficulty. The decision will CHRONIC INTERSTITIAL HEPATITIS 337 then depend principally upon the demonstration of the previous presence or absence of pericarditis. The typical picture of hyper- trophic or biliary cirrhosis of the liver is produced by that variety of the disease which has been designated also hypertrophic cirrho- sis of the liver toith jaundice. In this disorder the liver is greatly enlarged, and its lower border often extends considerably below the level of the umbilicus. Also its upper border may be dis- placed upward. At the same time the organ is characterized by increased resistance and hardness, although its surface appears smooth, and the liver does not undergo diminution in size. The spleen also usually exhibits considerable enlargement. Ascites-- is not present, but on the other hand jaundice is marked. The patients complain principally of a sense of pressure and of tension in the region of the liver and of derangement of gastro-intestinal activity. The disease usually pursues a slow course, and at times may persist for more than five years. Progressive emaciation, at times also cholemic manifestations, usually lead to death. In two cases I have observed the clinical picture of hypertrophic cir- rhosis of the liver with jaundice in which post-mortem examination dis- closed the existence of pseudofeukemia. Enlargement of the liver and of the spleen had resulted from pseudoleukemic new-growths, and the profound icterus from the pressure exerted by enlarged lymph-glands upon the hepatic ducts in the transverse fissure. Between portal and biliary cirrhosis of the liver there are various relations and gradations, so that a whole series of Varieties of cirrhosis of the liver has been described. The following sche- matic enumeration is presented : I. Alcoholic or portal cirrhosis of the liver. a. With atrophy of the liver, ascites, and enlargement of the spleen ; b. With hypertrophy of the liver, ascites, and enlargement of the spleen ; c. With jaundice. II. Hypertrophic or biliary cirrhosis of the liver, with jaundice. III. Biliary cirrhosis of the liver, ivith consecutive atrophy. a. With enlargement of the spleen ; b. Without enlargement of the spleen. In one of my patients a monolobular form of cirrhosis of the liver was suddenly superadded to a preexisting multilobular cirrhosis and caused death in the second week of the disease, being attended with enlargement of the spleen, but without jaundice and ascites; and in another, in wliich death resulted from cholemia, there Avas found on macroscopic examination the typical appearances of hypertrophic portal cirrhosis of the liver, while microscopic examination disclosed a most bpautiful example of monolobu- lar cirrhosis of the liver. Ascites M'as not present. The classifications sug- gested therefore scarcely indicate more than that every case of cirrhosis of the liver may possess peculiarities of its own, and should be carefully ex- amined. Upon what these peculiarities depend has, however, not yet been explained. Syphilitic cirrhosis of the liver is characterized especially by the constricting off of individual portions of the liver. It may be readily confounded with constricted liver and with tumors of the ■ 22 338 DIGESTIVE ORGANS liver. Little is known with regard to senile or arte r to-sclerotic cir- rhosis of the liver. It develops insidiously in elderly persons who perhaps may always have passed temperate lives, the liver being large and hard, and subsequently undergoing reduction in size. Ascites occurs and death results from excessive asthenia. Prognosis. — The prognosis of cirrhosis of the liver is unfa- vorable, tor there is no remedy capable of causing disappearance of the hyperplastic connective tissue, and, besides, the disease ex- hibits an undeniable tendency to progress. As a rule, the patients are at so advanced a stage of the disease when they come under observation for treatment that the outlook for therapeutic success is small. Nevertheless, isolated observations have been made in wliich it has been possible to check the progress of the disease, and to relieve distressing symptoms permanently, particularly the ascites. Treatment. — In the treatment causal therapy plays an im- portant part. The patients should be ^veaned from the use of alcohol, or if syphilis be the etiologic factor, potassium iodid (5.0 : 200 — 75 grains : 6|- fluidounces ; 15 c.c. — 1 tablespoonful — thrice daily), mercurous chlorid (0.5 — 1\ grains ; 1 such powder thrice weekly), or mercurial ointment (5.0 — 75 grains — to be used by inunction daily for 25 or 30 days) should be prescribed. In cases of arterio-sclerotic cirrhosis of the liver the employment of potassium iodid may be recommended. Among ssrmptomatic remedies potassium iodid and mercurous chlorid occupy first place. A milk-diet should be observed (1 or 2 quarts of thoroughly l)oiled milk in small amounts at intervals of from one-quarter to one- half an hoiu' throughout the day), as milk is an easily digestible and nutritious article of food, and it also stimulates diuresis. Local treatment will be required with especial frequency for the excessive ascitic accumuhdion. Generally little can be accom- plished with diuretics, laxatives, and diaphoretics. The most reliable measure is abdominal puncture. As a rule, the fluid natu- rallv soon reaccumulates, but there is no objection to repeating the puncture from time to time. It is properly becoming more com- monly the practice not to reserve puncture as a last resort, but to employ it early in order to avert threatening asphyxia. At times reaccumulation of the fluid does not take place after punc- ture, and recovery ensues. Courses of treatment at springs should be prescribed only when ascites is abseut or inconsiderable, so that the patient can move about. Carlsbad, Marienbad, Homburg, Kissingen, and Tarasp especially may be recommended. ACUTE YELLOW ATROPHY OF THE LIVER, Btiology. — Acute yellow atrophy of the liver is an exceedingly rare disease, and is attended with rapid fatty degeneration of the ACUTE YELLOW ATROPHY OF THE LIVER 339 liver-cells, with their disintegration and absorption, so that within a few days the liver becomes greatly diminished in size. The dis- ease develops generally under the influence of bacterial poisons (toxins) and perhaps also of putrefactive alkaloids (ptomains), although little of a definite nature is known in this connection. It has been maintained further that certain chemic poisons (phos- phorus, fungous poisons) may cause acute yellow atrophy of the liver, but under such circumstances there is probably resemblance rather than identity in the anatomic and clinical pictures. At times acute yellow atrophy of the liver develops in the sequence of infectious diseases, as, for instance, typhoid fever, pharyngeal diphtheria, enteritis, and syphilis. At other times the disease occurs as a complication of other diseases of the liver, as, for in- stance, cirrhosis and fatty liver. Occasionally small endemics of acute yellow atrophy of the li.ver have been observed in barracks, so that the suggestion of an independent infectious disease has been raised. It is known that the disease occurs with relative frequency during pregnancy, and with particular frequency between the fifth and the eighth month, and less commonly in association with parturition. Under such circumstances ptomains may be the exciting agents. Often a definite cause cannot be demon- strated — cryptogenetic atrophy of the liver. Occasionally fright, emotional disturbances of other kind, and alcoholism are assigned as causes. Experience has shown that acute yellow atrophy of the liver occurs more commonly in women than in men. Although the disease is most common at the vigorous period of life (from 25 to 45), on the other hand cases have been observed also in children and the aged. Anatomic Alterations. — On opening the abdominal cavity the liver is often not at all visible from having fallen back toward the vertebral column, and being covered in front by loops of intes- tine. The organ has often lost more than half in size and weight. The capsule of the liver, therefore, is wrinkled. The consistence of the oro^an is diminished, so that it can almost be shaken to and fro. On section the liver presents a more or less marked ochre- yellow color. In addition areas stained red are present, resulting from the ochre-yellow areas. Red markings are observed particu- larly in the left lobe of the liver, in wdiich the disease is prone to begin. On microscopiG examination attention is attracted particularly by the marked fatty degeneration of the liver-cells. The cells undergo disintegration, the masses of fat are partially absorbed, and eventually there remains a striated empty structure free from liver-cells. The blood-vessels also undergo fatty degeneration. The interlobular biliary passages stand out with marked distinct- ness, and appear hyperplastic. Cellular proliferation and round- cell accumulation also take place in the interlobular connective 340 DIGESTIVE ORGANS tissue, and cirrhosis of the liver has been observed to develop in the sequence of acute yellow atrophy. At times, but by no means constantly, bacteria have been found in the liver (Streptococcus pyogenes, Staphylococcus ])yogcne.s albus, pneumouiacoccus, Bacte- rium coli commune). If the liver has been exposed to the air for a Vvhile, a frost-like deposit at times takes place upon its sur- face, and this is found upon microscopic examination to consist of needles of tyrosin and spheres of leucin. In all probability acute yellow atrophy of the liver consists in a degenerative process involving the liver-cells, and to which secondarily inflammatory alterations (proliferation of the biliary passages, connective-tissue hyperplasia) are superadded. The remaining organs are generally characterized by their marked icteric hue. In addition, extrava- sations of blood occur in the viscera. Usually the glandular cells of the stomach, the intestine, the pancreas, the convoluted urinary tubules, often also the muscle-fibers of the myocardium and of the voluntary muscles, are in a state of fatty degeneration. The spleen and the portal and retroperitoneal lymph-glands are enlarged and softened. Symptoms, Diagnosis, and Prognosis. — Acute yellow atrophy of the liver often sets in with prodromes, consisting in symptoms of gastro-intestinal derangement. Then icteric discolor- ation of the skin and of the mucous membranes takes place, and this attains the highest possible degree of intensity within a short time. Soon symptoms are superadded of a condition that is designated cholemia, and which has recently been attributed to auto-intoxica- tion with abnormal metabolic products. Consciousness becomes more and more obscured, delirium develops, and the patients groan and often throw themselves about restlessly in bed, and from time to time exhibit clonic muscular contractions in individual extrem- ities or in all of the muscles. Often symptoms of blood-dissolution further appear, and there may be hemorrhages beneath the skin and the various mucous membranes. Amid progressive loss of consciousness the disease generally terminates fatally in the second week, although at times it may be protracted for from six to four- teen weeks. In the diagnosis of acute yellow atrophy of the liver the changes in the liver and in the urine are particularly important. On per- cussion, and to a certain degree also on palpation, the liver will be found from day to day to be growing smaller in size. The dulness yielded by the left lobe disappears earliest, and eventually the entire area of hepatic dulness may be reduced to a narrow band. The liver-dulness may even be wholly wanting, and be replaced by an area yielding a tympanitic note. The diminution in the area of liver-dulness progresses gradually from below upward. Pressure over the liver is in conspicuous degree painful. Diminution in the size of the liver may be simulated by the presence of intestine — ACUTE YELLOW ATROPHY OF THE LIVER 341 as, for instance, the transverse colon greatly distended with gas — between the surface of the liver and the abdominal and thoracic walls ; but generally such a condition is only a transient one, so that within a short time the liver-dulness is completely restored. Besides, the liver-dulness can frequently be elicited by pressing the plexiraeter firmly upon the abdominal wall, thus flattening the transverse colon upon the surface of the liver. Also, in the pres- ence of free perforative peritonitis disappearance of liver-dulness takes place when the gas thnt has escaped from the stomach or the intestine into the abdominal cavity insinuates itself between the liver and the thoracic and abdominal walls, but such a condition develops suddenly, and is, or at least may be, unattended with icterus, while peritonitic pain, abdominal distention, and the like, predominate. The urine is usually passed in small amounts, possesses a deep- brown, icteric hue, and generally contains albumin, fibrinous tube- casts, epithelial cells from the uriniferous tubules and the bladder, and round cells. Of particular importance is the occurrence of needles of tyrosin in the urinary sediment, and which usually lie together in sheaf-like arrangement, and of spheres of leucin, several of which are often coherent, and which are characterized by their double contour. Usually both of these substances are precipitated spontaneously. Should this not be the case, they can be precipi- tated by adding acetic acid to a drop of urine upon a slide, and permitting evaporation to take place. It may be remarked inci- dentally that leucin and tyrosin occur in the urinary sediment also in association with other severe varieties of jaundice — as, for instance, following phosphorus-poisoning — and at times also in the course of severe infectious diseases (small-pox). The amount of urea in the urine will be found diminished. Of abnormal urinary constituents, sarcolactic acid has further been isolated. All of these facts indicate that the metabolism is profoundly altered in cases of acute yellow atrophy of the liver. The disease is generally unat- tended with fever, and almost invariably terminates fatally with progressive asthenia and loss of consciousness. The prognosis is therefore hopeless. Treatment. — Causal treatment is applicable only when syph- ilis is an etiologic factor, and under such conditions inunctions of mercurial ointment (5.0 — 75 grains) may be employed, and j^otas- sium iodid (5.0 : 200 — 75 grains : 6 J fluidounces ; 15 c.c. — a table- spoonful — thrice daily) administered. The symptomatic treatment consists in the employment of stimulants, as, for instance : R Camphorated oil, 10.0 (2^ fluidrams). Dose : 1 c.c. (15 minims) subcutaneously thrice daily. The administration of from 1 to 2 quarts of boiled milk daily is advisable in order to increase the secretion of urine, and thus o42 DIGESTIVE ORGANS hasten the elimination of possible toxic metabolic products from the body. It may also be advantageous to stimulate the secretion of urine by permitting 500 c.c. (1 pint) of lukewarm physiologic salt-solution (0.7o jxt cent.) to flow into the rectum or beneath the skin several times daily. FATTY OR ADIPOSE LIVER, Ktiology. — Fatty liver is only of subordinate clinical sig- nificance. A distinction must be made between cachectic, toxic, infectious fatty liver, and that due to over-eating. Fatty liver due to over-eating occurs in association with obesity, and develops usually in persons who eat a great deal, partake excessively of carbohydrates and of alcoholics, and indulge insufficiently in phys- ical exercise. Cachectic fatty liver develops in the sequence of loss of blood or of discharges (protracted suppuration) and debili- tating diseases (pulmonary tuberculosis, carcinoma, chlorosis, per- nicious anemia, leukemia, etc.). Toxic fatty liver occurs in the train of certain intoxications, among which poisoning with phos- phorus, arsenic, and mercury may be particularly mentioned. Infectious fatty liver is that variety that develops not rarely in the sequence of acute infections diseases. Fatty liver occurs further in association with venous stasis in the form of the fatty nutmeg-liver, and more especially locally in connection with diseases of the liver in the neighborhood of carcinomatous abscesses and cirrhosis of the liver. A variety of physiologic fatty liver occurs in infants. It is a form of fatty liver due to over-feeding, and is dependent upon the use of milk containing much sugar in conjunction with insufficient bodily activity. Anatomic Alterations. — In cases of well-developed fatty liver the organ is enlarged and its margins blunt. It is light gray or yellowish gray in color. On section of the liver a fatty deposit adheres to the blade of the knife. On microscopic exami- nation the liver-cells are found filled with large and small fiit- globules. In addition some of them not rarely contain consider- able biliary coloring-matter. A distinction has lieen made between fatty infiltration and fatty degeneration of the liver, accordingly as the fat in the liver-cells has been deposited through the inter- mediation of the blood or has developed in the liver-cells them- selves from disintegration of their proto])lasm. Prolxdily the fatty liver due to over-feeding is a variety of fatty infiltration ; while the cachectic, toxic, and infectious forms, are, on the contrary, varieties of fatty degeneration. The view that fiitty infiltration and fatty degeneration are distinguishable from each other by the fact that in cases of the former the liver-cells are filled with large fat-globules, while in cases of the latter, on the contrary, the liver- cells are filled with numerous small and minute fat-globules, is AMYLOID LIVER 343 not correct. It has been pointed out that the diiferentiation between the two conditions can be made by chemic means, inasmuch as in the presence of fatty infiltration the amount of water in the liver is reduced (from 70 to 50 per cent.), because the fat has displaced the water of the liver-cells ; while in the presence of fatty degeneration the amount of water remains un- changed. Should fatty liver be an associated manifestation of general obesity, unusually large amounts of fat are found also in other organs and structures (subcutaneous connective tissue, epicardium, mesentery, epiploic appendices). Symptoms, Diagnosis, and Prognosis. — Patients with fatty liver due to over-eating not rarely complain of a sense of tension and of constriction in the region of the liver, and on pal- pation and percussion this organ will be found enlarged, resistant, smooth, witli blunt borders, and at times also tender on pressure. The remaining symptoms of general obesity will generally indi- cate that the manifestations just mentioned are dependent upon fatty infiltration of the liver. To what extent digestion and metabolism are thereby deranged is not definitely known. The prognosis depends upon whether the general obesity can be cor- rected or not. Cachectic, toxic, and infectious fatty liver may be wholly unattended with symptoms. Treatment. — The treatment of fatty liver consists in the treatment of the fundamental disorder, as, for instance, of that variet}" due to over-eating, in strict regulation of the diet. AMYLOID LIVER. Ktiology. — Amvloid degeneration of the liver may develop as a result of wasting discharges and cacliectic states of all kinds, as, for instance, protracted suppuration, particularly of bones and joints, of the kidneys and the pelvis, pleural empyema, chronic diarrhea, pulmonary tuberculosis, malarial and syphilitic cachexia. In rare instances it is impossible to ascertain the cause, so that the disease gives the impression of being an independent disorder. The condition occurs at all periods of life, and in children partic- ularly in the sequence of scrofulous — thus actually tuberculous — suppuration of the lymphatic glands, bones, or joints. Anatomic Alterations. — In cases of well-developed amyloid degeneration the liver is large, smooth, and hard — almost as if frozen. Its weight may be increased threefold. On section the margins exhibit an almost translucent aspect, and upon the cut surface the liver-substance can be scraped with the knife as if the organ were frozen. If tincture of iodin, or, still better, Lugol's solution (pure iodin, 0.5 — 7^ grains ; potassium iodid, 5.0 — 75 grains; distilled water, 200.0 — 6 J fluidounces), be poured upon 344 DIGESTIVE ORGANS the cut surface, the liver becomes stained dark brown or mahogany-brown in the amyloid areas. On viicroscopic examination of the liver the portions involved in amyloid degeneration can be recognized from their clear, waxy luster. They appear swollen and structureless, but, above all, they yield the amyloid reaction, being stained brown with Lugol's solution. If the sections are then placed in a watch-glass contain- ing dilute sulphuric acid, they assume a bluish or bluish-violet tint. Methyl-violet gives the areas involved in amyloid degenera- tion a bright-red tint, and they are thus sharply differentiated from the adjacent healthy tissue stained blue. Careful histologic examination discloses that the walls of the blood- vessels are first involved in the process of amyloid degeneration, and pri- marily the walls of the hepatic arteries, subsequently those of the inter- lobular capillaries and the branches of the portal vein. The liver-cells generally remain exempt, and according to some observers permanently so. Chemic examination of tlie amyloid material discloses that it contains nitrogen, and is a proteid substance. Th& source of this abnormal meta- bolic product is unknown. In all probability the amyloid substance is generated locally, for not rarely in the application of the amyloid test appearances are encountered in which a gradual transition in color is observed to take place from healthy to amyloid tissue. Some observers, however, assume that the amyloid substance is brought to the liver from without. If the amyloid degeneration of the liver is not well devel- oped, it can be recognized only with the aid of the reactions mentioned. Almost always other organs will also be found involved in the degenerative process, particularly the spleen, the adrenal bodies, the kidneys, and the raucous membrane of the intestine. Symptoms, Diagnosis, and Prognosis. — Amyloid de- generation of the liver will be susceptible of diagnosis only when the liver is large, hard, and smooth ; if the condition has been preceded by diseases that experience has shown are frequently followed by amyloid degeneration, and if enlargement and indu- ration of the spleen, edema of the skin, and marked albuminuria and diarrhea indicate simultaneous amyloid degeneration of the spleen, the kidneys, and the intestine. Amyloid liver is not attended with jaundice unless the biliary passages be obstructed by enlarged lymphatic glands in the transverse fissure. The patients are usually pallid in consequence of the conditions that are responsible for the amyloid disease. Recovery can scarcely be expected. Death occurs most commonly from progressive exhaustion. Treatment. — In the presence of amyloid disease preparations of iron, and particularly iron iodid, are generally prescribed, although these probably exert a useful influence upon the accom- panying anemia rather than ujiou the amyloid condition. In a CARCINOMA OF THE LIVER 345 prophylactic way it is important to suppress chronic suppuration, diarrhea, and wasting discharges of all kinds as rapidly as possible. CARCINOMA OF THE LIVER» Htiology. — Carcinoma of the liver is an extremely common disorder. Almost invariably the condition is one of secondary carcinoma. Cases of primary carcinoma of the liver are exceed- ingly rare. Most commonly secondary carcinoma of the liver develops in connection with carcinoma of the stomach, the new- growth extending directly from the stomach to the liver. Fre- quently, however, portions of the new-growth are conveyed from the stomach to. the liver as emboli through the blood-vessels, and thus give rise to secondary carcinoma in the liver. In addition to the stomach, the uterus, the rectum, the esophagus, and the mammary gland particularly are often the seat of primary carci- noma, which is often followed by secondary invasion of the liver. It should be pointed out, further, that secondary carcinoma of the liver develops at times in the sequence of carcinoma, of the gall-hladder. Often biliary calculi are found in the gall-bladder, so that it is reasonable to believe that these may act as the excit- ing cause of the new-growth in the gall-bladder. Naturally, also, they may have developed subsequently in the diseased gall-blad- der. Carcinoma of the liver occurs more commonly in women than in men. It usually develops after the fortieth year of life, and rarely earlier. Anatomic Alterations. — Carcinoma of the liver occurs in two varieties — namely, circumscribed and infiltrating. Circum- scribed cai^cinoma forms well-defined nodules that range in size from being scarcely visible to that of a man's head. The number of nodules varies greatly. At times the liver is so largely occupied by them that but little normal hepatic tissue is left. At the same time the size and the weight of the organ may reach more than six times the normal. Carcinomatous nodules situated at the surface of the liver often exhibit a depression or so-called umbili- cation. On section carcinomatous nodules usually present a juicy, whitish, or yellowish-white medullary structure, from which car- cinomatous juice or milk can be scraped with a knife. At times carcinomatous nodules are conspicuous for an abundance of ves- sels distended with blood, so that they present a reddish mottled appearance ; blood-lakes at times form in consequence of rupture of l)lood-vessels. Carcinomatous nodules may acquire a grayish or slaty color from the presence of pigment in large amount, and the condition is then designated pigmentary carcinoma. As in other organs, also in the liver, a distinction is made between fibrous carcinoma (scirrhus), medullary carcinoma, and colloid carcinoma (alveolar carcinoma), accordingly as the new-growth 346 DIGESTIVE OlKiANS contains much or little fluid or cavities filled with gelatinous or isinglass-like material. On rnici-oscopic examination the carcinoma is found to consist of masses of epithelioid cells with large nuclei separated from one another by a con- nective-tissue framework. These cells originate in part from the epithelial cells of the biliary passages, in part from the liver-cells. The tissue of an infiltrating carcinoma of the liver involves the interlobular connective tissue without sharp limitation, so that unless microscopic examination be made confusion with cirrhosis of the liver is possible. This variety of carcinoma occurs much less commonly than nodular carcinoma. Symptoms and Diagnosis. — In the diagnosis of carcinoma of the liver the demonstration of globular projections from the sur- face of the liver is almost of decisive significance. Such a condi- tion is naturally possible only when the new-growths are situated upon the surface of the liver. Carcinomata situated in the central portions of the liver are not accessible to diagnosis. Under favor- able conditions they may at best be suspected from the fact that the liver on palpation and percussion exhibits deep tenderness in circumscribed areas. As a rule, the carcinomatous projections from the surface of the liver can be detected only liy palpation, and but rarely can they also be seen if the abdominal walls are thin and deficient in fat. At times a depression or umbilication can be felt upon the surface of the growths, and in exceptional instances I have even seen this. The neoplastic nodules are often exceedinglv tender on palpation and on percussion. At times they are so soft as to exhibit fluctuation. Over highly vascular car- cinomata cardiac-systolic vascular murmurs may be audible. Of diagnostic significance is the respiratory mobility that the nodules exhibit together with the organ in which they are seated. Only when the liver has become greatly increased in size will the vigor of the diaphragm be insufficient to transmit the respiratory move- ment to the liver. With a liver the seat of extensive carcinoma- tous degeneration, not alone may the upper boundary of dulness begin unusually high, but also the lower boundary may extend into the small pelvis. Perihepatitic adhesions of the liver to the abdominal wall and to adjacent abdominal viscera may also pre- vent respiratory displacement of the liver. At the beginning of the disease it is highly important to palpate most carefidly the lower border of the liver throughout its entire extent, as it is just in this situation that carcinomatous nodules may be readily and dis- tinctly felt. Naturally, in doul)tful cases the surface of the liver will be examined repeatedly for projections. It is often possible in the course of the disease to detect newly forming nodules and to follow the growth of tliose already formed. In the differential diar/nosix it is important in the first place to determine that a tumor in the region of the liver is situated in CARCINOMA OF THE LIVER 347 that organ, and in the next place to decide as to its carcinomatous nature. In connection with the first point the respiratory dis- placement of the tumor is important, as this occurs in addition only in connection with tumors of the spleen, and generally not with tumors of the stomach, the kidneys, the intestine, or the mesentery. Besides, it should be noted whether the tumor is situated in the area of hepatic percussion-dulness, and whether it forms a continuous whole with this. The carcinomatous nature of a tumor of the liver will be rendered highly probable if the new-growth has developed spontaneously after the fortieth year of life, and has been attended with rapid emaciation. As compared with abscess of the liver, it should be noted that fluctuation is the rule when the accumulation of pus is situated superficially, while it is the excep- tion with carcinoma of the liver. Abscess of the liver is usually attended with febrile movement, while carcinoma of the liver is generally unattended with elevation of temperature. In addition, the etiology must be taken into consideration : carcinoma develops spontaneously, while abscess is preceded by traumatism, gall-stones, ulceration of the bowel or of the genitalia, or septicopyemia. Unilocular echinococcus of the liver likewise gives rise to a pro- jection from the surface of the liver, but, in contradistinction from that due to carcinoma, the former is attended with fluctuation, yields hydatid fremitus, and on exploratory puncture gives exit to clear watery fluid free from albumin, in which microscopic exam- ination discloses at times the presence of echinococcus-hooklets and echinococcus-scolices. Great difficulty may be encountered in the differentiation between carcinoma of the liver and multilocular echinococcus of the liver, as both diseases are attended with nodular enlargement of the liver, jaundice, and enlargement of the spleen. Multiloc- ular echinococcus of the liver is an exceedingly rare disease, and, therefore, in doubtful cases carcinoma of the liver will always be the more probable condition. The probability will be all the greater should the patient be of an age at which carcinoma is common and have become cachectic within a short time. In the differential diagnosis of carcinoma of the liver it is always of espe- cial importance if primary carcinoma be found in any other viscus. Gummatous nodules in the liver are not tender on palpation, and there must have been a history of previous syphilis. These tumors diminish and disappear upon treatment with mercurials and iodids. Should the liver be enlarged but present a smooth surface, the diagnosis of carcinoma of the liver will always be involved in doubt. Naturally, suspicion should invariably be aroused if jaun- dice develops in an elderly person without demonstrable cause, and if in the course of about four weeks this does not diminish, but rather increases in intensity, and if at the same time there should 348 DIGESTIVE ORGANS be rapid loss of strength. Jaundice is an exceedingly common, if not a constant, symptom of carcinoma of the liver, but I have noted its absence in a number of instances in which it would be most readily expected, namely, in the presence of carcinoma of the sail-bladder Avith extension to the liver. The development of jaundice in cases of carcinoma of the liver is explained by biliary stasis due to stenosis of the biliary passages in consequence of pressure exerted by the carcinomatous nodules. At times jaundice is de- pendent upon carcinomatous degeneration and enlargement of the portal lymphatic glands, with pressure upon the hepatic duct. The stools are frequently deficient in bile and clay-colored, though at times they retain their natural color, because the bile that enters the intestine is still sufficient to discolor the fecal mat- ter. It may also happen that periods in which the stools are free from bile alternate with those in which bile is present. A restor- ation of the lumen of the biliary passages is possible from the re- duction in size of the neoplastic nodules in consequence of fatty degeneration, so that the pressure exerted by them on adjacent structures varies. Among other sequelae of jaundice the patients often suffer in marked degree from itching of the skin — cutaneous pruritus — which especially disturbs rest at night and contributes materiallv to exhaustion. The skin is often the seat of extensive exanthemata and of bloody and encrusted fissures due to scratching. Enlargement of the spleen occurs in about one-tenth of all cases. Xot rarely abdominal dropsy — ascites — develops, and this may be due to various causes. At times it is dependent upon the general marasmus, and then there will also be cachectic edema of the skin of the lower extremities. In other instances the ascites is due rather to local causes and is unattended with edema of the extrem- ities. It may result from thrombosis of the portal vein, and from obstruction of the portal vein due to pressure exerted by enlarged carcinomatous lymph-glands in the transverse fissure. Carcinom- atous peritonitis, as a rule, gives rise to the same symptoms as ascites. It results from carcinomatous inoculation of the peri- toneum, and causes an accumulation of either serous or hemor- rhagic fluid, usually freely movable in the peritoneal cavity. Occasionallv excessive tenderness of the abdomen on manipulation is indicative of the presence of peritonitis. Whether the condi- tion be one of ascites or peritonitis, in either instance the presence of a large accumulation of fluid in the abdominal cavity may ren- der examination of the liver extremely difficult and even impossi- ble until the fluid has been withdrawn by puncture. Individuals suffering from carcinoma of the liver complain principallv of a sense of tension and a painful feeling in the right hypochondrium. Severe pain in the liver may also be present, such as is peculiar to almost all carcinomata, and is prone to occur par- ticularly at night. This may depend upon irritation of adjacent CARCINOMA OF THE LIVER 349 nerves. ' The appetite is generally wanting entirely ; the tongue is usually coated ; often the breath is fetid. The patients frequently exhibit eructation and vomiting in the absence of primary carci- noma of the stomach, and this may he attributed to the pressure exerted by the enlarged liver upon the stomach. In addition, in consequence of the cachexia the gastric juice is almost entirely deprived of its free hydrochloric acid, while the absorption-period of the stomach is prolonged and its motor activity is diminished. Occasionally the supraclavicular lymph-glands upon the left side are enlarsred and indurated, and sometimes also the inguinal glands. This condition may be associated with primary car- cinoma of the stomach, although I have observed glandular enlargement in connection with primary carcinoma of the liver also. As a rule, carcinoma of the liver is unattended with alteration in temperature. Nevertheless, there may be periods with elevation of temperature, and this may even assume a pro- nounced intermittent type. Definite statements as to the cJuration of carcinoma of the liver can hardly be made, as the disease begins most insidiously, and the time of its inception can scarcely be determined. In general a year may be stated to be the maximum duration, although death may occur much earlier from a rapidly growing neoplasm. Even when the disease sets in suddenly with jaundice it should not be forgotten that the jaundice has probably been preceded for some time by the development of carcinomatous tumors. Death may occur under most varied conditions. Often it is the result of jrrogressive ex- haustion. Occasionally evidences of blood-dissolution appear — hemorrhages into the skin and the mucous membranes, particu- larly also hemorrhage from the stomach (coffee-ground vomiting), in the absence of carcinoma of the stomach, and these may hasten the exhaustion. Occasionally the patients die rapidly in coma from carcinomatous intoxication, which may be dependent upon auto-intoxication. Excessive accumulation of fluid in the abdom- inal cavity may cause death by suffocation, but at the present day this can be averted by abdominal puncture — a less common occur- rence is rupture of a carcinomatous nodule through the abdom- inal wall or into the abdominal cavity, or into an adjacent organ, wdth its ofteu fatal consequences. Of less importance is extension of carcinoma of the liver along the round ligament to the umbil- icus, with the development of carcinoma and carcinomatous de- generation in this situation. It may be qttite difficult to discover the primary focus of disease. In any event a decision as to pri- mary carcinoma of the liver should not be reached too hastily, but stomach, rectum, uterus, esophagus, and mammary gland particu- larly should be carefully examined for a primary focus. Primary carcinoma of the stomach is often beyond recognition in the pres- ence of carcinoma of the liver, because the enlarged liver conceals 350 DIGESTIVE ORGANS the stomach and removes it from immediate examination, and the disturbances of gastric activity associated Avith carcinoma of the stomach (deficiency of hydrochloric acid in the gastric juice, de- layed absorption, enfeebled motor activity) may also be present in the absence of anatomic alteration in the stomach solely in conse- quence of the cachexia induced by carcinoma of the liver. I have even observed coffee-ground vomiting in several cases of carcinoma of the liver, while at the autopsy the stomach was found to be free from malignant disease. Prognosis. — The prognosis of carcinoma of the liver, like that of carcinoma elsewhere, is unfavorable. Although of late attempts have been made to remove new-growths of the liver by surgical means, but little good can be hoped for from operation in cases of carcinoma of the liver, because the lesion is almost always a secondary one, and only rarely are the conditions so favorable as to permit removal also of the primary neoplasm by operative measures. Treatment. — Xo specific remedy for the relief of carcinoma of the liver is known. Symptomatic treatment will include regu- lation of the diet, fats in particular being interdicted in the presence of jaundice. In other respects the treatment will depend upon particularly prominent symptoms that may be present. Among the remaining tumors of the liver, only sarcoma and adenoma are of clinical interest. Both varieties of new-growth give rise to the same symptoms as carcinoma of the liver, and are susceptible of differentiation only at autopsy, and at times only after microscopic examination of the tissue. Sarcoma of the liver, like carcinoma, is usually of secondary origin. Melanotic sarcomata occur at times in the sequence of sarcoma of the choroid, even though the diseased eye have been removed many years previously. Occa- sionally they give rise to melanuria, which is characterized by a brownish or blackish color of the urine when it is evacuated or after standing for a time, or on addition of oxidizing substances (chromic acid, dilute sulphuric acid, boiling with hydrochloric, sulphuric, or nitric acid). ECHINOCOCCUS OF THE LIVER. !Etioiv)g"y. — Echinococcus-cysts in the liver represent the measles of the tapeworm of the dog — Tcenia echinococcus. Echino- cocci are most readily acquired by those who come into frequent and intimate relation with dogs. Echinococcus is most prevalent in Iceland, where every seventh inhabitant is said to be the victim of the disease. Upon the Continent of Europe Pomerania and Mecklenburg are particularly notorious for the frequency with which echinococcus occurs among their inhabitants. The danger of infection is particularly great when the vicious practice of kiss- ing dogs is indulged in, or these animals are permitted to lick the hands or the face, for it is well known that dogs frequently lick tiie anus, so that it may readily hajipen that the ova of the Taenia echinococcus remain adherent to the snout, and they may, in the ECHINOCOCCUS OF THE LIVER 351 act of licking and kissing, become deposited upon the lips or gain entrance into the mouth of human beings. If, subsequently, with the ingestion of food echinococcus-eggs are swallowed by human beings, the ova, by means of their booklets, and probably by way of the gastric veins and the portal vein, pass from the stomach into the liver, where they develop into an echinococcus-cyst. In soiue instances they penetrate also into other viscera, although the liver is the organ most commonly invaded by echinococci. Another mode of infection for human beings consists in the inges- tion of echinococcus-ova with inadequately cleansed vegetables that have been contaminated by the feces of dogs containing such ova. Contamination of water also with the feces of infective dogs, and infection through the use of such water, may likewise take place. The especial frequency with which echinococcus-disease occurs in Iceland is due to the large number of dogs that are kept, to the intimate relation between the inhabitants and domestic animals, and to a lack of domestic cleanliness. Anatomic Alterations. — Echinococcus of the liver occurs in two forms — as a unilocular and as a multilocular echinococcus- FiG. 54.— Echinococcus-head, with retracted rostellum and crown of booklets ; magnified 275 times (personal observation, Zuricb clinic). cyst. The latter is an exceedingly rare condition that occurs with comparative frequency in Switzerland and in AVurtemburg. Unilocular echinococcus of the liver consists of a vesicle with a whitish, opaque, milk-glass-like wall, whose size may attain that of a man's head. It is usually possible to enucleate the cyst from the liver, leaving behind a connective-tissue capsule that has re- sulted in consequence of interstitial inflammation of the liver from the irritation exercised by the echinococcus-cyst upon the sur- rounding tissue. Incision of the echinococcus-cyst generally gives exit to a clear fluid. This resembles water, contains no albumin, but frequently succinic acid, and consequently on addition of a 352 DIGESTIVE ORGANS dilute solution of ferric chlorid assumes a brownish color. Not rarely small daughter-cysts are present in the fluid, and even in these granddaughter-cysts and greMt-gr and daughter-cysts, which may exhibit much the same })ecu]iarities as the mother-cyst. It is cliaractcristic of the echinococcus-niembrane that its cut margins become inverted. It may be readily recognized on microscopic examination from the fact that on transverse section it exhibits parallel lines or layers, which have been appropriately compared with the leaves of a book. Upon the inner surface of echino- coccus-cysts a glandular mass, the so-called germinal layer, is found as a rule. Upon this are situated brood-capsules with echiuococcus-heads (scolices), Avliich may be readily recognized from the presence of a rostellum and a crown of booklets and four suckers (Fig. 54). The booklets resist destructive influences for a long time, so that they are of great diagnostic significance. At times echinococcus-cysts occur without scolices — so-called sterile echi- nococcus-ci/sts or acephalocysts. Echinococcus-cysts may undergo suppura- tion. Often their contents are converted into a viscid, putty-like mass, in which echinococcus-hooklets are demonstrable. Although most commonly but one echinococcus-cyst is present in the liver, exceptions to this rule have been observed. Echino- cocci are most frequently seated in the right lobe of the liver. At times other viscera also, in addition to the liver, are the seat of echinococcus-cysts. Multllocukir echinococcus-cysts convert the liver into a multinodular, hard organ, which upon section exhibits numerous cysts or chambers filled with softened, pus-like, gelat- inous masses. Such alterations were formerly considered as due to soft carcinomata, from which, however, they can be distin- guished with certainty by the discovery in them of echinococcus- hooklets on microscopic examination. The condition is dependent upon the development of echinococci within previously formed vessels, most commonly the biliary passages and less commonly the portal vein or the lymphatics, and with the further develop- ment continually of new daughter-cysts side by side. Symptoms and Diagnosis. — Patients with unilocular echi- nococcHs of the liver complain frequently at first of a disagreeable' sense of tension and of fulness in the right hypochondrium, w hic^h may progress to marked pain. They experience a sense of con- striction, and suffer from dyspnea and palpitation of the heart. On examination, the liver is usually found enlarged, and its limits may be extended both above and below. It is, liowever, of ]iar- ticular importance to demonstrate the presence of a fluctuating prominence upon the surface of the enlarged organ, Mhich corre- sponds with the echinococcus-cyst. This naturally undergoes respiratory displacement with the liver. It is highly significant if the prominence yields hydatid fremitus on percussion. This consists in short-waved vibration, such as is yielded when a wire ECHINOCOCCUS OF THE LIVER 353 spring is tapped. The manifestation is, however, by no means frequently present. It is most distinetly appreciable if the per- cussion-hammer is permitted to rest upon the prominence for a few seconds following each blow, or if the middle three fingers of the left hand are placed upon the prominence, and the central one of these is percussed with a hammer or with the middle finger of the right hand. In rare instances the hydatid fremitus is asso- ciated wdtli a deep sonorous note on auscultation. In the differential diagnosis from other fluctuating prominences upon the surface of the liver, soft carcinomata and abscess of the liver particularly should be borne in mind. Carcinoma of the liver, however, occurs only in advanced life, is attended with rapid emaciation, and is usually associated with the presence of primary carcinoma in some other viscus ; while abscess of the liver is attended with fever, and the etiologic factors (gall-stones, ulcer- ation in the intestine and the genito-uriuary apparatus, septico- pyemia) should be taken into consideration. Exploratory punctm'e is an extreme means of differentiation, yielding in the case of echinococcus of the liver a clear, colorless, watery fluid, contain- ing no albumin, but booklets, and possibly even scolices and suc- cinic acid. Whenever possible, exploratory puncture should be avoided, as the contents of the cyst may readily leak into the abdominal cavity through the orifice of puncture, so that septic peritonitis may result, or, what is less dangerous, symptoms of auto-intoxication may appear in the form of widespread urticaria. At times sudden death has followed exploratory puncture, and this likewise has been attributed to auto-intoxication. Naturally, it will be possible to feel fluctuating prominences dis- tinctly upon the surface of the liver only when the echinococcus-cyst is applied directly to the abdominal wall. The conditions are less simple when the tumor is covered by the thoracic wall, although it may be that the cyst is applied to the wall with such j)ressure as to cause enlargement of some intercostal spaces, while those above and below are crowded together, and a visible projection fornia externally, which may yield fluctuation and hydatid fremitus. Occasionally echinococcus-cysts are situated in the neighborhood of the upper border of the liver, and are thus inaccessible to the eye and the hand. They can then be demonstrated only by care- ful determination of the upper border of the liver, which suddenly deviates from its horizontal course, and makes a marked, usually hemispherical deflection upward into the thoracic cavity. In con- tradistinction from encapsulated pleural exudates and subphrenic collections of pus, this projection will exhibit respiratory displace- ment. Here also exploratory puncture would be decisive in doubtful cases. All other manifestations attending echinococcus of the liver are rather of accidental and therefore of subordinate importance. Among these may be included jaundice, which de- 23 354 DIGESTIVE nncANS volops when pressure is exerted upon the larger hiliary passages; uacitcs, in consequence of pressure upon the trunk of" the portal vein ; and c/astro-intestinal disturbances, as a result of the crowding of the abdominal contents. The ilanger from a unilocular echinococcus-cyst of the liver depends [)rineipally upon its tendency to continued r/roicth. In consequence the diaphragm, the lungs, and the heart may be so greatly displaced upward that death will result from suffocation. Not rarely rupture of the echinococcus-cyst occurs into adjacent organs. It may take place into the stomach, as will be indi- cated by the vomiting of echinococcus-vesicles. Should rupture occur into the intestine, the urinary passages, or, after pre- vious adhesion between the lungs and the diaphragm, into the bronchial tubes, echinococcus-vesicles will appear in the stools, the urine, or the expectoration respectively. The expectoration under such conditions acquires a penetrating, aromatic odor, sug- gestive of prune-juice. At times it is also characterized by a red color, in consequence of the abundant presence of hematoidin- crystals. Rupture into the peritoneum, the pleura, or the peri- cardium will be followed by peritonitis, pleuritis, or pericarditis. Rarely rupture takes place into the hepatic veins or the inferior vena cava. Under such conditions echinococcus-vesicles may gain entrance into the right heart and the pulmonary artery, and cause sudden death from embolism of this artery. Rupture through the abdominal walls has also been observed. Should suppura- tion take place in an echinococcus-cyst, symptoms will appear sim- ilar to those of abscess of the liver, and often the nature of this collection of pus Avill be explained only by the discovery in it of echinococcus-hooklets. Echinococcus-cysts situated not upon the surface of, but within, the liver may be inaccessible to diagnosis during life. Under favorable conditions a probable diagnosis might be made in tlie presence of enlargement of the liver for which no other cause can be ascertained. The course of a itni- locular echinococcus-cyst of the liver is usually chronic, and may extend over several years. MultUocular ecltinococeus of the liver is generally attended with profound jaundice and enlargement of the spleen. The liver itself is enlarged, and feels unusually hard and nodular. The disease mav readily be confounded especially with carcinoma and with hvpertrophic cirrhosis of the liver. Carcinoma of the liver, how- ever, usually develops late in life, and in association with primary carcinoma in some other viscus ; and hypertrophic cirrhosis of the liver with jaundice is generally attended with increase in the size of the liver, with preservation of the smoothness of its surface. Death occurs generally with ]>rogressive exhaustion, but at times onlv after tlie lapse of more than ten years. Prognosis. — The prognosis of echinococcus of the liver is DISPLACEMENTS OF THE LIVER 355 under all conditions serious. It has recently been rendered less unfavorable for unilocular cysts, from the fact that cysts have been successfully removed by operative intervention. Treatment. — Prophylactic measures include domestic cleanli- ness, treatment directed to the expulsion of the Taenia echino- coccus in dogs, and the avoidance of licking by dogs. The kissing of dogs may be followed by most serious dangers. If echiuococcus-cysts have developed in the liver, they should be removed by operation. Recently atrophy of the cysts has been induced by injections of mercuric chlorid. Internal remedies (po- tassium iodid, ether) and affusions of a solution of sodium chlorid have been unattended with success. In the presence of a miilti- locular echinococcus of the liver, there is scarcely any other remedy than the relief of especially threatening or troublesome symptoms by the usual measures. Further, a large portion of diseased liver has in one instance been successfully removed by operative means. DISPLACEMENTS OF THE LIVER (HEPATOPTOSIS), In women who have borne children the liver is not rarelv found displaced downward and unduly mobile. Obviously relaxa- tion of the suspensory ligaments of the liver and of the abdominal walls is the cause of this condition. Enlargement of the liver, as a result of stasis, of fatty or amyloid degeneration, of the pres- ence of parasites or of neoplasms, is also capable of causing down- ward displacement of the liver in consequence of the increased weight of the organ. At times, however, the condition appears to be dependent upon congenital iceahness of the suspensory liga- ments of the liver, or such weakness may be acquired as a result of severe or protracted disease. Nervous influences also are of sig- nificance. Bodily over-exertion, expulsive efforts, and constric- tion by clothing favor the development of the condition. The degree of displacement of the liver is susceptible of great varia- tion. In aggravated cases the liver may be found in the pelvis, and in place of the normal hepatic dulness at the base of the right chest anteriorly a tympanitic percussion-note is obtained from the presence of intestine, and this will disappear when the liver is replaced in its normal situation. Such a condition is designated as movable or ivandering liver. Further, in forming an opinion as to the identity of a foreign body in the abdominal cavity from its shape great care must be observed, as errors have been made in mistaking a movable body in the abdomen for a wandering liver, while the autopsy has disclosed carcinoma of the omentum. It is especially important if one or two incisures (for the gall-bladder and the round ligament) are found in the lower border of the liver. At times the stretched round ligament also may be pal- 356 DIGESTIVE ORGANS pable tliroiigh the abdominal wall. Occasionally wandering liver is detected accidentally upon examination of the abdomen. If the patient on palpating the abdomen ha.s, perhaps, accidentally discovered the presence of a movable body, he is often so greatly distressed by the fear that the condition is due to a malignant neoplasm that a positive and reassuring opinion on the part of the phvsician will be required to convince the patient that the state of affairs is not serious. Some patients complain of a dis- agreeable, at times also painful, sense of traction and tension in the abdomen, and gradually become nervous and hysterical. Derangement of intestinal activity also may develop if loops of bowel are compressed or distorted. The prognosis is favorable with regard to life if the condi- tion is not dependent upon tumors or parasites, although it is often impossible to eifect a permanent cure. The treatment must generally l)e mechanical, attempts being made by means of abdominal bandages applied to the lower half of the abdomen to exert pressure upward, and thus to force the liver into its normal situation. Massage of the abdomen also ap- pears worthy of recommendation. Further, attention should be given to the general condition. Congenital displacement of the liver may occur in association with trans- position of the viscera. Under such conditions the liver will be situated in the left, and the spleen in the right concavity of the diaphragm. The dis- placement may involve only the liver and the spleen. As a rule, however, the remaining organs of the thoracic and abdominal cavities are correspond- ingly displaced. The condition is unattended with discomfort or danger. CONSTRICTED OR FISSURED LIVER. Constricted or fissured liver may result from tight lacing. The fissure formed is generally horizontal, and within it the serosa covering the liver is thickened, tendinous, and opaque. Beneath the fissure the liver-tissue may be entirely wanting, so that a por- tion of the liver may be completely constricted off. Often the latter is thickened and exhibits signs of blood-stasis. Most commonly the lowermost portion of the right lobe of the liver is constricted off, although at times the fissure may extend with- out interruption into the left lobe. Often the condition remains latent throughout life if the lower border of the liver does not extend considerably below the costal margin. Under other con- ditions a horizontal depression may be palpable upon the lower portion of the surfiice of the liver beneath the al)dominal wall. Below this depression the constricted portion of liver appears thickened, and at times can be reflected upward. Care must be taken to avoid confusion especially with a syphilitic lobulated liver. The condition is unattended with dano-er. Internal treat- CATARRH OF THE BILIARY PASSAGES 357 ment is unnecessary, and would also yield no result. Of late the constricted portion of the liver has been removed by operation in a number of instances. DISEASES OF THE BILIAKY PASSAGES. CATARRH OF THE BILIARY PASSAGES (CATAR- RHAL CHOLANGITIS AND CHOLECYSTITIS), Btiology. — Catarrli of the biliary passages is an exceedingly common disorder, and is induced particularly by infectious or toxic influences. Most commonly it is secondary to catarrli of the gas- troduodenal mucous membrane, the inflammatory process extending directly from the mucous membrane of the duodenum to that of the choledoch duet, and the more remote biliary passages. At times catarrh of the biliary passages arises in the sequence of acute or chronic infectious diseases, as, for instance, fibrinous pneu- monia, typhoid fever, erysipelas, pharyngeal diphtheria, and syph- ilis. Occasionally catarrh of the biliary passages occurs as an independent infectious disease. Of this character were especially certain epidemics of jaundice that have at times been observed in over-crowded dwellings (barracks, prisons), in the secpience of re- vaccination and the ingestion of spoiled food and drink. A num- ber of such epidemics have occurred particularly in the autumn months. At times children were attacked in especially large numbers. Among the toxic catarrhal staten of the biliary passages, that following phosphorus-poisoning should be mentioned particu- larly. This may, however, leave the larger biliary passages intact, and attack only the smaller intrahepatic biliary passages. The hypostatic catarrh of the biliary passages that occurs particularly in association with chronic disease of the heart and the respiratory organs is worthy of mention. AYhether circulatory and catarrhal alterations in the biliary passages are operative in connection with the jaundice that appears in some women shortly before and during the menstrual period — so-called menstrual icterus — is as yet unex- plained. Xot rarely gall-stones cause catarrh of the biliary pas- sages. Obviously the mechanical irritation of the mucous mem- brane of the biliary passages h\ the calculi is particularly favora- ble to the deposition of micro5rganisms, most commonly the Bac- terium coli, upon the mucous membrane, with the development of an inflammatory process. Not rarely diseases of the liver are at- tended with catarrh of the biliary passages, often because by causing obstruction of the biliary passages they give rise to biliary stasis, and the latter may be followed by inflammation, as under such circumstances bacteria readily gain entrance into the biliary passages, particularly the Bacterium coli. 358 DIGESTIVE ORGANS Anatomic Alterations. — In tlie presence of catarrli in the large hiliarv ducts the discliarge of bile is not rarely prevented by a p/«<7 of vnicus. At times, however, the phig has been forced into the intestine, so that its previous existence can only be recog- nized from the fact that the biliary passages are discolored only up to the point previously occupied by the plug, Avhile they are unstained for the remaining distance to the intestine. The raucous membrane is often conspicuous by reason of swelling and marked secretion of mucus. Stenosis of the biliary passages has given rise to biliary stasis, and thereby to the icteric manifestations in the liver and the remaining viscera that have been described on pp. 321 and 322. Catarrh of the intrahepatic biliary passages can be demonstrated in the smaller biliary channels only Avith the aid of the microscope, active desquamation of the epithelial cells j^ar- ticularly being found. Symptoms, Diagnosis, and Prognosis. — Catarrh of the biliary passages can be recognized only when in consequence of the formation of a plug of mucus and tumefaction of the mucous membrane, biliary stasis and hypostatic and resorptive icterus have developed, and which, from the nature of the causative factors, is also designated catarrhal jaundice. The symptoms are identically those that have been described on pp. 317—321 in the general con- sideration of jaundice, and in the diagnosis the essential point is to determine Avhether catarrh of the biliary passages is responsible for the jaundice. In this connection the history and the results of physical examination of the viscera are of great importance. Often previous dietetic error, nausea, vomiting, constipation, or diarrhea will leave no room for doubt that catarrh of the biliary passages has been preceded by gastroduodenal catarrh, and the condition is then designated gastroduodenal jaundice. When primary infectious catarrh of the biliary passages is present the pronounced involvement of the general condition is often striking. The liver and particularly the spleen are consideraljly enlarged. It is just in this variety of catarrh of the biliary passages that cholemia may readily develop, and death take place. The dura- tion and the course of catarrhcd jajindicc depend upon the caus- ative factors. Recovery from gastroduodenal jaundice usually takes place within one or two weeks, while the jaundice accom- panying incurable diseases of the liver persists until death. Also the prognosis depends naturally upon the character of the causative factors. Treatment. — In the first place, on account of the existing biliary stasis and jaundice the diet and the state of the bowels should be regulated in accordance with the rules laid down on pp. 322 and 323. Should the disorder be secondary to gastro-intestinal catarrh, the employment of acids is advisable. Attempts have been made, further, to cause expulsion from the biliary passages of pes- PUR ULEXT INFLAMMATION OF THE BILIARY PASSAGES 359 sible accumulations of mucns by pressure with the fingers upon the dilated gall-bladder not rarely distended Ijy accumulated bile, or by inducing contraction by means of the faradic current. It has been stated that as a result of this manipulation a gurgling murmur is appreciated, after which the biliary passages have become again patulous. Particularly troublesome symptoms of jaundice will require the treatment described on pp. 322 and 323. PURULENT INFLAMMATION OF THE BILIARY PASSAGES (PURULENT CHOLANGITIS AND CHOLECYSTITIS)* Purulent inflammation of the biliary passages scarcely occurs apart from the influence of bacteria, and according to previous ex- perience particularly of the Bacterium coli commune, the Strepto- coccus pyogenes, the Staphylococcus pyogenes albus and aureus, the pneumoniacoccus, and the typhoid-bacillus. The condition is usu- ally a secondary disorder, occurring particularly in connection with the presence of gall-stones or parasites in the biliary i^assages, and with infectious diseases, as, for instance, in the sequence of typhoid fever, and occasionally also after abscess of the liver and pylephle- bitis. Anatomically the disorder is characterized by inflammation of the mucous membrane of the biliary passages, with the presence of pus. Occasionally the gall-bladder particularly is filled ^vith pus, and distended thereby, the condition being designated empyema of the gall-bladder. The disease is exceedingly difficult of recog- nition. Particular diagnostic significance should be attached to the etiologic factors. In addition there will be the clinical picture of general septicopyemia (fever, enlargement of the spleen, meta- static inflammation in other organs, occasionally ulcerative endo- carditis). Of importance naturally are local alterations in the liver and the biliary passages, among which enlargement of the liver, jaundice, tenderness, and, in the presence of empyema of the gall- bladder, the demonstration of the enlarged gall-bladder, with tenderness on pressure, may be mentioned. The prognosis is grave, as death may result from septico- pyemia, or metastatic su])puration, or rupture of the biliarv ducts into the liver, with the formation of a liver-abscess ; into the portal vein or the hepatic veins ; into the abdominal cavity, with rapidly fatal peritonitis ; or into some other internal organ ; or through the abdominal wall in the presence of empyema of the gall-bladder. In tlie last-named event a biliary fistula may develop, from which occasionally numerous gall-stones are evacuated for a long time. The treatment of empyema of the gall-bladder is surgical. The gali-l)ladder should be opened — cholecystotomy — and pus and gall-stones evacuated ; or it should perhaps be entirely removed — cholecystectomy — tlie latter particularly when the wall of the gall- 360 DIGESTIVE ORGANS bladder is the seat of profound ulceration and alteration. Should the suppurative inflammation involve rather the biliary passages, it may also become necessary to expose these, to incise them, and evacuate the calculi — choledochotomy ; otherwise the only other remedy available Mould l)e to .sustain the strength of the patient as well as possible by means of the administration of large amoimts of alcohol, and to employ disinfectants, among which sodium salicylate (1.0 — 15 grains — every two hours) and salol (1.0 — 15 grains — every two hours) may be recommended. In addi- tion a hot cataplasm should be applied over the liver. DROPSY OF THE GALL-BLADDER. The conditions for the development of dropsy of the gall- bladder are provided whenever permanent occlusion of the cystic duct has been brought about. This occurs most commonly in the presence of gall-stones, either because a gall-stone has become impacted in the cystic duct or because in its progress it has injured the, wall of the duct, so that subsequently adhesions form at the site of injury. Under such conditions the bile is gradually ab- sorbed from the obstructed gall-bladder, while a colorless mucoid fluid takes its place. The amount of fluid may reach 40 quarts, so that the gall-bladder becomes correspondingly enlarged. Among the most important symptoms of dropsy of the gall- bladder is the presence of enlargement of the gall-bladder. The gall-bladder may be visible to the eye M'hen the abdominal wall is thin, and under other circumstances it may be palpable as a tensely distended, smooth, pear-shaped tiuuor. From a diagnostic point of view it should be borne in mind that the tumor undergoes respiratory displacement Avith the liver, is situated at the lower border of the liver, and that above it an incisure may be recog- nized, and that the dulness to which it gives rise passes over immediately into that of the liver. At times I have observed diagnostic difficulties to arise from the lodgment of the trans- verse colon between the lower border of the liver and the lower extremity of the gall-bladder, so that the tumor to which the latter gave rise was separated from the hepatic dulness by a tym]>anitic zone. Further, the tumor had the siiape of the kidney, and was readily movable in the abdominal cavity. Slight enlargement of the gall-bladder scarcely occasions discomfort, and at most may cause alarm in a patient who accidentally discovers the presence of a tumor in the abdominal cavity, and considers it carcinomatous. Excessive dropsy of the gall-bladder causes a sense of tension and pain in the region of the liver, and by displacement of the contents of the abdominal cavity may give rise not only to gastro-intestinal disturbances, l)ut, by displacement of the diaphragm upward, also to dyspnea, palpitation of the heart, and danger of suffocation. PARASITES IN THE BILIARY PASSAGES 361 Only surgical treatment is available. Puncture of the gall- bladder is not free from danger, because the contents of the viscus may escape into the abdominal cavity and give rise to fatal peri- tonitis. Incision of the gall-hladder — cholecystotomy — is attended with the possibility that fluid may reaccumulate in the gall-blad- der. Therefore recovery can be l)rought about most certainly by extirpation of the gall-bladder — cholecystectomy. CARCINOMA OF THE BILIARY PASSAGES, Carcinoma of the biliary passages is situated most commonly at the mouth of the choledoch duct or in the gall-bladder itself. Car- cinoma at the mouth of the choledoch duct gives rise to chronic jaun- dice, which usually terminates fatally with progressive exhaustion, and the cause of which is, as a rule, not recognized during life. Carcinoma of the gall-bladder gives rise to the development of a nodular, usually painful, and frequently extensive tumor, situated in the region of the gall-bladder, usually appearing as a pear- shaped swelling, and undergoing respiratory displacement with the liver. The percussion-dulness of the liver and that of the tumor are continuous. Frequently, but by no means constantly, jaundice is present. Often the neAv-growth extends to the liver, and a secondary neoplasm develops in this organ, ^vliich may attract the greater amount of attention. Death will probably occur within a year amid excessive asthenia. Like carcinoma in other organs, similar disease of the biliary passages usually occurs after the fortieth year of life. The causative factors remain, as a rule, un- recognized. The frequent association with gall-stones suggests that mechanical irritation may excite the development of car- cinoma. Nevertheless, the gall-stones may also have developed secondarily in consequence of biliary stasis. The significance of the gall-stones appears naturally to be supported by the fact that in cases of secondary carcinoma of the gall-bladder calculi do not occur in this viscus. The prognosis is unfavorable, as with carcinoma in other situations. Recently carcinoma of the gall-bladder has been suc- cessfully removed with the knife in a number of cases. Beyond such measures, symptomatic treatment alone will be applicable. PARASITES IN THE BILIARY PASSAGES. Parasites in the biliary passages are rare. Echinoeocci have already been mentioned in the consideration of multilocular echino- eocci of the liver. Flukes — Distoma hepaticum and Distoma lanceo- latum — may cause jaundice, purulent inflammation of the biliary passages, and suppuration in the liver, and are susceptible of recog- nition only when parasites or their ova are present in the stools. 362 DIGESTIVE ORGANS At times a sjjool-worm — Ascaris kimbricoides — may wander from the intestine into the biliary passages and eanse obstruction and jaundice, and at times suppuration in tlie liver or the formation of gall-stones. GALL-STONES (CHOLELITHIASIS;, Ktiology. — Extremely little of a definite nature is known as to the causes of gall-stones. Experience has shown that all those conditions favor the formation of gall-stones that cause biliary stasis. These include a sedentary mode of life and constrict- ing clothing. Thus, gall-stones have been frequently found in association with constricted liver. Further, they occur about four times as frequently in women as in men. What influence food may exert is unknown. If obesity predisposes to the formation of gall- stones, it is possible that biliary stasis is principally also the actual etiologic factor, as a result of the crowding in the abdom- inal cavity in consequence of the excessive fat in the omentum and the mesentery. Why gall-stones should be more common in certain regions than in others is as yet unexplained. Children but rarely suffer from gall-stones, which generally develop after the thirtieth year of life. Anatomic Alterations. — Gall-stones develop most com- monly in the gall-bladder, and much less commonly in the intra- hepatic biliary passages. Gall-stones in the hepatic duct, the cystic duct, or the choledoch duct have always migrated from the gall-bladder or the liver. Gall-stones consist either of bilirubin and lime-salts or of cholesterin, or they may be of mixed composi- tion, either layers of bilirubin and lime-salts and cholesterin alternating M^ith each other on cut section, or the one constituting the nucleus or the outer layer of the calculus. Bilirubin-calculi are brownish in color, while cholestcrin-calculi are white, upon section present a crystalline appearance with a radiate arrange- ment, and yield a greasy sensation to touch. Rarely, biliary calculi consist of calcium carbonate. They are whitish in color, and are characterized by great hardness. According to the size of biliary precipitates, a distinction is made between biliary sand and biliary calculi. The former possesses the character of sand and may attain the size of a pin-head. The size of gall-stones depends principally upon their number, for the more numerous the stones the smaller must they be. At times the entire gall-bladder is occupied by a single gall-stone, measur- ing several centimeters in length and reproducing the pear-shape of the gall-bladder. At times two or more gall-stones are present in the gall-bladder, and these may be in contact by a sort of articular surface. The number of gall-stones may reach many GALL-STONES 363 hundreds, and even thousands. Often, gall-stones that lie side by side in considerable number acquire peculiar shapes. They have been designated facetted gall-stones, and have been appropriately compared with the shape of the carpal bones. These peculiarities are not dependent, as has been supposed by some, upon the mutual attrition of adjacent angles and surfaces, but upon a failure in development at such points as contiguous stones, which originally possess a roundish shape, lie in contact. Such gall-stones generally exhibit extremely smooth surfaces, as if polished. In contradis- tinction from these there occur also globular calculi, with a multi- nodular surface, and these have been designated mulberry -calculi. Opinions are divided as to the mode of origin of gall-stones. In any event, the view is to be rejected that bilirubin or cholesterin is present in the bile in such excessive amount as not to be retained in solution, but to be precipitated. As experience has shown that biliary stasis favors the formation of gall-stones, there is much in favor of the view that the primary impulse in the formation of gall-stones is to be referred to bacteria, which, in the presence of biliary stasis, may readily gain entrance from the intes- tine into the biliary passages. In the first place, the Bacterium coli com- mune will suggest itself, because it is a constant inhabitant of the intestine. The bacteria excite catarrhal inflammation of the mucous membrane of the biliary passages, and for this reason some clinicians have employed the designation calculus-forming catarrh. The inflammatory products exert a decomposing influence upon the biliary acids, and as the biliary salts retain bilirubin and cholesterin in solution in the bile, these substances are pre- cipitated when decomposition of the biliary salts takes place. The precipi- tated constituents of the gall-stones do not simply crystallize together, but are held together by an organic mass. This material can be demonstrated when gall-stones are carefully dissolved. In some instances gall-stones have been found to develop around foreign bodies (prune-stones, blood-clots, ascarides). Symptoms and Diagnosis. — Many more persons suffer from gall-stones than is generally believed, because often the cal- culi are latent and occasion no symptoms. At times gall-stones are discovered accidentally, the gall-bladder, upon examination for some other cause, being found to be not only enlarged, but also filled with gall-stones. The latter will be recognized as hard, polyhedral bodies, which not rarely can be rubbed against one another with a palpable crackling sound, and yield the same sen- sation as when a bag filled with small pebbles or nuts is manipu- lated between the fingers. In cases in which the diagnosis was doubtful a sterilized needle has even been introduced into the gall-bladder, and observation made whether a hard body was en- countered with the point of the instrument. Rarely, the presence of gall-stones is disclosed by their passage through the biliary ducts without inducing symptoms, and their discovery accidentally in the stools. Gall-stones often give rise to hepatic colic. This results from the escape of the calculi from the gall-bladder, and their passage through the biliary ducts into the 364 DIGESTIVE ORGANS intestine. Under such conditions they readily become impacted in the biliary ducts, causing biliary stasis and pain, and giving rise to the clinical picture of hepatic colic. Calculi from the intrahepatic biliary ducts do not give rise to hepatic colic in their passage into the intestine, as they traverse channels that in com- parison with their site of origin become progressively larger as the intestine is approached. Frequently no especial causes for the occurrence of biliary colic are demonstrable, while in some instances anger and other emotional disturbances, bodily concus- sion, or physical over-exertion has been an antecedent condition. jNIenstruation, pregnancy, and the puerperium without doubt also favor the occurrence of attacks of hepatic colic. The principal symptom of biliary colic is pain. This is at times confined strictly to the region of the gall-bladder (exter- nal border of the right abdominal rectus muscle, just below the right costal margin), although it often radiates throughout a larger area, particularly toward the epigastrium, the right scapular region, and often also to the right arm. The pain increases par- ox vsmally to an unbearable degree, so that the patients cry aloud and groan, exhibit a painful and anxious expression, and are cov- ered with perspiration. Occasionally, there may be loss of con- sciousness and general clonic muscular spasm, obviously because the pain causes reflex spasm of the cerebral arteries, and thereby cerebral anemia. A chill likewise is not rarely induced by reflex influences, and this may be repeated several times. Vomiting also is a frequent svnqjtom dependent upon reflex influences. Often elevation of temperature takes place, although I would not attrib- ute this to nervous influences, but to inflammation of the biliary passages, and would consider it an indication of septic general in- fection. The occurrence of jaundice is of great importance, develop- ing on the average in the course of three days, as this length of time is necessarv for the blood to become sufticiently saturated with biliary coloring-matter in order to stain the skin and the mucous membranes yellow. The degree of jaundice varies ex- tremelv ; at times there is but slight yellowish discoloration of the conjunctivae. The jaundice naturally persists for some time after the attack of hepatic colic, until the biliary coloring-matter has been removed (principally through the urine). It is noteworthy that when the choledoch duct is obstructed bv a gall- stone enlargement of the gall-bladder in consequence of biliary stasis takes place but seldom. The duration of an attack of hepatic colic is susceptible of great variation, and fluctuates between a few hours and as many weeks. In the latter event the patients are never free from pain, although this at times becomes more severe. Under such conditions they . GALL-STONES 365 not rarely lose strength in an alarming degree. There are also great variations in the recurrence of attacks of hepatic colic. One must be prepared for this if gall-stones have not been found in the stools, in spite of the fact that these have been thoroughly dis- solved upon a sieve in a stream of water. To obtain assurance upon this point the stools must be continuously examined for at least a week after the pain has disappeared, as biliary calculi may remain for some time in the intestine. Gall-stones naturally will not be found in the stools if they slip back into the gall-bladder. The occurrence of facetted biliary calculi in the stools will justify the anticipation of recurrent attacks of hepatic colic, because such calculi are usually multiple in the gall-bladder. It is^ further, noteworthy that biliary calculi in the stools must by no means always have passed through the biliary passages, and it appears to occur not at all rarely that they give rise to iuflammation of the biliary passages and adhesions to the bowel, particularly the transverse colon, and then after perforation gain entrance into the bowel through a biliary-intestinal fistula. When gall-stones have entered the bowel the clanger is not always passed, for occasionally they may occupy the lumen of the intestine in such a peculiar manner, or a number of stones may be joined together by fecal matter into so large a mass, as to cause obstruction of the bowel and the development of ileus. In rare cases gall-stones in the cecum or the vermiform appendix give rise to typhlitis, appendicitis, perityphlitis, or paratyphlitis. Occasionally biliary calculi become so firmly impacted in the cystic duct or the choledoch duct that they cannot be moved either forward or backward. Such impaction of gall-stones is attended with the danger of inflammation, pressure-necrosis, and perforation of the gall-stones into the abdominal cavity, and this will gener- ally be followed by rapidly fatal peritonitis. Attacks of hepatic colic are not always attended with such readily recognized mani- festations as have been described. Occasionally they give rise to vomiting so severe and persistent as to arouse suspicion of ulceration of the stomach. At times, also, the pain is situated in the epigastric region, and this would appear to strengthen the suspicion of gastric ulcer. In other instances pain in the scapular region, about the right side of the chest, or along the right arm is such a conspicuous feature that gall-stones may be confounded with neuralgia. At times chills recur daily at the same hour, and the clinical picture is suggestive of intermittent fever, althougli malarial plasmodia are not found in the blood. If the pain radi- ates actively into the right iliac fossa, care will be necessary to avoid confusion with perityphlitis. In all doubtful cases attention should be directed to the occurrence of jaundice, which naturally often occurs in slight and scarcely appreciable degree. 366 DIGESTIVE ORGANS 111 addition to liepatic colic and its consequences, biliary calculi not rarely excite inflammatory alterafions in the biliary pa.s.s-ayr.s, suppuration and septicopyemia, and it is often exceedingly difficult to recognize them under such conditions. I have observed ulcera- tive endocarditisi, otitis media, and inflammation of the cerebral sinuses develop in the sequence of cholecystitis due to gall-stones. Occa- sionally abscess of the liver develops as a result of gall-stones. Also at times the gall-bladder becomes attached by adhesions to adjacent organs (stomach, intestines, urinary passages), ruptures into these, and evacuates its calculous contents into them, so that gall-stones may l)e vomited or be found in the urinary bladder. Occasionally adhesions to the abdominal wall form, with rupture of the gall-bladder externally, and at times numerous gall-stones are evacuated through the resulting external bilary fistula for a considerable length of time. Rupture of gall-stones into the lungs and the bronchi has also been observed. Pericholecystitis is a common sequel of gall-stones. Gall-stones may j^ersist at times throughout life. Only rarely is the disease terminated with a single attack of hepatic colic. Prognosis. — Hepatic colic is a serious condition under all circumstances, being attended M"ith numerous dangers, whether the calculi exhibit a migratory or a sessile tendency. It should not be forgotten in this connection, however, that gall-stones may excite the development of carcimoma in the gall-bladder. At times, also, connective-tissue hyperplasia develops in the neigh- borhood of the biliary passages within the liver, and gives rise to biliary cirrhosis of the liver. Treatment. — Patients with gall-stones generally seek profes- sional assistance at the time of an attack of hepatic colic, and for the relief of which the following measures may be adopted : Patients should remain in bed and apply a hot poultice over the region of the liver. They should partake of liquids only, such as weak tea, milk, and wine, diluted with water. If the pain is severe, a suhcutaneous injection of morphin should be given : R Morphin hydrochlorate, 0.3 (4-2 grains), Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose: From 0.25 (4 minims) to 0.5 (8 minims) subcutaneously. The patient should never be entrusted with morphin and a syringe for use upon himself because the danger and the tempta- tion are too gr^at to make injections when not necessary, and gradually to employ larger doses of the drug, and finally to become a morphin-habitue. Daily rectal injections of water at room-tem- perature may l)e recommended, as stimulation of intestinal peri- stalsis a})pears to favor the passage of the gall-stones through the biliary channels. GALL-STONES ■ 367 Enemata of oil have been advised by some physicians. Olive-oil (180.0 — 6 fluidounces) internally and glycerin have been recommended to facilitate the passage of gall-stones and for the relief of attacks of hepatic colic. "When an attack of biliary colic has been successfully relieved, efforts should next be made to effect solution of gall-stones still present, and to prevent the formation of new calculi. Oil of tur- pentine and ether in the form of Durande's remedy especially have been recommended as a solvent : B Oil of turpentine, 5.0 (75 minims), Ether, _ _ 20.0 ( 5 iuidrams).— M. Dose : 20 drops four times daily, A solvent action by this mixture can naturally be expected only upon cholesterin-calculi. JSTevertheless an undeniable effect upon bilirubin-calculi also is at times observed, but under such conditions the result must be attributed less to a solvent action than to the circumstance that the remedy stimulates the secretion of bile. Sodium salicylate acts in the same way : R Sodium salicylate, 1.0 (15 grains). Make 10 such powders. Dose : 1 powder thrice daily after eating. The administration of bile and its sodium-combination also favors the secretion of bile, and may be advised in the treatment of gall- stones. Courses of treatment with the waters at springs are much employed, particularly at Carlsbad, Marienbad, Tarasp, Kissingen, Homburg, Ems, Wiesbaden, and Vichy. That these waters are capable of exerting a solvent effect has not been demonstrated ; they do, however, influence favorably the catarrhal conditions of the gastro-intestinal mucous membrane and the biliary pass- ages, and in this way may prevent the formation of gall-stones. Persons in moderate circumstances may, with the same object in view, use artificial Carlsbad salt for periods of four weeks : R Artificial Carlsbad salt, 100.0 (3 ounces). Dose : 1 teaspoonful in a pint of tepid water, to be taken in four equal parts at intervals of ten minutes. Persons suffering from gall-stones should take considerable exer- cise, not wear constricting clothing, secure a daily evacuation of the bowels, and avoid all conditions capable of causing biliary stasis. Recently the operative treatment of gall-stones has occupied attention. Surgical intervention will be justified in the presence of impaction of a gall-stone in a biliary duct. With this end in view the abdomen should be opened, the stone located in the biliary duct, and an attempt made by gentle pressure to force its entrance 368 DIGESTIVE ORGANS into tlie intestine or the gall-bladder, or to crush it between the fingers — cholelithotripsy. Otlierwise, it would be necessary to incise the bile-duct — choledochotomy — extract the stone, and suture the margins of the wound. At times inn^acted calculi remain in situ without exciting inflammation, although the chronic hypo- static jaundice gives rise to alarming emaciation. Under such cir- cumstances choleci/denterostomy has been performed ; that is, an artificial communication has been established between the gall- bladder and the highest possible loop of small intestine. It may happen, of course, that the biliary passages are infected with bac- teria from the intestine, and become inflamed. Should there be a marked tendency to the formation of gall-stones, and should attacks of hepatic colic occur with such frequency as to make the life of the patient miserable, or should empyema of the gall- bladder have developed in consequence of the presence of gall- stones, this viscus has been incised — cholecy slot amy — or it has been removed — cholecystectomy. The latter operation is scarcely more dangerous than the first, and has the further advantage that no new gall-stones can form in the gall-bladder. Under the Avorst of circumstances the development of gall-stones in dilatations of the large biliary ducts would be possible. AYhen gall-stones have become impacted in the intestine, and symptoms of ileus have developed, abdominal section has been performed, the bowel in- cised, the calculus extracted, the intestine and the abdomen sutured, and cure effected in this wav. DISEASES OF THE BLOOD-VESSELS OF THE LIVER. THROMBOSIS OF THE PORTAL VEIN CPYLETHROMBOSIS;, Ktiology. — As in other blood-vessels, thrombi may form in the portal vein as a result of compression, of slowing of the blood- stream, and of marantic conditions. Fressure-thrombosis is observed in connection with tumors surrounding the trunk of the portal vein, as, for instance, carcinoma of the pancreas, stomach, or intes- tine, enlargement of the portal lymphatic glands, and at times also as a result of compression due to peritonitic adhesions. Tlirombosis of the portal vein due to slowing of the hlood-sfrraiii develops par- ticularly in association with certain diseases of the liver, most commonly chronic interstitial hepatitis and carcinoma of the liver. Marantic pylethrombosis is observed finally in the sequence of pro- tracted and del)ilitating diseases, among which chronic diarrhea, carcinoma, and pulmonary tuberculosis may be mentioned. Throm- bosis of the portal vein is a rather uncommon disorder. THROMBOSIS OF THE PORTAL VEIN 369 Symptoms, Diagnosis, Prognosis, and Anatomic Alterations.. — Obstruction of the trunk of the portal vein by a thrombus gives rise necessarily to increase in the blood-pressure in the portal area, and consequently to portal stasis. The latter is manifested by the occurrence of ascites, splenic enlargement, hypo- static catarrh of the stomach and the intestine, and hemorrhoids, at times of hemori-hage from the mucous membrane of the stomach and the intestine. Jaundice also may develop, and this has been ex- plained by the fact that in consequence of the thrombosis the blood-pressure in the intrahepatic branches of the portal vein has fallen so low that, contrary to the rule, bile can pass over from the biliary capillaries into the portal branches. It is therefore evident that the same conditions are present as in cirrhosis of the liver, and nothino; else would be expected, as in the latter disorder, also, the portal area is partially obstructed and partially constricted, although the process involves not the trunk of the portal vein, but its intra- hepatic branches. It has even been maintained that pylethrom- bosis gives rise to chronic interstitial hepatitis, but this view has not unjustly been contradicted. The diferential diagnosis between cirrhosis of the liver and pyle- thrombosis can scarcely ever be made with certainty. Excessive indulgence in alcohol is suggestive of cirrhosis, which, further, is rather a common disorder. Pylethrombosis may also be readily confounded with chronic-serous, tuberculous, and carcinomatous peri- tonitis, and in the diflPerentiation the points mentioned on page 336 should be borne in mind. The prognosis of pylethrombosis is not favorable, for even if, as in cirrhosis of the liver, venous collateral channels develop, for the purpose of conveying the portal blood to the general circula- tion, these will not suffice. The ascites increases progressively, and death appears unavoidable from asphyxia, cardiac paralysis, exhaustion, at times from excessive hemorrhage. The anatomic alterations are readily recognizable. On divid- ing the trunk of the portal vein this vessel will be found occluded by a fibrinous thrombus which at times may be followed far into the intrahepatic or the peripheral branches. Mural thrombi that have occasioned only stenosis of the portal vein are less com- mon. In addition the changes due to portal stasis are present. Treatment. — The treatment of portal thrombosis is mechan- ical. Abdominal puncture should be performed when the ascites becomes excessive. From internal remedies, such as digitalis, calomel, diuretin, urea, and other diuretics, and from laxatives, diaphoretics, or drastics, no permanent success can be hoped. Also absorption of the thrombus by medicaments cannot be effected. 24 370 DIGESTIVE ORGANS PURULENT INFLAMMATION OF THE PORTAL VEIN (SUPPURATIVE PYLEPHLEBITIS). ^Etiology. — Siij)])urative pylephlebitis is a nuiiiifestation of septicopyemia. It develops in the sequence of inflammation in the radicular distribution of the portal vein if bacteria gain en- trance into the portal vein from this point, excite inflammation of the wall of the vein, and in connection therewith give rise to the formation of a purulent thrombus contaminated by bacteria. Among the more common causes are dysentery, puerperal fever, carcinoma of the uterus, salpingitis, oophoritis, carcinoma of the rectum, proctitis and periproctitis, peritonitis, perityphlitis, abscess of the spleen, gastric ulcer, carcinoma of the stomach, and intes- tinal ulceration. In the newborn pylephlel)itis has been observed in the sequence of inflammation of the uml)ilicus. Anatomic Alterations. — The wall of the portal vein appears friable and readily torn in the diseased situation. On opening the vein a smeary, purulent, at times offensive-smelling, brownish thrombotic mass is found at this point. Often portions of the throml)us have become detached, and have found their wav into the liver, where they give rise to new foci of inflammation and suppuration. Collections of pus form also in other viscera, par- ticularly in the lungs. The spleen, as in many infectious diseases, is enlarged and soft. Symptoms, Diagnosis, and Prognosis. — The disease pursues the course of a septicopyemia. Repeated chills occur, and are followed by fever and sweating. The liver and the spleen are enlarged. Pressure over the liver induces pain. At times it has been possible to feel the portal vein through the abdominal walls as a thick cord. Often there is marked jaundice. Kot rarely foci of purulent inflammation appear in various parts of the body, as, for instance, the lungs, the pleura, the pericar- dium, and the joints. Lender the most favorable conditions the diagnosis can be made only with some degree of probability. The prognosis is unfiivorable, as recovery appears impossible. Treatment. — Efforts should be made to maintain the forces of the body as fully as possible, particularly by the use of alco- holics and stimulants. In addition, an ice-bag should be applied over the liver. ANEURYSM OF THE HEPATIC ARTERY. But a small number of cases of aneurysm of the hepatic artery have been recorded. The condition can be recognized with cer- tainty only when a swelling Avith exjiansile pulsation is palpable to the right of the median line, and over which a cardiac-systolic vascular murmur is audible. At times symptoms are present like DISEASES OF THE PANCREAS 371 those of biliary colic : Colicky attacks of pain, vomiting, and jaun- dice. In one case under my observation deatli resulted from inter- nal hemorrhage, the cause of which was found on post-mortem examination to be a ruptured aneurysm of the hepatic artery. The prognosis is unfavorable, for every aneurysm has a tendency to undergo enlargement and rupture. The treatment would be confined to the relief of particularly distressing symptoms. If the diagnosis is positive, persistent rest in bed and the application of an ice-bag would be indicated. VII. DISEASES OF THE PANCREAS. The diagnosis of disease of the pancreas is exceedingly difficult, for, in the first place, the organ is so concealed as to be accessible to physical examination only under especially favorable condi- tions, and, besides, no symptoms are known to be peculiarly dis- tinctive of disease of the pancreas. Acute and chronic inflammation of the pancreas is thus far only of anatomic interest. [Acute pancreatitis may be hemorrhagic, suppurative, or gangrenous. It is attended with pain in the superior abdominal region, usually of sudden onset and paroxysmal exacerbation ; generally with constipation, although diarrhea may supervene ; with abdominal distention, icterus, an anxious and pinched expression, a small and rapid pulse, and variable temperature. Death usually occurs in from two to five days, from collapse. In treatment morphin may be required for the relief of pain, and stimulants, possibly by enema, to overcome collapse. If the pancreas can be felt to be enlarged and the diagnosis is certain, operation and evacuation of septic material may be undertaken as soon as collapse has passed off. Chronic pancreatitis probably arises by extension from adjacent disease. It may set in gradually and without pain, or with severe epigastric pain, associated with nausea and vomiting, or followed by jaundice and perhaps also by a feeling of chilliness or a rigor. Tenderness is usually present in the umbilical region, and sometimes swelling of the pancreas can be made out. Appetite is usually wanting ; the taking of food is followed by epigas- tric discomfort, and loss of flesh and strength is marked. Albuminuria is common,, and glycosuria may be present. The temperature is variable. At a late stage hemorrhages may take place into the skin and from the mucous membranes, with death from asthenia. In diagnosis gall-stones in the choledoch duct, carcinoma of the head of the pancreas or of the liver and the bile-ducts, and chronic catarrh of the bile-ducts must be taken into consideration. The only treatment is surgical. — A. A. E.] In obese persons fat-necrosis occurs occasionally in the pancreas, and in connection therewith there may be hemorrhage into the pan- creas. Under such circumstances deatli takes place amid signs of shoek and progressive collapse, or the pancreas undergoes marked increase in size, exerts pressure upon the intestine, and gives rise 372 DIGESTIVE ORGANS to ileuH, or rupture into the abdominal cavity takes place, with the development of usually fatal peritonitis. At times calculi fonn in the excretory ducts of the pancreas — pancreatic sialolithiasis — and these may give rise to severe and painful attacks of pancreatic colic. Pancreatic cysts have been operated upon recently in a number of instances. Carcinoma of the pancreas may involve the tail, the body, the head, or the entire organ. jNIost commonly the head is the seat of the disease. Generally the new-growth is primary. The most reliable sign is the demonstration of a nodular tumor, somewhat above the level of the umbilicus, not connected with the stomach, the omentum, the colon, tiie kidneys, the liver, or the abdominal lymphatic glands. Carcinoma at the head of the pancreas often surrounds the portal vein and the choldeoch duct, and occasions irremediable ascites and jaundice. The prognosis is unfavorable and the treatment purely symptomatic. VIII. DISEASES OF THE PERITONEUM. INFLAMMATION OF THE PERITONEUM (PERITONITIS). etiology. — Inflammation of the peritoneum in human beings occurs almost unexceptionally as a result of the activity of bacteria, among which the Bacterium coli commune, the Streptococcus pyogenes, the Staphylococcus pyogenes albus and aureus, the pneumoniacoccus, the gonococcus, the Bacillus typhosus, the Ba- cillus tuberculosis, and some others have been demonstrated in the inflammatory lesions. Naturally it would be possible to excite peritonitis by means of strictly chemic poisons, as for instance, injections of oil of turpentine, tincture of iodin, and the like, into the abdominal cavity, but such an occurrence is only exceptionally to be anticipated in human beings. Infection of the peritoneum is usually brought about through certain contributory causes, which formerly, when the significance of bacteria was not understood, were considered the active and causative factors of the disease. Among these the greatest im- portance was attached to cold. Rcfrif/cratory (rheumatic) peri- tonitis is, however, among the less common varieties of the dis- ease. It has been observed after sleeping upon damp ground, and particularly in WM)men, at the menstrual period, following cold bathing. At times traumatism is followed by infection of the peritoneum and the development of traumatic peritonitis. INFLAMMATION OF THE PERITONEUM 373 Falls, blows, shocks, crushing, and punctured wounds of the abdomen, may be mentioned as particularly common causes of traumatic peritonitis. Peritonitis by extension probably occurs most commonly, and particularly in the sequence of inflammatory and ulcerative pro- cesses in any of the intestinal viscera, and in the vicinity of the peritoneum. It will suffice to mention a number of the more common disorders : ulcer, abscess, and carcinoma of the stomach, ulceration of the intestine, dysentery, carcinoma of the intestine, intestinal invagination and strangulation, typhlitis, appendicitis, abscess, carcinoma and echinoeoccus of the liver, absce.ss, carci- noma, echinococcus and infarction of the spleen, abscess and embolism of the kidney, paranephritis, impacted renal or biliary calculi, metritis, salpingitis, oophoritis, cystitis, prostatitis, strangu- lated hernia, suppurating inguinal glands, burrowing abscesses of the vertebrae, pleuritis, pericarditis, etc. These and similar dis- eases may cause peritonitis by rupture and evacuation into the abdominal cavity of material capable of exciting inflammation. Such a condition is designated perforative peritonitis. At times peritonitis develops in the course of infectious dis- eases, as, for instance, septicopyemia, erysipelas, fibrinous pneu- monia, typhus fever, and the like. Without doubt morbid altera- tions in the bodily metabolism diminish the resistance of the peri- toneum, and increase its susceptibility to inflammation. Among such disorders are uremia, pulmonary tuberculosis, the carcino- matous cachexia, and scorbutus. Feritonitis may be superadded to other diseases of the peritoneum, particularly tuberculosis and carcinoma. There are, however, cases in which no cause for the inflammation can be demonstrated — cryptogenetic peritonitis. The condition under such circumstances may often be an alimentary 'peritonitis, by which it is understood that bacteria migrate from the intestinal contents through the intestinal wall into the peri- toneal cavity and give rise to inflammation. Not at all rarely the statement is positively made that the symptoms of peritonitis have rapidly developed in the sequence of errors in diet (the ingestion of cold or spoiled beer, or of unripe fruit). Peritonitis may occur at any period of life ; it may develop even in the newborn in the sequence of septic infection of the umbilical wound. At times children are born with chronic syph- ilitic peritonitis. Peritonitis is most common, naturally, between the fifteenth and the forty-fifth year of life. Women are attacked more commonly than men, because diseases of the female genera- tive apparatus often constitute the source for inflammation of the peritoneum. Anatomic Alterations. — Inflammatory processes in the peritoneum pursue much the same course as inflammatory pro- cesses in other serous membranes, and, accordingly, a differentia- 374 DIGESTIVE ORGANS tion has been made between fibrinous, serous, purulent, and hemor- rhagic peritonitis. In addition there occurs putrid peritonitis, which results from a j)urulent peritonitis when the purulent exu- date becomes infected with the bacteria of putrefaction. Often mixed varieties of peritonitis occur, which may be designated sero- fibrinous, tibrinopurulent, etc., respectively. In accordance with the extent of the inflammation of the peritoneum a distinction is made between circamscribed (localized) and diffuse jjeritonitis. Further reference to circumscribed peritonitis will not be made here, because this is considered in other places as perityphlitis, perinepliritis, perihepatitis, perisplenitis, etc. Fibrinoits peritonitis is characterized by viyid redness and over-distention of the diseased peritoneum with blood. Here and there individual blood-vessels have ruptured, and punctate and sometimes larger extravasations of blood have taken place. Soon swelling, fatty degeneration, and desquamation of the endo- thelial cells of the peritoneum take place, and the serous mem- brane in these situation appears turbid and dull, like a plate of glass that has been breathed upon. The alterations in the endo- thelium render it possible for the exudate from the blood-vessels — containing considerable fibrin — to coagulate upon the surface of the peritoneum, and to form at first thin, cob-web like, and sub- sequently thicker, yellow, and opaque deposits. Through these fibrinous membranes numerous adhesions take place between the abdominal viscera, particularly loops of intestine. Should the process terminate in recovery, the fibrinous exudate may be entirely absorbed and disappear. ]\Iore commonly, it is true, the exudate is more or less extensively transformed into connective tissue, which forms peritoneal bands and adhesions between the individual abdominal viscera. At tiiues the entire mass of intes- tine and the remaining abdominal viscera are so firmly bound together that the whole constitutes an inseparable convolution, and the abdominal cavity is completely obliterated — obliterative peritonitis. Serous peritonitis is attended with an accumulation of slightly turbid, yellowish or yellowish-green fluid in the abdominal cavity. As a rule, the fluid contains flocculi of fibrin, and also the intes- tines and the remaining abdominal viscera are covered with fibrin- ous masses, so tliat the condition generally becomes one of sero- fibrinous peritonitis. Purulent infleomadtion of the peritoneum — suppurcdive peritonitis — occurs far more commonly than serous peritonitis, and this fact is probably indicative of the greater irri- tability of the peritoneum in comparison with some other serous membranes (pleura, pericardium). The peritoneum is rather com- parable with the meninges in this connection. The pus in the ab- dominal cavity presents the usual ai)}iearance, and it often reaches several quarts in amount. It becomes especially abundant in the INFLAMMATION OF THE PERITONEUM 375 true pelvis. In addition to pus fibrinous deposits are also encoun- tered, and these often bind the loops of intestine together. If adhesions are separated, deep pockets are often exposed filled with pus. Should absorption of the pus take place in the further course of the curative process, fibrinous deposits remain and subsequently undergo the same changes that have been described for fibrinous peritonitis. Putrid j^^^^iiomtis is characterized by the offensive odor of the pus, being irritating to both the nostrils and the eyes. The putrid material causes irritation of the skin of the dissector. On microscopic examination of the pus the pus-corpuscles are found in a state of partial degeneration. The pus contains in- numerable bacteria. Putrid peritonitis occurs, in addition to sep- ticopyemia, particularly in the sequence of rupture of the abdominal viscera. If the ruptured organ is a gas-containing viscus (esoph- agus, stomach, intestine), gas frequently escapes into the abdominal cavity, and the condition is designated pnewnoperitonitis. Hemor- rhagic 'peritonitis occurs in connection with tuberculosis and car- cinoma of the peritoneum, nephritis, and scorbutus. Symptoms and Diagnosis. — The symptoms of peritonitis vary in accordance with the nature of the inflammation. An account of the symptoms of diffuse, acute, purulent peritonitis, perforative peritonitis, and chronic peritonitis follows : Symptoms of Acute, Diffuse, Purulent Peritonitis. — A constant symptom of acute, diffuse, purulent peritonitis is pain. At first this may be purely local in the situation of the organ from which the inflammation of the peritoneum has originated, but soon it extends over the entire abdomen, and increases in such degree that the gentlest manipulation of the abdominal walls and the slight pressure of a thin sheet cannot be borne. The patient avoids speaking in a loud tone, deep breathing, or change in posture, in order to prevent aggravation of the pain. Not rarely, in spite of all precautions, the pain exhibits paroxysmal and colicky increase in severity, and this is frequently associated with audible gurgling in the abdomen and increased intestinal movement. The abdomen is distended like a drum and at times to the point of rupture, the overlying skin being glistening and smooth. The cause for this condition consists in marked distention of the intestine with gas— intestinal meteorism — and this in turn is dependent upon disturbed intestinal digestion and abnormal fermentation of the in- testinal contents. On percussion of the abdomen a uniformly loud tympanitic percussion-note is not rarely audible everywhere. In other instances areas of dulness appear in irregular distribution, in correspondence with accumulations of fluid exudate. Such dul- ness is most common in the dependent and lateral portions of the abdomen. Displacement of dulness with change in posture is scarcely observed, as the exudate is usually confined within cir- cumscribed cavities. As a rule, fluctuation cannot be elicited at 376 DIGESTIVE ORGANS all over exudatos, or but imperfectly. In' accordance with the degree of rueteorism the diaphragm, the lower borders of the lungs, and the heart are greatly displaced upward. The patient, therefore, complains frequently of dyspnea, a sense o^ fear, of oppres-non, and of palpitation of the heart. Vomiting usually occurs in consequence of irritation of the stomach. The vomited matter consists at first of the gastric contents, and its apj>earance accordingly varies with accidental conditions ; but later it frequently presents a greenish, bilious appearauce. With progressive exhaustion the vomiting ceases, and it is often replaced by troublesome eructation or singultus. Thirst is greatly increased, whereas the appetite is completely wanting. The tongue is often coated, but in other instances it presents a clean and strikingly red appearance, usually in consequence of frequent vomiting and slight irritation of its mucous membrane. At times the 6/"fa//i! is offensive. At the begin- ning of the disease the stools are generally thin and liquid, but subsequently marked constipation commonly exists. The urine is usually voided in diminished amount. The secretion is generally dark red (high-colored, saturated), frequently precipitates a brick- dust sediment, and contains much indican in consequence of de- rangement of intestinal digestion and increased decomposition of proteids in the intestine. Slight albuminuria also is not a rare occurrence. At times the patients complain of pain in the evacu- ation of urine and of retention of urine, svmptoms that are often associated w-ith pericystitis. The hofJUy temperature is elevated at times as high as 40° C. (104° F.) and above, although the course of the fever is irregular. Pulse and respiration are frequently more greatly accelerated than the height of the fever warrants, because, in addition to the eleva- tion of temperature, displacement of the lungs and of the heart and nervous influences are operative. The rapidity and the severitv with which the general condition suffers are noteworthy. The facial expression is painful and the features are distorted, the eyes become deeply sunken and surrounded by blue lines, and the chin and nose become sharply prominent. The course of acute diffuse j^^/'ifonitis may terminate fatally within a few days amid septic manifestations and progressive as- thenia, while in other instances the disease is prolonged for weeks and even for months, with numerous fluctuations, pursuing rather a subacute and even a chronic course. Often the outlook for recov- ery- appears most promising, but a renewed turn for the worse rapidly dispels hope. Among complications symptoms of ileus may be mentioned first, and amid which death may take place without mechanical obstruction of the l>owel being found upon post-mortem examination. The condition is therefore designated dynamic ileus, resulting from local paralysis of the musculature of the bowel. INFLAMMATION OF THE PERITONEUM 377 At times metastatic inflammatory processes appear in other situ- ations ; most commonly in the right pleural cavity, and at times also in the pericardial cavity. Under such circumstances it is often remarkable within how short a time a pleuritic effusion may be again completely absorbed when the peritonitis shows a dispo- sition toward improvement. Particularly serious are crrcumscribed collections of pus, which form especially between the loops of bowel. In the first place, they may readily give rise to renewed exacerbations of the peritoneal inflammation ; and besides, they may rupture into adjacent organs, as, for instance, into the intes- tine, the stomach, the genito-urinary passages, through the abdom- inal walls, and particularly through the umbilicus. Although natural recovery may follow such an accident, it is also possible for the pus to become infected with fecal matter or with urine and become putrid, and in this way cause death by septicopyemia. Rupture of pus into the large blood-vessels of the abdominal cavity is dangerous, for in addition to hemorrhage general septi- cemia may occur. Also when, contrary to experience, absorption of pus takes place, serious sequelce at times develop. The bowel may be so greatly displaced and distorted in consequence of peritoneal adhesions that stenosis and even obstruction — ileus — result. Similar conditions may also be brought about by loops of intestine slipping beneath peritonitic bands or being surrounded by them. Symptoms of Perforative Peritonitis. — The symptoms of per- forative peritonitis depend upon whether the inflammation of the peritoneum is free or encapsulated, and whether the rup- ture has taken place from a gas-containing or an airless viscus. In case of rupture of the stomach, the intestine, or the esophagus, in addition to particles of food, gas usually escapes into the ab- dominal cavity, and accordingly there develops a free or a saccu- lated pneumoperitonitis. With the development of a free pneumo- peritonitis the patient not rarely cries aloud that something has torn within the abdominal cavity, and he complains generally of indescribable pain in the abdomen. The abdominal walls are re- tracted, stretched with board-like hardness, and exceedingly tender to touch. It is noteworthy that outlines of loop.s of intestine beneath the abdominal walls are not visible, and that also no peristaltic movement of the bowel can be detected. Of particularly great diagnostic significance is the disappearance of the hepatic and the splenic dulness, which results in consequence of the rise of the escap- ing air and the displacement of the liver and the spleen from the thoracic and abdominal walls. This important sign will be absent only when the liver and the spleen have previously been immov- ably bound by peritoneal adhesions to the thoracic and abdominal walls. Frequently vomiting occurs, although its absence has been observed in case of rupture of the stomach, because at times in 378 DIGESTIVE ORGANS the efforts at vomiting the contents of the stomach pass more readily through the site of rupture into the abdominal cavity. The general condition is characterized in an unmistakahle man- ner by tiie signs of most profound exhaustion. The skin feels cool, the pulse is small and running, the voice is faint and hoarse, the face is pale, the eyes are sunken, retracted, and surrounded by gray rings, and the nose, tlie malar bones, and the chin stand out prominently. Consciousness is preserved. Death may result from putrid infection and progressive exhaustion within a few hours. At times it occurs as the result of asphyxia if the dia- phragm, the lungs, and the heart are displaced upward excessively in consequence of intestinal and peritoneal meteorism. Recovery as a result of internal medication and expectancy occurs most rarely, but life has been saved in a number of instances of late by surgical intervention. Sacculated pneiuno peritonitis occurs especially in connection with ulceration of the stomach and the intestine, when rupture of these viscera has been preceded by circumscribed peritonitis with adhesions, so that the escape of gastric or intestinal con- tents takes place into the previously closed cavity. The con- dition is exceedingly difficult of recognition. Circumscribed tenderness in tlie abdominal cavity should be looked for. Over this area a dull note will be elicited on percussion, in so far as the exudate is in contact with the abdominal walls, whereas a tympanitic percussion-note will be obtained over the gas-con- taining cavity. The fact is of especial importance if displacement of the percussion-boundaries in accordance with the position of the body can be demonstrated, under which conditions the tym- panitic percussion-note will always correspond with the highest point of the gas-containing cavity. It may also be possible that vigorous agitation of the body will elicit a sue cussi on-sound or a splashing sound, although there will be some hesitation in subject- ing the patient to such active manipulation. The formation of a sacculated pneumoperitonitis may take place so insidiously, as, for instance, in a case of typhoid fever, that even when the condition of the patient is most carefully followed the presence of the dis- ease may perhaps be recognized only at the autopsy. The subject of subphrenic pyopneumothorax has been considered on p. 167. If an airless viscus has ruptured into tlie peritoneal cavity (abscess of the liver or of the spleen, softened lymphatic glands, paranephritis, burrowing abscesses, and the like), or if an air- containing viscus has ruptured, and gas has accidentally not es- caped into the abdominal cavity, an acute diffuse peritonitis de- velops within the shortest possible time, if free rupture has taken place into the abdominal cavity. That the condition is one of perforative peritonitis will be indicated by the fact that tlie patients often designate with absolute positiveness a circumscribed area INFLAMMATION OF THE PERITONEUM 379 as the source of their trouble, and that not rarely also in the further course of the disease definite local disturbances become more pronounced in this situation, as, for instance, increased ten- derness and greater accumulation of exudate. Sacculated perforative peritonitis will be recognized from the presence beneath the abdominal walls of circumscribed dulness, which yields increased resistance and pain on palpation. As the condition may develop quite insidiously, it at times escapes diag- nosis. Occasionally it is recognized only from the sequelae, if rupture of the encapsulated pus takes place through the abdom- inal walls or into intestinal viscera. Symptoms of Clironic Peritonitis. — Among the chronic varie- ties of peritonitis peculiar clinical interest attaches to that which is attended Avith the formation of a serous, freely movable accumulation of fluid in the abdominal cavity — chronic-serous peritonitis. Usually without obvious cause more and more fluid gradually accumulates in the abdominal cavity. The abdomen increases progressively in size. Fluctuation can be elicited, and on percussion in the dorsal decubitus a tympanitic note is obtained over the upper portion of the abdomen corresponding to the loops of intestine floating upon the fluid, with dulness in the lateral portions. Change in jjosition is followed by displacement of the percutory phenomena, the uppermost portion of the abdomen yielding a tympanitic percussion-note, while a dull note is ob- tained over the lowermost portion. The intestines always tend to rise to the surface of the fluid. The physical phenomena are, on the whole, the same as those that attend ascites. Differen- tiation from ascites is possible only from the fact that causes for this condition are not demonstrable, and that the inflammatory fluid is characterized by the jiresence of a greater amount of albu- min (more than 4 per cent.) and a higher specific gravity (above 1014). Also tenderness of the abdominal walls and transient febrile movement are indicative of serous peritonitis. The dif- ferentiation from tuberculous-serous peritonitis is far more difficult. In favor of the latter disease would be the presence of tubercu- losis in other organs (particularly the intestine, the lungs, the lymphatic glands, the kidneys, the epididymis, the urinary pass- ages), or the detection of the thickened tuberculous omentum as a dense band passing transversely across the abdominal cavity. Even after the abdomen has been opened the diagnosis may still be doubtful, because at times nodular fibrous thickenings form upon the peritoneum in cases of chronic-serous peritonitis, pre- senting exactly the appearance of tubercles, and only differing from these histologically and bacteriologically. Chronic-serous peritonitis may pursue an afebrile course, and not rarely causes no other pain than that due to tension. Should the effiision of fluid be considerable, dyspnea and acceleration of cardiac action 380 DIGESTIVE ORGANS occur in consequence of displacement of the diaphragm, the lungs, and the iieart. The disease not rarely extends over many months, undergoes exacerbations and remissions, and is susceptible of cure. Prognosis. — The prognosis of all varieties of peritonitis is serious. Acute and perforative peritonitis must l)e considered particularly dangerous diseases, frequently causing death from exhaustion and septicemia, although the outlook for recovery has recently been improved in some varieties by surgical treatment. Treatment. — The treatment of peritonitis depends upon the variety of irijiainmation. In cases of acute, diffuse, purulent peri- tonitis the patient should be advised to observe as complete rest as possible, and invariably to use a bed-pan in the evacuation of the bladder and the bowels. The diet should be liquid and con- sist preferably of milk, coffee with milk, tea with milk, beef- soup, and wine diluted half with Avater. For the relief of the severe thirst, and in the presence of violent vomiting, small bits of ice may be sucked. For the inflammatory alterations in the abdominal cavity, not too heavy ice-bags should be applied to the abdomen. When the acute inflammatory .symptoms n)oderate the ice-bag should be replaced by hot cataplasms, which are more agreeable to most patients, and favor al^sorption of the effusion. Severe localized pain in the abdomen not rarely subsides speedily after the application of from 5 to 10 leeches to the abdomen. Among internal remedies the use of opium or morphin may be recommended : B Powdered opium, 0.03 (J grain), Sugar, 0.3 (4| grains).— M. Make 10 such powders. Dose: 1 powder every two hours. R Morphin hydrochlorate, 0.3 (4^ grains) ; Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose: 0.5 (8 minims) once or twice daily injected subcutaneously. Both morphin and opium are employed to place the bowel at rest. As a result the pain becomes less, and, besides, dissemina- tion of the pus throughout the entire abdominal cavity is pre- vented. Some patients do not bear o])ium well, and develop .severe pain, nausea, and delirium after its use, and for these mor- phin is better adapted. Opium or morphin shoidd be given until the abdomen becomes entirely free from pain on pressure. ]Many weeks may be required to attain this end. Should improvement in the conQ.^ Albumosuria can be recognized from the fact that the urine remains clear on boiling and addition of nitric acid, and becomes turbid only on cooling. If the turbid urine be again heated, it will again become clear. A practical method of examination for albumoses consists in performing Heller's test for albumin, and, if a white ring of albumin forms, heating the test-tube. If the ring is due* to albumoses, it disappears on heating ; while if due to serum-albumin and serum-globulin it becomes more intense. There is but one certain method of determining the amount of albumin in the urine, namely, boilinir the urine, completely sepa- rating the albumin by careful addition of dilute acetic acid, and then weighing it, after previous drying upon a previously weighed filter. Such a procedure requires far too much time for the general practitioner, apart from the fact that a drying chamber and chemic scales are necessary for its application. It is, therefore, a matter for congratulation that Esbach has described a sim- ple apparatus in the form of his albuminometer, by means of which the amount of albumin can be approximately estimated. Further, the de- terminations of albumin by means of carefully graduated Esbach alliuminometers often agree remarkably with the results of weighing. Esbach's albuminojneter (Fig. 55) consists of a test- tube of thick glass, which can be closed by a rubber stopper. The tube bears two principal marks, the upper of which is indicated by the letter R and the lower by the letter U. Below the U-line is a scale down to the bottom of the tube, the lowermost figure of which is 2 and the uppermost 7. In using the instru- ment the test-tube is filled with clear, filtered urine to the line U (urine) ; then Esbach's reagent, consisting, as described, of picric acid and citric acid (p. 389) is added up to the line R (reagent), and with the opening closed the whole is inverted several times for the pur- pose of thorough admixture. The instrument is per- mitted to stand for twentv-four hours at room-temper- ature (14° R.— 17.5° C— 63.5 F.). At the end of this time the level of the column of albumin that has been deposited at the bottom of the tube is read off. If, for instance, the level corresponds with the figure 3, this will indicate that 3 grams of albumin are present in 1000 c.c. of urine, therefore 0.3 per cent. In using the albuminometer of Esbach the follow- ing facts should be borne in mind : A knowledge of the percentage of albumin will naturally be of value if in addition tlie daily amount of urine is known, and there- from the total daily amount of albumin is estimated. The temperature of the room in which the albuminometer is kept should not be below 14° R. (17.5° C. — 63.5°F.), as otherwise the albumin will not be precipitated. Xow and then, although rarely, urine is encountered in which, in spite of the observance of all precautions, no precipitate of albu- min takes place, but a cloud of albumin floats in the upper layers of the Fig. 55. — Esbach's albuminometer; nat- ural size. ALB UMINUBIA 391 urine. Should the urine contain more than 0.7 per cent, of albumin, it should be diluted with an equal amount of water before it is introduced into the albuminometer. The patients shall not have used quinin, anti- pyrin, thallin, and potassium-salts, as picric acid, as has already been men- tioned, forms precipitates with these substances. The amount of albumin eliminated with the urine is susceptible of great variation in accordance with the causes of the albumin- uria. At times only traces of albumin will be present, with a scarcely appreciable turbidity of the previously clear urine, while in other instances the boiled urine may become a solid coagulum, which will not flow from the inverted tube. On careful inquiry into the clinical causes of alhuminuriay hematogenous albuminuria will be found, first, as a result of circu- latory disorders. Both anemia and venous hyperemia of the kid- neys are frequently attended with albuminuria. The nervous albuminuria that appears in the sequence of epileptic attacks, cerebral hemorrhage, tetanus, hysteria, progressive paralysis of the insane, etc., is often probably also due to disturbances in the renal circulation. Not rarely albuminuria is associated with anemic and cachectic states, although under such circumstances there is fre- quently a connection with hematogenous albuminuria, because in the course of the conditions named fatty degeneration readily develops, particularly in the epithelial cells of the convoluted uriniferous tubules. Nephrogenous cdbuminuria occurs particularly in association with diffuse inflammatory conditions of the kidneys, but also with all other possible diseases of the kidneys. Febrile or infectious and toxic cdbuminuria should further be mentioned as especial varieties of nephrogenous albuminuria. Febrile infectious diseases are frequently attended with albuminuria. The injury to the renal epithelium under such conditions is dependent proba- bly less upon the elevation of bodily temperature than upon the infection, as afebrile infectious diseases may, likewise, give rise to albuminuria. Probably bacterial poisons (toxins) are the sub- stances that cause irritation of the kidneys in the process of elimi- nation with the urine. Toxic albuminuria may be induced by many substances, whether introduced through the mouth, the rectum, or the skin. Among these may be mentioned mineral acids, carbolic acid, mercuric chlorid, phosphorus, arsenic, lead, cantharides, balsamics, and irritating applications to the skin of all kinds. Albuminuria occurs also at times after burns of the skin and chronic cutaneous eruptions, in all probability induced by the absorption of toxic substances from the skin. The danger from albuminuria does not reside in the loss of albumin, for an albuminuria with the loss of more than 20.0 grams of albumin daily is rare, and could easily be compensated for by the ingestion of several eggs or of meat. Therefore the prognosis of cdbuminuria depends solely upon the causa- 392 GEXITO-URINARY ORG ASS tive factors. When these are incurable so also is the allju- miuuria. In the treatment of albuminuria the nourishment and the mode of life play the most important part. No medicine is known capable of curing albuminuria, and tannic acid, fuchsin, brom- benzol, strontium lactate, and strontium bromid have been incor- rectly recommended as such. Patients with alljumiuuria should avoid -aW food and drinh capable of irritating the kidneys, particu- larly strong coffee and tea, alcoholics, sharp spices and acids, and asparagus. A milk-diet is particularly to be recommended : from 1 to 2 quarts of thoroughly boiled milk being taken in small amounts tliroughout the day. Meat should be taken only in mod- erate amount, and white meat (lamb, veal, poultry) particularly is to be preferred. Vegetables and light pastry may be recom- mended. Thirst should be relieved by acid or alkaline waters (Vichy, Bilin, Giesshiibel, Ems, Fachingen, etc.). The patient should wear flannel next to the skin, and take twice weeklv a bath at a temperature of 28° R. (35° C— 95° F.). All exposure to cold should be carefully avoided. In the winter the well-to-do should be advised to sojourn in an equable, warm southern climate. I have observed excellent results in a number of instances from a winter spent in Helouan, near Cairo. Bodily over-exertion should not be permitted under any circumstances, as it may cause a re- currence of a cured albuminuria. HEMATURIA. The presence of blood in the urine is designated hematuria when the urine contains sufficient hemoglobin to give rise to a dis- tinctly bloody hue. Two varieties of hematuria must, however, be distinguished, accordingly as red blood-corpuscles or, after previous solution of red blood-corpuscles, only free iiemoglobin is present in the urine. The latter condition is designated hemo- globinuria, as opposed to the more common occurrence of hema- turia. Hematuria is readily recognized from the distinctive color of the urine. In accordance with the number of red blood-corpus- cles present in the urine, and the transformation of their con- tained hemoglobin into methemoglobin, the urine exhibits a light- rose color, suggestive of the appearance of meat-infusion, or pre- senting a blood-red, brownish, or even blackish appearance. Should any doubt exist as to the nature of the condition, the urin- ary sediment should be examined for red blood-corpuscles, or Heller's blood-test should be ]ierformed. The red blood-corpus- cles in the urinary sediment, which often discloses the presence of blood by its brownish-color, are at times unchanged in form, alt!iough at other times (particularly in concentrated urine) thev HEMATURIA 393 exhibit thorn-apple processes, or they appear swollen and bi- convex, or lentil-shaped and even spherical. At times unusually small spherical red blood-corpuscles are encountered — so-called microcytes. Frequently red blood-corpuscles have yielded up their hemoglobin and appear as colorless discs of double contour — so-called" blood-shadows. At times, particularly in the hot summer months, ameboid movement and constrictions can on careful observation be detected in isolated red blood-corpuscles. Should tube-casts appear in the urine in association with renal hematuria, they may be covered with red blood-corpuscles or be entirely constituted of them (blood-clasts)., Tube-casts and epi- thelial cells from the uriniferous tubules also not rarely present a blood-stained or a brownish discoloration with hemoglobin. Rarely, hematoidin-crystals are present in urinary sediment. It is noteworthy that the red blood-corpuscles in the urine are almost never arranged upon one another in columns or in rouleaux, but are separated from one another, or lie in contact only at their borders. Hellers blood-test is performed as follows : Several cubic centimeters of urine are introduced into a test-tube, and potassium hydroxid is added in excess until the urine acquires an alkaline reaction. If the mixture be heated, the earthy phosphates are precipitated on boiling in the form of coarse flocculi, which after a time are deposited upon the bottom of the tube. In urine free from blood this precipitate appears gray, while in urine containing blood it acquires a reddish, brownish, or brownish-black'appear- ance. The test is so delicate that spectroscopic examination of the urine and Teichmann's blood-test are unnecessary. Bloody urine is necessarily albuminous, as the hemoglobin con- sists of blood coloring-matter and proteid. So long as the condi- tion is one of pure hematuria the urine contains only so much albumin as corresponds with the amount of blood present. The amount of albumin is increased when, in addition to hematuria, albuminuria also exists. The reaction of the urine depends upon the nature of the primary disease. In any event the presence of even quite a considerable amount of blood in the urine is never capable of rendering alkaline the naturally acid reaction of the urine. The causes of hematuria reside in alterations either in the kid- neys or in the urinary passages, and the character of the hematuria varies accordingly. With renal hematuria the blood is intimately admixed with urine, and retains the same color and character at the beginning and at the end of the act of micturition. Hemor- rhages from the pelvis of the kidney and the ureters disclose their origin frequently from the appearance in the urine of cylindric blood-clots, which represent casts • of the ureter. With hemor- rhages from the bladder the urine first voided is frequently less bloody than that evacuated last, because the blood, by reason of its 394 (iEXITO-UPiIXAIiY ORGANS weiglit, has collected in particular abundance in the fundus of the bhuldcr. Hemorrhages from the urethra, finally, are very slight, and often at the beginning of the act of micturition a few drops of blood make their apj)earance. With hemorrhages from the poste- rior portion of the urethra a few drops of blood are expelled only toward the close of the act of micturition, and often with painful tenesnuis. Renal hemorrhage occurs in connection with numerous diseases of the kidneys, as, for instance, acute nephritis, embolism of the renal artery, carcinoma of the kidney, renal tuberculosis, echino- coccus of the kidney, and injury of the kidney. At times renal hematuria is dependent upon alterations in the blood, among the causes of which leukemia, pseudoleukemia, pernicious aneuiia, scorbutus, purpura, and hemophilia may be mentioned. At times hematuria occurs in the course of infectious diseases if these assume the so-called hemorrhagic character, and give rise to hemorrhages of all kinds. Toxic hemorrhage from tlie kidney, such as may be observed folloAving the ingestion of cantharides, quinin, salicylic acid, potassium-salts, mineral acids, carbolic acid, etc., is worthy of especial mention. Hemorrhages from the pehis of the kidney and the ureter are induced most commonly by renal calculi, less com- monly by parasites, carcinoma, tuberculosis, or by rupture of an aneurysm of the renal artery. Hemorrhages from the bladder occur in connection with cystitis, vesical calculi, carcinoma, tuberculosis, parasites, and in the sequence of injuries (exterual and internal, with the catheter). At times the veins surrounding the neck of the bladder undergo dila- tation, forming so-called vesical hemorrhoids, which by rupture may give rise to profuse hemorrhage from the bladder. Hemorrhage from the urethra occurs in comiection with severe gonorrhea (so-called Russian gonorrhea), with impaction of urinary calculi and injuries with the catheter. Hematuria is but rarely attended with such profuse loss of blood that life is endangered by hemorrhage. Should life be threatened, the danger will depend rather upon the causes of the hematuria. The latter influence is responsible also for the fact that hematuria is of variable duration, and either terminates with a single attack or is frequently repeated. The treatment of hem(duria must be directed to the causative conditions. Under all circumstances bodily rest is indicated. Not much can be hoped for from hemostcdies. Hemoglobinuria indicates the occurrence of dissolved blood coloring-matter in the urine. Hemoglobinuria is invariably pre- ceded by hemoglol)inemia ; that is, red blood-corpuscles have first been dissolved in the blood and have given up their coloring-matter to the blood-plasma. Naturally the hemoglobinemia must have attained a certain decree of intensity before hemoo;lol)inuria occurs, HEMATURIA 395 for the spleen, the liver, and the lymphatic glands are capable of taking up the dissolved hemoglobin from the blood-plasma and utilizing it if the hemoglobinemia be but slight. Hemoglobinemia and liemoglobinuria are most commonly caused by the action of toxic substances upon the blood, either of chemic or of bacterial origin (toxins). Among chemic poisons potassium chlorate particu- larly is well knoAvn as a solvent for blood-corpuscles and as a cause for hemoglobinuria. A similar influence is exerted by quinin, mineral acids, carbolic acid, nitrobenzol, aniline-oil, copper sul- phate, hydrogen arsenid, etc. Hemoglobinuria can be induced in human beings by transfusion of blood from animals. Occasionally hemoglobinuria has been observed after the ingestion of fimgi, par- ticularly mussels. Among infectious diseases, in the sequence of which hemoglobinuria has been observed, typhoid fever, pharyn- geal diphtheria, malaria, acute miliary tuberculosis, small-pox, septicemia, and syphilis may be named. The hemoglobinuria attending afebrile cyanosis of the newborn, and following burns of the skin, should further be mentioned. At times hemoglobin- uria occurs in association with diseases of the blood, as, for instance, purpura and scorbutus. It has been observed also in the sequence of sunstroke and fat-embolism. Paroxysmal hemoglobinuria will be considered among the diseases of the blood. In cases of hemoglobinuria the urine presents a bloody appear- ance, at times like that of fresh blood, but often reddish-brown, as the urine frequently contains an abundance of methemoglobin. The urine in a thin layer is transparent ; it yields Heller's test for blood, although in the often brownish-discolored urinary sediment either no red blood-corpuscles at all are found or but a small number of usually discolored shadows, so that there will be no doubt that the condition is one of hemoglobinuria. Often the blood coloring-matter forms flocculent and filamentous brownish and greenish irregularly shaped masses, and tube-casts of com- pressed blood coloring-matter also appear. Such epithelial cells from the uriniferous tubules as may be present are frequently stained brownish or greenish by hemoglobin. At times crystals of hematoidin also are present. On boiling the urine a finely floc- culent precipitate of albumin does not occur, but there results a large, coherent coagulum of albumin, stained brownish by hemo- globin. Spectroscopic examination of the urine reveals, in addition to the two bands of oxyhemoglobin between the Fraunhofer lines D and E, the bands of methemoglobin, of which especially that between the lines C and D is usually distinct. Only rarely are the bands of methemoglobin alone visible. The prognosis of hemoglobinuria depends upon the causa- tive condition, and the same statement is applicable also to the treatment. 396 GENITO-URINARY ORGANS Hnnatinuria has rarely been observed, as, for instance, after pharyngeal diphtheria. Within recent years attention has been directed to hematnpor- phi/riiiui-ia, which has been observed particularly in connection with the toxic effects of sulphonal and trional, and with typhoid fever and mental disease. The prognosis is unfavorable. UREMIA. Ktiology. — Uremia is a symptom-complex that is not rarely observed in the sequence of diseases of the kidneys. In order to avoid repetition, it will not be without utility to precede a con- sideration of the individual diseases of the kidneys by a descrip- tion of uremia. The conditions for the development of uremia are always provided when the elimination of certain toxic sub- stances with the urine is interfered with. This occurs most com- monly when the amount of urine is diminished in abnormal degree, although uremia may occur also when the amount of urine is al)undant if the secretion contains a deficiency of toxic substances which are retained within the body. Uremia is accordingly the result of an intoxication, or, as it is now customary to designate it, an auto-intoxication, as the condition is dependent upon toxic substances generated by the body itself. The nature of the toxic substances is not known. The so-called urinous substances have been thought of (urea and its decomposition-product — ammonium carbonate — kreatinin, potassium-salts, sodium chlorid), but of late there has been a tendency to adopt the view that the responsible factors may consist in putrefactive alkaloids — ptomains. Although diseases of the kidneys constitute the most common cause of uremia, they are, however, not the sole cause. Diseases of the urinary passages, also, may be attended M'ith uremia if they interfere with the elimination of urine. Among diseases of the kidneys particularly acute and chronic interstitial nephritis give rise to uremia most commonly. It is noteworthy that at times severe irritation of one kidney may through reflex influences cause suppression of the function of the other kidney, and thereby give rise to uremia. A similar condition has been observed in con- nection with nephrectomy and the presence of a calculus in a ureter. In some cases uremia results from obstruction by a calculus, not of one ureter merely, but of each. Occlusion of both ureters may be caused by new-growths of the bladder, the rectum, and the uterus, as well as by tuberculosis of both ureters. Among dis- eases of the bladder paralysis of this viscus, and in connection therewith urinary stasis, may induce uremia. Even when the bladder becomes over-distended in consequence of .stupor there will be danger of uremia. This may develop also if the orifice of the bladder is obstructed by calculi, new-growths, or pressure from M'ithout. Finally, strictures, laceration, and compression of the urethra, and phimosis may be causes of uremia. Uremia may UREMIA 397 occur at any j^eriod of life. In children it develops most com- monly as a result of acute nephritis following scarlet fever. Symptoms and Diagnosis. — The symptoms of uremia con- sist particularly in nervous and inflammatory manifestations, the former being the result of irritation of the brain by the retained toxic substances, and the latter being due to the fact that the resist- ance of the tissues of the organism is diminished when the latter is saturated with excrementitious products. A most common symp- tom is headache — cephalalgia — which at times is diffused over the entire head, at other times is located in the forehead, the vertex, or the occiput, and at still other times exhibits a unilateral dis- tribution — uremic hemicrania. Obstinate neuralgia, particularly supra-orbital and occipital, is not rarely dependent upon uremia. Some patients complain of migratory muscular and articular pains. Vertigo, a sense of weight and pressure in the head, also are symp- toms of uremia. Frequently disorders of the special senses are present ; the pupils not rarely are unusually small — uremie myosis — and they react but sluggishly to light. At times sudden blind- ness occurs — uremic amaurosis — which may disappear in the course of a few hours or days. Many patients complain from time to time of deafness and tinnitus aurium. An important symptom of uremia is frequent and persistent vomiting — uremic hyperemesis — probably in consequence of irritation of the vagus. Consciousness is often obtunded. The patients lie for days, and even for weeks, in a state of stupor, and are often delirious. At times they become violent and maniacal, and enter into a pro- nounced psychopathic condition. When consciousness is lost the respiration often acquires a Cheyne-Stokes character. Uremic convulsions occur frequently. These are usually clonic, and but rarely tonic. They may involve circumscribed groups of nerves and muscles, and consist in briefly transient muscular twitching ; or there may be general clonic convulsions, with loss of conscious- ness, completely resembling an epileptic attack — uremic eclampsia. The duration and the number of the convulsions are susceptible of great variation. At times the attacks succeed one another at short intervals for days, the patient not returning to consciousness after the termination of the individual attack. At times they present the distinct character of cortical convulsions, beginning in a given extremity, and then, in accordance with the anatomic situation of the individual motor cortical centers, extending to the remaining extremity of the same side, and then to those of the opposite side. Rarely uremic paralysis occurs, in the form of monoplegia and hemi- plegia. Anatomic alterations may not be discernible in the central nervous system. In isolated cases I have observed circumscribed edema of the pia in the neighborhood of the central convolutions of the cerebral hemisphere on the side opposite to that of the hemiplegia. At times transitory paralysis 398 GEyiTO-URIXARY ORGANS l)ersists after uremic convulsions. I have, however, also observed perma- nent hemiplegia in consequence of cerebral hemorrhage during the con- vulsive seizure. Sometimes violent uremic tremor is noticeable. Some patients complain of paresthesia (crawling, prickling, a sense of cold). Particularly disagreeable is the often obstinate itching of the skin — cutaneous pruritus. Among the nervous mani- festations of uremia are attacks of intense dyspnea — uremic astlima. Attacks of uremic cardiac asthma have also been observed. Among the injiainmatory ^/jani'/e.s-to^ion.S' of nremia, diseases of the skin may be mentioned, and which have been dignified with the euphonious designation of uremicles. Among these belongs particularly chronic eczema, although I have also observed herpes zoster in the course of uremia. At times obstinate diarrhea occurs. This may be char- acterized by the putrid odor of the stools, which contain at times necrotic shreds of the intestinal mucous membrane. Some patients suffer from obstinate hoarseness, the cause for which may be found on laryngoscopic examination to be chronic edema of the laryngeal mucous membrane. In isolated rare instances I have observed yellowish necrotic deposits upon the laryngeal and pharyngeal mucous membrane, from which super- ficial uremic ulcers developed. A most serious manifestation is the occurrence of acute edema of the glottis, which may cause death by suffocation w'ithin a short time. At times symptoms of pneumonia appear suddenly. The serous membranes are particularly predisposed to inflamma- tion, so that uremic pleurisy or pericarditis, less commonly, peri- tonitis or meningitis, is encountered. The saturation of the body W'ith toxic, excrementitious substances in uremia is at times indi- cated by symptoms of blood-dissolution, which can scarcely occur otherwise than in consequence of impairment of the nutrition of the walls of the blood-vessels, so that these readily rujiture or become unduly permeable for red blood-corpuscles. Often fre- quent or profuse bleeding from the nose — uremic epistaxis — occurs; or there may be vomiting of blood — uremic hematemesis. Also cutaneous hemorrhage — uremic purpura — and bleeding from the gums have been observed. Uremic patients generally present a pallid complexion. The facial expression appears distorted, and the eyes often stare vacantly into distance. In many instances the expired air possesses a urinous odor, obviously resulting from decomposed urea, and thus from ammonium carbonate. In isolated instances of uremia following scarlet fever and cholera a Avhitish deposit has been observed to remain upon the skin after previous sweat- ing, and which upon chemic examination proved to be urea — so-called uridrosis. The bodily temperature is subnormal in the majority of cases, although elevation of temperature may occur when inflammatory processes arise, at times with uremic convul- sions, and at times also without demonstrable cause. Great atten- UREMIA 399 tion should be given to the state of the pulse, for some cases of uremia depend upcm attacks of cardiac failure, and this can be most certainly recognized from the smallness of the pulse and its deficiency in tension. At times the outbreak of an attack of uremia is preceded by unusual slowing of the pulse. The urine is gener- ally diminished in amount. If its elimination can be augmented, the large number of tube-casts in the urinary sediment is often striking, and which obviously had previously obstructed the uriniferous tubules. The course of uremia may be acute, subacute, or chronic. It may happen that apparently healthy persons are suddenly seized with uremic convulsions and death occurs. Perhaps examination of the urine after death will for the first disclose the fact that the patient has suffered from an unrecognized contracted kidney. The subacute cases may extend over eight weeks, and even more, while the chronic cases persist for months and years. In the latter event it is the rule for such marked improvement to occur at times that the patient believes himself cured. Death may take place in a uremic convulsion from cerebral or neural paralysis, or it may be due to edema of the glottis or of the lungs, or an attack of pneu- monia, of pleurisy, or of pericarditis may terminate life. At times exhaustion becomes excessive. The diagnosis of uremia is easy if adequate attention be di- rected to the eliminative relations of the urine and the presence therein of albumin. Otherwise confusion with diseases of the brain, epilepsy, meningitis, mental disease, cutaneous disease, disease of the stomach, and even other diseases, is scarcely to be avoided. Katurally a diagnosis of uremia will never be sufficient, but in every instance an effort must be made to determine the nature and the causes of the condition, because the treatment will be indi- cated accordingly. Anatomic Alterations. — No specific anatomic conditions are as yet known to be associated with uremia. At times, but by no means with particular frequency, edema and anemia of the brain are observed. The inconstancy of these conditions is un- equivocal testimony against the view that tlie nervous manifesta- tions of uremia are dependent upon edema and anemia of the brain. At times peculiar necrotic alterations and destructive pro- cesses take place upon the intestinal mucous membrane — uremic in- testinal ulcers. These have been attributed to irritation of the mucous membrane by ammonium carbonate resulting from the de- composition of urea excreted from the blood-vessels and deposited upon tlie mucous membrane. Prognosis. — The prognosis of uremia is always serious, although it depends largely upon the fact w^hether the causes are susceptible of removal or not. Accordingly, it is, for instance, more favorable in cases of acute nephritis, or of impaction of a 400 GEXITO-URIXABY ORGANS calculus, than in those of contracted kidney, because under the latter condition the disease is incurable. Treatment. — The treatment of uremia must always be an individualizing and causal one. Phimosis or stricture of the urethra should be at once relieved. In the presence of stupor or of paralysis of the bladder the urine should be systematically evacuated with a carefully sterilized catheter. In order to in- crease the secretion of urine and hasten the elimination from the body of possible toxic products of metabolism an abundance of inUk should be reconnuended. When stupor is present intestinal infusions of lukewarm milk or of physiologic salt-solution (0.75 per cent.) should be made tlirice daily. If the patient does not retain the infusion, even though not more than 300 c.c. of fluid have been used, subcutaneous infusion of salt-solution should be practised. If the secretion of urine does not improve, diuretics, diaphoretics, or drastics may be employed to cause increased elim- ination of water. Should these measures also fail, resort should be had to venesection. If the patient exhales a markedly urinous odor, lemonade and benzoic acid ivith camphor should be given in order to neutralize the ammonium carbonate : R Benzoic acid, 0.3 (4J grains); Camphor, 0.05 (f grain ); Sugar, 0.5 {7J grains). — M. Make 10 such powders. Dose : 1 powder everv two hours. Feebleness of pulse, faintness of heart-sounds, and other signs of cardiac weakness require the administration of large doses of digitalis : R Powdered digitalis-leaves, 0.1 (li grains); Diuretin, 1.0 (15 " ); Sugar, 0.5 [1\ " ).— M. Make 10 such powders. Dose : 1 powder every three hours. The last two indications can also be met by the following pre- scription : R Powdered digitalis-leaves, 0.1 (1^ grains) ; Benzoic acid, 0.3 (4} " ) ; Camphor, 0.05 (J grain ) ; Sugar, 0.5 (7^ grains).— M. Make 10 such powders. Dose : 1 powder every three hours. At times individual prominent symptoms will require symptom- atic treatment. Attempts have been made to control persistent eclamptic convulsions by continuous inhalation of chloroform. For uremic neuralgia phenacetin or anfipi/rin may be advised (1.0 — 15 grains — thrice daily). INIarkcd itchiuir of the skin niav l)e re- lieved by tepid baths (28° R.— 35° C— 95° F.)and inunctions of HYPOSTATIC KIDNEY 401 the skin with a carholated ointment (carbolic acid, 2.0 — 30 grains ; wool-fat and lard, each, 25.0 — | ounce), etc. HYPOSTATIC KIDNEY (VENOUS HYPEREMIA OF THE KIDNEY). etiology. — Hypostatic kidney develops when the escape of venous blood from the kidney is interfered with. The condition develops most commonly in the sequence of general venous stasis in connection with chronic diseases of the heart and the respiratory- organs. Enfeeblement of the right ventricle is invariably the source of the stasis in this connection. Less commonly hypostasis of the kidney develops in association with diseases of the abdom- inal cavity, as, for instance, abdominal tumors that exert pressure upon the inferior vena cava above the point of entrance of the renal veins. Finally, hypostatic kidney may develop as a result of local obstruction or occlusion of the renal veins, as, for instance, by thrombosis. Instances of the latter variety, which are as yet of little significance clinically, are distinguished from those of the two varieties first named by the fact that the arterial supply to the kidneys is unaltered, while under other conditions it is likewise interfered with. Anatomic Alterations. — Hypostatic kidneys are generally enlarged. Accordingly the capsule of the kidney appears dis- tended on section of the organ — retracts from the cut surface. The surface of the kidney appears smooth and presents a dark-red color. Frequently the greatly distended stellate veins upon it are conspicuous. Upon section of the kidney, although the cortex is deeply reddened and the Malpighian bodies often appear as dark-red granules, the reddish-black discoloration of the medullary structure is particularly marked. The consistency of the renal tissue appears increased, and this fact, in conjunction with the dark-red color, has given rise to the designation cyanotic induration of the kidneys. Microscopic examination discloses great over-distention with blood of the glomerular loops and of all of the veins. If the condition has existed for a long time, however, striate thickening of the glomerular capsules and of the membrana propria of the uriniferous tubules takes place. There may be also hyperplasia of the interstitial connective tissue. As a result of con- traction of the connective tissue the surface of the kidney acquires a nodular appearance, and often the capsule of the kidney is in places adherent to the surface of the organ. Such a condition is designated aXso cyanotic contracted kidney. At times extravasations of blood have taken place into the inter- stitial connective tissue, the Malpighian capsules, and the uriniferous tubules. At times, however, only the remains of hemorrhage are found, in the form of brownish granules of hemoglobin. Symptoms and Diagnosis. — Hypostasis of the kidney is attended with characteristic alterations in the urine. The amount 26 402 GENITO-URINARY ORGANS of urine is decreased (below 1500 c.c.), largely as a result of diminished arterial supply, for with occlusion of the renal veins alone the secretion of urine has rather been found increased. The urine is reddisii in color (high-colored, saturated), its reaction is strongly acid, and its specific gravity is increased (usually above 1020). The urine contains albumin, but only in small amount, and the urinary sediment isolated hyaline tube-casts, round cells, and at times also a few red blood-corpuscles. Often urates are precipitated as a pulverulent deposit — so-called brick-dust or lateri- tious sediment. In addition there occur edema of the lower extremi- ties, ascites, and other manifestations of stasis. In contradistinction from diffuse, acnte nephritis, in the diagnosis of hypostasis of the kidney it is to be borne in mind that the disorder is generally induced by chronic disease of the heart or the respiratory organs, and that the amount of albumin and the number of tube-casts and of red blood-corpuscles is usually small. The course of Jii/postcms of the kidneys is, as a rule, chronic, in accordance with the causa- tive conditions. Often exacerbations and remissions occur in con- formity with the functional activity of the right ventricle. Hypo- static kidneys as such scarcely ever cause death, which, as a rule, results in consequence of cardiac paralysis or of suffocation from excessive hydrothorax and hydropericardium. Prognosis. — The prognosis depends upon the curability of the causative conditions. Usually it is possible to increase the strength of the heart and to overcome the manifestations of stasis repeatedly. Subsequently, however, the remedies fail to exert their effect, and death is then unavoidal)le. Treatment. — The treatment is the same as that for weakness of the myocardium (pp. 23 and 24). DIFFUSE NEPHRITIS. ACUTE DIFFUSE NEPHRITIS. Ktiology. — Acute diffuse nephritis is either of infectious or of toxic nature. Infectious acute nephritis occurs most commonly in connection with infectious diseases. It is encountered with ]>artic- ular frequency in the sequence of scarlet fever and dipiitheria, but it may arise also in the sequence of other infectious diseases. Among the more frequent antecedent conditions may be mentioned fibrinous pneumonia, erysipelas, typhoid fever, acute articular rheu- matism, malaria, syphilis, etc. In relation to the connection between infectious diseases and acute neph- ritis, two possibilities may be considered ; namely, either the conveyance of specific bacteria or pyogenic cocci to the kidneys, with the development of inflammation ; or irritation of the kidneys in the elimination of bacterial poisons — toxins — through the kidneys. In accordance with previous experi- ence, the second possibility appears to be the more commonly effective. DIFFUSE NEPHRITIS 403 At times acute nephritis occurs as an independent infectious dis- ease. I have observed such occurrence repeatedly in members of a family and in servants in endemic distribution, and have demon- strated the presence of the Staphylococcus pyogenes albus in the urine. In the development of refrigeratory (^rheumatic) and trau- matic acute nephritis exposure to cold and injury are probably only contributing factors, favoring infection of the kidneys with bac- teria, among which the Streptococcus pyogenes has been recognized in some cases. Among the varieties of acute infectious nephritis belong also those arising by extension from adjacent disease. Thus, acute nephritis not rarely complicates gonorrhea, cystitis, pyelitis, or paranephritis. Toxic acute nephritis may be induced by the use of certain medicaments and poisons, among which maybe men- tioned cantharides, oil of turpentine, other balsamics, active diu- retics, potassium chlorate, potassium nitrate, quinin, sulphuric^ nitric, hydrochloric, and carbolic acids, mercuric chlorid, etc. In addition to the digestive tract, the injurious substances may gain entrance into the body in the act of respiration (oil of turpentine) through the air-passages, or by means of inunctions and the like. Irritating ointments containing carbolic acid, pyrogallic acid, and remedies for scabies are well adapted to induce acute nephritis. Possibly that form of nephritis that at times develops in the secjuence of chronic cutaneous eruptions and hums of the shin is a variety of toxic nephritis. Acute diffuse nephritis occurs at all periods of life. In children it develops generally in connection with diphtheria and scarlet fever. At times the primary disorders are so ill defined as not to attract attention, and the acute nephritis appears to be an independent disease. Anatomic Alterations. — In the presence of acute, diffuse nephritis the kidneys are enlarged, and their capsules are there- fore tensely distended, on section quickly retracting toward the hilus. The surface of the kidney is smooth and presents a greater or lesser number of small extravasations of blood. As a rule, the surface of the kidney is of a vivid, red color, although now and then pale kidneys are encountered. Upon section small extrava- sations of blood are appreciable, particularly in the cortex. At times the Malpighian bodies are conspicuous on account of in- crease in size, and marked distention with blood. The medulla of the kidney often presents a deep-red color. On microscopic examination of the kidneys all varieties of acute nephritis probably agree in the distention with blood of the blood-vessels and the vas- cular loops. Extravasations of blood are frequently encountered, at times in the interstitial connective tissue, at other times in the capsule, and at still other times, finally, within the uriniferous tubules. The involvement of the Malpighian bodies, the interstitial connective tissue, and the epithe- lium of the uriniferous tubules, in the inflammatory process, is susceptible of wide variations. Often the cavity of the capsule is filled with an albu- minous fluid, which has in part displaced the loops of blood-vessels from 404 GENITO-URINARY ORGANS the inner surface of the capsule. At times concentric thickenings of the capsule, resembling the layers of an onion, are appreciable, greatly dimin- ishing the cavity of the capsule, and at the same time compressing the vas- cular convolution. Cell-niulti])lication has, however, taken place also between the individual vascular loops. The nuclei of these loops are them- selves increased in number, here and there in a state of fatty degeneration, and in places the vessels are occluded by thrombi. Under such circum- stances the condition is designated gloinerulonephrUls, and these alterations are observed with particular frequency in connection with scarlet fever. More or less marked fatty degeneration has taken place in the epithelial cells of the convoluted uriniferoHS tubules. If the epithelial cells exhibit a marked ten- dency to desquamation, the condition has been described as acute desqua- mative nephritis. Frequently numerous uriniferous tubules are filled with tube-casts. Other tubules contain numerous round cells. Such a condi- tion has also been described as acute catarrhal nephritis. The interstitial connective tissue of the kidneys contains collections of round cells, which at times may be so large as to be visible to the unaided eye as small nodules. This condition has been designated also acute bjmphomatous nephritis. In the different varieties of acute diffuse nephritis at times one kind, and at other times other kinds of alterations preponderate. The question has been much disputed which of these alterations has been the earliest. In our opinion this is variable. Symptoms and Diagnosis. — Acute diffuse nephritis, like most diseases of the kiduey, is susceptible of recognition only from the alterations in the urine. Above all, the urine is con- spicuous from its bloody appearance and the hemorrhagic sedi- ment. At times the urine is light red in color, resembling meat- Avater, but frequently it is reddisli brown or brownish black from the presence of methemoglobin in considerable amount. On microscopic examination of the urinary sediment red blood-cor- puscles are generally found, presenting an unaltered appearance, or frequently a biconvex or a .spherical shape. At times ameboid movement and constrictions are observable. Often the red cells have yielded up their coloring-matter, so that they appear as colorless discs of double contour — so-called blood-shadows. Fre- quently accumulations and collections of the smallest granules and flocculi of blood coloring-matter are observed. Cylindric struc- tures also are not uncommonly present, ajiparently consisting of coherent hemoglobin. The urinary sediment often reveals the presence of blood by its brownish color. The amount of sediment is often quite considerable, so that it forms a dense cloudy precipi- tate. In addition to the red blood-corpuscles and hemoglobin, there occur in the sediment also round cells, epithelial cells from the uriniferous tubules, and tube-casts. The last are at times hyaline, at times granular, and are not rarely covered with round cells, epithelial cells from the uriniferous tubules, and red blood- corpuscles (Fig. 56). Although the presence of blood in the urine — hematuria — is a common symptom of acute nephritis, it is not unexceptional, and cases occur in which the urine is free from blood. Under such conditions the detection of albumin in the urine — albuminuria — DIFFUSE NEPHRITIS 405 and of tube-casts, round cells, and epithelium from the uriuiferous tubules in the urinary sediment is of special importance. The amount of albumin in the urine may be so considerable that on boiling and addition of nitric acid the urine solidifies into a firm coagulum. The average amount of albumin is about 0.5 per cent. In addition the physical properties of the urine should be given consideration in cases of acute nephritis, as the amount of urine is diminished (below 1500 c.c), its color deepened, and its specific gravity increased (about 1020). Naturally, hematuria cannot always be referred to acute nephritis. Renal hematuria is dis- tinguished from admixture of blood from the urinary passages from Q&M, Fig. 56. — Urinary sediment from a case of acute nephritis following fibrinous pneu- monia in a man, 42 years old ; containing blood-casts, red blood-corpuscles, round cells, and epithelial cells from the uriniferous tubules and lower urinary passages ; magnified 275 times (personal observation). the fact that the urine never contains clots of blood, but is inti- mately and uniformly admixed with blood. Renal hematuria occurs further in^onnection with embolism of- tbe renal artery, although this develops generally in association with valvular lesions of the heart, and the disorder sets in suddenly with pain referred to the kidney. In cases of hypostasis of the kidney the urine contains little if any blood, little alljumin, and few tube- casts, and, besides, the patients generally present chronic disease of the heart or the respiratorv organs. In cases of renal hemor- rhage from carcinoma and tuberculosis of the kidney the amount of albumin present in the urine is small, as is also the number of tube-casts, both at times even being: wantins;. Traumatic hemor- rhage from the kidneys presupposes an antecedent injury. 406 GENITO-URINARY ORGANS Local nlleralions in fJie J:i(Jnei/s arc often wanting in cases of acute nephritis. Some patients, liowever, complain of a sense of pressure, of tension, and of pain in the region of the kidneys and in the sacral region. Bimanual palpation of the kidneys often fails to induce the slightest unpleasant effect. A frequent symp- tom of acute diffuse nephritis is cutaneous edema. This often involves the face earliest, or even alone, the eyelids particularly becoming swollen, and giving rise to remarkable narrowing of the palpebral fissure. At times marked edema of the entire skin is the earliest sign of which the patient has taken notice. This may reach so considerable a degree that the skin appears distended to the point of rupture. Often accuraulation of JiuicJ takes place in the serous cavities, and hydrothorax and ascites particularly are not uncommon complications. It is noteworthy that the patient generally exhibits marked pallor, and examination of tlie blood dis- closes that within a short time diminution in the number of red corpuscles and in the percentage of hemoglobin takes place. The pressure in the aortic system undergoes rapid change, and the l)lood-pressure increases. As a result the aortic-diastolic sound becomes accentuated, often with a tympanitic-ringing character, and the radial pulse becomes tense. In explanation of this mani- festation irritation of the myocardium by metabolic products re- tained in the blood must be assumed. After a time hypertrophy of the left ventricle develops. The increased arterial blood-pressure appears with especial distinctness in pufse-tracings (sphygmograms). "While the reflux elevation becomes less, the first elevation due to elasticity becomes considerably increased. After complete recovery has taken place these manifestations are neutralized (Figs. 57 and 58).' The bodily temperature may remain unchanged, although as a rule it is elevated. At times the temperature reaches 39° C. Fiu. 57. — Pulse-tracins from a man. 22 years old. with acute refrigeratory nephritis, on the eighth day of the disease (personal observation, Zurich clinic). (102.2° F.) and above, and if at the same time there should be abdominal distention, diarrhea, and enlargement of the spleen, confusion with typhoid fever is possible ; but. naturally, the Widal blood-serum reaction will always be wanting in cases of acute nephritis. The patients c(im]ilain frequently of drawing pains in the muscles and the joints. Sleep often is disturbed ; while the DIFFUSE NEPHRITIS 407 appetite is lost, thirst is increased. Not rarely there are difficulty in the evacuation of urine, frequent vesical tenesmus, and pain in the act of micturition. The duration of acute nephi-itis is susceptible of great variation. In cases of infectious disease — as, for instance, fibrinous pneu- monia — acute nephritis is not rarely observed, disappearing within Fig. 58. — Pulse-tracing from the same patient (Fig. 57), after recovery had taken place, thirteen days later. one or two days ; and it is a remarkable fact that such speedy recovery may take place spontaneously although the primary dis- order continues unchanged or is perhaps even progressive. In other instances acute nephritis may persist for from four to eight weeks. Cases also occur in which the disease persists for more than eight months, so that the condition can scarcely be designated acute nephritis. Recovery generally takes place in such a way that the hematuria becomes less pronounced and disappears entirely for a time ; the albuminuria also slowly subsides, and likewise tube- casts and urinary sediment diminish, and finally the urine is free from all foreign elements. Often increased elimination of urine — polyuria — occurs with the onset of recovery, and the urine may have a low specific gravity (down to 1005). Not at all rarely it happens that exacerbations and remissions in the disease alter- nate with each other repeatedly. The dangers of acute nephritis consist especially in suffocation as a result of edema of the glottis or of the lungs, or of excessive effusions into the serous cavities, in inflammation of the skin and septicemia, in uremia, and in transformation into diffuse chronic nephritis. Injiammation of the skin may occur in consequence of marked cutaneous edema. The skin becomes reddened and rup- tures at numerous points, so that edematous fluid escapes ; at times erysipelas or gangrene of the skin develops, and, in consequence, absorption of the exciting agents of inflammation, general septico- pyemia, which may terminate fatally. Uremia frequently reveals itself earliest by headache and vomiting, until other uremic manifestations, particularly uremic convulsions, set in. The smaller the amount of urine eliminated, the greater is the danger of uremia. Experience has shown that the causes of acute nephritis also exert an influence upon the occurrence of uremia. Uremia is unfortunately common in con- 408 GENITO-URINARY ORGANS nection with scarlatinal nephritis, while it scarcely ever attends diphtheric nephritis. The transforination of acute into acute chronic nephritis is a rare occurrence. Under such circumstances the symptoms of acute chronic parenchymatous nephritis usually develop at first, witii diminished secretion of dark urine of increased specific gravity, containing a large amount of albumin and fattily degen- erated elements in the urinary sediment (fatty granules upon tube-casts, fatty granular cells, fattily degenerated epithelial cells), together with marked cutaneous edema. Gradually the symptoms of secondary contracting kidney may be superadded. Then the edema disappears, the urine becomes excessively al)un- dant (above 2000 c.c), with a low specific gravity, a small amount of albumin, and a scanty urinary deposit. Frequently death results from uremia. Prognosis. — Acute nephritis is ahvavs a serious disease. Xo remedy with even an approximately reliable action is known, and, besides, uremia may set in at any moment and bring grave dangers. The possibility of transformation into chronic nephritis is but small, so that the prognosis is not materially made worse thereby. Treatment. — No medicament capable of exerting a curative influence upon acute nephritis is as yet known. Astringents (also known as styptics or hemostatics) are without effect upon either the hematuria or the albuminuria, and also fuchsin, brombenzol, and strontium lactate, which have been recommended to diminish the eliminaticm of albumin, are without any effect. Recovery from acute nephritis can therefore be brought about only through appropriate dietetic measures. The patient should remain con- stantly in bed as long as hematuria and albuminuria are demon- strable, for an equable temperature is always essential for patients suffering from disease of the kidneys, as also is bodily rest, for hematuria and albuminuria may be aggravated as a result of incautiously getting out of bed and walking around. A tepid bath at a temperature of 28° R. (35° C. — 95° F.), morning and evening, is useful. The patient should remain in the bath for fifteen minutes, and is then dried with a warm towel, puts on a warm shirt, and returns to bed, which likewise has been pre- viously warmed by hot-water bottles. Sudden cooling of the body is always markedly injurious for persons suffering from disease of the kidneys. The bath-room should therefore be so situated that the patient need not pass through cold apartments to enter the bath. A milk-diet is the best for the patient, as milk is both nutritious and easily digested, acts as a diuretic, and does not irritate the kidneys. Well-boiled milk should be preferred, as it is better borne and less readily undergoes fermentation in the gastro-intestinal canal, and from one and a half to two quarts DIFFUSE NEPHRITIS 409 should be given daily, care being taken that the railk be swallowed slowly in small amounts at short intervals. Should the patient exhibit a distaste for milk, it may be mixed with weak tea or coifee or with beef-broth. All irritating articles of food should be avoided, as, for instance, strong coffee, strong tea, strong alco- holics, sharp condiments, vinegar, etc. Some meat, particularly white meat, may be permitted, and is without influence upon the excretion of proteids. ISIashed potatoes and rice-pap, oatmeal- gruel with milk, and stewed fruit may be allowed. If symp- toms of uremia appear, they should be treated according to the directions given on page 400. In the presence of marked cutaneous edema incisions or punc- tures should be made into the skin, if diaphoretic measures (injec- tions of pilocarpin, hot-air bath, hot bath) have not secured the desired result. If the edematous skin becomes inflamed, cata- plasms containing mercuric chlorid (1.0 : 1000) or aluminum acetate (1.0 : 100) should be applied. CHRONIC PARENCHYMATOUS NEPHRITIS. Anatomic Alterations. — Chronic parenchymatous nephritis is designated also large ivhite kichiey on account of the appearance of the diseased organ. The kidney is considerably enlarged, and its capsule is tense and is readily stripped from the surface of the organ. The surface of the kidney is smooth, and presents a light butter-yellow color. Upon section of the kidney the renal cortex also presents a butter-yellow color, while the medullary structure is characterized by a red color. If the cut surface be scraped with the blade of a knife, a fatty deposit is made. Microscopic examination of the kidney discloses particularly marked fatty degeneration of the epithelial cells of the convoluted uriniferous tubules, which are largely converted into fatty granular cells. Fatty degenerative processes occur also in the vascular loops of the Malpighian bodies, although in lesser degree. That the conditions present are inflammatory and not merely degenerative processes will be recognized from the fact that collec- tions of round cells are present here and there in the interstitial connective tissue. The uriniferous tubules are often tilled with tube-casts. Ktiology. — Little of a definite nature is known with regard to the causes of chronic parenchymatous nephritis. The condi- tion is usually an independent disease, as cases in which the affec- tion has developed from an antecedent acute nephritis are ex- tremely uncommon. Infectious and toxic influences are the prin- cipal causative factors. Thus, the disease has been observed in the sequence of malarial fever, pulmonary tuberculosis, syphilis, chronic suppuration, lead-poisoning, excessive indulgence in alcohol. The patients are usually adults. Symptoms, Diagnosis, and Prognosis. — Of all of the symptoms the alterations in the urine are the most important. 410 GENITO-URINARY ORGANS The urine is increased in amount, although on long-continued observation this may be found almost normal for days. The urine is dark reddish-yellow or yellowish-red in color, with an increased specific gravity (above 1020). The amount of albiuniii in the urine is often quite considerable (up to 5 per cent, and more). Generally the urinary sediment is abundant, and on microscopic examination it is found to be made up of tul)e-casts, round cells, and epithelial cells from the uriniferous tubules. Of particular importance is the presence of numerous fattily degen- erated cells, fatty graiudar cells, as well as fat-drops u})on tube- casts. The patients are conspicuous on account of pallor of the skin, and accordingly the blood is deficient in red corpuscles and hemoglobin. Marked cutaneous edema is present, and the face in consequence appears puffy and distorted. Also, the serous membranes are frecpiently filled with transudates. The disease generally begins insidiously, and often progressive pallor and cutaneous edema are the earliest conspicuous manifestations. Elevation of temperature does not occur except in the presence of complications. Increase in arterial blood-pressure takes place, although it is by no means so constant as in association with acute nephritis and contracted kidney. Most patients complain of loss of appetite and irregularity in the action of the bowels. The co?fr,s-e of the disease is generally chronic, and at times extends over several years. Occasionally acute exacerbations occur, in which the urine contains blood and entirely resembles that observed in acute nephritis. These exacerbations may in some cases occur with such frequency and persist for so long a time that the condition has been spoken of as chronic hemorrhagic ncpliritis. Recovery is almost impossible. Surgeons have re- ported isolated instances in which recovery took place after the removal of sujipurating parts. In some cases death ensues from progressive exhaustion. In others it results from excessive edema, which may give rise to asphyxia, cardiac para/ysis, edema of the lunr/s or of the glottis. It may also be induced by inflammation and gangrene of the skin, with consecutive septicopyemia second- ary to marked edema of the skin. At times chronic i)arenchymatous nephritis passes into second- ary contracted kidney in consequence of hyperplasia of the inter- stitial connective tissue. Under such circumstances the amount of urine becomes increased, and may even exceed the daily amount passed in health. The color of the urine becomes light yellow, the specific gravity falls below 1015, and the amount of albumin in the urine diminishes until only traces can be de- tected. The amount of urinary sediment also becomes small, and the fattily degenerated cells become less and less numerous. The cutaneous edema disappears, while hypertrophy of the lefl ventricle progressively develops, with a hard, wiry pulse. The DIFFUSE NEPHRITIS 411 patients not rarely die in consequence of uremia, which is quite unusual in association with pure chronic parenchymatous ne- phritis. Treatment. — The treatment for chronic parenchymatous ne- phritis is the same as that for acute nephritis (pp. 408 and 409). Nothing can be accomplished with drugs. The greatest import- ance should be attached to the mode of life. Causal treatment is indicated in cases of syphilis or lead-poisoning, and will then con- sist in the administration of potassium iodid (5.0 : 200 — 75 grains : Q^ fiuidounces; 15 c.c. — 1 tablespoonful — thrice daily). Sup- puration should be controlled as speedily as possible, and if by no other means by removal of diseased parts. CHRONIC INTERSTITIAL NEPHRITIS. Anatomic Alterations. — Chronic interstitial nephritis is so designated from its chronic course, and is attended particularly with inflammatory hyperplasia of the interstitial connective tissue. As a rule, but by no means invariably, the hyperplastic connec- tive tissue undergoes contraction after a time, as a result of which the kidneys are reduced in size. From this fact is derived the name contracted kidney. As the surface of the kidney is generally uneven and nodular, the condition is spoken of also as granular atrophy of the kidneys. Severed varieties of contracted kidney must be distinguished accordingly as the process is primary or second- ary, and, if primary, whether juvenile or senile {arteriosclerotic). Some clinicians make a distinction further between embolic contracted kidney and hypostatic contracted kidney. In embolic contracted kidney con- nective-tissue hyperplasia occurs in the sequence of embolism of the renal artery. Should several emboli be present in the kidney, the organ acquires a multinodular, irregular surface and an atrophic appearance. The condi- tion is almost always observed in association with valvular disease of the heart. It has already been pointed out that connective-tissue hyperplasia and contraction may occur in connection with hypostasis of the kidney. These two varieties are to be distinguished from cardiac conlracted kidney, because in this condition the kidney is involved only secondarily in the se- quence of disease of the heart, and the affection does not represent an inde- pendent disease of the kidney. Pi'imary or genuine juvenile contracted kidney occurs in indi- viduals less than forty years old. The capsule of the kidney is often so firmly adherent to the surface of the organ that it can be removed only with some laceration of the kidney. The kidneys are conspicuous for their smallness, at times being reduced as much as one-third in size and weight. The surface of the kidney is multinodular, and the individual prominences may be of approx- imately the same size. These consist of relatively healthy renal tissue, while the depressions between them result from contracted connective tissue. Here and there cystic cavities of varying size, filled with water, at times with colloid fluid, are present. The 412 GENITO-rniyARY ORGANS surface of the kidney is grayish red in color. On section it will be found that the kidney cuts with peculiar resistance and almost like leather. Tiie cut section, like the surface, is grayish red in color. The cortical tissue is diminished in amount, being in places contracted to a band one millimeter thick. The medullary sub- stance, together with the calices of the kidney, is also diminished. The pelvis of the kidney appears rather dilated. On 7)iieroscoplc examination the changes in the inferstidal connective tissue are especially conspicuous. There will be found here foci of round-cell accumulation, which form preferably in the neighborhood of the Malpigh- ian bodies, and the interstitial connective tissue besides appears increased, so that the uriniferous tubules are separated from one another by intervals of unusual size. The Malpighian bodies also participate in the connective- tissue hyperplasia, and their capsules are transformed into thick, striated, and cellular membranes. With progressive increase of connective tissue the capsular cavity becomes reduced, and finally complete connective-tissue obliteration of the capsule takes place. The uriniferous tubules do not re- main uninvolved in the processes described. Often they are constricted off by connective-tissue hyperplasia, at times in garland-like arrangement in several divisions. Should fluid collect in the constricted portions, cystic cavities form that are appreciable microscopically. For this purpose it is naturally necessary that they .shall have attained considerable dilatation. Only in recent years has attention been called to changes in the blood-vessels, which indicate that juvenile contracted kidney is in all probability of vas- cular origin. These consist in thickening of the intima of small arteries, which in places has led to closure of the lumen of the vessel — chronic oblit- erating endarteritis. In addition, thickeningof the muscular layer and depo- sition of hyaline masses take place. Senile or arteriosclerotic contracted kidney results from arterio- sclerosis of the renal artery and its branches, and is therefore of vascular origin. It generally develops in advanced life, because arteriosclerosis is a disease of that period. Also, in cases of arteriosclerotic contracted kidney the capsule of the organ is often adherent to the surface of the kidney. The sur- face of the kidney appears uneven and nodular, and often exhibits cystic cavities. The color of the kidney is rather gray than red. On section of the kidney its tough consistency is less marked than in the juvenile contracted kidney. The cortex in places is greatly diminished. ^Microscopic examination dis- closes particularly that the inter.stitial connective-tissue hy]ier- pla.sia is not uniform, but is focal in distribution, and that calcifi- cation is often present in the partially destroyed Malpighian bodies. Secondary contracted kidney develops from chronic parenchyma- tous nephritis as a result of a gradual washing out with the urine of the fattily degenerated epithelial cells from the convoluted uriniferous tubules, so that the tul)ules undergo partial collapse, while interstitial connective-tissue hyperplasia preponderates. Microscopically the secondary contracted kidney is characterized by the preservation of a yellowish or yellowish-gray color, the DIFFUSE NEPHRITIS 413 yellow areas corresponding to fattily degenerated epithelial cells in the convoluted uriniferous tubules, and the gray areas to the hyperplastic interstitial connective tissue. At times the kidney acquires a yellowish, mottled appearance, so that it has been de- scribed as a spotted or mottled contracted kidney. Further, the sec- ondary contracted kidney may be unchanged in size and possess a smooth surface, so that the interstitial connective-tissue hyper- plasia will be disclosed only on microscopic examination. Ktiology. — Chronic interstitial nephritis results in conse- quence of infectious, toxic, or involutional influences. The infec- tious varieties of contracted kidney include those that develop in the train of infectious diseases, such as malaria and syphilis. Urocys- titis and gonorrhea also at times cause contracted kidney. Toxic contracted kidney develops in consequence of the action of lead as the so-called plumbic contracted kidney. Disorders of metabolism, and particularly gout, may also be mentioned as causes. Arterio- sclerotic contracted kidney is a result of involutional processes that attend advanced age, but nothing further is known with regard to the actual processes concerned. In cases of secondary contracted' kidney the causes of the antecedent chronic parenchymatous neph- ritis must be taken into consideration, and these, as has been men- tioned, are usually of infectious or toxic nature. Contracted kid- ney occurs with exceptional rarity in children, and it is then usu- ally a secondary condition. Further, it is at times impossible to elicit a cause for the disease. Sometimes the disorder is hereditary, possibly because a morbid condition of weakness of the walls of the blood-vessels is inherited. Exposure to cold and to wet, and indulgence in alcohol, create a liability to the disease, and were con- sidered by earlier clinicians as the actual causes. Symptoms and Diagnosis. — Contracted kidney usually develops insidiously, and is unattended with cutaneous edema. It is therefore not uncommon for the disease to be discovered quite accidentally on examination of the urine. Naturally there are certain suspicious symptoms that should always stimulate an experienced and cautious clinician to subject the urine to careful examination. Among these may be mentioned palpitation of the heart, persistent head.ache, impairment of vision, repeated epis- taxis, persistent hoarseness, frequent vomiting, obstinate eczema, and itching of the skin. The majority of these symptoms are of uremic nature. Also, the sudden occurrence of eclamptic convul- sions or of cerebral hemorrhage is often dependent upon chronic interstitial nephritis. The urine is increased in amount, and instead of from 1500 to 2000 c.c. the daily amount may reach from 3000 to 6000 c.c. and even more. Often the patients are aroused from sleep by the fre- quent desire to evacuate the bladder. The urine is pale yellow in color, and often exhibits a distinct tendency toward a greenish 414 GENITO-URINARY ORGANS tint. Frequently the urine is slightly turbid, and, after shaking, the froth is retained upon its surface for a long time, a property that is often possessed by urine containing abnormal ingredients (albu- min, sugar, biliary coloring-matter). Tiie specific gravity of the urine is diminished (below 1015), at times as low as 1002. The reaction of the urine is feebly acid. Only a slight sediment is precipitated from the urine, and not rarely none at all, and this upon microscopic examination is found to contain hyaline and granular tube-casts of varying width. The amount of all)umin present is always small, but albumin may also he absent for days and weeks. Under such conditions it is possible to confound the disease with simple polyuria — diabetes insipidus — for in this disor- der also the amount of urine is increased and the specific gravity is diminished ; but polyuria is unattended with the alterations in the heart and the pulse, and usually also with the retinal changes that attend contracted kidney. Confusion with glycosuria — diabetes mellitus — is scarcely possible, because in this condition the specific gravity of the urine, which is increased in amount, is abnormally high. At times irritative states of the urinary passages, as, for in- stance, catarrh of the urinary bladder, gonorrhea, tuberculosis, cause increased secretion of urine, with a reduction in specific gravity, but the urinary sediment will not contain tube-casts, if albumin be present its amount will correspond with the admixture of pus or of blood with the urine, and changes in the circulatory apparatus and in the retina do not occur. The alterations in the circulatory apparatus take a conspicuous part in the clinical picture of contracted kidney. Hypertrophy of the left ventricle develops with great constancy in conjunction with a generally slight dilatation. The hypertrophy of the heart-muscle gives rise to a heaving and resistant apex-beat, and an accentu- ated, frequently tympanitic and ringing diastolic (second) aortic sound. Dilatation of the left ventricle gives rise to increased extent of the apex-beat, and to its displacement outside the left mammillary line and below the left fifth intercostal space. Further, after a time dilatation and hypertrophy of the right ventricle frequently also develop. The connection between contracted kidnetj and hypertrophy of the myocar- dium of fhe left side of tlie heart has not yet been definitely established. The conditions found in acute nephritis indicate that also here irritative influences due to toxic substances retained in the blood must be thought of. Endarteritic alterations similar to those that occur in the contracted kidney itself have, however, also been observed in the blood-vessels, and it is con- ceivable that the hypertrophy of the heart-muscle is attributable to these. The earlier view that the hypertrophy of the heart-muscle is a result of destruction of numerous blood-vessels in the diseased kidneys has properly been abandoned, for hypertrophy of the heart does not develop even after amputation of both lower extremities, although a far more extensive vascu- lar area is removed, and the blood-pressure in the aortic system is in con- sequence greatly increased. DIFFUSE NEPHRITIS 415 The hypertropliy of the left side of the heart is appreciable to the patient as distressing palpitation, which usually occurs particularly after mental and physical excitement, and after the ingestion of stimulating fluids (coffee, tea, alcohol). Reference has already been made to this complaint as one of the suspicious symptoms of contracted kidney. The hypertrophy of the muscle of the left side of the heart is manifested further in unusual hard- ness of the radial pulse, in correspondence with the increased blood-pressure in the aortic system. The pulse often feels like an irou wire, whence it has been designated also the iviry 'pulse. A trained hand can frequently detect the presence of contracted kidney from feeling the radial pulse. In the indse-tracing or sphygmogram the abnormal increase in blood- pressure is exhibited in the small size of the reflux elevation, and the un- usually marked character of the first, elasticity-elevation (Fig. 59). Further, the blood-pressure in the radial artery has been measured by means of the sphygmomanometer of v. Basch, and it has been found to be as high as 244 mm. of mercury instead of 160. Fig. 59. — Pulse-tracing from the right radial artery in a ease of chronic interstitial nephritis in a man 27 years old (personal observation, Zurich clinic). Retinal changes occur, according to my experience, in one-fifth of all the cases. Particularly characteristic are yellowish spots around the macula lutea, which result from sclerosis of the axis- cylinders in the retina, and larger spots in the neighborhood of the optic papilla, which depend principally upon fatty degenera- tion of the granular layers. These alterations constitute the con- dition of albuminuric retinitis. In addition, there are frequently also swelling of the optic papilla and retinal hemorrhages, venous hyperemia, and tortuosity of the veins. The mode of origin of these nutritive disturbances in the retina is unknown. Visual acuity may be preserved in spite of the retinal changes, but fre- quently complaint is made of obscuration and impairment of vision. Persons wnth contracted kidneys often present unusual pallor, which is dependent upon diminution in the number of red blood- corpuscles and in the percentage of hemoglobin. Rapid emacia- tion generally takes place, and the patients tire readily. The skin usually feels extremely dry, and exhibits a tendency to desquama- tion. Obstinate eczema also is frequently present. The bodily- temperature exhibits no noteworthy alteration. Although the 416 GENITO- URINARY ORGANS appetite is impaired, the sense of thirst is increased, obviously in consequence ot' tlie increased elimination of urine, and often the jxitient complains of dryness of the mouth and of stickiness of the tontjue. The course of contracted kidney is chronic, and not rarely extends over several years. Most patients die of uremia, which may set in suddenly and may terminate fatally within a short time, or in other instances be repeated from time to time. Occasionally cerebral heuiorrhage — encephahrrhagia — occurs in the first place, because in cases of contracted kidney the blood-vessels of the brain likewise often undergo degeneration, and also because hyper- trophy of the muscle of the left side of the heart, and the resulting increase in the blood-pressure in the arteries, increase the liability to rupture of blood-vessels. At times symptoms of iceakness of the heart-muscle appear. Gallop-rjiythm becomes audible over the heart, hypostatic edema develops, and finally cardiac paralysis and asphyxia. Xow and again acute exacerbations in the inflammatory process in the kidneys occur, and the urine contains blood and resembles that of acute nephritis. There is also a great tendency to inflammatorij processes in various organs, and death not rarely results, particularly from pneumonia. Prognosis. — Contracted kidney is an incurable disease, and the prognosis is accordingly grave. Albuminuric retinitis is an unfavorable symptom, for death usually follows within two years. Treatment. — The treatment is the same as that for acute nephritis. Well-to-do patients may be recommended a sojourn in Southern climates in order to escape the dangers of fluctuating and cold weather. Particularly a residence on the borders of the African desert (Helouan) often has a remarkably favorable influ- ence upon the albuminuria. PURULENT NEPHRITIS. Ktiology. — Purulent inflammation of the kidney probably occurs only as a result of the entrance of pyogenic micro- organisms into the kidney. Chemic irritation and suppuration in the kidney scarcely occur in human beings. In addition to the Streptococcus pyogenes and the Staphylococcus pyogenes aureus and albus, the Bacterium coli ])articularly has been shown to be capable of exciting suppuration, and this organism appears to play the principal part in the etiology of suppuration of the kidneys. Pneumoniacocci and typhoid-bacilli have also been found in isolated instances. Bacteria can gain entrance into the kidneys in any of three ways : namely, through the urinary passages, the blood-vessels, or the lymphatics. Infection of the kidneys by way of the urinary passages is probably the most common, and just under such conditions the Bacterium coli PURULENT NEPHRITIS 417 appears to be the exciting agent with particular frequency. Gonorrhea and stricture of the urethra, cystitis, and pyelitis are not rarely attended with purulent nephritis. The disorder occurs with especial frequency in association with renal and vesical cal- culi. Urinary stasis of whatever origin greatly favors infection of the kidneys. Not rarely this develops in the sequence of sur- gical operations upon the bladder or the urethra — as, for instance, after the introduction of sounds or catheters — and the condition has been designated surgical kidney. Naturally the danger of infection is particularly great if most scrupulous disinfection of the instruments employed is not practised. Infection of the kidneys by way of the arteries occurs in con- nection with suppuration of the kidneys of embolic origin. The suppuration associated with idcerative endocarditis is best known, but similar processes are probably operative when purulent ne- phritis develops in the sequence of other infectious diseases. The lymphatics will constitute the medium of infection particularly when inflammatory processes in the neighborhood (paranephritis) have extended to the kidney. Infectious agents may be intro- duced into the kidney directly through wounds inflicted by in- struments (dagger, knife, gun), but it should be borne in mind that suppuration of the kidney may occur also in consequence of closed injuries, as, for instance, a fall, a blow, or a contusion of the loin, and even after violent concussion of the body. At times it is impossible to elicit a cause for suppuration of the kidney — cry mitogenetic purulent nephritis. Some patients then attribute the condition to cold, but on careful inquiry they are usually able to give no definite information with regard to this factor. In any event, refrigeratory (rheumatic) suppuration of the kidney can be accepted only in the sense that the exposure to cold alone did not excite the suppuration, but merely favored infection of the kidneys through alterations in the circulation and the resulting diminished powers of resistance of the tissues. Sup- purative nephritis is an uncommon disease, which usually occurs after the fifteenth year of life, and is more common in men than in women. Anatomic Alterations. — In advanced cases of purulent nephritis little or none of the tissue of the kidney will be left^ so that the capsule of the organ, which frequently is thickened^ consists of a sac filled with pus. Under such circumstances the condition may be designated also pyonephrosis, or, if the pelvis of the kidney has actively participated in the inflammatory pro- cess, suppui'ative pyelonephritis. In less advanced cases the kidney contains one or more small foci of suppuration, which here and there exhibit a tendency to coalesce. The suppuration generally begins in the form of small, scarcely visible submiliary and mili- ary abscesses, the coalescence of which gives rise to larger and 27 418 GEMTO- Ulil^A li Y OIK iA SS larger acciinuilations of i)ii.s. In the presence of embolic abscesses of the kidney the infective enibolns can be fonnd at the center of the lesion. The cellnlar elements in the immediate vicinity of tl»e enibolns exhibit necrosis, and the peripheral boundaries of this necrotic area are surrounded ))y collections of round cells. Also, the uriniferous tubules are filled Avith bacteria, and not rarely form within the papillie of the kidney straight grayish-white lines converging toward the apex of the papillae. Purulent nc])hritis is at times bilateral, for both embolic processes and iniiauimatory processes arising by extension from the bladder are quite well capable of involving both kidneys in the morbid process. Symptoms and Diagnosis. — In the diagnosis of purulent nephritis three groups of symptoms particularly are important, namely, those of general septicopyemia, local alterations in the kidneys, and changes in the urine. The disease, like all other supi)nrative processes, is attended with fever, which at times is interrupted by chills. The fever freqnently exhibits a remitting type. There is a marked tendency to frequent, profuse, and debili- tating sweats. The patients generally soon become pallid, lose appetite, complain of increased thirst, and not rarely suffer from diarrhea. The local alterations in the kidneys consist, in the first place, in renal pain, which may occur spontaneously or be induced by pressure in the loin. Frequently the diseased organ can be felt on bimanual palpation, and it will be found to be enlarged. At times fluctuation is appreciable. As always in palpating the abdominal organs, the patient should lie with the head dependent and the lower extremities flexed at the hips and the knees, in order to relax the abdominal walls. The examination should be made only with warm hands, in order to avoid the rigidity of the abdom- inal muscles induced by cold. If necessary, the hands should be immersed in warm water. The patient should be engaged in conversation during the examination, in order to divert his attention therefrom. It may also be serviceable to have the patient lie upon the healthy side. Naturally, foci of suppuration in the kidney must have attained -a certain size before they can give rise to appreciable enlargement of the organ, and therefore such increase will not be present when the collections of pus are small. The associated pyelitis usually present may take a considerable share in causing enlargement of the kidney. It may also happen that the kidney is at times larger and at other times smaller, accordingly as the pus has free exit into the bladder or undergoes stagnation. In the presence of purulent nephritis the urine contains pus — pyuria — as soon as the purulent accumulation has ruptured into the urinary passages. Under such conditions the presence of albumin can i)e demonstrated in the urine, to an amount corre- sponding with the amount of })us. Larger amounts of albumin PURULENT NEPHRITIS . 419 and tube-casts will be present in the urine only when a diffuse inflammation of the kidney has been superadded to the purulent nephritis. Blood is not rarely present in the urine if blood-vessels are perforated in the process of destruction of the kidney. The presence of desquamated renal tissue — renal sequestra — is particu- larly significant ; but this occurrence is uncommon. The sequestra may at times attain the size of a pigeon's ego^, and on microscopic examination exhibit the structure of renal tissue. Often the amount of urine is increased in consequence of reflex irritation of the renal nerves. Under such circumstances the urine is light yellow in color and of a low specific gravity. The urine often undergoes alkaline fermentation. Kot rarely the patients complain of vesical tenesmus and of pain in the evacuation of urine. The diagnosis of suppuration of the kidney may be extremely difficult, because in the presence of small encapsulated foci of pus in the kidney local alterations in the kidney and in the urine may be absent. Should pyuria be present, the possibility of tubercu- losis of the urinary organs should be considered, although this would be attended with the presence of tubercle-bacilli in the urine. Purulent nephritis is distinguished from suppuration in the urinary passages by means of the local alterations in the kidney. The course of sujjpuration of the kidney may be acute, subacute, or j3hronic, and in the last-named event it may extend over many months. Among the complications renal colic should first be men- tioned. This results in consequence of temporary obstruction of the ureter by plugs of pus or exfoliated renal tissue, with the development of acute urinary stasis in the affected ureter and pelvis of the kidney. The patients then usually complain of sudden, severe pain in one loin, are at times seized with a chill and vomiting, and the bodily temperature rises to a higher level. The urine becomes diminished in amount and often quite clear, because it is secreted by the free healthy kidney. In consequence of acute urinary stasis in the pelvis of the kidney — acute hydro- nephrosis — the diseased organ either becomes palpable, or, if it has previously been palpable, it becomes increased in size. As soon as the obstruction to the flow of urine is removed the pain ceases, the temperature declines, and often remarkably large amounts of urine are evacuated, the fluid being now again purulent and turbid. Should the obstruction not be removable, there will be danger of uremia and urinary septicemia. Among the less common occurrences are paralysis of the lower extrem- ities — urinary paraplegia — which has been attributed to neuritis resulting by extension from the kidney. The situation becomes extremely grave when the accumulation of pus ruptures not into the urinary passages, but into the sur- rounding tissues. Rupture into the abdominal cavity usually causes rapidly fatal peritonitis ; rupture into the pararenal cellular tissue 420 GENITO-URINABY ORGANS gives rise to paranephritis. Rupture may take place also into the stomach, the intestine, the pleural cavity, or, after the previous formation of pleuritic adhesions, into the l)ronchial tul)es. At times the pus ruptures externally, and an external renal fistula is formed. Under such conditions extensive burrowing of the pus is possible. Long-continued suppuration of the kidney at times gives rise to amyloid disease and its dangers. At times death re- sults in consequence of progressive exhaustion or of urinary septi- cemia, the latter resulting from absorption of bacteria from the decomposed urine into the blood. Prognosis. — The prognosis of purulent nephritis has become more favorable within recent years from an appreciation of the fact that the disease is a surgical disorder which cannot be influ- enced by internal remedies. Nevertheless the disease is still a serious one. Treatment. — The single possible means by which an accumu- lation of pus in the kidney can be removed consists in neplurotomy or nephrectomy. Nephrotomy will suffice when the diseased organ still contains considerable healthy tissue. Otherwise nephrectomy should be performed, and the diseased kidney removed from the body. EMBOLIC INFARCTION OF THE KIDNEY. > !^tiology. — Embolic infarction of the kidney occurs princi- pally in connection with disease of the aortic or mitral valve, in consequence of the detachment of small thrombotic vegetations that gain entrance with the blood-current into the renal artery^ or more commonly into small branches thereof, and there become impacted. Only rarely is the condition dependent upon detached echinococcus-vesicles, or fragments of tumors of the myocardium, upon detached tlirombi from arteriosclerotic areas in the aorta or from aortic aneurysms, or upon thrombi from the pulmonary veins. Anatomic Alterations. — Emboli gain entrance most com- monly into the blood-current through the left renal artery, because this arises from the abdominal aorta at less nearly a right angle than the right renal artery. Only rarely does an embolus remain lodged in the trunk of the renal artery. When it does, necrosis occurs in almost the entire portion of the kidney cut off from its blood-supply. As a rule, emboli are swept into the smaller branches of the renal artery, where they give rise to the formation of wedge-shaped renal infarcts. These reach the surface of the kidney with a broad base, while their apices are directed toward the medullary aspect. The wedge-shaped area cut off from its blood- supply undergoes speedy coagulation-necrosis, and acquires a yel- lowish-gray color. Its boundaries appear blood-stained from the AMYLOID KIDNEY 421 presence of emigrated red blood-corpuscles. Subsequently fatty degeneration and absorption of the area may take place, so that only a small, superficial, depressed cicatrix remains upon the sur- face of the kidney. If the kidney is the seat of multiple emboli, it may acquire a multinodular appearance suggestive of contracted kidney, and the condition has been designated arteriosolerotic con- tracted kidney. At times calcification takes place in renal infarcts. Not rarely both kidneys are the seat of emboli. Symptoms and Diagnosis. — Embolism of the kidney may be recognized generally from the sudden occurrence of pain in the loin. Pressure in the same situation discloses also tenderness. A chill, followed by elevation of temperature and vomiting, often occurs in consequence of reflex irritation. The urine becomes bloody — hematuria — and not rarely contains also tube-casts and rather more albumin than corresponds to the amount of blood. In addition the demonstration of a source of embolism, thus generally a valvu- lar lesion of the heart, will be important in the diagnosis. The symptoms may disappear in the course of a few days, although re- currences are possible at any moment. Prognosis. — Embolic infarction of the kidney is not a serious disorder, providing the embolus does not contain bacteria nor pos- sess infectious properties, so that suppuration of the kidney is not to be feared. Treatment. — Rest in bed and a milk-diet should be prescribed, an ice-bag applied to the affected loin, and if the pain be intense a subcutaneous injection of morphin may be given. AMYLOID KIDNEY. etiology. — The causes of amyloid kidney are the same as those of amyloid disease of other organs — chronic wasting dis- charges and cachectic conditions of all kinds ; as examples may be mentioned suppuration of bones and joints, chronic diarrhea, pul- monary tuberculosis, syphilis, malaria, and carcinoma. Only rarely does amyloid kidney develop without appreciable cause. As the same causative factors are also capable of inducing chronic parenchymatous nephritis, it will be understood that both diseases occur together with great frequency. Anatomic Alterations. — Uncomplicated -amyloid kidney is extremely rare. In the presence of diffuse amyloid degeneration the kidneys present a pale-yellow or whitish appearance, whence the designation waxy kidney. The kidneys are increased in size. Their capsule is readily detached from the surface of the organ, and the latter presents a smooth appearance. The consistency of the organ is increased. The renal tissue at times presents an ap- pearance as if frozen, so that it can be shaved from sections of the kidney. Thin sections appear translucent in transmitted light. 4-J.2 GEMTO-L'HiyAHY (JllUASS If a solution of iodin and potassium iodid be poured upon the cut surface, tliis will assume a mahogany-brown tint. In the majority of cases the large white kidney already described will be encoun- tered, and the presence in this of areas of amyloid degeneration can be demonstrated from the appearance of the mahogany-brown color on addition of the solution of iodin and potassium iodid. On microscopic examination the amyloid tissue is characterized by its waxy luster and its swollen and structureless appearance. It yields, besides, the amyloid reactions with the solution of iodin and potassium iodid, with the solution of iodin and dilute sulphuric acid and methyl-violet described on pp. 343 and 344. The vascular loops in the ^Ialj)ighian bodies are attacked earliest; then the efferent vessels and the straight vessels are involved; and finally also the capillaries between the uriniferous tubules aud in the medulla of the kidney, the capsules of the Malpighian bodies themselves, the mem- brana propria, and the epithelial cells of the uriniferous tubules. Generally other organs also are the seat of amyloid degenera- tion, particularly the spleen, the cortex of the adrenal bodies, the liver, and the intestines. Symptoms and Diagnosis. — In the presence of uncompU- cated amyloid kidney the amount of urine is normal or slightly increased. The urine is pale yellow in color, and its specific gravity is diminished (from 1010 to 1015). The urine generally contains considerable albumin (up to 20 grams — 300 grains — daily), although isolated instances are on record in Avhich albumin- uria was absent throughout. The urinary sediment is generally slight, and at times contains remarkably wide cylinders of Avaxy luster. Some tube-casts may also yield the amyloid reaction, although this is not distinctive of amyloid disease of the kidneys, as it may occur also in connection with diffuse nephritis. As a rule, there is marked edema. The primary disorder itself \\'\\\ cause pallor of the skin. Death usually takes place in consequence of progressive exhaustion or of excessive edema. Should amyloid disease of the kidneys exist in association with chronic parenchy- matous nephritis, the symptoms of the latter will be the more con- spicuous, and there is no infallible symptom Ijy which the amyloid degeneration can be recoo;nized with anv deo-ree of certaintv. Amyloid kidney will be present, in all probability, if increased size and consistency of the spleen and the liver indicate amyloid degeneration of these organs. Should the intestine be involved in amyloid disease, diarrhea also will be present. Prognosis. — The prognosis of amyloid disease of the kidney is uutavoralile, as recovery appears impossil)le. Treatment. — In the first place, the same dietetic regulations should i)e prescribed as in diffuse nephritis (pp. 408 and 409). Among drugs, iron and iodin have been employed, as, for instance : R Sirup of iron iodid, Simple sirup, each, 50.0 (lo fluidounces). — M. Dose : 10 c.c. (a dessertspoonful) thrice daily. CARCINOMA OF THE KIDNEY 423 CARCINOMA OF THE KIDNEY. Ktiology. — Carcinoma of the kidney may be either primary or secondary. Often ilo cause is ascertainable for primary carci- noma of the kidney. The patients often attribute the condition to traumatism. Possibly renal calculi also may give rise to carcinoma of the kidney. Experience has shown that men are attacked oftener than women. Although carcinoma of the kidney occurs with particular frequency after the fiftieth year of life, it consti- tutes an exception as compared with carcinoma in other organs from the fact that it has been observed in numerous instances also in children within the first five years of life. Secondary carci- noma of the kidney results either through direct extension of the new-growth from the neighborhood, or through metastatic dis- semination from remotely situated organs. Not rarely it develops in the sequence of carcinoma of the testicle, even if the diseased organ was removed many years previously. Anatomic Alterations. — Primary carcinoma of the kidney generally develops only in one kidney, whereas secondary car- cinoma frequently appears in both organs. In cases of secondary carcinoma of the kidney the new-growths generally consist in cir- cumscribed nodules, whereas in cases of primary carcinoma diiFuse infiltration of the kidney takes place. Under these conditions the kidney may be greatly increased in size and weight, although it usually retains its shape in considerable degree. On section of the kidney the new-growth will at times present a dense fibrous appear- ance, with a deficiency of fluid, at other times a soft and medul- lary appearance, and at times be traversed by cavities containing colloid material, so that a distinction is commonly made between fibrous carcinoma (scirrhus), medullary carcinoma, and colloid car- cinoma (alveolar or gelatinous carcinoma). The neoplastic tissue is generally grayish white or yellowish white in color. At times it contains numerous blood-vessels, and then presents a reddish appearance. Also, blood-vessels may rupture and copious extrava- sations of blood take place into the carcinomatous tissue, and these, after having existed for a considerable time, acquire a reddish-brown, chocolate-like appearance. The carcinomatous cells are considered as offspring of the epithelial cells of the uriniferous tubules. Extensive careinomata of the kidney not rarely cause displacement of adjacent organs (liver, stomach, spleen, intestine). Symptoms and Diagnosis. — Carcinoma of the kidney may remain unrecognized so long as it does not undergo disintegration, and thereby give rise to alterations in the urine, or so long as demon- strable enlargement of the kidney is not present. Under the most favorable circumstances latent carcinoma may then be suspected from progressive emaciation and pallor, although doubt may remain as 424 GENITO-URINARY ORGANS to the scat of the disease. Carcinoma of the kidney frequently gives rise to hematuria, resulting from ])erforation of blood-vessels in the process of disintegration of the carcinomatous tissue. Hema- turia in advanced life, occurring without demonstrable cause, should always arouse suspicion of carcinoma of the kidney. The hemor- rhage may be abundant, persist for a long time, be repeated at short intervals, and as a result cause alarming anemia and serious loss of strength. Examination of the urinary sediment may prove of importance, for, although it is true that carcinoma-cells pre- sent in themselves nothing peculiar, it Avill nevertheless always be highly suspicious if many cells are present, and particularly cell-groups with multiple nuclei. The bloody urine is often evacu- ated without discomfort. In some cases, however, attacks of renal colic occur which result from temporary obstruction of the ureter by blood-clots of considerable size, or by aggregations of cells. The patients often complain persistently of severe pain in the loin, which is particularly prone to occur at night and disturb sleep. At times the patients are able to walk only with the body bent forward, at the same time avoiding with fear all possible rotation or flexion of the vertebral column. Pressure in the loin is generally painful. If the kidney has become increased in size in consequence of car- cinomatous proliferation, it at times gives rise to a considerable visible enlargement in the loin and of the abdomen. In diagnosis tlie detection on palpation of a tumor in the loin, which is usually nodular, painful, and hard, is important, although carcinoma of the kidney also may be fluctuating. If the carcinoma is of small size, it may at times be possible to reach it with the fingers by having the patient lie upon the healthy side of the body and make deep inspirations while bimanual palpation of the kidney is prac- tised. It is by no means always easy to determine with certainty that an ab- dominal tumor is of renal origin. It should be noted, in the first place, that the tumor in question is situated in the loin or has arisen therefrom. Besides, renal tumors do not undergo displacement with the respiratory movements, and generally retain the bean-shaped form of the kidney. They are separated from the lower border of the liver by a tympanitic zone on percussion, because the transverse colon passes between the two organs Finally, a sausage-shaped body usually passes over its anterior surface from below upward, and this may from time to time be seen to be the seat of peristaltic movement. This corresponds with the ascending or descending colon displaced from its normal situation. It becomes especially distinct on insufflation of the rectum with air, and on jjercussion it then yields a tympanitic note. Extensive tumors of the kidney displace the liver, the dia- phragm, the lungs, and the heart upward, and as a result cause marked dyspnea, palpitation of the heart, and a sense of constric- tion. Pressure upon the stomach and the intestines induces vomiting and irregularity in bowel-movement. Patients with car- CYSTIC KIDNEY 425 cinoma of the kidney usually undergo rapid emaciation and become exceedingly pale. Death results, as a rule, within a year in consequence of carcinomatous marasmus. At times complica- tions arise, such as 7'upture of the new-growth into the abdominal cavity, into blood-vessels, or externally. Rupture into the ab- dominal cavity is generally followed by rapidly fatal peritonitis, while rupture externally gives rise to an external renal fistula, and rupture into the blood-vessels to hypostatic edema. Pressure upon adjacent nerves may give rise to intercostal neuralgia or paralysis of one lower extremity. The tumor may also penetrate the vertebral canal through the intervertebral foramina, and cause spinal pressure-paralysis. Prognosis. — The prognosis of carcinoma of the kidney, like that of carcinoma in other organs, is unfavorable. The only hope for recovery depends upon early operation. Treatment. — Nothing can be accomplished in the treatment of carcinoma of the kidney by means of internal remedies. When the diagnosis has been established no time should be lost in the performance of nephrectomy. If the appropriate time for opera- tion has been neglected, or if the patient declines operation, all that remains is symptomatically to administer narcotics for the relief of severe pain, and styptics for the control of profuse hem- orrhage. In addition, an effort should be made to sustain the strength by means of a nutritious diet. In addition to carcinoma, sarcoma and adenoma of the kidney possess clinical significance. Both of these are indistinguishable from carcinoma during life. Sarcoma of the kidney is frequently of secondary origin and bilateral. Sarcoma of the kidney is observed also in children in the first five years of life. At times sarcomata contain transversely striated muscu- lar fibers (striocellular myosarcoma). Adenoma of the kidney not rarely originates from displaced elements of the adrenal gland. CYSTIC KIDNEY. Anatomic Alterations. — Cystic kidney consists in a trans- formation of one or often both kidneys into a multilocular struc- ture, which may attain considerable proportions and greatly dis- place adjacent organs. The individual cavities frequently contain fluid, at times also colloid material in which, remarkably, no urea, and at most uric acid, can be demonstrated. At times scarcely a trace of renal tissue can be recognized. The walls of the indi- vidual cavities consist of connective tissue. Their inner surface is lined with longitudinally arranged endothelial cells ; here and there collections of epithelial cells are present. The condition is probably always a congenital one, and it is often associated with other malformations (harelip, club-foot, absence of the renal pelvis and the ureter, absence of the duct of Botal). 420 GENITO-URINARY ORGANS Opinions are divided as to the 7node of origin of conrjenilal cystic kidney. According to the view of some, it results from urinanj staitis during fetal life, which may occur either in consequence of inflammatory alterations in the jjapillse of the kidney and obstruction of the uriniferoiis tubules, or from failure in the establishment of proper relations between the glomeruli and the convoluted uriniferous tubules and the deeper uriniferous tubules in the development of the kidney. Others consider the condition as a neo- plastic one {cyst adenoma). Both views are supported by certain evidence: the first, for instance, by the fact that congenital cystic kidney has been observed in association with congenital phimosis, and the second by the fact that congenital cystic kidney may suddenly increase in size in advanced life. Possibly both modes of development occur. Htiolog"y. — Nothing is known with rejrard to the causes of congenital cystic ki(hiev. At times several members of the same family are victims of the disease. Symptoms and Diagnosis.— At times cystic kidneys attain stich considerable proportions during fetal life as to cause obstruc- tion to labor, and delivery can be effected only after embryotomy. In other instances the children are born alive, but })resent so large a renal tumor that death soon occurs from asphyxia and cardiac paralysis. In still other instances no symptoms at all are present for years. Then, however, the kidney becomes greatly enlarged, and gives rise to symptoms and dangers in consequence. Such observations naturally often give the impression that the disorder has developed after birth. In the diagnosis the demonstration of a tumor of the kidney is important in the first place, and this has been discussed on p. 424. The tumor itself often presents a nodular surface, so that it may be readily mistaken for carcinoma of the kidney. In contradistinction from abscess and echinococcus of the kidney and hydronephrosis, fluctuation is, as a rule, not elicitable. Should exploratory puncture be decided upon, it is important to bear in mind that tirea will not be found in the fluid. The urine is frequently unaltered, although hematuria may occur periodically. Albuminuria is not rarely observed. The patients complain principally of a sense of tension and of pain in the loin and in the abdominal cavity. Dis])lacenient upwai^d of the liver, the spleen, the diaphragm, the lungs, and the heart gives rise to dyspnea and jDalpitation of the heart, and at times causes death by suffocation or paralysis of the heart. Some patients die from uremia in consequence of suppression of urine. Cystic kidneys may also rujiture, and thereby occasion serious dangers, as, for instance, perfoi'ative peritonitis. Prognosis. — The prognosis of cystic kidney is unfavorable, because the cysts have a tendency to undergo enlargement, and in conscfjuence to be attended with various dangers. Treatment. — The treatment of cystic kidney is surgical, and consists in puncture of the cysts or nephrectomy, although the latter should be performed only when the other kidney is healthy with certainty. ECHINOCOCCUS OF THE KIDNEY 427 ECHINOCOCCUS OF THE KIDNEY* Ktiology. — With regard to the cause of echinococcns of the kidney, the statements made upon pp. 350 and 351 concerning echinococcns of the liver are applicable. Human beings acquire echinococci by swallowing the ova of the tapeworm of the dog — Taenia echinococcns. An explanation is wanting for the fact that echinococcus-C3^sts develop at times in one and at other times in another organ. Anatomic Alterations. — Echinococcns of the kidney is generally unilateral, and, as experience has shown, it is most com- monly situated upon the left side. The cyst is unilocular, and it may at times be larger than an adult head, and, in addition to fluid, contain also daughter-cysts and granddaughter-cysts. Cho- lesterin-plates and crystals of uric acid, calcium oxalate, and ammonio-magnesium phosphate may frequently be demonstrated in the fluid. At times only small remnants of renal tissue are still present. The healthy kidney often appears hypertrophied. Symptoms and Diagnosis. — The diagnosis of echinococcus of the kidney is absolutely certain only when echinococcus-vesicles, echinococcus-scolices, or echinococcus-hooklets can be demonstrated in the urine. This will be possible only wdien the mother-cyst. has ruptured and evacuated its contents into the pelvis of the kidney. Under such conditions symptoms of renal colic (sudden pain, chill, fever, vomiting) frequently first appear, as long as the echi- nococcus-cyst causes obstruction of the ureter. Additional uri- nary disturbances occur when the echinococcns-cyst obstructs the urethra. At times the echinococcus-cyst is suddenly expelled forcibly for a considerable distance with a loud sound, and is suc- ceeded by turbid, milky urine resembling soapsuds. Expulsion of echinococcus-vesicles with the urine may be repeated at inter- vals of varying length, and for a period of years. In this way natural recovery may take place. Should expulsion of echino- coccus-cysts with the urine not take place, echinococcus of the kidney can be recognized only when a tumor of the kidney has developed. Should this be wanting, the cyst will remain con- cealed. The tumor of the kidney, the essential points in whose diagnosis have been stated on p. 424, is generally nodular and yields fluctuation, though not constantly. The differentiation from cystic kidney, abscess of the kidney, and hydronephrosis is often impossible. Exploratory puncture may yield the desired information from the discovery of echinococcus-scolices or echino- coccus-hooklets in the fluid. At times an echinococcus-cyst of the kidney undergoes suppuration, and the clinical picture may then even more closely simulate that of abscess of the kidney. Rupture of an echinococcus of the kidney into adjacent organs (stomach, intestine, pleural cavity, lungs, and bronchi), or into 428 GENITO-UBINARY ORGANS the abdominal cavity, or externally, may also take place at times. AVlien the kidney has undergone considerable increase in size symptoms of pressure upon adjacent organs will appear — gastric and intestinal disturbances, dyspnea to the point of asphyxia, palpita- tion of the heart, and cardiac paralysis. Prognosis. — The prognosis of echinococcus of the kidney is not unfavorable if the disorder is looked upon as a surgical one, and too nuich time is not consumed with internal treatment. Treatment. — Echinococcus-cysts cannot be destroyed by in- ternal remedies. Injections of mercuric chlorid (1 : 1000) into the echinococcus-cyst may possibly cause death and contraction. In the presence of an extensive echinococcus-cyst of the kidney, nephrotomy or nephrectomy should always be resorted to, accord- ingly as considerable healthy renal tissue is present or not. MOVABLE KIDNEY. etiology. — jNIovable kidney occurs with great frequency, particularly in pallid and emaciated women. Not rarely the kid- ney is forcibly displaced from its natural situation by pressure, particularly as a result of tight lacing, the wearing of constricting waist-bands, and the like. In men who from vanity wear corsets or tight belts movable kidney develops in the same way as in women. At times movable kidney is induced by heavy lifting and persistent expulsive effort, because the diaphragm as a result thereof exerts pressure upon the kidney. Wandering kidney is, therefore, com- mon in persons with chronic cough and constipation. In some cases the condition has been observed to develop in the sequence of a fall or a blow upon or an injury to the loin. At times wander- ing kidney occurs as a result of emaciation, as, for instance, after protracted febrile disease, or after reduction-cures, ol^viously be- cause as a result the capsule of the kidney likewise yields up some of its fat and its support of the kidney is lost. Occasionally wandering kidney appears after the puerperium, in consequence of relaxation of the abdominal walls and diminution in the intra- abdominal pressure. Increased weight of the kidney may also give rise to wandering kidney, as, for instance, when the organ is the seat of carcinoma or tuberculosis. At times the kidney is forcibly displaced from its situation, as, for instance, by tumors of the liver, the spleen, the pancreas, or in consequence of kyphoscoliosis of the vertebral column. In some cases nervous influences appear to be operative. Thus, movable kidney is not at all uncommon in cases of tabes dorsalis. The frequent association of wandering kidney and diseases of the female generative apparatus is likewise often referred to the nervous influence of the latter upon the kidneys. There is, probably, also, a congenital j^t'edisposition to wandering MOVABLE KIDNEY 429 kidney. The aflPection is rare in childhood, although isolated instances of congenital movable kidney are on record. Symptoms, Diagnosis, and Anatomic Alterations. — Many persons possess a movable kidney without suspecting the fact. The condition may be found accidentally on careful exam- ination of the kidneys. It can be detected with especial ease if, with the abdominal walls relaxed, bimanual palpation of the kid- neys is practised and deep inspirations are encouraged. Most com- monly the right kidney is movable, and this is diie to the fact that it is subjected to a certain degree of pressure by the superimposed liver. The left kidney is much less commonly affected, and least commonly both kidneys are movable. The mobility of the kidney may attain varying degrees of intensity. In the mildest cases the lower extremity of the kidney can just be felt on deep inspiration, and some clinicians even believe that this is a natural and not a morbid manifestation. In advanced cases the entire kidney can be felt, and be moved up and down in its fatty capsule. In the aggravated cases the kidney is wholly displaced from its normal situation, and may be found in the abdominal cavity, sometimes in the iliac fossa and even in the true pelvis. Some clinicians designate only cases of the last kind as wandering kidney or mi- g7'ating kidney. Under such circumstances the kidney may possess such a degree of mobility that it can be readily moved to and fro in the abdominal cavity. Naturally it may happen also that the organ becomes adherent in some abnormal situation, where it again becomes immovable. As a matter of course, marked downward displacement of the kidney is possible only when the organ possesses an abnorm- ally long mesonephron. At the same time the renal artery and vein must be unduly lengthened. At times the patients them- selves first notice a movable body in the abdomen accidentally, and come to the physician in great alarm, fearing the presence of carcinoma. Under such circumstances it often requires most earnest assurances in order to relieve them of this fear. In other instances the physician discovers the readily movable kidney accidentally in the course of an abdominal examination for some other purpose. That the body is the kidney will be recognized from the bean-shaped form of the tumor. Its surface is smooth, and pressure causes a dull, painful sensation. At times — according to my experience quite rarely — the loin upon one side will be found upon inspection to be depressed, and, on comparison with the opposite side, it will yield a tympanitic note on percussion, which will be replaced by a dull percussion-note when the mov- able kidney has been restored to its normal situation. At times pulsation of the renal artery can be felt in the hilus of the kidney. Not rarely the patient with wandering kidney applies to the 430 GENITO-URINARY ORGANS physician for the relief of various comphiint.s, as the cause for which tlie wandering- kidney is found. Indivi(hials with wander- ino- kidney often suffer from a liigh degree of nervousness. Fre- quently, complaint is made of disagreeable rather than painful drawing sensations in the abdominal cavity and in the loin. Often gastric disorders have developed, such as loss of appetite, eructa- tion, and vomiting. Investigation of the functions of the stomach often discloses the fact that the absorption-period for potassium iodid is retarded, and that the motor power of the stomach is diminished, so that the food remains in the stomach for a consider- able time. Often the gastric juice is deficient in hydrochloric acid. Less commonly, in my experience, there is an excess of hydrochloric acid in the gastric juice. After distention of the stomach with carbon dioxid the viscus will be found at an un- usually low level, so that, in addition to the displacement of the kidney — nephroptosis — there is also displacement of the stomach — gastroptosis. jS^evertheless, dilatation of the stomach may develop in connection with \vandering kidney either because, in the presence of right-sided wandering kidney, the pylorus becomes obstructed by pressure or traction, or because, in consequence of anemia and nervousness, the walls of the stomach imdergo relaxation. Often, there is obstinate constipation, which may increase to the decree of intestinal obstruction, and this mav at times be due to the pressure exerted by the movable kidney upon the bowel, and at other times to atony of the intestinal musculature. In some patients attacks of hepatic colic occur, with sudden pain in the region of the gall-bladder, jaundice, frequent vomiting, and at times also fever. The clinical picture deceptively resembles that of gall-stone colic, and results from acute biliary stasis caused by pressure or traction upon the ductus choledochus. Further, in consequence of biliary stasis and hypostatic catarrh in the biliary passages, gall-stones are not at all uncommon in association with Avandering kidney. At times peculiar attacks occur, which have been designated incarceration of a icandcring I'iclnei/. The patients complain of severe pain in the location of the wandering kidney, and the organ generally is also extremely sensitive to touch. The kidney often is greatly increased in size, and as, at the same time, the urine is diminished in amount, the enlargement of the organ may be dependent upon urinary stasis and acute dilata- tion of the pelvis of the kidney — paroxysmal hydronephrosis. Fever is present and vomiting is frequent. Such a condition may develop without demonstrable cause, although some patients attribute it to bodily over-exertion or to sudden change in posture. Obviously the disorder is dependent solely upon sudden occlusion of the ureter and acute urinary stasis, resulting from either twist- ing of the kidney about the long axis of its ureter or sudden displacement downward of the kidney and kinking of its ureter. MOVABLE KIDNEY 431 Generally the condition corrects itself in the course of a few days. At times it disappears rapidly if the kidney is restored to a more favorable situation through the adoption of a given position of the body or as the result of efforts at reposition. The occurrence of the change for the better is often manifested by the evacuation of large amounts of urine within a short time. At the same time the kidney becomes greatly reduced in size. It is noteworthy that in women the symptoms of wandering kidney are generally inten- sified at the menstrual period. I have had under observation women in whom wandering kidney could be demonstrated dis- tinctly almost only at the menstrual period. The demonstration of a wandering kidney during life is therefore of importance, because the condition might be readily overlooked after death if the kidney has accidentally been restored to its usual situation when the body is placed in the recumbent posture. Prognosis. — Wandering kidney is a troublesome and fre- quently an incurable condition, although, as a rule, it is not attended with danger to life. Symptoms of incarceration will only excep- tionally be followed by death from uremia. In the prognosis the observation is Avorthy of consideration that a wandering kidney exhibits a tendency to carcinomatous degeneration. Treatment. — As a prophylactic measure, the wearing of tight clothing and constricting waistbands and belts should be strictly forbidden. Not much can be accomplished with internal remedies in the treatment of movable kidney. Only in emaciated persons will rest in bed and a fattening diet sometimes be followed by replacement of a wandering kidney as soon as the fatty capsule of the organ has been sufficiently developed and gives the organ greater support. Naturally, this result can be expected only in cases that are not too far advanced. Individuals Avith wandering kidney should avoid bodily strain and secure an easy evacuation of the bowels daily. Women should not lace their clothing tightly, but should Avear it suspended from bands passing over the shoulders. The Avearing of an abdominal bandage mav be recommended, surrounding the abdomen from the umbilicus down- Avard, and by pressure forcing the kidney upAvard toward its natural position. Bandages Avith compresses, designed directly to force the kidney upward, rarely fit Avell. Often the movable organ slips from beneath the compress, and the bandage then does more harm than good. At times wandering kidney has been relieved by massage. In cases in which the symptoms are aggravated surgical treatment has been attempted. The most certain pro- cedure consists in removal of the moA^able kidney — nephrectomy ; but this Avill preferably not be undertaken, because it is not rarely obserA^ed that the function of the other kidney foils, and death results from uremia. As a rule, it will therefore suffice to suture the kidney in its normal situation — neplirojrhaphy. Naturally, 432 GENITO-URINARY ORGANS it may happen tliat after some time the kidney will again become movable, and permanent relief is not afforded. Such complications as may arise should be treated according to the usual rules. In cases of incarceration of a wandering kidney efforts should l)e made to replace the organ, hot cataplasms should be applied, warm tea should be drunk, and, if pain be considerable, morphia may be administered subcutaneously. Dystopia of the kidney is the designation given to an immovable displace- ment of the kidney which may be eitlier congenital or acquired. Congenital displacement of the kidney is generally left-sided. At times the organ is found in the true pelvis. By causing contraction of the pelvis, obstruction to labor may result. Acquired displacement of the kidney may occur in connection with wandering kidney if the organ becomes attached in an abnormal situation, but sometimes it occurs also as the result of pressure upon the kidney by adjacent organs. HORSESHOE KIDNEY. Horseshoe kidney results from the coalescence of the two kid- neys into a single organ. Generally the two lower poles of the kidneys are united, so that a semilunar or horseshoe-shaped body results, with its concavity directed upward. The ureters traverse the anterior aspect of the body downward. The coalescence of the kidneys is associated with their displacement, for generally the two organs are situated upon the anterior aspect of the lumbar vertebra. Occasionally, the kidneys coalesce at the margins of the hilus. In this way there results a disc-shaped or cake-shaped body, which may possess a single pelvis, but giving off two ureters. Symptoms are usually absent, and often the condition is discov- ered either accidentally on careful examination of the abdominal cavity, or possibly only upon post-mortem examination. The diagnosis is by no means easy, and other abdominal tumors must, in the first place, be excluded. Besides, it may be found that the loins are depressed, and on percussion yield a tympanitic note. ABSENCE OF THE KIDNEY. At times one kidney may be absent, and the knowledge of this fact is naturally of the greatest importance in considering the operation of nephrectomy. The condition may be congenital or acquired. Thus, the kidney has occasionally been found trans- formed into a mass of fat. Sitperniimerary J:idncys are without clinical significance. INFLAMMATION OF THE PARARENAL CONNEC- TIVE TISSUE (PARANEPHRITIS). Ktiology. — Inflammation of the loose and partly fatty con- nective tissue surrounding the kidney scarcely occurs other than as a result of the activity of bacteria, and among the exciting INFLAMMATION OF PARARENAL CONNECTIVE TISSUE 433 agents thus far isolated are the Streptococcus pyogenes, Staphylo- coccus pyogenes, Bacterium coli, tubercle-bacilli, pneumonia- cocci, and actinomyces. Exposure to cold may be a contributing factor in the development of infection of the pararenal connective tissue by bacteria, although the occurrence of a refrigeratory (rheumatic) paranephritis can scarcely be accepted as demonstrated with certainty. On the other hand, traumatic paranephritis un- doubtedly occurs. IN^ot only gunshot-wounds, stab-wounds, and open wounds generally may be mentioned in this connection ; but falls and blows upon and other injuries to the loin, and violent concussion of the body, and even heavy lifting, may be operative. At times paranephritis may follow antecedent infectious disease, as, for instance, typhoid fever and septicopyemia. Most commonly^ paranephritis arises by extension from adjacent inflammation. It often develops in the sequence of pyelonephritis (particularly witli urinary calculi), carcinoma, tuberculosis, and echinococcus of the kidney, and at times of embolism of the kidney. Paratyphlitis also may extend upward, and excite paranephritis. At times ulcers in the ascending or descending colon rupture into the pararenal connective tissue, and give rise to paranephritis. In addition, parametritis, periproctitis, carcinoma and tuberculosis of the vertebrse, abscess of the liver and of the spleen, duodenitis, psoitis, and purulent pleuritis may be mentioned as causative con- ditions. Men suffer most frequently from paranephritis. The disorder is less common in childhood than in adult life. Anatomic Alterations. — The principal alterations of para- nephritis consist in purulent infiltration of the pararenal connec- tive tissue, which, however, soon becomes transformed into a col- lection of pus. The latter generally does not become encapsulated, and often the pus is admixed with tissue-detritus. Not rarely it possesses putrid properties. The kidney is usually marked by great mobility. At times paranephritis is complicated by peri- nephritis, and inflammation, and even accumulation of pus, may take place within the capsule of the kidney. The inflammatory process may also extend to the tissue of the kidney itself, and cause purulent destruction of this organ. At times inflammation and erosion of the vertebrae and purulent infiltration and de- struction of adjacent muscular structures have been observed. Symptoms and Diagnosis. — The symptoms of paraneph- ritis are in part local and in part general. Only rarely does para- nephritis set in like an acute infectious disease, with a chill and high fever. Far more commonly the disease begins insidiously. Often, complaint is first made of pain in the loin, which is usually increased upon pressure. The patients generally assume a con- strained attitude, walking with the upper portion of the body bent forward and toward the diseased side ; or in bed they lie upon the diseased side, holding the vertebral column convex toward the 28 434 GENITO-URINARY ORGANS healthy side, with the lower extremity upon the diseased side flexed at the hip-joint and the knee-joint. The diattr(ilysis of the bladder depends upon the causative factors in the individual case. Prognosis. — Whether paralysis of the liladder is curable or not depends mainly upon the causative factors. If these be incurable, the principal danger consists in the readiness with which decomposition of the urine takes place and the frequently com- plicating inflammation of the bladder, and which in turn may give rise to pyelonephritis and urinary septicemia. IMPOTENCE IX THE MALE 463 Treatment. — In the presence of paralysis of the bladder attention should be given to systematic evacuation of the viscus. At times this end can be attained by pressure upon the bladder through the abdominal wall ; otherwise resort must be had to the introduction of a catheter, which naturally must be carefully sterilized. Artificial evacuation of the urine should be practised thrice daily. lu order to strengthen the muscular coat of the blad- der cold frictions should be applied over the bladder, subcutaneous injections of strychnin or of ergotin made, and the galvanic or the faradic current employed. In addition, careful attention ' should be given to the treatment of the causative conditions — causal therapy. IV. DISEASES OF THE MALE SEXUAL ORGANS. IMPOTENCE IN THE MALE. Ktiology. — Inability to effect coitus successfully is designated impotence in the male. At times the condition is dependent in a purely mechanical manner upon diseases of the penis, which prevent the introduction of the male organ into the vagina. The penis may be unduly short, or it may be rendered so from the presence of marked hydrocele or of scrotal hernia. Angular distortion of the penis in consequence of cicatrices or new-growths may cause impotence. Diseases of the testicles may give rise to impotence if the secretion of seminal fluid is abolished, for, as a rule, erection takes place only when the testicles secrete semen. At times im- potence in the male results from wasting discharges and exhaus- tion, and develops in the sequence of severe diseases, such as con- tracted kidney, diabetes mellitus, onanism, and venereal excesses. Toxic impotence may occur as a result of tlie protracted use of potassium bromid, camphor, lupulin, arsenic, salicylic acid, and morphin. At times impotence in the male is caused by nervous influences. Frequently it occurs in the course of tabes dorsalis. Xeurasthenia also is not rarely attended with impotence. Psychic impotence is particularly to be mentioned. This results from a fear on the part of the patient that he is not potent, and this para- lyzing dread either prevents entirely erection of the penis or per- mits but transient erection, or there occur premature discharge of semen and rapid flaccidity of the penis. Psychic impotence occurs at times in chaste persons, particularly on the first attempts at sexual intercourse. It occurs also in masturbators, in whom a guilty conscience exerts a paralyzing influence as soon as an attempt at normal sexual intercourse is made. Also, the dissolute 464 GENITO-URINARY ORGANS habitue of the brothel is at times attacked with psychic impotence in sexual intercourse with his wife. Psychic impotence may be manifested t)nly in sexual relations with certain women. Some men are capable of overcoming this by certain devices which are mostly repulsive to a healthy mind. Psychic impotence particularly has an injurious influence upon the mental state, and often induces suicide. Impotence in the male may be temporary or permanent, accord- ingly as the causative factors are curable or irremediable. The prognosis and the treatment also depend upon the nature of the cause. In the presence of neurasthenia, in addition to nervines, courses of treatment with cold water, in the mountains or at the seaside, will be necessary. In cases of psychic impotence the patient should by intelligent encouragement be imbued with confidence in his poteuce. Too frequent sexual intercourse and attempts at intercourse during alcoholic intoxication should par- ticularlv be avoided. Under such conditions also cold sponging of the hypogastrium and a sojourn in the mountains or at the seaside are often to be recommended. At times good results are secured from hypnosis and suggestion. Upon the latter probably depend the favorable effects reported from the employment of tablets of testicular tissue and injections of testicular fluid or of sperm. Applications of the galvanic and of the faradic current to the lumbar spine and to the sexual organs have also been made. STERILITY EST THE MALE, Sterility in the male is present if in spite of natural methods of coitus no seminal fluid is discharged into the vagina of the woman — so-called aspermatism ; or if the seminal fluid introduced does not contain fructifying spermatozoids — azoospermia. Aspermatism is most commonly due to obstruction of the semi- nal ducts ; less commonly it is caused by nervous disturbances. Aspermatism is often dependent upon stricture of the urethra in consequence of chronic gonorrhea. Disease of the prostate gland also not rarely causes aspermatism, as the enlarged gland may compress the urethra and thereby diminish its lumen, or as a result of contracting changes may give rise to such a deflection that the semen when ejaculated will not escape anteriorly, but posteriorly into the bladder. Disease of the seminal I'csicles may cause asper- matism by exerting pressure upon and diminishing the lumen of the ejaculatory ducts. At times phimosis is responsible for asper- matism if the urethra is, as a result, materially constricted. In- juries to the j)erineum are also capable of causing aspermatism through compression of the ejaculatory ducts. Occasionally the condition has been observed after operations for stone, if the ejaculatory ducts have been cut by. the surgeon's knife. Psychic aspermatism occurs principally in neurasthenic indi- INVOLUNTARY DISCHARGE OF SEMINAL FLUID 465 viduals ; coitus can be effecteil without difficulty, but ejaculation may not take place or onlv in intercourse with certain women, but not with others. This form of aspermatism occurs especially in masturbators and in men who have engaged excessively in illegit- imate sexual intercourse. Under such circumstances it may happen that ejaculation of seminal fluid fails to take place, especially in sexual intercourse with the wife. A variety of" jjhysiologic asper- matism occurs in healthy men who indulge in sexual intercourse at too short intervals. Aspermatism is readily recognizable from the fact that in sexual intercourse ejaculation of seminal fluid does not take place at all, or occurs only after the penis has become flaccid and has been withdrawn from the vagina. Should an ejaculation have taken place, but into the bladder, turbid urine containing many spermatozoids will be evacuated after the act of coitus. The duration and the prognosis, as well as the treatment of aspermatism vary in accordance with the causative factors. In cases of psychic aspermatism an endeavor should be made to im- prove the general condition, while the patient should be encour- aged with assurance, nervines be administered, courses of treat- ment with cold water, in the mountains and at the seaside, be pursued, and applications of electricity be made. Azoospermia is characterized by an absence of the secretion of the testicles, and therefore of fructifying spermatozoids, although in the sexual act secretion is discharged from the seminal vesicles and the prostate gland. The condition can be readily recognized on microscopic examination. The ejaculated fluid possesses the so-called seminal or spermatic odor, because this is due not to the secretion of the testicles — the true seminal fluid — but to that of the prostate gland. Azoospermia is a most common disorder. Most sterile marriages arc dependent upon azoospermia, and not upon the often insignificant displacements and other abnormalities of the unoffending wife. Gonorrheal urethritis is responsible for azoospermia with especial frequency if, in conjunction with gonor- rhea, bilateral orchitis or inflammation of the vasa deferentia de- velops, preventing the entrance of seminal fluid into the seminal vesicles and ejaculatory ducts. The condition is generally incurable. Spermatozoids will naturally be absent from the secretion of the gener- ative organs if the tissues of the testicles are seriously diseased and the normal function of the latter is suppressed. Such conditions are generally attended with impotence, and are therefore not included in azoospermia. INVOLUNTARY DISCHARGE OF SEMINAL FLUID (SPERMATORRHEA), Spermatorrhea consists in the discharge of secretion from the generative glands independently of the sexual act. The ejacu- 30 466 GENITO- URINARY ORGANS lated fluid may be derived i'vom the testicles, the prostate gland, tlie seminal vesicles, the glands of Littre or those of Cowper, TRUE SPERMATORRHEA. Symptoms and Diagnosis. — True .sjjernmtorrhea is attended with the discharge from the uretlira of testicular secretion, which is readily recognized on microscopic examination from the pres- ence of numerous spermatozoids. Occasionally these are imper- fectly developed, with a slender filament attached to the head. Their want of motility also is at times conspicuous. At times so-called seminal cells — large multinucleated cells — are present. If seminal fluid inconsiderable amount is admixed with the urine, the latter acquires a milky, fat-like appearance — lipuria — which disappears when the urine is agitated with ether, preferably after addition of potassium hydroxid. Involuntary discharge of seminal fluid occurs at night from time to time in every healthy man — nocturnal pollution. Under such conditions lascivious dreams generally occur, and with cus- tomary erection of the penis and a pleasurable sensation a discharge of seminal fluid takes place, and, as a rule, causes awakening. The occurrence is usually followed by a sense of great freshness on the following night. Such pollutions are repeated in difi'erent men at varying intervals, in some within from 4 to 8 weeks, in others within from 4 to 8 days, in accordance with the tempera- ment, the constitution, and the mode of life of the individual. Abnormal nocturnal pollutions are characterized by the reciu'- rence of seminal emissions during the same night or on several successive nights, by incomplete erection of the penis or its total absence, by the absence of voluptuous dreams, by failure to be awakened by the discharge, and the failure of the latter to be followed by a sense of freshness, but by one of exhaustion, with the association of headache, vertigo, pal])itation of the heart, a sense of constriction and of weakness in the legs. A more profound degree of the disorder is attended with semi- nal discharges also during the day and the waking hours — diurnal pollutions. These may occur upon any sexual excitement, how- over slight, as, for instance, in reading obscene books, in looking at voluptuous pictures, in contact with women, and even in looking at women or in thinking of sexual matters. This condition may eventually lead to_ permanent spermatorrhea, which is, however, a rare disorder. The latter is attended with the constant discharge of seminal fluid from tlie urethra and its accumulation in the ]>re- putial sac without any pleasural:)le sensation. Often this condi- tion is preceded for a time by spermafnrrltea attending micturition and defecation, the discharge of seminal fluid taking place only in association with those acts. Spermatorrhea exerts a most injurious psychic influence upon INVOLUNTARY DISCHARGE OF SEMINAL FLUID 467 the patient, and the more so as it is frequently observed in persons with an abnormally irritable and excited nervous system. The patients are worried particularly by the thought that they can never again be potent, and in many cases there is present in addi- tion the consciousness that the patient is himself responsible for the disorder as a result of sexual excesses and masturbation. The great fear of a gloomy future on the one hand, and the want of courage to renounce sexual abuse forever on the other hand, are often remarkable. Persons with spermatorrhea may for a long time preserve a healthy and even a vigorous appearance ; but, as a rule, they gradually grow paler and more emaciated, are troubled with sleeplessness and increasing exhaustion, become more and more neurasthenic, and some reach the insane asylum or commit suicide. Ktiolog^?-. — Spermatorrhea is a common sequel of sexual ex- cesses, both natural and unnatural — onanism. At times it occurs as a result of reflex irritation in the presence of gonorrheal ureth- ritis, phimosis, retained preputial sebum, worms, hemorrhoids, anal fissure, and the like. Occasionally the disorder is dependent upon disease of the central nervous system, as, for instance, tabes dorsalis or a transverse lesion of the spinal cord. Spermatorrhea occurs also at times during epileptic convulsions. In some cases spermatorrhea is ijiduced by conditions of general debility. It may therefore be observed in the sequence or course of typhoid fever, pulmonary tuberculosis, and diabetes. Members of families with an inherited nervous temperament and persons who have made themselves nervous by excessive mental activity or by excessive indulgence in alcohol, tea, or tobacco are undeniably predisposed to spermatorrhea. The prognosis and the treatment depend primarily upon the causative factors. Onanism and sexual excesses are to be avoided, and irritative conditions (gonorrhea, phimosis, worms, etc.) to be relieved. To subdue excessive sexual desire, anaphro- disiacs have been recommended (potassium bromid — 3.0 — 45 grains — at night in a wine-glassful of milk ; camphor or lupulin — 0.3 — 4i grains — four times daily). The mode of life is imjDortant. The evening meal should be light, and be taken three hours before bed- time. The bed should consist of a hard mattress and a light cover. The patient should try to sleep on his side, as experience has shown that pollutions readily occur in the dorsal decubitus. An effort should be made to make a moral impression on the patient, and to invigorate his general condition by cold baths or spongings, systematic walks, and in the summer by a sojourn in tlie moun- tains or at the seaside. The treatment of spermatorrhea has been largely undertaken by charla- tans. As a rule, a circular is first sent the patient arousing his fears, and finally a useless medicinal remedy or some form of apparatus is otiered at an extravagant price. Thus, alarms have been constructed for the purpose 468 GENITO-URINARY ORGANS of arousing the patient frona sleep on the approach of an impending pollution, and thus preventing the seminal discharges. Lallemand, who attributed spermatorrhea in all cases to chronic inflammation of the caput gallinaginis of the urethra, devised a caustic-carrier, and made applications of silver nitrate to the caput gallinaginis. The application of a cold bougie or y^sy- chrophore has been much practised. PROSTATORRHEA. Prostatorrhea is attended with the discharge from the urethra of turbid, milky secretion possessing a spermatic odor, and on microscopic examination containing cylindric epithelium, lamin- ated amyloid bodies, round cells, and gi'anules or scales of yellowish pigment. The occurrence of sperm-crystals is especially charac- teristic of prostatic secretion. They resemble asthma-crystals, but are four-sided, and not six-sided, double pyramids. These crys- tals are precipitated on addition of a 1 per cent, solution of ammo- nium phosphate to prostatic secretion. Prostatorrhea may occur in conjunction with inflammatory processes in the prostatic gland, which result frequently in consequence of gonorrhea or anemia, but also in the aged as senile hypertrophy of the prostate. The pros- tatic secretion makes its appearance not rarely after defecation, at times after coughing and expulsive efforts, or it is discharged exter- nallv if a finger is introduced into the rectum and pressure is made upon the prostate through the anterior wall of the bowel. The disorder is often the cause of unnecessary fear on the part of the patient, as the prostatic secretion is mistaken for seminal fluid, but the affection is wholly free from danger. Secretion from the seminal vesicles can be recognized from the presence of the bodies described by Lallemand and Trousseau, which resemble swollen sago-granules and consist of a globulin-substance. The glands of Cowper and of Littre in some cases secrete considerable fluid on erection. The .secretion, which contains round cells and epithelial cells in small number, on drying readily causes agglutination of the lips of the urethral meatus. V. DISEASES OF THE ADRENAL BODIES. ADDISON'S DISEASE. Symptoms and Diagnosis. — Addison's disease is attended with a dark discoloration of the skin and the mucous membranes and gradual Iv jirogressive asthenia. At times the discoloration of the skin and the mucous membranes is the earliest symjitom, while at other times anorexia, vomiting, irregularity in movement of the bowels, general malaise, and the like, have been present for .some time previously as prodromes. These prodromal .symp- toms are perhaps only the results of auto-intoxication dependent ADDISON'S DISEASE 469 upon disease of the adrenal bodies. The cutaneous alterations generally appear earliest in parts of the body exposed to the light ; then follow places subjected to pressure, or under normal condi- tions the seat of pigmentation. Eventually the discoloration in- volves the skin of the entire body. The dark color of the skin, which often is suggestive of the appearance of bronze, has helped to give the disease the name of hronze-disease. At the commence- ment of the discoloration of the skin small, dark sjDots appear ; these soon increase in size, coalesce with adjacent spots, and then discolor the skin uniformly throughout a considerable extent. The first alterations are usually observed in the face, which ac- quires a brownish hue, as if the skin had been burned by the rays of the sun ; subsequently the color becomes more like that of graphite, so that it may be confounded by the inexperienced clinician with cyanosis. The patient resembles a mulatto. Also, the hands and the forearms, in persons who go barefooted the dorsum of the feet and the legs, participate early in the cutaneous discoloration. The palmar aspect of the hands and the plantar aspect of the feet, however, as well as the nails of the fingers and the toes, remain unaltered, and are often conspicuous for their bright and pale appearance. On the trunk a dark, discolored cutaneous girdle is observed to encircle the junction of the abdo- men and the thorax, corresponding to the constriction induced by waist-bands and other articles of clothing. The nipples, the axillary cavity, the scrotum, and the penis are usually conspicuous for their dark-brown or black color. Of the mucous membranes, that of the oropharynx becomes affected particularly early, and especially upon the mucous membrane of the cheeks opposite the teeth a brownish or blackish oval or irregular area is frequently found whose borders often pursue an irregular, serrated course. Now and then, but on the whole uncommonly, small brownish or blackish spots are observed upon the conjunctiva, which may readily escape detection on account of their small size. In women similar alterations occur upon the mucous membrane of the labia minora and the vagina. Addison's disease is readily recognized from the discoloration of the skin and the mucous membranes. Long-continued employ- ment of silver nitrate may give rise to a dark discoloration of the skin — so-called argyria or argyrosis ; but the fact of the internal or external employment of this agent can be determined by inquiry into the history. The same statement is applicable to arsenical melanosis ; that is, that dark discoloration of the skin that appears in some persons after long-continued use of arsenic. The color of the skin in cases of Addison's disease differs from that observed in brunets and in those who live in the tropics in the fact that with the former general symptoms are present besides, and these will shortly be described. It is noteworthy, further, that in some 470 GENITO-URINARY ORGANS healthy persuns dark spots like those of Addison's disease occur upon the mucous membrane of the lips or the cheeks. Persons who have been infested for a long time with body-lice — Pediculi vestimentoruia — often present a brownish or l)lackish discoloration of the skin in c(jnsequenee of extravasation of blood at the points of biting — cutaneous nigrities — but the face and the mucous mem- branes escape. In persons of uncleanly habits the skin may present a brownish or blackish appearance due to dirt : but this can readily be removed by means of soap and water. Constitutional symptoms are generally not long absent. There is progressive loss of appetite, with nausea and vomiting and pro- gressive asthenia. Often debilitating diarrhea sets in. At times complaint is made of pain in one or both renal regions, and this often is increased on pressure. Also, pains in muscles and joints occur frequently. The action of the heart is generally accelerated, and the tension of the pulse is greatly diminished. The mental state is generally one of depression and dejection. At times ver- tigo, a sense of pressure in the head, tremor, convulsions, and paralysis occur. As a rule, the patients fail gradually with pro- gressive asthenia. In a number of instances I have observed the rather sudden development of coma, followed by death, the con- dition suffficestino; auto-intoxication. It is noteworthv that at times the constitutional symptoms and the comatose condition described may occur in the absence of discoloration of the skin and the mucous membranes, whereas an autopsy may disclose only disease of the adrenal bodies, thus auto-intoxication without bronz- ing. The duration of the disease extends at times over more than a year. ' Anatomic Alterations. — The dark discoloration of the skin and the mucous membranes persists after death. On microscopic examination of the skin brownish or blackish pigment-granules are found in the lowermost layers of cells of the rete Malpighii. Round and branched cells filled with pigment-granules occur also in the cutis. Of the internal organs, the adrenal bodies particu- larly attract attention, being diseased in tlie majority of cases, though not in all. Most commonly the condition is one of tuber- culous-caseous change, which in turn may be primary or second- ary ; less commonly there may be carcinoma, amyloid degeneration, gummatous nodules, hemorrhage, chronic fibrous inflammation, or even cchinococcus. At times the alterations are only unilateral, but in most cases they are bilateral. In addition to the alter- ations in the adrenal bodies, degeneration of ganglion-cells and nerve-fibers and connective-tissue hyperplasia in the solar plexus have been observed ; and because in some cases of Addison's dis- ease the adrenal bodies have appeared unchanged the opinion has been formed that the disorder is dependent upon disease of the solar plexus of the sympathetic system, and that the alterations ADDISON'S DISEASE 471 in the adrenal bodies are rather subordinate. Naturally, this view is not in accord with the fact that even expert observers have found the solar plexus intact. There raaining organs exhibit in part signs of emaciation. In cases of secondary tuberculosis of the adrenal bodies the same condition has been found in the lungs, the kidneys, the bones, and elsewhere. Ktiolog"y. — The causes of Addison's disease are often un- known, and the condition must then be designated cryptogenetic. At other times tuberculosis or carcinoma in other organs, antecedent syphilis, suppuration, or other wasting discharge, may suggest that the adrenal bodies are the seat of tuberculosis, carcinoma, gumma, or amyloid disease, with consequent development of Addison's dis- ease. At times the disorder is attributed to injuries in the renal region, and it is dependent upon hemorrhage. Generally adults are attacked by the disease, which is the more common in men. The pigment in the skin and the mucous membranes is derived from the transformation of hemoglobin, but the reason for the destruction of red blood-corpuscles in Addison's disease is unknown. It has been thought that in consequence of disease of the adrenal bodies certain substances are retained in the blood (pyrocatechin ? taurocholic acid ?), which cause marked destruction of red blood-corpuscles. In those cases in which the adrenal bodies are found unaltered it would be necessary to assume that the diseased abdominal sympathetic nerve exerted the same influence upon the activity of the adrenal bodies as if the adrenals themselves were diseased. Where the destruction of red blood-corpuscles and where the transformation of the hemoglobin takes place, and why the pigment is deposited precisely in the skin and the mucous membranes, are all questions to which at present satis- factory answers cannot be given. Prognosis. — The prognosis of Addison's disease is unfavora- ble, as the disorder invariably terminates fatally. Treatment. — Specific remedies for Addison's disease are not known. Of late, organotherapy has been attempted, and tablets of adrenal extract have been administered ; but the reports as to the results are contradictory and still too scanty to permit of a final opinion in one or the other direction. There thus remains scarcely any but symptomatic treatment. An endeavor should be made particularly to maintain, and if possible to improve, the general condition by means of nutritious food, codliver-oil, and preparations of iron or iodin. In the presence of antecedent svphilis the employment of mercurials and iodids would be in- cluded in the causal therapy. PART V. DISEASES OF THE NERVOUS SYSTEM. I. DISEASES OF THE PERIPHERAL NERVES. PERIPHERAL PARALYSIS. PRELIMINARY CONSIDERATIONS, Peripheral paralysis frequently comes under observation of the practitioner for treatment. Among the causative factors ex- posure to cold, traumatism, toxic influences, and infections mav be mentioned, and, accordingly, a distinction has been made between refrigeratory (rheumatic), traumatic, toxic, and infectious periph- eral paralysis. Toxic and infectious influences exhibit allied relations with each other in so far as infectious paralysis also is due to poisons, which, however, are of bacterial origin (toxins). As experience has shown, different nerves are involved in periph- eral paralysis with varying frequency. The nearer the surface and the longer the superficial course of a nerve, the more is it ex- posed particularly to the action of cold and traumatism, and the more frequently is it the seat of paralysis. Paralysis of the facial and of the radial nerve is, therefore, of common occurrence. In cases of toxic paralysis the remarkable and hitherto unexplained phenomenon is observed that definite nerves are generally paral- yzed by certain poisons. Thus, it is well known that lead-poison- ing peculiarly gives rise to bilateral radial paralysis. Peripheral paralysis can be readily recognized, for the paralyzed muscles are incapable of contraction and exerting their functional activity. In favor of the peripheral origin of a paralysis is the fact that only a few nerves and their related muscles are involved. Also, when all of the nerves and muscles of one extremity are paralyzed the condition is generally due to peripheral causes, which often are seated in the nerve-plexus controlling the paralyzed extremity. On the other hand, paralysis of both upper and lower extremities, or of all the lower extremities simultaneously — paraplegia — is m- dicative of a spinal origin, and paralysis of the arm and the leg 472 PERIPHERAL PARALYSIS 473 upon one side of the body — hemiplegia — is indicative of a cerebral origin. Great importance in the diagnosis and the prognosis of peripheral paralysis is attached to the electric irritability of the paralyzed nerves and muscles. If a nerve is injured anatomically in only a slight degree, if therefore the condition is one of slight peripheral paratysis, which, as experience has shown, generally subsides in from two to four weeks, the electric irritability of the affected nerves and muscles exhibits no alteration as compared with the healthy side, and both nerves and muscles react to the faradic and the galvanic current with equal current-strength as the corresponding muscles and nerves upon the healthy side. A peripheral paralysis of moderate severity subsides in the course of from four to eight weeks, and can be recognized from the pres- ence of partial degenerative electric reaction. This is manifested by the circumstance that for the stimulation of the diseased nerve- trunk by means of the faradic or the galvanic current (so-called indirect stimulation) considerably stronger currents are required than for the corresponding nerves of the healthy side. On direct stimulation of the paralyzed muscles the irritability to the faradic current will be found diminished, while that to the galvanic cur- rent is increased, and, besides, in contradistinction from healthy muscles, a considerably feebler galvanic; current is required to obtain anodal closure-contraction than kathodal closure-contraction. This condition is spoken of as a reversal of the normal contraction- formula, AnClC > KaClC. A severe peripheral paralysis either requires from eight to twelve weeks, or even more, for recovery to take place ; or only partial recovery takes place, the motility of only some muscles being restored, while others remain paralyzed ; or no improvement whatever ensues, but, on the contrary, the paralyzed muscles undergo progressive atrophy, become permanently shortened (con- tracture), and are periodically involved in involuntary contraction. On electric examination of a severe peripheral paralysis total de- generative electric reaction will be found. As compared with partial, total degenerative reaction is distinguished by the fact that the paralyzed nerve has lost its irritability completely to both faradic and galvanic currents. The manifestations on direct irri- tation of the muscles by means of the faradic or the galvanic current agree with those of partial degenerative reaction. Should recovery from a severe peripheral paralysis take place, it is dis- tinctive for voluntary muscular movement to occur earlier in the paralyzed parts than it is possible to induce it by electric stimula- tion of the previously paralyzed nerves. The character of the muscular contractions that take place in cases of severe and moderately severe paralysis upon stimulation with the galvanic current is further noteworthy. The muscular contractions are not 474 NERVOUS SYSTEM short and liglitning-like, but slow and protracted, and they re- semble per'idaltiG muscular iiiovements. This phenomenon is not less significant in the recognition of partial and total degenera- tive electric reaction than the reversal of the contraction-formula. In connection with both partial and total degenerative electric reaction, not only is the direct irritability of the paralyzed muscles to the galvanic current increased, but also the mechanical muscular irritability is augmented, so that even gentle percussion of the muscles is sufficient to induce active contraction. In precisely the same way as with galvanic muscular stimulation, also with mechanical irritation, it will be found that the muscular contrac- tion is not lightning-like, but slow and peristaltic. Division of nerves in animals has demonstrated that the manifestations of total degenerative electric reaction are dependent upon degeneration of the nerve-fibers (destruction of the medullary sheath and the axis- cylinder, multiplication of the nuclei in the nerve-sheath of Schwann). In consequence, the diseased nerve is incapable of transmitting, and of being stimulated by, the faradic and the galvanic current. The paralyzed muscles also undergo anatomic alterations. The individual muscle-fibers become smaller, and exhibit multiplication of the nuclei of the sarcolemma and increase of the intermuscular connective tissue. Under such conditions the diseased muscle loses its power of responding with contraction to brief stimulation by the faradic current, while the irritability to the galvanic current is increased. The electric irritability of the diseased nerve can be restored only if the degenerated nerve-fiber is reformed or regenerated. The axis-cylinders develop first. In this stage of regeneration the nerve- fibers are already capable of conducting impulses of the will ; but they become susceptible to electric stimuli only after the previously naked axis- cylinders are surrounded with a medullary sheath. The phenomena of degenerative electric reaction are not at once present with the onset of peripheral paralysis, but develop gradually only in the course of the second week of the disease, as some time is required for the nerve and its related muscles to undergo degenerative atrophy. Degeneration of peripheral nerves and muscles occurs not only in con- nection with diseases of peripheral nerve-trunks, but also when the large motor-trophic gangJion-ceUs in the anterior horns of the spinal cord are dis- eased. Disorders of the latter variety are designated also anterior polio- myelitis. Consequently, degenerative electric reaction is encountered also in the disease named. The ganglion-cell in the anterior horns of the spinal cord, its axis-cylinder process, and the distribution of the latter in the peripheral nerve-trunk to the related muscle form a continuous whole, or a neuron. The phenomena of degenerative electric reaction may be so interpreted as to indicate destruction of the spinal-peripheral neuron at its central point of origin or in the course of its peripheral distribution : in the first instance a degeneration of the whole neuron resulting, in the latter only of the peripheral portion beyond the focus of the disease. In the presence of disease of the ganglion-cells, accordingly, the phenomena of degenerative electric reaction will be present in the entire peri]ihcral distri- bution of the nerve, and in the presence of disease of the peripheral nerve- trunk itself only in the distribution of that portion of the nerve distal to the situation of the disease-focus. PERIPHERAL PARALYSIS 475 In the treatment of peripheral paralysis causal therapy should always be considered. When exposure to cold has been operative salicylic acid or sodium salicylate may be employed (1.0 — 15 grains — 1 powder every two hours until ringing in the ears occurs). Diaphoretics (hot infusions, pilocarpin subcutancously) and hot cataplasms, applications of cotton-wadding, and the like, have also been employed. Antecedent syphilis will require mer- curial inunctions and administration of potassium iodid (5.0 : 200 — 75 grains : 6^ fluidounces; 15 c.c. — 1 tablespoonful — thrice daily). Potassium iodid also may be employed in the treatment of toxic paralysis, for in cases of lead-poisoning it has been shown that potassium iodid aids in the elimination of lead from the body. Causal treatment occupies a conspicuous place, fin'ther, in all cases of traumatic peripheral paralysis. If nerves are injured by com- pression, the injurious influence should be removed. Paralysis of the nerves of the arms, for instance, develops at times in con- sequence of pressure induced by improperly constructed or badly fitting crutches, and under such conditions these supports must be dispensed with for the time and be properly adjusted after recovery has taken place ; or, after fractures of bone, nerves are sometimes surrounded by callus, and paralysis results from the pressure exerted. Under such conditions the only remedy consists in ex- posure of the callus by operatiou, its division with a chisel, and the setting free of the imprisoned nerve. At other times a nerve has been divided and paralyzed, and remains paralyzed, although the cut extremities of the nerve have iniited by means of a con- nective-tissue cicatrix. Under such conditions remarkably success- ful results have been at times obtained by excising the connective- tissue cicatrix and freshening the extremities of the nerve with the knife, and uniting them by means of suture. SpecijiG remedies in the treatment of peripheral paralysis are as yet unknown. It was formerly thought that the electric current was capable of accelerating the regeneration of diseased and degenerated nerve-fibers, but this is scarcely correct. Electric treatment also must be included among symptomatic measures. Also, in the purely symptomatic treatment of peripheral paralysis employ often is made of salicylic acid, sodium salicylate, and potassium iodid. In addition, inunctions of mercurial ointment, potassium-iodid ointment, veratrin-ointment, strychnin-ointment, alcoholic applications (camphorated spirit, spirit of formic acid, spirit of mustard, compound spirit of angelica, etc.), or subcutane- ous injections of strychnin nitrate (0.1 : 10 — 1^ grains : 2\ fluidrams ; from 0.25 to 0.5 — 4 to 8 minims — thrice daily) may be mentioned. Mechanical treatment with massage of the paralyzed muscles is advantageous in order to stimulate the nutrition of the muscles as much as possible, as these readily undergo atrophy due to inac- tivity in consequence of lack of use. The results of electric treat- 476 NERVOUS SYSTEM ment also are scarcely more than mechanical, inasmuch as after electric contractions paralyzed muscles emaciate less rapidly. As long as paralyzed muscles respond to the faradic current this should be employed, and with a well-moistened and firmly applied electrode movable from place to place, while the other (indifferent) electrode, as large as possible, is applied to the sternum, the indi- vidual paralyzed muscles are stimulated daily to contract for from ten to twenty times. Care should be taken to employ currents just strong enough to cause contraction of the paralyzed muscles, as currents of too great strength may produce electric contractures in the paralyzed muscles, which may not subside and may give rise to unfortunate disfigurement if, for instance, the muscles of the face are involved. If the paralyzed muscles do not respond to the faradic current, the galvanic current should be employed, preferably by labile application : the anode (+, positive pole) is applied to the sternum, and the more actively stimulating kathode ( — , negative pole) is stroked over each paralyzed muscle from ten to twenty times daily. If a permanent contraction take place in paralyzed muscles — contracture — an endeavor should be made by massage to prevent increase in the condition, and to render it more and more retrogressive. Also, the galvanic current by stabile (immovable) application is capable of overcoming muscular contractures. At times tenotomy may be serviceable. Certain kinds of paralysis will require orthopedic apparatus to neutralize more or less completely the loss of functional activity. MOTOR PARALYSIS OF THE TRIGEMINAL NERVE (PARALYSIS OF THE THIRD DIVISION OF THE TRIGEMINAL NERVE). The third or inframaxillary division of the trigeminal nerve contains motor nerve-fibers for the muscles of mastication (masse- ter, temporal, external and internal pterygoid). If these nerve- tracts are paralyzed, there will result motor or masticatory trigem- inal paralysis or paralysis of the muscles of mastication. The con- dition is rare, as the deep situation of the tliird division of the tri- geminal nerve affords protection from cold and external injury. Pressure-paralysis occurs with relative frequency in consequence of syphilitic or chronic inflammatory thickening of the meninges, particularly of the dura mater at the base of the brain, or of aneurysms of the cerebral arteries, or of syphilitic or tuberculous processes in the sphenoid bone, if these cause constriction of the oval foramen, through which the third division of the trigeminal nerve leaves the skull. Intracranial lesions usually involve the sensory as well as the motor branches of the trigeminal nerve, so that in addition to paralysis of the muscles of mastication there will also be trioeminal anesthesia. PARALYSIS OF THE FACIAL NERVE 477 In cases of unilateral paralysis of the muscles of mastication it will at once be noted that if the patient be requested to bring the teeth firmly together, the prominence and hardening of the con- tracted temporal and masseter muscles can be seen and felt only upon the healthy side, while these are wanting upon the diseased side. With each movement of mastication the lo%ver jaw is de- flected toward the paralyzed side, and if the patient be requested to move the lower jaw laterally he will be capable of doing this only toward the paralyzed side, but not toward the healthy side, as the latter movement must be performed by the paralyzed ptery- goid muscles. When paralysis of the muscles of mastication has existed for some time the temporal and masseter muscles may undergo wasting, and more or less deep excavations form upon the diseased side in the temporal region and in the cheek. Bilateral paralysis of the muscles of mastication is attended with drooping of the lower jaw and inability to bring the teeth together in mastication or to move the jaw laterally. PARALYSIS OF THE FACIAL NERVE, histiology.' — Peripheral paralysis of the seventh cerebral or facial nerve is one of the most common varieties of paralysis, because, by reason of its superficial and comparatively long course, the nerve is readily exposed to refrigeratory and traumatic influ- ences. Toxic paralysis of the facial nerve, as, for instance, from lead-poisoning, as well as infectious paralysis (following diphtheria, erysipelas, typhoid fever, syphilis, herpes zoster), is rare. Me- frigeratory (j'heumatic) paralysis of the facial nerve occurs with particular frequency when one side of the face is exposed to cold air, especially while the body is over-heated. Traumatic paralysis of the facial nerve occurs much more commonly. Even the new- born may be attacked by peripheral paralysis of the facial nerve, if delivery has been effected with forceps, and one blade of the instrument, by reason of improper application or of slipping, has exerted undue compression of the trunk of the nerve at the ear or at its division on the cheek. Paralysis of the facial nerve is often associated with disease of the ear. Tuberculous destruction of the petrous bone in particular frequently extends to the Fallo- pian canal and the contained trunk of the facial nerve, causing destruction of the latter. Occasionally the facial nerve is com- pressed or destroyed and paralyzed by enlargement or suppuration of the cervical or submaxillary lymphatic glands or of the parotid gland. Incised and contused wounds, operations upon the cheek, and severe blows upon the ear are capable of causing paralysis of the facial nerve. At times peripheral paralysis of the facial nerve is dependent upon pressure at the base of the skull, and it may be due to thickening of the dura mater of syphilitic or 478 NERVOUS SYSTEM chronic infiamniatory origin, or new-growths or aneurysms. Also, fractures of the skull may be followed by peripheral paralysis of the facial nerve, il' the nerve be compressed by hemorrhage or ruptured in Iracture of the petrous portion of the temporal bone. Members of nervous families and drunkards appear predisposed to })aralysis of the facial nerve in greater degree than others, proba- bly because the resistance of the nervous tissues to injurious iuHu- ences of various kind has been diminislied. Occasionally persons Fig. 60.— Facial expression of a man, 55 years old, presenting severe left-sided trau- matic peripheral paralysis of the facial nerve ; from a photograph (personal observation, Zurich clinic). are attacked with peripheral paralysis of the facial nerve a num- ber of times in tlie course of a few years, at times always upon the same side, and at other times upon one or the other side. Symptoms. — Of all of the symptoms of peripheral paralysis of the facial nerve, paralysis of the muscles of the face is found unexceptionally. The facial nerve, however, sends motor filaments also to the muscles of the palate and to the stapedius muscle, and accordingly paralysis of this nerve may be attended with PARALYSIS OF THE FACIAL NERVE 479 distortion of the uvula and the arch of the palate, and derangement of hearing. It should not be forgotten that the facial nerve re- ceives from the trigeminal nerve through the greater superficial petrosal nerve gustatory fibers, which leave the trunk of the facial nerve through the chorda tympani ; so that disorders of taste are possible in connection with facial palsy. Finally, the facial nerve contains secretory fibers for the lacrimal and the salivary glands, and accordingly derangement in the secretion of tears Fig. 61.— The same patient shown in Fig. 60, on laughing and of saliva is at times observed in connection with facial palsy. While paralysis of the muscles of the face is a constant symptom of paralysis of the facial nerve, the occurrence of the remaining symptoms depends upon the situation at which the trunk of the nerve is diseased. Even during rest the paralyzed side of the face is conspicuous for its smooth, flattened appearance, the absence of folds, the greater size of the palpebral fissure than upon the healthy side, the eversion of the lower eyelid, the fulness of the conjunctival sac with tears, and often the flow of tears over the 48U NER VO US SYSTEM lower lid across the cheek — so-called epiphora. The attention of the observer is particularly attracted by the unusual phenomenon that closure of the eyelids takes place only upon the healthy side, while the eye upon the diseased side remains constantly open (Fig. 60). The paralyzed side of the face appears drawn toward the healthy side. The difference between the paralyzed and the healthy side of the face becomes the more marked during laughter or on cryingj for the paralyzed side remains immobile, inanimate, Fig 62.— The same patient shown in Figs. 60 and 61, when an attempt is made to close the eyes. and mask-like, while the healthy side undergoes natural furrow- ing and alterations (Fig. 61). In order to study more carefully the paralysis of individual muscles, it is well to request the patient to perform given move- ments with the muscles of the face. It will at once be observed that the forehead, even during rest, is free from furrows, as com- pared with the healthy side. If the patient be requested to wrinkle the forehead, horizontal furrows appear only upon the PARALYSIS OF THE FACIAL NERVE 481 healthy side, ending at the middle line, while, in consequence of paralysis of the frontal muscle, no furrows are formed upon the diseased side. Paralysis of the corrugator muscle of the eyebrow is indicated by the fact that the brow upon the paralyzed side is lower than that upon the healthy side, and that on wrinkling the forehead vertical furrows become apparent only over the glabella upon the healthy side. The greater width of the palpebral fissure upon the diseased side is due to paralysis of the orbicular muscle of the eyelids. The action of the elevator muscle of the eyelid, innervated by the oculomotor, then preponderates, drawing the upper lid upward, so that in comparison with the healthy side the fissure appears reduced in size. To the same circumstance is due the eversiou of the lower eyelid — paralytic ectropion. Paraly- sis of the muscle of Horner, a portion of the orbicular muscle toward the nasal aspect, is attended with displacement of the lacrimal caruncle, so that the tears do not properly enter it and the duct continuous with it. This circumstance explains the fact that the eye upon the paralyzed side is constantly bathed in an excess of tears, and that frequently tears flow over the lower eye- lid and upon the cheek — so-called epiphora. In consequence, the nasal mucous membrane remains dry, and the patients complain of dryness and burning in the nose upon the paralyzed side, and also of impairment of the sense of smell. Marked disfigurement of the face results in consequence of absence of winking upon the paralyzed side, and even if the finger be applied to the eyeball or the cornea is touched reflex closure of the eye fails to take place. The disfigurement becomes particularly marked if the patient, when requested, attempts to close the eves, only the eye upon the healthy side being closed, while that upon the diseased side remains open — paralytic lagophthalmos — and be- tween the lids the white sclera and generally also a small portion of the cornea become visible as the eyeball is rolled ujjward and inward on closure of the eyes (Fig. 62). Frequently, on attempting to close the eyes, a narrowing of the palpebral fissure upon the paralyzed side is observed that has been attributed to syner- gistic relaxation of the elevator of the lids. The tip of the nose is deflected toward the healthy side, while upon the diseased side the entrance to the nares appears reduced in size. On deep inspiration the ala of the nose upon the diseased side is drawn toward the septum. Persons capable of moving the nasal aire voluntarily are able in the presence of facial paraly- sis to make such movement only upon the healthy side. Also, the buccal orifice and the chin are drawn toward the healthy side. The angle of the mouth is lower upon the paralyzed than upon the healthy side, in consequence of paralysis of the elevator muscle of the angle of the mouth. Whistling and distention of the cheeks 31 482 NERVOUS SYSTEM with air are impossible, because the lips cannot be closed upon the paralyzed side, and the air is thus permitted to escape from the mouth. Also in speakin^^, and particularly in the use of the labials (b, p, f, V, w), disturbances and secondary sounds are appreciable, and also in the articulation of certain vocal sounds (a, e). In eat- ing and drinking, the.ingesta readily escape between the paralyzed and separated li])s, so that some patients are compelled to perform these acts with the head thrown backward. In consequence of paralysis of the buccinator muscle the act of mastication is interfered with. The cheeks are not rendered sufficiently tense, and as a result the mucous membrane of the cheek is readily caught between the teeth in the act of chewing, and is bitten. Also, food readily finds its way between the mucous membrane of the cheek and the teeth, and must be re- moved with the fingers or by pressure upon the cheek from with- out. At times the base of the tongue appears lower upon the dis- eased than upon the healthy side in consequence of paralysis of the stylohyoid and digastric muscles. If the muscles of the soft palate are involved in paralysis of the facial nerve, the tip of the uvula is deflected toward the healthy side, and the arch of the palate not only assumes a lower level, as compared with the healthy side, but on active respiration flaps like a loose sail. Paralysis of the musculature of the cheek is revealed not only, as has been mentioned, by disturbances in mastication, but also by obliteration or depression of the nasolabial fold. In animated conversation, Avith respiratory movement, and during sleep the paralyzed cheek flaps to and fro like a curtain. Paralysis of the muscles of the auricle and of the occipital muscle is frequently demonstrable only with difficulty, because not many persons are capable of moving the auricle voluntarily. Naturally, the movements of the auricle would be wanting u])on the paralyzed side. Examination of the muscles by means of the faradic and the galvanic current could yet be practised, althougli alterations in electric muscular irritability would be ex])ected only in the presence of moderately severe paralysis. Involvement of the stapedius muscle in paralysis of tlie fiicial nerve will be indi- cated by excessive acuity of hearing — oxyokoia (Willisian hyper- acusis) — which is ox]i]ained by the preponderant action of tiie tensor tympani muscle. Paralysis of the jdatysma myoidcs can be recognized from the fact that on marked depression of the lower lip contraction of the platysma on the paralyzed side, Avith the formation of folds in the skin of the neck, does not occur. It is noteworthy that peripheral facial palsy is attended with absence of all reflex and associated movements. ^Movement of tlie fingers toward the eye or contact witli the cornea fails to induce closure of the lids, and in crying, laughing, and yawning the PABALYSIS OF THE FACIAL XERVE 483 paralyzed side remains immobile and inanimate. Disturbances of taste are only to be expected in association with peripheral facial palsy when the lesion is situated between the geniculate ganglion and the origin of the chorda tympaui. They involve always only the anterior two-thirds of the tongue, as the posterior third is sup- plied with gustatory fibers by the glossopharyngeal nerve. Often the patient complains of diminislied tactile sensibility of the tongue on the paralyzed side. Examination of tlie sense of taste is made most simply by dipping rolls of bibulous paper successively in solutions of common salt, vinegar, sugar, and quinin, and toucbing the anterior two-tbirds of tbe tongue upon one and tben upon tbe otber side. Tbe patient should retract the tongue into the mouth only after he has appreciated a distinct gustatory sensation. Bitter solutions are tested last, because they leave an after-taste for a long time. It is advisable to test the sense of taste also by means of the galvanic current and a gustatory electrode. Some patients complain of dryness of the mouth upon the para- lyzed side, and this condition is associated with disorders in the secretory branches of the facial nerve to the salivary glands. If the nerve-fibers for the lacrimal gland upon the paralyzed side are also involved, secretion of tears takes place on crying only upon the healthy side. Sensory disturbances are wanting in cases of pure facial palsy. Nevertheless, cutaneous anesthesia is now and then observed upon the paralyzed side, and particularly if, as a result of the action of peripheral, injurious influences, in addi- tion to the fibers of the facial nerve, also the terminal fibers of the intimately related trigeminal nerve are involved. The occurrence of facial palsy is at times preceded by pro- dromes, such as vertigo, headache, mental confusion, ringing in the ears, impairment of hearing, and pain in the ear. At other times the paralysis follows immediately upon the action of the injurious influence (cold, injury). Often the attention of the pa- tient is directed by his friends to the distortion of the face and the paralysis of the facial nerve. In other instances he is induced by a sense of tension, impaired motility, difficulty in eating, speak- ing, and whistling, to resort to the use of a mirror, when the alteration upon one side of the face is noticed. At times the disorder is discovered quite accidentally on using the mirror in the performance of the toilet. Whether the paralysis is of mild degree, of moderate severity, or profound can be determined alone by electric examination (p. 473). Should there be no electric appa- ratus at hand, the mechanical irritability of the paralyzed muscles should be tested, for increased mechanical muscular irritability and tardy muscular contractions are indicative of a moderately severe or a profound paralysis. After the paralysis of the facial muscles has existed for some time muscular icasting gradually ensues — atrophy due to inactivity. Profound paralysis of the facial nerve may persist through- 484 NERVOUS SYSTEM out the remainder of life, but often only partial improvement ensues, some muscles of the face regaining their motility, while others, on the other hand, remain paralyzed permanently. Per- sistent muscular contraction may readily develop in paralyzed muscles — muscular contracture — and the previously smooth and unfurrowed paralyzed side of the face now becomes distorted by unusually deep furrows. Involuntary contractioTis also occur frequently in the paralyzed muscles, and these may also be in- duced voluntarily by slight cutaneous irritation. Often an abnor- mally increased tendency to associated movements is noticeable. Fig. 63.— Facial expression in a case of bilateral facial paralysis: from a photograph (personal observation, Zurich clinic). On closure of the eyes, for instance, twitching occurs at the angle of the mouth, or, on puckering the lips, contraction of the palpebral fissure. Long-continued paralysis of the facial nerve may be fol- lowed by disease of the eye, for in the absence of winking, and if the cornea is not moistened with tears and cleared of foreign bodies from the air, there will be danger of inflammation of the cornea (keratites), rupture of the cornea, and loss of the eyeball (pan- ophthalmitis). Among rare complications of peripheral facial palsy, vasomotor and trophic disturbances appear at times upon the paralyzed side, such as pallor of the PARALYSIS OF THE FACIAL NERVE 485 skin, grayness of the hair, labial, lingual, and pharyngeal herpes. The herpes may precede the paralysis or follow it after the lapse of a few days. At times hyperidrosls appears upon the paralyzed side. Peripheral paralysis of the facial nerve is generally unilateral — -facial hemiplegia ; bilateral paralysis of the facial nerve — -facial diplegia — is encountered but rarely. Either the latter is the result of tuberculous disease of both petrous bones, paralysis in- volving at first the one and then the other facial nerve ; or it is associated with lesions at the base of the skull, and here at times simultaneously if the basal disease involves both facial nerves at /i-'riiil^ Fig. G4. — The same patient as in Fig. 63, on attempting to close the eyes. the same time ; or both nerves may be affected in quick succession by cold or external injuries. Further, examples are known also in which the facial nerve upon one side was paralyzed as a result of peripheral influences, and that upon the opposite side as a result of central influences, the arm and the leg being involved addi- tionally in the paralysis in association with the latter, with the development of the clinical picture of cerebral hemiplegia. In the presence of facial diplegia the face has lost its power of ex- pression upon both sides, remains inanimate, and resembles a mask. The patients may be heard to laugh or shout or cry, but 486 NERVOUS SYSTEM the facial expression remains rigid and unaltered. The upper lip not rarely droops like a proboscis, while the lower lip is everted. The imperfect closure of the lips prevents in marked degree the ingestion of nutriment, because food and drink readily escape from the mouth. Often the patients introduce the food deeply into the pharynx with the fingers, a spoon, or a specially devised wooden spatula, in order to facilitate swallowing. AMien the patient is requested to close the eyes both palpebral fissures persist (Figs. 63 and 64). Anatomic Alterations. — Little is known with regard to the anatomic alterations of peripheral fiicial paralysis, because the disorder is not fatal, and because if death should result accident- ally from other causes the removal of the nerve and the facial muscles will not be permitted on account of the unavoidable mutilation of the fice. In severe cases of rheumatic or traumatic paralysis of the facial nerve destruction, fatty degeneration, and disappearance of the medullary sheaths and axis-cylinders, and multiplication of the nuclei of the sheaths of Schwann, have been found in the peripheral portions of divided nerves. The connec- tive tissue of the nerves has generally been unaltered. Fatty degeneration had taken place in the paralyzed facial muscles. Mild facial paralysis is perhaps attended with scarcely more than active over-distention of the vessels with blood, and slight exudation into the connective-tissue nerve-sheath, Avith compression of the nerve-fibers, with- out extensive nerve-degeneration. Therefore, these conditions are suscep- tible of speedy involution. Diagnosis. — The recognition of peripheral facial palsy is easy on account of the striking distortion of the face. In con- tradistinction from central facial paralysis, all of the facial muscles are involved, while with central facial paralysis the branch to the forehead remains uninvolved, so that the patient is capable of wrinkling the forehead and eyebrows, and of closing the eyes. In addition, with central paralysis reflex and associated move- ments are preserved ; phenomena of degenerative electric reaction are wanting ; and, finally, the arm and the leg are, as a rule, involved, so that a condition of hemiplegia exists. Only with disease of the bones does facial jwralysis preserve its peripheral character if the lesion involves the intrapontine facial path from the point of exit of the facial trunk at the posterior peduncle of the pons to the facial nucleus, or the latter itself. Other pontine symptoms (interference with swallowing, contracted pupils, dif- ficulty in articulation) will then usually be present also, and fre- quently also paralysis of the extremities. The seat of peripheral facial paralysis can be readily deter- mined with the aid of the accompanying diagram representing the course of the facial nerve (Fig. 65). 1. If the lesion is situated outside the stylomastoid foramen, the PARALYSIS OF THE FACIAL NERVE 487 paralysis will be confined to the muscles of the face alone (Fig. 65,1). 2. A lesion in the loivermost portion of the Fallopian canal will be attended in addition with paralysis of the posterior auricular nerve, and consequently of the muscles of the auricle and the occip- ital muscle (Fig. 65, 2). 3. When the lesion is situated above the point of origin of the chorda tympani nerve there will be, in addition to paralysis of the -nap. Fig. 65.— Diagram of the distribution of the facial nerve :/c, trunk of the facial nerve; ac, trunk of the auditory nerve ; pai, internal auditory canal ; Gg, geniculate ganglion'; psm, greater superficial petrosal nerve ; sip, stapedius nerve ; cht, chorda tympani ; Jst, styloid foramen ; nap, posterior auricular nerve ; bv and sth, nerves for the digastric and. stylohyoid muscles ; gsz, facial branches ; trg, trg', trg", trg"', trunk and three branches of the trigeminal nerve ; Gsp, sphenopalatine ganglion ; Ig, lingual nerve. muscles of the face and of the auricle, also disturbances in the sense of taste and of the secretion of saliva (Fig. 65, 3). 4. If the facial nerve is diseased between the point of origin of the stapedius nerve and the geniculate ganglion, disorders of hear- ing (oxyokoia) will be observed, in addition to paralysis of the muscles of the face, the auricle, and the occipital muscle, and to disturbances in the sense of taste and in the secretion of saliva (Fig. 65,4). 5. Disease of the geniculate ganglion itself will be attended, in addition to paralysis of the facial muscles, the muscles of the au- ricle, the occipital muscle, disturbances in the sense of taste, in 488 NERVOUS SYSTEM the secretion of saliva, and in the sense of Iiearing, also with j)(ir((/i/fiis of the ui-ii/a and auppreasion of tlie .secretion of tears, as the fibers of tlie facial nerve governing the functions last named leave the path of the nerve at the geniculate ganglion, in order to join the path of the trigeminus through the greater superficial petrosal nerve (Fig. 65, o). 6, Lesions aboce the geniculate fjangJion will be attended with all of the manifestations of facial palsy except disturbances in the sense of taste. There will thus be present paralysis of the uvula, derangement in the secretion of tears, in the sense of hearing, in the secretion of saliva, paralysis of the facial muscles and those of the auricle, and the occipital muscle. The prognosis and the treatment will be governed by the rules laid down on pp. 475 and 47(3. PARALYSIS OF THE SPINAL ACCESSORY NERVE. In the discussion of peripheral paralysis of the spinal accessory nerve the motor accessory fibers that enter the vagus, and supply especially the muscles of the larynx and the pharynx, and pass to the cardiac plexus, are omitted from consideration. The condi- tion to be described is attended only with jmrali/sis of the sterno- mastoid and the trapezius. Most commonly, paralysis of the spinal accessory nerve is of traumatic origin, as this nerve pursues a long and superficial course upon either side of the neck. Stab-wounds, operation-wounds, suppurating cervical lymphatic glands, destroy- ing the trunk of the spinal accessory nerve, are relatively frequent causes of such paralysis. Nevertheless, paralysis of the spinal accessory nerve is one of the less common varieties of periplieral paralysis. At times paralysis of the spinal accessory is dependent upon disease of the cervical vertel)rse, as it sends numerous root- iilaments to the level of the seventh cervical vertebra. In the presence of unilateral paralysis of the sternocleidomastoid muscle the head and the chin acquire an abnormal position, in con- sequence of predominant activity of the healthy sternomastoid. The head and the chin are directed toward the parali/zed side, and the chin is elevated. Rotation of the head in the opposite direction is greatly interfered with. AVhen the patient lies upon his back and attempts to raise his head the contracted sternomas- toid becomes apparent beneath the skin only upon the healthy side of the neck. Also, on deep inspiration only the healthy and not the paralyzed sternomastoid undergoes contraction. If the paral- ysis has existed for some time, a depression in the course of the neck is observed upon the paralyzed side, resulting from inactivity- atrophy of the paralyzed sternomastoid. At times the healthy sternomastoid undergoes contracture, with the development of spasmodic torticollis, which greatly prevents rotatory movement of PARALYSIS OF THE HYPOGLOSSAL NERVE 489 the head. In the presence of bilateral paralysis of the sternomas- toid the patient is almost wholly incapable of raising his head from the recumbent posture. Paralysis of the trapezius muscle is indicated, on inspection of the patient from the front, by the fact that the supraclavicular fossa, upon the paralyzed side is unusually deep, and the shoulder is lower. Viewed from the posterior aspect the scapula upon the paralyzed side is lower than upon the healthy side. At the same time, the scapula upon the paralyzed side stands off a greater dis- tance from the vertebral column, its upper and outer angle being drawn markedly forward and downward by the weight of the arm, while the inferior angle is more closely approximated to the verte- bral column. 3Iovement of the scapula is rendered difficult, as it can be accomplished only by contraction of the elevator of the angle of the scapula. The act of approximating the scapula to the vertebral column is rendered difficult, and is possible only through the agency of the rhomboid. Elevation of the arm above the hori- zontal level is attended with difficulty, because the scapula is imper- fectly fixed. Further, the external free border of the paralyzed trapezius does not form a straight line, but a curved line, with its convexity directed toward the vertebral column. In the presence of bilateral paralysis of the trapezius the back appears unusually wide. In addition, the conditions just described are present on both sides. PARALYSIS OF THE HYPOGLOSSAL NERVE. Peripheral paralysis of the hypoglossal nerve gives rise to paralysis of the tongue — glossoplegia. The paralysis of the tongue in turn is characterized in part by disorders of mastication and in part by disorders of speech, and accordingly it may be divided into masticatory and articulatory glossoplegia. Hypoglossal palsy is most commonly of traumatic origin, resulting especially from punctured and incised wounds, or from pressure exerted by en- larged lymphatic glands or other tumors of the neck. I have recently treated a woman with hypoglossal paralysis in the sequence of syphilis, induced by gummatous hyperplasia upon the dura at the base of the skull. After a course of treatment with inunctions of mercurial ointment and the internal administration of potassium iodid complete recovery ensued. Unilateral hypoglossal paralysis is attended with deviation of the tip of the tongue toumrd the paralyzed, side in consequence of preponderant action of the healthy genioglossus muscle. The dorsum of the tongue is the more greatly arched upon the para- lyzed side. The diseased half of the tongue exhibits more marked furroioing of its surface, and often also active fibrillary twitching. In chewing, the food readily remains upon the paralyzed half of 490 NERVOUS SYSTEM the tongue, and the patients often complain in consequence of imperfect distribution of the food in tlie mouth and of defective taste. In the act of deglutition deficient propulsion of the food is appreciable, and the approximation of the tongue to the palate is incomplete, so that food may readily return into the mouth. The swallowing of saliva may also be interfered with, and the patient in consequence often permits dribbling from the mouth. In speak- ing, the imperfect articulation, particularly of the lingual letters (d, t, s, sch, 1, r, k, g, ch), will be noted. If the paralysis has existed for some time, unilateral atrophy of the tongue takes place. In cases of bilateral hypoglossal paralysis the tongue is con- verted into an immobile muscular mass. The formation of a bolus is scarcely possible, and speech is reduced to an inarticulate grunt or jargon, so that the patient can often make himself understood only in writing. MULTIPLE OR COMBINED PARALYSIS OF CEREBRAL NERVES. In the presence of multiple or combined paralysis of cerebral nerves several cerebral nerves may be paralyzed together. At times almost all of the cerebral nerves upon one side are paralyzed, while in other instances some nerves may be paralyzed upon one side and others upon the opposite side of the body. Such a con- dition is most commonly associated with lesions at the base of the skull, which extend gradually and involve one nerve after the other. Particularly, syphilitic, carcinomatous, and tuberculous lesions of the meninges and the cranial bones are the etiologic factors. Less commonly, aneurysms of the cerebral arteries or fracture of the base of the skull is the cause of the disorder. At times multiple paralysis of cerebral nerves occurs in the sequence of infectious diseases, as, for instance, after pharyngeal diphtheria. It occurs occasionally, also, in the course of polyneuritis. Injuries in the iqjper poiiion of the cervical region are likewise capable of causing paralysis simultaneously of several cerebral nerves. In the dif- ferential diagnosis paralysis due to lesions of the nuclei of the cerel)ral nerves in the medulla oblongata and in the pons is par- ticularly to be taken into consideration. The etiology and the mode of development of the palsy afford the principal means of distinction in the differential diagnosis. PARALYSIS OF THE PHRENIC NERVE. The phrenic nerve, wdiich receives fibers from the third and fourth cervical nerves, is paralyzed at times in consequence of injuries, as, for instance, fractures, luxations, neoplasms of the cervical vertebrae, tumors, abscesses, punctured and incised wounds PARALYSIS OF THE PHRENIC NERVE 491 of the neck. Infectious paralysis of the phrenic nerve has been observed also in the sequence of diphtheria and influenza. Toxic paralysis has been noted in the sequence of poisoning with lead, alcohol, carbon monoxid, and opium. At times refrigeratory paralysis is observed. It is noteworthy that paralysis of the diaphragm is much more commonly of myopathic than of neuro- pathic origin ; that is, dependent not upon disease of the phrenic nerve, but upon disease of the diaphragm itself. Such a condi- tion occurs particularly in association with diaphragmatic pleurisy and peritonitis, because the inflammation of the serous membrane readily extends to the muscular structure of the diaphragm, whose function is thereby deranged. Paralysis of the diaphragm may involve a number of circumscribed areas, or be unilateral or bilateral. Bilateral or comjjlete paralysis of the diaphragm is a most dangerous disorder, as death may result from asjjhyxia. During quiet breathing symptoms may naturally be absent, but these appear at once upon active bodily exercise, as, for instance, in ascending stairs. It is noteworthy that the type of respiration is purely costal, and that principally the upper portion of the thorax moves in the act of breathing, while the lower remains immobile and appears unusually full. In contrast with normal conditions inspiratory retraction and expiratory protrusion of the epigastrium take place. The upper border of the liver is unusually high, and scarcely participates in the respiratory movements. The latter, however, are reversed as compared with the normal. The liver ascends with inspiration, as does also its lower border, whose movement frequently can be followed with the finger. All ex- pulsive efforts (coughing, defecation, heavy lifting, vomiting, loud and continued speaking or singing) are difficult and incomplete. Even slight catarrhal states of the air-passages may at times be attended with danger of asphyxia, because in consequence of deficient cough and expectoration accumulation of secretion in the air-passages readily takes place. The greater the embarrassment of respiration the more rapid becomes the act of breathing and the greater the cyanosis. To overcome the dangers of paralysis of the diaphragm electric treatment particularly is to be advised. The phrenic nerve will be found in the angle formed between the sternomastoid and the omohyoid muscles. In this situation upon either side an electrode is placed, and a strong faradic current is passed through the dis- eased nerve, with interruption by means of a suitable device corre- sponding to the rhythm of normal breathing. Contraction of the diaphragm will be recognized from the fact that air enters the air- passages with a gurgling sound and the epigastrium bulges with inspiration. 492 NERVOUS SYSTEM PARALYSIS OF THE RADIAL NERVE. Htiology. — As the facial is the most commonly paralyzed of the cerel)ral nerves, so among the nerves of the arm the radial is by far the most commonly affected by peripheral paralysis. Its long and superficial course affords a favorable point of attack for external injurious influences. Only rarely is radial paralysis due to refrigeratory or infectious causes. Radial paralysis of toxic orir/in is distinctly more common. For a long time it has been known particularly that under the influence of lead (saturnism) radial paralysis occurs not rarely. This saturnine paralysis of the radial nerve is characterized by its bilateral distribution. Toxic radial paralysis may, however, occur also as a result of the action of alcohol. It has often been observed after injections of ether, antvpyrin, and osmic acid beneath the skin of the forearm. Traumatic radial paralysis is the most common variety. Sleep- paralysis is the best known form, occurring during sleep when the patient places the forearm (usually tlie right) in such a posi- tion that the radial nerve is compressed, and as a result is para- lyzed. At times the patient has supported himself upon his arm, resting the upper arm upon a sharp edge, or permitting the arm to hang over a sharp edge (arm of a chair or edge of tlie bed), or the patient has slept with the arm beneath the head, the upper arm being thereby unduly compressed upon its dorsal aspect, or the lateral decubitus is assumed in sleep, and the radial nerve of the arm placed beneath the body is injured by pressure. The deeper the sleep the less will the inconvenience of a given posture be appreciated^ and the greater, therefore, is the danger of press- ure-paralvsis. Laborers who take a midday nap in tlieir work- places, and drunkards, are therefore attacked by sleep-paralysis with particular frequency. Another important variety of trau- matic paralysis of the radial nerve is known as crutch-palsy. This develops at times even Mithin a few hours after the use of an unsuitable crutcli, particularly if this be too short or too long, or unpadded, and is supplied with unsuitable supports for the hands. Of all the nerves of the arm, the radial in particular is peculiarly exposed to the danger of compression by a crutcli on account of its posterior situation in the axilla. A few other varieties^ of traumatic radial parali/sis may be mentioned. Radial paraly^^is after shackling of the upper arm has been designated prisoners^ palsy. Coaclrrnen's palsy has been observed in a number of in- stances in Russian coachmen who have wrapped the horses' reins too firmly about the upper arms, and have then, usually in a drunken state, fallen asleep. A bandage-palsy also has been described by Russian physicians, occurring in infants when the arms are too firmly bandaged to the trunk, and the infants are. besides, permitted to lie upon one side of the body for too long a time. Water-carriers' palsy of Rennes arises from the carrying of heavy water-jugs, through the handles of which the upper arras are passed, "the vessels being co'mpressed against the abdomen. In the same PARALYSIS OF THE RADIAL NERVE 493 way the carrj'ing of heavy bundles by means of straps or ropes wound about the upper arms may give rise to radial paralysis. Under some conditions the application of Esmarch's rubber tube to the arm is followed by peripheral pressure-paralysis of the radial nerve, and an improperly applied plaster- of-Paris bandage may also have the same effect. The designation narcosis- paralysis has been applied to cases of radial palsy that have developed during narcosis, in the course of an operation, in consequence of compres- sion of the radial nerve by the head of the humerus in lifting the arm upward. Naturally, punctured, incised, contused, and gunshot wounds may cause injury and paralysis of the radial nerve. Occasionally radial paraly- sis develops in the sequence of luxation or fracture of the humerus. In the latter event the radial nerve may be lacerated and paralyzed by the ex- tremities of the fractured bone, or it may be surrounded by callus and be paralyzed by compression. Examples of traumatic radial paralysis could be largely multiplied. Drummers' pjaralysis may yet be mentioned, involv- ing most commonly the long extensor of the thumb and resulting from over-use of the muscles in beating the drum. Anatomic Alterations. — Little is known Avith regard to the anatomic alterations attending peripheral radial paralysis, be- cause the disorder in no sense is dangerous to life. In a case of radial paralysis following typhus fever neuritic alterations were found, and in a case of recent lead-palsy I succeeded in finding throughout the entire nervous system only degenerative atrophy of the fibers of the radial nerve. Symptoms and Diagnosis. — Individuals with radial paral- ysis attract attention at once by the position of tlie hand and the fingers. When the arm is raised vertically the hand is flexed upon the palm, and at the same time pronated. The thumb is adducted and slightly flexed, and the remaining fingers likewise are flexed upon the palm (Fig. 66). If the patient be directed to Fig. 66.— Position of the fingers and the hand in a case of peripheral radial paralysis— sleep-paralysis ; from a photograph (personal observation, Zurich clinic). practise dorsal flexion with the paralyzed hand, this will be found impossible on account of paralysis of the radial and ulnar extensors of the carpus. As a result of paralysis of the common extensor of the fingers the patients are unable to perform dorsal flexion of the basal phalanx of the fingers. Extension of the fingers is not 494 NERVOUS SYSTEM at all possible, as extension of the second and third phalanges, which are supplied by the interosseous muscles (with synchronous flexion of the basal phalanges), can take place only if the basal phalanx has been previously flexed upon the dorsum. Extension of the lingers can, however, be effected when the basal phalanges have been passively placed in dorsal flexion. Extension of the thumb cannot be effected because the long and short extensors of this digit are paralyzed ; abduction also is greatly limited in consequence of paralysis of the long abductor of the thumb. The abolition of movement in the fingers and the thumb causes great difficulty in the execution of all fine manipulations (draw- ing, writing, buttoning). The grasp of the hand is extremely feeble, because, in consequence of paralysis of the extensors of the fingers, the points of attachment for the flexors are not sufficiently distant. If the forearm and the hand are placed upon a horizontal support, the patient will be unable to abduct the hand toward the radial or the ulnar aspect, as the long and short radial extensors of the carpus and the ulnar extensor of the carpus are paralyzed. AVhen, however, the hand is held in the dependent posture these movements can be executed by the corresponding flexors. Often radial paralysis is limited to the muscles already mentioned, as the nerve-filaments for the long and short supinators and the triceps leave the trunk of the nerve quite high up, and are fre- quently situated above the point of injury. Involvement of the short supinator in radial paralysis' is attended with inability to execute supination of the forearm when this member is held in the dependent posture. Paralysis of the long supinator may be recognized by the absence of contraction of the muscle named when resistance is offered to flexion of the forearm held in a posi- tion midway between pronation and supination. Paralysis of the triceps, finally, is attended Avith inaljility to extend the flexed forearm, or to offer resistance to passive flexion of the forearm. The alterations in electric irritability of the paralyzed nerves and muscles vary in accordance with the severity of the palsy. In the presence of slight and moderately severe paralysis the elec- tric current is a convenient means for determining the seat of the paralysis, for if the course of the radial nerve be followed with the electrode of a faradic current muscular contractions will be wanting above the seat of the lesion, and will be observed only below this point on stimulation of the nerve. After the paralysis has existed for some time atrophy from icant of use develops in the paralyzed muscles. Although the radial is a mixed nerve, sensory disturbances may be wanting in a case of radial paralysis because the sensory branches are given off from the trunk of the nerve at so high a level that they are generally situated above the lesion, or because neighboring nerves assume the function of the paralyzed radial PARALYSIS OF THE MEDIAN NERVE 495 branches. When sensory disturbances are present these involve the dorsal aspect of the upper arm (posterior superior cutaneous nerve), that of the forearm (posterior inferior cutaneous nerve), and that of the hand and the fingers between the thumb and the middle of the middle finger. The terminal phalanges naturally remain unaffected, as these are supplied with cutaneous branches by the median nerve. Vasomotor and trophic disorders occur but exceptionally, as, for instance, nodular thickening of the extensor-tendons or thickening of the digital articulations. The onset of paralysis of the radial nerve is often sudden, the patient awaking from deep sleep therewith. In other instances, however, the condition is preceded by prodromes — paresthesia, such as a sense of contraction, of the crawling of ants, of coldness and stiffness, and the like. The duration of radial paralysis generally is exceedingly long. Even mild sleep-palsies may persist from four to six weeks. Repeated radial paralysis may occur in laborers and drunkards if compression of the nerve is repeated during sleep. Plumbic paralysis of the radial nerve likewise may readily recur if the individual is again exposed to the action of lead. PARALYSIS OF THE MEDIAN NERVE. etiology. — Peripheral paralysis of the median nerve is, like that of the radial nerve, generally of traumatic origin. The median nerve is injured with particular frequency just above the wrist-joint, upon the radial aspect of the palmar surface of the forearm by incised wounds, as, for instance, by fragments of glass, while injuries of the trunk of the nerve in the internal bicipital sulcus are much less common. Nevertheless, crutch-paralysis, prisoners^ 'paralysis, and narcosis-paralysis of the median nerve, as well as paralysis in consequence of luxation and fracture of the humerus, have been observed. At times median paralysis has been observed after excessive muscular contraction. In this group is included drummers' paralysis, which involves especially the flexor of the thumb, and naturally much more commonly the long exten- sor of the thumb supplied by the radial nerve. Refrigeratory and infectious paralysis of the median nerve is uncommon. Symptoms and Diagnosis. — The extent of the paralysis naturally depends upon the seat of the lesion. If the median nerve is injured just above the wrist-joint, the muscles of the thenar eminence are paralyzed, with the exception of the adductor of the thumb, supplied by the ulnar nerve, and in consequence of loss of function on the part of the short abductor of the thumb, the short flexor of the thumb, the opposing muscle of the thumb, the power of abduction and flexion of the thumb is partially and the opposing action of the thumb is wholly abolished. When 496 NERVOUS SYSTEM the paralysis has existed for some time atrophy of the thenar mus- cles takes place. As the action of the abductor of the thumb, supplied by the ulnar nerve, preponderates, the thumb becomes permanently approximated to the hand, and its terminal phalanx is markedly flexed upon the dorsum through the action of the long and short extensors of the thumb. As a result there develops a form of hand that has been designated the ape- hand. There are paralyzed, in addition, the first and second lumbrical muscles, which effect palmar flexion of the second and third phalanges of the index-finger and the middle finger, with synchronous dorsal flexion of the basal phalanx. The sensibility of the skin is lost upon the radial aspect of the palmar surface of the hand to a median line passing through the fourth finger. Upon the dorsal aspect of the finger cutaneous sensibility is wanting Fig. 67.— Claw-hand following paralysis of the left ulnar nerve as the result of a punctured wound ; from a photograph (personal observation, Zurich clinic). in the terminal phalanges of the thumb and of the second and third fingers. Not rarely trophic alterations occur, particularly glossy finger, vesication of the skin, thickening and fracture of the nails. A lesion in the course of the internal l)icipital sulcus causes paralysis of all of the muscles upon the palmar surface of the fore- arm, in addition to the muscles already named, with the exception of the ulnar flexor of the carpus, which is supplied by the ulnar nerve. The patient is, therefore, unable to flex the terminal pha- lanx (paralysis of the deep flexor of the digits) and the second phalanx (paralysis of the superficial flexor of the digits). This is particularlv noticeable in the second and third fingers, and less so in the fourth and fifth, as the deep flexor receives besides branches from the ulnar nerve. Palmar flexion of the hand can be effected only with difficulty, and with synchronous abduction toward the ulna (from contraction of the ulnar flexor of the carpus). In con- sequence of paralysis of tlie radial flexor of the carpus abduction of the hand toward the radius is impossible if the hand is in a PARALYSIS OF THE ULNAE NERVE 497 position of palmar flexion. Paralysis of the round pronator and of the quadrate muscle prevents pronation of the dependent arm, while with the forearm flexed the long supinator (supplied by the radial nerve) will efi:ect .pronation of the forearm. PARALYSIS OF THE ULNAR NERVK etiology. — Refrigeratory and infectious par^alysis of the ulnar nerve is uncommon. The condition is generally dependent upon traumatic influences, which coincide with those of traumatic radial paralysis. Sleep-palsy, crutch-palsy, narcosis-palsy, and prisoners' palsy involving the ulnar nerve have been observed. At times pressure-paralysis of the ulnar nerve has been noted in certain artisans (clockmakers, glassworkers) as a result of long-continued support of the arm upon the elbow. Symptoms and Diagnosis. — Paralysis of the ulnar nerve is attended with paralysis of the muscles of the hypothenar emi- nence (abductor, flexor, and opposing muscle of the fifth digit), and consequently the little finger is incapable of executing the corresponding movements. Paralysis of those portions of the deep flexor of the digits passing to the ring-finger and the little finger prevents plantar flexion of the terminal phalanx of these fingers. Plantar flexion of the hand is impaired, and can be performed only toward the radial but not toward the ulnar aspect (paralysis of the ulnar flexor of the carpus). The interosseous muscles are paralyzed, and as a consequence the patients are unable to perform plantar flexion of the basal phalanx of the fingers, and at the same time to extend the other two phalanges. In the presence of paralysis of the ulnar nerve the third and fourth lumbrical muscles are further paralyzed. In consequence extension of the basal phalanx with synchronous plantar flexion of the other two phalanges is wanting. Sensory disturbances are present on the palmar aspect of the hand toward the ulna from a median line passing through the ring-finger. On the dorsal surface of the hand and the fingers the sensory disturbance extends to a median line passing through the middle finger and upon the ulnar side of this line. After the paralysis has existed for some time atrophy of the paralyzed muscles takes place from disuse. This is appreciable particularly in the muscles of the hypothenar eminence, which presents a thin and flattened appearance, and in the interosseous spaces, which present unusually deep depressions. At times a claw-hand develops. This results from dorsal hyperextension of the basal phalanges of the fingers by the common extensor of the digits, while in consequence of paralysis of the lumbrical muscles the flexors of the fingers cause such marked palmar flexion of the other two phalanges that at times the nails are dug into the palm 32 498 NERVOUS SYSTEM of the hand. As the first and third himbrical muscles are not involved in paralysis of the ulnar nerve, the claw-position is gen- erally more pronounced in the fourth and fifth fingers (Fig. 67). PARALYSIS OF THE MUSCULOCUTANEOUS NERVE. Paralysis of the musculocutaneous nerve occurs with extreme rarity. Paralysis of the biceps of the arm is most commonly attended with loss of flexion of the forearm or with incomplete flexion in pronation from the action of the long supinator supplied by the radial nerve. PARALYSIS OF THE AXILLARY NERVE. !^tiolog3''. — Paralysis of the axillary nerve is most commonly of traumatic origin (fall, blow, contusion of the shoulder, pressure by a crutch, luxation or fracture of the head of the humerus). At times it occurs as a complication of inflammation of the shoulder- joint, perhaps from extension of the inflammatory process to the nerve. Refrigeratory and toxic paralysis of the axillary nerve (lead-poisoning, diabetes mellitus) are also known. Symptoms and Diagnosis. — Paralysis of the axillary nerve is attended with paralysis of the deltoid muscle. Although the axillary nerve sends fibers to the small round muscle, no disturb- ance of function is observed in this muscle, as it receives nerve- fibers also from the suprascapular nerve. \^ hen the deltoid muscle is paralyzed the patient is unable to elevate the arm to the hori- zontal level. The muscle undergoes gradual atrophy, the shoulder becomes flattened and thin, and a flail-joint develops at the shoul- der, in consequence of the traction of the arm and the deficient resistance of the paralyzed deltoid muscle. Sensory disturbances may be present upon the upper, outer, and posterior aspect of the arm. COMBINED PARALYSIS OF THE NERVES OF THE ARM AND THE BRACHIAL PLEXUS. By combined paralysis of the nerves of the arm is understood simultaneous paralysis of several nerves of this member. The cause may be situated in the upper arm or the forearm or in the brachial plexus. The last situation is particularly adapted for the develop- ment of combined paralysis of the nerves of tlie arm, because here the paths for the various nerves to the arm lie so closely together that even a small lesion is capable of injuring several nerves at the same time. Constrictions of the arm, fractures, luxations, and the pressure of a crutch are well adapted to injure several nerves of the arm at the .same time in their course through the member. PARALYSIS OF THE NERVES OF THE ARM 499 Paralysis of the brachial plexus also is generally of traumatic origin, and occurs particularly in consequence of pressure in asso- ciation with luxation of the humerus, dislocation or fractures of the clavicle, and neoplasms of the neck. At times it has been observed to set in abruptly, in an apoplectifonii manner, spon- taneously, or after excessive strain. On post-mortem examination hemorrhage into the brachial plexus has been observed in a number of instances. In all cases of brachial paralysis motor disturbances invariably preponderate ; sensibility may be wholly unaltered. In accordance with the seat of the lesion several varie- ties of paralysis of the brachial plexus can be distinguished, namely, an upper, a lower, and a mixed variety, the last including the manifestations of the other two. The upper variety of paralysis of the bracMal plexus involves the fifth and sixth cervical nerve-roots. It includes ErVs j?aral- ysis of the brachial j)lexus, which is attended with paralysis of the deltoid, the biceps, the internal brachial, and the long supinator, and also at times of the supraspinous, infraspinous, and short supinator. Erb showed that two or three centimeters above the clavicle, at the level of the transverse process of the sixth cervical vertebra, just behind the external border of the sternomastoid muscle there is a point — Erb's supraclavicular point — con-espond- ing to the fifth and sixth cervical nerve-roots, electric stimulation of which induces contraction of the muscles involved in Erb's paralysis of the brachial plexus. Parturitional or obstetric paralysis also belongs in this category. This is observed in the newborn when during labor it has been necessary to free the arms or apply the fingers over the clavicles, or introduce a hook or the fingers into the axillary cavity. Ob- stetric palsy may result also from slipping of the forceps and pressure upon the brachial plexus. Generally, in addition to the paralysis there is found luxation or fracture of the humerus or fracture of the clavicle or of the scapula. The muscles involved are the same as those that suffer in Erb's palsy. Recovery is not impossible. The lower variety of paralysis of the brachial plexus involves the distribution of the eighth cervical and the first dorsal nerve. The muscles paralyzed include those of the thenar and hypothenar eminences, the interosseous, and at times also some of the flexors of the forearm. Oculopupillary symptoms (contraction of the pupil, narrowing of the palpebral fissure, retraction of the eye- ball) will be especially conspicuous. These depend upon the cir- cumstance that the communicating branch of the first dorsal nerve transmits oculopupillary fibers from the cervical cord to the path for the cervical sympathetic. Sensory disturbances may be ob- served especially in the distribution of the median and the ulnar nerve and on the inner aspect of the upper arm. ' 500 NERVOUS SYSTEM PERIPHERAL PARALYSIS OF THE SCAPULAR MUSCLES. PARALYSIS OF THE SERRATE MUSCLE. Ktiology. — The greater untericn- serrate niusele receives fibers from the lung thoracic nerve, a branch of the brachial plexus. Peripheral paralysis of the serrate muscle is not unconmion, as the nerve pursues a superficial and long course on the side of the neck and the lateral aspect of the chest. Most commonly paralysis of the serrate muscle is of traumatic origin, as, for instance, from Fig. 68.— Position of the scapula with the arm dependent in a case of paralysis of the right serrate muscle in consccjuence of muscular over-exertion in a weaver for fourteen years (personal observation, Zurich clinic). punctured or incised wounds of the neck, or from the carrying of heavy weights upon the shoulder. At times paralysis of the ser- rate muscle results from muscular over-exertion. I have seen such a condition after the mowintr of hnv and after lono--continued weavino;. Paralysis of the serrate muscle has been observed also after too long-continued planing and sawing. Infectious paralysis of the serrate muscle has been reported in the sequence of typhoid fever, diphtheria, erysipelas, and other infectious diseases. Befrigeratory jiaralysis of the serrate muscle is also known. Almost always the PERIPHERAL PARALYSIS OF THE SCAPULAR MUSCLES 501 condition occurs in adults, and more commonly in men than in women. Symptoms and Diagnosis. — Paralysis of the serrate muscle is attended with an abnormal position of the scapula, which is apparent even with the arm at rest and dependent, but becomes more conspicuous when the arm is held in front of the body or is elevated vertically. When the arm is dependent the inferior angle ///^' -^"^ ^ ^^ III ^\: Fig. 69.— The same patient as shown in Fig. 68, with the arm elevated in front. of the scapula is removed from the dorsal aspect of the chest (from preponderant action of the biceps, the lesser pectoral, and the coracobrachial). The inner border of the scapula is more closely approximated to the vertebral column upon the diseased than upon the healthy side (from preponderant action of the rhomboid and the trapezius), and the inferior angle of the scapula is more closely approximated to the vertebral column than the upper and inner angle. In consequence, the inner border of the scapula is directed 502 NERVOUS SYSTEM from above and without downward and inward. The entire scapula occupies a higher level upon the diseased than upon the healthy side (Fig. 68). If the arm is raised in front of the body, the internal border of the scapula becomes so greatly removed from the dorsal aspect of the chest that the hand can be easily inserted between the chest-wall and the border of the scapula (Fig. 69). At the same time tiie scapula becomes still more closely approxi- mated to the vertebral column. This approximation becomes the Fig. 70.— The same patient as shown in Figs. 68 and 6l>, with the arms elevated vertically. greater if the arm is raised to a vertical position (Fig. 70). Ele- vation of the arm slowly above the horizontal level is possible only with difficulty, and can be effected with greater ease only if the scapula has previously been put in proper position by the hands and is there held during the act of elevating the arm. All movements of the arm forward (pushing, crossing) are rendered difficult, and the patient is unable to offi?r any resistance to retrac- tion of the scapula. Gradually the serrate muscle may undergo PERIPHERAL PARALYSIS OF THE SCAPULAR MUSCLES 503 atrophy from disuse, the thorax becoming flattened on its lateral aspect and the otherwise readily visible serrations of the muscle being lost. As a prodrome of paralysis of the serrate muscle, pain at times appears in the shoulder, and subsequently may be replaced by cutaneous anesthesia. Paralysis of the serrate muscle is gen- erally unilateral. Traumatic bilateral serrate paralysis may be observed if heavy weights are carried lirst upon one shoulder and, after paralysis lias developed, subsequently upon the opposite shoulder, or if at first one of the muscles and then the other is unduly strained. PARALYSIS OF THE GREATER AND LESSER PECTORAL MUSCLES. The greater and lesser pectoral muscles are supplied by the anterior thoracic nerve. Paralysis of these muscles is uncommon, and is characterized by impairment of adduction of the upper arm upon the paralyzed side, and absence of muscular elevation in the infraclavicular region on attempted adduction. The patient is able only with difficulty to place the hand upon the healthy shoulder, and to clap the hands. Little resistance is oifered to passive abduction of the upper arm. Atrophy of the paralyzed muscles is attended with the development of a marked depression in the infraclavicular region. PARALYSIS OF THE RHOMBOID AND THE ELEVATOR OF THE ANGLE OF THE SCAPULA. The rhomboid and the elevator of the angle of the scapula are supplied by the dorsal nerve of the scapula from the brachial plexus. Derangement of function appears in connection with paralysis of the muscles named only when the trapezius is paral- yzed at the same time. Under such conditions paralysis of the rhomboid prevents approximation of the scapula to the vertebral column, while paralysis of the elevator of the scapula prevents movement of the scapula upward. PARALYSIS OF THE BROAD DORSAL MUSCLE. Paralysis of the broad dorsal muscle, supplied by the subscap- ular nerves of the brachial plexus, is attended with difficulty in adduction of the arm to the chest, but particularly in the move- ment of the arm and the hand toward the gluteal region. PARALYSIS OF THE INTERNAL ROTATORS OF THE ARM. The internal rotatcjrs of the arm include the subsca2)ular and the greater round muscle, both of which are supplied by the sub- scapular nerves of the brachial plexus. When the muscles named are paralyzed the action of the external rotators of the arm (infra- 504 NERVOUS SYSTEM spinous, lesser round muscle) preponderates, so that the palmar aspect of the arm and the hand is directed forward, and the arm cannot be rotated inward on request. All of the movements of the hand directed to tlie opposite side of the body are, therefore, rendered difficult. If atrophy of the subscapular occurs, crackling sounds are audible on movement of the scapula, but these are present also in some healthy persons. PARALYSIS OF THE EXTERNAL ROTATORS OF THE ARM. The external rotators of the arm, the infraapiiioas and the lesser round muscle, are supplied by diiferent nerves, namely, the infraspinous by the suprascapular and the lesser round by the axillary. Paralysis of both muscles is attended Avith internal rotation of the arm from preponderant action of the internal rota- tors, so that the ulnar border of the arm is directed forward. External rotation of the arm is impossible. When the infra- spinous muscle upon the right side is paralyzed the movements necessary in writing and sewing are greatly interfered with. Atrophy of the infraspinous muscle gives rise to a depression in the infraspinous fossa. PERIPHERAL PARALYSIS OF THE MUSCLES OF THE BAOC Paralysis of the lumbar extensor muscles is attended with marked convex curvature of the vertebral column forward in standing — lordosis — a vertical line through the dorsal vertebrae passing far behind the sacral promontory. In the sitting posture, however, marked h/pJwsis develops in the lumbar region, and the upper portion of the body inclines so far forward that the patient is compelled to support his arms upon the thighs in order not to fall over. In the dorsal decubitus the kyphosis disappears. If the patient be seated upon the floor and attempts to arise, he will slowly climb up upon his own extremities with rotatory move- ments of the body. The waddling, duck-like walk is, further, peculiar. Paralysis of the extensors of the back is attended with paralytic kyphosis in the standing posture, which disappears in the dorsal decubitus. Unilateral paralysis will give rise to para- lytic scoliosis. Paralysis of the extensors of the neck is attended with drooping forward of the head. PERIPHERAL PARALYSIS OF THE ABDOMINAL MUSCLES. Unilateral paralysis of the abdominal 7nuscles is attended with retraction of the umbilicus toward the healthy side with each expiration. Bilateral jMralysis of the abdominal muscles prevents PERIPHERAL PARALYSIS OF THE OBTURATOR NERVE 505 all expulsive and expiratory movements (cough, sneezing, strain- ing at stool). The hand applied to the abdominal wall fails to detect contraction during the movements named. Change from the recumbent to the sitting posture is possible only with the aid of the arms. In standing, the abdomen protrudes greatly for- ward. In walking, the upper portion of the body is bent forward, and the lumbar portion of the vertebral column is the seat of lordosis. A vertical line through the cervical vertebrae will pass in front of the sacral promontory, as the pelvis is bent greatly forward. Simultaneous paralysis of the abdominal muscles and the muscles of the back is attended with impossibility of maintain- ing the upright posture. PERIPHERAL PARALYSIS OF THE CRURAL NERVE, Paralysis of the crural nerve of refrigeratory, toxic, or infec- tious origin is uncommon ; most frequently it is of traumatic origin. The causes may reside within the vertebral canal (hemor- rhage) or consist in disease of the vertebral column (fracture, tuberculosis, new-growth) or inflammation or a new-growth in the true pelvis. Aneurysms of the femoral artery and punctured and incised wounds may also be mentioned as causes for the paral- ysis. Paralysis of the iliopsoas muscle prevents flexion of the thigh upon the abdomen, and paralysis of the quadriceps extensor of the thigh renders impossible extension of the flexed thigh or resistance to passive flexion. Naturally, the patellar tendon-reflex is wanting. Such sensory disturbances as may be present are dis- tributed upon the anterior and inner aspect of the thigh, and in the course of the greater saphenous nerve, also along the inner aspect of the leg and the inner border of the foot. Atrophy of the paralyzed muscles from disuse is attended with wasting of the thigh upon its anterior aspect. The paralysis of the muscles named is attended further with disturbances in walking and in changing from the sitting to the standing posture. PERIPHERAL PARALYSIS OF THE OBTURATOR NERVE. Peripheral paralysis of the obturator may result from the same causes as paralysis of the crural nerve, and at times both nerves are paralyzed simultaneously. Occasionally paralysis of the ob- turator nerve is observed after difficult labor or after incarcera- tion of an obturator hernia. The abductors of the thigh particu- larly are paralyzed, so that the patient is unable to move the abducted member to the middle line, or to throw it over the healthy member in the recumbent or sitting posture. In conse- quence of paralysis of the external obturator, external rotation of 506 NERVOUS SYSTEM tlie lower extremity also is embarrassed. Sensory disturbances may be present upon the internal aspect of the thigh. PERIPHERAL PARALYSIS OF THE GLUTEAL NERVES, Paralysis of the gluteal nerves is attended with difficulty in rotation of the thigJi botli inward (middle and lesser gluteus, inter- nal obturator, tensor of the broad fascia) and outward (greater gluteus). Abduction of the leg is interfered with (greater and mid- dle gluteus). Walking, particularly ascending stairs, is rendered difficult, because the iliopsoas and the greater gluteus are com- pelled to fix the trunk upon the thigh and to maintain the equi- librium, and the action of the iliopsoas preponderates in the pres- ence of paralysis of the greater gluteus. In consequence of paral- ysis of the greater gluteus change from flexion of the body for- ward to the upright posture is impossible. Atrophy of the gluteal muscles from disuse is characterized by flattening and w^asting of the buttocks. PERIPHERAL PARALYSIS OF THE SCIATIC NERVK Ktiology. — Peripheral paralysis of the sciatic nerve may in- volve the trunk of the nerve or individual branches. In the lat- ter event peroneal is more common than tibial paralysis. The tntnh of the sciatic nerve often suffijrs from traumatism, "while refrigeratory, infectious, and toxic paralyses are observed much less commonly. The trauuiatic causes are approximately tlie same as those for peripheral paralysis of the crural nerve. Isolated jialsies of the peroneal nerve have been observed in a number of instances in laborers compelled to occupy a stooping posture for a long time in their work (potato-pickers, stone-setters, asphalters). Symptoms and Diagnosis. — In cases of paralysis of the trunk of the sciatic nerve flexion of the leg upon the thigh is im- possible (paralysis of the l)iceps of the thigh, the semitendinosus, the semimembranosus). External rotation (internal obturator, gemelli, pyriform) and aljduction of the thigh also are restricted. In walking the extremity remains straight and is not flexed at the knee-joint. In the presence of peroneal paralysis the tip and the outer border of the foot are directed downward (pes varo-equinus). In walking the patient must lift the foot high, in order to avoid scraping the floor with the toes, and the foot is brought down upon its outer border. Dorsal flexion of the foot and the toes is im- possible. Paralysis of the tibial nerve prevents plantar flexion of the foot and the toes, and, from the preponderant action of the antagonists, gradually gives rise to pes calcaneus — club-foot. In addition, in consequence of paralysis of the posterior tibial muscle, abduction of the foot is greatly impaired (posterior tibial). MOTOR TRIGEMINAL SPASM. 507 PERIODIC PARALYSIS. The designation periodic paralysis has been applied to a condi- tion in which persons are periodically paralyzed for hours in the upper and lower extremities, and at tin:ies also in a number of cerebral nerves. The electric irritability of the paralyzed nerves and muscles is greatly diminished, or even at times . abolished. The disease is hereditary. It has been thought to be dependent upon auto-intoxication. SPASMODIC DISORDERS OF MOTOR NERVES (HYPERKINESIS). Muscular spasm may be either tonic or clonic. With tonic spasm there is persistent contraction of the muscle, which may re- main shortened and hard for hours and at times for days. Clouic spasm is attended with intermittent muscular contractions usually appreciable to the eye and the applied hand and capable of enu- meration. If tonic muscular spasms are attended with pain, they are designated cramps. MOTOR TRIGEMINAL SPASM, Motor trigeminal spasm is known also as masticatory spasm, be- cause it involves the muscles of mastication. Tonic spasm of the muscles of mastication gives rise to the clinical picture of trismus or lockjaw. The jaws are clinched tightly and the patient is unable to separate them, speaking through the teeth, and the contracted temporals and masseters are usually visible and palpable beneath the skin as muscular masses of board-like hardness. Naturally, persistent trismus is attended with the danger of starvation, so that it becomes necessary for purposes of artificial nutrition to in- troduce an esophageal tube between the teeth or into the nose, or to administer nutrient enemata. Most commonly trismus results in consequence of reflex irritation from the irruption of teeth and periostitis of the lower jaw. It is quite a constant symptom of tetanus, although here it is probably due to central irritation. The best-known examples of clonic spasm of the muscles of masti- cation are the chattering of the teeth on exposure to cold and to emotional influences, and the grinding of the teeth in cases of men- ingitis and in teething children. In the first event particularly the masseters and the temporals are involved, in the latter the pterygoids. At times spasm of the muscles of mastication is asso- ciated with trigeminal neuralgia. In the treatment an attempt will be made first to remove the causative factors. In addition, subcutaneous injections of morphin. 508 NERVOUS SYSTEM applications of the galvanic and the faradic current, and in the presence of trismus even gradual separation of the jaws by the introduction of wedges. SPASM OF THE MUSCLES OF THE FACE (PSOROSPASM). Symptoms, Diagnosis, and Prognosis. — ]Most commonly clonic spasm of the muscles of the face is ol)served. If all of these 7nuscl('s are involved, the condition is generally unilateral. Spon- taneously and particularly on emotional disturbance active con- tractions take place in the various muscles of the face, giving rise to marked and disfiguring grimaces. Wrinkling of the foreiiead, blinking of the eyes, distortion of the cheeks, puckering of the lips, and dilatation of the mouth alternate irregularly with one another, and the appearance resembles the distortions of the facial muscles induced by faradization of the facial nerve. At times pressure -points are discovered over the supraorbital or the infra- orbital nerve, the spinous or the transverse processes of the cer- vical vertebrae, the condyles of the radius or the ulna, the mucous membrane of the buccal or the nasal cavity, pressure upon which causes cessation of the spasm. The number of paroxysms of spasm varies ; often they are repeated within a few minutes. The individual paroxysm is of widely varying intensity, extent, and duration. At times there is but a transitory, lightning-like con- traction of the muscles of the face. The stapedius, the muscles of the palate, and the salivary secretory nerves do not, as a rule, participate in the clonic muscular spasm. The contractions usually cease during sleep, altliough I have ol)served them to per- sist in cases of cerebral hemi])legia. The disorder is annoying, but not dangerous. Not rarely it persists throughout life. Re- covery can be expected only when the causative factors are dis- coverable and are capable of removal. Partial clonic spasm of the muscles of the face occurs also in healthy persons following great mental excitement, as, for instance, involuntary wrinkling of the forehead, the play of the alfe of the nose, and the twitching of the lips. The best-known of the varieties of partial clonic spasm of the facial muscles is clonic spasm of the sphincter of the eyelids — nictitation — which is observed with particular frequency in association with diseases of the eyes themselves. Tonic spasm of the facial muscles is most commonly partial, and involves with preference the sphincters of the eyelids. With the onset of such spasm — blepharospasm — the eyelids snap together like the lid of a chest, and remain closed until the attack termi- nates. The duration of an attack varies between minutes, hours, and weeks. Naturally, the patient is unable to see during the SPASM OF THE MUSCLES OF THE FACE 509 attack, and if this occur on the crowded street the patient may be exposed to serious danger. It is noteworthy that at times points are discoverable upon the body, as, for instance, over the supra- orbital and infraorbital nerves, the cervical vertebrae or elsewhere, on pressure upon which the muscular spasm ceases and the closed eyelids separate. The disorder may be extremely obstinate and persist throughout the whole of life. !^tiology. — Spasm of the facial muscles is observed with particular frequency in nervous persons. At times the disorder is inherited, although some members of the family perhaps will not suffer from spasm of the facial muscles, but from certain central neuroses (hysteria, neurasthenia, epilepsy, chorea, psychopathy, etc.). At times the disorder is due to traumatism. Thus, it has been observed to develop in the sequence of contusion of the trunk of the facial nerve, as a result of the pressure exerted by enlarged lymphatic glands or by an aneurysm of a cerebral artery. Frequently it occurs in consequence of reflex irritation, as, for instance, in association with trigeminal neuralgia, and diseases of the eyes and the teeth. It has been observed also in women with disease of the uterus or the ovaries, and in persons with intestinal worms. In children the habit of imitation plays an important part ; that is, previously healthy persons who are brought much in contact with those presenting facial spasm are attacked by the same disorder. Also originally voluntary grimaces may gradually be converted into involuntary facial spasm. Experience has shown that men are attacked by spasm of the facial muscles more com- monly than women. The disorder occurs less commonly in child- hood. Anatomic Alterations. — But little is known with regard to the anatomic alterations attending spasm of the facial muscles. In any event the latter may occur in the absence of any change in the fibers of the facial nerve, so that the disturbances present must be of a purely functional nature. Treatment. — In the first place, an effort should be made to remove any causative factors present — causal therapy — considera- tion being given particularly to facial spasm of reflex origin. The rapidity with which the spasms cease after removal of the causative conditions is often surprising. Unfortunately, such cases are the less common. As a rule, one is compelled to resort to symptomatic treatment. In nervous persons success may be attained by means of 2i judicious mode of life and the administration of nervines, par- ticularly hromids. Narcotics also, particularly subcutaneous injec- tions of morphin, have been largely used. At times psychic treat- ment will be indicated, particularly in children, li jyressure-points can be demonstrated, applications of the galvanic current through the anode should be made to them. Recourse has been had also to nerve-section (neurotomy), nerve-excision (neurectomy), and nerve- 510 NERVOUS SYSTEM stretching ; but generally the twitchings cease only so long as the facial paralysis persists, generally recurring with the disappear- ance of the paralysis. SPINAL ACCESSORY SPASM. Wliat has been said concerning spasm of the facial muscles is applicable also to the causes of spinal accessory spasm. At times disease of the cervical vertebrce is responsible for the disorder. In children it has been observed at the period of dentition. Unilateral clonic sjmsm of one sternomastoid is attended with periodic twitch- ing movements of the head, the face and the chin being rotated toward the healthy side, the chin elevated, and the occiput re- tracted. Unilateral tonic spasm of the sternomastoid is attended with persistence of this position during the attack and immobility of the head — spasmodic torticollis. Bilateral clonic spasm of the sternomastoid is attended with various manifestations, accordingly as the spasmodic muscular contractions of the sternomastoid occur alternately or synchronously. In the first instance the head is in- volved in rotatory movements, in the latter in nodding movement. Bilateral tonic spasm of the sternomastoid is attended with retrac- tion of the head. In addition to the sternomastoid, the trapezius also is involved in cases of accessory spasm. Unilateral clonic spasm of the tra- pezius is attended with elevation of the scapula and retraction of 'the head. The symptoms of bilateral clonic as well as of tonic spasm of the trapezius may be understood without further description. A striking and varying picture of alterations in the movements of the head and the shoulder results when both the sternomastoid and the trapezius are involved in the spasm, although it is easy to separate the picture into its individual constituents. With regard to the prognosis and the treatment, the same statements are applicable as were made concerning spasm of the facial muscles. HYPOGLOSSAL SPASM. Hvpoglossal spasm is attended with spasm^ of the tongue — glossospasm — and accordingly as this occurs in the act of chewing or of speaking a distinction is made between m a sticatoi'i/ and artic- idatorj/ spasm of the tongue. The spasm may be clonic or tonic and unilateral or bilateral. The disorder can be readily recog- nized, and attacks particularly hysterical and nervous persons. In accordance with the character of the spasm, either the mastica- tory or the articulatory movements are interfered with. If the tongue is retracted for a considerable length of time, danger of suffocation may arise. SPASM OF THE DIAPHRAGM 511 SPASM OF THE CERVICAL AND SCAPULAR MUSCLES. Spasm of the Inferior Oblique Muscle of the Head. — This muscle rotates the head in the horizontal level, without elevating or depressing the chin. If the disorder be unilateral and clonic, the head is rotated horizontally toward the dis- eased side, while in the presence of bilateral alter- nating muscular spasm ro- tatory movements of the head from side to side occur — rotatory spasm or tic. Unilateral tonic spasm keeps the head constantly turned toward one side, and resistance is encountered when an attempt is made to restore the head to its normal position. Spasm of the splenius mus- cle of the head also gives rise to an abnormal position of the head. The muscle turns the head toward the diseased side, while the face and the chin are approxi- mated to the shoulder. The contracted muscle is visible beneath the anterior border of the trapezius, and the sternomastoid appears relaxed upon the diseased side and stretched upon the healthy side (Fig. 71). When spasm of the rhomhoid is present the scapula becomes approximated to the vertebral column, and cannot be moved freely outward. Elevation of the arm above the horizontal level is attended with resistance. The contracted muscle is visible and palpable in the interscapular space. Spasm of the elevator of the scapula is attended with elevation of the scapula, particularly its inner upper angle. The head is retracted. The contracted muscle appears in the clavicular fossa at the side of the anterior border of the trapezius. Fig. 71.— Position of the head in the presence of spasm of the right splenius muscle of the head. SPASM OF THE DIAPHRAGM. Clonic spasm of the diaphragm, also designated hiccough, is the best-known variety. While the diaphragm contracts suddenly and air endeavors to enter the air-passages, the chink of the 512 NERVOUS SYSTEM glottis closes and then a gurgling sound is heard. The condition may corae to an end with a few contractions of the diaphragm, but in some cases it persists for days and weeks, and the patient complains of pain and disagreeal)le sensations along the points of attachment of the diaphragm. Children are predisposed in marked degree to clonic spasm of the diaphragm, which may occur after overloading the stomach and after hearty laughter. The same causes may give rise also to clonic spasm of the diaphragm in adults. At times the disorder occurs in association with dla~ phragmatic pleurisy or peritonitis, or with irritation of the j^hrenio nerve by mediastinal tumors. Disease of the brain (meningitis, hemorrhage, softening) also is at times attended with spasm of the diaphragm. Occasionally this occurs in cases of hysteria. Reflex clonic spasm of the diaphragm has been observed in connection with diseases of the stomach, the intestine, the kidneys, the liver, and the sexual organs. Further, there are cases ivithout obvious etiologic factors. In treatment efforts should be directed first to the removal of the cause — causal therapy. Among symptomatic measures expulsive efforts with closure of the chink of the glottis, rapidly successive swallowing of w-ater, the introduction of a sound into the esopha- gus, constriction of the lower portion of the thorax Avith simulta- neous strong flexion of the head, and the like, have been recom- mended. Among medicaments, nervines and narcotics particularly have been employed. In cases of hysteria psychic treatment is indicated. I have effected cure by means of regular and slow counting. Tonic spasm of the diaphragm has been observed as a result of exposure to cold and in the sequence of infectious diseases (par- ticularly rheumatism, tetanus). At times it is dependent upon disease of the brain (epilepsy, hysteria). It may be recognized from the want of movement in the greatly distended lower portion of the thorax in respiration, while the upper portion is engaged in active and labored breathing. The lower border of the heart and of the lungs is unusally low, and exhibits no movement with respi- ration. Respiratory movement of the lower border of the liver is likewise not demonstrable. The epigastrium bulges forward. If speedy relief be not afforded, death will result from suffocation. A subcutaneous injection of morphin should be given or chloro- form-narcosis be induced in order to overcome the tonic spasm of the diaphragm. If these measures do not succeed, faradization of the phrenic nerves should be practised. SPASM OF THE ABDOMINAL MUSCLES. Spasm of the abdominal muscles is generally of central origin. Clonic spasm of the abdominal muscles has occasionally been NEURALGIA 513 observed in connection with hysteria ; tonic spasm — recognizable from the hardness, tension, and contraction of the abdominal walls — occurs in connection with tetanus and meningitis. MUSCULAR SPASM IN THE UPPER AND THE LOWER EXTREMITIES. The muscles of the arms and the legs are but rarely involved in tonic or clonic spasm. The condition when present can be readily recognized. CRAMPS. The best-known example of tonic, painful muscular spasm is cramp in the calf of the leg. The patient complains suddenly of intense pain in the calf of one leg and at the same time the mus- cles in this situation are thickened and contracted with board-like hardness. As a rule, the pain ceases in the course of a few seconds, although a sense of weakness persists for some time. Occasion- ally extravasations of blood beneath the skin are observed in the region of the calf. Nervous and anemic individuals are greatly predisposed to the disorder. At times it develops in the sequence of over-use on the part of the calf-muscles in standing, walking, swimming, turning, dancing. The cramps in the calves that are observed in cases of Asiatic cholera and diabetes mellitus appear to be dependent upon toxic influences. Cramps in the calves develop not rarely in persons with varicose dilatation of the veins of the leg. The cramp can be overcome by vigorous rubbing, by alcoholic frictions, and by subcutaneous injection of morphin. Be- sides, attention should be given to the causative conditions. NEURALGIA. PRELIMINARY CONSIDERATIONS. Neuralgia — nerve-pain — is characterized by its distribution in the course of diseased sensory nerves. Either the pain occurs in attacks or it is greatly increased paroxysmally. The number and the duration of the attacks of pain are susceptible of wide varia- tion. The pain is described by the patient as gnawing, burning, and crushing, and not rarely becomes so intense that even strong men are made to groan and are incapacitated from all physical and mental occupation. Not rarely rest at night is greatly disturbed. The pressure-points of Valleix are peculiar to many varieties of neuralgia. It has been found that certain points in the course of the diseased nerve are particularly sensitive to pressure. The pressure-points are definite for the individual nerves, being gen- erally situated at places where the nerve is superficial and rests 33 514 NERVOUS SYSTEM upon bone, so tliat it is readily accessiljle to the compressing finger. Cutaneous sensibility in tlie distribution of the diseased nerve is frequently altered. At the beginning there is frequently hyperesthesia, which is subsequently followed hy anesthesia. At times vasomotor, secretory, and trophic d'lsturbances are present. It may also happen that severe pain radiates throughout an exten- sive cutaneous area, and it may give rise to clonic or tonic muscular spasm. Anatomic alterations may be wanting in the nerve even though the neuralgia have lasted for years, while in other instances neuritic changes are found ; and accordingly a distinction can be made between neurotic and neuritic neuralgia. Further, the dif- ferential diagnosis generally is extremely difficult during life, and often impossible. Among the causes for neuralgia are the same conditions that have been named as causes for peripheral paralysis, and accord- ingly refrigeratory {rheumatic), traumatic, infectious, and toxic neu- ralgia may be distinguished. It has also been maintained that reflex neuralgia occurs, developing in the sequence of antecedent disease in remote organs, particularly in the female generative organs. Such nerves as lie superficially and pursue a long course or pass through narrow bony canals are readily exposed to injury. The sciatic and the trigeminus are, therefore, attacked by neu- ralgia with particular frequency. Among the infectious forms of neuralgia the malarial variety is especially well known, and this mav be the sole manifestation of malarial infection, and is charac- terized by its intermittent occurrence. It is remarkable that typically recurring neuralgia, so-called masked intermittent, may occur in regions free from malaria and attack persons A\ho have never lived in malarial regions, so that doubt as to the malarial nature of some cases of intermittent neuralgia appears justified, doubt that may perhaps be removed by examination of the blood for malarial plasmodia. In addition to malaria, syphilis is yet a common cause for neuralgia. Among the toxic varieties of neu- ralgia may be included the uremic, the gouty, and the diabetic, and Avhich more appropriately may be designated autotoxic. Experience has shown that members of nervous families and pale, nervous, debilitated individuals are attacked by neuralgia with particular frequency and readiness. Women are more greatly predisposed to neuralgia than men. The curability of neuralgia, depends essentially upon its causes. At times it persists throughout life, and embitters the existence of the patient to such a degree as to induce suicide. The treatment of neuralgia should be, in the first place, causal. Should exposure to cold have been operative, resort may be had to diaphoretics, hot fomentations, applications of cotton batting, and the internal administration of salicylic acid or sodium NEURALGIA 515 salicylate (1.0 — 15 grains — every two hours), of antipyrin (1.0 — 15 grains — thrice daily), or phenacetin (1.0 — 15 grains — thrice daily). AVhen syphilis is the etiologic factor inunctions of mer- curial ointment (5.0 — 75 grains — daily), and internally potassium iodid (5.0:200 — 75 grains : 6^ fluidounces; 15 c.c. — one table- spoonful — thrice daily) may be prescribed. Malarial influences will indicate the employment of quinin hydrochlorate (from 1.0 to 5.0 — from 15 to 75 grains — to be given three hours in advance of the expected paroxysm). At times surgical intervention will be required for the removal of the cause of neuralgia, as, for instance, in the removal of a tumor exerting pressure upon a nerve, and the like. Among symptomatic measures subcutaneous injection of morpliiii is the most reliable, but in cases of obstinate neuralgia there Avill be risk that the patient will demand progressively increasing doses, and become a morphin-habitue, particularly if he be entrusted with a syringe and a solution of morphiu : R Morphin hydrochlorate, 0.3 (4J grains) ; Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose : From 0.25 to 0.5 (4 to 8 minims) subcutaneously. Even when malarial infection is not suspected quinin hydro- chlorate (from 1.0 to 5.0 — from 15 grains to 75 grains — in tablet) is a useful remedy. In addition, nervines and narcotics of all kinds have been employed. It will suffice to mention a few ex- amples from which success may most likely be expected : R Bitter-almond water, Solution of potassium arseuite, each, 5.0 (75 minims). — M. Dose : 10 drops thrice daily after eating. R Atropin sulphate, 0.01 (i grain) ; Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose : 0.25 (4 minims) subcutaneously. R Solution of cocain hydrochlorate, 0.5 : 10.0 (7i grains : 2^ fluidrams). Dose: 0.5 (8 minims) subcutaneously. R Exalgin, • 0.3 (4i grains) ; Sugar, 0.5 (7J " ).— M. Make 10 such powders. Dose : 1 powder thrice daily. R Tincture of gelsemium, 20.0 (5 fluidrams). Dose : 10 drops thrice daily. R Butyl chloral hydrate, 5.0 (75 grains) ; Glycerin, 20.0 (5 fluidrams) ; Distilled water, 130.0 (4 fluidounces).— M. Dose : 15 c.c. (1 tablespoonful) every five or ten minutes until half the prescription is used. Alcoholic frictions and narcotic and irritating ointments have also been considerablv used. It is a matter of indiifereuce with 516 NERVOUS SYSTEM regard to the results whether spirit of mustard, spirit of camphor, spirit of formic acid, or compound spirit of angelica be employed. Chloroform-liniment also may be used : R Chloroforii), 10.0 (2^ fluidrams) ; Ammoniated liniment, 40.0 (10 " ). — M. Apply with friction. The following examples of narcotic and irritating ointments may be given : R Morphin hydrochlorate, 0.1 (1^ grains); Wool-fat, Lard, each, 5.0 (75 " ).— M. For inunction. R Extract of belladonna, 2.0 (30 grains) j Wool- fat. Lard each, 5.0 (75 " ).— M. For external application. R Veratrin, 0,3 (4^ grains) ; Wool-fat, Lard, each, 25.0 (6 drams).— M. For inunction. Leeches, wet cups, and applications of ice to the nerve and hot fomentations have also been employed considerably. Some pa- tients are greatly relieved by the employment of the galvanic cur- rent. The current should not be too strong and the anode (+ pole, copper-pole) should be applied to the affected nerve. The ap])li- cation should be repeated daily, but should not be continued longer than from three to five minutes. Treatment with the faradic brush may also yield good results. In obstinate and distressing cases resort has been had to surgical measures, and nerve-stretching, nerve-section (neurotomy), nerve-resection (neurectomy), and re- cently also the extraction of exposed nerves by means of forceps have been practised. Unfortunately, all of these efforts are attended either with no result or too frequently with only a tran- sient result. Any effect will be wanting if the operation fails to reach the seat of the neuralgia, and this may happen all the more readily as no remedy is known that is capable of determining with certainty the seat of neuralgia. Neuralgia cured by operation re- curs readily after the divided or exsected nerve has united or reformed, and this may happen even Avhen remarkably long por- tions of the nerve have been removed. Great care should there- fore be exercised in promising a successful result. TRIGEMINAL NEURALGIA. histiology. — Trigeminal neuralgia is one of the commonest varieties of neuralgia, as the branches of the trigeminal nerve pass through several bony canals and in part lie superficially, so that TRIGEMINAL NEURALGIA 517 they may be readily aifected by injurious influences. Refrigera- tory trigeminal neuralgia occurs with certainty, and it may develop, among other conditions, when individual branches are exposed to a draft of cold air or to rain. Among the forms of infectious neuralgia the best known is that of malarial origin. Trigeminal neuralgia, however, occurs not at all rarely in connection with typhoid fever, syphilis, and influenza. Toxic trigeminal neuralgia has been observed as a result of the action of lead, mercury, and iodin, and in cases of gout and of diabetes. Traumatic trigeminal neuralgia occurs frequently. Among the causes, contusions and stab-wounds of the nerve, periostitis of the cranial bones, com- pression by a neoplasm, the extension of neoplastic proliferation into the trunk of the nerve, inflammatory processes in the teeth or the jaw, in the nose or in the frontal sinuses, and in the eye and the ear. At times trigeminal neuralgia is dependent upon disease at the base of the skull (syphilitic inflammation and thickening of the meninges, tumors, aneurysms of the cerebral arteries). Chil- dren generally are exempt from trigeminal neuralgia, excepting alveolar neuralgia (toothache). Women are attacked more fre- quently than men, and pale and nervous persons in greater num- ber than the robust. Symptoms and Diagnosis. — Trigeminal neuralgia is, as a rule, unilateral. Naturally, after the lapse of a certain time it may gradually extend to the opposite trigeminal nerve, while the nerve first involved becomes free from pain. Only rarely are all three branches of the trigeminal nerve simultaneously attacked by neur- algia, and such a circumstance must be indicative of a basal origin, as the branches lie close together in this situation. Most commonly only a few branches of the trigeminal nerve are affected by neur- algia. Of all of the branches of the trigeminal nerve the supra- orbital is most commonly attacked. At times the neuralgia is preceded by certain paresthesias (a sense of crawling or of coldness or of stiflness) as prodromes. The pain may possess a burning, boring, or crushing character, and at times attains an unendurable intensity. The duration of an attack of pain and the frequency of its recurrence vary ex- tremely. The individual attack of pain sets in at times without recognizable cause, but at other times it is excited by emotional disturbances, a draft of air, glaring light, eating, drinking, or the like. In the course of the aifected nerve Valleix's pressure-points can generally be demonstrated. Cutaneous sensibility is at first generally heightened, but subsequently becomes diminished or, less commonly, lost. Vasomotor disturbances are at first indicated by arterial spasm and pallor of the skin, and soon vascular dilata- tion occurs, with corresponding redness and warmth of the skin. Among secretory disturbances increased secretion of tears, of nasal mucus (at times bloody), of saliva, and of perspiration has been 518 NERVOUS SYSTEM observed. Trophic disturbances are less common, and they may consist in increase or diminution in the fatty layer of the skin, coarseness, graying, and loss of the hair, eruptions of herpes, iritis, glaucoma, or neuroparalytic ophthalmia. Severe attacks of pain are at times attended with clonic muscular spasm in the face and at times also in the extremities. When the causative conditions are incurable the disorder may persist for many years, and even throuo-hout the ^vhole of life. The fear of an attack of neuralgia in eating, sleeplessness at night, and seclusion result in physical and moral depressi(m, and may lead to suicide. For those familiar with the anatomic distribution of the trigeminal nerve there is no Fig. 72.— Distribution of the trigeminal nerve upon the face. difficulty in determining with certainty the branch of the nerve that is tiie seat of neuralgia. For ready recognition reference may be made to Fig. 72, and we shall confine ourselves to the following diagnostic points : In cases of sujjraorbital neuralgia the pain radiates from the supraorbital margin to the frontal region, toward the root of the nose, and into the upper eyelid. The most constant pressure-point is situated just below the supraorbital foramen in the roof of the orbit. Infraorbital neuralgia is attended with pain radiating from the infraorbital margin along the cheek to the upper lip and the lateral CERVICO-OCCIPITAL NEURALGIA 519 aspect of the nose. The distinctive pressure-point is at the infra- orbital foramen. Lingual neuralgia or glossalgia is attended with severe pain in one-half of the tongue, and often with coating of part of the tongue, together with thickening of this half of the tongue and increased secretion of saliva. The diagnosis should never be considered complete with the localization of the neuralgia, but in every instance an effort should be made to determine the causative factors. Prognosis. — The prognosis depends upon the curability of the causative factors. Treatment. — The treatment is the same as that described on pp. 514-516. In obstinate cases resort has been had to com- pression and even to ligation of the common carotid artery, but without certainty as to the result. CERVICO-OCaPITAL NEURALGIA* Ktiology. — From the cervical plexus, formed from the highest four cervical nerves, five sensory nerves are given ofF: the greater and the lesser occipital, the great auricular, the inferior subcuta- neous of the neck, and the supraclavicular, of which any one may be attacked alone by neuralgia, or in rare instances all may suffer together. Most commonly neuralgia of the greater occipital is present, and the condition is for brevity's sake designated occipital neuralgia. The causes for the varieties of neuralgia under con- sideration have already been mentioned several times. Occipital neuralgia is observed particularly after injuries to the scalp, and further in association with syphilis and uremia. At times cervico- occipital neuralgia is dependent upon disease of the cervical verte- brae (tuberculosis, tumors) or upon disease of the spinal membranes or of the cervical cord itself. Symptoms and Diagnosis. — OccijMal neuralgia is attended with pain radiating from the occiput to the parietal bone. A pressure-point is situated at the point of exit of the occipital nerve between the mastoid process and the atlas. Occasionally there appear at the time of the attack of pain redness of the face, secre- tion of tears, contraction of the pupils, and vomiting. The hair may fall out and nodules may form beneath the scalp. The duration of the disorder depends upon the nature of the causative factors. Neuralgia of the lesser occipital nerve is attended with pain in the lateral aspect of the occiput and extending to the ear. A pressure-point is situated at the point of exit of the nerve just behind the mastoid process. In cases of neuralgia of the great auricular nerve the patients complain of pain above the mastoid •process, upon the posterior aspect of the auricle, and in the parotid gland, while neuralgia of the inferior subcutaneous nerve of the 520 NERVOUS SYSTEM neck is attended with pain in the anterior, inferior, and median portions of the neck, and neuralc/ia of the supraclavicular nerve with pains in the region of the acromion, the shoulder, and tlie upper portion of the thorax. PHRENIC NEURALGIA* The designation plirenic neuralgia has been given to pain occur- ring paroxysmally in the course of the phrenic nerve and at the points of attachment of the diaphragm, and often giving rise to marked difficulty in breathing. The occurrence of such a variety of neuralgia has not without reason been doubted. Among the causative factors that have been named are disease of the heart, aneurysm of the aorta, disorders of the liver, the kidneys, the in- testine and the spleen, pleurisy, pericarditis, and peritonitis. CERVICOBRACHIAL NEURALGIA. Neuralgia involving the sensory nerves of the brachial plexus (from the fourth to the eighth cervical and the first dorsal nerve) occurs frequently. Generally it is of traumatic origin (contusion, compression, incised, punctured, and gunshot wounds, and the likej. Often several nerve-tracts are involved at the same time. At times vasomotor and also trophic disturbances occur (herpes, abnormal growth of hair, glossy fingers). At times muscular weakness and atrophy are superadded to neuralgia. DORSO-INTERCOSTAL NEURALGIA. Ktiology. — The twelve dorsal nerves, after leaving the verte- bral canal through the intervertebral foramina, divide into poste- rior and anterior branches. The posterior nerve-roots or dorsal nerves are distrii)uted upon the skin of the back down to the sacrum, and are rarely the seat of neuralgia. The anterior nerve- roots or intercostal nerves, however, are attacked all the more fre- quently, and the causative factors, as with other neuralgias, are principally exposure to cold, injury, infection, and intoxication. Among the injuries it should be noted that some cases are depen- dent upon disease of the vertel)ral column (tuberculosis, carci- noma), and that intercostal neuralgia may at times be secondary to pleurisy, possibly because intercostal nerves become compressed and irritated by connective-tissue cicatrices. Often intercostal neuralgia precedes or is followed by herpes zoster. Malaria has also been ol^served to be a causative factor. Symptoms and Diag^nosis. — Intercostal neuralgia is gen- erally unilateral, most commonly left-sided, and, as a rule, attacks several contisfuous intercostal nerves at the same time. The CRURAL NEURALGIA 521 nerves between the fifth and the ninth are involved with especial frequency. The pain is characterized by its radiation about one- half of the chest. Pressure-points are present close to the vertebral column, in the axillary region, and close to the margin of the sternum, and are designated as vertebral, lateral, and sternal points respectively. Hyperesthesia and subsequently anesthesia of the skin are observed frequently. Among trophic disturbances herpes occurs not rarely. The patient often complains of dis- turbed sleep and of difficulty in breathing, laughing, sneezing, and coughing, because the pain is excited or intensified by these acts. Accurate limitation of the pain in the course of the inter- costal spaces and the absence of pleuritic friction-sounds and of alterations in the ribs readily distinguish intercostal neuralgia from muscular rheumatism, dry pleurisy, and inflammation of the ribs. Neuralgia of the mammary gland or mastodynia also is a variety of inter- costal neuralgia, because in addition to tbe supraclavicular nerves the mam- mary gland receives branches also from the second to the sixth intercostal nerve. The disorder is most common in women, particularly hysterical and anemic women, and it develops at times in the sequence of injury to the gland or of unduly protracted lactation. At times small indurations — so-called neuralgic nodes — are present in the painful gland. The disorder is attended with attacks of unbearable pain in one breast or in both. At times a colostrum-like fluid is secreted during an attack of pain. The attack occasionally persists for more than an hour. The obstinacy and the severity of the pain have induced some patients to have the gland ampu- tated. LUMBO-ABDOMINAL NEURALGIA. Lumbo-abdominal neuralgia includes involvement of the ilio- hypogastric, ilio-inguinal, lumbo-inguinal, and external spermatic nerves, which originate from the four upper lumbar nerves. The painful area extends over the lumbar and gluteal regions, the scrotum or the labia majora, and the anterior aspect of the thigh. A pressure-point is frequently found at the middle of the crest of the ilium. At the time of the attack of pain there may be pria- pism, discharge of seminal fluid, or leukorrhea. In addition to exposure to cold, disease of the vertebral column, exudates and tumors in the pelvis, and displacements of the uterus particularly give rise to lumbo-abdominal neuralgia. CRURAL NEURALGIA. Crural neuralgia is uncommon, and when it occurs is generally of traumatic origin. Disease of the vertebral column, exudates and tumors in the pelvis, aneurysms of the femoral artery, and crural hernias have been named as causes of crural neuralgia. The pains are distributed especially upon the anterior and inter- nal aspect of the thigh, and, in the course of the greater saphenous nerve, along the inner aspect of the leg and the inner border of 522 NERVOUS SYSTEM the foot to tlic groat toe. Pressure-points may be present as fol- lows : A crural point, just below Poupart's ligament, correspond- ing to the point of exit of the crural nerve ; a knee-point on the inner aspect of the knee-joint; a plantar point, in front of the internal malleolus ; and a toe-point, at the base of the great toe. OBTURATOR NEURALGIA. Obturator neuralgia may set in suddenly in connection with strangulated obturator hernia, and is therefore of diagnostic im- portance. The pain extends along the inner aspect of the thigh to the knee. Generally the adductors of the thigh are paralyzed at the same time. NEURALGIA OF THE EXTERNAL CUTANEOUS NERVES OF THE THIGH. The pain extends upon the outer aspect of the thigh to the knee. I have observed this variety of neuralgia frequently in individuals who have supported one knee upon the other for long periods of time. SCIATIC NEURALGIA. Ktiology. — Among all of the varieties of neuralgia sciatic neuralgia, also designated sciatica, occurs most commonly. The nerve may readily suffer from exposure to cold and traumatism on account of its superficial position and its long course, but infec- tious and toxic neuralgia of the sciatic nerve is also known. Working in the damp (as in digging canals, Avorking in the woods or in fortresses, sleeping in damp rooms and in the open air, and the like) is often followed by sciatica. Among the traumatic causative factors may be mentioned a fall, a blow, or contusion involving the gluteal region, heavy lifting and long standing, fractures and luxations of the thigh, neoplasms and exudates in the vicinity of the sciatic nerve, displacements and neoplasms of the nterus and the ovaries, parametric and perimetric exudates, pregnancv, fecal accumulation in the rectum, tumors of the pelvic bones, luxations, fractures, and tumors of the vertebrae, hemor- rhage, inflammation, and tumors of the spinal membranes, and the like. Among the varieties of toxic sciatic neuralgia those occurring in the course of diabetes mclHtus mnst be included, and Avhich at times are bilateral and exceedingly obstinate. Bilateral and usually resistant sciatica is observed not rarely in cases of tabes dorsalis. The disease generally attacks adults, and men more commonly than women. Anatomic Alterations. — But few reports have been made SCIATIC NEURALGIA 523 as to the anatomic alterations attending sciatica. In some cases the nerve is said to have been uninjured — neurotic sciatica — while in others it has been inflamed — neuritic sciatica. At times car- cinomatous masses have penetrated the nerve from the neighbor- hood, and have developed within it. In a case of sciatica follow- ing purpura I found extensive hemorrhage into the nerve. At times collections of serous fluid have been reported as present in the nerve-sheath. Symptoms and Diagnosis. — Sciatica is frequently recog- nized without difficulty, because the patient Avill indicate with his finger accurately the course of the sciatic nerve as the painful area. The pain extends from the point of exit of the sciatic nerve in the region of the hip down to the toes. Naturally, partial sciatica occurs at times, so that perhaps the pain extends only along the posterior aspect of the thigh, or along the calf of the leg, or is present only on the plantar aspect of the foot. Accordingly as the pain radiates from above downward or in the reverse direction a distinction has been made between descending and ascending sciatica, although this is not of much practical value, as many patients state that the pain occurs simultaneously throughout the whole course of the sciatic nerve. The number, duration, and severity of the attacks exhibit great variations. Pressure-points are present at the side of the sacrum, at the level of the posterior superior iliac spine, at the lower border of the gluteus correspond- ing to the point of exit of the sciatic nerve from the sciatic notch, at a point just behind the greater trochanter, at the middle of the posterior aspect of the thigh (bifurcation of the posterior cuta- neous nerve of the thigh), in the popliteal space (tibial nerve), at a point just below the head of the fibula (peroneal nerve), and at a point each behind the external and the internal malleolus. Vasomotor and trophic disturbances are not common. Standing and walking cause increase in the severity of the pain, and for this reason the patient shields the neuralgic extremity. It is, therefore, not surprising that muscular atrophy from disuse slowly takes place. Rapid degenerative muscular atrophy occurs when the sciatica is of neuritic origin. Under such conditions cutaneous anesthesia and impairment, and even abolition, of the knee-jerk may readily be present. On standing, it is not rarely observed that the spinal column undergoes lateral curvature — scoliotic sciatica. Generally the convexity of the curva- ture is directed toward the diseased side and less commonly toward the healthy side. An uncommon complication is the presence of sugar in the urine. The duration of sciatica varies between a few weeks and many years. Some patients are never relieved of their disorder. Also, relapses occur readily and repeatedly. The danger of confound- ing sciatica and coxitis is particularly great. In the diagnosis of 524 NERVOUS SYSTEM the latter tlie distinetive position of the lower extremity (flexion of tiic thigh and the leg with rotation outward) and the circum- stance that kicking and rotatory movements of the thigh are pain- ful in the presence of sciatica and usually are greatly interfered with, while they are free and unattended with pain in the presence of sciatica, must be taken into consideration. Prognosis. — Sciatica is an obstinate and even an incurable disorder, but it is not attended with any immediate danger to life. Naturally, the patients may become greatly debilitated in conse- quence of pain and persistent insomnia, and also nervous. Treatment. — In treatment an endeavor should first be made to meet the causal indications in the usual manner according to the suggestions already laid down. Under all circumstances rest in bed and an equable temperature are particularly serviceable measures. No specific remedy for sciatica is known, so that the treat- ment must be conducted upon the lines indicated on pp. 514-516. In chronic cases courses of treatment with baths have been re- sorted to, and indifferent thermal, saline, or sulphurous baths par- ticularly have been recommended. At times I have secured suc- cessful results by means of bloodless stretching of the sciatic nerve, the extended extremity being flexed as strongly as possible at the hip-joint and moved toward the abdomen. SPERMATIC NEURALGIA. Spermatic neuralgia is attended with pain in the testicle and the epididymis, radiating in the course of the spermatic cord to the lumbar region. At times swelling of the testicle also occurs. Among the etiologic factors may be mentioned onanism, other sexual excesses, antecedent gonorrheal epididymitis, injuries, anemia, and neurasthenia. Further, excessive sexual continence has been thought to cause the disorder. The testicle should be supported with a suspensory bandage, narcotic ointments be applied by inunction, in the presence of severe pain an injection of mor- phin be made, electricity be employed, and the general condition be treated. In obstinate cases the painful testicle has been re- moved. Neuralgia of the glans and the penis, the scrotum, the labia viajora, the urethra, ?in(!i the, perinenm ha?, also been described. Among the causative factors are exposure to cold, injuries, and sexual excesses. COCCYGODYNIA. Neuralgia of the coccyx — coccygodynia — is attended with severe pain in the coccygeal region, which becomes increased to an intol- erable degree on sitting, walking, and expulsive effort. The disorder generally occurs in women, and is attributed to injuries. ANESTHESIA 525 difficulty in labor, or exposure to cold. Further, in many instances the condition appears to be really not a neuralgia, but an inflam- matory condition of the coccyx. In obstinate and painful cases the coccyx has been removed. ARTICULAR NEURALGIA. Articular neuralgia occurs especially in pallid, nervous, or hys- terical individuals. It may develop spontaneously or after ex- posure to cold or as a result of injury. Most commonly the knee- joint or the hip-joint is the seat of the disorder. In contradis- tinction from anatomically demonstrable arthritis, the patient usu- ally keeps the extremity extended and avoids all movement. After the disorder has persisted for some time muscular atrophy from disuse may result. It is often exceedingly difficult to distinguish articular neuralgia from arthritis. The treatment should be directed against the general condition. In addition, the patient should be encouraged to use the joint. At times it is necessary to insist upon such use of the joint. Occasionally recovery takes place abruptly. ANESTHESIA. Sensory disturbances of the skin and the mucous membranes are attended with either total or only partial loss of sensibility, and accordingly a distinction is made between anesthesia and hy- peresthesia. Accordingly as all varieties of sensation or but a single variety is lost the result will be total, or payiial anesthesia, although the condition can be recognized only from a careful study of all varieties of sensation. In what follows cutaneous anesthesia alone will be considered, although naturally conditions of anesthesia and hyperesthesia may occur wherever there are sensory nerves, as, for instance, in muscles, joints, fascia, tendons, periosteum, and internal viscera. Cutaneous sensibility includes both the sense of touch and com- mon sensation. Each of these principal divisions can be sub- divided into several subgroups, and accordingly the following scheme of examination may be adopted : Tactile Sensibility : Contact-sense ; Pressure-sense ; Localization-sense ; Time-sense ; Temperature-sense. 526 XER VO US SYSTEM Common Sensibility : Pain-seiise ; Electric sensibility ; The sense of tickling. In investigating cutaneous sensibility it should be a rule to employ the simplest methods of examination. In order not to distract the attention of the patient, it is well for him to keep his eyes closed during the examina- tion, and if possible to assume a comfortable recumbent posture. Contact- sensibility is tested by touching or stroking the skin with a blunt body (the finger, a hair-brush, a bit of wood, a swab of cotton, a roll of paper). For purposes of comparison, symmetric portions of the skin or in the presence of para-anesthesia higher or lower portions should be tested successively. The test-agent should be neither too warm nor too cold, as the patient might confound the thermal sensation with that of contact. The simplest mode of testing the pressure-sense consists in making a varying degree of pressure upon the skin with the finger, or by placing upon the part to be tested a rather large coin at the temperature of the body and gradually adding more coins, and noting whether the patient is able to distinguish slight differences in weight. In making this examination the arms and the legs should be supported upon a firm base. The sense of localization con- sists in the ability of the patient to designate correctly tlie points upon the skin touched or to indicate them with his finger. In addition, it includes the recognition of the area of contact. The latter is determined by means of a pair of compasses or an esthesiometer (Figs. 73 and 74). In using either instrument, two movable points are applied simultaneously to the skin. The degree of separation f'CiiJ _ of the points can be varied. The size of the tactile area consists in the smallest distance between the points at which the two are appreciated not as one, but as two. Examination of the time-sense is of little value. B& J, ..I., ..].,.. uem Fig. 73— Compasses for testing sensibility. Fig. ~i. — Esthesiometer. It is made by means of vibrating cords, on the sound- ing-board of which a healthy individual is capable of di.stinguishing the discontinuity of 1500 vibrations per second. An adequate method for testing the tevi- perature-sense for practical purposes consists in blowing upon the skin and then breathing upon the skin, or by the application of test-tubes, one of which is gently warmed in the flame. Paradoxic disturbances of the temperaiure-sense are manifested at times in the confusion of hot with cold, and vice versa. For testing the sense of pain, needle-prick and the pulling of hairs are sufficient. The electric sensibiliti/ of the s/:in is tested by means of a dry metallic electrode connected with a faradic current, and the aji- preciation of the beginning prickling must be separated from the actual perception of pain. The sensation of tickling and of itching can be readily excited by touch with the finger upon the sole of the foot, the palm of the hand, in the axillary cavity, etc. Cutaneous anesthesia results from disease of either the periph- eral receptive apparatus (sensory nerve-termination) or the periph- eral sensory nerve-trunks, thus the conducting apparatus for ANESTHESIA 527 sensory stimuli, or of the central receptive stations in the spinal cord or the brain, and it is by no means always easy to determine the seat of the disease with certainty. The demonstration of peripheral injuries to the skin itself or to the peripheral nerve- trunks is of particular importance in this connection. In addition, a study of the reflex processes is of great importance, as these are abolished in the presence of peripheral anesthesia, whereas they persist if the anesthesia is of central origin. As many nerve- trunks are of mixed character, it should not be surprising that often motor paralysis and anesthesia occur in association. etiology. — The causes for cutaneous anesthesia include the same agencies as give rise to paralysis and neuralgia, and, accord- ingly, a distinction can be made between refrigeratory, traumatic, toxic, and infectious cutaneous anesthesia, to which vasomotor anes- thesia may be added. That cutaneous anesthesia may result from exposure to intense cold is indicated by the action of the ether- spray, which is employed upon the skin to render minor operations painless. The skin becomes anesthetic also when more consider- able portions of the extremities are frozen. Traumatic cutaneous anesthesia occurs when a sensory nerve is compressed or contused. Toxic cutaneous anesthesia develops, for instance, when strong alka- lies or acids are applied to the skin. Cutaneous anesthesia occurs also as a result of the action of lead and of carbon monoxid. Narcotics (morphin, cocain) may likew^ise diminish the sensibility of the skin. Infectious cutaneous anesthesia develops in the sequence of infectious diseases when inflammation of a sensory nerve has occurred. Preservation of cutaneous sensibility depends further upon normal circulation of the blood, and the influence of cold, already mentioned, is probably due in part to resulting circulatory altera- tions. At times, however, such vasomotor cutaneous anesthesia develops spontaneously in consequence of spasm of the muscular coat of the vessels. Cutaneous anesthesia develops also after ligation of the extremities to the degree of pulselessness, and in conjunction with the occurrence of embolism or thrombosis of the main artery of an extremity and with thrombosis of the principal vein. Cutaneous anesthesia can be readily demonstrated by means of the tests already described. ' The patient becomes conscious of the condition from his failure, in the presence of anesthesia in the hands, to feel a body grasped with these members, and which, therefore, he readily permits to fall, particularly if the guidance of the eyes is removed. Individuals with cutaneous anesthesia iu the feet are not distinctly conscious of the resistance of the floor in Avalking. As a result, the gait may become imcertain and awk- ward. The patient walks with the feet held far apart, swinging them in walking, raising them unduly high, and he presents an ataxic 528 NERVOUS SYSTEM gait — peripheral pseudotabes. Anesthesia of the skin and the trunk is attended with failure on the part of the patient to appre- ciate the presence of his clothing as well as the resistance of chairs or beds. Whether the condition is one of para-anesthesia, hemi- anesthesia, or anesthesia of an entire extremity or of only a single nerve, can be readily determined from the extent of the impair- ment of sensibility. Symptoms. — At times there may be paresthesia in addition to cutaneous anesthesia, including a sense of tingling, of cold, and of stiffness. Some patients also complain of severe pain in the insensitive areas — dolorose anesthesia. This phenomenon may be explained by the fact that, for instance, a tumor by pressure may interrupt the conductivity of a sensory nerve, while, at the same time, the central termination of the nerve is irritated, and this irri- tation gives rise to pain, which, in accordance wdth the law of eccentric conduction, is referred to the peripheral distribution of the nerve. Often motor, vasomotor, and trophic disorders occur when cutaneous anesthesia is dependent upon disease of a mixed nerve. The prognosis and the duration of the disorder vary with the nature of the causative condition. In the treatment of cutaneous anesthesia, in addition to removal of the causative factors — causal therapy — cutaneous irri- tation plays an important part. This may be effected by means of spirituous aj^plications (spirit of mustard, camphorated spirit, spirit of formic acid, compound spirit of angelica) or the electric brush of a faradic current or the kathode of a galvanic current. TRIGEMINAL ANESTHESIA. Ktiology. — Peripheral trigeminal anesthesia occurs prin- cipally as a result of exposure to cold and of injury. Punctured and incised wounds, neoplasms, and disease of the cranial bones are well adapted to cause trigeminal anesthesia. At times the condition is dependent upon abnormal conditions at the base of the skull (tumors, aneurysms, meningitic thickening), which exert compression upon and cause paralysis of the trunk of the trigeminal nerve. Under these conditions not individual, but all of the branches of the trigeminal nerve are involved in the anes- thesia, and motor trigeminal paralysis (paralysis of the masticatory muscles) may be superadded. Symptoms and Diagnosis. — Unilateral trigeminal anes- thesia is attended with loss of cutaneous sensibility upon one side of the face and tlio anterior aspect of the auricle. When a glass or a spoon is carried to the mouth a sensation is perceived as if these objects were divided at the middle line, because one- half of the lip is insensible. Sensation is lost also upon the con- DISEASE OF THE OLFACTORY NERVE 529 junctiva, the cornea, and the nasal and buccal mucous membrane. Touching the eye causes no movement of the lid and no flow of tears through reflex influences. The secretion of tears is diminished. Tickling the nose upon the diseased side does not excite sneezing. Pungent olfactory impressions (ammonia, acetic acid) also are not appreciated. The sensibility of the buccal mucous membrane likewise is lost upon one side. The sense of taste is, as a. rule, abolished upon the anterior two-thirds of the tongue. At times unilateral coating of the tongue and diminuticm in the secretion of saliva have been observed. The facial expression is frequently characterized by relaxation upon the diseased side, because the trigeminal nerve exercises a reflex influence upon the tone of the facial muscles. Vasomotor and particularly trophic disorders also occur. Among the latter inflammation of the cornea and of the whole eye — neuroparalytic ophthalmia — has long been known, although of late there is a growing tendency to adopt the view that this inflammation of the eye is not dependent upon the influence of trophic nerve-fibers, but that in consequence of defi- cient sensibility of the cornea winking is infrequent, so that foreign bodies from the air, and particularly bacteria, remain upon the eye and cause inflammation. Peripheral is diiferentiated from central trigeminal anesthesia by the unaltered persistence of the reflexes with the latter. Prognosis. — The prognosis depends upon the curability of the causative condition. Treatment. — The treatment should be conducted according to the rules given on p. 528. In addition, the eye should be pro- tected by means of a suitable bandage. PERIPHERAL DISEASE OF THE NERVES OF SPECIAL SENSE. DISEASE OF THE OLFACTORY NERVE. Peripheral disease of the olfactory nerve is attended either with morbidly increased acuity of the sense of smell — hyperosmia — or with diminution and even loss thereof — hyposmia and anosmia, or with jmrosmia; that is, subjective appreciation of odors in the absence of odorous substances. Hyperosmia is generally of central origin, and occurs with par- ticular frequency in association with hysteria. Patients thus af- fected are capable of smelling substances that another with normal olfactory organs is incapable of appreciating ; or they arc greatly annoyed by olfactory impressions of not excessive intensity, and at times are seized with excitement, convulsions, or syncope. Hyposmia and anosmia are common accompaniments of acute and chronic inflammation of the nasal mucous membrane. The 34 530 NERVOUS SYSTEM condition has been frequently observed also in connection with nasal polvpi. It often develo])s in the sequence of protracted ether-inhalation, as, for instance, in collectors of insects. It may occur as a result of traumatic influences in the presence of tumors of the ethmoid bone from pressure upon the fibers of the olfactory nerve or in the presence of fracture of the ethmoid bone or the skull. Tumors and menino-itic thickenintj at the base of the skull, as well as tumors, hemorrhage, and softening in the frontal region of the brain close to the islandofReil, may cause anosmia through pressure upon or injury of the olfactory nerve. At times anosmia develops in advanced life, in consequence of involution of the olfactory bulb. Further, anosmia may be congenital in conse- quence of absence of the olfactory nerves. The condition may be unilateral or bilateral, and in many persons is detected purely by accident. Bilateral loss of the sense of smell is attended with dis- turbance in the sense of taste for all such articles of food and drink whose taste is dependent on their aroma. Parosmia is frequently of central origin (mental disease, hysteria, epilepsy), although it may also occur as a result of peripheral in- fluences, in connection with acute and chronic inflammation of the nasal mucous membrane. The condition generally found is one of a sense of disagreeable olfactory impressions (caxiosniki), which not rarely gives rise to hallucinations in the insane. At times parosmia is associated with anosmia, a condition corresponding with painful anesthesia and susceptible of a similar explanation ; that is, interruption of conduction on the one hand, and stimula- tion of the central extremity of the olfactory nerve on the other hand. Disturbances of the sense of smell can be tested with the aid of pleasantly smelling (oil of cloves, oil of rose) and disagree- bly smelling substances (assafetida), as the disorder may be partial and not complete. Pungent odors (ammonia, acetic acid) should be avoided, as this variety of olfactory impressions is transmitted through the trigeminus. First one naris and then the other is tested, while the nasal orifice not being examined is carefully closed. The treatment of all varieties of olfactory disturbance con- sists essentially in efiPorts to cure the fundamental disorder. DISEASE OF THE GUSTATORY NERVR Disorders of the sense of taste on the anterior two-thirds of the tongue are dependent upon disease of either the trigeminal or the facial nerve, while those on the posterior third are dependent upon disease of the glossopharyngeal nerve. Further, it is also con- tended that the fibers for the sense of taste from the trigeminal nerve are derived from the trunk of the glossopharyngeal nerve. That the facial nerve itself contains no nerves of taste, but that DISORDERS OF THE PERIPHERAL ^'ERVES 531 these pass at intervals from the trunk of the trigeminal nerve into that of the facial nerve has already been mentioned on pp. 479 and 487 in the consideration of peripheral facial palsy. The morbid disorders of the sense of taste are manifested in a manner anal- ogous to those of the sense of smell, and they are designated hy- pergeusia, hypogeusia, and parageusia. Hypergeusia consists in an ability to detect the taste of sub- stances even when present in small amounts. More pronounced gustatory impressions may give rise to conditions of excitement, convulsions, or syncope. Hypergeusia is generally of central origin, and is encountered with particular frequency in association with hysteria. Hypogeusia and ageusia involving the anterior two-thirds of the tongue is most commonly unilateral in association with peripheral facial jJcdsy if the lesion is situated between the geniculate gan- glion and the giving oif of the chorda tympani nerve. In other instances unilateral hypogeusia or ageusia is observed in associa- tion with trigeminal anesthesia or with injuries of the lingual nerve. Finally, the condition may involve the posterior third of the tongue in the presence of disease of the glossopharyngeal nerve. Persons with a heavily coated tongue often complain of impair- ment of the sense of taste, or this may develop after the ingestion of food that is unduly hot or irritating. Parageusia is observed principally as a result of central causes, in the insane and the hysterical. The patient generally complains of a bad taste, although the mouth is empty. The tests for the sense of taste are described on p. 483. The treatment of disorders of the sense of taste is comprised in the relief of the primary disorder. INFLAMMATORY AND DEGENERATIVE DIS- ORDERS OF THE PERIPHERAL NERVES. PRELIMINARY CONSIDERATIONS. Inflammatory and degenerative disorders of the peripheral nerves are generally designated neuritis. It should, however, be borne in mind in this connection that inflammatory processes are by no means always operative, but it is difficult anatomically to make a sharp distinction between nerve-inflammation and nerve- degeneration. Nevertheless, neuritis plays a most important part at present in the domain of nervous diseases. !^tiology. — The causes for inflammatory and degenerative disorders of the peripheral nerves are exposure to cold, traumatism, infection, and intoxication. To what extent bacteria are concerned in these processes is as yet undetermined. It is highly probable that cold and injury act only as contributory influences for infec- 532 NERVOUS SYSTEM tion of peripheral nerves ■with bacteria, while in the development of infectious and toxic neuritis the injurious influence of toxins (bacterial poisons) or chemic poisons upon the nervous structures may be operative. The anatomic alterations involve eitlier the interstitial connective tissue of the nerves — interstitial iieuritiii — or the nerve- fibers themselves — parenchymatous neuritis. In addition, mixed varieties of the two principal classes mentioned occur — mixed neuritis; and these again may be separated into several subdivisions accordingly as the connective tissue and the nervous structure are affected simultaneously by the inflammatory irritant or the inflam- matory process begins in one portion of the nerve and then in- volves the other secondarily. Interstitial neuritis in its acute form is often indicated macro- scopically by the thickened and unusually reddened appearance of the nerve, with loss of its transverse striation (bands of Fon- tana). Here and there extravasations of blood may have taken place, and these may be present both in the external nerve-sheath and upon transverse section of the nerve. The presence of numer- ous extravasations of blood has given rise to the designation Jiem- orrhagic or apoplectiform neuritis. On microscopic examination of the nerve the blood-vessels are found greatly dilated, tortuous, and distended with blood. Tlieir walls often appear thickened and swollen and glistening. The nuclei of the vessel-wall are in places increased in number and involved in fatty degeneration. In addition, the interstitial connective tissue is increased. At the same time it contains numerous cells and round cells. In rare cases an accumulation of pus takes place in the nerve — suppu- rative neuritis. This may occur particularly when foreign bodies and toxic substances have penetrated into the nerve, and also when suppurative in- flammation in the neighborhood of the nerve has extended to the latter. In the presence of chronic interstitial neuritis the nerve fre- quently presents a brownish, almost black color, due to the remains of pigment from preceding hemorrhage. The nerve generally feels denser than normal, in correspondence with an increase in the interstitial connective tissue. At times the inflammatory areas appear as nodular enlargements — nodose neuritis. It is note- worthy that a neuritis by no means always extends throughout the entire course of a nerve, but involves only a single small portion or several portions, and accordingly a distinction should be made between diffuse, circvmsrrihed, and multiple or insular neuritis. The neighborhood of joints and the points of deflection of nerves constitute especially favored situations for insular neuritis. At times a neuritis that is at first insular exhibits a tendency to ex- tend progressively in tlie course of the nerve, and even to the spinal cord, and the condition is then designated migratory neuritis. Parenchymatous neuritis can be diagnosed with certainty by DISORDERS OF THE PERIPHERAL NERVES 533 means of microscopic examination. In teased preparations of fresh nerve-tissue or in such tissue stained with osmic acid fibers will be found whose medullary substance and axis-cylinder appear granular and involved in fatty degeneration, and often also ab- sorbed, so that the empty nerve-sheath remains. In the latter multiplication of the nuclei takes place. On transverse section of hardened nerves empty sheaths will be found in greater or lesser number, and frequently containing but a single nucleus. French physicians have pointed out that parenchymatous neuritis also at times involves the nerve-fibers for only short distances, and this condi- tion has been designated segmental neuritis. The symptoms of neuritis will naturally vary accordingly as the inflammatory process involves motor, sensory, or, as occurs most commonly, mixed nerves. At the beginning of the disease irritative symptoms are not rarely present, but these are shortly followed by paralytic phenomena. Therefore, infiammation of motor nerves is often at first attended with twitching and rigidity in the related muscles, but these are soon replaced by progress- ively increasing weakness and paralysis. The muscles rapidly undergo wasting, as they participate in the degenerative process, and together Avith the diseased nerves are generally tender upon pressure. Both nerve and muscle exhibit degenerative electric reaction. In the distribution of the diseased nerves the tendon- reflexes are at times increased at first, but generally diminution and disappearance of reflex movement soon occur. After neuritic muscular paralysis has existed for some time muscular contrac- tures and deformities readily develop. Infiammation of sensory nerves is attended with especial fre- quency with paresthesias : a sense of coldness or the creeping of ants (formication), prickling and sticking of the skin, marked neuralgic pains. Often cutaneous hyperesthesir is present at the beginning of the disorder, but this subsequently is replaced by anesthesia. In cases of infiammation of mixed nerves, in addition to the motor and sensory disturbances described, vasomotor and trophic disturbances are at times observed, as, for instance, pallor or cyan- otic discoloration of the skin, accordingly as an irritative or a paralytic condition of the vasomotor nerves is present, coldness of the skin, hyperidrosis or anidrosis, thickening of the epidermis, abnormally increased desquamation of the epidermis, excessive growth of hair, thickening and fragility of the nails, glossy fin- ger, herpes or pemphigus-like cutaneous eruptions, articular swelling, etc. The course of a neuritis may be acute, subacute, or chronic. Acute neuritis at times sets in abruptly — aj)oplectiform neuritis. In other instances it develops, like an acute infectious disease, 534 NERVOUS SYSTEM with rigor, fever, and enlargement of tlie spleen. Chronic neuritis may result from an acute neuritis or it may develop insidiously in an independent manner. At times neuritis begins first in a single nerve or in a few nerves, and then extends progressively to a larger number — polyneuritis. Under such circumstances it may happen that the alterations are first observed in the nerves of the lower extremity, gradually invading nerves at successively higher levels — ascending neuritis. Should cereijral nerves also become involved, the disease becomes a- serious one, and death may readily take place in consequence of paralysis of the vagus-accessory nerve. Even when cerebral nerves are not involved neuritis is a serious disease in relation to its curability. While recovery is always possible, it is not certain, and under all circumstances much patience is necessary on the part of both patient and phy- sician. The diagnosis of neuritis is not particularly difficult. Inflam- mation of motor nerves is most likely to be confounded with ante- rior poliomyelitis, for in this disease also, as the lesion of the motor-trophic ganglion-cells in the anterior horns of the spinal cord is soon associated with degeneration of the related nerves and muscles, degenerative muscular atrophy and degenerative electric reaction occur ; but poliomyelitis is unattended with sensory dis- turbances, and the diseased nerves and muscles are also usually free from pain on pressure. Neuritis is distinguished from other diseases of the spinal cord by the fact that the liladder and the rectum are almost always uninvolved witli the former, while, on the other hand, nerve and muscle exhibit degenerative electric reaction. The treatment of neuritis should be directed, in the first place, to the causative factors — causal therapy. In a case of refrigeratory neuritis, for instance, warm baths, salicylic acid, sodium salicylate, also diaphoretics (pilocarpin hydrochlorate) Avill be employed. Causal indications may be present also in a case of traumatic neuritis. Antecedent syphilis will require the employment of mercurial preparations and potassium iodid, and the like. The symptomatic treatment is the same as that in cases of peripheral paralysis (p. 475) and of cutaneous anesthesia (p. 528). Baths, salicylates, antipyrin, massage, and electricity are the most impor- tant remedies. MULTIPLE NEURITIS, Ktiology. — ^Multiple neuritis, also known as polyneuritis, occurs at times like an independent infectious disease, and is then often referred, as a matter of convenience, to exposure to cold, the occurrence of which, however, cannot be confirmed on careful inquiry. At times cases of such infectious polyneuritis have been MULTIPLE NEURITIS 535 observed to occur in groups and in almost epidemic distribution. It must, nevertheless, be admitted that exposure to cold may be followed by multiple neuritis, at least in the sense that the exposure favors infection of peripheral nerves. At times multiple neuritis has been observed to develop in the sequence of traumatism, which at times has been of apparently insignificant character, as, for instance, riding upon rough roads. Multiple neuritis occurs with particular frequency in the sequence of infectious diseases. It has long been known and greatly feared in connection with pharyngeal diphtheria, but it may occur also in conjunction with typhoid fever, herpes zoster, dysentery, pneumonia, pulmonary tubercu- losis, and particularly syphilis. Septic diseases, and particularly puerperal fever, at times give rise to multiple neuritis. A com- plete description of toxic multijAe neuritis will not be attempted here, because it will be taken up in detail in succeeding sections. On the other hand, attention is to be directed to the occurrence of multiple neuritis in consequence of auto-intoxication. This condi- tion is observed in connection with diabetes mellitus and gout, and possibly also cases of marasmus belong in this category, as, for instance, in association with carcinoma. With the exception of post-diphtheric paralysis, multiple neuritis is generally a disease of adults. Anatomic Alterations. — Multiple neuritis may be of inter- stitial, parenchymatous, or mixed character, and nothing need be added to what has been stated on p. 532 concerning neuritis in general. Symptoms and Diagnosis. — Multiple neuritis may pursue an acute or a chronic course. If it occurs as an independent acute infectious disease, it sets in at times with a chill, followed by ele- vation of temperature to as high as 40° C. (104° F.), and even higher. Often enlargement of the spleen is present. Above all, paralysis occurs, generally involving isolated nerves of the lower extremities at first, soon rendering the entire extremity helpless, and then extending to the upper extremities. Cerebral nerves also may be involved. Paralysis of the vago-accessory nerve is attended with great acceleration of pulse. Paralysis of degluti- tion may occur. At times paralysis of the hypoglossal and facial nerves has been observed. On one occasion I observed sudden blindness in consequence of inflammation of the optic nerve. By reason of the ascending character of the paralysis the disease is strongly suggestive of acute ascending spinal paralysis, but in cases of multiple neuritis the paralyzed nerves and muscles ex- hibit, in contradistinction from spinal paralysis, degenerative elec- tric reaction. In addition, nerves and muscles are generally tender on pressure, and the paralyzed muscles soon undergo de- generative atrophy. Sensory disturbances are frequently present. Vasomotor and trophic disturbances (coldness and cyanotic dis- 636 NERVOUS SYSTEM coloration of the skin, edema, articular swelling) also are observed. At times active delirium appears, and the patient may die in coma. The bladder and the rectum are, as a rule, uninvolved. In some instances I have observed recovery from acute multiple neuritis, although after a considerable time a second and even a third attack occurred — recurrent polyneuritis. Chronic multiple )ieurifis is often unattended with fever, but in other instances periodic febrile movement occurs. The paralysis develops slowly in the course of weeks or months, and at times exhibits also an ascending character. The disease may be readily confounded with chronic anterior poliomyelitis, as in this disease also degenerative electric reaction is found in the paralyzed muscles, but it is unattended with sensory disturbances, and the nerves and muscles are not tender to touch. In some cases chronic multiple neuritis originates from an acute neuritis, the fever ceas- ing and the new paralysis developing but slowly. Long-continued paralysis is frequently attended with contractures that give rise to deformities in the extremities. Prognosis. — The prognosis of multiple neuritis is always serious. If the disease pursues an ascending course, there will be danger of death from paralysis of cerebral nerves. In the pres- ence of chronic multiple neuritis a long time may be expected to elapse before the diseased nerves will be regenerated and the paralysis will have disappeared. Treatment. — The treatment of multiple neuritis should be conducted upon the lines laid down on p. 475. TOXIC NEURITIS. SATURNINE PARALYSIS. Ktiologfy. — Of the toxic varieties of neuritis, that due to lead- poisoning lias been known longest. It occurs most commonly in certain artisans who in the pursuit of their avocation are exposed to chronic lead-poisoning. Among these are particularly painters, potters, printers, file-cutters, shot-molders, workmen in lead-mines, etc. Lead-poisoning may result accidentally from the use of pre- .served food kept in receptacles containing lead, of Avater trans- mitted through lead-pipes, of cosmetics containing lead, of snuff wrapped in lead-foil, etc. Rarely, lead-poisoning may result from carelessness on the part of the physician in consequence of the administration of preparations of lead in too large amounts or for too long a period. Symptoms and Diagnosis. — The symjitoms of saturnine paralysis usually appear only after the patient has been exposed to the action of the metal for a considerable length of time. As a rule, other symptoms of lead-poisoning have already been pres- TOXIC NEURITIS 537 ent, particularly the presence of a bluish-gray lead-line at the margin of the gums, together with anemia and colic. Bilateral radial paralysis, with preservation of the function of the supinators, is distinctive of lead-paralysis. The palsy generally develops gradually, and the patient complains at first of weakness in the hands and fingers, which eventually passes over into paralysis, and in spite of all devices renders the hand incapacitated for work. When the forearms are held horizontally the hands fall in palmar flexion, and at the same time the fingers are flexed and the thumbs adducted. Dorsal flexion of the hands, extension of the fingers, abduction and extension of the thumb, abduction and adduction of the hands toward the ulna or the radius, can be effected imperfectly, if at all. Of the extensors of the fingers, those of the index-finger and the little finger are involved late, so that both of these fingers can at first be relatively well engaged in dorsal flexion. Supination and extension of the forearm remain unaffected. Only rarely is lead-palsy widespread — generalized lead-paralysis. Under such circumstances the muscles of the upper arm, the shoulder, the back, and the lower extremities also may be involved. Even the muscles of the face and the larynx and the diaphragm are at times paralyzed. The paralyzed muscles become the seat of degenerative atrophy, and both nerve and muscle exhibit degenerative electric reaction. The tendon-reflexes are abolished in the paralyzed parts, and gradually muscular eontractures take place. Diseased nerves and muscles are generally tender on pressure. At times some of the tendons become thickened — hypertrophio tenosynovitis. Paresthesia and hyperesthesia, less commonly anesthesia, also occur. The duration of the paralysis depends upon the degree of the disturbance, and more accurately upon the degenerative electric re- action. Advanced paralysis requires many months for recover}^ Frequently relapses occur, often because the patients resume their former employment ; less commonly relapses occur in spite of avoidance of contact with lead. Anatomic Alterations. — Upon the basis of personal obser- vation I should consider lead-paralysis the consequence of a degenerative inflammation of j^eripheral nerves. Paralysis of long standing may be complicated by secondary atrophy of the related trophic-motor ganglion-cells in the anterior horns of the spinal cord. The paralyzed muscles exhibit reduction in the size of their mascle-fibers, proliferation of the sarcolemma-nuclei, and increase in the interstitial connective tissue. Prognosis. — Although lead-palsy is, as a rule, not a fatal disease, the prognosis with regard to permanent recovery is not favorable, because patients resume their injurious pursuits without observance of the necessary precautionary measures, or are even 5138 NERVOUS SYSTEM satisfied witli an improvement in tlie paralysis and return to their work too quickly. Treatment. — For the load-paralysis itself sulphur-baths should be employed (potassium sulphid, 150.0 — 5 ounces — to a full bath at a temperature of 28° R. — 35° C. — 95° F.), massage of the para- lyzed muscles be practised, or instead electric treatment, and thrice weekly subcutaneous injections of strychnin be made : R Strychnin nitrate, 0.1 {l\ grains); Glycerin, Distilled water, each, 5.0 (75 minims). — M. Dose : 0.25 (4 minims) subcutaneously. Internally potassium iodid (5.0 : 200 — 75 grains : 6|- fluidounces ; 15 c.c. — 1 tablespoonful — thrice daily) should be administered to eliminate the lead present in the system. As a prophylactic measure it is important that the patient shall never take a meal in the room in which lead is manipulated. Also, before eatino;, the mouth and the pharynx should be rinsed with water to remove lead-dust that may be present, and the hands should be freed from adherent particles of lead by washing. Experience has shown that drunkards are more susceptible to lead-poi.soning than others. In isolated cases jjaralysis has been observed among those exposed to the action oi mercury, zinc, and copper, and this also is in all probability the result of a degenerative neuritis. ARSENICAL PARALYSIS. Arsenical paralysis is observed most commonly after acxde arsen- ical poisoning. The extensor muscles of the leg, particularly the peronei, are generally first attacked, although the arms — with pref- erence the extensors of the forearms — may also be involved. In one case I observed paralysis of the bladder and of the vagus. The paralyzed muscles rapidly undergo wasting and, together with the related nerves, are tender on pres.sure and yield degen- erative electric reaction. The tendon-reflexes are abolished in the distribution of the paralysis. Gradually muscular contractures develop. Often the paralyzed parts become the seat of severe neuralgia. Nevertheless, cutaneous anesthesia becomes more and more marked, and as a result the gait becomes ataxic — peripheral pseudotabes. Little is known with regard to the anatomic alterations, although the occurrence of a degenerative neuritis is most prol)able. The prognaosis is not unfavorable, although, naturally, many months may elapse before complete recovery takes place. The treatment is the same as that for lead-paralysis. Paralysis with symptoms similar to those dependent upon plumbic and arsenical poisoning has been observed also after poisoning with phosphorus, carbon monoxid, and carbon disulphid. TOXIC NEURITIS 539 ALCOHOLIC PARALYSIS. Htiology. — Alcoholic paralysis occurs principally in drinkers of spirit. In one instance I have observed the condition even in a boy. Symptoms and Diagnosis. — The paralysis almost always develops gradually, although I have repeatedly observed a sudden (apoplectic) onset. Not rarely the paralysis has been preceded by severe neuralgia, which may also persist in association with the paralysis. The extensors of the legs and the forearms are involved in the paralysis earliest and most constantly. Gradually all of the muscles of the extremities may be affected, and even cerebral nerves, particularly the vagus, are at times involved. Paralysis of the bladder and the rectum is uncommon. The diseased nerves and muscles are tender on pressure, undergo wasting, and exhibit degenerative electric reaction. Contractures slowly de- velop. The tendon-reflexes are abolished in the paralyzed parts. Cutaneous sensibility is frequently impaired and peripheral pseudo- tabes may readily develop. At times marked swaying of the body occurs when the eyes are closed — Bracht-Romberg's symptom. Con- traction of the pupil — myosis — and sluggish reaction to light may be present. Paralysis of the ocular muscles is uncommon. The disorder is at times attended with slight febrile movement. Pro- gressive alcoholic marasmus, often associated with stupor, occa- sionally leads to a fatal termination. Two patients under my observation died in consequence of complicating miliary tuber- culosis. The duration of the disease may be extended over many months. Anatomic Alterations. — Degenerative atrophy of the nerve- fibers is found in the diseased nerves, and in the muscles atrophy of the muscle-fibers, increase in the sarcolemma-nuclei, and multi- plication of the interstitial connective tissue. At times the degen- erative process has extended from the nerves to the spinal cord, in which degenerative areas develop in the posterior columns and atrophy of the ganglion-cells in the anterior horns takes place. Prognosis. — Kecovery from extensive alcoholic paralysis is wholly possible, but requires a long time. Treatment. — The treatment is the same as that for lead- paralysis (p. 538). Abstinence from alcohol is highly important. At times paralysis has been observed after the ingestion of spoiled rye — ergot-poisoning or ergotism — and of spoiled maize — pellagra — and this must in all probability be considered the sequel of a toxic neuritis. 540 NERVOUS SYSTEM II. DISEASES OF THE SPINAL CORD. PRELIMINARY DIAGNOSTIC CONSIDERATIONS. In the diagnosis of disease of the spinal cord two points must be taken into consideration — in the hrst place, the seat, ana, in the second, the anatomic nature of the spinal disorder, \yith regard to the seat of the disease a correct diagnosis is possible only from a knowledge of the clinical anatomy and physiology of the spinal cord. A brief resume of these subjects may therefore be given. The spinal cord extends downward to the junction between the first and the second lumbar vertebra, whence it follows that all foci of disease below the second lumbar vertebra may involve the Cauda equina, but not the spinal cord itself. Also, there is no danger from the introduction of instruments into the vertebral canal, as, for instance, in the practice of lumbar puncture, of in- flicting injury upon the spinal cord, if this be undertaken below the second lumbar vertebra. Of the several segments of the spinal cord, the cervical portion is included between the first cervical and the second dorsal vertebra, and attains its greatest size at the level of the fifth and sixth cervical vertebrse. The dorsal cord is in- cluded between the second and the tenth dorsal vertebra, and the lumbar cord between the tenth dorsal and the second lumbar vertebra, its greatest size corresponding with the level of the twelfth dorsal vertebra. In order to form a proper conception of the vertebral column it should be recalled that the spinous process of the seventh cervical vertebra projects markedly backward, whence the name vertebra prominens, and for which reason it can be readily recognized. If three contiguous spinous processes project conspicuously backward, the middle one may be considered as belonging to the seventh cervical. It is accordingly easy to localize accurately visible or palpable alterations in the vertel^ral column. Should, however, such external indications be absent, it will be necessary, in order to deter- mine the level of disease in the spinal cord, to observe whether, on percussion of the vertebral column or on passing over it a sponge wrung out of hot water or by means of the kathode of a galvanic current, a circumscribed point of pain can be demonstrated ; or, if cutaneous anesthesia be present, an attempt should be made to fix its upper limit at the side of the vertebral coliunn. In the latter event, naturally, it should be borne in mind that the indi- vidual nerve-roots pursue a longer course in tiie vertebral canal, before they reach the intervertebral foramina and make their exit, the lower the level at wliich they leave the spinal cord. There- fore, the upper limit of the anesthetic cutaneous area will approxi- DISEASES OF THE SPINAL COED 541 mately correspond with the level of the focus of disease only when this is situated in the upper portion of the spinal cord. The area of cutaneous anesthesia at the side of the spinal column will occupy a lower level than the seat of the disease if this be situated in the lower portion of the spinal cord. In general, the following rules will be found to hold good : Foei of disease below the twelfth dorsal vertebra {lower lumbar cord) are attended with anesthesia in the lower extremities, except upon the outer and inner aspects of the thighs and the inner aspect of the legs (external cutaneous nerve of the thigh, obturator, crural, and saphenous nerves). Foci of disease betiveen the tenth and the eleventh dorsal vertebra {tipper lumbar cord) are attended with anesthesia of the whole of the lower extremities. In the presence of foci of disease at the level of the eighth dorsal vei'tebra {point of exit for the terdh dorsal nerve) the anesthesia extends to the level of the umbilicus. Foci of disease between the fifth and the seventh dorsal vertebra {points of exit for the sixth and seventh dorsal nerves) give rise to anesthesia at the level of the ensiform cartilage. Foci of disease at the level of the first dorsal vertebra give rise to anesthesia to the level of the nipples. Foci of disease betiveen the fourth and the fifth cervical vertebra give rise to anesthesia to the level of the clavicles. Foci of disease at the level of the upper cervical vertebrce give rise to anesthesia in the arms. For the comprehension of certain diseases of the spinal cord it is important to know that the relation between the dura mater and the spinal column differs from that between the dura mater and the bones of the skull, as in the cranium the dura is closely applied to the inner surface of the bones, while in the spinal canal it is separated from the inner surface of the vertebrae by loose con- nective tissue containing considerable fat and numerous veins. It therefore not rarely happens that foci of disease develop in the vertebral canal that may involve the spinal cord in coiLsequence of pressure or by extension of inflammatory processes. In transverse sections of the spinal cord two varieties of tissue may be distinguished by differences in color, an outer or white sub- stance and an inner or g)ru/ substance. The white matter of the spinal cord consists principally of medullated nerve-fibers, and is rather a conducting organ, while the gray matter contains numer- ous ganglion-cells, and may be considered the seat of a series of spinal centers. In each half of the spinal cord an anterior and a posterior horn can be distinguished in the gray matter. The two sides of the gray matter are connected by means of the gray commissure. The shape of the gray matter of the spinal cord has not inappropriately been compared with the letter H, although it 542 NERVOUS SYSTEM 2 Vk will be readily discerned that the shape of the H varies in the dif- ferent segments of the cord. It is well to train the eye to recog- nize from the shape of the gray matter the segment of the cord to which it belongs. In the lumbar segment the anterior and pos- terior horns are club-shaped (Fig. 75, 5, 6, 7), while in the dorsal region both horns are exceedingly small (Fig. 75, 4), and in the cervical portion the anterior horn particularly assumes a serrated appearance (Fig. 75,1, 2,3). _ Both in the white and in the gray matter of the spinal cord definite, associated groups of nerve-fibers or of ganglion-cells can be distin- guished, and these have been designated also systems of the spinal cord. They have been dis- covered in part by developmental methods, in part by experimental means, and from a study of diseases of the spinal cord. In the anterior horns of the spinal cord the large multipolar ganglion-cells, which are gener- ally arranged in three groups close together, form a connected system. Among their processes the axis-cylinder process in particular is of great importance, for soon after leaving the ganglion- cell it becomes surrounded by a medullary sheath and enters the anterior nerve-root of the spinal cord, then the peripheral motor nerve- trunk, and finally the related muscle-fiber. Ac- cordingly, ganglion-cell, axis-cylinder process, peripheral nerve-fiber, and muscle constitute a continuous and uninterrupted whole, which has been designated a neuron, or, more accurately, a spinal-peripheral neuron or a neuron of the first degree. Disease of the ganglion-cells of the anterior horns is knoM'n also as anterior poliornyelitis (7ro?M^, gray). The characteristics of such disease are relaxed (flaccid) paralysis of the cofd°"natura^'^size^'^i^ related musclcs, rapid degenerative muscular I'omniencement, 2, mid- atrophv, degenerative electric reaction in the die, and 3, termination it ^ i i t^' !> xi paralyzed nerves and muscles, abolition oi the reflexes, preservation of cutaneous sensibility and of the muscular power of the bladder and the rectum. The ganglion-cells in question possess trophic-motor functions. If they are destroyed, the related axis-cylinder processes undergo de- generation, which extends to the muscle-fibers. Degenerated nerves and muscles yield degenerative electric reaction. These Fig. 75. — Transverse of the cervical enlarge nient ; 4, middle of the dorsal cord ; 5, com- mencement, 6, middle, and 7, termination of the lumbar enlarge- ment (from personal preparations). DISEASES OF THE SPINAL CORD 543 ganglion-cells do not possess sensory functions. The reflexes are abolished in the region controlled by the area of disease, because the transference of sensory stimuli to the motor paths within the spinal cord has been rendered impossible in consequence of the disease of the ganglion-cells. In the gray matter of the dorsal portion of the spinal cord at the junc- tion between the anterior and posterior horns there is an associated group of ganglion-cells bearing the name of the column of Clarke or the vesicular column. It is known that the fibers for the lateral cerebellar tract of the spinal cord, shortly to be mentioned, have their origin here, but nothing is known definitely with regard to their function. The following columns or fiber-systems may be distinguished in the white substance of the spinal cojxl on either side : 1. The direct or anterior pyramidal tract, 2. The crossed or lateral pyramidal tract, 3. The lateral cerebellar tract, 4. Gowers' column or the antero-lateral fasciculus, 5. The postero-exterual or Burdach's column, 6. The postero-internal or GolFs column, 7. The antero-lateral remnant. The crossed or lateral pyramidal tracts are situated in the lateral columns of the spinal cord, and are separated from the periphery of the cord in tfie cervical and dorsal regions by the lateral cere- bellar tracts, while in the lumbar region they reach the periphery and at the same time assume a wedge-siiaped appearance (Fig. 76, 2psb). . These tracts contain the largest portion of the motor fibers, which pass from the motor cortical centers in the anterior and posterior central convolutions, through the corona radiata, the internal capsule, the cerebral peduncle, the pons, and the medulla oblongata into the spinal cord, where they enter into re- lations with the motor-trophic ganglion-cells in the anterior horns, and from these conduct voluntary impulses to the periphery of the body. Each individual nerve-fiber of these tracts originates from the axis-cylinder process of a motor pyramidal cell, and continues without interruption to the lateral pyramidal tract of the spinal cord. Here the individual nerve-fiber passes into the gray matter of the spinal cord and breaks np into numerous ramifications. The latter come into contact with the ganglion-cells by means of sim- ilar ramifications (protoplasmic processes), M'hich suffice for the transmission of voluntary impulses. The pyramidal cell, with its axis-cylinder process and the ramification of the latter in the gray matter of the spinal cord, is likewise designated a neuron, and it is described as a neuron of the second degree or a cerebrosp>inal neuron. Thus, the entire motor pyramidal (corticorauscular) tract, from the cerebral cortex to the muscle, is constituted of two neurons, which are connected within the anterior horn of the spinal cord by contact. The lateral pyramidal tract is known also as z. 'i'P 7 vsr Level of the first cervical nerve r2psh ^ 4 6,-/,S ^^^'S Third cervical nerve ■ Sixth cervical nerve — i Third dorsal nerve I Sixth dorsal nerve Twelfth dorsal nerve Fourth Ittmbar nerve — »«, Fig. <6.— Diagrammatic representation of tlu irin, ijal columns of the spinal cord • Ipvs, anterior pyramidal tracts (direct); 2;).sh. lateral pyramidal tracts (crossed) Ssi-ft lat- eral cerebellar tracts: Unk,, postero-external (Bnrdnch'si wodee^aped column '5i!-» postero-internal (Goll's) column ; 6, Gowers' column : 7,;r. anterolateral remnant divid- cofum • &r!?"nd-bundles of the anterior column and the remnant of the lateral 544 DISEASES OF THE SPINAL CORD 545 the crossed pyramidal tract because the motor fibers from the cere- bral hemisphere upon one side largely pass over within the pyra- midal decussation in the medulla oblongata to the lateral pyra- midal tract of the opposite half of the spinal cord. From what has been said, it will therefore be understood that destruction of the pyramidal tract at any point in its course must be followed by motor paralysis. Should the disease be situated above the pyra- midal decussation the paralysis will occur upon the opposite side of the body ; but if, on the other hand, the disease is situated below the decussation, thus in the spinal cord itself, the paralysis will occur upon the same side. In contradistinction from paral- ysis resulting from anterior poliomyelitis, evidences of degenerative muscular atrophy and degenerative electric reaction are wanting in the paralyzed members; besides, the reflexes are preserved, because degeneration of the peripheral nerves and muscles and interruption of the spinal reflex arc do not occur, while, on the other hand, a tendency to spasm and muscular contracture is present, with exaggeration of the tendon-reflexes. The direct or anterior pi/ramidcd tract is situated in the anterior column of the cord,' just beside the anterior longitudinal fissure (Fig. 76, Ipvs). It is of subordinate importance and at times is wholly wanting. It is known as the direct pyramidal tract because it contains those portions of one corticomuscular pyramidal tract that do not cross over in the pyramidal decussation to the lateral pyramidal tract of the opposite half of the cord, but remain upon the same side, in order to enter the anterior pyramidal tract, and only within the spinal cord to pass over to the other side of the cord through the intermediation of the anterior spinal commissure. Various differences occur in the relation between the anterior and the lateral pyramidal tracts. At times the anterior pyramidal tract is wholly wanting, or, as occurs less commonly, it preponderates over the lateral pyramidal tract. The lateral cerebellar tract (Fig. 76, Sksb) is situated in the lateral columns of the cord close to the periphery, while inter- nally it adjoins the lateral pyramidal tract. As has been men- tioned, its fibers originate from the ganglion-cells of the columns of Clarke, and as the latter are present only in the dorsal cord, it will be understood that the lumbar cord contains no lateral cere- bellar tract. The lateral cerebellar tract can be followed upward into the restiform body of the medulla oblongata, and thence into the superior vermiform process of the cerebellum. Coordinative functions are attributed to this tract, although this is based upon conjecture rather than upon fact. A small portion of the white substance of the spinal cord sit- uated posteriorly in the angle between the lateral cerebellar and the lateral pyramidal tract, and extending forward along tlie periphery of the cord as a narrow band to the neighborhood of the 35 546 NERVOUS SYSTEM anterior longitudinal fissure, is known as the column of Gowers or the anterolaleral fasciculus. Gowers believes this tract to conduct centripetally. The columns of Bur da ch and of Goll in the posterior columns of the spinal cord are separated with particular distinctness in the cervical cord by a depression (posterior intermediate fissure). The columns of Goll contain fibers from the posterior spinal nerve- roots. The nerve-fibers that enter at the lowermost level are dis- placed progressively further forward and inward by those that enter at higher levels. Above, the fibers terminate in the nucleus funiculi gracilis, and they pass from here to the tegmentum, the quadrigeminate bodies, and the optic thalami. The nerve-fibers of the columns of Burdach reach the nucleus funiculi cuneati and the olive at the same level as the nucleus funiculi gracilis. As a unilateral lesion of the spinal cord gives rise to anesthesia upon the opposite side of the body, it must be concluded that the spinal sensory paths undergo decussation Avithin the cord. This takes place in the posterior aud perhaps also in the anterior spinal com- missure. The anterolateral remnant includes those nerve-fibers that are situated in the anterior and lateral columns of the spinal cord and do not belong to the pyramidal tracts, the lateral cerebellar tracts, and Gowers' tract (Fig. 76, Irsi-). They are considered to be short spinal paths whose function consists in connecting the ganglion- cells in the gray matter of the spinal cord with one another. Disease of the spinal cord is revealed by disturbances in the function of the cord. The nature of these disturbances will de- pend upon the seat of the disease. iSIotor, sensory, vasomotor, secretory, trophic, and reflex disturbances may be present. Spinal paralysis indicates disease either of^ the large ganglion- cells in the anterior horns of the spinal cord, or of the lateral pvramidal tracts. In each instance the character of the paralysis is different, as has been mentioned on pp. 542, 545. Sensory disturbances will be present when the posterior columns of the cord or the posterior horns are diseased. It is believed that the fibers for painful and thermal sensibility pass through the horns, while the fibers for tactile sensibility pass through the pos- terior columns. Vasomotor disturbances are not uncommonly associated with disease of the spinal cord. The vasomotor nerve-paths are be- lieved to pa.ss from the brain to the lateral column of the spinal cord, then to enter the anterior horn, and to extend from this through the anterior nerve-roots to the periphery of the body. In addition, there are spinal vasomotor centers, which are capable of acting independently of the brain, but nothing definite is known with regard to their situation. Trophic disturbances occur, as has been mentioned, in muscles, ANEMIA OF THE SPINAL CORD 547 fascia, bones, and joints in connection with anterior poliomyelitis. The posterior horns of the spinal cord also are credited with trophic functions, as trophic, that is, acute, gangrene of the skin, independent of pressure and infection, has been observed in con- nection with posterior poliomyelitis. Alterations in the reflexes are manifested at times in exaggera- tion, at other times in abolition of reflex movement. The former occurs, for instance, in association with spastic spinal paralysis ; the latter in association with tabes dorsalis. The spinal cord is necessary for the occurrence of the reflexes, because the transfer- ence of reflex irritation from the sensory to the motor paths takes place within the gray matter of the cord. Every interruption of the reflex arc will be attended with abolition of reflex movement, and this may naturally result from disease of the sensory or of the motor path or of the spinal cord. Exaggeration of reflex movement is often attributed to the withdrawal of the inhibitory activity of nerve-flbers entering the spinal cord from the brain. The diseases of the spinal cord may be divided into two natural groups, namely : the diseases of the structwe of the cord and those of the spinal membranes. The diseases of the spinal cord proper may be in turn irregular in distribution — atypical or asystematic diseases of the spinal cord ; or they may remain confined to definite systems — typiccd or systematic diseases of the spinal cord. In the latter event a single system or several systems may be involved, and a distinction is accordingly made between single and combined system-diseases of the sjnnal cord. Diseases of the spinal cord in which it has not yet been possible to discover anatomic alterations are designated /?mcf?07ia^ diseases of the spinal cord, or neuroses of the spinal cord. DISEASES OF THE SPINAL CORD. Atypical or Asystematic Diseases of the Spinal Cord. ANEMIA OF THE SPINAL CORD. The condition of anemia of the spinal cord is without clinical significance. Naturally, it will appear in the course of general anemia, such as may occur in consequence of excessive hemorrhage, in association with certain diseases of the blood (chlorosis, leukemia, pseudoleukemia, pernicious anemia), and following debilitating diseases (carcinoma, pulmonary tuberculosis, suppuration, chronic diarrhea). Such patients not rarely complain of spinal symptoms, such as paresthesia, hyperesthesia, or anesthesia, tremor, undue readiness of fatigue, and the like, symptoms that have been at- tributed to anemia of the spinal cord. Spinal anemia due to more especially local causes has been observed in connection with embo- 548 NERVOUS SYSTEM limi and thrombosis of the abdominal aorta. Under such circum- stances there develop, in consequence of anemia of the hinibar cord, paraplegia and anesthesia in the lower extremities, paralysis of the bladder and the rectum, and abolition of reflex movement and electric irritability. Absence of pulsation in the femoral artery is distinctive of this condition. In consequence of an in- adequate supply of blood giingrene of the lower extremities soon develops, and death occurs as the result of septicemia. In all cases of anemia of the spinal cord the treatment will consist principally in relief of the primary disorder. HYPEREMIA OF THE SPINAL CORD. Hyperemia of the spinal cord may result from increased arterial supply or obstructed venous exit, and a distinction is accordingly made between arterial and venous hyperemia of the spinal cord. Little of a definite nature is known concerning both conditions, and they are therefore as yet of no clinical significance. Arterial hyperemia of the spinal cord may develop as a result of traumatism, infectious diseases, sexual excesses, and certain in- toxications (alcohol, amyl nitrite) ; while venous hyperemia oj the spinal cord develops in conjunction with stasis resulting from chronic disease of the heart, lungs, or liver, and convulsive dis- orders (tetanus, epilepsy, uremia). Among the Sjntnptoms of hypereniia of the spinal cord a sense of traction in the sacral region, rigidity of the spinal column, girdle-sense, drawing and pain in the lower extremities, paresthesia, hyperesthesia, and anesthesia, and twitching and paralysis of the muscles have been mentioned. Xo characteristic symptom is known, and generally the diagnosis is made, in the presence of spinal symptoms in association with demonstrable causes of hyperemia of the spinal cord, by attributing the former to the latter. The treatment should lie directed less to the circulatory dis- turbances in the spinal cord than to the primary disorder. HEMORRHAGE INTO THE SPINAL CORD. Htiologfy. — Hemorrhage into the spinal cord or hematomyelia includes only such extravasations of blood as take place suddenly into the substance of a healthy spinal cord. Such hemorrhage is rare, and is to be carefully distinguished from the more common hemorrhage that takes place into inflamed and softened spinal tissue, and is designated hematomyelitis. Hemorrhage into the spinal cord may result from injury — traumatic spinal hemorrhage. The causative factors include not only concussion and injury of the vertebral column, but also heavy lifting, strong expulsive HEMORRHAGE INTO THE SPINAL CORD 549 efforts, and the like. Exposure to cold is likewise not without influence ; at least, a jwitient under my cure was sei/x'd with hemorrhage into the spinal cord at a hathing- resort as a cold douche was directed against the vertebral column. Of import- ance are processes in the sexual sphere, particularly venereal excesses and amenorrhea. Suppression of hemorrhoidal bleeding also has been stated to provoke a tendency to spinal hemorrhage. Excessive indulgence in alcohol appears to be not without influ- ence. Cases, however, occur also in which no exciting cause for the spinal hemorrhage can be demonstrated. The disorder develops most commonly in men between the twentieth and the fortieth year of life. Anatomic Alterations. — Hemorrhage into the spinal cord may be classified according to the external appearance into transverse, longitudinal, and circumscribed. In cases of transverse hemorrhage into the spinal cord the extravasation involves the entire transverse section or it may be confined accidentally to one-half of the cord — unilateral hemorrhage. After incision of the dura the extravasation of blood can frequently be distinguished beneath the pia as a dark, reddish-black collection, which at times pushes the pia outward and projects above the level of the adjacent healthy spinal tissue. At times the pia and even the arachnoid are suffused with blood. Blood may also be ad- mixed with the cerebrospinal fluid, and impart to this a reddish, bloody appearance. On section through the hemorrhagic focus the appearances vary with its age. In recent cases it consists of a soft bloody mass, constituted of red blood-corpuscles and dis- integrated spinal tissue. The older the lesion the more con- spicuous on microscopic examination are fatty degeneration and disorganization of the injured nerve-fibers. There are present numerous fatty granule-cells, which are nothing more than emi- grated colorless blood-corpuscles, which have become laden with the not readily absorbed fat for the purpose of hastening its absorption. Older hemorrhagic foci are appreciable even to the unaided eye from their reddish-brown appearance, and they are likely to present a more firm consistence. Microscopically, in addition to fatty granule-cells, red blood-corpuscles are found in various stages of disorganization. Here and there granules, needles, and plates of precipitat(>d hematoidin are also present. Gradually a hemorrhagic extravasation may undergo complete absorption, and there will remain in its place a cavity filled with serous fluid whose wall is constituted by proliferated neuroglia — apoplectic cyst. In addition, secondary degeneration of the spinal cord occurs above and below the hemorrhagic extravasation : above, ascending degeneration of the columns of Goll, the lateral cere- bellar tracts and Gowers' bundle ; below, descending degenera- tion of the lateral and anterior pyramidal tracts. Only rarely will 550 NERVOUS SYSTEM it be possible on microscopic examination to find the rnptured spinal vessel responsible for the hemorrhage. If the blood-vessels exhibit any change, this generally consists in secondary prolifera- tion of nuclei and in fatty degeneration. Miliary aneurysms, which are as a rule responsible for hemorrhage into the brain, seldom occur in the spinal cord. Tubular hemorrhage into the spinal cord extends especially in the longitudinal axis of the cord, and at times attains a length of several centimeters. Naturally, the white matter of the cord oifers considerably more resistance to the extension of the hemor- rhage than the grav matter. Circumscribed hemorrhages into the cord consist of small extravasations of l)lood tliat involve only certain small portions of the cord. The gray matter of the cord is more susceptible to all varieties of hemorrhage on account of its greater abundance of blood-vessels, and it is, therefore, a rela- tively common seat of circumscribed spinal hemorrhage. Small extravasations of blood in the spinal cord may disappear and leave only a brownish or yellowish cicatrix consisting of neuroglia — apoplectic cicatrix. Symptoms and Diagnosis. — The sudden occurrence of spinal symptoms is distinctive of all varieties of hemorrhage into the spinal cord. In other respects the symptoms vary in accordance with the extent and the situation of the extravasation. Transverse hemorrhage in the lumbar or dorsal cord is attended with suddenly developed paraplegia in the lower extremities. At the same time there is anesthesia. The tendon-reflexes, particularly the knee-jerks, are generallv enfeebled for the first few days, and this is thought to be due to the general concussion of the spinal cord induced by the hemorrhage ; subsequently the tendon-reflexes become exag- gerated. The tendon-reflexes remain permanently abolished only when the hemorrhage destroys the lumbar cord and thereby inter- rupts the spinal reflex arc. In the latter event paralysis of the bladder and of the rectum is present from the outset, as the spinal centers for the bladder and the rectum in the lowermost portion of the lumbar cord are destroyed ; also in cases of transverse hemorrhage into the dorsal cord paralysis of the bladder and the rectum appears after the lapse of some time. The detrusor of the bladder suffers first, and the patients are capable of emptying the viscus only incompletely and with difficulty. Subsequently paral- ysis of the sphincter of the bladder is superadded, and the reten- tion of urine at first present is succeeded by incontinence. Bacteria from the air and the urethra readily gain entrance into the bladder, and cause fermentation of the urine and readily excite cystitis, pyelonephritis, and urinary septicemia. Incontinence of urine also is attended with the danger of cutaneous irritation, of bed-sores, and of septicemia. In cases of transverse hemorrhage in the upper portion of the spinal cord symptoms of paraplegia of the arms HEMORRHAGE INTO THE SPINAL CORD 551 occur in addition' to the symptoms described. Heniorrha<^c hij^li up may even give rise to bulbar symptoms if the nuclei of the cerebral nerves on the floor of the fourth ventricle or the intra- medullary nerve-roots of individual cerebral nerves are involved in the morbid process. With the occurrence of hemorrhage into the spinal cord the patients frequently complain of severe pain in the spinal column, which is probably dependent upon sudden distention of the pia mater by the extravasated blood. The bodily temperature remains unchanged, although at times slight elevation of temperature takes place in from three to five days, and this has been designated reac- tionary fever, and has been considered the sequel of an inflammatory reaction on the part of the spinal tissues surrounding the extrava- sation. If the transverse section of the spinal cord is wholly destroyed by the hemorrhage, recovery or even improvement cannot be anticipated, as regeneration of spinal tissue does not take place. Improvement can be hoped for only when part of the symptoms result from pressure exerted by the extravasated blood, and this pressure ceases after absorption of the blood has taken place. After transverse hemorrhage into the spinal cord has existed for some time mitscidar contractures and exaggeration of the tendon- reflexes gradually develop in the paralyzed extremities, conditions that are commonly attributed to secondary degeneration of the lateral pyramidal tracts, although this has scarcely been demon- strated with any degree of certainty. The principal dangers from the disorder are bed-sores and septicemia and urinary decomposi- tion, cystitis, pyelonephritis, and urinary septicemia. Unilateral hemorrhage into the spinal cord sets in suddenly with the symptoms of a unilateral lesion of the spinal cord. Accordingly, paralysis is found upon the side of the hemorrhage and anesthesia upon the opposite side. Circumscribed hemorrhage into the anterior horns of the spinal cord is attended with symptoms of anterior poliomyelitis (flaccid paralysis, degenerative muscular atro])hy, degenerative electric reaction, abolition of the reflexes) ; and into the posterior horns, with partial anesthesia, particularly with loss of painful and of thermal sense. Prognosis. — The prognosis of hemorrhage into the spinal cord is unfavorable, because such destruction of the cord as is effected is permanent. At times gliosis is .said to have devel- oped in tlic sequence of spinal hemorrhage. Treatment. — For the control of hemorrhage into the spinal cord and to avert reactionary inflammation in the spinal tissue an ice-bag should be applied to the vertebral column at the site of hemorrhage. Success can scarcely be expected from the inter- nal administration of hemostatics. To hasten absorption of the 552 NERVOUS SYSTEM .blood, sorbefacicnts, particularly potas.siimi iodic! (5.0 : 200 — 75 grains : G^ liuidouuces ; 15 c.o. — 1 tablespoontul — thrice daily), are often prescribed, but it is at least doul)tful whether they have any effect. If symptoms of paralysis of the bladder and tiio rectum appear, attempts should be made in the pres- ence of retention of urine to secure evacuation of the bladder thrice daily l\v means of compression of the bladder through the abdominal -wall. The catheter should be resorted to only when the procedure mentioned proves unsuccessful, and in that event most rigid disinfection of the catheter must be secured. If incon- tinence of urine has developed, the urine should be collected in a suitable receptacle. The skin of the buttocks and the vicinity should be thoroughly cleansed morning and evening of all con- tamination, and -washed with alcohol in order to avert bed-sores. It is, further, important to change the posture of the body several times during the day. If, in spite of these precautions, redness and discoloration of the skin appear, the surface should be covered with smoothly applied adhesive plaster, and the patient should be placed upon a hair mattress or a water-bed. If a bed-sore be present when the patient comes under observation, it should be covered with cotton that has been immersed in camphorated wine, or the patient should be placed permanentlv in a M'arm bath at a temperature of 28° R. (35° C\— 95° F.). Xot much will be accomplished Avith electric treatment of the spinal lesion and the paralvzed muscles. Massage of the paralyzed muscles should preferably be recommended in order to maintain the nutrition of the muscles and to avert the development of contractures. ACUTE INFLAMMATION OF THE SPINAL CORD (ACUTE MYELITIS;. Htiology. — Acute inflammation of the s])inal cord probably develops generally as a result of the activity of bacteria, and those influences that have hitherto been considered as the causes of the disease are probably without other significance than that of contributory agencies for the infection. Among these belong par- ticularly exposure to cold, traHinatism, and jweceding infectious dis- ease. Also, states of hy])eremia of the spinal cord appear to favor infection of the cord. In women sym]>toms of spinal inflamma- tion appear at times at the menstrual period, particularly if men- struation be a])sent or delayed. ^lyelitis is even reported to have been observed after profound emotional disturbance ; for instance, after severe fright. Inflammation of the spinal cord may arise by extension from disease of the verteljral column (carcinoma, tuberculosis). Acute neuritis also extends at times to the spinal cord. Acute myelitis ACUTE lyFLAMMATIOX OF THE SPINAL CORD 553 is a rather uncommon disease, which attacks men somewhat more frequently tlian women, and which occurs particularly in adults. Anatomic Alterations. — An acutely inflamed spinal cord is characterized In' remarkable softness, so that the condition may be spoken of as injiammatory spinal softening or injiaMinatory myelomalacia. It should naturally be remembered that precisely the same alterations may take place if the circulation and nutri- tion of the spinal cord are cut off as a result of embolism or thrombosis of Ijlood-vessels. There then occurs necrotic spinal softening or necrotic myelomalacia, although little of a definite nature is known with regard to this. In accordance with the duration of the disease the softened spinal cord presents a varying color, and accordingly a distinction has been made between red, yellow, and gray softening of the spinal cord. In the presence of red softening the color of the cord is due to the fulness of the vessels with blood and diapedesis of red blood-corpuscles. When numerous extravasations of blood occur the condition has been designated hematornyelitis or hemorrhagic myelitis. Destruction of migrated red blood-corpuscles, transformation of their hemo- globin, and progressive fatty degeneration of the nervous elements gradually give rise to the appearances of yellow softening of the spinal cord, Avhich when the hemoglobin is wholly absorbed is succeeded by gray softening. The degree of softening is most variable. In some cases the inflamed spinal tissue presents an almost fluid consistence. At the same time it may happen that smaller foci of inflammation are gradually absorbed, and in their place a spinal cyst filled with serous fluid remains. Should the disease pursue a chronic course, induration or sclerosis of the previously softened tissue at times takes place. Rarely, cases of acute myelitis occur in which accumulations of pus take place in the spinal cord — abscess of the spinal cord, purulent myelitis. On microscopic examination of softened spinal tissue, fatty granule-cells, degenerated nerve-fibers and ganglion-cells, red blood-corpuscles, emigrated colorless red blood-corpuscles, swelling and proliferation of glia-cells and altered blood-vessels are found in abundance. The vessels exhibit disten- tion with blood, thickening of their walls, multiplication and fatty degen- eration of their nuclei, and often also the presence of round cells and fatty granule-cells in considerable number in the adventitial lymph-sheaths. Often the blood-vessels are surrounded by a collection of colorless blood- corpuscles. The nerve-fibers exhibit disintegration, fiitty degeneration, and atrophy of medullary sheaths. Their axis-cylinders often |)resent marked swelling and enlargement, which may be seen with especial dis- tinctness upon transverse section of the hardened spinal cord, and often increase and diminution in size occur alternately in garland-like arrange- ment. Finally, disintegration and disapi)earance of the axis-cylinders takes place. The ganglion-cells become swollen, not rarely present vacu- oles, lose their processes, and eventually contract to small, roundish struc- tures, not rarely stained deeply brown. If the inflammation has existed for some time, laminated amyloid bodies also occur. Acute myelitis most commonly involves the gray substance 654 NERVOUS SYSTEM of the cord, perhaps because the large number of blood-vessels in this situation readily permits the entrance of numerous bacteria. Siiould the inflammation be confined to the gray matter of the spinal cord, the condition is spoken of as central myelitis or polio- myelitis. It is naturally the rule for the inflammatory process to extend from the gray to the white matter of the cord. Observa- tions of inflammation of the white substance of the cord exclu- sively are rare, and are known as leukomyelitis. Should the in- flammatory process involve especially the peripheral layers, the disease is designated perimyelitis. With this condition inflamma- tion of the spinal meninges is frequently associated — acute myelo- meningitis. The distribution of acute myelitis is extremely variable. At times it takes place principally throughout a transverse extent, so that the entire transverse section of the cord is involved in the inflammatory focus — transverse myelitis. An especial form of transverse myelitis consists in involvement of one-half of the spinal cord only. In some instances the inflammatory process exhibits a tendency rather to extend longitudinally, and at times it involves the entire length of the spinal cord — diffuse myelitis. Small myelitic areas, which are often recognized only on micro- scopic examination of the hardened spinal cord, are known as circumscribed myelitis, and if a number of such areas are present in the spinal cord separated from one another the condition is designated disseminated or insular or multiple myelitis. Experi- ence has shown that the luml)ar and dorsal portions of the cord are the most common seats of inflammation. Symptoms and Diagnosis. — Acute myelitis not rarely begins, like an acute infectious disease, with a chill, followed by fever, with elevation of temperature to 39° or 40° C. (102.2° or 104° F.) and above. In some cases a sense of drawing in the back, a feeling of stiffness in the vertebral column, and paresthesia in the extremities appear as prodromes. Symptoms of spinal paralysis soon aj^pear, and these correspond most frequently with the clinical picture of transverse myelitis in the lumbar or dorsal cord. The patients complain of a sense of weakness in the lower extremities and are compelled to go to bed, and even within a short time flaccid paralysis of the extremities has developed. Painful jerking or muscular contractions also occur from time to time in the paralyzed parts. Complaint is frequently made of paresthesise in the paralyzed muscles, ]Dar- ticularly the crawling of ants (formication), sticking, prickling, burning, and also sensations of cold. The anesthesia is always more marked in the lower extremi- ties. The tendinous and cutaneous reflexes are wanting when the lower portion of the lumbar cord is involved in the inflammatory process, and its functional activity is suppressed. When the in- flararaatorv foci are situated at a hig'her level the reflexes remain ACUTE INFLAMMATION OF THE SPINAL CORD 555 unchanged or are even unduly increased. Disease in the lower portion of the lumbar cord is from the first attended with jjaridly ascending character ; or the initial fever gradually sub- sides, but after the lapse of several weeks death occurs as a result of septicemia or of urinary infection ; or the disease assumes a chronic course and persists for months or years. Under the con- ditions last named a portion of the paralytic phenomena may dis- appear in so far as these are dependent rather upon compression than upon actual destruction of nervous elements. Complete recovery is scarcely to be expected. Further, the disease exhibits a great tendency to relapjse, in consequence of insignificant inju- rious influences. The diagnosis of acute transverse and of progressive myelitis is not difficult. In contradistinction from hemorrhage into the spinal cord, importance should be attached to the fact that the symptoms do not set in suddenly, but successively. In the pres- ence of acute spinal meningitis irritative symptoms predominate, particularly pain. The presence of rigidity of the neck also is of importance. Spinal ascending (Landry's) paralysis is unattended with sensory disturbances, as well as paralysis of the bladder and the rectum. Multiple neuritis is attended with degenerative mus- cular atrophy and degenerative electric reaction in the paralyzed nerves and muscles, while the bladder and the rectum usually remain unaffected. From the clinical course described such cases of acute myelitis will naturally deviate in which the inflammatory process is confined to one-half of the spinal cord or to small cir- cumscribed areas. In the first event, the symptoms of a unilateral lesion of the spinal cord appear acutely (paralysis and hyperes- thesia upon the side of the lesion, and anesthesia upon the opposite side), while in the latter they depend upon the varying seat of the inflammatory focus. Prognosis. — The prognosis of acute myelitis is grave, as there is always immediate danger (urinary infection, septicemia, paral- ACUTE INFLAMMATION OF THE SPINAL CORD 557 ysis of cerebral nerves), or the disease pursues a chronic course ; complete recovery can scarcely be expected. Treatment. — In the presence of acute myelitis an ice-bag, or, still better, the ice-sac of Chapman, should be applied to the verte- bral colunan. For the control of the fever, and thereby to diminish the flow of blood to the spinal cord, sodium salicylate or phenacetin should be prescribed : R Sodium salicylate, 1.0 (15 grains). Make 10 such starch-capsules. Dose : 1 powder every two hours. R Phenacetin, 1.0(15 grains); Sugar, 0.5 (7i " ).— M. Make 10 such powders. Dose: 1 powder thrice daily. The diet should be exclusively liquid, and a milk-diet is the best. Strong coffee or tea and wine and alcoholics should be for- bidden. Daily evacuation of the bowels should be secured, and to this end some stewed fruit (apple-sauce, prunes) should be given at the midday meal. If necessary, laxatives should be prescribed, and glycerin-enemata are particularly to be recommended. It is important for the position of the patient to be changed every two hours, in order to avoid persistent pressure upon the same part of the skin. Care should also be taken to have the sheet always free from creases and that it does not contain dry bed-crumbs. The entire body should be cleansed with tepid water at least once daily, and the back and the sacral region should be rubbed with some form of spirit, cologne- water, or lemon-juice, in order to increase the resistance of the skin. If inflammation of the skin and bed-sores threaten in spite of these measures, the skin should be covered with smoothly applied adhesive plaster, and the patient should be placed upon an air-mattress or a water-bed. The great- est consideration should be given to such paralysis of the bladder and the rectum as may be present. If retention of urine occur, an effort should first be made to evacuate the bladder by pressure through the abdominal walls, and only if this fails should resort be had to the use of the catheter, which must be most scrupu- lously disinfected. If dribbling of urine be present, a proper receptacle should be provided. If the skin is soiled by urine or feces, it should at once be cleansed and washed with a solution of mercuric chlorid (1.0 : 1000). If a bed-sore be present when the patient comes under observation, it should be dressed with cotton that has been immersed in spirit of camphor or the patient should be placed in a permanent tepid bath (30° C— 24° R.— 86° F.). The foregoing directions for the care of the patient are of far greater importance than any medicament. It is at least question- able whether antiphlogistics (mercurials, leeches, cups), sorbefacients (potassium iodid), or nervines (bromids, belladonna, ergot, arsenic, 558 NERVOUS SYSTEM preparations of gold or silver, strychnin, etc.) are capable of ex- erting any effect. Also the utility of electric treatment of the spinal cord and the paralyzed muscles is doubtful. On the other hand, resort is generally had to massage of the paralyzed muscles, in order to maintain their nutrition and avert the development of contractures. CHRONIC INFLAMMATION OF THE SPINAL CORD (CHRONIC MYELITIS)* ^Etiology. — Chronic myelitis is dependent upon the same causes as acute myelitis, and accordingly a distinction has been made principally between refrigeratory, traumatic, and infectious chronic myelitis. Among the infectious varieties syphilitic mye- litis should be particularly mentioned. Without doubt, alcoholism also plays an etiologic role, and under such circumstances the myelitis would be considered toxic. Anatomic Alterations. — Spinal tissue in a state of chronic inflammation is characterized generally by increased hardness or sclerosis. Not alone do the diseased areas feel unusually hard, but they also appear gray, translucent, and shrunken. It is note- worthy that the spinal cord may appear unaltered in the fresh state, although after hardening in preparations of chromic acid, as, for instance, Miiller's fluid, the inflammatory areas can be recog- nized readily from their light-yellow color. On microscopic examination hyperplasia of the neuroglia and destruction of nerve-fibers and ganglion-cells will be found in the inflamed areas. Of the nerve-fibers, the medullary sheaths first undergo granular disintegration and fatty degeneration. The disappearance of the axis-cylinders is often preceded by marked swelling. The ganglion-cells undergo contraction to round and often greatly pigmented structures, without processes. The blood-vessels appear dilated in places, are distended with blood, exhibit striated and thickened walls with many nuclei, and are surrounded on their outer surface by collections of round cells. The adventitial lymph-spaces also not rarely contain round cells. Fatty granules are encountered only in small number, in contradistinction from acute myelitis, while amyloid bodies are present in considerably greater number. Chronic myelitis exhibits the same distribution as acute mye- litis. Disease of the gray matter is known as chronic central mye- litis or chronic poliomyelitis, while disease of the white matter is designated leukomyelitis. Should the chronic inflammatory process remain confined to the peripheral layers of the white matter of the spinal cord, the condition \s de^iirniited. a]so chronic perimyelitis. Under the conditions last named the spinal membranes are fre- quently involved in the inflammatory process, and particularly the pia mater and the arachnoid undergo thickening and adhesion — chronic myelomeningitis. For the same reasons that are applicable to acute myelitis a distinction can be made between chronic transverse myelitis, unilateral myelitis, circnmscrihed, diffuse, and c/i ron ic myelitis. Symptoms, Diagnosis, and Progfnosis. — When chronic CHRONIC INFLAMMATION OF THE SPINAL CORD 559 myelitis occurs as an independent disorder it generally develops gradually. Pains in the course of the vertebral column, a sense of constriction, shooting pains in the arms and the legs, pares- thesise in the lower extremities, and at times also vesical disturb- ances are often complained of as prodromes. Most commonly chronic myelitis is situated in the lumbar or dorsal cord, and in conformity with this fact the more serious disturbances generally appear first in the lower extremities. The legs become readily fatigued in walking, the knees often give way, and the patient stumbles over slight irregularities or elevations upon the floor. Fatigue and weakness in the lower extremities progress graduallv in such a way that the patient shortly resorts to the use of crutches for support. Eventually complete paralysis ensues, and the patient is kept permanently in bed or in a chair. To the motor paralysis sensory disturbances are generally superadded, most commonlv more or less marked and complete anesthesia. Vasomotor and trophic alterations may also be present. The tendinous and cutane- ous reflexes are abolished when the inflammation has interrupted the functional activity of the lumbar cord. Exaggeration of the reflexes occurs in connection with transverse myelitis of the dorsal cord when secondary degeneration of the lateral pyramidal tracts takes place below the inflammatory focus. Then muscular con- tractures generally develop, most commonly in the flexors of the thigh and the leg. The bladder and the rectum frequently exhibit disturbances. At times retention and incontinence of urine alter- nate. Some patients complain of priapism or of impotence. Chronic myelitis is generally unattended with fever. At times transitory febrile movement occurs, during which the inflammatory process advances. At times it extends from below upward — chronic ascending myelitis. To the paralysis of the lower extremities there is then superadded paralysis of the arms, and should the process extend to the medulla oblongata and the pons Varolii there will develop paralysis of various cerebral nerves (hypo- glossal, vago-accessory), which may lead to a fatal termination in consequence of paralysis of deglutition or of the heart. The duration of the disease may extend over many years. Re- covery is possible in cases that are not too far advanced. Gen- erally, however, it is not complete. The principal dangers are cystitis and urinary infection or bed-sores and septicemia. Treatment. — The treatment of chronic myelitis is the same as that of acute myelitis. The well-to-do may, in addition, under- take courses of treatment at the baths during the summer. There may be mentioned indifferent baths (Gastein, Pfaffers, Ragatz, Wildbad), saline baths (Nauheim, Rehme, Kissingen, Reichen- hall, Rheinfelden, Bex), sulphur-baths (Aachen, Baden in Aargau, Baden near Vienna, Schinzach, Stachelberg, Leuk, Lenk, Serneus), and peat-baths (Marienbad, Franzensbad, Elster, Cudowa, Steben). 560 NERVOUS SYSTEM MULTIPLE CEREBROSPINAL SCLEROSIS, Etiology. — Little of a reliable nature is known with regard to the causes of multiple cerebrospinal sclerosis. Exposure to cold, traumatism, antecedent infectious disease, and intoxications (alcohol, lead, phosphorus, carbon raonoxid) are considered causes of the disorder. At times the disease has occurred as a sequel of the puerperium. In some cases heredity has been observed ; in others, several mem- bers of a family have been attacked — familial form. The disorder generally de- velops between the fifteenth and the thirty- fifth year of life. It occurs but rarely in childhood, although isolated cases of con- genital midfiple sclerosis hay e been reported. Anatomic Alterations. — Multiple cerebrospinal sclerosis is characterized by the formation of foci of neuroglia, which -j^^ are distributed throughout the entire central J ^^^ nervous system in varying size, number, and arrangement. The white nervous matter everywhere appears particularly favored by the foci (Fig. 77). The indi- vidual foci can be readily recognized, for when of sufficient size they are sharply differentiated from tlie surrounding healthy structure by their reddish-gray or grayish color. Generally they feel indurated, whence the term sclerosis. Often they can be detected through the pia mater, so that the brain and the spinal cord present I ^^^^ ^ g^^yish, mottled appearance. On trans- verse section of the spinal cord they fre- quently become depressed. The size of the foci may attain several centimeters ; but, on the other hand, it may be so inconsider- -«p^ able that the smallest foci can be recog- ^ ^^ nized only with the aid of a microscope. Often they are present side by side in large number and above one another, while in other instances they occur in but small number. Their distribution follows no rule, and no case resembles another. In the medulla oblongata sclerotic areas are not rarely found in the nuclei of indi- vidual cerebral nerves. Similar changes have been observed also in the trunk of cerebral nerves. Fig. 77. — Transverse sec- tions of the spinal cord from a case of multiple cerebro- spinal sclerosis, in a man 3.5 years old: a-d, cervical por- tion ; f-k, dorsal portion : l-n, lumbar portion ; natural size; hardened in Muller's fluid (personal observation, Zurich clinic). MULTIPLE CEREBROSPINAL SCLEROSIS 561 Microscopic examination ^\?,c\o?,es proliferation of the neuroglia and destruc- tion of the nerve-fibers in the sclerotic areas. It is noteworthy that the axis-cylinder offers resistance for a long time, so that naked axis-cylinders may be found in the areas. The blood-vessels further exhibit alterations, which consist in thickening of their wall, nuclear proliferation, fatty degen- eration and the presence of round cells, fatty granule-cells, and also yellow- ish flakes of pigment in the adventitial lyniph-sheaths. The cells in the sclerotic foci have been thought to consist, in part, of emigrated colorless blood-corpuscles. Fatty granule-cells, and particularly amyloid bodies, are frequently encountered in the sclerotic areas. In all probability multiple cerebrospinal sclerosis must be considered as a form of disseminated chronic myelitis, the inflammatory irritant being brought to the spinal cord through the blood-vessels. Symptoms. — The distinctive symptoms of multiple cerebro- spinal sclerosis are generally preceded by prodromes of an indef- inite character. These include vertigo, headache, paresthesias, neuralgia, disturbances of the bladder, and paroxysmal vomiting (gastric crises). The disease can be recognized only when typical symptoms make their appearance, including intention-tremor, scan- ning speech, nystagmus, and apoplectiform attacks. Intention- tremor may be recognized from the fact that when the patients wish to execute a movement the members set in action begin to tremble actively or generally to shake, and in greater degree the more nearly they approach the consummation of the act. If the patient attempts to touch with his fingers a body held before him, the arms and hands are thrown to and fro. TJie introduction of a needle into a previously made perforation is scarcely possible, because the fingers and the needle are too actively moved to and fro upon the paper. On attempts to carry a glass or a spoon to the mouth the contents are partially spilt by the sliaking of the arm, and the rattling of the teeth can be heard. Writing, sewing, dressing, buttoning are naturally disturbed in marked degree, and they may even be rendered impossible. On sitting erect, in AA^alk- ing, and in the use of a stick the oscillating and tremulous move- ments may be readily observed. Opinions are divided as to the 7node of origin of intention-tremor. It has been thought that the naked axis-cylinders in the sclerotic areas are capa- ble of transmitting the impulses of the will only interruptedly. According to others, transverse radiation is believed to be possible from non-medul- lated nerve-fibers, and thus to disturb the normal transmission of volitional impulses. It is less probable that intention-tremor is dependent upon the presence of sclerotic areas in definite portions of the brain, as the phenom- enon is a most constant and early manifestation, so that it would be neces- sary to assume the presence invariably of early disease of definite portions of the brain, Avhereas the disorder is characterized especially by the irreg- ular distribution of the foci of disease. Scanning speech is characterized, in the first place, by the ar- ticulation of the individual syllables of a word in jerks and with pauses, and, besides, by the peculiar, monotonous, singing, and high-pitched character of the voice. The disturbances of speech .36 562 NERVOUS SYSTEM are thought to be dependent upon intention-tremor of the muscles of articulation and of the larynx or of the vocal bands. Not rarely most marked distortion of the face is observed on attempts to speak. A patient under ray care was capable of speaking only by holding the lower jaw firmly with her hands, and keeping it at rest. Sudden dilatation of the chink of the glottis and trem- ulous movements of the vocal bands during phonation have also been observed on laryngoscopic examination. The nystagmus is likewise due to intention-tremor of the ocular muscles. It can be readily recognized from the horizontal to-and- fro movement of the eyes that takes place when a finger is moved to and fro in a horizontal direction, and which becomes the more marked the further the finger is moved outward. Rarely, twitch- ing movements in a vertical direction or rotatory movements occur — vertical and rotatory nystagmus. Nystagmus occurs rather less constantly than intention-tremor and scanning speech, and is present in about one-half of the cases. Apoplectic attacks occur still less commonly. Consciousness is lost, and wdien it is restored the patient finds himself paralyzed upon one side of the body or in one member ; but, as a rule, the paralysis disappears in the course of a few days. There is a dis- position to attribute such attacks, wdiich not rarely are attended with elevation of temperature and are at times accompanied also bv eclamptic convulsions, to the development of new sclerotic areas. The typical symptoms of multiple cerebrospinal sclerosis must be distinguished from the more accidental nervous disturbances, which vary accordingly as one or another portion of the central nervous system is the seat of the sclerotic process, and is thus thrown out of function. As of the anatomic alterations, it may likewise be said of this group of symptoms that one case scarcely resembles wholly any other. Of diagnostic significance are particularly atrophic changes in the optic nerve, which preferably involve the temporal half of the optic papilla. At times disturbances occur also in other cerebral nerves (paralysis of the ocular muscles, of the trigeminus, of the vagus, tinnitus aurium, impairment of hearing, immobility of the tongue, etc.). Frequently motor disturbances appear, particularly paresis or paralysis in the lower extremities. These are often associated with muscular spasm and exaggeration of the tendon- reflexes. The gait becomes spastic-paretic, and the clinical picture resembles that of so-called spastic spinal paralysis. Sensory dis- turbances, generally partial anesthesia, are also not uncommon occurrences. At times jKiralysis of the bladder develops, which may subside, subsequently, however, to reappear. If groups of ganglion-cells in the anterior horns of the spinal cord are destroyed by the sclerotic process, muscular paralysis with degenerative atrophy and degenerative electric reaction may MULTIPLE CEREBROSPINAL SCLEROSIS 563 result. When paralysis has existed for some time muscular con- tractures may develop, frequently earliest in the adductors of the thighs, subsequently in the flexors of the thighs, the legs, and the feet. Extensive foci in the vicinity of the posterior columns of the spinal cord render the gait ataxic, and under such conditions confusion with tabes dorsalis may arise. Vasomotor and trophic disturbances have been observed, but are among the less common manifestations. The mental condition not rarely suffers. The patients become more and more apathetic, forgetful, and finally demented. Sometimes uncontrollable laugh- ter is observed at an early stage, long-continued laughter of an unusually hearty, almost boisterous character being induced on slight provocation. Uncontrollable crying also may occur. The course of multiple cerebrospinal sclerosis frequently ex- tends over many years, and often remissions and exacerbations in the symptoms alternate. Death results from accidental disease (pulmonary tuberculosis, pneumonia, etc.), or from excessive ex- haustion, or from urinary infection in the presence of paralysis of the bladder, or from septicemia in consequence of bed-sores, or from bulbar paralysis (paralysis of swallowing and of respiration). Diagnosis. — The diagnosis of multiple cerebrospinal sclero- sis is easy in typical cases. Naturally, emphasis must be placed upon the fact that there is a neurosis of the central nervous system — so-called pseudosclerosis — which may exactly reproduce the clinical picture of multiple sclerosis, although upon post-mortem examination the central nervous system may be found unchanged. The occurrence of atrophy of the optic nerve is distinctive of cerebrospinal sclerosis. Intention-tremor occurs at times also in association with cerebral tumors, mercurial poisoning, and hysteria ; but under such conditions the remain- ing symptoms of multiple sclerosis will be wanting. Should the typical symptoms of the disease already described be absent, it will scarcely be possible to make the diagnosis with certainty. The disease may then be readily confounded with chronic myelitis, tabes dorsalis, spastic spinal paralysis, and amyo- trophic lateral sclerosis. Confusion with paretic dementia is also possible. Further, it should be borne in mind that no invariable relation exists between the severity of the morbid manifestations and the extent of the anatomic alterations. Prognosis. — Multiple cerebrospinal sclerosis is an incurable disease, and from this point of view the prognosis is unfavorable. It is true that at times such remarkable improvement occurs as to encourage the hope of recovery, but this proves deceptive. There is, however, no immediate danger of death. Treatment. — No specific remedy for multiple sclerosis is known, and, in general, the rules should be followed that have been laid down on p. 485 for the treatment of myelitis. 564 NERVOUS SYSTEM TUMORS OF THE SPINAL CORD. Tumors of the spinal cord are not uncommon : gliomata, sarco- mata, carcinomata, myxomata, cholesteatomata, gummata, and tuber- culomata have been ol)served. Anatomic Alterations. — Tumors of tlie spinal cord are generally of spherical form, l)ut at times they involve the entire transverse section or one-half or a still smaller section of the spinal cord, or they may extend throughout the length of the cord from above downward. At times they are clearly defined from the surrounding spinal tissue by a connective-tissue capsule, but at other times they gradually merge into the structure of the cord. Often the latter is softened at the point of junction. In the tumors themselves softening and the formation of cavities may also take place. In tumors well supplied with blood-vessels ex- tensive hemorrhage may suddenly occur, with destruction of the neoplastic tissue and of the adjacent tissue of the cord. The causes for tumors of the spinal cord are often unknown. At times traumatism, pregnancy, and the puerperium are named as causes. At times the tumors are of metastatic origin. Gum- mata and tuberculomata are sequels of syphilis and tuberculosis respectively. The diagnosis of a spinal tumor is scarcely ever possible. This is a matter of course for cases in which spinal symptoms are wholly wanting. The same condition also prevails at times in connection with relatively extensive neoplasms if these displace rather than destroy the nervous elements of the cord. Under other circumstances, in accordance with the seat and the extent of the new-growth, symptoms of transverse interruption or of a unilateral lesion of the cord, of anterior poliomyelitis, syringo- myelia, spastic spinal paralysis, tabes dorsalis, and the like, may be present, and only the autopsy may reveal the causes for the spinal disturbances. The progtiosis is serious. Death results generally from progressive exhaustion, in the presence of paralysis of the bladder from urinary infection and in the presence of bed-sores from sep- ticemia. Specific treatment is applicable only when syphilis is present, but otherwise the treatment applicable to myelitis should be em- ployed (p. 557). CAVITIES IN THE SPINAL CORD (SYRINGOMYELIA AND HYDROMYELIA). Anatomic Alterations. — The presence of cavities in the spinal cord is at times due to morbid dilatation of the central canal, and the condition is then designated hydromyelia. It is CAVITIES IN THE SPINAL CORD 565 characterized by the presence in places of cylinclric epithelium upon the walls of the cavity. The disorder has been observed particu- larly in connection with tumors in the posterior fossa of the skull, and it has been attributed to stasis. Most cavities in the spinal cord result from gliosis (gliomatosis) ; that is, prolifer- ation of neuroglia first takes place, which not rarely extends throughout the entire length of the spinal cord, and even through the medulla ob- longata, and then by the softening of this tissue a cavity results — syrin- gomyelia. Less commonly cavities result from softening of myelitic foci or of tumors of the spinal cord. Hydrorayelia and syringomyelia are by no means always easily and with certainty distinguishable from each other, for when syringomyelia is present rupture into the central canal occasionally takes place, and there may be subsequent dilatation of the central canal, and the walls of the cavity then likewise present cylindric epithelium in places. The cavity in a case of syringomyelia may involve the entire spinal cord and also the medulla oblongata, and it may terminate in the fourth ventri- cle, or it may develop for only a short distance at a single yioint or at several points in the spinal cord. Most commonly the cervical cord is the seat of the disease, and in this situation the cavity usually attains its greatest size. In the course of the spinal cord the cavity often al- ters its position (Fig. 78). At times it is situated between the posterior columns of the spinal cord, while at other times it involves the gray mat- ter of the cord, now in the neighbor- hood of the anterior horns, where it causes destruction of tiie lars^e mo- tor-trophic ganglion-cells, then in the neighborhood of the posterior Medulla oblonsata Cervical nerve, l-2~ Cervical nerve, 1-2 — Dorsal nerve, 1-2- Dorsal nerve, 2-3 — Dorsal nerve, 4- Dorsal nerve, 8-0- Dorsal nerve, lf-11 — Dorsal nerve, 11-12 1 Lumbar nerve, 3-4 — Lumbar nerve, 4-5- — Lumbar nerve, 4-5- Fig. 78.— Syringomyelia in a woman 29 years old ; natural size (personal ob- servation). 566 yERVOUS SYSTEM horns, in other situations in the middle portion of the gray matter, etc. The size of the cavity varies from the scarcely visible to such an extent that the tip of the little finger can be readily introduced. Under the latter condition the entire transverse section of the cord is increased in size. The spinal cord not rarely resembles a fluctu- ating sac oscillating to and fro, and which on incision gives exit to a generally clear and but rarely flocculent or blood-stained fluid, and which collapses after evacuation. The cavity is generally provided with a membrane formed of dense neuroglia. The blood- vessels are generally thickened and obstructed by thrombi, condi- tions that are associated with the softening of the neuroglia and the formation of the cavity. Often yellowish and brownish pig- ment is encountered in the neighborhood of the cavity. The adjacent columns of the spinal cord are not rarely sclerotic. Btiology. — Syringomyelia is probably in many cases de- pendent upon developmental defects in the spinal cord that undergo further development as a result of accidental influences. The latter include particularly traumatism and antecedent infectious disease. Hereditary and familial occurrence of syringomyelia has also been observed. The condition generally appears in adults. Symptoms. — An extensive cavity in the spinal cord may be w^holly unattended with symptoms. Among the distinctive mani- festations of syringomyelia are progressive muscular atrophy, partial loss of sensibility, and vasomotor and trophic changes. Progressive muscular atrophy generally begins, like typical spinal muscular atrophy, in the muscles of the thenar and hypo- thenar eminences and in the interosseous muscles. Xext, the extensor muscles upon the dorsal aspect of the forearm and the deltoid are involved. The muscles waste progressively, become correspondingly weaker, exhibit fascicular (fibrillary) contractions and deg-enerative electric reaction. The condition can scarcelv be differentiated from chronic anterior poliomyelitis, upon which spinal progressive muscular atrophy depends, if partial anesthesia also is not present. The development of the symptoms is readily explained by the fact that the cavity has destroyed the large motor-trophic ganglion-cells in the anterior horns of the spinal cord. Partial anesthesia occurs in cases of syringomyelia together with or independently of progressive muscular atrophy, and is due to destruction of the posterior horns of the spinal cord, through which pass the paths for painful and thermal sensibility. It is not surprising, therefore, that loss of painful and thermal sensibility occurs. Needle-pricks are often appreciated only as touch. Often the skin is marked by the wounds of burns, which are frequently acquired from contact with a stove, the attention of the patients not being attracted to their wounds by the pain, but by the odor, of burning tissue. At times cold is felt as warm, and vice versa. SPINAL COMPRESSION-PARALYSIS 567 Among the trophic disorders ulceration, particularly on the fingers, should be mentioned, occurring and persisting without pain. At times also the terminal phalanges are exfoliated with- out pain. Often the phalanges become peculiarly shortened and thickened. Not rarely contracture of the aponeurosis of the hand is observed. Marked kyphoscoliosis in the upper dorsal portion of the spinal column frequently develops. At times painless fissures form upon the fingers. Bullae also often form, suggestive of herpes or pemphigus. At times a perforating ulcer develops. Spontaneous fracture of bones and alterations in joints are also known to occur. Among vasomotor manifestations erythema, edema of the hands or feet, anidrosis and hyperidrosis may be mentioned. Not rarely inequality of the pupils exists. Bulbar symptoms also develop when the cavity has invaded the medulla oblongata. Among the symptoms may be mentioned atrophy of the tongue, unilateral facial atrophy, paralysis of deglutition, paralysis of the muscles of the vocal bands, accelerated action of the heart, glycosuria, and polyuria. At times paralysis of the ocular muscles develops. Optic neuritis and contraction of the visual field also have been observed in a number of instances. At times the patients have exhibited ataxia or a spastic-paretic gait. The course of syringomyelia is chronic. Death results from accidental diseases, progressive marasmus, bulbar paralysis, bed- sores, or septicemia. Diagnosis. — The recognition of syringomyelia is easy in typical cases. Some of the symptoms are suggestive of nervous leprosy, but this disease occurs only in the tropics, and can be recognized bacterioscopically from the presence of leprosy -bacilli. The symptom-complex described by Morvan, and designated Morvan^s disease, and which is characterized especially by inflam- mation and painless exfoliation of the terminal phalanges, is only syringomyelia. Prognosis. — Syringomyelia is an incurable disease, and its prognosis is therefore unfavorable. Life may, however, be main- tained for many years. Treatment. — The treatment is limited to the relief of partic- ularly troublesome or dangerous symptoms. SPINAL COMPRESSION-PARALYSIS. Etiology. — Spinal pressure-paralysis results most commonly in consequence of disease of the spinal column. Tuberculosis of the vertebrae particularly, carcinoma of the vertebrae less com- monly, give rise to spinal pressure-paralysis. The condition may result also from luxation or fracture of the vertebrae, from arthritic or syphilitic exostoses, from thickening of the odontoid process, 568 NERVOUS SYSTEM and the like. At times processes that exert pressure upon the spinal cord enter the vertebral canal from without ; for instance, cheesy-tuberculous inflammation extending from the pleural cavity through the intervertebral foramina into the spinal canal ; carci- nomatous changes in the kidney, which have followed the same path in their extension ; aortic aneurysm, first perforating the vertebral column and then compressing the spinal cord ; and dis- integrating carcinoma of the esophagus, which injures the spinal cord after destruction of the vertebral column. Pressure upon the spinal cord sometimes arises from the spinal membranes, and occurs particularly in connection with meningeal hemorrhage, inflammation, and neoplasm. Disease of the spinal cord itself is also easily capable of exerting injurious pressure upon the dis- eased organ, particularly progressively growing tumors of the spinal cord. Spinal pressure-paralysis may occur at any period of life. Thus, it is not rarely induced in children by tuberculosis of the vertebrae. Anatomic Alterations. — Spinal pressure-paralysis is fre- quently attended with alterations in the vertebral column, partic- ularly kyphosis (gibbus). Under such conditions it may be inferred that stenosis of the vertebral canal is responsible for the compression of the spinal cord, although snch an occurrence is but seldom actually encountered. In the majority of cases the inflam- mation of the vertebrae or in the vicinity gives rise to inflamma- tion upon the outer surface of the spinal dura niater — external spinal pachymeningitis — and the pressure upon the spinal cord results as a secondary consequence. In the presence of tubercu- losis of the diseased vertel)r8e it is the rule, for instance, that in the vicinity of the diseased vertebrae thick, cheesy-tuberculous masses are present upon the outer surface of the dura, and these represent the actual cause of the compression. The eifects of the alterations named upon the spinal cord itself are variable. In some cases the spinal cord appears compressed, diminished in size, marked by a deep constriction, and not rarely hardened or sclerotic, although these occurrences are rather infrequent. More commonly either the spinal cord exhibits no alteration in size at the point of com- pression or it is widened, and on touch is found nnusually soft. On transverse section it rises above the level of the cut surface, appears of grayish or reddish-gray color, and its cut surface fails to ])resent the usual appearance or presents it but imperfectly. Also, after the spinal cord has been hardened in Miiller's fluid the confused appearance of the cut surface is visible, and even more distinctly than in the fresh state. Besides, it will be found, if the disease has existed for a considerable length of time, that second- ary degeneration of the anterior and lateral pyramidal tracts below and of the columns of Goll, the lateral cerebellar tracts, and Gowers' bundle above the point of compression has taken place. SPINAL COMPRESSWN-PABALYSIS 569 Microscopic examination discloses degeneration of nerve-fibers at the point of compression. Often naked axis-cylinders, whose medullary sheaths have been destroyed by granular disintegration and fatty degeneration, are conspicuous for their marked swelling. The neuroglia appears increased and generally contains numerous fatty granule-cells. The blood-vessels are often greatly distended and markedly tortuous. Here and there collec- tions of round cells are present in the neighborhood of the blood-vessels. In the gray matter of the spinal cord the ganglion-cells undergo swelling at first, and frequently present vacuoles ; subsequently they shrink into small structures without processes. It was formerly believed that all of these symptoms were inflammatory, and therefore the designation compres- sion-myelitis has also been employed ; but this is inappropriate, because the alterations are often in the main the results of anemic states and venous stasis, which necessarily are followed by the alterations in the meninges. Symptoms and Diagnosis. — The symptoms of spinal press- ure-paralysis are frequently preceded by prodromal local alterations in the vertebral column, particularly circumscribed spinal pain, appearing spontaneously or upon pressure, and distortion of the spinal coliunn, and at times also burrowing abscesses. Patients also often complain of a constricting girdle or hoop-like sensation about the trunk, which is induced by irritation of posterior nerve- roots. The distinctive symptoms of compression of the spinal cord t!onsist in signs of transverse interruption of the functions of the cord. At first these are incomplete, and involve the motor paths alone or principally, whilst subsequently sensory disturbances also become apparent. The predominance of motor symptoms is ex- plained by the fact that pressure-paralysis of the spinal cord is often associated with disease of the vertebral column, and this generally arises from the bodies of the vertebrae, which are in close proximity to the motor paths of the spinal cord. Besides, as has been determined by experiments upon animals, the motor nerves offer less resistance to pressure than the sensory nerves. Frequently the clinical picture begins with weakness in the lower extremities, which more or less quickly becomes transformed into complete j9ara/?/sis and compels the patients to remain in bed. The paralysis is at first flaccid. If the focus of pressure is situated in the upper portion of the cervical cord, the arms in addition to the legs will be paralyzed. The tendon-reflexes, as well as the cutane- ous reflexes, are generally increased. Often vesical disturbances are present, consisting at first in retention of urine (detrusor- paralysis), and subsequently in incontinence of urine (sphincter- paralysis). In consequence there may arise the danger of alkaline decomposition of the urine, cystitis, pyelonephritis, urinary infec- tion, bed-sores, and septicemia. Paralysis of the rectum also occurs frequently, and increases the danger of bed-sores and septicemia. The patients often complain of muscular twitching in the paralyzed members, and this may occur spontaneously or result from reflex irritation on palpation of the extremities, and is at times attended with severe pain. Not rarely severe shooting j^ain occurs parox- 570 NERVOUS SYSTEM ysmally in the paralyzed extremities. Paresthesice (formication, tingling, prickling, burning, a sense of cold) also occur. Cutaneous- anedhesia, in conjunction with paralysis, indicates almost total transverse interruption of the spinal cord. At first it is often in- complete, subsequently, however, becoming complete. Should demonstrable alterations in the vertebral column be absent, it will be important to determine the upper limit of anesthesia in order to localize the seat of pressure. Vasomotor and trophic disturb- ances (abnormal color of the skin, anidrosis, hyperidrosis, the for- mation of blisters) are not rarely observed. The course of the disease is generally chronic ; either there is a tendency to progressive aggravation, or periods of improvement and exacerbation frequently alternate with each other. Recovery is not impossible when the focus of pressure disappears and the compression of the spinal cord itself has not given rise to altera- tions in the substance of the cord of too serious a nature. When paralysis has existed for a considerable length of time, muscular contractures often develop, at first generally in the extensors, but subsequently in the flexors of the thighs and the legs. The diagnosis of a transvei^se lesion of the spinal cord is in itself generally easy, but insurmountable difficulties may arise in endeavoring to attribute the disturbance to spinal compression. In this connection the fact whether local alterations in the ver- tebral column (painful pressure-points, but especially deformities of the spinal column) are present or not, is particularly important. Should these be absent the diagnosis will remain doubtful. The de- termination of the nature of the compressing influence is also fre- quently attended with difficulty,, In early life pressure-paralysis of apparently spontaneous origin, with a projection of the verte- bral column, generally depends upon tuberculosis of the vertebrse. The presence of painful anesthesia is to a certain degree distinc- tive of carcinoma of the vertebrse. The patient under such cir- cumstances complains of the most intense pain in the extremities, whose cutaneous covering is totally insensitive. The condition is explained by the fact that the pressure of the new-growth upon the posterior spinal nerve-roots has interrupted the transmission of sensory impulses from the periphery to the brain, although irritation of the central terminations of the nerve-roots induces severe pain that is referred to the periphery. In order to deter- mine the cause of pressure-paralysis all the organs in proximity to the vertebral column should be examined most carefully. Progfnosis. — The prognosis of spinal pressure-paralysis is unfavorable under all conditions. Progressive exhaustion, paral- ysis of the bladder and urinary infection, bed-sores and septi- cemia, are the principal dangers. Some of the causes of compres- sion (carcinoma, aneurysm of the aorta) render the prognosis unfavorable by reason of their incurable nature. UNILATERAL LESIONS OF THE SPINAL CORD 571 Treatment. — Causal treatment should be employed when the pressure is of syphilitic origin, and it should consist in inunctions of mercurial ointment and the internal administration of potas- sium iodid (5.0:200 — 75 grains : Gg^ fluidounces ; 15 c.c. — 1 tablespoonful — thrice daily). Rest is necessary under all cir- cumstances. In addition, an ice-bag should be applied contin- uously over the focus of disease, and massage of the paralyzed members should be practised. Internally, potassium iodid may be essayed. Recently the vertebral column has been opened in several instances, and the compressing focus of disease removed. UNILATERAL LESIONS OF THE SPINAL CORD. etiology. — A unilateral lesion of the spinal cord is one that interrupts the functions of one-half of the cord. It may be caused Uppermost hy- peresthetic Anesthesia. Uppermost liypeves- thetic zone. Anesthesia (in conse- quence of injury to the sensory nerve- roots). Paralysis of motility and of the vasomo- tor nerves and hy- peresthesia. Fig. 79.— Diagram illustrating the symptoms of a unilateral lesion of the left half of the dorsal cord. by a punctured wound of the spinal cord, although it may develop also in connection with inflammation, hemorrhage, new-growths, and compression of the cord. Syinptoms and Diagnosis. — Unilateral lesions of the spinal 572 NERVOUS SYSTEM cord give rise to striking and readily recognized symptoms, namely, paralysis and cutaneous hyperesthesia upon the side of the injury and anesthesia upon the opposite side. Accordingly, spinal hemiplegia and crossed anesthesia are distinctive of a uni- lateral lesion of the spinal cord. Upon the paralyzed side the muscular sense, motor power, and electromuscular sensibility are diminished. Vasomotor and at times trophic disturbances also are observed. Reflex irritability is unaltered or increased. If the cutaneous hyperesthesia is traced upward, a narrow band of cutaneous anesthesia will be detected surrounding the trunk upon the paralyzed side from the middle line to the vertebral column, and referable to injury of posterior nerve-roots. Above this band is a hyperesthetic zone surrounding the trunk entirely (Fig. 79). The distribution of the phenomena described depends upon the seat of the disease, and at times is confined to the lower extremi- ties, while at other times it involves also the arms. In the pres- ence of disease of the cervical cord symptoms of paralysis of the sympathetic (contraction of the pupils, narrowing of the palpebral fissure, retraction of the eyeballs, redness and increased heat of one side of the face) are at times superadded. Occasionally paral- ysis of the bladder is present, with its sequelae and the develop- ment of bed-sores. ^Yith a lesion that progressively extends the clinical picture of a unilateral lesion may gradually disappear. The symptoms of a unilateral lesion of the spinal cord may be explained by the fact that a portion of the nerve-fibers in the spinal cord are uncrossed, while others are crossed. The uncrossed fibers (motor, vasomotor, trophic, muscular and dynamic sense, and muscular sensibility) must therefore be paralyzed upon the side of the lesion, and the uncrossed (sensory fibers) upon the uninjured side. The progtiosis and the treatment will depend upon the underlying diseases. System- Diseases of the Spinal Cord. SINGLE SYSTEM-DISEASES. TABES DORSALIS (POSTERIOR SPINAL SCXEROSIS; LOCOMOTOR ATAXIA). Btiology. — Tabes dorsalis is one of the most common, and at the same time by reason of its incurable character one of the most dreaded, diseases of the spinal cord. Most cases are sequels of syphilis. Those syphilitics are especially liable to the disease in whom the original disorder was not thoroughly treated. Generally many years have elapsed before the symptoms of tabes appear in the sequence of syphilis, but in isolated cases I have observed the symptoms as early as the second and the third year. Not alone TABES DOBSALIS 573 acquired, but at times also hereditary syphilis is believed to give rise to tabes dorsalis. Nothing is known concerning the intimate connection between tabes dorsalis and syphilis. It might, for instance, be supposed that syphilis induces a lessened resistance on the part of the spinal cord toother injurious influ- ences, which formerly were considered as the actual fundamental causes; or it is also possiljle that poisons (toxins) of the, as yet unknown, bacteria of syphilis cause injury to the tissues of the cord. Under either condition it must naturally be assumed that the nerve-fibers of the posterior columns of the cord or, in accordance with the most recent views, the posterior spinal nerve-roots are particularly susceptible to the injurious influences of the syphilitic poison. Although syphilis is the principal cause for tabes dorsalis, it cannot be considered as the sole exciting factor. Other infectious diseases also (typhoid fever, pneumonia, diphtheria, small-pox) may act as causes. The occurrence of toxic tabes dorsalis also has been recorded, developing after intoxication with ergot (ergotism) or spoiled maize (pellagra) and excessive indulgence in tobacco. At times tabes dorsalis develops in the sequence of traumatism, particularly concussion of the spinal column. The injurious influ- ence of cold cannot be wholly denied. Upon the other hand, nothing definite is known with regard to the etiologic significance of emotional disturbances, suppression of perspiration, and the like. Tabes dorsalis occurs most frequently between the thirtieth and fortieth years of life, and ten times more commonly in men than in women. Anatomic Alterations. — The distinctive anatomic lesion of tabes dorsalis consists in gray degeneration of the posterior columns of the spinal cord. This condition, however, appears to be second- ary and dependent upon disease of the intervertebral ganglia, and, in addition, the remainder of the nervous system also (cerebrum, cerebellum, peripheral nerves) may be involved. The latter fact explains the variability in the clinical picture. After opening the dura mater gray bands are often visible through the translucent pia mater, traversing the entire length of the spinal cord and diminishing in size from below upward, and being obscured from view only when the pia mater upon the posterior aspect of the cord is thickened, and hence rendered opaque. The related por- tions of the spinal cord situated between the posterior nerve-roots and the posterior columns of the cord frequently are remarkably small and generally feel indurated (sclerotic). On transverse sec- tion of the cord the posterior columns appear gray and slightly translucent. While this change involves the entire extent of the posterior columns in the lumbar region, including the columns of Burdach as well as those of Goll, toward the cervical portion it gradually becomes confined to the postero-internal or columns of Goll (Fig. 80). If the changes in the spinal cord are followed from below upward, they can still be recognized in the delicate 574 NERVOUS SYSTEM columns bounding the fourth ventricle, and at times they can be detected also in the peripheral layers of the pons Varolii and the qiiadrigeniinal bodies. It is noteworthy that islets of medullated nerve-til)ers always persist also in the most anterior portions of the posterior columns in the lumbar cord close to the gray com- missure. The difference in the ajipearanee of the anterior and the posterior spinal nerve-roots is striking, for while the former gen- erally preserve their usual size and natural, medullary-white ap- pearance, the latter are thin, gray, and almost translucent. On microscopic examination disappearance of the nerve-fibers and increase of the neuroglia are found in the diseased posterior columns. In all probability the atrophy of the nerve-fibers is the primary change, to which the increase in the neuroglia is added secondarily. In the hyperplastic neuroglia, which in advanced cases acquires a fibrillated ajjpearance, isolated fatty granule-cells and numerous amyloid bodies are not rarely present. The blood- vessels are often thickened and in places obliterated. Anatomic alterations are encountered also in the columns of Clarke and in the zone of Lissauer, in addition to the jjosterior columns of the cord. In the columns of Clarke, particularly when the spinal cord is stained by Weigert's hematoxylin-method, the disappearance of the finer nerve-fibers is conspicuous, while the ganglion-cells appear unaltered. Also in the zone of Lissauer, which forms the peripheral boundary of the posterior horns, atrophy of nerve-fibers with a double contour has taken place. Disappear- ance of the nerve-fibers, and in lesser degree of the ganglion-cells, occurs also in the posterior horns of the spinal cord. Examination o^ \\\e posterior spinal nerve-roots discloses atrophy and disappearance of the nerve-fibers and increase of the con- nective tissue. Atrophic disappearance of the ganglion-cells and connective-tissue proliferation have been demonstrated likewise in the intervertebral ganglia, although the alterations in the posterior nerve-roots not rarely predominate. In the cerebral cortex and in the cerebellum disappearance of nerve-fibers, in the latter also that of the ganglion-cells and blood-vessels, has been described. De- generation and disappearance of the ganglion-cells in the nuclei of the cerebral nerves is noteworthy, but also in individual cerebral nerves themselves degeneration and disappearance of nerve-fibers and hyperplasia of the connective-tissue occur in their trunks as well as in their intramedullary course. Degeneration and dis- appearance of nerve-fibers in the peripheral nerves should not be overlooked. These alterations occur particularly in the finer cutaneous branches, but are observed also in the larger nerve- trunks. It has already been pointed out that the lesions of tabes dorsalis are dependent upon degenerative and not inflammatory alterations in the nerve- fibers of the spinal cord. It appears that this nerve-degeneration does not begin primarily in the spinal cord, but originates in the ganglion-cells of the intervertebral ganglia. As is well known, each of these ganglion-cells TABES DORSALIS 575 gives off a process, whicli soon divides into two branches, one of which enters a peripheral nerve and the other the posterior column of the spinal cord. As a result of morbid activity on the part of the ganglion-cells de- generation and atrophy take place in the branch passing to the spinal cord, and these may bring about the anatomic alterations of tabes in the poste- rior columns. In harmony with this view is the fact that the alterations become more restricted to the columns of GoU the higher up in the cord they are situated, as fibers from the nerve-roots entering the lowermost portion of the cord become gradually displaced toward the median portion of the posterior column as they ascend. Just why the process begins in the intervertebral ganglia of the lumbar cord has not yet been determined. Only rarely does tabes dorsalis begin in the cervical cord, when the disease may be confined to the postero-external (Burdach's) columns. The condi- tion is then designated cervical tabes dorsalis. Symptoms. — Among the symptoms of tabes dorsalis a dis- tinction should be made between constant (typical) and accidental symptoms. The former particidarly are of diagnostic significance, and they alone depend upon the typical seat of the disease, while the accidental symptoms vary accordingly as in the individual case one or another portion of the nervous system becomes in- volved. The typical symptoms of tabes dorsalis include absence of the knee-jerks, reflex pupillary immobility, swajring station, and ataxic gait. Ahsence of the knee-jerks, also known as Westphal's symptom, is one of the earliest and most constant signs of tabes dorsalis, and there should always be some hesitancy in making a diagnosis of tabes dorsalis if the knee-jerks are preserved unchanged. The phenomenon is explained by the fact that in the presence of tabes dorsalis the spinal reflex arc is interrupted. This interrup- tion was formerly believed to occur in the posterior columns of the spinal cord at the junction of the dorsal and lumbar portions, within the so-called root-entrance zone. In accordance with more recent views with regard to the development of tabes dorsalis, however, it is probable that the interruption of the spinal reflex arc occurs in the degenerated posterior nerve-roots, and the second, third, and fourth lumbar roots are those especially involved, I have been able to demonstrate by clinical observation that also in cases of cervical tabes the knee-jerks may be absent if in addition to the tabes inflammation of the crural nerves also exists. In view of the great significance of absence of the knee-jerks in the diagnosis of tabes dorsalis it is exceedingly important to avoid all sources of error in the examination. The extremity to be examined must be perf^ectly relaxed, and is either crossed over the opposite member or is permitted to hang witbout constraint over the edge of a chair or of the bed. It is highly useful to employ the expedient of Jendrassik, the patient during the examination forcibly pull- ing his clasped hands apart or forcibly squeezing the finger of the exam- iner. By means of such devices the attention of the patient is involuntarily diverted from the examination of the knee-jerk and the member is relaxed unconsciously. The suspicion of tabes dorsalis will be increased if in addition to absence of the knee-jerks there is also reflex pupillary immobility. This sign is known also, after its discoverer, as Robertson's symp- 576 NERVOUS SYSTEM torn. This is developed by having the patient look toward the sky from a bright window while light is excluded from the eyes by means of the hands held before the eyes. If now one or both hands are suddenly re- moved from before the eyes, contraction of the Middle of the olive — ^BS^I^^^ pupils on exposure to light fails to take place. The size of the pupils re- mains the same in the dark Just below the pyramidal £^^ and on exposure to light. decussation W^P^Ss n^, ^ -n ihe sensory pupillary re- action likewise is wanting ; Upper cervical portion -- «^i ^}]f^ i^'.^" pricking the skin ^w.^rirvnaf clilatatiou 01 tlic pupil lails to take place. The reac- Cervical enlargement fi^^^B ^^^^ ^^ ^^^^ pupil in ac- commodation, however, is preserved, so that the pu- Lower cervical portion - B^^^B pil'' become dilated in dis- tant vision, while they be- ^B^zESJBM come contracted in near Lower cervical portion ^MwW^B vision ®0f less diagnostic signifi- cance is the fact that the pu- pils are not rarely contracted ^^^^ — spinal mijosis — or are un- Mid-dorsal portion ^S^m equal. eWhen the eyes are closed the body sicays m arkedly — Bracht-Rom- Commencementofthelum- .^Sf& ^^^'9 Symptom. This not bar enlargement " ^|^^^ rarely becomes so marked that the patients are in Middle of the lumbar en- ^^ danger of foiling. Often largement ^|^^ tlie patient has noticed Mgf^ the symptom first when Lowermost lumbar portion -^^ in washing the face he has Fig. 80.— Transverse sections of the spinal cord been compelled tO cloSC hlS presenting advanced degeneration of the posterior eyCS columns from a man r>'2 years old. The degenerated ^ ' , areas are light, as they appear in the spinal cord AtaXlCL IS SO Constant a hardened in Mliller's fluid. , j? j. i i i* Natural size; from transverse sections of the SymptOm OT taOCS (lOrsallS spinal cord hardened in Midler's fluid (personal +i,„f fKo rliooooo line olcrv observation, Zurich clinic). ^"^^ l^''^ Clisease lias dlbO been designated progres- sive locomotor ataxia. It can be recognized in walking from the fact that the patient holds the legs far apart and brings the feet down upon the heels, raising the extremities unnecessarily high, and at the TABES DORSALIS 577 same time making awkward and jerky movements. The gait is also appropriately characterized as sfringhalt-like. If the patient be requested to place one foot in advance of the other in walking, or if he make an attempt to walk upon a crack in the floor or upon a chalk-line, he will be able to do any of these with extreme difficulty and awkwardness, if at all. On lying in bed the ataxia of the legs will be shown by the fact that in elevating one of the members it will oscillate to and fro and be thrust beyond the mid- dle line toward the opposite side. All ataxic disturbances are increased in the dark, when the patient is unable to guide the movements with the aid of vision. Ataxic movements are not uncommon also in the arms. They may be readily recognized if the arms are widely separated when the eyes are closed and an attempt is made to bring the finger-tij)S together. In ataxic patients to-and-fro movements in the air will follow for some time before the finger-tips are brought in contact. Much discussion has taken place as to the mode of origin of the ataxia. In our opinion the view of Leyden is the most likely, and according to which the ataxia is the result of sensory disturbances, not alone cutaneous sensi- bility, but particularly also the sensibility of the deeper structures (muscles, tendons, fascia, joints), being affected. Possibly disturbances in the reflex paths in the spinal cord may be operative. Some clinicians have attributed the ataxia to disease of deffnite spinal tracts supposed to possess coordinative activity (lateral cerebellar tracts), but nothing is known with regard to the existence of such tracts. The typical symptoms of tabes clorsalis thus far considered de- velop slowly, and generally with prodromes. The latter include with especial frequency pain in the course of one or both sciatic nerves, at times attacks of headache and vomiting, vertigo, and the like. Among the accidental symptoms of tabes dorsalis sensory dis- turbances particularly predominate, and this can be readily under- stood from the fact that the morbid process develops especially in the sensory sections of the cord ; but motor, trophic, secretory,, and vasomotor manifestations, together with visceral disturbances, also occur not at all rarely. In view of the great variability in the symptoms, a brief consideration of the most important of them must suffice. Sensory disturbances are scarcely ever wholly absent. Often the patients complain of paresthesise, particularly the crawling of ants, prickling, burning, a sense of cold, and shooting pains. Often complaint is made of a painful girdle- sense about the trunk, and but seldom of pain in the vertebral column itself. Cutaneous anesthesia is frequently encountered, at times total, at other times partial. The anesthesia is generally most pronounced on the soles of the feet, and progressively dimin- ishes toward the trunk. Often the patients complain of not feel- ing the floor beneath their feet, and in M^alking they appreciate a 37 578 NERVOUS SYSTEM sensation as if tliey were treacling upon wool, or were going about in rubber shoes or on pigs' bladders. At times poltjesthesia is observed, the application of a needle upon tlie skin being felt as a multiple irritation. Quite often the conduction of sen- sory stimuli is retarded, at times more than ten seconds elapsing before the patient indicates that he feels the prick of a needle. Duplicate sensations are occasionally observed. Either a single needle-prick is felt by the pa- tient at first as touch and after some time as pain, or at first slight and after a few seconds a more marked perception of pain occurs. Not rarely the sensory impression persists for a long time. Frequently disturbances of the muscular sense are demonstrable, and when the eyes are closed the patient is incapable of deter- mining which of the two members placed at different levels is the higher, which is the more flexed, and the like. Paralysis plays a rather subordinate part in the clinical picture of tabes dorsalis. At any rate, it has nothing to do with the occurrence of the ataxia, for in spite of marked ataxia the motor power in the lower ex- tremities may be unaltered. At times paralysis in the distribution of certain nerves (peroneal, radial) appears early. This has been attributed to periplieral neuritis, which may gradually subside and undergo perfect recovery. Muscular contractures and muscular twitching are less common manifesta- tions. Among trophic disorders the tabic articular changes especially have long attracted attention. The large joints are attacked with especial frequency, particularly the knee-joints. As a rule, the joints become enlarged, and they are at the same time but little, if at all, tender to touch, and after the articular enlargement has sub- sided deformity and ankylosis may persist because the articular extremities are greatly distorted. Among other trophic disorders in the course of tabes dorsalis there may be mentioned abnormal fragility of the bones, an ujidue tendency to laceration on the part of certain tendons, particularly the Achilles tendon, hemiatrophy of the tongue, perforating ulcer of the foot, herpes zoster, thickening af the nails, loss of the teeth, the nails, and the hair, etc. Vasomotor and secretory disorders are revealed by unusual red- ness and heat of the skin, by hyperidrosis, increased secretion of saliva and of tears, and the like. Among the visceral disturbances of tabes dorsalis the visceral crises deserve first mention. These consist in sudden attacks of pain and functional disturbance in certain organs. Gastric crises are the most common and the best known. These consist in attacks of severe epigastric pain with profuse vomiting, which may persist for days, and is at times attended with an excess of hydrochloric acid. If the attacks are repeated in quick succession, the patient may become exhausted in an alarming degree. Often such patients are treated for years for chronic gastric catarfh, and are sent each summer to health-resorts TABES DORSALIS 579 before the real nature of the gastric disorder is recognized. At times gastric crises deviate from the typical picture described in so far as they are attended either with severe epigastric pain alone or only with profuse vomiting without such pain. Among other visceral crises intestinal crises may be mentioned. These are attended with paroxysmal attacks of diarrhea, usually accompanied by colic. Rectal crises are attended with burning pain in the rectum. Renal crises suggest the clinical picture of renal colic, and are attended with severe pain in the loin, but they are generally unattended with albuminuria and hematuria. Laryngeal crises are characterized by attacks of cough and dyspnea resembling whooping-cough or laryngismus stridulus. Pharyngeal, bronchial, cardiac, clitoral, and urethral crises also have been described. Among other visceral manifestations ocular changes deserve first place on account of their diagnostic importance. Not rarely optic atrophy develops, and may give rise to gradual blindness. At times blindness occurs early, so that the patients must bear the burden of their disease for many years in a blind state. Paral- ysis of the ocular muscles is often present, and it may disappear after a time, being probably more frequently dependent upon peripheral neuritis than upon disease of the nuclei of the nerves. Paralysis of the laryngeal muscles also is not rarely observed in the course of tabes dorsalis. The statement that tabic patients present valvular lesions of the heart with especial frequency I am unable to confirm from personal observation. Frequently, and at times early, symptoms of paralysis of the bladder occur. These may appear and disappear repeatedly in the course of the disease. Eventually they may persist, and then are attended with the dangers of urinary infection and of bed-sores. In men impotence not rarely occurs early. Women, however, may, in spite of ad- vanced tabes dorsalis, conceive and bear children in the usual manner. The course of tabes dorsalis is chronic, and the disease often extends over many years. Attempts have been made to distin- guish several stages of the disease, although all such divisions are somewhat artificial and of slight practical value. Should the ataxia in the lower extremities become excessive, the patients will be unable to move about alone, even with the aid of a cane, and will be compelled to remain constantly in bed. At times in at- tempts at walking the patient may stumble over his own feet and fall to the ground. After the patient has been confined to bed for a long time atrophy of the muscles of the lower extremities develops from disuse, with a condition of weakness and the devel- opment of muscular contractures. At times apoplectiform attacks occur with hemiplegia, the latter disappearing ; but if dependent upon thrombosis of cerebral arteries the paralysis may persist. The mental state of the patient is often stated to be an abnormally ciieer- ful one. I should rather describe it as one of fatalistic resignation. Psychic disturbances occur, and predominate from the outset in 580 NERVOUS SYSTEM cases in wliicli tabes dorsalis occurs in connection with progressive paralysis of the insane. Death takes pkice in consequence either of accidental disease (pneumonia, puhiionary tuberculosis) or of progressive exhaustion, or of urinary infection or septicemia ; at [times also with the occurrence of a soporose state of sudden onset. I Diagnosis. — In the diagnosis of tabes dorsalis reliance should be placed upon the four typical symptoms : Absence of the knee- jerks, reflex pupillary ihimobility, unsteadiness in station, and 'ataxia. Confusion with peripheral pseudotabes may readily occur 'when this condition develops as a result of polyneuritis. Peripheral pseudotabes occurs with particular frequency and distinctness in connection with alcoholic, diabetic, postdiphtheric, and toxic poly- neuritis. Although the reaction of the pupils may be exceedingly sluggish in the presence of polyneuritis, reflex jiupillary immo- bility scarcely ever occurs, and the presence of the latter, there- fore, is always indicative of tabes dorsalis. Tabes dorsalis Mill scarcely be confounded with cerebellar ataxia, because the knee- jerks are preserved in the presence of cerebellar disease. Heredi- tary ataxia often develops during childhood, and is attended with nystagmus and articulatory disturbances. Prognosis. — The prognosis of tabes dorsalis is unfavorable with regard to recovery, although life does not appear to be im- mediately threatened, and if the patient does not come under pro- fessional observation too late material improvement may at times be brought about. Treatment. — As syphilis is the cause of tabes dorsalis in the majority of cases, it might be supposed that in such cases causal therapy with mercurial inunctions (5.0—75 grains — daily) and potassium iodid (5.0 : 200 — 75 grains : 6 J fluidounces ; 15 c.c. — 1 tablespoonful — thrice daily) would yield good results. Too much, however, should not be expected in this connection. Im- provement fails to take place in the majority of cases, or under the most favorable circumstances it is but slight. This is prob- ably due to the fact that the patients generally come under pro- fessional observation too late, and that under the most favorable circumstances preparations of mercury and of iodin are capable only of arresting the morbid process or checking the course of the dis- ease, and not of effecting recovery. Such nerve-fibers as are already degenerated are lost forever. Nevertheless, antisyphilitic treatment should always be advised, and it should even be repeated from time to time. Among internal remedies, I have in a number of cases observed surprising results from the use of ftUver nitrate, while the remaining large number of nervines have been dis- appointing : R Silver nitrate, 0.3 (4J grains) ; Aluminum hydrate, sufficient to make 30 pills. Dose : 1 pill thrice daily. SPASTIC SPINAL PARALYSIS 581 Gymnastic exercises with tlie lower extremities, and if neces- sary also with the upper extremities, are to be warmly recom- mended. Tlie patient is, for instance, instructed to walk several times daily upon certain lines and figures, and as a result the ataxic disturbances not rarely subside, and the power of locomo- tion is greatly improved. I have in a number of cases also observed material improvement in the power of locomotion as a result of treatment by suspension. Not much can be accomplished by courses of treatment at the baths (saline, sulphurous, indiiferent baths, courses of treatment with cold water). Well-to-do patients may be advised to pass the winter in mild climatic resorts (Riviera), in order to be in the open air as much as possible. A sea-voyage also may be recommended. For neuralgias, antipyrin (1.0 — 15 grains — thrice daily) or phenacetin (1.0 — 15 grains — thrice daily) may be employed. At times subcutaneous injections of morphin must be resorted to. These constitute also the most reliable means of relieving severe visceral crises. The faradic and the galvanie current will not aiford any material relief. SPASTIC SPINAL PARALYSIS. l^tiology and Anatomic Alterations. — Disease of the lat- eral pyramidal tracts is believed to be the cause of spastic spinal paralysis. Although the clinical picture of spastic spinal paral- ysis is by no means rare, it has been shown that it generally results in consequence of other diseases of the spinal cord, while it occurs with exceeding rarity as an independent disorder. It is encountered with especial frequency in connection with myelitis, spinal pressure-paralysis, multiple cerebrospinal sclerosis, com- bined system-disease of the spinal cord, and syphilitic spinal paralysis. Spastic spinal paralysis develops not rarely in children when in consequence of protracted or artificial labor, or during teething, or after infectious diseases cerebral paralysis occurs, at times in the form of monoplegia, at other times of hemiplegia, and at still other times of paraplegia. The condition is known also as spastic rigidity of the extremities or Little's disease. Exposure to cold, infectious diseases, and alcoholism are mentioned as causes of independent spastic spinal paralysis, although actually little of a definite nature is known in this connection. Symptoms, Diagnosis, and Prognosis. — The symptoms begin generally in tlie lower extremities. Muscular weakness de- velops, and may progress to marked paralysis. At the same time muscular contractures appear, jjarticularly in the extensors and the adductors of the thigh and in the flexors of the foot. The gait assumes the character that has been designated spastic-paretic. The tendon-reflexes are abnormally increased. Sensibility and the 582 NERVOUS SYSTEM functions of the bladder and the rectum, however, remain undis- turbed. The spudk-pa.rctic gait is characterized by a peculiar rigidity of the lower extremities, which in talking are applied firmly to the o-round like stilts. The extremities are scarcely flexed at the hip and the knee, and the thighs can be moved in front of each other only with great difficulty on account of adductor-C(>ntrac- ture, so that often the pelvis is greatly rotated in walking. Con- tractures of the muscles of the calf often give rise to pes equinus, so that the patient in walking first applies the toes to the ground, and in consequence of exaggeration of the tendon-reflexes the legs are set into tremulous and agitated movement. If the morbid process advances, contractures gradually develop in the flexors of the thigh and the leg, and these render walking wholly impos- sible. Exaggeration of the knee-jerks will be manifested by marked and persistent contraction in the extensor of the thigh after even a slight blow with the plexor. At times reflex muscular twitching occurs as well in members not percussed. Ankle-clonus also is ex- aggerated ; and if with the leg extended dorsal flexion of the foot is practised suddenly, active flexion and extension of the foot take place, which not rarely can be prevented intentionally by rapid dorsal flexion of the great toe.^ If the arms are involved, active reflex muscular contraction will follow percussion of the extensor tendons of the forearm or the tendon of the triceps. The peri- osteal reflexes also are abnormally increased. The duration and the curability of the symptoms depend upon the nature of the primary disorder. In cases of independent spinal paralysis complete recovery has been observed at times in the course of a few weeks. Treatment. — Treatment should be directed, in the first place, to the primary disorder — causal therapy. In cases of independent spastic spinal paralysis hot baths, nervines, electricity, and mas- sage have been employed. DISEASE OF THE GANGLION-CELLS OF THE AN- TERIOR HORNS r ANTERIOR POLIOMYELITIS). Poliomyelitis indicates only inflammation in the anterior horns of the spinal cord, btit the structures upon which the characteristic features of the clinical picture depend are the multipolar, motor- trophic ganglion-cells in the anterior horns, whose destruction is followed by flaccid paralysis of the related muscles, rapidly de- veloping degenerative muscular cdrophy, degenerative electric reac- tion in the diseased nerves and muscles, abolition of the reflexes, ^ Irritation of the sole of the foot induces extension of the great toe and per- haps also of the remaining toes. — A. A. E. DISEASE OF GANGLION-CELLS OF ANTERIOR HORNS 583 with preservation of cutaneous sensibility and of the functions of the bladder and the rectum. In accordance with the course of the dis- ease and the age of the patient, several clinical varieties may be distinguished, namely : acute spinal paralysis of childhood ; acute, subacute, and chronic spinal paralysis of adults; spinal progres- sive muscular atrophy. ACUTE SPINAL PARALYSIS OF CHILDHOOD. l^tiology. — Acute spinal paralysis of childhood is one of the most common diseases of this period of life, and experience has shown that it is more common in boys than in girls, and that it occurs especially at the period of dentition, and from that time on to the fourth year of life. There is a tendency at the present day, and not without reason, to assume the occurrence of infection in many cases, as in the first place the entire course of the disorder corre- sponds in many respects with that of an acute infectious disease, and in addition the disease occurs at times in endemic or epidemic distribution. Besides, exposure to cold, traumatism, fright, and emotional disturbances generally, difficult dentition, and antecedent infectious disease are assumed to be causative factors. Anatomic Alterations. — The alterations of acute spinal paralysis of childhood arise from the blood-vessels of the anterior horns. These are dilated and extremely tortuous, ruptured in places, and presenting in their adventitial lymph-sheaths, as well as outside of these, accumulations of round cells. The ganglion- cells are swollen, plump, in part deprived of their processes, and they are likewise surrounded by round cells. In the fresh state the inflammatory area presents a blood-red and softened appear- ance. Subsequently it becomes converted into a sort of cicatricial, sclerotic, and contracted tissue, which contains but a few, if any, ganglion-cells, and may persist throughout the rest of life. Even after the lapse of many years the disease-focus is recognizable from the contraction and diminution in size of the anterior horn. The disease is at times unilateral and at other times bilateral, and it may appear as a small, circumscribed focus or as an extensive process, or as a number of disseminated foci. In the anterior nerve-roots related to the foci of disease degeneration and disap- pearance of nerve-fibers are found — alterations that may be traced in the peripheral nerves to the muscles. In the muscles atrophy of muscular fibers takes place, with increase in the connective tissue, the latter being not rarely well supplied with fat-cells. The atrophic muscular fibers are characterized by an abundance of sarcolemma-nuclei, and often also by unusual distinctness of their transverse striation. Other muscle-fibers exhibit fibrillation and vitreous degeneration. In addition to atrophic muscle-fibers, here and there also hypertrophic fibers are present, which not rarely contain vacuoles and accumulations of nuclei. 584 NERVOUS SYSTEM Symptoms. — Should acute spiual paralysis of childhood de- velop like au acute infectious disease, it begins suddenly, or, after a sense of general malaise has been present for a few days, with high fever, delirium, stupor, general clonic spasm ; and if, after the lapse of some hours or a few days, consciousness returns and the fever has disappeared, the paralysis is noticed. In other instances naturally the paralysis has developed quite insidiously and without antecedent febrile prodromes. The child may have appeared perfectly well on retiring, and awakes on the following morning paralyzed. Under such conditions there is great danger that the paralysis will be overlooked by the family for some time, and possibly it is discovered only by accident. Most commonly in cases of spinal paralysis of childhood the lower extremity, and with especial frequency the left, is the seat of the paralysis, and even in the leg the condition is often one of partial paralysis only, involving preferably the distribution of the peroneal nerve. In other instances, in accordance Avith the seat of the focus of inflam- mation, there may be paraplegia of the lower or of the upper ex- tremities, total paraplegia, hemiplegia, or crossed hemiplegia. In- volvement of the cerebral nerves, as, for instance, the facial nerve, is extremely rare. At times a portion of the paralysis subsides in the course of a few days — so-called temporary para/i/sis — a manifestation that is dependent upon the fact that some ganglion-cells are not de- stroyed, but are unduly compressed, so that they resume their functional activity after absorption of inflammatory products has taken place and the excessive pressure has been removed. It does occasionally happen that the paralysis wholly disappears, but this is exceedingly rare, and those parts that are paralyzed after the lapse of four weeks, experience has shown, remain always paralyzed. The muscular paralysis is invariably of flaccid type, so that the paralyzed members can be moved passively to and fro without resistance. Toward the end of the first week emaciation becomes noticeable in the paralyzed muscles, and this increases from week to week ; it appears and advances too rapidly to be explained as the result of atrophy from disuse. In conjunction with progressive wasting degenerative electric reaction in the paralvzed muscles and the related nerves and increased meclianical muscular irritability occur. Sensory disturbances are wanting as a rule. At times para- lyzed nerves and muscles are sensitive to pressure. Older chil- dren occasionally complain also of a sense of dragging and even of painful sensations along the vertebral column at the onset of the disease. As the spinal reflex arc has been interrupted by the disease of the ganglion-cells of the anterior horn, it will be understood that all reflex movement will be wanting in the paralyzed parts. Vasomotor disturbances are frequently present. DISEASE OF GANGLION-CELLS OF ANTERIOR HORNS 585 The skin of the paralyzed member presents a cyanotic appear- ance and generally feels cool. Trophic disturbances likewise have been observed. The skin of the paralyzed parts frequently pre- sents an unusually thick layer of adipose tissue, which in part conceals the marked wasting of the paralyzed muscles. Also, in the muscles themselves active deposition of fat takes place, Mdiich in part neutralizes the loss of actual muscular tissue. It is note- worthy also that the bones are notably retarded in growth, are thin and unusually brittle, and when the child has grown up the paralyzed member at times forms only a small appendage. Even tendons, fascise, and blood-vessels in the distribution of the mus- cular paralysis fail to grow normally. The functional activity of the bladder and the rectum does not suffer. Muscular contractures develop frequently in the course of the disease, and they may give rise to marked deformities and in- terference with the function of the paralyzed members. Abnormal demands upon the healthy muscles, the weight of the bed-cloth- ing, and similar circumstances are the causative factors for such muscular shortening. Under such conditions club-foot of any variety may develop, as well as spinal curvature, flail-joint, and the like. Poor patients may pass through life as cripples, and utilize their infirmity as a means for exciting the sympathy of those in better circumstances. They often devise ingenious appa- ratus for the purpose of neutralizing the functional disturbance in the legs or the arms, as, for instance, supports, upon which they can move about, rolling vehicles, and the like. The course of the disease is chronic, and the patients often attain advanced age. Occasionally symptoms of spinal progressive mus- cular atrophy develop at a later period. Other patients become idiotic and epileptic. Some are greatly burdened by excessive obesity, to which many patients are predisposed by sedentary pur- suits and deficient activity. DiagtiosiS. — The recognition of acute spinal paralysis of childhood is easy. The disease might most readily be confounded with acute polyneuritis, but with the latter nerves and muscles are generally sensitive to pressure, and, in addition, various sensory disturbances are present. Parturitional or obstetric palsies (p. 499) have existed from birth, and in cases of spastic spinal paralysis the tendon-reflexes are exaggerated. Prognosis. — Although, as a rule, the disorder is unattended Mnth danger to life, nevertheless the prognostic outlook is not favorable, because the paralysis does not subside and nmscular contractures and deficient growth of the bones increase the in- firmity. Treatment. — The treatment varies with the stage of the dis- ease. During the prodromal febrile period a hot bath (28° R. — 35° C. — 95° F. for fifteen minutes) should be given, an ice-bag 586 NERVOUS SYSTEM applied to the head, and, if the child can swallow, phenacetin (0.8 — 4^ grains — twice daily) or antipyrin (0.3 — 4^ grains — twice daily) administered internally. The application of an ice-bag to the vertebral column may also be advised. For the paralysis, massage should be practised daily. At the same time varied passive movements of the joints should not be omitted, in order to prevent as much as possible the development of contractures. The application of electricity to the spinal cord and to the para- lyzed muscles will be attended with as little success as the internal administration of the various nervines. Little also is to be ex- pected from baths (saline or sulphurous or indifferent thermal baths). On the other hand, surgical and orthopedic measures may yield good results in the presence of contractures. ACUTE, SUBACUTE, AND CHRONIC INFLAMMATION OF THE GANGLION-CELLS OF THE ANTERIOR HORNS IN ADULTS (ACUTE, SUBACUTE, AND CHRONIC POLIOMYELITIS OF ADULTS). Acute anterior poliomyelitis of adults in its clinical course most closely resembles acute spinal paralysis of childhood. It is, on the whole, a rare disease, which experience has shown is more common in men than in w^omen, and which generally occurs before the thirtieth year of life. It has been observed in the sequence of infectious diseases (puerperal fever, gonorrhea). I have had under observation individuals in whom the affection gave the impression of being an independent infectious disease. Exposure to cold, ti-au- matism, over-exertion, and alcoholic and venereal excesses also are capable of acting as causes. The disease begins with feb7'ile pro- dromes. Often a chill occurs at the beginning, followed by high fever, stupor, and delirium — a condition that often persists for one or two weeks. Clonic convulsions are, however, commonly absent, perhaps because the motor cortical centers are more resist- ant in adults than in children. 3Iuscular jxirali/sis then generally sets in suddenly, and, as in cases of spinal paralysis of children, it is of flaccid type, is attended with rapid degenerative wasting, degenerative electric reaction, and increased mechanical irrita- bility, with loss of the cutaneous and tendinous reflexes, while sensibility and the functions of the bladder and the rectum exhibit no derangement. At times the paralyzed nerves and muscles are sensitive to pressure, and the overlying skin is often mottled blue and feels cold. Further, the paralysis at times subsides in part — temporary paralysis — and in individual rare cases the paralysis has disappeared entirely. The paralysis disappears especially from such muscles as exhibit no degenerative electric reaction. The distribution of the paralysis varies, as with spinal paralysis of childhood, between monoplegia, paraplegia, hemiplegia, and paral- DISEASE OF GANQLION-CELLS OF ANTERIOR HORNS 587 ysis of individual neuromuscular areas. Cerebral nerves are but rarely affected. After the paralysis has existed for some time muscular contractures may develop. Disturbances in growth of bones, tendons, fasciae, and blood-vessels do not occur, because the members of the patient are fully developed. The diagnosis, the prognosis, and the treatment are the same as for acute spinal paralysis of childhood. Subacute and chronic anterior poliomyelitis of adults is due to the same causes as the acute variety, is likewise one of the less common diseases of the spinal cord, and develops generally between the thirtieth and the fiftieth year of life. The disorder sets in in- sidiously without antecedent febrile manifestation, most commonly in the extensors of the leg, tlien slowly invading the muscles of the trunk and the arms, and even those supplied by the cerebral nerves. Less commonly the onset is marked by paralysis in the arms, and this may then extend to the legs. The disease is pro- gressive in course, although it may happen that the paralysis sub- sides spontaneously in part or at times even entirely — temporary paralysis ; although, on the other hand, danger exists that the dis- ease may involve cerebral nerves (hypoglossal, vago-accessory, glossopharyngeal), and death resnlt from inspiration-pneumonia or paralysis of respiration or of cardiac action. Accordingly as the muscular paralysis develops within a few weeks or many months a distinction is made between subacute and chronic polio- myelitis. The character of the paralysis is that already described for anterior poliomyelitis (flaccid paralysis, rapid degenerative muscular atrophy, degenerative electric reaction, abolished reflexes, preservation of cutaneous sensibility, retained functional activity of the bladder and the rectum). AVhen the paralysis has existed for some time muscular contracture may develop. The duration of the disease may extend over four years. The anatomic alterations consist in disappearance of the large motor-trophic ganglion-cells in the anterior horns. In addi- tion, changes in the blood-vessels (thickening of the wall, nuclear nuiltiplication and hyperplasia of the neuroglia) may occur. De- generation and atrophy of nerve-fibers also have been found in the anterior nerve-roots and in the peripheral nerves. In some cases areas of degeneration have been found in some columns of the cord and disappearance of ganglion-cells in the columns of Clarke. The diagnosis is not always easy. Subacute and chronic anterior poliomyelitis is distinguished from spinal progressive mus- cular atrophy hj the fact that progressive muscular atrophy gener- ally begins in the muscles of the hand, that atrophy of the muscles precedes paralysis, and that the atrophy involves the muscles only in bundles (fascicular), and not totally as in cases of anterior polio- myelitis. Amyotrophic lateral sclerosis is attended, in addition to muscular wasting and contractures, especially with exaggeration 588 XERVOUS SYSTEM of the tendinous and periosteal reflexes. Finally, in the presence of progressive polyneuritis sensory disturbances are generally pres- ent in addition to motor disorders. The prognosis and the treatment are the same as for acute spinal paralysis of childhood. SPINAL PROGRESSIVE MUSCULAR ATROPHY. Ktiology. — Little of a definite nature is known with regard to the etiology of spinal progressive muscular atrophy. The dis- ease, which is uncommon, occurs more frequently in men, and, as a rule, develops only after the thirtieth year of life. Among the causati ve factors exposure to cold, over-exertion', traumatism, and antecedent infectious disease have been mentioned. In exceptional instances spinal progressive muscular atrophy has been observed in persons that in early life had suffered from spinal paralysis of chUdhood. On the other hand, heredity, in contradistinction from the myo- pathic form of progressive muscular atrophy, is not of especial etiologic significance. Anatomic Alterations. — There is a great deficiency in good and reliable anatomic descriptions. The disease is characterized by disappearance of the large motor-tropliic ganglion-cells in the anterior horns of the spinal cord. At the same time the ganglion- cells frequently become filled with yellowish or yellowish-brown, granular pigment, undergo progressive contraction to small round- ish structures without processes (so-called pigmentary degenera- tion of the ganglion-cells), and finally undergo c(miplete destruc- tion, while neuroglia takes their place. The destruction of each ganglion-cell is necessarily followed by degeneration of the entire spinal-peripheral neuron, and accordingly degeneration and atrophy of the nerve-fibers can be traced in the related anterior nei-ve-roots of the spinal cord and in the peripheral nerves to the muscles. The diseased muscles exhibit marked atrophy and a light, usually brownish color. The loss of individual muscle-fibers can be seen with especial distinctness on transverse section, while the inter- stitial connective tissue is abnormally increased and generally contains many nuclei. In many places muscle-fibers are replaced by remains of granular, yellow or brownish pigment. Here and there abnormally dilated blood-vessels with thickened walls can be seen. In addition to atrophic muscle-fibers a greater or lesser number of hypertrophied muscle-fibers are present, and which not rarely exhibit vacuoles and nests of nuclei. The disapi^earance of the muscuhir fibers occurs in various ways. Mus- cular fibers can be seen that are characterized by marked diminutiveness, distinct transverse striation, and an abundance of sarcolemma-nuclei. Other muscle-fibers, on the other hand, exhibit arranular turbidity, fatty degenera- tion, fibrillary or discoid disintegration or fibriUation as in the case of vitreous muscular degeneration. DISEASE OF GAXGLIOX-CELLS OF AXTERIOH HORNS 589 Symptoms. — Muscular atrophy and the muscular weakness and muscular paralysis dependent thereon generally appear first in the small muscles of the hand, in the thenar and hypothenar eminences, in the interosseous and the lumbrical muscles. Then the extensors upon the dorsal aspect of the forearm are involved, next the deltoid muscle, and only subsequently the muscles of the upper arm. The process may gradually extend to the muscles of the trunk. The muscles of the leg either remain exempt or are involved only late. Not rarely the disease extends from the ganglion-cells of the anterior horns of the cervical portion of the spinal cord to the ganglion-cells of the nuclei of the cerebral nerves on the floor of the fourth ventricle, which have the same functions as the ganglion-cells of the spinal cord. The nuclei of the hypoglossal, vago-accessory, glossopharyngeal, and facial nerves especially are involved, and, accordingly, to the symptoms of spinal progressive muscular atroj)hy the clinical picture of chronic progressive bulbar paralysis is superadded. JSTaturally, the reverse may happen ; that is, progressive bulbar paralysis develops first, the disease of the ganglion-cells extending from the nuclei of the cerebral nerves to the ganglion-cells of the cer- vical cord, with the development secondarily of spinal progressive muscular atrophy. The muscles of the right hand are involved somewhat earlier than those of the left. Only in left-handed persons and in those whose work requires greater use of the left hand does the disorder begin in this hand. In either event the other hand also is soon involved, and the disease then exhibits a symmetric distribution. The disorder usually sets in insidiously. The patients generally note at first undue readiness of fatigue and awkwardness in the movements of the fingers, and on more careful examination it will be found that the thenar and hypothenar eminences have lost their fulness and are flattened, so that the subjacent metacarpal bones can be readily reached. The thumb is often abducted and ex- tended, so that the so-called ape's hand results, as long as the extensors of the thumb and the long adductor upon the dorsal aspect of the forearm remain intact. Interosseous spaces of unusual depth upon the dorsum of the hand result from atrophy of the interosseous muscles, and disappearance of the lumbrical muscles will be disclosed by apparent excavation of the palm of the hand and prominence of the tendons of the flexors of the fingers beneath the skin of the palm. Weakness of the interossei often gives rise to the claw-hand. The more marked the muscular atrophy the greater is the weakness of the wasted muscles and the more pronounced is the functional disturbance in the fingers. Muscular wasting in the extensors upon the dorsal aspect of the forearm gives rise to an appearance of emaciation and flattening. The interosseous space between the ulna and the radius often is 590 NERVOUS SYSTEM distinctly recognizable as a deep depression, and the borders of the radius and the ulna can be readily palpated (Fig. 81). The supinators long remain intact, undergoing atrophy only when the biceps and the internal brachial in the upper arm are involved. In the presence of atrophy of the deltoid the region of the shoulder Fig. 81. — A man, 52 years old, with s]iinal prri-res.-i ve muscular atrophy ; from a photograph (persoual observation. Zurich clinic). appears flattened, and the head and the neck of the humerus are readily accessible through the skin. At times a depression between the head of the humerus and the acromion process is appreciable on ocular inspection. This is indicative of a flail-joint, which results from the fact that the deltoid is so greatly weakened in its powers that the forearm by reason of its weight drops downward and its DISEASE OF GANG LION-CELLS OF ANTERIOR HORNS 591 articular head is separated from the glenoid cavity. The weakness of the deltoid muscle is characterized particularly by an inability to raise the arm to the horizontal level at all perfectly or for more than a short time. Of the muscles of the upper arm, the triceps remains uninvolved the longest. An exceedingly common symptom of spinal progressive atrophy is fascicular (fibrillary) muscular contraction. This consists in sud- denly occurring and rapidly disappearing muscular twitching, in- volving isolated muscle-bundles. At times it is so persistent and distributed among so many muscles that these appear to be in a condition of constant restlessness. In other cases, however, a long time elapses before the muscular twitching becomes visible. It can often be induced artificially by percussion, by blowing upon the skin or spraying it with cold water. Nothing of a definite nature is known with regard to its development. It occurs tran- siently also in healthy persons under the influence of cold, as, for instance, on removal of the clothing. Degenerative electric reaction is present in the atrophied muscles, although the exam- ination requires skill and attention, as the atrophy, and accord- ingly also the degenerative electric reaction, are often present only in bundles of muscles. All reflex movements (cutaneous, tendinous, and periosteal reflexes) are wanting, or at least are enfeebled, in the distribution of the affected muscles. Cutaneous sensibility remains unchanged, but not rarely the diseased nerves and muscles are sensitive to pressure. Vasomotor disturbances occur frequently, and give rise to cyanotic discoloration and cold- ness of the skin, particularly in the fingers, hands, and forearms. At times trophic disturbances occur, as, for instance, thickening and brittleness of the skin, abnormal growth of hair, pemphigus, herpes, thickening of tendons or joints. The functions of the bladder and the rectum remain undisturbed. The disease pursues an extremely slow course and sometimes extends over many years. The greater the number of arm-muscles that waste and become incapacitated functionally the greater is the degree of helplessness of the patient. Muscular contractures also develop gradually. If the extensors of the back are involved in atrophy and paralysis, the patient eventually will be unable to assume the erect position unaided. If bulbar symptoms are super- added, the tongue undergoes wasting, becomes movable with diffi- culty, and exhibits fibrillary contractions, and difficulties in speech and in the formation of a bolus develop as a result of hypoglossal paralysis. Difficulty in swallowing, paralysis of the laryngeal muscles, and acceleration of the action of the heart occur (paral- ysis of the glossopharyngeal and vago-accessory). The muscles of the face, and especially those of the lips and the cheeks, become thin, atrophied, and stiff", and movable with difficulty (facial palsy). The complication is of serious significance, because 592 NERVOUS SYSTEM death may result rapidly in consequence of inspiration-pneumonia or paralysis of respiration or of cardiac action. Diagnosis. — The diagnosis of spinal progressive muscular paralysis can scarcely be considered difficult. Confusion might most likely occur with myopathic and neural progressive muscular atrophy; that is, with those varieties of progressive muscular wasting and paralysis dependent upon disease of the muscular structure itself or of the peripheral nerves. In the differential diagnosis it should be borne in mind that myopathic and neural progressive muscular atrophy are frequently hereditary, begin at times in early life, and frequently commence in the muscles of the legs or the facial muscles, or in the muscles of the shoulder-girdle. The same muscular changes as occur in spinal muscular atrophy are observed also in syringomyelia, but the latter is attended besides with partial anesthesia and trophic disorders. Spinal progressive muscular atrophy is distinguished from subacute and chronic ante- rior poliomyelitis by the fact that in the former muscular atrophy appears first, and then weakness and paralysis of the atrophic mus- cles while in poliomyelitis paralysis appears first, and then atrophy of the paralyzed muscles occurs. Chronic polyneuritis does not pursue the typical course of spinal progressive muscular atrophy, and it is generally attended also with sensory disturbances. Occa- sionally muscular atrophy complicates antecedent arthritis. Under such circumstances only a few muscles in the vicinity of the in- flamed joint are involved. Prognosis. — Spinal progressive muscular atrophy is an in- curable disease of progressive course and distribution. The prog- nosis is therefore unfavorable. Life naturally may be preserved for many years, particularly if bulbar symptoms do not occur. Treatment. — Internal remedies are without effect. In the first place, massage of the affected muscles may be recommended. At least, no more can be accomplished by electric treatment of the muscles. Baths (indifferent, saline, sulphurous) have also been employed. COMBINED SYSTEM-DISEASES OF THE SPINAL CORD. HEREDITARY ATAXIA. Ktiology. — Hereditary ataxia is an uncommon disease, first carefully studied by Friedreich, and therefore known also as Friedreich^ s ataxia. The disorder is generally an hereditary or familial one, and boys are more commonly attacked than girls. Mental disease and alcoholism in the parents, as well as antecedent infectious disease, have been named as causative factors. Symptoms and Diagnosis. — The disease generally begins AMYOTROPHIC LATERAL SCLEROSIS 593 ill chilclhoocl (between the third and the seventh year) or at the period of puberty. The most conspicuous symptom is the mark- edly ataxic gait, whicli is suggestive of the staggering of an intoxi- cated person. Marked swaying of the body is noticeable particu- larly on standing — static ataxia. The ataxia soon extends from the legs to the arms. In walking the head is involved in active oscillation. The muscles of articulation and the ocular muscles also are involved in the ataxia, with the development of ataxic anarthria and ataxic nystagmus. Swaying of the body when the eyes are closed is frequently, though not invariably, present. The knee-jerk is almost always absent. The foot often exhibits deform- ities, and the great toe is generally in a position of dorsal flexion. Spinal curvature also is frequent. In contradistinction from ordi- nary tabes dorsalis sensory disturbance, visceral crises, paralysis of the bladder and the rectum, trophic changes, reflex immobility of the pupils, paralysis of ocular muscles, and optic atrophy are almost always wanting. The disease pursues a chronic course, and at times may extend over more than thirty years. Death usually results from some accidentally intercurrent disease. Anatomic Alterations. — Disappearance of nerve-fibers and proliferation of neuroglia are found in the spinal cord in the poste- rior columns, in the lateral pyramidal tracts, in the lateral cerebellar tracts, and in the tracts of Gowers (Fig. 82). Disappearance of ganglion-cells and of nerve-fibers has been observed also in the columns of Clarke. The posterior spinal nerve-roots are often thin, atrophic, and gray. Nerve-degeneration has been observed also in peripheral nerves. Recently attention has been called by several observers to atrophy of the cerebelliun, and there is a tendency to ascribe the staggering gait to this condition (cerebellar ataxia). There is much in favor of the view that the anatomic alterations result from defective development of individual por- tions of the spinal cord and the cerebellum. Prognosis and Treatment.— There can be no hope of therapeutic success, and the prognosis is therefore unfavorable with regard to recovery. AMYOTROPHIC LATERAL SCLEROSIS. Ktiologfy. — Amyotrophic lateral sclerosis is a rare disease, which is observed more comraonly in women than in men, and generally appears between the thirti/-fifth and the fiftieth year of life. Exposure to cold, traumatism, and emotional disturbances have been mentioned as causative factors. Lead-poisoning also is thought to be responsible for the disease. Isolated observations have been made pointing to the hereditary and familial occurrence of the disorder. Anatomic Alterations. — The affection represents a disease 38 594 NERVOUS SYSTEM of the motor-lateral pjrramidal tracts and the motor-trophic ganglion- cells in the anterior horns of the spinal cord, and accordino;ly con- sists in a combination of" the symptoms of lateral sclerosis and those of chronic anterior poliomyelitis. The disease of the lateral pyramidal tracts, which consists in loss of nerve-fibers and in- crease of neuroglia, occurs first, and may at times be followed toward the brain throughout the entire motor or corticomuscular path to the motor ganglion-cells of the cerebral cortex. Likewise the disease of the ganglion-cells of the anterior horns (atrophy, disappearance of ganglion-cells, and proliferation of neuroglia) causes degeneration and atrophy of nerve-fibers in the anterior spinal nerve-roots, and in the peripheral nerves to the muscles. The muscles themselves also may exhibit degenerative atrophy. The entire motor path from the cerebral cortex to the peripheral muscle-termination is thus involved in cases of amyotrophic lat- eral sclerosis, and the alterations consist in degenerative atrophy of the cerebrospinal and spinal-peripheral motor neuron. In iso- lated cases the anterior (direct) pyramidal tracts, and even the columns of Goll, also have been found degenerated. Disappear- ance of ganglion-cells of the posterior horns of the spinal cord has likewise been observed. Symptoms and Prognosis. — In accordance w-ith the motor alterations, the clinical manifestations consist of a combination of the symptoms of spastic spinal paralysis (paralysis, contracture, exaggeration of the tendinous, periosteal, and cutaneous reflexes) and those of chronic anterior poliomyelitis (muscular atrophy, degenerative electric reaction in the atrophied muscles). The disease begins in the arms, and extends tiience to the muscles of the trunk and the lower extremities. In the latter only spastic- paretic, and not atrophic, alterations become apparent. It is noteworthy that the atrophy of the ganglion-cells of the anterior horns may extend to the nuclei of the hypoglossal, vagus-acces- sory, glossopharyngeal, and facial nerves, and less commonly also to those of the trigeminus and the abducens, so that symptoms of progressive bulbar paralysis develop. The disease often begins with paresthesise in the arms, partic- ularly with pain, formication, burning, and a sense of coldness. To these weakness and even paralysis of the muscles of the arms become superadded. At the same time muscular contractures also develop. The arms become adducted to the thorax, the forearms are flexed at the elbow-joint, and, particularly, marked flexor- contracture develops, with associated pronation in the joints of the hand and flexor-contracture of the fingers. Tlie tendinous and periosteal reflexes are abnormally increased. To the symp- toms described, muscular atrophy is su])eradded. This frequently begins in the small muscles of the fingers and the hand, then extends to the extensor muscles upon the dorsal aspect of the AMYOTROPHIC LATERAL SCLEROSIS 595 Cervical portion Dorsal portion — forearm, invades the deltoid and other muscles of the upper arm, and latest, if at all, involves the flexor-muscles of the forearm. It is noteworthy that the muscles do not undergo fascicular atro- phy or wasting in bundles, but throughout their entire extent. The atrophic muscles exhibit fas- cicular (fibrillary) contractions and degenerative electric reaction. Should the changes in the spinal cord extend downward from the cer- vical portion, the patients complain of stiffness in the back if the mus- cles in this situation become in- volved. Involvement of the mus- cles of the lower extremity will be indicated by weakness and a spas- tic-paretic gait. The patients make short, stumbling steps, scrape the feet upon the ground in walking, move the legs rigidly like stilts, and in consequence of contracture of the abductors push one thigh before the other with difficulty. At the same time the knee-jerk and ankle-clonus are greatly in- creased. Cutaneous sensibility and the functions of the bladder and the rectum exhibit no alteration. Should bulbar symptoms appear, the tongue undergoes atrophy, with the development of disturb- ances in the formation of the bolus and in articulation (hypo- glossal paralysis). The muscles of the chin and the cheek undergo wasting and become rigid. The masseteric reflex is exaggerated. In consequence of vago-accessory and glossopharyngeal paralysis dif- ficulty in swallowing, paralvsis of the laryngeal muscles, and tacliy- cardia occur. Inspiration-pneumonia and paralysis of respiration or of the heart are, therefore, frequent causes of death. The dis- order generally terminates fatally in from one to three years. Recovery has been observed but rarely. The progfnosis is grave. Diagnosis. — In the diagnosis care should, in the first place, be observed to avoid confusion with spinal progressive muscular Lumbar portion of the spinal cord Fig. 82.— Anatomic alterations in the spinal cord from a case of hereditary ataxia ; the diseased areas are shaded (after Friedreich and Schultze). 596 NERVOUS SYSTEM atrophy, although in cases of tlie latter, conversely from amyo- trophic lateral sclerosis, the atrophy precedes the muscuhir paral- ysis, and the reflex movements are diminished or even al)olished. Amyotrophic lateral sclerosis is generally distinguishaljle from syringomyelia from the presence of partial sensory loss and trophic disturbances in the latter. In the presence of hypertrophic cervical pachymeningitis irritative symptoms (pain) preponderate, and, in addition, other sensory disturbances occur and bulbar symptoms are wanting. Treatment. — Good results are reported from the administra- tion of potassium iodid (5.0 : 200 — 75 grains : Q\ fluidounces ; 15 c.c. — 1 tablespoonful thrice daily) and sulphurous baths (potassium sulphid, 150 — 5 ounces — to a full bath at a temperature of 28° E,. _35o c.— 95° F.). Secondary Degeneration of Individual Columns of the Cord. — Secondary degeneration of the spinal cord is rather of anatomic than of clinical interest, so that a brief reference to the subject must suffice. The reason for its occurrence is found in the cir- cumstance that, in accordance with the so-called law of Waller, the peripheral portions of nerve-fibers that are separated from their trophic centers undergo degeneration and atrophy. Three varieties of secondary degeneration of the spinal cord may be distinguished, namely, an ascending, a descending, and a mixed form. Descending secondary degeneration of the spinal cord always de- velops when the corticomuscular or motor pyramidal tract is inter- rupted at any point in its course, so that the motor paths toward the peripheral side of the focus of disease are cut oif from their trophic center, the motor pyramidal cells in the motor cortical center in the anterior and posterior central convolutions of the cerebrum. This condition occurs most commonly as the result of cerebral hemorrhage, which generally takes place into the internal capsule. The degenerated pyramidal tract may be visible in ad- vanced cases to the naked eye in the middle portion of the foot of the related cerebral peduncle and in the pons. Within the pyram- idal decussation of the medulla oblongata the greater portion of the degenerated nerve-fibers cross over into the lateral (crossed) pyramidal tract of the opposite half of the spinal cord, and only a small portion remain upon the same side and continue their course in the anterior (direct) pyramidal tract (p. 597, Fig. 83). In the cervical and dorsal portions of the spinal cord the lateral pyramidal tracts are se})arated further from the periphery of the cord by the lateral cerebellar tracts. In the lumbar region, how- ever, the lateral pyramidal tracts reach the periphery of the cord and terminate at about the level of the third or fourth sacral nerve. In some cases the direct pyramidal tract is wholly wanting, as, for AMYOTROPHIC LATERAL SCLEROSIS 597 instance, in the accompanying illustration, while in other cases, on the contrary, it may be larger than the crossed pyramidal Cerebral peduncle Pons Middle of the olive Pyramidal decussation Middle of the cervical enlargement Middle of the dorsal segment Middle of the lumbar enlargement Conus medullaris Fig. 83.— Descending: secondary degeneration of the right lateral pyramidal tract in conseqnence of hemorrhagic encephalbmalacia of the left internal capsule; hardened in Miiller's fluid ; natural size (personal observation, Zurich clinic). tract. Anatomically, there results degenerative atrophy of nerve- fibers, to which proliferation of the neuroglia becomes superadded. Further, even marked degeneration is frequently not distinguish- 598 NER VO US SYSTEM Middle of the olivary body ' Middle of the pyramidal decussation Uppermost portion of the ___ cervical cord Middle of the cervical en- largement Lower portion of the cervi- cal cord 1 cm. above the point of compression ^i^JI Point of compression (fourth dorsal vertebra^ 1.5 cm. below the point of compression Middle of the dorsal cord Lower portion of the dorsal _ cord Middle of the lumbar en- largement Con us medullaris Fig. 84.— Compression-myelitis in a man, 62 years old,' resulting from tuberculosis of the fourth dorsal vertebra: natural size; hardened in Miiller's fluid (personal observation, Zurich clinic). able in the fresh cord, although it at once becomes most distinct after hardening in Miil- ler's fluid. Descending secondary degeneration of the spinal cord is be- yond the possibility of diagnosis. In patients with this lesion muscu- lar contractures and ex- aggeration of the reflexes are often present ; but it has not been demon- strated that these phe- nomena are dependent upon the secondary de- generation in the cord. Both manifestations might be the result of long-continued paralysis, without etiologic relation to each other. Ascending secondary- degeneration of the spi- nal cord is in its pure form a rare disorder. It has been observed in isolated cases in associa- tion with neoplasms com- pressing the roots of the Cauda equina. It has also been developed experi- mentally in animals by division of the posterior nerve-roots of the spinal cord. In the immediate neighborhood of the site of injury degeneration was found in the postero- external or columns of Burdach, but the degen- eration extended upward into the postero-internal or columns of Goll, and it was observed that the degenerated nerve-fibers ACUTE ASCENDING SPINAL PARALYSIS 599 at progressively higher levels more closely approached the pos- terior median fissure and advanced forward. Mixed secondary degeneration of the spinal cord develops after transverse lesions of the cord. Below the seat of disease the lateral and the anterior pyramidal tracts upon either side undergo degeneration. Above the transverse lesion, however, ascending degeneration takes place in the columns of Goll, in the lateral cerebellar tracts, and in the bundles of Gowers in front of the latter (p. 598, Fig. 84). As is well known, the intervertebral gan- glia represent the trophic centers for the columns of Goll, and the columns of Clarke those for the lateral cerebellar tracts. As the columns of Clarke extend only down to the lower part of the dorsal cord, transverse lesions in the lumbar cord will not be fol- lowed by secondary degeneration of the lateral cerebellar tracts. Further, diffuse (traumatic) degeneration of the spinal cord will occur in the immediate neighborhood of the seat of disease, and the columnar degeneration will begin a slight distance beyond. FUNCTIONAL DISOKDEKS OF THE SPINAL CORD OR NEUROSES OF THE SPINAL CORD. ACUTE ASCENDING SPINAL PARALYSIS* Symptoms, Prognosis, and Anatomic Alterations. — Acute ascending spinal paralysis, also known as Landry's paral- ysis, either sets in suddenly or is preceded by slight chill, febrile movement, pain in the back and in the extremities, and paresthe- sise as prodromes. The patient is conscious of weakness in one lower extremity or perhaps simultaneously in both, and the weak- ness soon gives place to marked flaccid paralysis. While at first only the muscles of the foot are involved, soon those of the leg and then those of the thigh become paralyzed, and then the paral- ysis extends to the abdominal, dorsal, and thoracic muscles, to the arms, and finally also to the tongue, the pharyngeal muscles, and the vago-accessory nerve, with the development of difficulty in breathing and accelerated heart-action. Other cerebral nerves (facial, abducens) are rarely involved in the paralysis. Occasionally death takes place within a few days as the result of inspiration- pneumonia or respiratory or cardiac paralysis, while in other instances it is deferred for several weeks. The paralyzed muscles exhibit unchanged electric irritability, and waste, if at all, only after the paralysis has existed for some time (atrophy from disuse). The bladder and the rectum are not involved in the paralysis. Sensory disturbances are wanting or are present only in insignificant degree. The cutaneous and tendinous 600 NERVOUS SYSTEM reflexes remain unaltered, or become gradually enfeebled after the disease has existed for some time. Trophic alterations are Mant- ing, while vasomotor disturbances (discoloration of the skin, sweats) occur at times. Fever is not present, as a rule. Consciousness is preserved until death occurs. In numerous instances enlargement of the spleen and albuminuria were present, so that the appearance of an infectious disease was created. Unfortunately, the disease terminates fatally in the majority of cases. Improvement and recovery take place l)ut seldom. It is distinctive of the disease that alterations in the nervous system capable of explaining the occurrence of the paralysis cannot be found. Diagnosis. — The recognition of acute ascending spinal paral- ysis is not ditiicult if the typical symptoms are borne in mind. At times acute ascending myelitis simulates the disorder, but the former is generally attended with sensory disturbances, paralysis of the bladder and the rectum, and changes in the tendon-reflexes. Acute ascending polyneuritis also may give rise to confusion. It should be noted that in the presence of the latter disease degener- ative electric reaction appears early in the paralyzed nerves and muscles, that the tendon-reflexes disappear, and that the muscles imdergo degenerative atrophy within a short time. Ktiology. — Exposure to cold and emotional disturbances, but with greater propriety antecedent infectious disease, are named as causes of acute ascending spinal paralysis. The disorder is most common between the twentieth and the fortieth year of life, and in men. Treatmetlt. — Inunctions of mercurial ointment (5.0 — 75 grains — daily) have been made, particularly if syphilis had previously been present. No good is to be expected from nervines. The galvanic current also, applied to the vertebral column, would scarcely be capable of controlling the disease. Should paralysis of deglutition develop, it will be necessary to nourish the patient by means of the stomach-tube. REFLEX PARALYSIS. Reflex paralysis Avas looked upon until within recent years as a by no means rare occurrence, and it was observed particularly in the sequence of diseases of the female generative apparatus, the kidneys, and the bladder (urinary paraplegia), and the intestines (dysentery, intestinal worms). Its occurrence was attributed to paralysis of the functions of the spinal cord, in consequence of irritative conditions in various organs. It has, however, been shown recently that most cases of reflex paralysis are due to neu- ritis and myelitis that have developed by extension from the dis- eased organs. Nevertheless, reflex paralysis does appear to occur, and in support of this view it may be pointed out that some forms INFLAMMATION OF THE SPINAL DURA MATER 601 of paralysis disappear with surprising rapidity after removal of the fundamental disorder. PSYCHIC PARALYSIS. Psychic paralysis results from the influence of profound emo- tional disturbances, particularly fright, whence also the name of Jright-paralysis. Paraplegia has been observed also as a result of imagination. Further, myelitic alterations may take place as a result of fright. The treatment consists in encouraging suggestion and in making a mental impression on the patient. DISEASES OF THE SPINAL MENINGES. INFLAMMATION OF THE SPINAL DURA MATER (SPINAL PACHYMENINGITIS). Inflammation of the spinal dura mater may involve either the outer or the inner aspect of this membrane, and accordingly a dis- tinction is made between external and internal spinal pachymenin- gitis. Naturally, it may happen that an external pachymeningitis in particular may extend to the inner aspect of the dura, and thus give rise to internal pachymeningitis. EXTERNAL SPINAL PACHYMENINGITIS. !^tiolog"y. — External spinal pachymeningitis occurs most com- monly as the result of vertebral disease (tuberculosis, carcinoma). At times inflammatory processes have invaded the vertebral canal through the intervertebral foramina or, after destruction of the vertebrae, through abnormal o])enings, and such a condition has been observed in connection with cheesy-tuberculous pleurisy, car- cinoma of the esophagus, syphilitic ulceration of the pharynx, and deep bed-sores. It is doubtful if the disease may result from exposure to cold. Anatomic Alterations. — The anatomic alterations vary with the causative factors. In some cases purulent, at times (in the presence of bed-sores) smeary and putrid, deposits are found upon the outer aspect of the spinal dura, beneath which the tissue of the dura is vividly reddened and swollen. At the same time accumulations of pus may have formed in the loose fatty connective tissue between the dura and the vertebral column (spinal peri- pachymeningitis). When the meningitis is tuberculous, cheesy deposits are not rarely found upon the spinal dura, and which may be several centimeters thick, and may exert considerable pressure upon the spinal cord and its roots. In cases pursuing a chronic 602 NERVOUS SYSTEM course dense, cicatrix-like thickening occurs upon the outer aspect of the dura mater, and often also connective-tissue adhesions to surrounding structures. Symptoms, Diagnosis, and Prognosis. — The disease is attended with stiffness and pain in the vertebral column. Pressure, percussion of the vertebral column, the passage of a sponge dipped in hot water, induce pain at the site of the inflammation. Xot rarely complaint is made of girdle-sense in consequence of irrita- tion of posterior nerve-roots. If spinal nerve-roots are compressed by inflammatory products to such a degree as to suffer loss of func- tion, paralysis and anesthesia result. Often the clinical picture of spinal pressure-paralysis is developed. In diagnosis the demonstration of spinal deformity is im- portant, as this often indicates involvement of the dura. Never- theless, the diagnosis is rather a matter of probability. The prognosis varies with the nature of the primary disorder. Recovery is possible. Treatment. — In the treatment rest, application of ice, and administration of potassium iodid are particularly deserving of consideration. Recently, surgical treatment has also been attempted (opening of the vertebral column and removal of cheesy masses). INTERNAL SPINAL PACHYMENINGITIS. Internal spinal pachymeningitis may appear in one of two forms : either as hypertrophic internal spinal pachymengitis or as hemorrhagic internal spinal pachymeningitis. Hypertrophic internal spinal pachymeningitis is a rare disease, which has been attributed to exposure to cold, syphilis, and alcoholic excess. It is characterized by connective-tissue thickening of the dura, and not rarely also of the arachnoid and the pia, so that the spinal cord becomes surrounded by a thick band of connective tissue. The process is generally circumscribed, and is situated in the cervical portion of the cord ^vith relative frequency, so that the condition has been designated cervical hypertrophic pachymenin- gitis. The dangers consist, in the first place, in irritation of the nerve-roots passing through the diseased tissue, and subsequently in paralysis. Besides, the clinical picture of spinal pressure- paralysis may be superadded in the presence of excessive com- pression of the spinal cord. The patient complains principally of sdjfness and pain in the vei'tebr-al column, and often also of a constricting, girdle-like feeling in the upper portion of the chest. In addition, there appear neuralgia in the arms and various forms of 2)<'i''<'sfhesia' (formica- tion, burning). Also, muscular twitching is not rarely observed in the arms. At times trophic disturbances occur (thickening of the epidermis, formation of vesicles). All of these manifestations result from irritation of the nerve-roots. Paralysis of the spinal INFLAMMATION OF SOFT MEMBRANES OF SPINAL CORD G03 nerve-roots is attended with cutaneous anesthesia and loss of tlie reflexes, and generally gives rise first to paralysis of the muscles supplied by the median and ulnar nerves. The action of the extensors of the hand and the fingers therefore becomes predomi- nant, and gives rise to contracture and fixation of the hand in dorsal flexion and to claw-fingers. The paralyzed muscles rapidly undergo atrophy and exhibit degenerative electric reaction. Finally, the clinical picture of sjjinal 2:)ressure-paralysis may be superadded. Paraplegia develops in the lower extremities, the tendon-reflexes become exaggerated, and paralysis of the bladder and the rectum occurs. The disease often extends over years, and is at times susceptible of recovery. It is distinguished from spinal progressive muscular atrophy by the predominance of the sensory disturbances at the beginning of the disorder, a circumstance that is of importance also in the differentiation from amyotrophic lateral sclerosis, in which disease, besides, the reflexes are exaggerated. Therapeu- tically, employment may be made especially of potassium iodid internally and local applications of iodin and the ice-bag. Hemorrhagic internal spinal pachymeningitis may occur, together with a similar process of the cerebral dura, particularly in the insane and in alcoholics, and is attended either with thin, vascular membranes that can be scraped ofl" with a knife, or with blood-sacs of considerable size (hematomata), which upon section are found to consist of discrete collections of blood of varying age, separated from one another by membranes. Only hematomata at times give rise to symptoms by exerting pressure upon the spinal cord and the nerve-roots. Also, blood-vessels at times rupture suddenly in individual membranes, with profuse hemorrhage, which may com- press and paralyze the spinal cord. The diagnosis cannot be made with certainty. INFLAMMATION OF THE SOFT MEMBRANES OF THE SPINAL CORD (SPINAL MENINGITIS). Inflammation of the soft membranes of the spinal cord involves the arachnoid, but especially the pia. Arachnitis and piitis are grouped together under the designation meningitis (leptomenin- gitis), and a distinction is made between acute and chronic spinal meningitis. ACUTE INFLAMMATION OF THE SOFT MEMBRANES OF THE SPINAL CORD (ACUTE SPINAL MENINGITIS). Anatomic Alterations. — Acute spinal meningitis is almost always 'purulent in character. The pia especially is infiltrated and covered with yellowish-green masses of pus, which are particularly abundant upon the posterior aspect of the spinal cord, because the 604 NERVOUS SYSTEM patients generally occupy the dorsal decubitus. In this situation at times the pus envelops the entire spinal cord in a coherent membrane, while upon the anterior surface it is present in insular and disseminated areas. The pia and the arachnoid exhibit, besides, vascular hyperemia. The veins are greatly distended Avitli blood, dilated, and markedly tortuous. Here and there vessels have ruptured, and generally small extravasations of blood have taken place. The cerebrospinal fluid is generally increased, and, besides, it is usually flocculeut and turbid and slightly purulent. The spinal cord is in many cases unaltered ; in others it appears hvperemic and soft, and at times it may even contain small abscesses. Purulent inflammation of the pia often extends to the spinal nerve-roots. On microscopic examination the tissue of the pia and the arachnoid is found swollen aud thickened, and containing innumerable round cells. The blood-vessels are greatly dilated and filled with red blood-corpuscles. Their walls are thickened and infiltrated with round cells. In preparations stained with aniline dyes bacteria can be discovered in places in recent cases. The cerebrospinal fiaid contains large numbers of pus-corpuscles. These fre- quently form small masses admixed with fibrin, and correspond with the flakes of pus appreciable to the unaided eye. The syAnal cord not rarely is wholly unafiected. At times nerve-fibers in proximity to the pia are in- flamed and swollen. The inflammatory process may, however, invade the septa that penetrate the spinal cord from the pia. The spincd nerve-roots also are but slightly involved in the inflammatory process in some cases, while in others degeneration of nerve-fibers, round-cell accumulations, and vascular hyperemia may be encountered. Htiology. — Purulent spinal meningitis occurs most commonly in association witli purulent cerebral meningitis, and the condition is then designated purulent cerehrosjnnal meningitis. This aifection occurs at times in epidemic distribution as an independent infec- tious disease, and will receive detailed description in the considera- tion of the infectious di.seases. Here only those cases Avill be discussed in which the inflammation is confined to the soft mem- branes of the spinal cord. The affection under such conditions is often due also to local causes and to extension from adjacent injlam- rnatory processes. The inflammatory irritant may enter the spinal cord from without, and therefore spinal meningitis is at times observed in association with deep bed-sores over the sacrum, with suppuration in the pelvic connective tissue as a result of puerperal septicemia, and at times also with pleural empyema. Puncture of or injection into the dural sac also is capable of exciting purident spinal meninoitis if unclean instruments or fluids containing bac- teria or irritating substances are employed. In the same way operative measures, with opening of the vertebral canal, and punc- tured and gunshot wounds and traumatism of other kinds may give rise to acute spinal meningitis. At times the disease is dependent upon inflammatory processes in the vertehrse or the spinal cord. INFLAMMATION OF SOFT MEMBRANES OF SPINAL CORD Q05 Occasionally acute spinal meningitis develops in the course of infectious diseases (septicemia, pneumonia, erysipelas, typhoid fever, etc.). Exposure to cold also is said to be a cause, but probably it is only a contributory factor for the infection of the meninges. In the majority of cases the excitants of the inflammation are bacteria, especially the Streptococcus pyogenes and the Staphylococcus pyogenes albus and aureus. The Meningococcus intracellularis has been demon- strated as the cause of epidemic cerebrospinal meningitis. Inflammation of the spinal meninges in consequence of purely chemic irritation is pos- sible, but is probably rare. Symptoms and Diagnosis. — Local symptoms are decisive in the recognition of spinal meningitis. The patient complains frequently at first of stiffness and pain in the vertebral column, and also pressure upon and percussion of the vertebrae, as well as move- ment of the vertebral column in sitting erect and in rotation of the body, excite pain. The occurrence of rigidity of the neck (tortiooUis, ivry-neck) is of especial diagnostic importance, and is dependent upon irritation and contracture of the muscles of the neck. Under such circumstances the head may be strongly re- tracted, and it may be impossible to flex it upon the chest. On the other hand, rotation and dorsal flexion of the head are not interfered with. Often the muscles of the back also are in a state of permanent contracture, and the vertebral column appears curved with its convexity forward, so that the fist can be easily placed between the body and the bed. Contracture of the abdominal muscles causes scaphoid retraction of the abdomen. Often a sense of constriction about the trunk, and even a painful girdle-sense, may appear, and this is indicative of irritation of the posterior nerve- roots. Radiating pains in the lower extremities and muscular twitching also are symptoms of irritation of tlie nerve-roots. Generally there is cutaneous hyperesthesia. The irritability of the vasomotor nerves also is increased, so that even slight cutaneous irritation is sufficient to induce active and persistent reddening of the skin. Irritative manifestations are thus present throughout the entire clinical picture. Naturally, these may be followed by para- lytic phenomena in the progress of the disease. Muscular paral- ysis develops ; cutaneous hyperesthesia is replaced hy anesthesia; paralysis of the bladder and the rectum appears ; the exaggeration of the reflexes is followed by tb.eir diminution and disappearance. Pupillary alterations occur often, inequality of the pupils with especial frequency. Little diagnostic importance is to be attached to the genercd manifestations. The disease is almost always at- tended with elevation of the bodily temperature, although the inten- sity and the type of the fever are subject to no definite rule. Tlie duration of the disease at times extends over only a few days, while in other instances the disorder is protracted over a few weeks, and gradually assumes a rather chronic course. 606 NERVOUS SYSTEM Prognosis. — The prognosis of acute spinal meningitis is grave. The principal danger consists in extension of the inflammatory process to the cerebral membranes, and death from increasing cerebral pressure or from paralysis of the vagus. Naturally, death may result, apart from these conditions, from progressive exhaustion, from paralysis of the bladder and urinary infection, or from septicemia in consequence of the fundamental disorder. At times muscular paralysis persists for a long time. Treatment. — In the first place, the application of Chapman's ice-bag to the vertebral column is to be recommended in the treat- ment of acute spinal meningitis. Internally, antipyrin (1.0 — 15 grains — 4 times daily) or phenacetin (1.0 — 15 grains — thrice daily) may be prescribed for the relief of the pain. If this be intense, subcutaneous injections of morpbin may be necessary. Scarcely any therapeutic etfect will be yielded by lumbar puncture. The patient should be placed at rest in bed, and receive only liquid diet, prefer- ably a milk-diet. CHRONIC INFLAMMATION OF THE SOFT MEMBRANES OF THE SPINAL CORD (CHRONIC SPINAL MENINGITIS). Anatomic Alterations. — Chronic spinal meningitis is attended with connective-tissue tbickening of the pia and the arach- noid. Often connective-tissue adhesions have formed between the pia, the arachnoid, and the dura. The morbid process usually occurs in circumscribed foci, is most markedly devek)ped upon the posterior aspect of the spinal cord, and involves with especial fre- quency the lumbar cord, and least commonly the cervical cord. At times the pia particularly presents a brownish or blackish dis- coloration, indicative of antecedent hemorrhage. Calcareous plates not rarely form, particularly in the arachnoid columns. The cerebrospinal fluid is either unchanged or increased in amount. At times it appears slightly turljid. On microscopic examination of the spinal cord the unusually marked development of tlie pial septa not rarely attracts attention. Often nerve-fibers in the neighborhood of the pia are degenerated, and at times there is complete marginal degeneration of tlie white substance of the spinal cord. The spinal nerve-roots also often exhibit thickening of the pia, and on microscopic examination present connective- tissue hyperplasia and nerve-degeneration. Ktiology. — In the etiology of chronic spinal meningitis the same causative factors are operative as in that of acute meningitis (pp. 604 and 605). At the same time it may happen that acute inflammation occurs at first, which slowly passes into the chronic form, or, in other instances, chronic spinal meningitis develops independently from the outset. Si/philis, alcoholism, and chronic diseases of the spinal cord (chronic myelitis, tabes dorsalis) par- HEMORRHAGE INTO THE SPINAL MEMBRANES 007 ticnlarly are considered especially common causes of chronic spinal meningitis. Symptoms and Diagnosis. — The symptoms of chronic spinal meningitis are identical with those of acute meningitis, except for the absence of fever and the duration of the disease often for several years. Irritative symptoms are present at the beginning, and consist in stiffness and pain in the vertebral column, rigidity of the neck, a girdle-sense, radiating 'pains in the lower extremities, paresthesias, muscidar twitching and contractures, cutaneous hyperesthesia, and exaggeration of the reflexes. After a time 2:>aralysis develops if the spinal cord, and particularly the nerve-roots, are degenerated. The muscles are rather paretic than paralytic, and undergo degenerative atrophy and exhibit degener- ative electric reaction. The reflexes become enfeebled or dis- appear. Cutaneous anesthesia develops, and frequently paralysis of the bladder and the rectum occurs, with the development of urinary infection, bed-sores, and septicemia. At times the dis- order assumes an acute character. By extension of the inflam- matory process to the meninges of the brain and the medulla oblongata death may result from excessive cerebral pressure or from respiratory or cardiac paralysis. Prognosis. — Recovery from chronic spinal meningitis is not impossible. Nevertheless, the prognosis is serious, particularly in the presence of paralysis of the bladder and the rectum. Treatment. — Causal treatment is indicated when there is a history of alcoholism or of syphilis. In the case of drunkards alcohol should be withdrawn, and syphilitics should be treated wdth inunctions of mercurial ointment and the internal adminis- tration of potassium iodid. Symptomatically the use of warm baths (28° R.— 35° C— 95° F.) should be recommended. Saline baths also may be employed. Mercurial inunctions and potassium iodid also have been employed in non-syphilitic cases, but yield no definite results. AMien muscular paralysis develops resort should be had to massage and electricity. HEMORRHAGE INTO THE SPINAL MEMBRANES. lEtiology. — Hemorrhage into the membranes of the spinal cord is only of subordinate clinical significance. It occurs at times as the result of traumatism, and not alone after punctured, incised and gunshot wounds and fractures and luxations of the vertebrae, but also after concussion, powerful expulsive efforts, and heavy lifting. It is often a sequel of circulatory disturbances. It occurs particularly in conjunction with convulsive disorders (eclampsia, epilepsy, tetanus). Chronic diseases of the heart and of the res- piratory organs also at times cause meningeal hemorrhage, w-hich occasionally accompanies inflammation of the meninges, the spinal 608 NERVOUS SYSTEM cord, or the vertebral column. Xot rarely meningeal hemorrhage occurs in the course of infectious diseases, apparently because the vessels become abnormally })ermeable to the blood-corpuscles as the result of the infective process. Sometimes blood passes from the intermeningeal spaces of the brain into the corresponding spaces of the spinal cord. It may also happen that an aortic aneurysm ruptures into the vertebral canal and pours its contents into the intermeningeal space. A similar result has been observed also from rupture of tlie vertebral artery and the spinal artery. At times it is not possible to discover a cause for the condition — cri/ptor/enetic meningeal heniorrhage. Anatomic Alterations. — Meningeal hemorrhage can be readily recognized, and in accordance with its age presents a bright-red or a brownish-red appearance. In size it varies from punctate and barely visible spots to extravasations that may extend throughout the entire length of the spinal cord. Should absorption take place, brownish pigment-spots, subsequently be- coming black, often persist. In accordance with the seat of the hemorrhage several varieties are distinguished. EpuJural hemor- rhage occurs upon the outer aspect of the dura, particularly in the fatty connective tissue that separates the dura from the inner aspect of the vertebral canal. Subdural hemorrhage (formerly designated also arachnoid) occurs in the narrow, capillary space between the dura and the arachnoid. In this category belongs the internal hemorrhagie pachymeningitis described on p. 603. Sub- arachnoid hemorrhage is not rarely the result of extravasation of blood into the corresponding portion of the brain, and together with cerebrospinal fluid may be present in the interstices of the arachnoid. Subpial hemorrhage can be conceived as resulting only from dis- placement of the pia from the structure of the cord by the blood. Symptoms and Diagnosis. — The sudden onset and the predominance of irritative symptoms are distinctive of meningeal hemorrhage. Naturally, these features can be expected only if the extravasation of blood is sufficiently large to cause irritation of the meninges and the spinal nerve-roots. Hemorrhages of smaller amount may be unattended with symptoms and fail of recognition during life. At times a sense of drawing and other unusual sensations in the vertebral column have preceded the occurrence of the hemorrhage for a day or even longer, as jwo- dromes. The occurrence of a hemorrhage of considerable amount is attended with severe pain in tlie vertebral column, whose seat corresponds with that of the hemorrhage, and is probably depen- dent upon the sudden distention of the meninges. The patient is conscious of stiffness and generally of increase in the pain on move- ment of the vertebral column. Should the hemorrhage be seated in the cervical cord, rigidity of the neck may develop. Irritation of posterior nerve-roots may cause a girdle-sense about the trunk, NEOPLASMS OF THE SPINAL MENINGES 609 and often also radiating pains in the lower extremities. Pares- thesise, hyperesthesia, muscular twitching and contractures are not rarely present. Hemorrhage of sufficient extent is capable of causing paralysis of spinal nerve-roots and the spinal cord by compression. Under such circumstances cutaneous anesthesia, muscular paralysis with degenerative atrophy and degenerative electric reaction, enfeeblement or abolition of reflex movement, and paralysis of the bladder and the rectimi may develop. The distri- bution of the manifestations described depends up(ni the seat and the extent of the hemorrhage. In contradistinction from spinal hemorrhage, meningeal hemorrhage is distinguished by the pres- ence of irritative symptoms at the beginning. Prognosis. — The prognosis should be guarded. Danger re- sides in the fact that hemorrhage at a high level may injure the nerve-roots in the medulla oblongata. Bulbar symptoms (disturb- ance in articulation and in deglutition) develop, and in connection with which paralysis of the vago-accessory nerve may give rise to a fatal termination through paralysis of respiration or of the heart. At times meningeal hemorrhage may be complicated by menhigith, with its serious dangers. Should paralysis of the bladder and the rectum develop, the danger of urinary infection, bed-sores, and septicemia arises. At times ^9ara?2/s?s remains permanently. Com- plete recovery is, however, by no means impossible. Treatment. — The application of a Chapman ice-bag to the vertebral column should be directed; a diet, principally of milk, be prescribed ; the use of coffee, wine, tea, and alcoholics be interdicted ; and free, easy evacuation of the bowels be provided for. Severe pain should be relieved by phenacetin (1.0 — 15 grains — thrice daily), antipyrin (1.0 — 15 grains — four times daily), or subcutaneous in- jection of morphin. Persistent paralysis will require massage, which is to be preferred to the application of electricity. After the disappearance of all irritative symptoms baths may be of ad- vantage, particularly saline baths. NEOPLASMS OF THE SPINAL MENINGES* Anatomic Alterations. — Xeoplasms of the spinal meninges arise, as a rule, from the dura mater, and generally are spherical in shape. They vary in size, although they rarely exceed 5 cm. in length. Fibromata, lipomata, myomata, sarcomata, psammomata, melanomata, neuromata, tuberculomata, gummata, enchondromata, osteomata, carcinomata, and lymphangiomata have been observed. By reason of the small size of the vertebral canal, extensive de- velopment of the neoplasm is possible only by penetration of the new-growth through the intervertebral foramina and prolifer- ation externally, or by compression of the spinal cord and the nerve-roots. At times neoplasms have formed a deep excavation 39 610 NERVOUS SYSTEM in the spinal cord, while in other instances the cord and adjacent nerve-roots are flattened. As a result of the compression soften- ing of the spinal cord may readily result. Below and above the point of compression secondary degeneration occurs after a time : above in the column of Goll, the lateral cerebellar tracts, and the bundle of Gowers, and below in the lateral pyramidal tracts. Ktiology. — Syphilis is definitely known as the cause for gum- mata, and tuberculosis for tuberculomata. Otherwise, nothing is kno\vu with regard to the etiology. Traumatism, pregnancy, and the puerperium are further included among the causative condi- tions. Malignant neoplasms (sarcoma, carcinoma) at times arise by metastasis from antecedent neoplasms in other organs. Ex- perience has shown that men beyond tJie fortieth year of life are most commonly attacked. Symptoms and Diagnosis. — Neoplasms of the spinal men- inges give rise to morbid manifestations only if at first they irri- tate the membranes, and subsequently cause paralysis as a result of excessive compression of the spinal cord or the spinal nerve- roots. The irritative symptoms are the same as those that have been mentioned in previous sections : Pain and a sense of stiffness in the vertebral column, a sense of constriction, shooting pains in the extremities, hyperesthesia, paresthesia, muscular twitching and contracture. In the presence of spinal pressure-paralysis the clinical picture, in accordance with the existing conditions, may be that of total transverse lesion of the spinal cord (paraplegia, para-anesthesia, exaggeration of the reflexes, paralysis of the blad- der and the rectum), or that of a unilateral lesion of the cord, or a circumscribed injury of the cord. In the last event motor or sensory paralysis will predominate accordingly as the tumor com- presses the spinal cord from in front or behind. Compression of the nerve-roots also will cause paralysis of motility and sensibility. It is distinctive for the paralyzed muscles to undergo rapid degen- erative atrophy, with degenerative electric reaction and abolition of reflex movement. The duration of meningeal neoplasms extends at times over sev- eral years. The dangers consist in a complicating meningitis, in excessive exhaustion, in the presence of paralysis of the bladder and the rectum, in cystitis and urinary infection, and in bed-sores and septicemia. The diagnosis of neoplasms of the spinal meninges is attended with unusually great difficulty. There is generally a gradual development of the symptom-complex of meningeal irri- tation. The presence of neoplasms in other organs is a matter of great importance, thus rendering probable the existence of meta- static new-growths. In contradistinction from tumors of the spinal cord itself, irritative symptoms predominate in the presence of spinal neoplasms. The nature of the neoplasm is generally in- NEOPLASMS OF THE SPINAL MENINGES 611 volved in doubt, except in the case of metastatic growths. With regard to the seat of the disease, local changes in the vertebral col- umn and the distribution of the symptoms are decisive. Tumors of the Cauda equina not rarely are attended with circumscribed cutaneous anesthesia of the perineum, the scrotum, the penis, and the posterior aspect of the thigh. In addition, paralysis of vari- ous muscles and the bladder and the rectum, and abolition of re- flex movement, occur. Prognosis and Treatment. — Although meningeal tumors have recently been successfully removed by surgical means after opening the vertebral column, the prognosis is nevertheless serious, in the majority of cases. Causal therapy should be employed in cases of syphilis (mercurial inunctions, internal administration of potassium iodid). In a few rare cases cysticerci and echinococci have been found in the spinal meninges, and the latter have been removed by operation. INDEX TO VOLUME I. Abdominal dropsy, 382 muscles, peripheral paralysis of, 504 spasm of, 512 Acephalocysts, 352 Acoria, 240 Addison's disease, 468 treatment, 471 Adrenal bodies, diseases of, 468 Affrictus perieardiacus, 54 Ageusia, 531 Agonal edema, 124 Albumin in urine, determination, 390 Albuminoraeter, Esbach's, 390 Albuminuria, 387 accidental, 388 causes, 391 false, 388 hematogenous, 388 in pneumonia, 136 nephrogenous, 388 pathologic, 388 persistent, 388 physiologic, 387 renal, 388 tests for, 388 Boedecker's, 389 boiling-nitric-acid, 388 Galippe's, 389 Heller's, 389 Panum's, 389 transitory, 388 treatment, 392 Albumoses in urine, 389 Alcoholic paralysis, 539 Amaurosis, uremic, 397 Amoeba coli, 292 Anachlorhydria, 240 Anacidity, 240 Anadenia, gastric, 214 Anemia, bothriocephalus, 297 brickmakers', 311 miners', 311 tunnel, 311 Anesthesia, 525 cutaneous, 525 infectious, 527 paresthesia with, 528 refrigeratory, 527 toxic, 527 Anesthesia, cutaneous, traumatic, 527 treatment, 528 vasomotor, 527 dolorose, 528 trigeminal, 528 neuroparalytic ophthalmia with, 529 Aneurysm, wall of, 66 Angina, 184 circumscribed, 187 complications, 187 diffuse, 187 lacunar, 187, 188 parenchymatous, 187, 189 pectoris, 63 phlegmonous, 187 superficial, 186, 188 treatment, 189 Anguillula intestinalis, 315 stereo ralis, 315 Ankylostomiasis, 311 treatment, 314 Ankylostomum duodenale, 311 Anosmia, 529 Anterolateral remnant, 546 Ante-stomach, 199 Anthrax, pulmonarv, and bronchiecta- sis, 109 Aorta, aneurysm of, 65 diagnosis, 70 neuralgia in, 69 paralysis from, 69 pressure-phenomena, 69 rupture, 69 symptoms, 67-70 treatment, 70 varieties, 65 diseases of, 65 embolism of, 72 gangrene and, 72 isthmus of, constriction and occlusion of, 71 Aortic insufficiency with valvular dis- ease, 37 obstruction with valvular disease, 38 Ape-hand, 496 Aphonia, spastic, 94 Appendicitis, 257 complications, 261 613 614 INDEX TO VOLUME I. Appendicitis, diagnosis, 263 symptoms, 260 treatment, 264 Arachnitis, 603 Arachnoid hemorrhage, 608 Arm and brachial plexus, nerves of, paralysis of, 498 external rotators of, paralysis of, 504 internal rotators of, paralysis of, 503 Arsenical paralysis, 538 Arytenoid muscles, paralysis of, 90 Ascaris lumbricoides, 301 mystax, 303 Ascites, 382 cachectic, 382 chylous, 383 fatty, 383 ■ hypostatic, 382 treatment, 385 Aspermatism, 464 Asthma, cardiac, 30 dyspeptic, 215, 236 hay-, 78 Asthma-cigarets, 117 Asthma-crystals, 115 Asthma-spirals, 115, 116 Ataxia, Friedreich's, 592 hereditary, 592 spinal cord in, 595 locomotor, 572. See also Tabes dor- salis. origin of, 577 Atrophy, spinal progressive muscular, 588 syringomyelia and, 592 treatment, 592 Auricle, muscles of, paralysis of, 482 Axillary nerve, paralysis of, 498 Azoospermia, 464, 465 BAcrLLl of diphtheria and fibrinous rhinitis, 77 Back, muscles of, peripheral paralvsis of, 504 Bacteria of bronchopneumonia, 125, 126 Bacteriuria, 457 Balantidium s. Paramcecium coli, 293 Balsamics in bronchial catarrh, 103 Biernier's change in pitch, 165 Biliary calculi, 362 passages, carcinoma of, 361 catarrii of, 357 diseases of, 357 echinococci in, 352 parasites in. 361 purulent inflammation of, 359 sand, 362 Bladder, detrusor of, paralysis of, 462 sphincter of, paralysis of, 462 urinary, abscess in, 450 Bladder, urinary, carcinoma of, 455 desquamative catarrh of, 451 diseases of, 448 foreign bodies in, 457 hyperesthesia of, 460 hypertrophy of, 450 treatment, 455 inflammation of, 448. See also Urocystitis. neuroses of, 458 paralysis of, 461 parasites of, 457 purulent catarrh of, 451 spasm of, 460 Blepharospasm, 508 Blood in urine, 392 Blood-shadows, 393 Boedecker's test for albuminuria, 389 Boiling in chest, 124 Bostock's catarrh, 77 Bothriocephalus latus, 293, 297 Bothriocephalus anemia, 297 Bowel, intussusception of, 271 nomenclature, 272 treatment, 274 ob.struction of, 275 effect on general condition, 280 diagnosis, 278 symptoms, 278 treatment, 283 stenosis of, 275 diagnosis, 278 symptoms, 278 treatment, 283 Box-note, 114 Brachial plexus and arm, paralysis of nerves of, 498 Bracht-Rombeig's symptom, 539, 576 Bradycardia, paroxysmal, 63 with fat heart, 30" Brain, diseases of, hiccough and, 512 Brickmakers' anemia, 311 Bronchi, diseases of, 96 Bronchial asthma, 113 treatment, 116 catarrh, 96 bacteria and, 97 dry, 98 moist, 98 rales in, 98 symptoms, 98-101 treatment, 102 coagulum, 104 constriction. 111 croup, 103 dilatation, 106 treatment, 110 ulcers. 97 Bronchiectasis, 106 complications, 109 diagnosLs, 108 INDEX TO V0LU3IE I. 615 Bronchiectasis, symptoms, 108 treatment, 110 Bronchiolitis, 100 and alveolar emphysema of lungs, 118 Bronchitis, fibrinous, 103 treatment, 106 putrid, 100 Bronchoblennorrhea, 100 Bronchopneumonia, 125 Bronchorrhea. 100 Bronchostenosis, 111 Bronze-disease, 469 Bubbling murmurs, 166 Bucardia, 27 Bulimia, 240 Burdach's column, 546 Cacosmia, 530 Cadaveric position, 91 Calculi, biliary, 362. See also Gall- stones. carbonate-, 441, 446 cvstin-, 442, 446 indigo-, 442, 446 mulberry-, 363, 441, 446 oxalate-* 441, 446 phosphatic, 441, 446 renal, 441 treatment, 446 uratic, 441, 446 xanthin-, 442, 446 Caput Medusse, 335 Carbon-dioxid narcosis, 127 Carcinosis, miliary, 150 Cardia, carcinomata of, 224 spasm of, 236 Cardiac insufficiency, 17. See also Myo- cnrclium, vjeakness of. intermittency, 63 neuroses, 61 Cardiorhexis, 34 Cardiospasm, 236 Catarrh, acute gastro-intestinal, in in- fants, 247 treatment, 250 autumnal, 77 Bostock's, 77 calculus-forming, 363 drunkards', 212 Cecum, inflammation of, 257. See also T)/phlitis. Cell, heart-failure, 20 Cercomonas coli, 293 intestinalis, 293 Cerebellar tract, lateral, 545 Cerebral arteries, embolism of, 43 nerves, multiple paralysis of, 490 Cerebrospinal sclerosis, multiple, 560 nystagmus in, 562 treatment, 563 Cervical muscle, spasm of, 511 Cestodes, 293. See also Tapeworms. Cheyne-Stokes breathing in fat lieart, 30 Chlorosis, tropical, 311 Cholangitis, catarrhal, 357 purulent. 359 Cholecystitis, catarrhal, 357 purulent, 359 Choledoch duct, carcinoma of mouth of, 3G1 Cholelithiasis, 362. See also Gall-stones. Cholemia, 320, 340 Cholera nostras s. europsea, 243 Chorditis, tuberous, 83 vocalis hypertrophica inferior, 83 Chylopericardium, 60 Chylothorax, 170 Cicatrix, apoplectic, 550 Circulatory organs, diseases of, 17 Cirrhosis, portal. 333 Cirsomphalos, 335 Clarke's column, 543 Claw-hand, 496, 497 Coccygodynia, 524 Coccvx, neuralgia of, 524 Colic, hepatic. 362 intestinal, 291 mucous, 255 renal, 444, 445 treatment, 447 Column of Burdach, 546 of Clarke, 543 of GoU, 546 of Gowers, 546 Compensation, derangement of, venous stasis with, 42 Compression-myelitis, 569, 598 Compression-paralysis, spinal, 567 general paralysis with, 569 treatment, 571 Contact-sensibility, testing of, 526 Contraction, fascicular muscular, 591 Contraction-formula, normal, reversal of, 473 Convulsions, uremic, 397 Coprostasis, 276 Cor adiposum, 29 bovinum, 27 hirsutum, 53 Coryza, 73 complications, 74 hay-, 78 treatment, 76 Cough in bronchial catarrh, 99 laryngeal, 95 Cramps, 513 Crico-arytenoid muscles, posterior paral- ysis of, 90 Cricothyroid muscles, paralysis of, 92 Croup, bronchial, 103 616 INDEX TO VOLUME I. Crural nerve, peripheral paralysis of, 505 Crutch-palsy, 492 Cutaneous sensibility, 525 Cyanosis, congenital, 46 Cysticercus cellulosse, 293 Cystoplegia, 461 Cystospasm, 460 Damoisean's curves, 155 Dextrocardia, 34 Diaphragm, paralysis of, 491 spasm of, 511 Diarrhea, dentition, 248 fatty, 255 nervous, 290 summer, of infants, 247 Diarrhcea ablactatorum, 248 Digestive organs, diseases of, 175 Digitalis-leaves for cardiac insufficiencv, 23 Diplegia, facial, 485 Diplococcus pneumoniae s. lanceolatus. 129 Dittrich plugs, 101 Dorsal muscle, broad, paralysis of, 503 Dro[)sy, abdominal, 382 Drum-stick fingers, 46, 110 Drunkards' catarrli, 212 Drunkards, morning vomiting of, 214 Duodenitis, acute catarrhal, 244, 245 chronic catarrhal, 255 Duodenum, round ulcer of, 266 Dura mater and spinal column, relation of, 541 spinal, inflammation of, 601 Dyspepsia, nervous, 241 Dystopia ventriculi, 233 EcHixococcrs-CYSTS, sterile, 352 Eclampsia, uremic. 397 Electric-sense of skin, testing of, 526 Empyema pleurae necessitatis, 157 Endocarditis. 47 chronic, 36 contracting, 47 cryptogenetic, 47 fetal, and heart-disease. 46 recurrent contracting, 47 ulcerative, 47 and puerperal fever, 47 and typhoid fever, 49 treatment, 49 verrucose, 47, 49 and rheumatism, 50 and scarlet fever, 50 Endocardium, diseases of, 35 inflammation of, 47. See also Endo- cnrclitif^. Enormitas cordis, 27 Enteralgia, nervous, 291 Enteritis, membranous, 255 Enteroptosis, 288 Enterorrhagia of newborn, 288 Enterostenosis, 275. See also Bowel, sleiiosis of. Enuresis, diurnal, 458 nocturnal, 458 Epidural hemorrhage, 608 Epigastrium, restless movements in, 23i) Erb's paralysis of brachial plexus, 499 supraclavicular point, 499 Ergotism, 539 Ergot-poisoning, paralysis from, 539 Eructation, 211 nervous, 235 Esbach's albuminometer, 390 reagents, 389 Esophagism, 204 Esophagitis, catarrhal, 200 phlegmonous, 201 Esophagomalacia, 202 Esophagus, carcinoma of, 191 complications, 195 diagnosis, 196 paralvsis of recurrent larvngeal from, 193 treatment, 196 catarrh of, 2U0 dilatiition of, 199 dimensions of, 194 diseases of, 191 diverticula of, 197 pulsion-, 198 traction-, 198 paralysis of, 203 peptic ulcer of, 201 softening of, 202 spasm of. 204 spontaneous rupture of, 202 stenosis of, 196 and carcinoma, 192, 193 thrush of, 203 Esthesiometer, 526 Eiat mamelonne, 213 Expectorants, 102 Exploratory puncture, apparatus, 160 Extremities, arteries of, embolism of, 43 Evebrow, corrugator muscle of, paraly- sis of, 481 Eyelids, orbicular muscle of, paralvsis of, 481 Face, muscles of, spasm of, 508 paralysis of muscles of, 478 Facial nerve, diagram of distribution, 4.^7 paralysis of, 477 diagnosis, 486 treatment, 488 Fasciculus, anterolateral, 546 Fecal concretions, true, 259 INDEX TO VOLUME I. 617 Fecal concretions, false, 258 Finger, drumstick, AQ, 110 Fistula, bimucous intestinal, 281 pulmonary, 166 Four-glass test, 210 Fremissement cataire, 36 Fremitus, bronchial, 98 Friedreich's ataxia, 592 Fright-paralysis, 601 Gat-ippe's picric-acid test, 389 Gall-bladder, carcinoma of, 361 dropsy of, 360 empyema of, 359 Gall-stones, 362 facetted, 363 treatment, 366 Ganglion-cells of anterior horns, disease of, 582 in adults, inflammation of, 586 pigmentary degeneration of, 588 Gangrene and embolism of aorta, 72 from perichondritis of larynx, 88 Gastralgia, nervous, 238 Gastrectasis, 227 treatment, 231 Gastric catarrh, acute, 210 chronic, 212 treatment, 215 hypertrophic, 213 juice, digestive power of, 206 hydrochloric acid in, 207, 209 hypersecretion of, 241 lab-ferment in, 210 pepsin in, 209 Gastritis, chronic atrophic, 213 cystic, 214 polypous, 213 phlegmonous, 216 purulent, 216 Gastro-intestinal catarrh, acute, in in- fants, 247 treatment, 250 Gastroptosis, 229, 233 Gastrosuccorrhea, 241 Gastroxynsis, 242 Genito-urinary organs, diseases of, 387 Glans penis, neuralgia of, 524 Gliomatosis, 565 Glomerulonephritis, 404 Glossoplegia, 489 Glottis, edema of, 85 disease of larynx and, 86 spontaneous, 86 spasm of, 93 phonatory, 94 rachitis and, 94 Gluteal nerves, peripheral paralysis of, 506 Gmelin's test for biliary coloring-matter, 319 " Golden vein," 286 GoU, column of, 546 Gowers' column, 546 Gray matter of spinal cord, 541 Giinsburg's phloroglucin-vanillin solu- tions, 207 Gustatory nerve, disease of, 530 Hagen-Brandt's formula to abort acute coryza, 76 Hand, ape-, 496 claw-, 496, 497 Hay-asthma, 78 Hay-coryza, 78 Hay-fever, 77 Head, muscles of, spasm of, 511 Heart, acquired valvular disease of, 35 cardiac manifestations with, 37 diagnosis, 43 embolic alterations, 42 spontaneous recovery, 44 symptoms, 37-43 treatment, 45 venous stasis with, 42 beer-, Munich, 28 chronic aneurysm of, after mycocar- ditis, 33 dilatation of, 24 acute, blood-pressure and, 25 and cardiac insufliciency, 27 and pericarditis, 57 diminished resistance of heart- muscle and, 24 treatment, 28 echinococcus of, 34 fat, 29 anemic, 30 cachectic, 30 plethora and, 30 hypertrophy of, 28 'toxic, 29" new-growths of, 33 0X-, 27 right-sided, 34 rupture of, 34 thrombosis of, 51 villous, 52 Heartburn, 211 Heart-disease, congenital 45 Heart-failure cells, 20 Heart-murmurs, localization, 43 Heart-pain, nervous, 63 Hellei-'s nitric-acid test, 389 test for hematuria, 393 Helminthiasis, intestinal, 292 Hematemesis of newborn, 288 Hematinuria, 396 Heraatomyelia, 548 Hematomyelitis, 548, 553 Hematoporphyrinuria, 396 618 INDEX TO VOLUME I. Hematuria, 392 Heller's test, 393 Hemiplegia, iacial, 485 Hemoglobinuria, 392, 394 Hemopericai'diiim, 60 HemopneuDiopericardium, 58 Hemopneumotliorax, 162 Hemoptysis and fibrinous bronchitis, 105 Hemorrhoidal nodules, inflammation of, 286 Hemorrhoids, 284 blind, 286 mucous, 286 treatment, 287 Hemothorax, 170 Hepatic artery, aneurysm of, 370 embolism of, 43 Hepatitis, chronic interstitial, 331. See also Liver, cirrhosis of. suppurative, 327 treatment, 330 Hepatoptosis, 355 Herpes with pneumonia, 137 Hiccough, 511 Horns, anterior, ganglion-cells of, dis- ease of, 582 in adults, inflammation of ganglion- cells of, 586 Hunger, disorders of sense of, 240 Hydromyelia, 564 Hydronephrosis, 435 and pyelitis, 440 partial, 436 treatment, 438 varieties, 437 Hydropericardium, 59 Hydropneumopericardium, 58 Hydropneumothorax, 162 diagnosis, 166 encapsulated, 162, 167 subphrenic, 167 treatment, 168 Hydrothorax, 169 Hypaciditv, 208, 240 Herperacidity, 208, 209, 240 Hyperacusis, Willisian, 482 Hyperchlorhydria, 240 Hypergeusia, 531 Hyperkinesis, 507 Hy parosmia, 529 Hypertropliy, cardiac, eccentric, 24 Hypochlorhydria, 240 Hypogeusia, 531 Hypoglossal nerve, paralysis of, 489 spasm, 510 Hyposmia, 529 Icterus, 315. See also Jaundice. viridis, 324 in cardiac insufficiency, 20 Ileocolitis, 244 Ileus, 275. See also Bowel, obstructixm of. paralytic, 277 Iliopsoas muscle, paralysis of, 505 Impotence in male, 463 Infants, acute gastro-intestinal catarrh in, 247 treatment, 250 fatty liver in, 342 feeding of, with milk substitutes, 252 Inferior oblique muscle of head, spasm of, 511 Intention-tremor, 561 Intestinal crises, 291 Intestine, animal parasites of, 292 atony of, 289 carcinoma of, 267 treatment, 270 catarrli of, acute, 242 symptoms and diagnosis, 244 treatment, 246 chronic, 252 treatment, 256 diseases of, 242 hemorrhage of, in newborn, 288 nervous spasm of, 290 neuroses of, 289 motor, 289 sensory, 290 peristaltic unrest of, 290 polypi of, 270 protozoa in, 292 relaxation of muscular coat of, 289 sarcoma of, 270 worms of, 293 Intussusception, 271 Intussusceptum, 271 Intussuscipiens, 271 Invagination, 271 Isthmus aortse persistens, 71 of aorta, constriction and occlusion of, 71 Itching-sense, testing of, 526 Jaffe's test for indican in urine, 281 Jaundice, 315 catarrhal, 358 cutaneous, 318 diagnosis, 321 difi'usive, 316 due to pjeiochromia, 316 due to polycholia, 3i6 gastroduodenal, 317, 358 hepatogenous, 316 hvpertrophic cirrhosis of liver with, 337 menstrual, 357 of mucous membranes, 318 toxic, 317 treatment, 322 Jejunitis, 244, 246 INDEX TO VOLUME L 619 Kidneys, absence of, 432 adenoma of, 425 amyloid, 421 arteriosclerotic contracted, 411, 421 atrophy of, granular, 411 carcinoma of, 423 contracted, 411 cyanotic, 401 diagnosis, 413 hypertrophy of myocardium and, 414 pulse-tracing of, 415 symptoms, 413 treatment, 416 cyanosis of, 22 cyanotic induration of, 23, 401 cystadenoma of, 426 cystic, 425 diseases of, 387 dystopia of, 432 echinococcus of, 427 embolic infarction of, 420 horseshoe, 432 hypostatic, 401 in cardiac insufficiency, 19 large white, 409 movable, 428 treatment, 431 pelvis of, calculi in, 441 treatment, 446 carcinoma of, 447 dilatation of, 435 treatment, 438 varieties, 437 diseases of, 435 inflammation of, 438 parasites of, 448 sarcoma of, 425 spotted, contracted, 413 suppuration of, 416 treatment, 420 surgical, 417 venous hyperemia of, 401 wandering, 264, 428 incarceration of, 430 treatment, 431 Labia inajora, neuralgia of, 524 ivaennec's cirrhosis of liver, 333 Lagophthalmos, paralytic, 481 Laryngeal cough, 95 mucous membrane, anesthesia of, 95 sensory disorders of, 95 Laryngitis, catarrhal, 79 treatment, 83 granular, 82 hemorrhagic, 81 Larynx, abscess of, 85 catarrh of, 79 treatment, 83 disease of, 79 Larynx, disease of, edema of glottis and, 86 hyperesthesia of, 95 muscles of, paralysis of, 89 treatment, 92 mycosis of, 96 pachydermia of, 82 papillomata of, 83, 84 paresthesia of, 95 perichondritis of, 87 polypi of, 83, 84 ulcers of, treatment, 84 Lead-paralysis, 536 Leptothrices, pulmonary, 101 Leukomyelitis, 554 chronic, 558 Leukoplakia oris, 181 Lientery, 245, 254 Little's disease, 581 Liver, abscess of, 327 treatment, 330 adenoma of, 350 adipose, 342 amyloid, 343 atrophy of, acute yellow, 338 treatment, 341 cryptogenetic, 339 granular, 332 blood-vessels of, diseases of, 368 carcinoma of, 345 treatment, 350 cast of, 325 cirrhosis of, 331 alcoholic, 332, 334-336 arteriosclerotic, 334, 338 atrophic, 332 diagnosis, 334 hypertrophic, 332 biliary, 333, 337 Laennec's, 333 monocellular, 334 monolobular, 333 multilobular, 333 senile, 334, 378 symptoms, 334 syphilitic, 334, 337 treatment, 338 constricted, 355 contracted, 331. See also Liver, cir- rhosis of. diseases of, 315 displacements of, 355 echinococcus of, 350 treatment, 355 fatty, 342 degeneration of, 342 infiltration of, 342 fissured, 355 hypostatic, 323 in cardiac insufficiency, 20 induration of, cyanotic, 23 G20 INDEX TO VOLUME I. Liver, mold of, 325 movable, 355 nutmeg, 323, 324 cyanotic, 23 sarcoma of, 350 serous coat of, inflammation of, 325 suppurative inflammation of, 327 treatment, 330 syphilitic lobulated, 334 venous hyperemia of, 323 wandering, 355 Localization, sense of, 526 Locomotor ataxia, 572. See also Tahes dorsalis. Lower extremities, muscular spasm in, 513 Lung, abscess-formation of, bronchiec- tasis and, 108 atelectasis of, 121 brown induration of, 22 carcinoma of, 149 catarrhal inflammation of, 125 treatment, 128 cirrhosis of, 139 treatment, 142 diseases of, 117 echinococcus of, 151 edema of, 123 agonal, 124 emphysema of, alveolar, 117 bronchiolitis and, 118 complications, 119 treatment, 120 interstitial, 120 vicarious alveolar, 119 fibrinous inflammation of, 128. See also Pneumonia, fibrinous. gangrene of, 144 complications, 147 treatment, 148 hypostasis of, 122 new-growth of, 149 sarcoma of, 149 slaty induration of, 140 suppuration of, 142 tumors of, 149 Male, impotence in, 463 sexual organs, diseases of, 463 sterility in, 464 Mammary gland, neuralgia of, 521 MarechaFs test for biliary coloring- matter, 319 Mastication, muscles of, paralysis of, 476 spasm of muscles of, 507 Masticatory spasm, 507 Mastodynia, 521 Median nerve, paralysis of, 495 Mediastinitis, 173 Mediastinopericarditis, 53 Mediastinum, abscess of, 174 Mediastinum, diseases of, 171 inflammation of, 173 interstitial eunihysema of, 174 tumors of, 171 Megalogastria, 229 Megastomum entericum, 293 Melanosis, villous, 253 Melasicterus, 318 Melena of newborn, 288 Meningeal hemorrhage, 607 Meninges, spinal, diseases of, <101 neoplasms of, 609 Meningitis, cerebrospinal, 604 purulent, in pneumonia, 13G spinal, 603 acute, 603 chronic, 606 Merycism, 237 Mesenteric artery, embolism of, 43 Miners' anemia, 311 Miserere, 273, 280 Mitral insufficiencj' with valvular dis- ease, 39 obstruction M'ith valvular disease, 40 stenosis with valvular disease, 40 Molimina, hemorrhoidal, 286 Morbus coeruleus, 46 Morvan's disease, 567 Motor nerves, spasmodic disorders of, 507 inflammation of, 533 trigeminal spasm, 507 Mouth, diseases of, 175 inflammation of, 175 thrush of, 179 jMulberry-calculi, 363, 441, 446 Munich beer-heart, 28 Murmur, bubbling, 166 endocardial and pericardial, 56 nun's, 313 presystolic, 40 Muscular contraction, fascicular, 591 spasm, 507 Musculocutaneous nerve, paralysis of, 498 Mycosis nasi, 79 pharyngis leptothricia, 190 Mycotic bronchial plugs, 101 Myelitis, acute, 552 anesthesia with, 554 ascending, 555* bed-sores with, 556 diagnosis, 556 gangrene of skin in, 555 treatment, 557 central, 554 chronic, 558 ascending, 559 central, 558 circumscribed, 554 compression-, 569, 598 INDEX TO VOLUME I. 621 Myelitis, diffuse, 554 hemorrliagic, 553 multiple, 554 purulent, 553 transverse, 554 Myelomalacia, inflammatory, 553 necrotic, 553 Myelomeningitis, acute, 554 chronic, 558 Myocarditic cicatrices, 31 Myocarditis, 31 chronic, 32 aneurysm after, 33 treatment, 33 varieties, 32 Myocardium, diseases of, 17 weakness and, 21 echinococcus of, 34 hyperirritability of, after pericarditis, 56 hypertrophy of, and contracted kid- ney, 414 inflammation of, 31 tumors of, 33 weakness of, 17 and dilatation of heart, 27 diseases and, 21 in pericarditis, 55 senile, 22 toxic varieties, 22 treatment, 23 venous stasis with, 42 Myomalacia cordis, 31 Myosis, uremic, 397 Myositis from trichinae, 307 Narcosis, carbon-dioxid, 127 Nasal mucous membrane, catarrh of, from coryza, 75 fibrinous inflammation of, 77 fungi on, 79 molds on, 79 Neck, inferior subcutaneous nerve of, neuralgia of, 519 Nematheliminthes, 301 Neoplasmata pericardii, 60 Nephritis, acute desquamative, 404 lymph omatous, 404 chronic hemorrhagic, 410 interstitial, 411 diagnosis, 413 pulse-tracing of, 415 symptoms, 4l3 treatment, 416 parenchvmatous, 409 diffuse, 402 acute, 402 pulse-tracings, 406 treatment, 408 urinary sediments from, 405 purulent, 416 Nephritis, purulent, cryptogenetic, 417 treatment, 420 Nephrolithiasis, 441 diagnosis, 443 symptoms, 443 treatment, 446 Nerve, electric irritability of, 474 Nerve-pain, 513 Nerve-roots, spinal, changes in, in tabes dorsalis, 574 paralysis of, 602 Nervous system, diseases of, 472 Neuralgia, 513 articular, 525 cervicobrachial, 520 cervico-occipital, 519 crural, 521 dorso-intercostal, 520 anesthesia with, 521 hyperesthesia with, 521 glossalgia, 519 in aortic aneurysm, 69 infraorbital, 518 lingual, 519 lumbo-abdominal, 521 malarial form, 514 neuritic, 514 obturator, 522 occipital, 519 of coccyx, 524 of external cutaneous nerves of thigh, 522 of glans penis, 524 of great auricular nerve, 519 of inferior subcutaneous nerve of neck, 519 of labia majora, 524 of mammary gland, 521 of penis, 524 of perineum, 524 of scrotum,, 524 of supraclavicular nerve, 520 of urethra, 524 phrenic, 520 sciatic, 522. See also Sciatica. spermatic, 524 supraorbital, 518 syphilis and, 514 treatment, 519 trigeminal, 516 varieties, 514 Neuritis, 531 apoplectiform, 532 ascending, 534 hemorrhagic, 532 interstitial, 532 migratory, 532 mixed, 532 multiple, 534 paralysis with, 535 recurrent, 536 622 INDEX TO VOLUME I. Neuritis, nodose, 532 parenchymatous, 532 segmental. 533 suppurative, 532 toxic, 536 treatment, 534 Neuron, 542 cerebrospinal, 543 of second degree, 543 Neuroses, cardiac, 61 Newborn, melena of, 288 Nictitation, 508 Nocturnal pollution, 466 Nodes, singers', 82 Nose, catarrh of, 73 chronic atrophic. 75 hypertrophic, 75 complications, 74 ozena with, 76 treatment, 76 diseases of, 73 Nucleo-albumins in urine, 389 Nun's murmur, 313 Nutmeg-liver, 323, 324 cyanotic, 23 Obstetric paralysis, 499 Obturator nerve, peripheral paralysis of, 505 _ GEsophagomycosis oidica, 203 Oidium albicans, 180 Olfactory nerve, disease of, 529 Ox-heart, 27 Oxyuris vermicularis, 303 Ozena with chronic coryza, 76 Pachtmexingitis, spinal, external, 601 internal, 602 Pain-sense, testing of, 526 Palate, soft, catarrh of, 184. See also A ngina. diseases of, 184 Palsy, bandage-, 492 coachmen's, 492 crutch-, 492 prisoners', 492 water-carriers'. 492 Pancreas, calculi in ducts of, 372 carcinoma of, 372 cysts of, 372 diseases of, 371 fat-necrosis in, 371 hemorrhage into, 371 inflammation of, 371 Pancreatitis, 371 Panum's test for albumin, 389 Parageusia, 531 Paralysis, acute spinal, of childhood, 583 alcoholic, 539 Paralysis, arsenical, 538 compression-, spinal, 567 general paralysis with, 569 treatment, 571 drummers', 493 fright-, 601 from aortic aneurysm, 69 from ergot-poisoning, 539 lead-, 536 motor, of trigeminal nerve, 476 narcosis-, 493 obstetric, 499 of axillary nerve, 498 of broad dorsal muscle, 503 of cerebral nerves, multiple, 490 of corrugator muscle of eyebrow, 481 of diaphragm, 491 of elevator of angle of scapula, 503 of external rotators of arm, 504 of facial nerve, 477. See also Facial nerve, paralysiis of. of hypoglossal nerve, 489 of iliopsoas muscle, 505 of internal rotators of arm, 503 of median nerve, 495 of muscles of auricle, 482 of face, 478 of mastication, 476 of musculocutaneous nerve, 498 of nerves of arms and brachial plexus, 493 of orbicular muscle of eyelid, 481 of pectoral muscles, 503 of phrenic nerve, 490 of platysma rayoides, 482 of radial nerve, 492 of rhomboid, 503 of serrate muscle, 500 of spinal accessory nerve, 488 nerve-roots, 602 of sternocleidomastoid muscle, unilat- eral, 488 of tibial nerve. 506 of tongue, 489 of trapezius muscle, 488, 489 of ulnar nerve, 497 periodic, 507 peripheral, 472 muscular contractions in, 473 of abdominal muscles, 504 of crural nerve, 505 of gluteal nerves, 506 of muscles of back, 504 of obturator nerve, 505 of scapular muscles, 500 of sciatic nerve, 506 treatment, 475 pressure-, 476 psvchic, 601 reilex, 600 saturnine, 536 INDEX TO VOLUME I. 623 Paralysis, sleep-, 492 spinal, 546 acute ascending, 599 spastic, 581 temporary, 584, 586 uremic, 397 Paranephritis, 432 Pararenal connective tissue, inflamma- tion of, 432 Paratyphlitis, 257, 259 diagnosis, 263 symptoms, 263 treatment, 266 Parosmia, 530 Pectoral muscles, paralysis of, 503 Pellagra, paralysis from, 539 Penis, neuralgia of, 524 Pepsin in gastric juice, 209 Peptones in urine, 389 Pericardial cavity, gas in, 58 friction, 54 synechige, 53 Pericarditis, 52 and dilatation of heart, 57 circumscribed, 53 diagnosis, 55, 56 difiuse, 52 dry, 52 external, 53 hemorrhagic, 53 humidn, 52, 53 hyperirritability of myocardium after, 56 myocardial weakness in, 55 prognosis, 57 purulent, 53 putrid, 53 serofibrinous, 53 sicca, 52 spontaneous, 52 treatment, 57 with effusion, 52, 53 Pericardium, alterations of blood in, 60 chyle in, 60 diseases of, 52 dropsy of, 59 inflammation of, 52. See also Peri- carditis. tumors of, 60 Perichondrium of larynx, inflammation of, 87 Pericystitis, 450 Perihepatitis, 325 Perimyelitis, 554 chronic, 558 Perineum, neuralgia of, 524 Peripheral disease of nerves of special sense, 529 nerves, degeneration of, 474 diseases of, 472 Peripheral nerves, inflammatory and degenerative disorders of, 531. See also Neurilb^. paralysis, 472 muscular contractions in, 473 treatment, 475 Peritoneum, carcinoma of, 386 diseases of, 372 echinococcus of, 386 inflammation of, 372. See also Peri- tonitis. Peritonitis, 372, 375-380 alimentary, 373 by extension, 373 chronic, symptoms, 379 cryptogenetic, 373 difl'use, 374, 375 fatty, 383 fibrinous, 374 hemorrhagic, 375 obliterative, 374 perforative, 373, 377 purulent, 374, 375 ])uti'id, 375 rheumatic, 372 serous, 374, 379 suppurative, 374 symptoms, 375-380 traumatic, 372 treatment, 380 Perityphlitis, 257 complications, 261 diagnosis, 263 symptoms, 260 treatment, 264 Peroneal nerve, palsy of, 506 Pettenkofer's test for biliarv coloring- mntter, 319 Pharyngitis, catarrhal, 184 chronic atrophic, 189 circumscribed, 187 complications, 187 diffuse, 187 granular, 188 parenchymatous, 189 superficial, 186, 188 treatment, 189 Pharynx, catarrh of, 184 diseases of, 184 Phloroglucin-vanillin solution, Giinz- burg's, 207 Phrenic nerve, paralysis of, 490 Phthisis pituitosa, 101 ventriculi, 213 Pica, 240 Piitis, 603 Pilimictio, 458 Platyhelminthes in intestine, 293 Platysma myoides, paralysis of, 482 Plethora and fat heurt, 30 Pleura, cachectic edema of, 169 624 INDEX TO VOLUME I. Pleura, carcinoma of, 170 diseases of, 152 dropsy of, 169 ecliinococcus of, 171 iutiamniation of, 152. See also Pleurisy. Pleural cavity, blood in, 170 chyle in, 170 hypostatic edema of, 168 exudates, influence on other organs, 156 Pleurisy, 152 auscultation in, 155 cryptogenetic, 153 diagnosis, 158 diaphragmatic, 158 dry, 153 fibrinous, 153 hemorrhagic, 153 inspection in, 154 interlobular, 158 moist, 153 multilocular, 158 palpation in, 155 percussion in, 155 pulsating, 158 purulent, 153 rupture of pus in, 157 serous, 153 treatment, 160 Pleuropneumonia, fibrinous, 130 Pneumatotherapy for pleurisy, 161 Pneumococcus of bronchopneumonia, 125 of Friinkel, morphology, 128 Pneumonia, abortive, 134 afebrile, 134 aspiration-, 126 in perichondritis of larynx, 88 asthenic, 135 bilious, 135 catarrhal, 125 treatment, 128 croupo\]s, 128. See also Pneumonia, fbrinovK. dissecting, 140 ephemeral, 134 erratic, 135 fibrinosa cruciata, 131 duplex, 131 fibrinous, 128 anomalies, complications, and se- quelfe, 134 delirium in, 136 diagnosis, 137 incubation-period, 132 of children, 135 prune-juice sputum in, 136 symptoms, 132 treatment, 138 foreign-body, 126 Pneumonia, intermittent, 135 interstitial, 139 treatment, 142 lobar, 1.30 malignant, 135 massive, 1.30 progressive, 134 protracted, 134 pulmonary abscess after, 142 recurrent, 135 serous, 124 totalis, 131 typhoid, 135 wandering, 135 Pneumopericardium, 58 Pneumoperitonitis, 375, 377 sacculated, 378 Pneumothorax. 162 closed, 167 diagnosis, 166 ojien, 167 transitional, 167 treatment, 168 valvular, 167 Poikilocytosis, 313 Poliomyelitis, 554 anterior, 474, 542, 582 chronic, 558 of adults, 586 Pollution, nocturnal, 466 alarms for, 467 Polyneuritis, 534 paralysis with, 535 recurrent, 536 Portal vein, purulent inflammation of, 370 thrombosis of, 368 Precordium. pains in, 63 Pressure-sense, testing of, 526 Presvstolic murmur, 40 Proctitis, 244, 246 chronic catarrhal, 255 Propeptones in urine, 389 Prostatorrhea, 468 Protozoa in intestine, 292 Prune-juine sputum in pneumonia, 136 Pseudo-apoplectic attacks in fat heart, 30 Pseudocroup, 81 Psorospasm, 508 Ptvalism, 182 false, 183 idiopathic, 184 primary, 184 Puerperal fever and endocarditis, 47 Pulmonary abscess. 142 from perichondritis of larynx, 88 artery, aneurysm of, 152 fistula, 166 insufficiency with valvular disease, 42 obstruction with valvular disease, 42 INDEX TO VOLUME I. 625 Pulmonary orifice, congenital stenosis of, 45 stenosis witli valvular disease, 42 Pulse, cervical venous, conditions mis- taken for, 41 in aortic aneurysm, 68 Pulsus inspiratione intermittens s. para- doxus, 112 Pyelitis, 438 and iiydronephrosis, 440 calculous, 442 Pyelonephritis, 438 suppurative, 417 Pylephlebitis, suppurative, 370 Pylethrombosis, 368 Pylorus, incontinence of, 237 insufficiency of, 237 spasm of, 236 Pyonej)hrosis, 417 Pyopericardium, 53 Pyopneumopericardium, 58 Pyopneumothorax, 162 sacculated, bronchiectasis and, 109 Pyramidal tract, anterior, 545 crossed, 543 direct, 545 lateral, 543 Pyrosis, 211 Rachitis and spasm of glottis, 94 Eadial nerve, paralysis of, 492 Eats, trichinous, 306 Reactionary fever, 551 Recurrent laryngeal nerves, paralysis of, 91, 92 from carcinoma of esophagus, 193 Regurgitation, nervous, 235 Reumant, anterolateral, 546 Renal artery, aneurysm of, 434 em hoi ism of, 43 calculi, 441 treatment, 446 sand, 441 Respiration in bronchial catarrh, 99 Respiratory organs, diseases of, 73 Retinal artery, embolism of, 43 Retinitis, albuminuric, 415 Rheumatism, acute articular, and endo- carditis, 50 Rhinitis, catarrhal, 73 chronic atrophic, 75 hypertrophic, 75 complications, 74 ozena with, 76 treatment, 76 fibrinous, 77 Rhomboid muscles, spasm of, 511 paralysis of, 503 Robertson's symptom, 575 Rumination, 237 40 Salivation, 182 Satiety, disorders of sejise of, 240 Saturnine paralysis, 536 Scanning speech, 561 Scapula, elevator of angle of, paralvsis of, 503 spasm of, 511 Scapular muscles, peripheral paralysis of, 500 vScarlet fever and verrucose endocarditis, 50 Sciatic nerve, peripheral paralvsis of, 506 Sciatica, 522 ascending, 523 descending, 523 neuritic, 523 scoliotic, 523 sugar in urine in, 523 Sclerosis, amyotrophic lateral, 593 treatment, 596 cerebrospinal, multiple, 560 nystagmus in, 562 treatment, 563 Scrotum, neuralgia of, 524 Seminal fluid, involuntary discharge of, 465. See also Spermalorrhea. Sensibility, compasses for testing, 526 cutaneous, 525 Sensory nerves, inflammation of, 533 Seropneumopericardium, 58 Seropneumothorax, 162 Serrate muscle, paralysis of, 500 Sexual organs, male, diseases of, 463 Sialodochitis, fibrinous, 184 Singers' nodes, 82 Singultus, 211 Siphon, stomach, soft-rubber, 232 Situs viscerum perversus s. inversus, 34 Skin, electric sensibility of, 526 Slaty induration of lung, 140 Sleep-paralysis, 492 Spasm, muscular, 507 rotatory, 511 Spasmus glottidis ablactatorum, 94 Spastic rigidity of extremities, 581 Spastic-paretic gait, 581, 582 Special sense, nerves of, peripheral dis- ease of, 529 Speech, scanning, 561 Spermatorrhea, 465 charlatans' treatment, 467 permanent, 466 true, 466 Spinal accessory nerve, paralysis of, 488 spasm, 510 colinnn and dura mater, relation of, 541 compression-paralysis, 567 general paralysis with, 569 treatment, 571 626 INDEX TO VOLUME I. Spinal cord, abscess of, 553 acute inflammation of, 552. See also Myelitis, acute. anatomy, 540 anemia of, 547 anterior horns of, 542 circumscribed hemorrhage into, 551 cavities in, 5G4 chronic inflammation of, 558 columns of, diagram of, 544 diseases of, 540 asystematic, 547 atypical, 547 combined system, 592 divisions of, 547 rules for diagnosis, 541 symjitoms, 546 system, 572 typical, 572 functional disorders of, 599 gray matter of, 541 hemorrhages into, 548 circumscribed, 550 treatment, 551 tubular, 550 hyperemia of, 548 in hereditary ataxia, 595 neuroses of, 599 physiology, 540 secondary degeneration of, 596-599 single system-diseases of, 572 soft membranes of, inflammation of, 603-606 softening of, 553 systems of, 542 transverse lesion of, diagnosis, 570 section of, 542 tumors of, 564 unilateral lesions of, 571 white matter of, 541 columns of. 543 dura mater, inflammation of, 601 membranes, hemorrhage into, 607 meninges, diseases of, 601 neoplasms of, 609 meningitis, 603 acute, 603 treatment, 606 chronic, 606 pachymeningitis, external, 601 internal, 602 paralysis, 546 acute ascending, 599 of childhood, 583 spastic, 581 progressive muscular atrophy, 588 treatment, 592 sclerosis, posterior, 572. See also Tahes dorsalis. softening, 553 Spleen, infection-, acute, 131 Splenic artery, embolism of, 43 Splenius muscle of head, spasm of, 511 Sputum, globular, 100 prune-juice, in pneumonia, 136 Sputum-cocci, 129 Sputum-septicemia, cocci of, 129 Stasis, urine of, 19 Stenocardia, 63 Stenosis, aortic, with valvular disease, 38 Sterility in male, 464 Sternocleidomastoid muscle, unilateral paralysis of, 488 Sternomastoid, spasm of, 510 Stimulants in cardiac insufficiency, 24 Stomach, absorptive power of, 205 ante-, 199 atony of, 238 carcinoma of, 222 treatment, 226 dilatation of, 227 treatment, 231 yeast-cells and sarcinse from vomitus of, 230 diseases of, 205 displacements of, 233 entire, tonic spasm of, 236 fungus of, 223 hypermotility of, 236 motor activity of. 206 musculature of, tonic spasm of, 236 nervous tormina of, 236 neuroses of, 234 mixed, 241 motor, 234 secretory, 240 sensory, 238 peristaltic unrest of, 236 suppurative inflammation of, 216 ulcer of, latent. 218 round, 217 treatment, 220 Stomach-contents, acetic acid in, 209 acidity of, 207, 208 butyric acid in, 209 examination of, 207 hydrochloric acid in, 207 lactic acid in, 209 organic acids in, 209 Stomach-siphon, soft-rubber, 232 Stomatitis, aphthous, 178 catarrhal. 175 oidica. 179 ulcerative, 177- Stomatomycosis sarcinica. 181 Stringhalt gait, 577 Struma, substernal. 172 Subacidity, 240 Subarachnoid hemorrhage, 608 Subdural hemorrhage, 608 INDEX TO VOLUME I. 627 Subpial liemorrhage, 608 Suffocation in perichondritis of larynx, 88 Superacidity, 240 Supraclavicular nerve, neuralgia of, 520 Syncope, total, in pleurisy, 157 Syringomyelia, 564 anesthesia witli, 566 atrophica, 566 Tabes dorsalis, 572 absence of knee-jerk in, 575 ataxia in, 576 cervical, 575 course of, 579 cutaneous anesthesia in, 577 diagnosis, 580 gastric crises in, 578 gymnastics for, 581 intestinal crises in, 579 paralysis with, 579 spinal nerve-roots in, 574 syphilis and, 572 treatment, 580 Tachycardia, paroxysmal, 61 Tactile sensibility, 525 Taenia echinococcus, 350 mediocanellata s. saginata, 293 saginata, 297 solium, 293, 299 Tapeworms, 293 heads of, 299 ova of, 295 proglottides of, 295 treatment, 298 Temperature sense, testing of, 526 Tenesmus, anal, 246 Test, Boedecker's, for albuminuria, 389 boiling-nitric-acid, 388 for acidity of gastric contents, 208 for albuminuria, 388 four-glass, 210 Galippe's picric-acid, 389 Gmelin's, for biliary coloring-matter, 319 Heller's, for hematuria, 393 nitric-acid, 389 JaflTe's, for indican in urine, 281 Marechal's, for biliary coloring-mat- ter, 319 Panum's, for albumin, 389 Pettenkofer's, for biliary coloring- matter, 319 Test-breakfast, 207 Test-meal, 206 Thigh, external cutaneous nerves of, neuralgia of, 522 Thorax, barrel-like, in emphvsema of lungs, 118 examination of, in bronchial asthma, 114 Thrush-fungus, 180 Thyro-arv-epiglottic muscles, paralvsis of, 92 Thyro-arvtenoid muscles, paralvsis of, 90 Tibial nerve, paralysis of, 506 Tie, rotatory, 511 Tickling-sense, testing of, 526 Time-sense, testing of, 526 Tongue, black, 182 geographical, 182 hairy, ]82 paralysis of, 489 spasm of, 510 Tormina, nervous intestinal, 290 of stomach, 236 Torticollis, 605 Trabecular degeneration, 107 Trachea, diseases of, 96 Trapezius muscle, paralysis of, 488, 489 spasm of, 510 Tremor, intention-, 561 Trichina spiralis, 305 Trichinae, muscle-, 305 Trichiniasis, 305 diagnosis, 310 symptoms, 308 treatment, 310 Trichocephalus dispar, 304 Trichomonas intestinalis, 293 Tricuspid insufficiency with valvular disease, 40 obstruction with valvular disease, 41 stenosis with valvular disease, 41 Trigeminal, motor spasm of, 507 nerve, distribution of, 518 motor paralysis of, 476 Tunnel anemia. 311 Typhlitis, 257 diagnosis, 263 stercoral, 259 symptoms, 262 treatment, 265 Typhoid fever, endocarditis and, 49 Uffelmann's reagent, 209 Ulcer, fecal, 278 stercoral. 278 Ulnar nerve, paralysis of, 497 Uncinaria duodenalis, 311 Upper extremities, muscular spasm in, 513 Uremia, 396 treatment. 400 Uremides, 398 Ureter, carcinoma of, 447 diseases of, 435 Urethra, neuralgia of, 524 Uridrosis, 398 Urinary bladder. See Bladder, urinary. Urine, albumin in, 387 628 INDEX TO VOLUME I. Urine, albumin in, determination, 390 albumoses in, 389 blood in, 392 icteric, 318 indican in, Jaffe's test for, 281 nucleo-albnmins in, 389 of stasis, 19 peptones in, 389 propeptones in, 389 sugar in, in scoliotic sciatica, 523 unconscious evacnation of, 458 Urocystitis, 448 acute, 450 chronic, 452 croupous, 450 hemorrhagic, 451 mucous, 451 pseudodiphtheric, 450 pseudomembranous, 450 suppurative, 451 treatment, 453 Vagus, neurosis of, 113 Valvular disease, acquired, 35 insufficiency, relative, 35 Ventricles, dilatation and hypertrophy of, 24 diagnosis and symptoms, 26 hypeitrophy of, 29 Vermiform appendix, inflammation of, 257. See also Appendicitis. Vertebra prominens, 540 Vertigo, gastric, 214 Vesicular columns, 543 Volvulus, 277 Vomiting, blood-, in newborn, 288 fecal, 273, 280 morning, of drunkards, 214 nervous, 234 periodic, 242 "Wandering kidney, 264 AVeaning, spasm of glottis and, 94 Westphal's symptom in tabes dorsalis, 575 White matter of spinal cord, 541 Williams' tracheal note, 155 Willisian hyperacusis, 482 Wintrich's change in pitch, 164 Worms, flat, sucking, 301 tapeworms, 293 of intestine, 293 round, 301 Anguillula intestinalis, 315 stercoralis, 315 Ankylostomum duodenale, 311 seat-" 303 spool-, 301 Trichina spiralis, 305 whip, 304 Wry-neck, 605 Xanthopsia, 320 Yeast-cells and sarcinje from vomitus of gastric dilatation, 230 Yellow vision, 320 Catalogue SL Medical Publications W. B. SAUNDERS 6 COMPANY PHILADELPHIA W 925 Walnut Street S< 8« S«