HANDBOOK OF Practical Medicine BY v / Dr. HERMANN EICHHORST, PROFESSOR OF SPECIAL PATHOLOGY AND THERAPEUTICS AND DIRECTOR OF THE UNIVERSITY MEDICAL CLINIC IN ZURICH VOLUME II DISEASES OF THE DIGESTIVE, URINARY, AND SEXUAL APPARATUS ONE HUNDRED AND SIX WOOD ENGRAVINGS NEW YORK WILLIAM WOOD & COMPANY 1886 Copyright by WILLIAM WOOD & COMPANY 1886 TABLE OF CONTENTS. DISEASES OF THE DIGESTIVE APPARATUS. PART I. PAGE Diseases of the Buccal Cavity and Salivary Glands, the Soft Palate, and the Pharynx, ..... 1-26 1. Catarrhal inflammation of the buccal mucous membrane. Catarrhal stomatitis, ..... 1-4 2. Ulcerative stomatitis, ...... 4-7 3. Aphthae. Aphthous stomatitis, .... 7-9 4. Leucoplacia oris, ....... 9-10 5. Sprue. Stomatomycosis oidica, .... 10-14 Appendix: a. Leptothrix buccalis, .... 13 b. Stomatomycosis sarcinica, ... 14 6. Salivation. Ptyalism, ...... 14-17 Appendix: Diminution of salivary secretion, . . 17 7. Fibrinous inflammation of the excretory ducts of the salivary glands. Sialodochitis tibrinosa, ... 17 Appendix: Mechanical retention of saliva, ... 17 8. Catarrhal inflammation of the soft palate and mucous mem- brane of the pharynx. Angina and catarrhal pharyn- gitis, ....... 17-22 9. Chronic catarrh of the soft palate and pharynx, . . 22-25 10. Mycosis pharyngis leptothricia, .... 25-26 PART II. Diseases of the (Esophagus, ...... 26-50 1. Stenosis of the oesophagus, ..... 26-33 2. Dilatation of the oesophagus, ..... 33-37 3. Catarrhal inflammation of the oesophagus, . . 37-39 4. Phlegmonous inflammation of the oesophagus, . . 39-40 5. Corrosive inflammation of the oesophagus, . . 40-41 6. Round ulcer of the oesophagus, ..... 41 7. Cancer of the oesophagus. ..... 41-44 8. Hemorrhages from the oesophagus, .... 44-45 9. Perforation of the oesophagus, .... 45-47 10. Spontaneous rupture of the oesophagus, . . . 47-48 11. Softening of the oesophagus. (Esophagomalacia, . . 48 12. Sprue in the oesophagus. (Esophagomycosis oidica, . . 49 13. Paralysis of the oesophagus, ..... 49-50 14. Spasm of the oesophagus. (Esophagismus, . . . 50-51 IV TABLE OF CONTENTS. PART III. PAGE Diseases of the Stomach, ...... 51-105 A. Gastric affections associated with anatomical lesions, . 51-100 1. Hemorrhage of the stomach, ..... 51-56 2. Acute gastric catarrh. Acute gastritis, . . . 56-59 3. Chronic gastritis, ...... 59-04 4. Purulent gastritis. Gastritis phlegmonosa, . . 61-66 5. Toxic gastritis. Gastritis venenata, . . . 66-67 6. Round ulcer of the stomach, .... 67-75 Appendix: a. Hemorrhagic erosions, ... 75 b. Follicular ulcers, .... 75 7. Cancer of the stomach, ..... 75-82 Appendix: a. Gastric polypi, .... 82 b. Sarcoma, ..... 83 8. Dilatation of the stomach. Gastroectasia, . . 83-94 » 9. Incontinence of the pylorus, .... 94-95 10. Degenerative changes in the stomach, ... 95 11. Atrophic changes in the stomach, .... 95 12. Softening of the stomach. Gastromalacia, . . 95-96 13. Rupture of the stomach. Gastrorhexis, . . . 96-97 14. Animal and vegetable parasites in the stomach, . 97-98 15. Foreign bodies in the stomach, .... 98 16. Changes in the shape and position of the stomach, . 98-100 B. Functional Diseases of the stomach. Neuroses of the stomach, 100-105 ' 1. Rumination. Merycismus, .... 100 2. Peristaltic restlessness of the stomach, . . . 101 3. Hypersecretion of the gastric mucous membrane, . 101 4. Nervous pain in the stomach. Gastralgia, . . . 101-104 5. Nervous dyspepsia. Neurasthenia gastrica, . . 104-105 Appendix: Periodical vomiting, . . . . 105 Nervous gastroxynsis, . . . 105 PART IV. Diseases of the Intestines, . ... . . . 105-171 1. Acute intestinal catarrh, ..... 105-112 Appendix: a. Cholera morbus, ..... 112-114 b. Acute gastro-intestiual catarrh of infants, . 114-118 2. Chronic intestinal catarrh, ..... 118-123 Appendix: Phlegmonous enteritis, .... 123 3. Inflammation of the caecum and vermiform appendix and sur- rounding parts. Typhlitis, perityphlitis, and paratyphlitis, 123-127 4. Stenosis and occlusion of the intestines. Entero-stenosis and ileus, . . ..... 127-136 6. Round ulcer of the duodenum, ..... 136-137 6. Intestinal cancer, ...... 137-140 Appendix: a. Polypi, . . . . . . 141 b. Lipoma, ..... 141 c. Angioma, myoma, sarcoma, . . . 141 7. Animal parasites of the intestines. Helminthiasis, . . 141 Protozoa, ........ 141-143 a. Amoeba coli, ...... 142 b. Cercomonas intestinalis, .... 143 c. Trichomonas intestinalis, .... 143 d. Balantidium coli, ...... 143 Flat worms. Platodes, ..... 143-151 a. Bothriocephalus latus, ..... 145-146 b. Taenia solium, ...... 146 c. Taenia saginata, ...... 146-147 Appendix: a. Taenia nana, .... 151 b. Taenia flavo-punctata, . . . 151 c. Taenia cucumerina, . . . 151 d. Taenia madagascariensis, . . 151 e. Bothriocephalus cordatus, . . 151 TABLE OF CONTENTS. V PAGE Roundworms. Nematodes, ..... 152-159 Ascaris lumbricoides, ..... 152-155 Appendix: Ascaris mystax, .... 155 Oxyuris vermicularis, ..... 155-157 Tricocephalus dispar, ..... 157-158 Anchylostomum Uuodenale, .... 158 Anguillula intestinalis and stercoralis, . . . 158-159 Appendix: Trematodes, .... 159 8. Intestinal hemorrhage. Enterorrhagia, . . . 159-163 Appendix: Melaena neonatorum, .... 163-164 9. Haemorrhoids. Phlebectasia-haemorrhoidalis, . . . 164-168 10. Nervous intestinal pain. Enteralgia, . . . 168-169 Appendix: 1. Nervous constipation, .... 170 Nervous diarrhoea, . . . . 170 2. Embolism of the mesenteric artery, . . 170 PART V. Diseases of the Liver, ....... 171-228 A. Diseases of the biliary passages, .... 171-191 1. Stenosis and occlusion of the bile-ducts, . . . 171-178 2. Catarrh of the bile-ducts. Cholangitis et cholecystitis catarrhalis, ...... 178-181 3. Purulent inflammation of the bile-ducts, . . . 181 4. Gall-stones. Cholelithiasis, .... 181-190 5. Parasites of the biliary passages, . . . . 190 a. Ascaris lumbricoides, .... 190 b. Echinococci, ...... 190 c. Liver fluke. Distomum hepaticum, . . 190 6. Dropsy of the gall-bladder. Hydrops cystidis felleae, . 190-191 7. Empyema cystidis felleae, . .... 191 8. New growths in the biliary passages, ... 191 B. Diseases of the parenchyma of the liver, . . . 191-225 1. Hyperaemia of the liver, ..... 191-194 2. Perihepatitis, ...... 194-195 3. Suppurative hepatitis. Abscess of the liver, . . 195-201 4. Chronic intestinal inflammation of the liver. Cirrhosis of the liver, ...... 201-207 5. Acute yellow atrophy of the liver, .... 207-211 6. Fatty liver, ....... 211-213 7. Waxy liver, ....... 213-216 8. Cancer of the liver, ..... 216-220 Appendix: a. Sarcoma, ..... 220 b. Adenoma, ..... 220 c. Fibroma, etc., . . . 220 9. Echinococcus of the liver, .... 220-224 10. Changes in the position of the liver, . . . 224-225 11. Changes in the shape of the liver. Tight-laced fissure, 225 C. Diseases of the blood-vessels of the liver, . . . 226-228 1. Stenosis and occlusion of the portal vein, . . 226-227 2. Suppurative inflammation of the portal vein, . . 227-228 3. Aneurism of the hepatic artery, .... 228 PART VI. Diseases of the Pancreas, ...... 229-230 1. Hemorrhage, . . ... . . . 229 2. Pancreatitis, ........ 229 3. Cancer, ........ 229 Appendix: Diseases of the mesenteric and retroperitoneal glands, ........ 230 VI TABLE OF CONTENTS. PART VII PAGB Diseases of the Peritoneum. ...... 230-242 1. Inflammation of the peritoneum. Peritonitis, . . 230-237 2. Dropsy of the peritoneal cavity. Ascites, . . . 237-242 3. Cancer of the peritoneum, ..... 242 4. Parasites of the peritoneum, ..... 242 SECTION IV. DISEASES OF THE URINARY AND SEXUAL APPARATUS. PART I. Symptomatically Important Changes in the Urine, . . 243-257 1. Albuminuria, ....... 243-245 2. Haematuria, ........ 245-252 3. Haetnoglobinuria, . . . . . . 252-254 4. Pyrocatechinui'ia, ....... 254 5. Melanuria, ....... 254 6. Chyluria, ........ 254-255 7. Lipuria, ........ 255 8. Fibrinuria, ........ 255 9. Hydrothionuria, ....... 255 10. Oxaluria, ........ 256 11. Cystinuria, ....... 257 PART II. Diseases of the Renal Parenchyma, ..... 258-308 1. Uraemia, ........ 258-263 2. Ischaemia of the kidneys. ...... 263-268 3. Passive congestion of the kidneys, .... 265-268 4. Bright’s disease, ....... 268-290 a. Acute diffuse nephritis,' ..... 268-276 b. Diffuse chronic parenchymatous nephritis, . . 276-281 c. Diffuse chronic interstitial nephritis, . . . 281-290 5. Suppurative nephritis, ...... 290-293 6. Paranephritis, ....... 293-296 Appendix: Perinephritis, . . . . 296 7. Embolism and hemorrhagic infarction of the kidneys, . 296-297 8. Waxy kidneys, ....... 297-299 9. Cloudy swelling and fatty degeneration of the kidneys, . 299-300 10. Cancer of the kidney, ...... 300-303 Appendix: a. Sarcoma, ..... 303 b. Adenoma, ...... 303 c. Fibroma, ..... 303 d. Cavernoma, ..... 303 e. Lymphangioma, .... 304 11. Cystic kidneys, ....... 304-305 a. Congenital cystic kidney, .... 304 b. Cyst-formation in chronic intestinal nephritis, . . 304 c. Other forms of cysts, ..... 304 12. Echinococcus of the kidneys, ..... 305-306 Appendix: Pentastomum denticulatum, . . . 306 Cysticercus cellulosse, .... 306 13. Movable kidney. Floating kidney, .... 306-307 Appendix: Abnormally low position of the kidney, . . 307 14. Anomalies in the shape and number of the kidneys, . 307-308 a. Lobulated kidneys, ...... 307 b. Horse-shoe kidneys, ..... 307 c. Absence of a kidney, ...... 308 d. Supernumerary kidneys, ..... 308 Appendix: Aneurism of renal arteries, . . . 308 TABLE OF CONTENTS. VII PART III. PAGE Diseases of the Renal Pelvis and the Ureters, . . . 308-326 1. Hydronephrosis, ...... 308-310 2. Pyelitis, ...... . 310-315 3. Renal calculi. Nephrolithiasis, .... 315-323 Appendix: Renal infarction, ..... 323-324 4. Tumors in the pelvis of the kidney and ureters, . . 324 5. Parasites in the pelvis of the kidney and ureters, . . 325-326 PART IV. Diseases of the Bladder, ...... 326-345 A. Anatomically demonstrable diseases of the bladder, . . 326-340 1. Cystitis, ....... 326-335 2. Cancer of the bladder, . . . . . 335-338 Appendix: mucous polypi, lipoma, myxoma, etc., . 338 3. Parasites in the bladder, ..... 338-339 4. Foreign bodies in the bladder, .... 339-340 B. Functional diseases (neuroses) of the bladder, . . . 340-345 1. Nocturnal enuresis, ...... 440-342 2. Hyperaesthesia of the bladder, .... 342 3. Spasm of the bladder, ..... 342-343 4. Paralysis of the bladder, ..... 343-345 PART V. Diseases of the Male Sexual Apparatus, . . . 345-355 1. Male impotence, ....... 345-346 2. Male sterility, ....... 346-347 а. Aspermatism, ....... 346 б. Azoospermia, ...... 347 3. Spermatorrhoea, ....... 347-351 a. True Spermatorrhoea, ..... 347-350 b. Prostatorrhoea, ....... 350 Appendix: Diseases of the suprarenal capsules, . . 351-355 Bronzed skin, Addison’s disease, . . . 351-355 Hemorrhage into the suprarenal capsules, . 355 HANDBOOK OF PRACTICAL MEDICINE. SECTION III. DISEASES OF THE DIGESTIVE APPARATUS. PART I. DISEASES OF THE BUCCAL CAVITY, THE SALIVARY GLANDS, THE SOFT PALATE, AND THE PHARYNX. 1. Catarrhal Inflammation of the Buccal Mucous Membrane— Catarrhal Stomatitis. 1. Etiology.—Catarrh of the buccal mucous membrane may be primary or secondary, acute or chronic. Primary stomatitis is generally the result of thermal, mechanical, or chemical irritants. It is doubtful whether stomatitis alone may be the result of a general cold, but it may be produced by too cold, and especially by too hot ar- ticles of diet. Among the mechanical irritants may be mentioned the sharp edges of the teeth, which give rise to an inflammation of the mu- cous membrane of the tongue or cheeks. In infants, stomatitis is some- times the result of violent sucking, particularly if the mother’s breast does not contain much milk. It is sometimes produced by too early feeding with solid food. Continued talking and shouting are also said to produce stomatitis. Among chemical causes may be mentioned the internal or local em- ployment of preparations of iodine, bromine, arsenic, lead, mercury, and, according to Guipon, the prolonged administration of nitrate of silver. In some cases it is produced by mineral acids or other irritating substan- ces and gases. In drinkers and smokers it is the result of the irritation produced by alcohol and tobacco. It also occurs in infants whose mouth is not kept clean, and in which particles of milk are allowed to decompose. It is also produced occasionally by an irritating secretion from the nipple of the mother’s breast. It may also be produced by vomiting, especially if the vomited matter is very acid. This is often most marked in dilatation of the stomach. Secondary stomatitis is sometimes propagated from adjacent organs, 1 2 sometimes is associated with infectious diseases, or is the result of vari- ous disturbances of the general condition. Stomatitis often accompanies dentition in children, and in adults ia observed not infrequently in inflammation of the alveolar process, or with the cutting of the wisdom teeth. It may be associated with inflam- mation of the salivary glands, or of the mucous membrane of the nose, pharynx, or larynx. It is observed very often in gastric affections. The affection may develop in all febrile conditions, especially in the infectious diseases (typhoid fever, measles, scarlatina, variola, erysipelas, phthisis, syphilis, etc.). It is sometimes communicated by the milk of cows or goats who are suffering from foot rot. It is not infrequent in chlorosis, anasmia, and scurvy, and is ob- served occasionally as the result of stasis in diseases of the heart and lungs. II. Symptoms and Anatomical Changes.—In acute stomatitis there is usually, at first, a feeling of heat, dryness, and burning in the mouth. In nursing infants, these sensations are manifested by the fre- quent introduction of the finger into the mouth. The inflamed mucous membrane is hot, and is often sensitive to the touch. At first the buccal secretion is extremely scanty because the excre- tory ducts of the mucous follicles are occluded on account of the inflam- matory swelling. At a later period, there is often a very profuse flow of saliva; in infants this often runs in a constant stream from the mouth, and produces erythematous inflammation of the integument of the chin. In adults the secretion flows backward and then passes into the stomach. The buccal fluid is usually acid, more rarely neutral, but, according to Bohn, it is never alkaline. As a rule, the secretion is at first tough, vitreous, transparent; later it becomes more fluid and cloudy, and is richer in cells. The salivation is explained in part by increased activity of the mucous follicles, but mainly by reflex stimulation of the salivary glands. Perverse sensations of taste appear very early. Many patients com- plain of a flat, pasty taste, a sensation which may be resolved into sev- eral components, inasmuch as the tactile sensibility of the mucous mem- brane and the delicacy of taste are both impaired. Some patients complain of a bitter or foul taste, and the latter may be associated with a foul odor from the mouth. All these changes are the result, in part, of desquamation of the epithelium which accumulates within the buccal cavity and, mixed with debris of food and fungoid vegetations, under- goes decomposition. The anatomical changes may be studied in detail in the living sub- ject. The inflammation is more often circumscribed than diffuse. The inflamed parts are extremely red, either uniformly or in an aborescent manner. At the same time the mucous membrane is unusually swollen; this is particularly well marked if the cheeks or tongue are affected. The tongue then seems to be broader, and its edges show the indentations of the teeth. In some cases the mucous follicles take a more prominent part in the swelling, and this is recognized particularly on the mucous mem- brane of the lips and the border between the hard and soft palate. In these localities, we find small elevations, sometimes of a pearl-gray color, and upon pressure these often discharge a mucous or slightly puriform secretion. A red vascular areola is often seen around these nodules. In very rare cases, rupture of the follicles gives rise to superficial losses of substance. Stomatitis is generally accompanied by very active loosening and DISEASES OF THE BUCCAL CAVITY, ETC. DISEASES OF THE BUCCAL CAVITV, ETC. 3 desquamation of the epithelium. The cells often accumulate on the in- flamed parts and form white, smeary, partly removable patches, or a more diffuse deposit. It is found very often on the gums, inner surface of the lips, and on the tongue, upon which it forms grayish, yellowish, or brownish masses, or the color may depend on the character of the food. The swollen papillae fungiformes sometimes project upon the sur- face of the tongue, and, as the epithelium of the papillae is easily re- moved, numerous red prominences, hardly as large as the head of a pin, are found upon the otherwise coated tongue. The coating of the mouth consists, in addition to debris of food, chiefly of pavement epithelium, often in large coherent masses; the cells contain fat granules. In addition, we find, bacteria, particularly rod- shaped ones, pus-corpuscles (either scattered or in groups), occasionally red blood-globules and, according to Miquel, cholestearin crystals and Fig. 1. Coating of the mouth in chronic stomatitis, containing desquamated epithelium, threads of lepto- thrix, mucous and pus-corpuscles. Magnified 275 diameters. lime salts (Fig. 1). Brown granular pigment is observed free or in- closed in epithelial cells. As a rule, the general condition of the patient is very little affected. The bodily temperature is hardly at all elevated unless the primary dis- ease is pyrexial. In infants, however, the temperature may rise con- siderably as the result of stomatitis, and general convulsions are ob- served occasionally, but it is doubtful whether they depend upon the stomatitis. There is often a feeling of increased thirst, and anorexia may be present, even though the stomach is unaffected. The foul taste and odor from the mouth occasionally give rise to nausea and even vomit- ing. As the ingestion of food increases the burning sensation in the mouth, infants sometimes refuse the breast for days, and emaciation and loss of strength are necessary consequences. The disease does not 4 DISEASES OF THE BUCCAL CAVITY, ETC. often last more than a week. Chronic stomatitis either develops as such from the start, or follows relapsing acute attacks. The symp- toms are similar to those of the acute form, except that they are less violent. After it has lasted for some time, permanent thickening of the submucosa sometimes follows as a result of the inflammatory hyper- plasia. III. Diagnosis and Prognosis.—The diagnosis is easy, but we must be careful not to regard every coating on the tongue as evidence of stomatitis. A coating often forms during the night upon the pos- terior half of the tongue of perfectly healthy individuals, as the result of dryness and imperfect desquamation of the epithelium. In the new-born a sort of physiological congestion of the buccal cavity develops during the first few days of life. This is produced by the irritation of the atmosphere, the movements of sucking and the in- gesta, and should not be mistaken for stomatitis. The prognosis as regards life is good, but serious symptoms sometimes develop in nursing infants. Complete recovery does not always occur; for example, in the case of drinkers and smokers. IV. Treatment.—In addition to the removal of the cause the in- flamed membrane must be treated locally. Washing the mouth with cold water often proves sufficient. The food should not be too hot, cold, hard, spiced, or irritating in other respects. Einsing the mouth with chloride of potash (gr. Ixxv. : 1 vij., every two hours; especially after meals) is regarded, in some measure, as a specific. In little children a soft piece of linen is dipped into the solution and applied every two hours The following mouth-washes may also be mentioned: Salicylate of soda ( 3 ss.: § iiiss.); carbolic acid ( 3 ss.: 3 iiiss.); liq. alumin. acetic, (gr. Ixxv.: § iiiss., one tablespoonful in a cup of water), the latter espe- cially if there is a disagreeable fcetor ex ore. In chronic stomatitis applications of corrosive sublimate (gr. vij.: 3 xiv.) or nitrate of silver (gr. xv.: 3 vij.-xiv.) have been recommended. 2. Ulcerative Stomatitis. (Stomacace.) I. Etiology.—Inflammation, at first of the gums, then ulcerative degeneration and a foul stench from the mouth are the chief symptoms of the disease. It occurs sometimes sporadically, sometimes epidemically (especially in overcrowded and badly ventilated barracks, prisons, or- phan asylums, and hospitals). In the epidemics .described by French military surgeons, the officers escaped almost entirely, and the privates suffered most, because the former Avere better fed and lived under more favorable hygienic condition. Larrey reports that the disease broke out among Napoleon’s troops after the battle of Eylau, probably from drinking snow-water. Telluric and climatic influences are not unimportant. For example, the disease occurs with remarkable frequency on the coast of Holland and, according to Vauvray, in Port Said. The disease is most frequent in summer, and its outbreak is said to be specially favored by the occur- rence of a hot spell after prolonged rains. It is more frequent in the cities than in the country, and particularly in the low, damp dwellings of the poor. Aniemic and feeble individuals, convalescents, those suffering from phthL'is, diabetes, scurvey, scrofula, and rachitis, are specially predis- 5 posed to the disease. Children manifest a marked predisposition to this as to most other diseases of the mouth. Among one hundred and six cases observed by Bohn, eighty-four occurred in children. It is observed most frequently from the age of four to ten years. The development of the disease depends upon the presence of teeth, so that infants prior to the period of teething, and toothless old people are entirely exempt. Bohn mentions an obstinate case of this disease which was cured by the extraction of the teeth. The parasitic and infectious character of the disease has not been proven. There is no doubt that it often attacks several children of the same family, that it occurs epidemically in institutions, and not infre- quently appears in separate houses at the same time, but it may be claimed that the same bad hygienic influences are acting upon all the affected individuals. But we must confess that to us the clinical history of the disease suggests an infectious disease. As a rule, a direct cause cannot be demonstrated in the sporadic cases. Toxic stomatitis is a special form of the disease. It is produced most frequently by the internal or external administration of mercury, but lead, phosphorus, and copper may act in the same way. It develops so much more readily from the administration of mer- cury the larger the doses and the more rapidly administered. It hardly ever occurs in chronic mercurial poisoning because very small quantities are gradually absorbed. Certain individuals suffer from sto- matitis after extremely small doses of the remedy. Children possess a certain degree of resistance to its influence, although calomel, which is so much used in children, is especially apt to produce stomatitis. II. Symptoms and Anatomical Changes.—The ordinary (non- toxic) form of the disease generally begins with a feeling of rawness and burning in the mouth, which is especially annoying on taking food. The first objective signs always appear upon the gums. As a rule, the lower jaw is affected, often upon one side alone (particularly the left side). During the further course of the disease, the lower jaw continues to be more affected than the upper, and the latter may remain entirely un- affected. Redness and swelling of the mucous membrane are first observed on the free edge of the gum, especially at the point of contact of two adja- cent teeth. The free edge of the gum is loosened and swollen, and bleeds on slight contact. After one or two days, a yellow, smeary, pasty coating forms. This gradually increases in amount and if removed discloses an ulcer, usually with sharp edges and a grayish, speckled base. A large part of the gums may be converted gradually into a pasty, gray, or brownish necrotic pulp, which consists of epithelium, pus-corpuscles, red blood-globules, bacteria, and granular detritus. Bohn also observed a sort of algae. These changes generally appear first at one of the incisor or canine teeth, and gradually extend backwards or between the teeth to that por- tion of the gums which is adjacent to the tongue. The process may be interrupted by the absence of a tooth. The same process is found occasionally upon the mucous membrane of the cheeks and the edges of the tongue. Careful examination shows that these ulcers are, to a certain extent, casts of others which are found upon corresponding parts of the external and internal surfaces of the gums—hence a sort of local infection. The cheeks and lips are not infre- DISEASES OF THE BUCCAL CAVITY, ETC. 6 DISEASES OF THE BUCCAL CAVITY, ETC. quently swollen. Secondary facial erysipelas may develop or, after re- covery and cicatrization, the mucous membrane of the cheek, edge of the tongue, and gums may remain adherent to one another. In addition, a nauseous foetor ex ore is noticeable. The patients often infect the whole room within a few minutes. As a rule, the neighboring lymphatic glands (submaxillary, submental, cervical) are enlarged, indurated, often tender on pressure and during mastication. The salivary glands are occasionally swollen and inflamed. They are almost always stimulated to increased secretion, and discolored, stinking, often bloody saliva runs almost uninterruptedly from the usually open mouth. The flow of saliva also continues during sleep, the fluid wets the pillow and the patient’s sleep is disturbed, partly by the stench, partly by the discomfort arising from the wet pillow. The saliva may also flow backwards into the larynx and give rise to attacks of cough and suffocation. The more actively the destruction of the gums progresses, the more the teeth are laid bare. They begin to loosen, and in severe cases may be readily removed with the fingers, without causing pain. The inflamma- tory process occasionally extends to the lower jaw, in which it produces inflammatory and necrotic changes. The remainder of the buccal mucous membrane is often in a condition of catarrhal inflammation, and the tongue is coated, broadened, and its edges present indentations produced by the teeth. The hard palate and the floor of the mouth rarely are affected. Under very unfavorable conditions, however, wide-spreading necrotic changes may develop in these parts and give rise to death after pyaemic symptoms (chills, high fever, loss of consciousness, meteorism, etc.). The process never extends to the pharynx. In certain cases the patients have a very cachectic appearance,but, as a rule, the general condition is very little affected. There is usually very little or no fever, the chief complaints referring to the pain in the mouth, foetor ex ore, perverse sensations of taste, antipathy to food and drink, and the annoyance caused by the salivation. Ulcerative stomatitis may be acute or chronic. The acute form runs its course in one or two weeks, the chronic form lasts for months. The latter develops from the former if slowly healing ulcers are left over, or it appears as a chronic affection from the beginning. Mercurial stomatitis is often preceded by peculiar sensations of taste, generally described as metallic by the patient. A sensation is felt as if the teeth were too long or loose; in addition, there is marked salivation. Finally, redness of the buccal mucous membrane, active desquamation of epithelium with its accumulation into smeary white masses upon the gums and lips, disagreeable foetor ex ore, and finally ulcerative destruc- tion (which may first affect the mucous membrane of the cheeks or tongue) become noticeable. III. Diagnosis and Prognosis.—The diagnosis is so easy that a mistake is hardly possible. The previous history will serve to distin- guish ordinary stomatitis from the toxic form. The prognosis is almost always favorable, and an unfavorable termination is hardly ever ob- served except as the result of gross carelessness. IV. Treatment.—We should first endeavor to remove the cause of the disease. Among local remedies, chlorate of potash occupies the first rank, and renders all other remedies unnecessary. The mouth should be washed with a solution of the potash salt gr. lxxv.: § vij. every two hours. DISEASES OF THE BUCCAL CAVITY, ETC. 7 Vogel administers it internally, and holds that it is very rapidly excreted in the saliva. Feuvrier recommends that small crystals of the salt be taken into the mouth. If there are ulcers on one side, the patient should sleep upon the unaffected side in order to prevent the growth of the ulcer from prolonged pressure of the cheek against the gums. Carbolic acid (gr. xxx.: 5 iiiss.), permanganate of potash (gr. xv. : 3 iiiss., one teaspoonful to a cup of water), liq. alumin. acet. (gr. Ixxv. : 3 iiiss., one tablespoonful to a cup of water), etc., have also been recom- mended. The ulcers may be cauterized with the solid stick. If children are unable to gargle, the chlorate of potash may be given internally, or applied with a brush. Special attention should be paid to the diet (meat broths, milk, eggs, diluted wine, beer). 3. Aphtha. Aphthous Stomatitis. I. Etiology.—Aphthous stomatitis is chiefly a disease of childhood, and is observed most frequently from the tenth to thirtieth months of life. In certain children, the cutting of each tooth is accompanied by an outbreak of aphthae. It is much less frequent during the period of second dentition. The disease is observed frequently among the children of the poor, who attach little weight to keeping the mouth clean. A decided pre- disposition is also manifested by anaemic, rachitic, and scrofulous chil- dren. Inflammations and other irritations of the buccal mucous membrane may also produce aphthae. This category includes catarrhal and ulcera- tive-stomatitis, sprue,-catarrhal and diphtheritic angina, sharp edges of the teet’h, inveterate smoking, etc. In certain cases, the development of the disease is associated with infectious diseases or certain local diseases. It occurs in scarlatina, measles, fibrinous pneumonia, typhoid fever, gastric, intestinal, and uterine affections. Aphthae appear in some women during menstrua- tion, in others during the puerperal condition or the period of lactation. The affection develops not infrequently in an epidemic form, and contagious influences can occasionally be demonstrated. The epidemics appear most frequently in the summer, then in the autumn, particularly after severe changes in the weather. Bohn denies the contagious character of aphthae. Brief mention may be made of the following case: The servant of a teacher visited her family in a remote village in which an epidemic of aphthae was prevailing. Two days later, the servant, who had returned to service, was taken sick with aphthous stomati- tis, and, a few days later, the child under her care. Then two of the other chil- dren were affected, and ten days later other cases appeared in the village. It has been claimed by various writers that aphthae may be conveyed from animals to man. II. Symptoms axd Anatomical Changes.—In nursing infants, aphthous stomatitis begins not infrequently with mild prodromal symp- toms: slight fever, irritability, increased thirst, increased salivation, pain on nursing. The characteristic changes depend upon the formation of round, white or yellowish patches, which are surrounded by a red zone, are slightly elevated, and cannot be removed from the mucous membrane. These patches may develop within a few hours. They vary from the size of a pea to that of a lentil, in some places 8 diseases oe the buccal CAVITE, ETC. are merely punctate. When they increase in size, they coalesce, and give rise to irregular, jagged patches, which are found particularly at the edges of the tongue and at the junction of the mucous membrane of the lips and gums. A considerable extent of mucous membrane may undergo the aphthous change. If the development of aphtlne is associated with the eruption of the teeth, the white patches are found first or exclusively at the site of the new tooth. Under other conditions, the patches appear with special frequency at the tip of the tongue, its lower surface and edges, the mucous membrane of the lips, and border of the gums. They are also found on the hard palate, uvula, and tonsils. According to certain authors, aphthae sometimes occur upon the intestinal mucous membrane. Fresh eruptions often appear after the outbreak of the original crop. Aphthae never form vesicles; they are the result of a fibrinous inflam- matory process in the mucous membrane, the fibrinous exudation being deposited immediately beneath the epithelium of the mucous membrane. The white patches consist of finely granular fibrin, which contains a few round cells. Recovery generally occurs from desquamation, more rarely from absorption of the exudation, but cicatrices are left over in all cases. If desquamation takes place, the epithelial cover first ruptures. The fibrinous exudation gradually loosens at the edge, and often rolls up. Finally, it is cast off entirely, and a shallow, at first congested portion remains, which is very rapidly covered with epithelium, and restitutio ad integrum is complete. The disease usually lasts one to two weeks. It is serious only in weak, poorly-nourished children, because the movements of suckling and mas- tication cause pain, so that the little ones are unwilling to nurse, and their nutrition is impaired still more. The aphthae sometimes develop near the excretory ducts of the sali- vary glands, occlude one or the other duct (generally Wharton’s duct), and give rise to tension, pain, and swelling of the gland on account of the stasis of saliva. If the duct is made permeable by a fine sound, a large amount of saliva is discharged, and the symptoms rapidly disap- pear. Baillard and Bouchut have observed necrotic changes in a few cases. Relapses often occur in adults. . III. Diagnosis.—The diagnosis is easy. The following mistakes are possible : a. Clumps of casein which have remained in the mouth in little children. The red areola is absent, and the lump is readily removed. b. Stomatitis is characterized by fcetor ex ore, a tendency to hemor- rhage, and degeneration of the tissue of the mucous membrane. c. Sprue is easily recognized by the characteristic fungus. d. In herpes of the buccal mucous membrane vesicles are present, from which, upon puncture, a fluid exudes. IV. Treatment.—Apart from the removal of the causes, treatment consists of the use of chlorate of potash, either as a gargle or by applica- tion with a brush, or internally (gr. xlv.: 3 iiiss., a teaspoonful to table- spoonful every two hours). Other remedies are unnecessary. The following have been recom- 9 mended : Brushing with muriatic acid, nitrate of silver, corrosive subli- mate, borax, lime water, etc. 4. Leucoplacia Oris. 1. In leucoplacia oris we find whitish, gray, yellowish, or yellowish- gray patches, which are especially frequent on the tongue, but also ap- pear upon the lips, mucous membrane of the cheeks, gums, hard palate, uvula, velum palati, and tonsils. Sometimes there are a few scattered plaques which hardly project above the level of the surrounding parts, sometimes the patches are distinctly elevated, especially at the edges, sometimes they form almost papillomatous excrescences. Occasionally they are almost horny in consistence, coalesce with one another, and cover a large part of the buccal cavity. On microscopical examination, the epithelial cells are found to have undergone marked proliferation, the upper layers are loosened and swol- len, the lower are not thoroughly developed. The papillae of the mucous membrane appear flattened, the vessels are dilated, and the subepithelial tissue is infiltrated with numerous round cells. The disease has been recently described under different names, such as pityriasis, ichthyosis, psoriasis, tylosis, teratosis linguae et oris, lichenoid. 2. The causes are : irritation of the mucous membrane by tobacco, alcohol, defective teeth, gastric disturbances, gout, syphilis. It is often associated with diseases of the skin (psoriasis, lichen planus, eczema, ichthyosis, syphilides, and epithelioma of the lower lip). It is more fre- quent in men than in women (among twenty-six cases collected by Mor- ris, twenty-two occurred in men, four in women). It is said to be remarkably frequent among the natives of India. It is rarely observed during childhood, and is usually observed between the ages of twenty and sixty years. 3. The symptoms sometimes consist merely of the visible changes in the mucous membrane. Some patients experience a feeling of rawness while eating. Impaired gustation and a hypochondriacal mood are occa- sionally observed, the latter being the result of the patient’s belief that his stomach is constantly disordered on account of the supposed coating on the tongue. As a rule, the disease runs a chronic course (sometimes more than thirty years). 4. The diagnosis is easy, since sprue, aphthae, and cauterization of the mucous membrane maybe excluded by the history, acute course, and microscopical examination. 5. The prognosis is doubtful. Numerous cases have been reported in which the disease was followed by epithelial cancer of the tongue (thirty-one times among sixty-eight cases reported by Weir). 6. Existing causes of the disease should be removed. Carlsbad, Vichy, and similar waters may be employed, and, if necessary, anti- syphilitic remedies. The following remedies have also been recom- mended: Arsenic (Fowler’s solution, aq. amygdal. amar., aa § ss., M. D. S. 5-10 drops t. i. d. after meals), hyoscyamus (aq. amygdal. amar., 3 v.; ext. hyoscyami, gtt. xx. M. D. S. 15 drops every two hours), or gargles of chlorate of potash, borax, salicylic acid, cauterization with chromic acid (one part to five) every three or four days. After excision of the patches, they often return in the cicatrix. The disease is often made worse by the use of iodide of potassium. DISEASES OF THE BUCCAL CAVITY, ETC. 10 DISEASES OF THE BUCCAL CAVITY, ETC. 5. 6'prue. Stomatomycosis Oidica. I. Etiology.—Sprue in the buccal cavity depends upon the prolifer- ation of a fungus, oidiuni albicans (probably saccharomyces albicans is more correct) upon the mucous membrane of the mouth. It is observed most frequently in the new-born, especially from the second to eighth weeks of life. In adults it is generally the result of protracted exhausting diseases (phthisis, cancer, diabetes, leukaemia, typhoid fever, etc.). In the new-born it is so much more apt to develop the more the gen- eral care of the patient, especially the cleansing of the mouth, is neglected. It is generally found in large maternity hospitals, foundling asylums, among the children of the poor, and in damp, poorly-ventilated houses. Feeble children, particularly those who are weakened by chronic diar- rhoea, have a special predisposition to the disease, for if the movements of nursing and deglutition are not very strong, and the mouth is not kept very clean, particles of food are apt to remain in the buccal cavity. They here decompose, and afford a favorable soil for the proliferation of the fungus. The disease is more frequent among bottle-fed infants than among those nursed at the breast. The majority of cases occur during the summer. Imperfect cleaning of the nipple of the bottle is often an exciting cause. Sprue is sometimes produced by placing the child at the breast of a nurse whose own child suffers from sprue, and whose nipple is not kept clean. The fungus has also been found in the air of the room in which there were children who suffered from the disease. Berg produced sprue by inoculation on the buccal mucous membrane. I have recently observed a very peculiar case of this disease. The patient, a girl of 20 years, has always been pale and weak. For one and one-half years, the tongue has presented a diffuse, light yellowish-gray coating which is two millimetres thick, and can be easily removed. It consists of spurs and threads of oidium albicans. Salivation is so marked that the fluid is constantly running from the mouth. Sleep is disturbed on account of the salivation. The patient suffers from anorexia. No- thing abnormal can be discovered in the internal organs. The pecu- liar features of the case are: The age of the patient, the idiopathic origin of the disease, and the uselessness of all remedies which have been employed. II. Symptoms.—If the development of the fungus is slight, all symp- toms may be absent. Profuse development of the fungus has a serious significance, both on account of the usually dangerous primary affection, and also on account of the danger produced by the sprue itself. The tip and sides of the tongue are generally the first to be affected, then follow the mucous membrane of the cheeks, lips, gums, hard palate, velum palati, and uvula. In severe cases, sprue is found in the pharynx, oesophagus, and upper part of the larynx. It is sometimes so abundant in the oesophagus as to give rise to occlusion of the canal. Cough and attacks of suffocation have been observed in sprue of the larynx. Beubold showed that mucous membranes which are provided with cylindrical or ciliated epithelium offer a vigorous resistance to the prolif- eration of sprue. Only in exceptional cases is it found in the stomach, nose, or those parts of the air passages which are provided with ciliated epi- thelium. The fungus is sometimes found in the contents of the stomach 11 and intestines, but in such cases it has simply been swallowed. It may also be aspirated into the deeper air passages, and give rise to putrid bronchitis or pneumonia. Sprue appears, at first, as a whitish or bluish-white, thin coating of the mucous membrane. On careful examination, it is found that, upon the tongue, it is situated mainly in the spaces between the fungiform papillae and on the mucous membrane near the excretory ducts of the follicles. These punctate spots gradually increase in size and thick- ness, and larger grayish-white or yellow, later brownish or blackish patches are formed, which finally coalesce with one another. At first, the patches cannot be removed by gentle rubbing, because they are situated beneath the uppermost layer of epithelium. At a later period, the epithelial layer bursts, the smooth surface becomes rough DISEASES OF TIIE BUCCAL CAVITY, ETC. Fia. 2. Oidium albicans from the mouth of a child aet. 9 months. Magnified 275 times, and uneven, and the deposit is removed, in part spontaneously, in part by mechanical means. The deposit consists chiefly of spores and threads of the fungus (Fig. 2). The spores are round or oval, with a distinct contour, very retrac- tile, sometimes uniformly finely granular, sometimes containing one or two larger nuclei. They may be scattered or collected into irregular masses, or arranged into so-called colonies. The thallus threads are elongated, straight, or slightly curved threads which vary in width. The broader ones contain transverse striations, while the narrower ones have a less distinct contour and hardly any transverse striae. The width of the threads varies from 0.003-0.005 mm. The inside appears finely granular, and in places contains oval cavities. In many threads inden- tations are visible. Here or immediately beneath the transverse septa we not infrequently find spores sprouting out laterally; some of these 12 DISEASES OF THE BUCCAL CAVITY, ETC. are converted into thallus threads. The same process may again take place from the latter. In addition to the fungus we find desquamated cells of pavement epithelium and a few round cells. In some places the fungus has pene- trated between the epithelium cells, or the threads are covered with individual epithelial cells. Rees states that the spores sometimes pene- trate the epithelium cells and proliferate within the latter. The development of sprue is not infrequently preceded by inflamma- tory changes in the mucous membrane. The latter is red, dry, hot, and sensitive to the touch. The infants often cry while nursing, and adults complain of burning and pain while eating. Afterwards salivation becomes profuse, and the mixed secretion of the mouth always has an acid reaction. Zweifel found that in the new-born the saliva contained no ptyalin. Infants affected with sprue often suffer from profuse and obstinate diarrhoea, the cause of which is not always clear. The diarrhoea some- times precedes the sprue, and favors the development of the latter by the exhaustion it produces; in other cases it is an accidental complica- tion; and in a third series of cases it is assumed that the fungus is swal- lowed, produces decomposition of the ingested milk, and thus causes the diarrhoea. The duration of the disease depends upon the care devoted to the patient. As a rule, it may be relieved in one or two weeks. III. Anatomical Changes.—The fungus enters between the upper horny layers of epithelium, proliferates in the middle layer of the epithe- lium, where it gives rise, as the result of compression, to disappearance of the cells with the exception of the nuclei, while the upper layers of epithe- lium are merely flattened. In a few places the fungus may pass into the submucous tissue, and may even enter the blood-vessels and lymphatics. The vessels are congested, but, as a rule, inflammatory changes are absent. Zenker’s case shows that it is possible that the fungus may be carried away by the current of blood, after it has entered the vessels, to the periphery; for example, to the brain, where it may act as an embolus and continue to proliferate. According to Rees and Grawitz, the fungus of sprue is really identical with saccharomyces mycoderma which is often found upon alcoholic and many fermenting substances. At all events, it is not identical with oidium lactis, which produces the acid fermentation of milk. The fungus is very widely diffused, and a slight preparation of the mucous membrane alone seems to be necessary in order to allow the pro- liferation in the buccal cavity of the numberless spores which are floating in the air. Haussmann states that sprue is found in the vaginae of eleven per cent of pregnant women, and thinks it is conveyed to the new-born during delivery. But this does not explain the striking fact that the new-born are usually free from the disease for the first few weeks. IV. Diagnosis.—With the aid of the microscope the diagnosis is easy. Patches similar to sprite are found when sarcina develops on the buccal mucous membrane, but this is distinguished by the shape of the fungus (vide Fig. 4, p. 14). V. Prognosis.—The prognosis is not always favorable. In some cases sprue is an unpleasant complication of a disease which is in itself dangerous, in others it may produce serious results by giving rise to dis- DISEASES OF THE BUCCAL CAVITY, ETC. 13 turbance of nutrition, diarrhoea, occlusion of the oesophagus, or disease of the larynx, bronchi, and lungs. VI. Treatment.—The prophylaxis is very important. In children the mouth should be cleaned after each meal, or after vomiting, and the bottle and its nipple should also be carefully cleaned and kept in water when not in use. After the child has nursed, the nipple of the mother’s breast should be carefully washed. In adults, likewise, the mouth should be carefully cleaned after each meal. If sprue has formed, the mouth should be washed with borax every two hours (B Sol. natri biborac., gr. lxxv.: § vij. D. S. Externally). Chlorate of potash has no effect in this disease. The application of muriatic acid, nitrate of silver, chloride of iron, or alum is necessary Fig. 3. only in very obstinate cases. Kehrer claims that weak solutions of borax favor the development of oidium albicans. Appendix. It is not surprising that the mouth, with its warm, moist atmosphere and its decomposing fragments of ingesta, should offer a favorable soil for the development of low organisms. A large number of mould fungi and bacteria may be found in every mouth, particularly in the coating of the tongue and the tartar of the teeth. \Ve will here refer somewhat in detail to two varieties. a. Leptothrix buccalis. This fungus—included by some among the algae, by others among the schizomycetes—forms long threads, which usually project from a mass of granules and rods. The threads are sometimes uninterrupted, sometimes appear to be made of small divisions arranged like a rosary (Fig. 3). They are found abundantly in the tar- tar and, according to Leber and Kottenstein, play an important part in dental caries. On the application of iodine they assume a blue color. Spirochsete plicalilis is also found in the tartar. Leptothrix buccalis from the tartar of the teeth. Magnified 275 diameters. 14 DISEASES OF THE BUCCAL CAVITY, ETC. 1). Stomatomycosis sarcinica has been observed a number of times by Friedreich in patients who were enfeebled by chronic diseases. The fungus was sometimes present in such masses as to form small white patches. They are easily recognized by their square shape and charac- teristic grouping. A black coating on the tongue has recently been described, in which fungus threads and spores were found by Lanceraux (glossophyton according to Dessoir). The disease is insignificant, but is occasionally obstinate. A. Fraenkel has recently obtained bacteria, similar in appearance to pneumococci, from the mouth of healthy individuals. When pure cultures were made and inoculated upon rabbits, the animals died of septicaemia. Fraenkel proposes for this bacterium the term coccus of Fig. 4. Stomatomycosis sarcinica. After Friedreich. sputum-septicaemia. The comma-iike bacillus of the mouth is not identical with KoclPs comma-bacillus of Asiatic cholera. 6. Salivation. Ptyalism. I. Etiology.—Ptyalism means increased secretion of saliva; as a general thing the saliva flows, in part, from the open mouth. It occurs most frequently as the result of reflex irritation of the nerves of the salivary glands, and hence it is generally observed as a symptom of most diseases of the mouth (stomatitis, dental caries, denti- tion, inflammation of the maxilla, etc.). I recently treated a boy of ten years in whom the disease lasted three months after an attack of mumps. Both parotid glands secreted very profusely, especially the one which had been affected. The occurrence of salivation after the administration of mercury, more rarely of iodine, gold, silver, copper, lead, and arsenic, is probably the result of reflex irritation of the nerves of the salivary glands by preceding stomatitis. Substances which have a sharp taste (tobacco, condiments, etc.) may also give rise to increased secretion of saliva as the result of irritation of the buccal mucous membrane. Ptyalism may also be produced by trigeminal neuralgia. In some cases, the reflex irritation is produced by remote organs. Frerichs produced ptyalism in dogs by irritation of the gastric mucous membrane. Clinically it is found that ptyalism is a frequent accompa- 15 niment of many gastric and intestinal diseases (gastric catarrh, ulcer and cancer, cardialgia, worms, etc.). It was formerly held that diseases of the pancreas, spleen, and liver gave rise to salivation, but this has not been proven. Diseases of the genital organs (uterus and ovaries) not infrequently give rise to ptyalism. Stark reports two cases in which insane women suffered from salivation whenever they were affected with nympho- mania. Men and women have complained to me not infrequently that they suffered from salivation immediately before and during coitus. Some women suffer from very annoying ptyalism during pregnancy. The disease is sometimes the result of irritative conditions of the cen- tral nervous system. It is well known that certain gustatory sensations may produce ptyalism, and this is also true of violent emotions. Le- pine and Bochefontaine have shown that irritation of the anterior part of the cerebrum in dogs caused increased secretion of the submaxillary gland. Ptyalism is not infrequent in hypochondriacal, hysterical, and insane individuals. Paulicki reports the case of a melancholiac who suf- fered for five years from salivation, which occurred every other day from 8 a.m. to 9 p.m.; it was associated with diaphoresis and profound depres- sion. The affection has been observed a number of fimes in diseases of the medulla and pons, which contain the first centre for the salivary nerves. Certain vegetable substances may produce ptyalism by action on the nerve centres (jaborandi or its alkaloids, pilocarpine, physostigmine, nico- tine, digitalis). Sometimes it is the result of irritation of the peripheral nerves, espe- cially diseases of the middle ear which affect the chorda tympani. Some individuals suffer from ptyalism if they hear very high and shrill notes. According to some writers, it is observed occasionally in certain infectious diseases (typhoid fever, intermittent fever, dysentery). The cause of salivation sometimes remains unknown (idiopathic ptyalism). II. Symptoms.—The normal daily amount of saliva varies from two hundred to fifteen hundred ccm. In practice, the disease is very easily recognized if disturbances of deglutition (pseudo-salivation) can be excluded. The patients state that saliva accumulates very quickly and in large amounts in the mouth. Speech is thereby interfered with, and the pa- tients must often swallow the saliva, and finally are compelled to expec- torate very frequently, or to allow the saliva to run from the open mouth. There is occasionally a feeling of tension in the region of the glands, and they may be found somewhat swollen and hard. Some pa- tients also complain of a sensation of warmth in the glands'. On account of the various changes which may have been present in the mouth, the mixed buccal secretion does not always possess the same qualities. In cases of diseases of the mouth, the fluid is often acid, cloudy from profuse desquamation of epithelium, often foul-smelling and bloody or dirty in color. The symptoms of ptyalism may be produced experimentally by the administration of jaborandi or pilocarpine (0.01 subcutaneously), and the secretion can be collected separately by the introduction of canulae into the excretory ducts of the salivary glands. The saliva which first es- capes has an alkaline reaction, after a while it becomes neutral or even DISEASES OF THE BUCCAL CAVITY, <$TC. 16 DISEASES OF THE BUCCAL CAVITY, ETC. acid. The reaction often varies from time to time, but if the experi- ment is continued for any length of time, the saliva tends permanently to remain acid. This is also true of ptyalism which results from other causes. The amount of fluid may be very considerable (as much as eleven thousand com. in twenty-four hours, according to some old reports). After a time, the fluid deposits a sediment* composed of epithelial cells, a few mucous and pus corpuscles, crystals of carbonate of lime, and amor- phous albuminoid granules. In some cases, the saliva does not contain rhodankalium and ptyalin. A clinical distinction should be made between transitory and contin- ued ptyalism. The former lasts only a few hours or days, and presents a favorable prognosis, since it subsides upon the removal of the cause. Protracted ptyalism may persist for months, years, even for life, is often very unyielding under treatment, and may prove a source of danger. The affection gives rise, as a rule, to disturbed sleep, either because the saliva is constantly flowing from the mouth, wetting the pillow, and thus rousing the patient very often, or because it flows into the larynx, and causes attacks of cough and suffocation. If the saliva flows into the pharynx, the patient will be disturbed by frequent acts of deglutition. Erythema of the integument of the chin is produced occasionally by the overflowing saliva. Digestive disturbances are often produced. The ingestion of the large amounts of saliva, mixed with air bubbles, gives rise to a feeling of fulness and distention in the region of the stomach, and interferes with gastric digestion. Constipation is generally, diarrhoea rarely, observed. The saliva accumulated in the stomach is occasionally vomited, espe- cially in hard drinkers, who generally reject in the morning the saliva which has accumulated in the stomach over night. If the secretion is very profuse, diuresis may be scanty, or the relative amounts of urine ;and saliva vary on alternate days. In one of my cases, a slight degree of polyuria lasted for a number of days after the salivation was relieved. The patients may emaciate, their appearance becomes almost cachetic, and occasionally they die from exhaustion—less as the result of ptyal- ism than of the causes which have given rise to it. III. Diagnosis.—The disease is easily recognized, but we should never be satisfied with the diagnosis of ptyalism, since this is only a symptom of various diseases. IV. Prognosis.—This always depends upon the etiology, for while salivation is almost physiological in some cases (dentition of childhood), and in others may be relieved by removing slight causes (local diseases of the mouth), it may also constitute a very obstinate and serious dis- ease (affections of the central nervous system). V. Treatment.—As a matter of course, the causes should be re- moved whenever possible. If this cannot be done (for example, in dis- eases of the central nervous system), almost the only rational measure is the administration of sulphate of atropia, gr. pulv. althaeae, q. s. ut ft. pil. No. xx. D. S. 1 pill t. i. d.; or atropiaB sulph., gr. : 3 iij., 4 to 1 syringeful subcutaneously. This remedy possesses an inhibitory influ- ence upon the secretory nerves of the salivary glands. Very little can be expected from the use of astringent mouth washes, or the internal ad- ministration of astringents. The use of opium is recommended by many. DISEASES OF THE BUCCAL CAVITY, ETC. 17 Appendix. Little is known concerning diminution of the salivary secretion. It may be produced artificially by the administration of quinine. Patients complain not very infrequently of a peculiar dryness in the mouth. This is observed in diabetes mellitus and insipidus, and small contracted kid- neys, i. e., diseases which are associated with an abnormally profuse ex- cretion of urine. Similar complaints are made in febrile diseases. Dryness of the mouth also appears occasionally as a symptom of old age, and in hysterical, hypochondriacal, and anaemic individuals. Buxton recently described diminished secretion of saliva after an attack of mumps, and, at the same time, impairment of taste. Drinks should be offered frequently to febrile patients, and the lips and tongue smeared with vaseline. In a few other cases I have employed pilocarpine internally and subcutaneously, with temporary benefit. Buxton obtained relief from the application of one electrode to the back of the neck and the other to Steno’s duct. 7. Fibrinous Inflammation of the Excretory Duct of the Salivary Glands. Sialodochitis Fibrinosa. Kussmaul was the first to call attention to this disease; it has been observed in Steno’s duct and the duct of the submaxillary gland. At first, retention of saliva results; the affected gland becomes painful, tender on pressure, and swollen. Fever, inflammatory phe- nomena, and erysipelatous changes in the skin were observed in one case, absent in two others. Pressure or catheterization of the duct dis- charged some purulent, flocculent, occasionally foul-smelling masses and fibrinous casts of the duct. In addition to fibrin and round cells, Weber found bacteria in the expressed plugs. In Kussmaul’s case, the disease had lasted ten years, and was attributed to pressure. Relapses were fre- quent, and were preceded for a few days by a salty taste in the mouth. Treatment consists in the removal of the plug in the duct by pressure or catheterization. Appendix.—Mechanical retention of the saliva is sometimes the re- sult of aphthous or diphtheritic changes near the opening of the excre- tory ducts, and which occlude these ducts. Occlusion of the canals may also be brought about by salivary calculi and foreign bodies. Verneuil thinks that this may also be the result of spasm of the muscular coat of the ducts. If the saliva is retained in the gland, the organ en- larges, the patient experiences a feeling of tension, and later of pain, and the integument appears tense and shining. These symptoms rapidly subside if the excretory duct is made permeable by the passage of a sound. 8. Acute Catarrhal Inflammation of the Soft Palate and Mucous Mem- brane of the Pharynx. Angina, and Catarrhal Pharyngitis. I. Etiology.—This disease is generally accompanied by disturbance of deglutition, The act of swallowing is painful and produces the sen- sation as if the inflamed region were narrowed (hence the term angina). The anginal disturbances are partly the result of local narrowing from the swelling of the inflamed tissues, partly of hyperassthesia of the mu- cous membrane, partly of paresis of the muscular tissue of the soft pal- ate and pharynx from infiltration of the muscles with inflammatory 18 DISEASES OF TIIE BUCCAL CAVITY, ETC. transudation. These disturbances are particularly severe when the soft palate is affected by the inflammation, because this part forms a natural narrowing of the tract. In some cases, the soft palate and pharynx are affected simultaneously, in others only one or the other is inflamed, and finally circumscribed parts may alone be attacked. Hence the terms angina et pharyngitis diffusa et circumscripta. The disease may be primary or idiopathic, secondary or symptomatic. Primary angina and pharyngitis include the rheumatic, traumatic, thermic, and toxic forms. Rheumatic angina not infrequently follows a wetting, when strong winds and changeable weather are prevailing, particularly in the spring and autumn. Nevertheless the question has been raised whether tiie term infectious angina should not be substituted for rheumatic angina. At all events, careful examination often shows that the supposed expo- sure cannot be proven to have been the cause of the disease. Further- more, the local changes are not infrequently preceded for days by febrile prodromata—a feature which could hardly be expected in a local disease resulting from a cold. Furthermore, the general symptoms and local changes are often strikingly disproportionate to one another; in addi- tion, the disease is found to occur in epidemics, and cases of infection are observed. The epidemic outbreak and infection are apt to occur in schools, barracks, hospitals, etc. The bacterium of rheumatic angina has not yet been discovered. Neverthe- less, we believe that a cold hardly acts in any other way than by favoring the development of bacteria. The predisposition to infectious angina is very unequally distributed. Children are affected with special frequency, and distinct predisposition is manifested until the twentieth to twenty-fifth years. Feeble, anaemic, and scrofulous children are prone to the disease. Heredity occasionally plays a part in the etiology, and in some cases a predisposition is ac- quired. This is especially true of individuals who are improperly clothed, who enervate their constitution by avoiding cool baths and fric- tions, live in rooms which are excessively warm, and do not exercise in the open air. Why in one individual this organ, in another that one, constitutes the locus minoris resistentias is unknown. Catarrh of the soft palate and pharynx may be produced in a mechan- ical way by foreign bodies, such as fish-bones and other sharp substances which have injured the mucous membrane or have been wedged into it. The inhalation of dust may have the same effect. The disease is also produced by too loud or continued speaking and singing (preachers, teachers, singers, officers, etc.). Among the thermal irritants are excessively hot or cold articles of diet, the inhalation of hot vapors. Chemical irritants may have a direct or indirect action. In the lat- ter event, the toxic substance is first received into the blood-vessels and then is deposited upon the mucous membrane, where it gives rise to irri- tation. Direct action is observed after the ingestion of acids, alkalies, and other irritating substances; indirect action is observed after the in- ternal administration of mercury, bromine, iodine, arsenic, antimony, gold, silver, lead and copper, belladonna and veratrine. The secondary catarrhs of the soft palate and pharynx include inflam- mations which are propagated from adjacent parts, and those which oc- cur during the course of certain infectious diseases. 19 DISEASES OF THE BUCCAL CAVITY, ETC. The former variety is observed in stomatitis, inflammation of the nasal mucous membrane and larynx, and in gastric catarrh. The older physicians very often assumed the existence of a “gastric” angina, be- cause coated tongue, vomiting, and anorexia often make their appear- ance in angina and pharyngitis. We must be careful, however, not to mistake the effect for the cause. Among the infectious diseases, angina and pharyngitis are observed regularly in scarlatina; indeed, the angina may be the sole manifestation of scarlatina. Angina also occurs in variola, measles, and roetheln, and is often observed in typhoid, typhus, and relapsing fever, more rarely in fibrinous pneumonia. It is also observed in facial erysipelas, but we must here differentiate between a secondary angina and one which is propagated directly from the external skin to the mucous membrane. Inflammation of the soft palate and pharynx may occur as an indepen- dent erysipelas of the mucous membrane, independently of cutaneous erysipelas. The French have called attention to the relations between acute articular rheumatism and angina; the latter may either precede or follow the articular affection. Syphilis very often gives rise to catarrhal angina and pharyngitis. Intermittent fever also exerts an influence in this direction, and a num- ber of cases of intermittent angina have been described. According to Niemeyer, visceral gout is sometimes manifested as a catarrhal angina (vide Yol. IV.). II. Symptoms and Anatomical Changes.—Acute catarrhal angina and pharyngitis not infrequently run the course of an acute infectious disease. The scene opens with a violent chill, followed by high fever (40° C. or more). After a while the patient complains of difficulty and pain in swallowing. A few days later, the fever subsides quite suddenly, not infrequently after an outbreak of perspiration, but a feeling of marked weakness persists for some little time. Epileptiform convul- sions may occur in children at the time of the chill and high fever. The severity of the general symptoms often exhibits a striking disproportion to the local changes, a very slight circumscribed redness of the mucous membrane sometimes being associated with general symptoms of a seri- ous character. The symptoms just sketched occur particularly in so-called rheumatic angina; when it is the result of other causes, the disease often develops very gradually, and the subjective symptoms are more prominent. The chief subjective symptom is the disturbance of deglutition. This is often particularly annoying on account of the increased produc- tion of saliva and mucus, which stimulates the patient to repeated deglu- tition. Occasionally there is a sort of tenesmus of deglutition. The more diffuse and intense the catarrh, and the greater the swelling of the inflamed parts, the more difficult and painful are the movements of deglutition. The pain is sometimes so great that the patient refuses food. Speaking may also give rise to a feeling of tension and pain, on account of the traction on the structures of the soft palate. In cases in which the uvula is markedly inflamed, the enunciation of the letter r is especially impaired. Spontaneous pains are often felt; they are located immediately behind the angle of the lower jaw, but sometimes radiate into the region of the ear. The head is often held stiffly or obliquely, the latter when the inflam- 20 DISEASES OF THE BUCCAL CAVITY, ETC. mation is unilateral; the head is then inclined towards the diseased side. Rotatory and nodding movements are followed by severe pain. The jaws are sometimes almost immovable, a narrow fissure being left between them. Every active or passive effort to open the mouth gives rise to severe pain, and articulation is thus interfered with. If the tonsils are swollen, the speech becomes nasal in character. Saliva some- times flows in an almost constant stream from the open mouth. If the disease is complicated with stomatitis, the saliva may be cloudy, even tinged with blood, and very foul smelling. A disagreeable fcetor ex ore is often observed. The submaxillary glands near the angle of the lower jaw are usually enlarged and tender to the touch. Some authors state that the enlarged tonsils may be felt from the outside, but they seem to have been mis- taken for swollen lymphatic glands. The movements of mastication are generally painful and difficult. To examine the throat, the patient is placed in front of the window, the mouth opened as wide as possible, and the head directed upward so that the light falls full into the pharynx; the tongue is then depressed with a spoon or spatula. The view is generally improved if the patient says a or ah. The examination is difficult in little children, and an assistant may be required to hold the little one and compress the nostrils. When the child opens his mouth to breathe, the spatula should at once be intro- duced. The inflammatory changes have been divided into superficial, paren- chymatous, and lacunar, although these forms may not be entirely dis- tinct from one another. In superficial catarrh, the inflamed mucous membrane is reddened and swollen. The redness is sometimes uniform and diffuse, sometimes in patches, sometimes hemorrhagic in places; its intensity varies greatly, and it may even have a bluish tinge. The swelling is especially marked in those places in which the submucous tissue is abundant and loose. The uvula may be thickened into a shapeless mass, and lengthened so that its tip rests on the base of the tongue, and gives rise to nausea and vomiting. The pillars of the palate may be swollen to such an extent that the tonsils appear very small in comparison. If the tonsils in par- ticular are inflamed and swollen, they may almost touch one another in the median line. When one tonsil is alone affected, the uvula is pushed towards the opposite side. In the beginning, the secretion of the mucous membrane is often diminished, so that the inflamed parts appear very dry. At a later period, the secretion is increased, and the parts are cov- ered with a vitreous or slightly puriform, cloudy mucus. The follicles of the mucous membrane may be swollen. This is shown by the nodular appearance of the mucous membrane; the small, grayish granules corresponding to the enlarged follicles which are filled wfitli secretion. The rupture of individual follicles gives rise to super- ficial losses of substance. Vigorous desquamation of the epithelium of the mucous membrane sometimes takes place. The swollen epithelial cells sometimes remain upon the mucous membrane as grayish deposits, and to the inexperienced eye may look like diphtheritic deposits. The inflamed -parts also present a great tendency to hemorrhage, and this may be produced by contact during examination. In parenchymatous (phlegmonous) angina, not alone the surface of the mucous membrane, but the tissue proper of the membrane or the in- 21 DISEASES OF THE BUCCAL CAVITY, ETC. terlacunar connective tissue of the tonsils is involved. Hence the ten- dency to the formation of abscesses. Clinically, this form of the disease is characterized by very severe general symptoms. Anatomically it is characterized by considerable swelling of the inflamed parts. If the ab- scess opens spontaneously, there is danger of suffocation if the perfora- tion occurs during sleep and the pus flows into the larynx. In some cases the pus perforates externally. Cases have been reported in which the carotid was eroded, and fatal hemorrhage ensued. In other cases, external fistulae formed, with inflammation of the subcutaneous tissue of the neck and passage of pus into the thorax. Phlegmonous angina may also give rise to oedema of the glottis, which proves fatal unless we inter- fere quickly and actively. The patients feel very much relieved immediately after spontaneous or artificial discharge of the pus. Suppuration generally continues two to four days, and then recovery follows. The pus sometimes has a nau- seous odor. The lacunar inflammation affects the tonsils alone. The border of the lacunae is found to be very red, and at the same time the secretion of the follicles is increased. The lacunae contain a thick, puriform, later caseous secretion, which varies from the size of a pin’s head to that of a pea, has an extremely foul odor when squeezed, and is composed chiefly of rod-shaped bacteria, drops of fat, needles of the fatty acids, choles- tearin crystals, and a few lymph-corpuscles. Complications occur not infrequently in catarrhal angina and pharyn- gitis. If the tonsils are very much swollen, the naso-pharyngeal space may be narrowed to such an extent that respiration is possible through the mouth alone. But if the tonsils are almost in contact, the slit for the current of air may be too narrow, the patients suffer from dyspnoea and danger of suffocation, and cyanosis and signs of cerebral congestion make their appearance. These symptoms are especially dangerous in infants at the breast, because they render nursing difficult or impossible. Pulmonary conges- tion, bronchitis, and pneumonia are apt to develop because the infants are unable to breathe well with the mouth. Many patients complain of impaired hearing and ringing in the ears. This is sometimes the result of mechanical narrowing of the opening of the Eustachian tube, sometimes of catarrh of the mucous membrane of the tube. The latter may lead to otitis interna, and thus give rise to serious symptoms and dangers. Gastric symptoms (vomiting, anorexia, constipation) occur very often in the course of catarrhal angina, and not infrequently the disease begins with such symptoms. I have repeatedly found albumin and casts in the urine; haematuria has also been observed. Cerebral symptoms (convulsions, delirium, clouded consciousness) are especially frequent in children. The disease generally lasts only a few days. Many so-called ephem- eral fevers of childhood are the result of catarrhal angina. The disease rarely lasts more than one to two weeks. One attack predisposes the patient to a relapse. It is sometimes found that the relapses chiefly or exclusively affect the former site of disease. Furthermore, the relapses often present the same character of inflammation (superficial, phlegmonous, lacunar) as the original at- tack. The following sequelae may occur : transition into chronic inflamma- 22 diseases of the buccal cavity, etc. tion, hyperplasia of the tonsils, in very rare cases paralysis of the pharynx or general paralysis. III. Diagnosis and Prognosis.—The diagnosis can be made at once from a mere inspection of the parts. The prognosis, as regards life, is almost always good. Danger arises only in children if there is an unusually high fever. The prognosis as regards permanent recovery is not so good, since relapses occur repeatedly in many cases. IV. Treatment.—Prophylaxis is an important part of treatment. If the patients have been coddled and enervated, the constitution should be gradually hardened by cold frictions and exercise in the open air, and by salt-water baths in summer. Individuals who are required to strain their vocal organs should spare them as much as possible. The inhala- tion of dust should be prevented by suitable apparatus, etc. The treatment of acute angina and pharyngitis is causal, local, and symptomatic. The causal treatment purposes a speedy removal of the causes (iodine and mercury in syphilis, quinine in intermittent fever, etc.). In local treatment, inhalations and applications with the brush seem to us to be more suitable than gargles. We may employ solutions of chlorate of potash (gr. lxxv.: 1 vij.), alum, muriate of ammonia, bicarbonate of soda, etc. Abortive treatment by the application of a strong solution of nitrate of silver (gr. xv.: 3 ss.-i.) is not always successful. Compression may be ap- plied to the throat in the following manner : a cloth dipped in tepid water is wrung out and placed around the neck; it is then covered with a dry cloth, and finally with a piece of oiled silk. If an abscess forms, the pus should be removed as early and freely as possible with the aid of the knife. In relieving fever, preference should be given to antipyrin ( 3 i.-ij. to 3 xiv. of water by enema). B. Fraenkel obtained very rapid success from the use of quinine (gr. x.-xv.) in lacunar angina. 9. Chronic Catarrh of the Soft Palate and Pharynx. Chronic Catarrhal Angina and Pharyngitis. I. Etiology.—Chronic catarrh of the soft palate and pharynx is a frequent and annoying complaint, and not infrequently interferes seri- ously with the patient’s ability to work. The inflammation may be diffuse or limited to a few parts of the palate and pharynx. The disease is observed most frequently from the twentieth to the thirty-fifth years; it is rare in childhood. Men are more frequently affected than women. A feeble, nervous constitution predisposes to the malady. Hereditary influence is said to have been observed in a number of instances. Mackenzie and Lemon maintain that a very large pharynx predisposes to the disease. Chronic catarrh sometimes develops as the result of repeated relapses of an acute attack. In other cases, the disease appears in a chronic form from the beginning. All those causes which have been mentioned in the previous section may also act as the etiological factors in that form of chronic catarrh which follows repeated acute attacks. The following are the causes of that variety which is chronic from the beginning : a. Constant and loud talking and singing ; the disease is often ob- served in teachers, preachers, singers, actors, etc. DISEASES OF THE BUCCAL CAVITY, ETC. 23 b. Immoderate use of alcohol is not an infrequent cause. The less diluted the alcohol, the more apt is the disease to develop. c. Inveterate smoking, especially cigarette smoking, is also an etiolo- gical factor. It must be remembered, however, that a number of causes .act together in some of these cases. . d. Inhalation of dust has also been mentioned as a cause, but Mac- kenzie thinks that its efficacy has been overestimated. This statement does not agree with our own experience. e. The disease is sometimes observed as the result of chronic stasis in chronic diseases of the heart and lungs. /. It is sometimes the result of other chronic diseases, viz., Bright's disease, malaria, syphilis, phthisis, scrofula, gout, chronic rheumatism of the muscles and joints, etc. g. In some cases, the disease is propagated from other parts (catarrh of the nose, larynx, stomach, oesophagus). h. According to certain authors, the disease may develop in a reflex manner (?), especially as the result of uterine diseases. II. Symptoms and Anatomical Changes.—The majority of pa- tients who suffer from diffuse catarrh of the soft palate and pharynx are annoyed by a feeling of dryness, tickling, and a feeling as if a foreign body were present in the throat. This is particularly noticeable on awaking in the morning and, as a rule, is so marked in talking and singing as to seriously interfere with these acts. At the same time, the chronic laryngitis, which is generally produced by the same causes which have given rise to the pharyngitis, interferes with the clearness and timbre of the voice. An unusual secretion of mucus often compels the patient to hawk and cough a good deal. If the mucus is very tough, movements of strangling and vomiting are not infrequently produced during expectoration. In many patients, these symptoms are especially severe in the morning after rising. Others attempt to get rid of the mucus by swallowing it. The tonsils may be very considerably enlarged as the result of chronic inflammation. The speech then assumes an unpleasant nasal character, the patients are often forced to breathe through the mouth, many suffer from dyspnoea during sleep, and are disturbed several times a night. On account of the narrowness of the opening of the Eustachian tube, the patients often complain of difficulty of hearing and ringing in the ears —symptoms which may also result from propagation of the catarrh of the pharynx to the Eustachian tube without marked affection of the tonsils. The uvula may also undergo hyperplasia, often projects upon the base of the tongue, and thus gives rise to strangling, nausea and vomiting. Tonsillar hypertrophy and hyperplasia sometimes constitute an inde- pendent affection, the result of circumscribed chronic inflammation. Among other forms of circumscribed catarrhs, Schmidt makes special mention of chronic lateral pharyngitis; it often produces very annoying symptoms, and is readily overlooked on account of its concealed position. Chronic catarrh is also divided into the superficial, parenchymatous, and lacunar varieties. In chronic superficial catarrh, the mucous membrane, as a rule, has a brownish-red or grayish-red color. Some of the vessels of the mucous membrane are occasionally found in a condition of varicose dilatation. The secretion of mucus is increased so that the patients are compelled to 24 DISEASES OF THE BUCCAL CAVITY, ETC. hawk frequently, and are especially hindered in singing and speaking. The masses of mucus occasionally contain specks of blood, and for this reason the disease is often mistaken for pulmonary phthisis. The pro- duction of mucus is sometimes so considerable that the posterior wall of the pharynx shines as if coated with varnish. In other cases, the secre- tion dries into greenish-gray crusts, especially at night, when the patients breathe through the open mouth. During the day, the patients experi- ence an annoying sensation of tickling, or as if a foreign body were situated in the upper part of the pharynx and, after vigorous strangling move- ments, the crusts are expectorated. The mucous membrane not infrequently appears uneven and granular (pharyngitis granulosa). The individual elevations generally have a grayish color, the furrows between them appear congested. The mucous membrane is sometimes extremely dry so that the patients are annoyed by a scratching, burning feeling; sometimes it is coated with tough, vitreous, or puriform mucus which necessitates frequent hawking and swallowing. These changes occur earliest, and to the most marked extent, upon the posterior surface of the pharynx. In very many cases, pharyngitis granulosa is a follicular affection, i. e., there is a chronic inflammatory hyperplasia of the follicular appa- ratus of the mucous membrane. Saalfeld has recently described pro- liferation of the lymphoid tissue of the mucosa around the excretory ducts, hypertrophy of the mucous glands, dilatation of the duct within the region of swollen tissue, so that the slit-shaped opening is seen at the apex of each granule; the mucous membrane around the granules is either unchanged or is thickened and infiltrated with cells. Chronic parenchymatous catarrh includes the hyperplasiae, especially of the tonsils and uvula, which have been previously discussed. In chronic lacunar catarrh, yellow, stinking plugs—thickened products of inflammation—are found in the lacunae of the tonsils. The plugs are occasionally calcified, forming tonsillar calculi which sometimes attain the dimensions of a pea. These plugs may be hawked up by the patient. Anxious individuals may regard the yellow masses as tubercles which have been expectorated from the lungs. A single lacuna may be alone affected, but this may bt the starting-point of frequent acute, inflammatory ex- acerbations. The disease sometimes gives rise to intolerable foetor ex ore. The patients themselves may perceive the foul odor, and I have treated a number of patients who suffered in consequence from an antipathy to food, and from gastric and intestinal catarrh, all of these symptoms rapidly disappearing after the primary affection was relieved. Among the complications and sequelas, bronchial asthma merits special mention (vide Yol. I., page 228). According to Kauchfuss, pharyngitis granulosa in children sometimes maintains a tendency to pseudo-croup (vide Yol. I., page 180). Individuals who are affected by chronic angina often suffer from acute and febrile exacerbations, and also exhibit a tendency to diphtheria. The disease often lasts for years, sometimes for an entire lifetime, if the etiological factors cannot be removed (teachers, clergymen, smokers,, etc.). III. Diagnosis and Peognosis.—The diagnosis is so easy that, further remarks are unnecessary. The prognosis is not grave so far as regards danger to life, but the- disease is not very amenable to treatment, and has a tendency to relapse.. Hope of permanent relief can hardly be entertained in the. case.' of tlroso 25 DISEASES OF THE BUCCAL CAVITY, ETC. individuals whose occupation renders the removal of the causes im- possible. TV. Treatment.—The causal treatment should occupy the first rank. Teachers, clergymen, etc., should abstain from the use of the voice as much as possible. Local treatment should also be taken into consideration. Simple superficial catarrh may be treated by the methods described on page 4. Good results are sometimes obtained from brushing the pharynx with tinct. iodi., tinct. gallarum, equal parts. The applications should be made daily, and immediately followed by gargling with water. The treatment is discontinued for a few days if pains and violent inflamma- tion develop. This plan of treatment may also be adopted in pharyngitis granulosa. Application of liq. ferri sesquichlorat, ( 3 iss.: 3 i.), zinc, chlorat. ( 3 ss_ :§i.), iodoform., acid, tannic., aa gr. xxvij., spirit, vin. dil. 3 xiv. Fig. 5. Threads of leptothrix and epithelium from the deposits in mycosis pharyngis leptothricia. Iodine- preparation. After Hering. Magnified 630 diameters. have been recommended. Some authors prefer the application of pow- ders, for example, alum or tannic acid. In advanced cases, each individual granule should be destroyed with caustics, such as nitrate of silver, chromic acid, or sulphate of copper. The galvano-cautery has also been employed with excellent results. Surgical interference is the best treatment for hypertrophy of the tonsils and uvula. 10. Mycosis Pharyngis Leptothricia. 1. This disease gives rise to the formation of yellowish patches (occa- sionally looking like horn), which are situated mainly in the crypts of the tonsils and base of the tongue. Inflammatory changes are absent, and there may be no subjective symptoms. Some patients complain of tickling, a feeling of a foreign body, and dryness in the throat. 26 DISEASES OF THE OESOPHAGUS. The changes are often discovered accidentally. The disease is entirely benignant, though very obstinate. Only fourteen cases have been hitherto observed. 2. If small particles of the deposits are treated with a five-per-cent solution of potash, and then teased, they are found to be composed, in part, of threads of leptothrix which turn blue on the addition of tinc- ture of iodine (Fig. 5). Cocci in zooglcea masses are also present. It is doubtful whether similar deposits are produced by other fungi. 3. The prognosis should be made with caution, because the fungus is apt to return very rapidly if mechanically removed. One case was rap- idly relieved by smoking. Very little effect has been obtained by direct applications, gargles, or cauterization. Galvano-cautery and tonsillotomy afforded at least temporary relief. PAKT II. DISEASES OF THE OESOPHAGUS. 1. Stenosis of the (Esophagus. I. Etiology.—Stenoses of the oesophagus are the result of abnormal •conditions’within the lumen of the tube, of diseases of its walls, or of morbid changes in adjacent organs Sintra-oesophageal, interstitial, and extra-oesophageal stenoses). Intra-oesophageal stenosis is the result, in most cases, of the ingestion of foreign bodies or abnormally large boluses of food. But even large, hard foreign bodies may be present in the oesophagus, although symp- toms of stenosis are entirely absent. Not a few cases have been reported in which foreign bodies in the oesophagus were found upon autopsy, al- though no symptoms were produced during life. Oidium albicans may proliferate upon the mucous membrane of the oesophagus to such an ex- tent as to occlude completely the lumen of the canal. Polypi which project from the wall of the oesophagus into its lumen may be regarded as on the border-line between the interstitial and intra-oesophageal causes of stenosis. Among the interstitial causes, the most frequent ones are cancer and cicatrices, the latter being generally produced by poisoning with acids or alkalies. The cicatrices are always preceded by ulcerative changes in the wall of the organ. The toxic cicatrices are the most important on ac- count of their frequency; in many cases they do not form until weeks after the poisoning. Stenosis has sometimes been observed after the ingestion of a too hot bolus, evidently as the result of ulceration (from the burn) of the oesophageal mucous membrane. Deglutition of a very hard and sharp morsel may act in the same way. The disease has also been observed a few times after small-pox, which is attended occasionally with the formation of pustules on the oesophageal mucous membrane. Ulcers resembling the round gastric ulcer have been found occasionally in the lowermost part of the oesophagus. These are probably the result of digestion of the mucous membrane by gastric juice which has passed into the oesophagus during an attack of vomiting (peptic ulcers), and, according to Debove, may terminate finally in cicatricial stenosis. (Eso- DISEASES OF THE OESOPHAGUS. 27 phageal stenosis is sometimes the result of syphilitic ulcerations follow- ing destruction of gummata in the walls of the organ; the canal may also be narrowed by the projection of gummata into the lumen. In very rare cases cicatrices and stenosis are produced by tubercular ulcerations. Abscesses in the walls of the oesophagus may act in the same man- ner as tumors of this region. In these cases the symptoms of stenosis have been known to disappear suddenly after rupture of the abscess. It has been justly questioned whether stenosis may be produced by hyper- trophy of the oesophageal muscular tissue. But the stenosis is occasion- ally the result of a congenital defect of development. The lumen of a circumscribed portion of the tube is unusually small, though the walls may be almost entirely unaffected. In these cases, the patients have generally suffered since childhood from difficulty in deglutition, espe- cially if the bolus of food is too large. Those forms of stenosis which are the result of muscular spasm (spas- tic strictures) are associated with changes in the walls of the oesophagus. Extra-oesophageal stenoses may be the result of numerous diseases, of which the following are the most important. Enlargement of the thyroid gland, whether the result of struma or of a true neoplasm (particularly cancer) sometimes gives rise to stenosis. The lateral prolongations of the gland often surround and constrict the oesophagus, and Huber reports a case in which the stru- mous degeneration affected only the lateral horns of the gland, but no swelling had been noticed anteriorly during life. The stenosis is also produced by enlargement of the cervical tracheo-bronchial and medias- tinal glands, and by inflammation of the mediastinal and cervical cellu- lar tissue. Gallard reports a case following a metastatic cancer in the connective tissue between the trachea and oesophagus (primary cancer in the stomach). The stenosis is sometimes the result of verte- bral changes: abscess in tuberculosis of the vertebrae, tumors, exostoses, and marked lordosis of the spine. It has also been observed as the result of dislocation of the hyoid bone and clavicle, excessive length of the styloid process and ossification of the stylo-hyoid ligaments. Among the diseases of the respiratory apparatus, cancer of the lungs and pleura gives rise to oesophageal stenosis with relative frequency. Stenosis has also been observed after inflammatory changes and thicken- ing of the arytaenoid and cricoid cartilages, though these really affect the lower end of the pharynx. Thickening and ossification of the cricoid car- tilage has also been described as a cause of oesophageal stenosis. This is also claimed with regard to enlargement of the thymus gland, but has not been proven with certainty. Van Swieten mentions stenosis as the result of retraction of the apex of the lung. In certain cases oesophageal stenosis is produced by changes in the circulatory apparatus (extensive pericarditis, hypertrophy of the heart, aneurisms of the aorta, subclavian or carotid arteries). It was formerly assumed that stenosis of the oesophagus was produced by rhythmical filling of the right carotid in cases in which this vessel, contrary to the rule, took its origin from the aorta below the left subcla- vian and passed to the right side of the body either between the oesopha- gus and spinal column or between the oesophagus and trachea. Iiyrtl held, however, that this was conceivable only when that portion of the vessel which passes transversely across the oesophagus is in a condition of aneurismal dilatation. If this condition is not present, any changes which may be produced must be looked for in the circulatory organs. It 28 DISEASES OF TIIE (ESOPHAGUS. is evident that the act of deglutition will be able, by means of compres- sion, to interrupt, temporarily, the circulation in the right carotid. This harmonizes with the fact that the right radial pulse has been known to disappear during the act of deglutition, that some patients complained, at this time, of palpitation, anxiety, and syncopal attacks, and that, upon autopsy, the portion of the right carotid, which was situated centrally from the oesophagus, was in a condition of aneurismal dilatation. Zenker’s case presented analogous conditions. The patient, a very short man, died suddenly, and no cause of death could be ascertained. It was found that itlie aorta passed over the right bronchus and then passed between the oesophagus and spinal column to the left side of the latter. Hence it is possible that temporary occlusion of the aorta oc- curred during the act of deglutition, and that this proved fatal by giving rise to sudden anaemia of the brain. II. Anatomical Changes.—Stenosis of the oesophagus affects most frequently the lower third, next the region of the bifurcation of the trachea. As a rule, there is only one stenosis, more rarely two or more. The length of the stenosed portion varies considerably. Cases in which the entire organ is narrowed are rare, and occur generally after the action of caustic poisons. The degree of stenosis may be so marked that a fine sound is passed through with difficulty, and cases have been reported in which cicatricial structures had converted the en- tire oesophagus into a solid connective-tissue strand. Annular stenoses are apt to give rise to symptoms at a very early period, while the effects of stenosis may be compensated for a long time if only a portion of the transverse section of the oesophagus is affected, or if it is compressed upon one side alone. In the latter event, oesophageal adhesions, and hence inability of the organ to move to one side, may be a source of great danger. The oesophagus is usually dilated and sometimes forms a diverticu- lum above the site of stenosis. The muscular coat is often hypertro- phied and the mucous membrane in a condition of chronic catarrh. Be- low the stenosis the organ is usually collapsed and its walls atrophic, while the mucous membrane presents numerous longitudinal folds. We will not describe the anatomical changes which constitute the causes of the stenosis. III. Symptoms.—The most prominent symptom is difficulty in de- glutition (dysphagia mechanica). This develops suddenly (foreign bodies, cases of spastic stricture), or appears gradually and keeps on increasing for weeks and months (the latter is by far the more frequent). At first the patients have a feeling as if a large solid bolus had stuck fast in a certain spot. Gross errors are made by the patients with regard to localization. They endeavor to prevent the disagreeable sensation by masticating the food very finely or mixing it with a large amount of saliva, or by taking a sip of water to wash it down. After a certain length of time, however, all these manoeuvres fail. Some patients at- tempt to obtain relief by making repeated movements of deglutition after swallowing a morsel, by making certain rotatory and nodding move- ments with the head and spinal column, or by stroking the side of the neck with the fingers. Pain is always felt while the food is passing the site of stenosis. Sometimes the first morsel produces severe symp- toms, but subsequent ones pass more easily. If deglutition is not performed with sufficient caution, great anxiety- and dyspnoea may occur after a number of morsels have been swallowed- DISEASES OF THE (ESOPHAGUS. 29 This is owing to the fact that the food accumulates above the stenosis, and distends the oesophagus so that the latter compresses the air passages situated in front of it. Perhaps it is partly the result of mechanical irritation of the recurrent nerves which are situated close to the oeso- phagus. These symptoms subside as soon as the food has been regur- gitated or has passed into the stomach. Regurgitation of solid food is also a frequent, almost constant symp- tom of oesophageal stenosis. If the stenosis is situated high up, regur- gitation takes place very soon after ingestion. If it is situated lower down, and especially if a diverticulum has formed, hours may elapse before the food is regurgitated. The regurgitated food appears macer- ated and swollen, has a neutral reaction, and is mixed with pus-corpus- cles and desquamated pavement epithelium, often with fungus spores and threads. Loquet observed violent singultus in oesophageal stenosis, particularly when the stenosis was situated below the diaphragm. If the stenosis continues to increase, the patients are compelled to re- strict themselves to fluid nourishment, and finally, ingestion through the mouth becomes impossible. Examination with the sound and auscultation afford remarkably valuable aid in the recognition of the disease. In examination with the sound we find an obstruction, which is over- come with difficulty or not at all, at the site of stenosis. In the latter event, a sound must be chosen which is sufficiently small to be passed into the stomach. The situation of the stenosis can be determined by measuring the distance between the apex of the sound, where the ob- struction is felt, and the point at which the sound corresponds to the row of teeth. The situation of the stenosis in the body is then found by ap- plying the sound externally along the buccal cavity and spinal column, and partly from our knowledge of the various dimensions of the oeso- phagus. Length of the oesophagus, . . . . .25 cm. Distance from the teeth to the beginning of the oesophagus, 15 “ Length of the cervical portion of the oesophagus, . 5 “ “ “ dorsal “ “ “ . 17 “ Distance between the beginning of the oesophagus and the point at which it crosses the left bronchus, . . 8 “ Distance between the teeth and the point at which the oeso- phagus crosses the left bronchus, . . . . 23 “ Length of abdominal portion of the oesophagus, . . 3 “ The red English sounds are preferable to the French ones because they are more durable and less apt to break. The olive-tipped sounds should be selected. Mackenzie recommends that the transverse section of the sound should be oval, corresponding to the shape of the oesopha- gus. The anterior third of the instrument should be dipped in warm water for one to two minutes before introduction, in order to make it more pliable, and it should also be smeared with glycerin, albumen, butter. A sound should not be introduced until we are certain that the con- striction is not the result of an aneurism, since the latter maybe perfo- rated by the instrument and produce rapid death from hemorrhage. IS’or should it be employed if acute inflammatory changes are present. In introducing the sound, the patient should sit on a chair and brace himself firmly against its back; the head is slightly raised, the mouth 30 DISEASES OF THE CESOPIIAGUS. opened wide, and a cork placed between the teeth. The physician then bends the end of the sound slightly downwards. The patient is then directed to protrude the tongue slightly, the index finger of the left hand is introduced as far as the base of the tongue, and the sound, which is held like a pen by the right hand, is pushed in over the left index finger. At the first attempts, the patients often suffer from nausea or even vomiting, or they stop breathing. Much can be done by calmly reassuring them. If an obstacle is en- countered, the sound should be held quietly for a few seconds, then withdrawn a little, and again pushed forwards. In some indivi- duals the involuntary contraction of the oeso- phagus causes a temporary obstruction to the passage of the instrument. If the obstruction is permanent, we are justified in making a di- agnosis of stenosis. Smaller sounds should then be employed until we succeed in passing the stricture. We should not be satisfied until the sound has passed into the stomach, since stenoses which are situated more deeply may otherwise be overlooked. If the stenosis is very marked, it may be impassable-except to catgut filiform bougies. Whalebone sounds with removable olive-sliaped ivory tips are not much employed at the present time. Sainte-Marie and Ferrie have constructed special instruments to measure the length of the stenosis. Sainte-Marie placed upon the sound a compressible olive-shaped tip, while the posterior extremity terminated in a mano- meter, which was filled with a colored fluid down to the zero point. When the sound reached the stenosis, the manometer rose on account of the compression of the tip, and did not fall to zero until the obstruction was passed. Ferrie fastened to the tip of the sound a little sac of goldbeater’s skin. The sac col- lapsed when the sound met the obstruction. The sound was then passed through the ob- struction, and the sac was distended by blowing into the sound, which was then withdrawn. The beginning of the lower portion of the ste- nosis could be recognized by the obstruction felt in withdrawal. The length of the stricture is the difference in the lengths of the sound in the first and second positions. If fluid is swallowed by the patient, and if, at the same time, we place the index finger upon the hyoid bone, in order to recognize the beginning of deglutition by the upward move- ment of the bone, the sound produced is only heard when the oesopha- gus is ausculted alongside the spine as far as the site of stenosis. Lower down the sound is entirely absent, or is heard only after a certain interval—after the fluid has gradually passed through the stricture. Fig. 6. CEsopliageal sounds, a, Eng- lish sound with olive shaped tip b, French sound with sharp tip. DISEASES OF THE (ESOPHAGUS. 31 Abnormal gurgling sounds, which sometimes last a few minutes, are heard not infrequently above the stenosis. This method of examina- tion is especially valuable when no bougie is at our disposal, or when the presence of an aneurism is suspected. The cervical portion of the oesophagus is ausculted on the left side alongside the larynx, from the lower border of the cricoid cartilage to the region of the clavicle. Pharyngeal sounds are heard more frequently in this region than good oesophageal sounds. The thoracic portion of the oesophagus is ausculted immediately to the left of the spinous pro- cesses, from the seventh cervical to the ninth dorsal vertebra. The stomach begins at the tenth, sometimes at the ninth dorsal vertebra. Waldenburg successfully examined the organ (cesophagoscopy) by means of an arrangement of mirrors. Ziemssen distended the oesophagus by means of an effervescent mix- ture, in order to determine, by means of auscultation, dilatation of the oesophagus above the stricture. If the occlusion of the organ becomes complete, the condition of the patient is truly distressing. He emaciates to a skeleton, the abdomen is sunken, the bowels are constipated for many days, and the amount of urine diminishes to an extreme degree. In a case of sulphuric acid poisoning under my care, not more than 3.5 gm. of urea pro die were passed during the last week of life. The patients often lie for days more dead than alive. The respirations are not infrequently extremely slow and irregular, and we must be on our guard against mistaking this condition for death, especially since the heart sounds are unusually feeble and the pulse barely perceptible. In one case under my observation, respiratory intervals of one and a half minutes occurred during the last two days of life. Complete occlusion of the stenosis sometimes occurs suddenly. Ac- cording to Mosetig, this is apt to occur when the kernels of fruit which have been swallowed are deposited above the stenosis. The patients sometimes attribute sudden complete occlusion to external causes. A patient who was suffering from stenosis as the result of cancer, became unable to swallow anything a few hours after catching cold while help- ing to extinguish a fire. Sudden stenosis, or temporary complete occlu- sion has been observed in oesophageal cancer without any previous symptoms. Exacerbation and improvement of the stenotic symptoms sometimes alternate with one another. According to Koenig, the symptoms of stenosis which occur in women suffering from goitre occasionally grow worse at the period of menstruation, when the goitre enlarges. Tem- porary improvement may occur in cancerous strictures if portions of the cancer break off and render the passage freer. A few striking cases of cicatricial stricture have been reported, in which sudden and permanent improvement occurred, even after the operation of gastrotomy had been contemplated. In some cases, death results from perforation into the mediastinum or air passages, pneumonic changes, or gangrene of the lungs (the two latter produced by the passage into the larynx of ingested particles of food which had been regurgitated). IV. Diagnosis.—The diagnosis is usually made with facility from the subjective symptoms, the results of exploration with the sound, and auscultation. As a matter of course, we should also endeavor to aseer- 32 DISEASES OF THE OESOPHAGUS. tain the cause of the stenosis. This depends upon the previous history of the other symptoms. V. Prognosis.—The prognosis depends in part upon the cause; for example, it is unfavorable in cancer and aneurism. It also depends upon the degree of stenosis. VI. Treatment.—Tieatment should be directed against the cause itself and against the stenosis as such. The former requires, according to circumstances, the use of antiphlogistics, antisypliilitics, absorbents, nervines, narcotics, and surgical interference. The local treatment belongs properly to the domain of surgery. In cicatricial stricture, gradual dilatation with larger and larger sounds should be adopted. The sound should be introduced daily, every other day, or once or twice a week, according to the intensity of the irrita- tive symptoms produced by the operation. It should be kept in situ for a few minutes to a few hours, and this plan of treatment should be continued for a long time. Good results are often obtained from the use of distensible bougies, which are allowed to remain in the oesophagus, and, when they grow thicker, mechanically dilate the organ. The employment of forcible rupture of the oesophagus and of internal cesophagotomy has been abandoned. Strictures of the cer- vical portion are sometimes incised from the outside (external cesopha- gotomy). In other cases, the oesophagus is opened from the outside below the stricture, and an oesophageal fistula is made in order to nourish the patient. Gastrotomy, i. e., the making of a gastric fistula through which to nourish the patient, has been performed successfully in a number of instances. Of twenty-seven operations performed from 1876 to 1883, fourteen (fifty-two per cent) were successful (under anti- septic precautions). In one case, Trendelenburg introduced into the gastric fistula of a boy a rubber tube which was provided above with a funnel-shaped at- tachment. The boy chewed his food with the teeth, then spat it into the funnel, and then passed it into the stomach with the aid of a spoon. Careful sounding may also have a surprisingly good effect, and make the passage permeable for a few days in stenosis produced by cancer. Great care must be exercised, however, in order to prevent perforation. In stenosis produced by thickening of the cricoid cartilage, Wernher has advised that the larynx be lifted forwards and upwards during the act of deglutition in order to render possible the entrance of the bolus into the oesophagus. The character of the diet is very important in all forms of oesophageal stenosis. We may recommend milk, eggs to which salt, sugar, wine, liquor, coffee or tea has been added, beef-tea (mixed with an egg or milk), pigeons or chickens cooked into a soup which has been strained through a cloth, wine, beer, beer soup with egg, cocoa, chocolate. So long as pulpy substances can pass the site of obstruction, we should order scraped meat and ham, Leube-EosenthaFs meat solution, thin porridge of potatoes, peas, and lentils. It has recently been proposed to keep soft sounds permanently in the oesophagus in order to facilitate the passage of food into the stomach. If the passage of food through the oesophagus is no longer possible, and cesophagotomy or gastrotomy is impracticable, wre must endeavor to maintain life by artificial nourishment through the rectum. This method is not capable of maintaining life permanently, for, in the most favorable cases, only one-fourth of the amount of albumen DISEASES OF THE (ESOPHAGUS. 33 necessary for nutrition is absorbed from the rectum. Eggs are absorbed only to a very slight extent; their absorption is increased by the addition of salt, but this gives rise to such irritation of the gut that the enemata are not retained. Beef juice and peptones are partly absorbed, but they are borne very poorly, and irritate the mucous membrane. Experiments have recently been made with injections of blood, but no positive results have yet been obtained. As a good mixture for nutritive enemata we can recommend meat soup mixed with an equal amount of milk and starch, but the soup should not be very salty; the injection should have the temperature of the body, and not exceed two hundred to three hun- dred cubic centimetres in amount. It is best to introduce it slowly through a rubber tube with a funnel attachment. Still better are Leube’s meat-pancreas injections, which are made in the following man- ner: 3 v. to x. meat are chopped fine, 3 xiv. to 3 iiiss. finely-chopped pancreas, which is free from fat, are added, and then mixed into a fine porridge with \ iij. to ivss. lukewarm water. This mixture, at the temperature of the body, is then injected into the rectum. This mass is sometimes digested so thoroughly that the faeces are almost entirely normal in appearance. Mackenzie has recently recommended the follow- ing mixture: Boiled mutton or chicken, § v.; milk, 3 xiv.; fat, 3vi.; brandy, § ss.; water, 3 iij. This is strained, rubbed into a porridge, and injected twice a day at a temperature of 35° C. Once a week, the rec- tum is cleared out about three to four hours before the injection of the nutritive enemata. The attempt has been made to secure artificial nourishment by subcu- taneous injections of oil, cod-liver oil, milk, beef juice, yolk of egg, defibrinated blood, and syrup. 2. Dilatation of the (Esophagus. Dilatation of the oesophagus may extend over the entire length of the organ (total dilatation), or only over small portions (partial dilatation). Sometimes the dilatation affects only a circumscribed portion of the transverse section of the organ (diverticulum). The latter variety is divided into pulsion and traction diverticula, according as the diverti- culum is produced by a force from within or by traction from without. Dilatation of the oesophagus sometimes develops as an independent dis- ease, sometimes from previous stenosis (primary and secondary dilata- tion). a. Primary total dilatation has been described as a congenital condi- tion; this is, perhaps, the result of imperfect development of the muscular coat and congenital atony of the entire wall of the organ. In other case£, the condition is acquired in later years as the result of a blow on the chest, lifting a heavy load, the sticking fast of a hot bolus, ingestion of a large amount of hot water, perhaps chronic catarrh of the oesophagus which has developed primarily or has been propagated from the stomach. Habitual vomiting has also been mentioned as a cause of this condition. The dilatation is sometimes quite uniform and cylindrical, some- times spindle-shaped, the greatest amount of dilatation being generally situated in the middle of the thoracic portion. The oesophagus is occa- sionally elongated, and may be thrown into loops like the intestines. Luschka describes a case in which the organ was 46 cm. long (normal length 25 cm.), and 30 cm. in circumference (normal circumference 7.5). The dilatation is sometimes so great that a man’s arm can be intro- 34 DISEASES OF THE (ESOPHAGUS. duced into the organ. The mucous membrane is not infrequently in a condition of chronic catarrh, and occasionally presents superficial losses of substance; the epithelium may be very much thickened, almost warty. The muscular coat is often very thin in cases of congenital dila- tation. In one case, Klebs found fatty degeneration of the muscular fibres, and Stern describes an infiltration of the mucosa and muscular coat with round cells. In other cases, the submucous and muscular coats have been found thickened. As a rule, the first symptoms develop from the ages of fifteen to twenty years. The prominent symptoms are difficulty of deglutition and regurgitation of food. The patients may feel that the food does not reach the stomach. They have difficulty in swallowing, may take only small amounts of food at a time, and these must be moistened with large amounts of water; or they employ spoons and other instruments to push the food into the first part of the (esophagus. Davy’s patient could only swallow if he assumed a position midway between the dorsal and sit- ting position, and allowed the right arm to hang over the back of the chair. Ingestion of food is sometimes followed by a sense of oppression, fear of suffocation, palpitation, and attacks of syncope—the result of pressure of the food which remains in the (esophagus upon the heart, lungs, and adjacent nerves. After a time, the food is regurgitated. It is often very little changed, in other cases it appears macerated. The regurgitated masses are usually alkaline or neutral in their reaction—a proof that they have not been in the stomach. The starchy ingredients of the food may be converted into sugar. The partly decomposing masses in the oesophagus often give rise to a pestilential fcetor ex ore. The disease often lasts five to ten years. Emaciation occurs so much more slowly the larger the amount of food which passes into the stomach, but death from starvation finally occurs. In Ogle’s case, the fatal termination was accelerated by pressure of the dilated oesophagus upon the thoracic duct. The diagnosis depends upon the fact that, in persons who present the symptoms just described, the oesophageal sound can not alone be passed into the stomach without obstruction, but that lateral movements of the sound enable us to recognize an unusually wide lumen. It must be re- membered, however, that if the dilated oesophagus is elongated and con- voluted, the passage of the sound into the stomach may meet with great difficulty. Distention with carbonic acid may enable us to distinguish an unusually wide tympanitic zone along the spinal column. For this purpose, we may give the patient a teaspoonful of tartaric acid in half a wineglassful of water, then an equal quantity of bicarbonate of soda. It should also be remembered that distention of the oesophagus with food will produce dulness on percussion along the spine, and that this dis- appears as soon as regurgitation has occurred. The prognosis is unfavorable. The treatment consists chiefly in the administration of nutritious fluid food, which should be given often, but in small quantities. Nour- ishment by means of the oesophageal sound or enemata, or perhaps gastrotomy may become necessary under certain circumstances (vide page 32). b. Primary partial dilatation of the oesophagus is generally congenital. 35 DISEASES OF THE (ESOPHAGUS. This category includes the so-called “ praestomach,” which is a circum- scribed dilatation immediately above the cardiac end of the stomach. c. Secondary dilatation of the oesophagus develops whenever a steno- sis is present in any part of its course. The stasis of food above the constriction may give rise to gradual dilatation of the organ, but this occurs only in rare cases. It has also been stated that stenosis of the pylorus may produce secondary dilatation of the oesophagus, particularly if the walls of the stomach are unyielding. Secondary dilatation is gen- erally the result of acquired stenoses, rarely of congenital stenosis, espe- cially if situated near the cardiac end. The wall of the oesophagus is thickened, occasionally the individual muscular strata are separated from one another, and in such places the wall is thinned. The anatomical changes mentioned in the remarks on primary dilatation are also noticeable. The symptoms are generally concealed by those of oesophageal ste- nosis. A diagnosis of dilatation secondary to a stenosis may be made if regurgitation occurs quite a while after the food is ingested, and if a sound can be moved freely to the sides ajbove the constriction. The diagnosis may also be facilitated by distention of the oesophagus with carbonic acid, or the appearance of dulness on percussion alongside the spinal column. The prognosis depends upon the primary affection, and the treatment is the same as that of oesophageal stenosis. d. Pulsion diverticula are rarely observed. Almost all of them are situated at the transition of the pharynx into the oesophagus, indeed they may be regarded as diverticula of the pharynx. As a rule they take their origin from the posterior wall of the organ, either in the median line or on one side. They form sacculated projections which at first press downwards between the spinal column and posterior wall of the oesophagus, but later appear on one or both sides between the oesophagus and larynx. Their size varies from that of a pea to that of a child’s head. The lining mucous membrane is generally in a condition of chronic in- flammation, is often thickened, and here and there presents epithelial losses of substance. According to Zenker and Ziemssen, the diverticu- lum possesses no muscular coat, but this is not true of all cases. The disease is by far more frequent in men, and, as a rule, the first symptoms appear after the age of forty years. But this does not imply that the predisposition is not congenital. On the contrary, it appears to be generally the result of a circumscribed defective development of the muscular coat. In Fere’s case, the muscular coat was absent in a cir- cumscribed locality. Under such circumstances the food and foreign bodies will gradually dilate the oesophagus and may produce a diverticu- lum at the congenitally weak spot. The following have been mentioned as the exciting causes of this form of the disease : ingestion of foreign bodies, injury in the region of the neck, wearing a tight collar, poisoning with alkalies. In some cases no cause can be discovered; and even those mentioned are not above criticism. Zenker and Ziemssen showed that the formation of these diverticula is favored by certain physiological changes. For example, calcification of the cricoid cartilage narrows the passage from the lower part of the pharynx to the upper part of the oeso- phagus. As the muscular coat is very thin in the lower part of the pharynx, the stasis of food in this locality may produce gradual dilata- tion. The symptoms develop very slowly. At first the food is retained in 36 DISEASES OF THE (ESOPHAGUS. the diverticulum only at intervals. As it increases in size it sometimes appears, after eating, as a tumor on one or both sides of the neck. Some patients can empty it by stroking the tumor. This manipulation may be attended by peculiar clucking sounds or, as in Betz’s case, by a sound as if air were being pressed through a narrow opening. Similar sounds are sometimes audible during the ingestion of food, and are heard occasionally at a considerable distance. The more the diverticulum is filled with food, the more its opening approximates the median line of the oesophagus, while at the same time the increasing dimensions of the part situated below the opening com- press the oesophagus. If the diverticulum is sufficiently large, pressure upon the heart, trachea, bronchi, and recurrent nerves may give rise to marked dyspnoea, danger of suffocation, and palpitation of the heart. The food is regurgitated, partly in a macerated, partly in a decomposed condition, some time after it is ingested, and fcetor ex ore is often notice- able. The diverticulum sometimes receives the largest proportion of the food, so that the patients are exposed to the danger of death from starva- tion. The diagnosis is based principally upon the appearance of a tumor in the neck after the ingestion of food, and the spontaneous development of murmurs while food is being swallowed. The tumor gives a dull or dull tympanitic percussion sound, and often disappears after stroking. Under certain circumstances the diagnosis may be rendered still more certain by cautious distention of the oesophagus with carbonic acid, if a tumor then appears which is tympanitic on percussion. It is especially characteristic of the formation of a diverticulum that, in examination with the sound, the instrument sometimes passes into the stomach, some- times into the diverticulum. If two sounds are introduced, it is some- times found that one enters the diverticulum, the other passes into the stomach. The more the diverticulum is filled with food, and accordingly the more its opening corresponds to the course of the oesophagus, the more likely it is that the sound will enter the diverticulum. The prognosis is grave, inasmuch as the disease is not very amenable to treatment, though the patients often attain old age. Proper nourishment, especially fluid food, is the first requisite in treatment. If the symptoms of impermeability of the canal become very marked, we may nourish the patient by the aid of the oesophageal sound. Finally, it may be necessary to perform gastrotomy. The text- books on surgery should be consulted with regard to the removal of the diverticulum itself. e. Traction diverticula are situated most frequently near the bifur- cation of the trachea. They are usually associated with disease of the bronchial and tracheal lymphatic glands. As the result of periadenitic inflammation, an adhesion forms between the inflamed glands and the outer wall of the oesophagus. If the glands undergo retraction, the oesophagus experiences a local traction outwardly. The same effect may be produced by callous inflammation in the mediastinum, which has developed either spontaneously or as the result of tuberculosis of the spine, or pleurisy. These diverticula are usually single, rarely multiple, and do not at- tain large dimensions. They involve either the anterior or lateral wall of the oesophagus, and their apex, which is usually funnel-shaped, may point upwards, dcTwnwards, or horizontally. Their depth is generally 37 DISEASES OF THE (ESOPHAGUS. two to eight mm., rarely twelve mm. The muscular coat is sometimes present, sometimes absent. On account of the small size of the diverticula, disturbances of de- glutition may not be produced. The chief danger arises from the ten- dency to perforation. This may be produced by sharp foreign bodies which have been caught in the diverticulum, by food which has decom- posed in the same situation; occasionally the cause of perforation remains unexplained. The results of perforation are not always alike. In some cases, the oesophagus is brought into communication with a cavity which is filled with a mass of softened lymphatic gland. Further perforation then occurs into a bronchus, and the softened masses are then expectorated, or are aspirated into the deeper air passages, and produce pneumonia or pulmonary gangrene. In the first event, recovery is conceivable, A communication with a pulmonary cavity, and the formation of a fistula, sometimes takes place, or purulent, ichorous pleurisy, pneumopericarditis, or pericarditis develops, or erosion of a large vessel (aorta, pulmonary artery). Traction diverticula occur at all ages, and equally in both sexes. Their development can generally be traced to the period of childhood. As a rule, the patients are scrofulous, phthisical, or inhale a good deal of dust, since all these conditions are apt to produce inflammation of the tracheo-bronchial glands. The condition is hardly recognizable during life, unless the signs of perforation occur, and all other causes may be excluded. 3. Catarrhal Inflammation of the (Esophagus. I. Etiology.—Catarrhal inflammation of the oesophagus is some- times of mechanical, thermal, or chemical origin, sometimes it is propa- gated from adjacent parts, sometimes it is produced by constitutional diseases. Thus acute catarrh may be produced by the ingestion of hard, sharp bodies, by the unskilful use of the oesophageal sound, by the ingestion of too hot or too cold articles of food, of acids, alkalies, or other irritating substances. (Esophagitis is sometimes the result of frequent vomiting, especially if the vomited matters are very acid. Catarrh of the mucous membrane is often observed above the site of a stricture as the result of the violent irritation produced by the stagnant and decomposing food. Chronic oesophageal catarrh is also produced in hard drinkers and in- veterate smokers, in the latter as the result of the ingestion of saliva mixed with irritating tobacco juice. It is sometimes found that the catarrh extends to the oesophagus from the pharynx or stomach, and also from inflammations of the spine, medi- astinum, pericardium, even of the larynx or bronchi. Acute catarrhal oesophagitis is often observed in acute infectious dis- eases (measles, scarlatina, typhoid fever, variola, cholera,‘diphtheria,etc.). Chronic oesophagitis is kept up not infrequently by chronic respiratory and circulatory diseases. It is also observed in syphilis and phthisis. II. Anatomical Changes.—The catarrh may be acute or chronic, circumscribed or diffuse. Acute oesophageal catarrh is characterized by loosening and profuse desquamation of the epithelium, which becomes opaque and whitish. Congestion is not prominent, because it is partly concealed by the condi- tion of the epithelium cells. The mucous follicles are sometimes swollen. 38 DISEASES OF THE (ESOPHAGUS. They form small, gray, transparent elevations, situated generally in lon- gitudinal rows upon the folds of the mucous membrane, and discharging upon pressure a mucous or muco-purulent fluid. They are often sur- rounded by an areola of injected vessels. At the beginning of the catarrh, the mucous membrane is occasionally very dry, but later it is generally covered with an abnormally abundant mucous or muco-purulent secretion. Very violent catarrh may give rise to superficial, but usually not very extensive losses of substance. These are produced sometimes by active desquamation of the epithelium, sometimes by shallow ulceration of the follicles, the latter being situated occasionally in longitudinal rows. Catarrhal erosions and ulcerations cicatrize, but do not often give rise to stenosis. In very rare cases, abscess and gangrene have been ob- served as complications and sequelae. It should be remembered that the mucous membrane of the new-born is physiologically congested, probably as the result of 'rritation produced by the food during the first few days of life. Some authors attribute it to changes in the foetal circulation. In chronic oesophageal catarrh, the mucous membrane has a brownish- red or grayish-red color. The epithelium is thickened, the mucous membrane covered with a tough, vitreous, or puriform secretion. Super- ficial ulcers are often present. Zenker and Ziemssen deny the occurrence of blackish or slate-colored pigmentation of the mucous membrane as the result of long-standing catarrh. One of the sequelae is dilatation of the oesophagus, probably from relaxation and hypertrophy of the muscular coat. Zenker denies that this hypertrophy may become so excessive as to lead to stenosis of the canal. In other cases, the mucous membrane becomes hypertrophic, and gives rise to the formation of polypoid or papillary proliferations. The hypertrophy sometimes extends to the peri-oesophageal cellular tissue. III. Symptoms and Diagnosis.—The disease is latent in many cases, but occasionally the patients complain of pain, varying in intensity from a dull feeling of pressure to a marked burning or pricking pain. The pain may be felt in the cervical region, between the scapulae, beneath the sternum or epigastrium, or in the breast without any definite locali- zation. The inflammation cannot be localized from the site of the pain. The pains sometimes arise spontaneously, or on making various move- ments of the spine (so that the patients often hold the head stiff and immovable), or on percussion of the spinous processes, or touching the lateral portion of the neck. Deglutition generally produces pam (odyn- phagia), which is not infrequently especially severe when the bolus passes a certain locality. Violent pain may also be produced by the introduction of a sound, and, under such circumstances, it may be diffuse or circumscribed. Difficulty in deglutition is sometimes the direct result of the pain, but it may also be produced by reflex spasm of the muscular coat of the oesophagus. The patients experience the terrifying sensation as if the food remains sticking in one spot; they endeavor ineffectually to force it down; their terror increases; not infrequently reflex spasms of the muscles of the respiration occur, and even general convulsions. After vain attempts at deglutition, the bolus is regurgitated, occasionally coated with a muco-purulent or bloody mass. The sensation of the pres- ence of a foreign body is sometimes experienced. 39 DISEASES OF THE (ESOPHAGUS. In examination with the sound, numerous epithelium cells of the mucous membrane often adhere to the fenestra of the instrument. The examination is painful, and often causes reflex spasm, so that the sound is held fast until the spasm relaxes. If the examination is performed carefully, the presence of streaks of blood upon the sound would favor the diagnosis of ulceration of the mucous membrane. Examination with the sound should not be employed, however, except in cases of urgent necessity. The epithelium is sometimes desquamated to such an extent that it is expelled in the shape of a tube. Recovery occurred in a case of this kind reported by Birch-Hirsehfeld. Slight fever is sometimes present. The feeling of thirst is often greater than would be expected from the intensity of the fever. IV. Treatment.—We should first attempt to remove the causes of the disease, and then directly combat the inflammation. If the pain is violent, an injection of morphine should be made into the side of the neck, or under the integument of the back near the spinal column, or narcotics may be given internally. The inflammation may be combated by the ingestion of pieces of ice, or small swallows of milk and ice. Not much can be expected from external derivatives (leeches, cups, blisters, mustard poultices, etc.). Solid food should be prohibited, and, if necessary, nutritive enemata employed. In chronic catarrh, we may resort, if the patient is free from pain, to the introduction of a sound smeared with an astringent salve (R Acid, tannic., gr. xv.; vaselin., 3 iij.; or argent, nitric., gr. viiss.; vaselin., 3iij.). The operation should be performed after supper, and in the morning before breakfast. 4. Phlegmonous Inflammation of the (Esophagus. This very rare disease leads to the formation of pus in the sub- mucous connective tissue of the oesophagus. In the beginning, this tissue appears infiltrated with pus, and accordingly thickened; later it contains circumscribed accumulations of pus. The abscess often pro- trudes into the lumen of the oesophagus, and causes stenosis. The epi- thelium over the abscess may be partly desquamated, and the mucous membrane is often congested. The muscular coat generally presents a normal appearance, though the microscope often reveals slight infiltra- tion with pus. Perforation of pus occurs towards the inside alone; it not infrequently raptures in several places at the same time. If recovery occurs, these openings generally cicatrize, but in some cases they remain open, the cavity of the abscess becomes lined with epithelium, and thus a sort of intraparietal diverticulum is produced. This may persist for a long time without causing any special disturbance. The inflammation has been known to extend from the submucous layer of the oesophagus to that of the stomach and vice versa. The following are the causes of the disease: impacted foreign bodies, acute oesophagitis produced by poisons, perhaps diphtheria of the canal, variola, phthisis, phlegmonous gastritis. The most frequent cause is suppuration in the vicinity of the canal, inasmuch as it extends to the submucous layer and there produces secondary suppuration. This cate- gory includes: tuberculosis of the spine, abscess of the lymphatic glands, and suppuration of the cartilages of the larynx. In some cases, the abscess perforates not only into the oesophagus, but also into other cavi- 40 DISEASES OF TIIE (ESOPHAGUS. ties, for example, the air passages, thus producing an abnormal eorm munication between the oesophagus and air passages. In some cases, no cause can be ascertained. The disease can hardly be recognized during life. 5. Corrosive Inflammation of the (Esophagus. Corrosive oesophagitis is that form of inflammation which is produced by toxic irritants—usually by mineral acids and alkalies. The degree of inflammation depends on tlie nature of the poisonous substance and its degree of dilution. The changes sometimes involve the entire circumference of the organ, sometimes they appear in a band which runs along its entire anterior surface. In cases of relatively brief action of the poison, the changes may be confined to the upper layers of epithelium. These are found corrugated, desquamated, whitish, desiccated, and present a certain resemblance to a croupous membrane. In poisoning with alkalies we usually find a peculiar smeary, soap- like mass, produced by marked swelling of the epithelium. If the irritation is more marked, the inflammation extends to the submucous connective tissue and phlegmonous oesophagitis is produced. If the irritant action is very intense, necrosis of all the layers of the oeso- phagus is produced, so that we find brittle, pulpy, reddish-brown or blackish shreds of tissue. The inflammation and necrosis extend not in- frequently to the parts around the oesophagus. When the changes affect the epithelium alone, restitutio ad integrum is the usual result, unless death is threatened by lesions of other organs. If the submucous layer is affected to a considerable degree, stenosis may be expected after the occurrence of cicatrization. Death generally takes place rapidly if extensive necrosis has been produced. After poisoning with tartar emetic the changes consist of simple inflammation; in other cases, of ulceration or pustulation of the oesophageal mucous membrane. The symptoms of corrosive oesophagitis consist of pain, difficulty in deglutition, increased thirst, cough, and strangling. The latter act ex- pels desquamated and mortified shreds of the wall of the organ. In some cases, almost the whole of the mucous membrane (even together with a portion of the gastric mucous membrane) has been desquamated in continuity. Cauterization and necrosis within the mouth and pharynx and upon the lips are noticeable, and sometimes excoriations run from the angles of the mouth across the cheeks, evidently because the poison ran out of the mouth. It is a notable fact that, in some cases,, pain is experienced only at the outset, and later may disappear almost entirely. The diagnosis follows from the clinical history and the appearances of the buccal cavity. If the history cannot be obtained, the application of blue and red litmus paper to the bticcal mucous membrane will decide whether the poison is an acid or alkali. The prognosis depends on the degree of destruction, but it should always be made with caution, since the development of stenosis does not occur, as a rule, until the lapse of many weeks. The inflammation should be treated by giving small pieces of ice, milk and ice, and by external applications of ice. Morphine may be given internally or subcutaneously to relieve the pains. In poisoning with acids, we may give magnesia (gr. lxxv. to a glass of milk and ice, one DISEASES OE THE OESOPHAGUS. 41 tablespoonful every ten minutes), in order to neutralize the poison, and diluted vinegar in ice-water in poisoning with alkalies. The patient should be nourished by means of rectal injections. 6. Round (Peptic) TJlcer of the (Esophagus. Ulcers which are entirely similar to round gastric ulcers are some- times found in the lower part of the oesophagus. These will be produced if active gastric juice enters the oesophagus during the act of vomiting, and remains there a sufficient length of time to exercise a digestive and destructive effect. The symptoms are also similar to those of the round gastric ulcer, viz., haematemesis, bloody passages, perforation of the wall of the oesophagus, formation of cicatrices and stricture. The treatment is the same as that of the round gastric ulcer. 7. Cancer of the (Esophagus. I. Anatomical Changes.—Cancer of the oesophagus is almost al- ways primary; secondary cancer is rare, and generally extends from the stomach, more rarely from the pharynx. The primary cancer is situated occasionally in the mediastinum. Primary cancer of the oesophagus is almost always a flat pavement- epithelium cancer, sometimes hard, sometimes juicy. The occurrence of scirrhus or encephaloid cancer in this locality is doubtful. It is situated generally in the lower third of the canal, then in the middle, and least frequently in the upper third. The sites of predilection are the portion immediately above the cardiac end of the stomach, the point where the canal crosses the left bronchus and the region behind the cricoid cartilage. All these places are particularly subject to irritation during deglutition. The cancer may appear in patches (insular), or in the shape of a girdle (cingular). The former constitutes the beginning of the disease; the latter form produces stenosis in two ways: by preventing dilatation of the oesophageal wall, and by proliferation into the lumen of the canal. As a rule, there is but one growth, which varies from three to ten cm. in height. In rare cases the entire canal is involved in the cancer- ous process. In one case, Zenker found that the middle of the organ, over an extent of four cm., was alone free from the cancerous degeneration. Carmalt states that not alone the epithelial cells of the mucous mem- brane, but also those of the excretory ducts of the mucous glands prolif- erate into cancer cells. The muscular coat adjacent to the cancer is generally hypertrophic; later it becomes infiltrated with masses of the neoplasm. The oesophagus is sometimes dilated above the tumor, but this dilata- tion is not so frequent as is generally believed. The tracheo-bronchial and mediastinal lymphatic glands are usually enlarged and cancerous. The deeper cervical glands are more rarely affected, the peripheral cer- vical glands usually escape. If necrosis of the cancer occurs, a previous stenosis may disappear. As a rule, however, the improvement is only temporary. The necrosis is sometimes so extreme that careful observation is necessary to discern 42 DISEASES OF THE (ESOPHAGUS. the remains of the cancer, and Rokitansky even believed that recovery was possible from the formation of a cicatrix. In some cases, the ulcerative degeneration spreads to adjacent organs, and may lead to abnormal communication with the air passages, lungs, pleura, pericardium, cavities of the heart or the large vessels. Perforation occurred twenty-seven times among forty-four cases col- lected by Petri. The following table of fifty-three cases of perforation is furnished by Schneider : Perforation into the trachea, . . . .21 times. “ “ “ lungs, . . . . 16 “ “ “ “ bronchi, . . . . 16 “ The neoplasm may be propagated in various ways. It often spreads directly to adjacent organs, viz., the stomach, pharynx, pleura, lungs, bronchi, trachea, mediastinal cellular tissue, pericardium, myocardium, aorta, and vertebrae. The vertebrae are sometimes perforated and the spinal cord may be compressed. The cancer may also extend from the mediastinum into the spinal canal through the intervertebral foramina. In other cases, the growth spreads by dissemination, probably through the agency of the lymphatic channels. In this way, the tumor extends to the mucous membrane of the oesophagus itself, the pleura, pericardium, and peritoneum. True metastasis takes place occasionally, and secondary nodules are observed in the lungs, liver, kidneys, suprarenal capsules, pancreas, medulla of the bones, and lymphatic glands. II. Etiology.—Primary cancer of the oesophagus is a disease chiefly of old age, being most frequent from the age of forty to sixty years. In the majority of cases, it occurs in the male sex. The influence of heredity is questionable. Burning during degluti- tion, injury from foreign bodies, abuse of alcohol, and chronic diseases of the stomach, are mentioned as exciting causes. C. Neumann reported a case in which the cancer followed an ulcerative and cicatricial process. III. Symptoms.—As a rule, the symptoms develop slowly and gradu- ally, and our attention may first be attracted by the signs of oesophageal stenosis. At the same time, we are often struck by the emaciation and cachectic appearance of the patient. The disease sometimes begins with very violent pains, which are partly spontaneous, partly the result of the act of deglutition. I recently treated a man who suffered from the most violent pains for nearly a year before the signs of stenosis were demonstrated. The patient located the pain in the lower part of the oesophagus, although examination with the sound and the autopsy showed that the cancer was situated in the upper third of the canal. In. some cases the pains occur only at night; they radiate occasionally into the limbs and along some of the intercostal spaces. Phonation is interfered with in not a few cases, on account of paraly- sis of the recurrent laryngeal nerves; the act of coughing and straining also suffers under such conditions. The paralysis of the vocal cords is more often unilateral, but can hardly be recognized, except with the aid of the laryngoscope. Sometimes the tumor compresses the nerves, some- times it proliferates into them. The paralysis may be a very early symptom and even precede the signs of stenosis. If the cancer is situated in the cervical part of the oesophagus, it may be visible as a painful, infiltrated swelling; when it extends to the pharynx it may be visible through the buccal cavity. Examination with 43 DISEASES OF THE (ESOPHAGUS. the sound should he resorted to if the cancer is situated more deeply. In this manner we first determine the situation and degree of an oeso- phageal stenosis. The particles which remain adherent to the fenestras of the sound* should be carefully examined, since they can he recognized very often as fragments of cancer, on account of the so-called pearly globules (Fig. 7) which they contain. The regurgitated masses also contain particles of cancer, in addition to food, pus, and blood. The presence of numerous epithelial cells with two nuclei is also suspicious, even if the pearly globules are absent. The sound should be introduced carefully, in order to avoid perforation and hemorrhage. Auscultation furnishes signs similar to those obtained in oesophageal stenosis (vide page 31). Fig. 7. Pearly globule from cancer of the oesophagus, which had remained in the fenestra of the sound. Magnified 275 diameters. The majority of patients complain of great thirst. If the oesophagus is markedly stenosed, the food regurgitates, the patient’s hunger is never satisfied, and he grows weaker and weaker. The digestive power of the stomach is very much diminished, and the food may remain un- digested for many hours. Riegel showed that the carcinoma destroys the hydrochloric acid of the gastric juice, and thus makes the lat- ter inefficient. The patients generally complain of obstinate constipa- tion. An increased amount of indican is often found in the urine (if a test tube is filled with equal amounts of urine and hydrochlo- ric acid, and one to three drops of a fresh solution of chloride of lime are added, the urine will assume a reddish or bluish color). The amount of urea is diminished. Marchand states that asthma-like or stenocardic attacks are occasionally observed. Pulmonary phthisis develops not infrequently. Marantic oedema and venous thrombosis develop not in- frequently with the increasing loss of power. 44 diseases of the oesophagus. The disease may last many months. According to Lebert, the average duration is thirteen months. The fatal termination results from starvation, associated with the signs of increasing oesophageal stenosis (these symptoms fnay improve temporarily if portions of the growth are cast off on account of ulcera- tion), from increasing marasmus, a fatal hemorrhage, oesophageal perfo- ration, or complicating pneumonia, pulmonary gangrene, pleurisy, and pericarditis, or severe spinal paralysis. Some patients present symptoms of pyaemia. IV. Diagnosis.—The diagnosis consists of the demonstration of a stenosis and the recognition of its cancerous character. Concerning the former problem, we refer to the remarks on oesophageal stenosis (Vol. II., page 31). The carcinomatous character of the stenosis is recognized from the previous history, the associated symptoms, general cachexia, age, and the presence of fragments of cancer in the vomited masses or upon the sound. V. Prognosis.—This is unfavorable, as in all other forms of cancer. VI. Treatment.—Special attention should be paid to a suitable diet (vide Vol. II., page 32). The pain may be relieved by narcotics. Careful sounding not infrequently produces marked diminution of the disturbances of deglutition for a considerable period. Ziemssen advises the daily use of the sound. Surgical text books must be referred to for detailed information con- cerning operative procedures. Resection of the oesophagus may only be performed if the cancer is situated in the cervical portion of the oesophagus. This is also true of oesophagotomy. Early gastrotomy seems to be more advisable, even if it is intended to follow this operation by resection of the oesophagus. 8. Hemorrhages from the (Esophagus. Hemorrhages may take place either into the tissue of the oesophagus itself, and then possess merely an anatomical interest, or upon the free surface of the mucous membrane, in which event they may be recognized during life, if circumstances are specially favorable. The hemorrhage is very rarely the result of external injury, much more frequently of injury internally by ingested foreign bodies. As a rule, it does not take place immediately after the ingestion of the foreign body, but ulceration of the mucous membrane first occurs, and this con- stitutes the immediate cause of the hemorrhage. If it takes place from vessels of the oesophagus itself, it is less serious than if the large ves- sels near the organ are eroded (aorta, pulmonary artery, carotid, sub- clavian, intercostal arteries, vena cava, hemiazygos, and even the cavities of the heart). Unskilful use of the sound may also produce traumatic hemorrhage, and this may prove serious if the patient is suffering from a vascular cancer of the oesophagus or from aortic aneurism. Closely allied to traumatic hemorrhages are those produced by irritant poisons. Ulcerative processes of the oesophagus may also give rise to hemorrhage, either from the vessels of the oesophagus itself or adjacent large vessels which have undergone perforation. Spontaneous rupture and softening of the oesophagus also give rise to hemorrhage. In some cases it is the result of varicose dilatation of the oesophageal veins, either from rupture of the veins or from the extension of an ulcerative process of the mucous membrane to the subjacent veins. This condition is observed most fre- DISEASES OF THE (ESOPHAGUS. 45 quently in cirrhosis of the liver, because the coronary veins of the stomach, and the veins of the lower part of the oesophagus attempt to convey a part of the blood of the portal vein to the vena azygos, independently of the circulation in the liver. Klebs noticed varicose veins in the submucosa of the oesophagus in syphilitic hepatitis, and Zenker observed a similar- condition in tight-laced fissure of the liver and marked senile atrophy. Old age, in itself, seems to predispose to varicose dilatation of the oeso- phageal veins. In some cases the cause of the development of the varices cannot be recognized. (Esophageal hemorrhages sometimes originate in surrounding parts, for example, in aneurisms of the aorta. The symptoms of oesophageal hemorrhage consist of haematemesis and evacuation of black or bloody masses in the stool. The latter occur only when the hemorrhage is very profuse. Rapid death sometimes follows with signs of internal hemorrhage (pallor and coolness of the skin, imperceptible pulse, nausea, failure of the senses). Sometimes the first hemorrhage proves fatal, at other times the hemorrhage ceases, and death occurs in a subsequent attack. The diagnosis can be made only when gastric and intestinal hemor- rhage can be excluded. The prognosis depends on the primary cause and the abundance of the hemorrhage. The treatment consists of the ingestion of small pieces of ice, and the application of an ice-bag to the praecordial region and to the left of the spinal column; several subcutaneous injections daily of Ergotinum Bom- belon (one-half syringeful diluted with an equal amount of water) should be made to the left of the spine, and five to ten drops of liq. ferri sesqui- chlorat. in a tablespoonful of water should be given every two hours. Symptoms of collapse should be combated bv subcutaneous injections of camphor (camphorae, gr. xv.; olei amygdalar., 3 iij. M. I). S. One syringeful t. i. d.), and the administration of champagne and ice. For days no food except iced milk should be administered by the mouth, and the strength should be maintained by nutritive enemata. 9. Perforation of the Oesophagus. 1. Perforation of the walls of the oesophagus may occur from within outwards (primary) or vice versa (secondary). This process is more fre- quent in males, and at an advanced age. The thoracic portion of the oesophagus is most frequently affected, especially the part which is adja- cent to the bifurcation of the trachea. This is owing, in part, to the fact that diseases of the bronchial and tracheal lymphatic glands play a prominent part in the etiology of the disease. Among the causes of primary perforation of the oesophagus we must first mention traumatism. Thus it occurs not very rarely in examina- tion with the sound, which penetrates the wall of the oesophagus, and enters a false passage (mediastinum, pleural sac, pulmonary cavity, etc.). Eras reported a case occurring in a mountebank who was able to pass three swords (fifty to fifty-five cm. in length) into the oesophagus. On one occasion the trick failed, and the point of one sword entered the mediastinum. Foreign bodies may lead to perforation either directly or indirectly. In the latter event perforation is preceded by ulceration. In some cases perforation depends upon toxic influences, or upon various forms of ulcerative processes (catarrh, diphtheria, tuberculosis, cancer, syphilis, etc.). (Esophagomalacia will be discussed later. 46 Secondary perforation of the oesophagus is produced most frequently by cheesy and softened bronchial and tracheal lymphatic glands. In other cases it follows cold abscesses resulting from tuberculosis of the spine, or retropharyngeal abscess, phthisical cavities, pulmonary gan- grene, or cancer. It is produced occasionally by diseases of the trachea, as in Steffen's case in which a tracheotomy canula, which had been left in too long, destroyed the posterior wall of the trachea, and finally per- forated the oesophagus. Zenker observed perforation of the oesophagus by prominent tracheal cartilages as the result of excessive pressure of the trachea backwards by a goitre. Zenker also observed perforation by a gangrenous cyst of the thyroid gland. Finally, aortic aneurisms some- times perforate into the oesophagus. 2. As a rule, there is but one point of perforation; more rarely there are several adjacent ones. The opening is sometimes round, sometimes slit-shaped, and in the latter event may be several centimetres in length. In some cases the perforation occurs gradually and spontaneously, in others it is produced slowly, sometimes by the act of vomiting. 3. As a matter of course, the perforation causes an abnormal communi- cation between the lumen of the oesophagus and adjacent organs. Hence the symptomatology is extremely variable. If the perforation takes place into the connective tissue of the mediastinum and neck, inflamma- tory and gangrenous processes are the inevitable result. The pus may then rupture externally, giving rise to an external oesophageal fistula, through which pass pus, ichorous fluid, and particles of food. In perfo- ration into the large vessels, fatal hemorrhage occurs, attended usually with hematemesis. If the oesophagus opens into the air passages, deglu- tition is generally followed, in a little while, by violent cough and par- ticles of food are expectorated. In one case, Obernier saw the commu- nication by the aid of the laryngoscope. Water mixed with powdered charcoal was given the patient to drink, and the particles of charcoal could then be seen in the trachea. Such communications are usually followed by pneumonic or gangrenous changes in the lungs, the result of aspiration of particles of food. If a communication has been formed between the oesophagus and a pulmonary cavity, a sound, whose introduc- tion formerly soon met with an obstruction, apparently passes farther into the oesophagus, because it passes through the opening into the cavity. In addition, the ingestion of fluid may produce increased tho- racic dulness by filling the cavity, and this again changes to a tympanitic percussion note when the fluid is expectorated. If a colored fluid has been ingested, the sputum will present a corresponding color. In addi- tion, ichorous processes will soon develop in a cavity which previously had not produced a putrid secretion. If the cavity is gangrenous, its secretion may pass into the oesophagus, so that expectoration is replaced by putrid evacuations. If a communication forms between a previously healthy lung and the oesophagus, gangrenous changes develop in the lung. In one case I found, for a week, very numerous, colorless, dou- ble-contoured bacteria in the sputum, and then the sputum became gangrenous (vide Fig. 8). The patient suffered from oesophageal cancer which had perforated into the right lung. In one case Lesser found numerous cells of ciliated epithelium in the sputum, after the perfora- tion into the lung had occurred. Communication with the pleural or pericardial cavities is shown by the development of pneumothorax and pyopneumothorax, or pneumopericardium and pyopneumopericar- dium, but these lesions may also precede the perforation. Cutaneous DISEASES OF THE (ESOPHAGUS. DISEASES OF THE (ESOPHAGUS. 47 emphysema rarely follows perforation of the oesophagus, because the perforation is generally preceded by inflammation in the mediastinum which prevents the entrance of air. The beginning and end of the disease may be almost coincident, es- pecially if a large vessel has been opened. In other cases the patients complain, at the time of perforation, of pain, anxiety, a sensation as if something had burst internally, and collapse. The perforation some- times occurs so slowly that it may be overlooked, and according to Vigla, it may persist for several months. 4. The prognosis depends partly on the primary disease, partly on the mode of perforation. Recovery is possible. Fig. 8. Fungus spores from the sputum in a case of oesophageal cancer which had penetrated into the lung. Magnified 600 diameters. 5. The strength must be maintained by nutritive enemata, in order to allow cicatrization to occur. 10. Spontaneous Rupture of the (Esophagus. 1. Spontaneous rupture of the oesophagus, i. e., that form which is not preceded by injury or disease, is extremely rare. Only fourteen cases have been reported. The majority of the cases occurred in men, many of whom were ad- dicted to excesses, particularly in the use of alcohol. Two cases also presented symptoms of pyaemia. The rupture was often preceded by vomiting; in one case while the patient was ironing, in another during defecation. 2. The accident always occurred suddenly. The patients cried out that something had burst internally, and complained of intolerable pain in the lower part of the spine and between the shoulders; in addition, 48 DISEASES OF THE (ESOPHAGUS. fear of impending death, pale face, cool extremities, and imperceptible pulse. Nausea and vomiting were frequently observed at the onset, oc- casionally hsematemesis. Cutaneous emphysema soon occurred, at first around the neck, then over larger areas. Death generally occurred in col- lapse within twenty-four hours; in one case life was maintained for a week. 3. The rupture was generally longitudinal, beginning not far from the cardiac end of the stomach, more than five cm. in length, affected all the coats of the organ, and usually led first into the mediastinum and then into one or both pleural cavities. The latter contained the contents of the stomach. In one case two longitudinal perforations were present, in another the opening was circular. Zenker showed that enormous force is necessary to rupture the oeso- phagus, and he believes that cesophagomalacia was present in the cases under consideration. 4. The diagnosis is always difficult. It may possibly be made if there .is a sudden development of haematemesis, pleural effusion, pneumo- thorax, and cutaneous emphysema. At the same time we must be able to exclude previous disease of the oesophagus, perforation of the stomach, and other causes of internal hemorrhage. 5. The prognosis is bad. If the pains are very violent, treatment must be confined to the use of narcotics and to the administration of stimulants to relieve the collapse. All remedies should be administered subcutaneously. 11. Softening of the CEsopliagus. (Esophagomalacia. 1. Softening of the oesophagus almost always affects the lower part of the canal. It is generally associated with gastromalacia. If the mucous membrane is alone affected, it is converted into a soft gelatinous mass of a grayish, yellowish, brownish, or blackish-green color. If all the coats are affected, there is danger of rupture. This takes place most frequently into the left pleural cavity; even the lung may be implicated. Softening processes and ecchymoses are sometimes found upon the aorta and in the posterior mediastinum. In the majority of cases the lesion is produced post-mortem as the result of digestion by the gastric juice. But some cases are of vital ori- gin, or at least have developed during the agony. This is especially true of those cases known as brown softening, and the infarctions, which are often observed, also indicate a vital origin. For, if the contents of the stomach, especially the gastric juice, regurgitate into the oesophagus, self- digestion will readily take place as soon as the circulation is partly inter- rupted. The gastric juice then unfolds its digestive action because it is not neutralized by the alkaline blood. 2. The diagnosis during life is always difficult, if not impossible, es- pecially since such patients may not be moved much in order to avoid rupture of the oesophagus. Under the most favorable circumstances the condition may be recognized by ligematemesis and sudden signs of pneu- mothorax or hydropneumothorax. 3. (Esophagomalacia is especially apt to develop in basilar meningitis and chronic cerebral diseases in general; also whenever the death strug- gle is prolonged. 49 DISEASES OF THE (ESOPHAGUS. 12. Sprue in the (Esophagus. (Esophagomy costs oiclica. 1. Oidium albicans, when it appears upon the oesophageal mucous membrane, is almost always propagated from the buccal cavity and pharynx. It is observed in feeble individuals suffering from acute or chronic diseases (cholera infantum, phthisis, diabetes, typhoid fever, pyaemia, etc.). 2. It sometimes appears in the form of more or less large, irregular patches, as long stripes, or as complete casts of the oesophagus. It may also proliferate to such an extent as to fill the canal with a solid plug. According to Bompard, the fungus develops particularly in the upper and lower parts of the canal. It rarely extends into the oesophagus, since cylindrical and cili- ated epithelium seem to resist its proliferation. Grawitz attributes the immunity of the stomach to the acid reaction of its mucous mem- brane. Sprue sometimes extends into the larynx and deeper air passages. The masses of fungus appear as white, yellow, or yellowish-gray de- posits upon the mucous membrane, and may be removed. The sub- jacent mucous membrane is occasionally congested, and may even present superficial ulceration. Wagner noticed that the fungus penetrated between the uppermost layers of epithelium, and then proliferated freely in the succulent mid- dle layers, where it gave rise to atrophy, so that sometimes only the nuclei of the cells remained. Wagner also noticed that it entered the mucosa, and even the blood-vessels. Zenker found the fungi in the ves- sels of the brain, whither they had probably been carried as emboli, and had then continued to proliferate. 3. In many cases sprue of the oesophagus presents no symptoms. In others there are disturbances of deglutition which occasionally end in symptoms of complete occlusion. Emboli in the brain may give rise to grave cerebral symptoms. 4. The diagnosis can only be made when fungi are found in the vom- ited matters, and it is certain that they do not come from the mouth or pharynx. In examination with the sound, masses of the fungus may remain in the fenestra. 5. The prognosis is often unfavorable on account of the primary dis- ease, but the fungus itself may give rise to severe symptoms (dysphagia, aphagia, cerebral symptoms). Slight proliferations possess no signifi- cance. 6. Treatment consists of the prophylactic measures against the devel- opment of sprue in the mouth (vide Vol. II., page 13). If there is difficulty of deglutition, the fungus should be removed mechanically by the administration of emetics. 13. Paralysis of the (Esophagus. 1. Little is known concerning this affection. Its causes include diseases of the brain and cervical cord (hemorrhage, tumors, multiple sclerosis, bulbar paralysis, ataxia, progressive general paralysis). A few cases have been produced by compression of both pneumogastric nerves by swollen lymphatic glands. Diphtheria, syphilis, lead poisoning, alcoholism, cold, ingestion of hot food, and mental excitement have also been mentioned as etiological factors. Hysteria is a rare cause. 2. The symptoms consist of difficulty of deglutition. In addition, we 50 DISEASES OF THE (ESOPHAGUS. sometimes notice a feeling of oppression, palpitation, dyspnoea, partly the result of excitement, partly the result of pressure of the oesophagus (which is distended by the food) upon the heart, lungs, and recurrent laryngeal nerves. Large, firm boluses are often swallowed more readily than small, fluid ones. Some patients swallow better in the upright position, others help the bolus along with the aid of a stick. Regurgita- tion of food sometimes occurs or the latter enters the stomach with a rumbling noise.. In examination with the sound, the tip of the instru- ment is found to be freely movable on all sides. Auscultation shows that deglutition is slowed. 3. The prognosis depends upon the cause. 4. We must secure suitable nourishment for the patient and, if neces- sary, use the oesophageal sound for this purpose. The faradic current sometimes produces good effects, but the current should not be too strong in order to avoid irritation of the pneumogastrics. One pole is applied to the cervical spinous processes, the other within the oesophagus, either by means of a laryngeal electrode (vide vol. I., Fig. 50), or a similar but longer and more flexible one. The current should be applied shortly be- fore dinner. 14. Spasm of the (Esophagus. (Esophagismus. 1. Spasm of the oesophagus occurs in many central neuroses (hysteria, hypochondria, epilepsy, chorea, tetanus), and is an important symptom of hydrophobia. It is observed occasionally in very nervous individuals who, having been bitten by a dog, live in dread of the onset of hydro- phobia. Mental excitement (fright, terror, joy) is also mentioned among the causes. In many cases it has a reflex origin. Sudden spasm occurs not infrequently, even in robust individuals, during examination with the oesophageal sound. (Esophagismus may be produced by imperfectly masticated food, foreign bodies or very hot food; also by inflammation and cancer of the organ. Pharyngeal polypi, pharyngitis granulosa, and chronic angina may also give rise to the disease. It also occurs in diseases of the stomach and intestines, and is observed particularly in women who are suffering from uterine diseases. It occurs occasionally during pregnancy and lactation. In some cases the disease has been attributed to injury of the breast; also to poisoning with belladonna and stramonium. Romberg observed it during arthritis. 2. The disease is characterized by a disturbance of deglutition, asso- ciated with a feeling of constriction and occasionally of pain. If the spasm affects the upper part of the oesophagus, the food is regurgitated at once. In addition there may be a feeling of oppression, palpitation, dyspnoea, sometimes loss of consciousness, and general convulsions. The spasm sometimes occurs at the mere thought of eating. The affection may last for days, weeks, or even months. In examination with the sound a resistance is encountered which often ceases suddenly. On auscultation, the sound produced by degluti- tion can only be followed as far as the site of spasm, but the latter often changes. The diagnosis is usually easy. The prognosis is almost always fa- vorable, except in hydrophobia, or when the disease is the result of ana- tomical lesions of the central nervous system. Therapeutic measures should be directed mainly against the primary disease. In addition, we may attempt to relieve the spasm by the sub- 51 cutaneous administration of narcotics. The application of the constant current is often indicated (cathode to the cervical spine, anode within the oesophagus, a feeble current one to two minutes daily). Kecovery is sometimes effected by careful repeated introduction of the sound. DISEASES OF THE STOMACH. PART III. DISEASES OF THE STOMACH. A. GASTEIC AFFECTIONS ASSOCIATED WITH ANATOMICAL LESIONS. 1. Hemorrhage of the Stomach. I. Etiology.—Hemorrhage is probably much more frequent than appears, since, as a rule, a diagnosis can only be made if the hemorrhage is not too slight in extent. The following are the causes of the dis- ease : a. Injuries, chemical and thermal irritants. This category includes a blow or fall upon the gastric region, ingestion of sharp substances or of hot food, acids, alkalies, or other irritating substances. b. Diseases of the vessels of the stomach. These include varicose or aneurismal dilatation of the vessels of the mucous membrane, and embolic processes. c. Ulcerative affections of the walls of the organ, particularly hemor- rhagic erosions, round gastric ulcers, cancer, phlegmonous gastritis, and also tubercular ulcerations. d. Excessive arterial fluxion of the mucous membrane. Hence hemorrhage occurs not infrequently in violent gastritis. This category also includes the vicarious gastric hemorrhage which takes the place of menstrua- tion, and is also said to occur at times instead of an habitual flux. e. Stasis in the portal vein which impedes the flow of blood from the gastric veins, or local stasis in the mucous membrane of the stomach. This is sometimes the result of occlusion of the trunk of the portal vein (pylephlebitis) or of some of the branches within the liver, as the result of cirrho- sis, tumors, pigment emboli in protracted intermittent fever, dilatation of biliary capillaries following stasis of bile, sometimes the result of circulatory disturbances following chronic diseases of the respiratory or circulatory apparatus. The causes of local stasis include protracted or violent vomiting or straining (childbirth). Gastric hemorrhage is also said to occur occasionally in pregnant women as the result of stasis. /. Nervous influences (vaso-inotor?). It has been shown that injury of the central nervous system may produce hemorrhage of the stomach in animals. This has also been observed during the course of hysteria and general paresis of the insane. g. Aneurisms and abscesses which rupture into the stomach, or per- foration of a gastric ulcer or cancer into the cardiac cavities or the large vessels. Thus gastric hemorrhage has been observed from rupture of aneurisms of the aorta or coeliac axis, perforation of a cold abscess following vertebral caries, per- foration of a round gastric ulcer into the left heai't. 52 DISEASES OF TIIE STOMACH. h. Infectious diseases. Gastric hemorrhage occurs occasionally in yellow fever, small-pox, measles, scarlatina, etc,, when the signs of so-called dissolution of the blood make their appearance. It has been observed occasionally in intermittent fever. Kron re- ported a case in which it appeared every third day, and ceased after the adminis- tration of quinine. Sometimes it does not appear until the period of malarial cachexia. It is associated generally with grave changes in the blood, resulting in abnormal permeability of the walls of the vessels and excessive diapedesis of red blood-globules. i. Blood diseases. Gastric hemorrhage is observed in haemophilia, morbus maculosus Werlhofii and scurvy, and also in progressive pernicious anaemia. The connection between the hemorrhage and the primary disease is probably the same as in the diseases mentioned under li. Jc. Poisons. This category includes poisoning with acids, alkalies, phosphorus, arsenic, etc. and also uraemia and cholaemia. Gastric hemorrhage is most frequent from the fifteenth to the for- tieth years of life. It is extremely rare in childhood. A special form of the disease, known as melaena neonatorum, occurs in the new-born, and will be discussed later. The disease is more frequent in women than in men, because the round ulcer, which is the chief cause of gastric hemorrhage, is especially frequent in the female sex. Moreover, menstruation is not without in- fluence on the development of gastric hemorrhage. The hemorrhage sometimes appears to be spontaneous, sometimes it is preceded by bodily or mental excitement, overloading of the stomach, ingestion of indigestible food, etc. II. Anatomical Changes.—The anatomical changes, so far as re- gards the hemorrhage, depend upon the abundance of the latter, if it is very profuse, the stomach is found tense, and the contents shine through with a bluish or blackish color. Upon opening the organ we find blackish clots, which sometimes present the shape of the stomach. If the blood is removed, and the mucous membrane wrashed with water, the surface is found to be very pale. This is also true of the other viscera. When the hemorrhage has not been the immediate cause of death, fatty degeneration of the heart-muscle, kidneys, and other glands can often be demonstrated. The source of the hemorrhage cannot always be discovered, particu- larly in capillary hemorrhages. In other cases, an eroded vessel is found, sometimes partly occluded by a thrombus. The site of the hemorrhage can sometimes be ascertained by the injection of a colored fluid into a main artery. If the hemorrhage is small in extent and has developed gradually, the contents of the stomach are chocolate-colored, like coffee grounds, inky and sooty, exactly like the vomited matters. The lesions which give rise to the hemorrhage cannot be discussed here. If the hemorrhage has been profuse, bloody, blackish or tarry contents are often found in the intestines, sometimes in the upper air-passages, into which they have passed during the act of vomiting. III. Symptoms.—Slight hemorrhages often occur without any symp- DISEASES OF THE STOMACH 53 toms. The blood-globules are then entirely dissolved by the gastric juice, and leave no recognizable traces. But if the hemorrhage is larger in amount, this change can no longer be effected by the gastric juice, and the evacuations from the bowels assume a bloody character. The patients usually discharge tarry, blackish, sometimes soft, sometimes very hard masses, which often have a pestilential odor. The stools should therefore be examined in all conditions which may possibly give rise to gastric hemorrhage, particularly when sudden pallor of the skin, small pulse, syncopal attacks, etc., arouse the suspicion of hemorrhage. The evacuations are sometimes accompanied by colicky pains and tenesmus. In many cases gastric hemorrhage is attended by hasmatemesis. If the hemorrhage is small in amount, the vomited masses consist of mucus, or chiefly of food, mingled with dots and streaks of fresh blood. If the hemorrhage is more profuse, but the blood has remained for some time in the stomach, the coloring matter of the blood is converted into liae- matin by the hydrochloric acid of the gastric juice, and the vomited masses have a brownish, chocolate, or inky color. This is most frequent in cancer of the stomach, but is also observed in gastric ulcer, cholfemia, poisoning, etc. Under the microscope tve find discolored, dentate or de- generated red blood-globules, mixed with food (vide Fig. 9). If the hemorrhage is very profuse, brownish-black, non-aerated clots, usually of an acid reaction, are vomited together with articles of food. Several pounds may be vomited. If a large artery has been opened, the blood occasionally has a bright, arterial appearance, and the red blood-globules are usually found unchanged. Gastric hemorrhage may occur without haematemesis, and the latter is some- times observed in cases in which the blood does not really originate in the stomach, for example, in profuse intestinal hemorrhage, or when blood flowing from the nose, pharynx, oesophagus, or air passages has been swallowed and then vomited. Vomiting of blood and bloody evacuations are often associated with one another. During the hemorrhage many patients experience a sensation as if something warm were flowing into the stomach. Not infrequently, there is a feeling of abnormal abdominal pulsations. The patients often com- plain of a feeling of constriction or fulness in the gastric region. A feeling of warmth soon ascends along the oesophagus, a tendency to vomit follows, a sweetish taste in the mouth becomes noticeable, and the patient finally vomits blood. If the haematemesis is very violent, masses of blood sometimes burst from the mouth and nose. The blood not infrequently enters the air passages, and gives rise to cough or danger of suffocation. The accident always exerts a depressing influence upon the patient. The symptoms usually begin or are accompanied or followed by signs of rapid loss of blood. The patients grow as pale as death. They com- plain of faintness, dizziness, ringing in the ears, spots before the eyes, a film over the eyes; the pulse grows small, occasionally imperceptible. If the hemorrhage is very considerable, death may occur, though not a drop of blood escapes by vomiting or an evacuation from the bowels. There is almost always a tendency to relapse, so that many patients experience a number of attacks. 54 DISEASES OF THE STOMACH. The sequelae of a profuse gastric hemorrhage may last a long time. For weeks, the patients continue to be as pale as death. (Edematous swelling of the ankles, eyelids, and conjunctiva often develops within a few hours. There is marked apathy and somnolence, and at the same time inability to sleep at night. The pulse is not infrequently markedly dicrotic. Systolic anaemic murmurs develop in the heart. In one case I observed a pericardial friction murmur, which I attempted to explain by subpericardial extravasations of blood. Venous murmurs are heard over the bulb of the internal jugular vein, and over the crural vein im- mediately below PouparPs ligament. A systolic arterial sound is heard on auscultation of the larger arteries. The blood obtained on pricking the tip of the finger has a serous color, and contains scanty red blood- globules, .which are very pale and irregular in size and shape (poikilocy- tosis). A strikingly large number of elementary corpuscles are found Flo. 9. Coffee-grounds vomited matters in a woman set. 32 years, suffering from cancer of the stomach. The red blood-globules have lost their color, and form colorless circles, sc, sarcina ventriculi: hf, a group of yeast cells. Enlarged 275 diameters. occasionally in the blood. The white corpuscles are sometimes slightly increased in number (leucocythsemia). Marked desquamation of the skin, loss of hair, and albuminuria are less frequent events. In a number of cases, I observed intolerable foetor ex ore, marked dryness of the mouth, and unquenchable thirst. Amau- rosis has been observed in a number of cases after profuse losses of blood, particularly after hsematemesis. Its causes are unknown, but it has been attributed to central hemorrhages, oedema of the sheath of the optic nerve, serous infiltration, and circulatory disturbances in the retina. The latter are proven by the retinal hemorrhages observed in some cases. Neuroretinitis, and later, atrophy of the optic nerve, have also been seen. The visual disturbances develop a few days after the hemor- rhage, and, after a while, may subside more or less completely. They are said to be present particularly in those cases in which pain in the occiput and stiffness of the neck developed after the heematemesis. 55 DISEASES OF THE STOMACH. IV. Diagnosis.—When the hemorrhage is so profuse that death ensues before the occurrence of haematemesis or bloody evacuations, a probable diagnosis can only be made when the signs of internal hemor- rhage suddenly develop in a patient who had long presented gastric symptoms. If bloody evacuations alone occur, the statements of the patient may onlv be accepted if he presents an anaemic appearance. Blackish stools, which are erroneously supposed to contain blood, are passed after the administration of ferruginous preparations and bismuth. In doubtful cases, water, which is poured over the stool, will assume a bloody color if the stool contains blood. Or we may employ the microscope or spec- troscope. As a matter of course, the passage of a bloody stool is not proof of a gastric hemorrhage. Such a conclusion is only warranted when we can exclude intestinal hemorrhage and the passage of blood into the stomach. The presence or absence of gastric symptoms must be employed not infrequently in making a differential diagnosis. Mistakes may also be made concerning haematemesis. I recently observed a questionable case of cancer of the stomach, in which an ominous sooty mass was vomited, and seemed to favor the diagnosis. On microscopical examination of the vomited matter, it was found to contain, not blood-globules, but crystals of bismuth. Iron preparations may also give rise to pseudo-haematemesis. Blackish-red and blood-like vomiting may also occur after eating cherries, beets, sausage, claret, etc. A mistake is hardly possible if the physician sees the vomited matter. In doubtful cases, the previously mentioned tests will decide. Malingerers sometimes swallow blood, and then vomit it with the aid of emetics, but signs of acute anaemia are absent in such cases. The individual is apt to contradict himself or lays a trap for himself by exag- gerating the symptoms in the attempt to appear sick. A mistake is possible in the new-born, inasmuch as they may swal- low blood, while nursing, from a wound of the nipple, or it may have entered the mouth from the genital passages of the mother during de- livery. For the differential diagnosis of haematemesis and haemoptysis, vide Yol. I., page 256. Haematemesis may be attributed to gastric hemorrhage only in those cases in which hemorrhages from the nose, pharynx, oesophagus, or intestines can be excluded. The amount of the hemorrhage may enable us to judge whether it has come from a large or small vessel. The hemorrhage may be assumed to be arterial if the blood is bright red. V. Prognosis.—Death is rarely an immediate result of profuse hemor- rhage from the stomach. It has also been observed a number of times in round gastric ulcer that the pains, feeling of fulness, anorexia, and nausea diminished after a gastric hemorrhage. Furthermore, haematem- esis has been known to cause diminution of ascites resulting from cir- rhosis of the liver. Nevertheless, gastric hemorrhage is not a favorable symptom. Its causes often possess a grave significance, and the symp- tom itself enfeebles the organism and accelerates the failure of the vital energies. VI. Treatment.—After a gastric hemorrhage occurs, the patient should be placed in bed, relieved of all tight articles of clothing, and kept absolutely quiet. A subcutaneous injection of ergotinum Bombe- 56 DISEASES OF THE STOMACH. Ion (one-half syringeful with an equal amount of water) should be made in the region of the stomach, an ice-bag applied to the epigastrium, and small pieces of ice swallowed. If syncopal attacks make their appear- ance, the head should be held as low as possible, the face and chest sprinkled with cold water, ammonia or ether held to the nostrils, a mus- tard poultice applied to the calves, and camphor (gr. xv., ol. amygdalar. 3 iij., one syringeful) injected subcutaneously. For days the patient should take nothing but milk and ice; if inanition threatens, nutritive enemata should be ordered (vide page 33). When death from hemor- rhage threatens, transfusion has been performed. But apart from the fact that transfusion of blood is no longer regarded as a rational proce- dure, Czerny and Kussmaul report a case of intestinal hemorrhage in which, after transfusion had been performed, renewed hemorrhage and death ensued. Transfusion with a solution of common salt is being more employed at the present time. Caution should be exercised in the internal administration of styptics as they often produce vomiting. The following may be mentioned: B Plumb, acetic., gr. f; opii, gr. y every two hours. — B Acid, tannic., gr. iss.; opii, gr. T3¥; every two hours.—B Eiq. ferri sesquichlorat., 3 iij.; five to ten drops in water, repeated a number of times. — B Seri lact. aluminat., f xvi.; one wineglassful every fifteen to thirty minutes.— B 01. terebinthin., five to ten drops in water, repeated several times. Intermittent haematemesis should be treated with quinine (gr. xv.- xxx. daily in a single dose). If symptoms of suffocation occur, the finger should be introduced into the introitus laryngis, in order to remove any clots which may be present. The anaemic symptoms which are left over require nutritious, light diet, particularly in a fluid form. Iron preparations should be adminis- tered with caution, and only when gastric symptoms are no longer present. 2. Acute Gastric Catarrh. {Acute Gastritis.) I. Etiology.—Acute gastritis is sometimes primary, sometimes sec- ondary to other diseases. Errors in diet constitute the most frequent cause of acute primary gastritis. It is an every-day experience that overeating produces acute gastric catarrh, particularly if the individual usually eats sparingly. In such cases the gastric juice is too small in amount to digest the excess of food, and, in addition, the power of the muscular coat of the stomach is often too slight to propel the food at the proper period into the intes- tines. Hence fermentation of the food and irritation of the gastric mucous membrane. Errors in the quality of the food may also produce the disease; for example, ingested foreign bodies (fruit pits, fish-bones, nails, hair), in- digestible food (fatty articles, leguminous plants, particularly when they are not properly hulled), spoiled food (tainted meat, bad wine or beer, water from stagnant pools, etc.), unripe vegetables, and fruit. Some individuals possess an idiosyncrasy with regard to certain arti- cles of food, and their ingestion is always followed by acute gastritis, even when the patient is unaware of the nature of the food he has eaten. Acute gastritis sometimes depends upon errors with regard to the 57 DISEASES OF THE STOMACH. period of eating. Thus it has been observed as the result of prolonged fasting. It may be produced by mechanical, thermal, and chemical irritants. Among the mechanical irritants should be included hasty eating, in which the food is imperfectly masticated. This category also probably includes cases which have been reported as the result of eating cheese (Meschede), and raspberries with the larvae of dipterae (Gerhardt), The disease may also be produced by the ingestion of very hot or very cold articles. A remarkable case of this kind is reported by Spry. While the watch- man of a light-house was looking upwards at the burning of his tower some molten lead fell into his mouth, and then into the stomach. At his death, which occurred a few days later, the lead was found in the stomach, while the sole anatomical changes were those of gastritis. Chemical irritants include chiefly the poisons (acids, alkalies, caustics, tartar emetic, etc.). Toxic gastritis also includes those forms which are observed in uraemia, cholaemia, gout, and alcoholic excesses. Acute gastric catarrli may also be the result of a cold. Among the causes we must also mention injuries to the gastric region, as in lifting heavy loads, frequent and excessive straining. A great influence is exerted by the nervous system, which probably acts by producing disturbances in the secretion and character of the gas- tric juice, thus interfering with digestion, and facilitating decomposition of the food. Thus many individuals suffer from acute gastritis after any violent emotion, or after coitus. Acute gastritis sometimes occurs almost in an epidemic form. This is observed very often in midsummer, but also in the autumn and spring, when it is often associated with influenza. It is probably the result of infectious influences. Primary acute gastritis is more frequent in men than in women. Catarrh of the gastric mucous membrane alone is more frequent in adults than in children, but gastro-intestinal catarrh is more frequent in the latter. The relation between the two diseases is readily understood. The imperfectly digested and partially decomposed food which passes from ther stomach into the intestines produces inflammation of the mu- cous membrane of the latter. Certain individuals present a special tendency to gastric catarrh. This is observed in conditions of anaemia and convalescence, in chlorosis, phthisis, syphilis, cancer, hysteria. Very slight causes will produce acute gastritis when the circulation is impaired in consequence of diseases of the heart, lungs, or liver. In some cases there is an hereditary predis- position to the disease. Secondary gastritis is observed in many febrile and infectious diseases. It sometimes opens the scene, and in children it not infrequently takes the place of the initial chill. It is more frequent in some infectious diseases than in others. It is an almost constant prodrome of scarlatina, and is also very frequent in erysipelas. Acute gastritis develops not infrequently after affections of the mouth, salivary glands, and pharynx. For example, in salivation when large amounts of saliva are swallowed, or when putrid, purulent secretion is swallowed in affections of the pharynx. It is observed also in putrid bronchitis and pulmonary gangrene, more rarely in pulmonary abscess or in empyema which has ruptured into the lungs. In rare cases, acute gastritis is propagated from the intestines, but it- more frequently accompanies peritonitis. 58 DISEASES OF THE STOMACH. II. An atomical Changes.—Acute gastritis is rarely fatal, so that our knowledge of the anatomical lesions is based partly on theory, partly on experiments. The pyloric part of the stomach is affected chiefly or exclusively. The mucous membrane is unusually red, loosened, swollen, and covered with vitreous or slightly cloudy mucus. This is usually re- moved with difficulty. The redness may be uniform, in patches, or arborescent. Small extravasations are observed occasionally, and the mu- cous masses may be streaked with blood. Some of these phenomena, especially the hypersemia, may disappear in part after death. On the other hand, physiological hypergemia may be found in autopsies on individuals who died suddenly during digestion. Furthermore, catarrhal swelling should not be mistaken for cadaverous softening and macera- tion. Ebstein produced gastritis experimentally by feeding starving dogs with whiskey. On microscopical examination, the simple and compound pepsin glands presented appearances similar to those observed during digestion. The peptic cells were not appreciably changed, the mucous cells were opaque, granu- lar, shrunken, partly fatty and stained very deep by reagents. The cylindrical cells were in a mucoid condition. Numerous round cells were accumulated in the interglandular connective tissue. In addition, Ebstein found dilatation of the blood-vessels, swelling of the endothelium of the lymphatics, proliferation of the nuclei and desquamation. III. Symptoms and Diagnosis.—Anorexia is the chief symptom of acute gastritis. The mere thought or sight of food often produces nausea. Many patients have a longing for highly-spiced, pungent articles of food. Thirst is almost always increased. Nausea and vomiting are observed almost constantly. The vomited matters consist at first of partly unchanged, partly decomposed food. Later, we find a tough, stringy, mucoid fluid, which is vomited with diffi- culty. It is sometimes streaked with blood. Finally, the patients vomit a yellow, greenish-gray, or greenish-black biliary fluid which has an in- tensely bitter taste. The act of vomiting is very often preceded by a sort of “ imperative idea.” The mind is continually recurring to certain articles of food, the conception of which intensifies the nausea. Many patients are very much annoyed by singultus. The gases dis- charged are sometimes odorless, sometimes sour-smelling, or they have a sulphuretted hydrogen stench, or an indefinable nauseous odor. Rancid gases, or very acid gastric contents, may give rise to a burning feeling (heart-burn, pyrosis) in the stomach, or in the oesophagus (after vomit- ing). The patients generally complain of fulness and distention of the epigastrium. There is sometimes a feeling of pressure and even pain, which may be confined to the epigastrium, or may radiate towards the spine and scapulae. In some cases, pain is produced by the ingestion of food. As a rule, the tongue is coated. There is not infrequently a stale, pasty taste in the mouth, with increased secretion of saliva and fcetor ex ore. Herpes (small, light-yellow vesicles which dry into brownish- yellow crusts) sometimes forms upon the lips. The bowels are almost always constipated. Diarrhoea occurs only when the inflammation extends to the intestinal mucous membrane. The urine is usually diminished in quantity. It has a dark color, and, on cooling, often deposits a bright-red sediment of urates. In one case. Senator noticed an odor of sulphuretted hydrogen in the sediment. Nervous disturbances are often very noticeable. Complaints are DISEASES OF THE STOMACH. 59 made of a feeling of dnlness in the head, abnormal sensations of pressure, throbbing in the frontal or occipital region. The patients fall into a melancholy mood, and sometimes feel so miserable that they are apprehensive of a serious illness. Their thoughts are often confused, and there is often an inability to perform any mental effort. A feeling of vertigo is often experienced, and is sometimes so severe that the patient is unable to stand. Praicordial terror and palpitation of the heart occur occasionally. The temperature may be normal, or there is a slight rise. In some cases, the fever is extremely high, and delirium and eclampsia may develop, particularly in children. If the fever continues for some days, it may be mistaken for typhoid fever. This is differentiated by the demonstration of an error of diet, or other obvious cause, the usually sudden onset, unusual course of the fever, and the more rapid and sudden termination. Acute gastritis may last from a few hours to several days, or even two weeks. One attack predisposes to a relapse, and if repeated attacks occur, the condition may become chronic. IV. Prognosis.—The prognosis is favorable, except in those cases in which the cause produces an irreparable lesion. V. Treatment.—Rational diet will often prevent the development of acute gastritis. After the disease has developed, the causal factors should first be considered. Emetics are indicated when the stomach is overloaded; for example, apomorphine (gr. iss. : 3 iij., i—£• syringeful subcutaneously). The com- bination of ipecacuanha (gr. vij.) with tartar emetic (gr. f) (one powder every ten minutes until emesis is produced) is less serviceable, because it irritates the gastric mucous membrane. Ipecacuanha alone (gr. vij. overy ten minutes) should only be ordered in children. If the stomach is distended with gas, and the patients complain of eructations of irritating gases, we may order a few glasses of selters water; or sodium bicarb., sodium salicylic., aa 3 i. (as much as can be placed on the tip of a knife, every two hours); or sodium bicarb., gr. vij.; resorcin, gr. iss. (one powder every two hours). Laxatives may be recommended if we suspect that the decomposed gastric contents have entered the intestines. For example, calomel and jalap, aa gr. v.; or inagnes. ust., 3 iij.; aq. destill., q. s. ad f vij. M. D. S. one tablespoonful every hour; or pulv. liq. comp., two tablespoonfuls in water. Violent gastric pains are relieved by warm poultices and injections of morphine in the region of the stomach. The latter are also useful when vomiting occurs from excessive peristalsis of the stomach. But if there are no special indications, we may confine ourselves to dietetic measures alone. For one or more days the patient should be restricted to water, soup, or weak meat soup, weak tea, good wine, or water; at the most boiled milk. In addition, acid, hydrochlor. dil., gtt. v., in one-half wineglassful of lukewarm water t. i. d., half an hour after meals. 3. Chronic Gastritis. I. Etiology.—Chronic gastritis either develops from a relapsing acute catarrh, or it is chronic from the beginning. It is remarkably frequent in drunkards, particularly in those who 60 DISEASES OF THE STOMACH. imbibe alcohol in the purest form possible. No small proportion of drunkards fall a prey to chronic gastritis, while others perish from degeneration of the heart muscle, chronic inflammation of the liver and kidneys, or pneumonia. The disease is very often the result of irrational diet, the result of irregularity of the meals, or excessive haste in eating. This is especially true of certain professions, such as medicine and law. Imperfect teeth also predispose to chronic gastritis. It is often found among the poor, whose chief nutriment consists of vegetables which must be taken in large amounts to meet the needs of the body. In this case over-burden- ing of the stomach and easily decomposed food are the two chief injurious factors. The disease is common in other protracted gastric affections, for ex- ample, round ulcer and carcinoma. Indeed, the symptoms of gastritis may entirely conceal those of the primary affection. Chronic gastritis is also the result of circulatory disturbances. It occurs in diseases of the portal vein, in many hepatic affections, particu- larly cirrhosis, and in all conditions which interfere with the outflow of blood from the inferior vena cava (valvular diseases, changes in the heart muscle, pulmonary emphysema, etc.). It often develops in certain constitutional diseases, such as anaemia, chlorosis, phthisis, cancer, syphilis, Bright’s disease, etc. In such cases also the gastric symptoms may occupy the most prominent part. It is more frequent in adults, particularly in males, and is found par- ticularly among those who follow sedentary occupations. II. Anatomical Changes.—Abnormal color and swelling of the mucous membrane and excessive secretion are the most important changes. They affect chiefly the pyloric portion. The mucous membrane is usually brownish-red or grayish-red. A few large and unusually dilated vessels are often seen beneath the mucous membrane. Sometimes we find scattered extravasations of blood and superficial losses of substance. If the catarrh has lasted for some time, the mucous membrane assumes a grayish-black or slate-gray color. This is the result of metamorphosis of the pigment of the extravasated blood- corpuscles, and its deposition in the interglandular tissue, the cells of the glands, and mucous membrane. In rarer cases the mucous membrane is unusually pale. The loosening and swelling of the membrane are often marked. The surface is covered with thick masses of mucus, sometimes vitreous and translucent, sometimes cloudy and slightly purulent, sometimes tinged with blood or colored gray or brownish. Chronic gastritis also gives rise in many cases to thickening from inflammatory hyperplasia, affecting chiefly the interglandular connective tissue. The compression produces atrophy of numerous glands. In addition, their long diameter is often shortened (so-called atrophic pig- ment induration). The submucous and muscular layers often taken part in the inflam- matory hyperplasia. The muscular fibres may increase in size to such an extent that the muscular layer attains a thickness of two cm. This increase in thickness is generally confined to certain parts of the muscu- lar tunic. If it is confined to the pylorus it may give rise to stenosis, which in its turn causes stagnation and decomposition of food and dilatation of the stomach. Even the serous layer is occasionally thickened; in places it is opaque and rough. The surface of the mucous membrane is very often uneven and nod- ular. Sometimes there are numerous large prominences, sometimes the surface has a finely nodular appearance (etat mamellonne). This condition is sometimes produced by submucous accumulations of fat, or inflammatory hyperplasia of the lymph follicles. Ebstein attaches importance to inflammatory hypertrophy of the interglandular connec- tive tissue. In some cases Jones found partial atrophy and fissures in the mucous membrane, in others he attributes the condition to excessive contraction of the smooth muscular fibres. Rindfleisch believes that the surface has grown so large that it can no longer be spread in a uniform layer over the inner surface of the stomach. Ziegler describes hyper- plasia of the submucosa in the prominent parts of the mucous membrane. Secondary changes sometimes develop. These include cystoid de- generation of some of the glands from occlusion of the excretory duct, and an accumulation of mucoid fluid within the gland. The mucous membrane is sometimes elongated into pendulous outgrowths (so-called polypi of the stomach). As many as thirty may be present. If situated at the gastric orifices they may produce symptoms of stenosis. Less prominent, but more numerous proliferations give rise to that form of the disease which has been described as gastritis prolifera or verrucosa. III. Symptoms.—The symptoms are almost identical with those of acute gastritis, but they are less severe. The majority of patients com- plain of a feeling of fulness and tenderness in the epigastrium, some- times intensified to violent pain. The patients suffer from loss of appetite, but boulimia may be noticed at irregular intervals. There is a frequent desire for strongly spiced articles of food. Thirst is sometimes increased, but not so often as in acute gastritis. Vomiting is also less frequent. The vomited matters are sometimes unchanged, sometimes in a con- dition of fermentation. Bilious vomiting is also observed. Yeast fungus and sarcina ventriculi are found not infrequently with the microscope. Morning sickness often occurs in drunkards. The vomited matter is mucous and stringy, usually alkaline and consists chiefiy of saliva which is excreted in increased amount on account of reflex irritation of the nerves of the salivary glands, and is swallowed during the night. The patients sometimes vomit peculiarly tough, vitreous, gum-like masses, which are the result of mucous fermentation of the hydro- carbons. There are frequent eructations of odorless or rancid gases, and some- times a small amount of the gastric contents passes into the mouth at the same time. This is associated not infrequently with a feeling of great relief. Heart-burn (pyrosis) very often persists for hours after- wards. The tongue may be entirely clear, but, as a rule, it has a thick, gray, yellowish or brownish coating, and its edges contain the impressions of the teeth. The saliva is generally increased in amount. Foetor ex ore is often observed. The patients often complain of a stale, foul taste in the mouth. The gastric region may be distended, and is often sensitive on pres- sure, most markedly in the region of the pylorus. The urine is scanty, high-colored, often deposits a brick-red sediment DISEASES OF THE STOMACH. 61 62 DISEASES OF THE STOMACH. on cooling, and contains an excessive amount of oxalate of lime and phosphates. The bowels are usually constipated unless enteritis is also present. In the latter event, diarrhoea may alternate with constipation. The patients complain not infrequently of palpitation and praecordial terror which, according to French writers, may give rise to dilatation of the right ventricle. It is assumed that reflex irritation from the stomach causes contraction of the pulmonary vessels in the tracts of the vagus and sympathetic, and that this causes increased pressure in the pulmo- nary artery. Stenocardic and asthmatic symptoms are occasionally observed. The patients often feel as if they are suffering from some severe dis- ease. They put no trust in their mental or physical powers, and regard their condition as hopeless. Many suffer from vertigo (vertigo e stomaclio laeso), and this seems to confirm their suspicions of an incurable disease of the brain or spinal cord. The dizziness is often felt only in the morning. In one case, Leube was able to produce this symptom by pressing upon the patient’s stomach while in the recumbent position, and then allowing him to stand up. If the disease lasts for a long time, the general nutrition becomes impaired. The signs of dissolution of the blood sometimes develop, and numerous hemorrhages appear upon the skin and mucous membranes. Eczema and urticaria appear occasionally. If the gastric catarrh is secondary to a serious affection, death may ensue as the result of increas- ing marasmus. The disease lasts for months or years, with frequent remissions and exacerbations. IY. Diagnosis.—It is often difficult to decide whether chronic gas- tritis is an independent affection or is dependent on cancer or ulcer of the stomach. Hypertrophy of the walls of the stomach may develop to such an extent as the result of catarrh that the thickened greater curvature or pylorus may be felt on palpation, but in such cases the prominence is smooth. The age of the patient and the long continuance of gastric symptoms without cachexia may also be useful in differential diagnosis from cancer. The absence or infrequency of vomiting favors the diag- nosis of simple catarrh. According to Bamberger, an abundance of sarcina ventriculi in the vomited matters is indicative of cancer. When a gastric tumor is not demonstrable, a cancer may be over- looked. Our suspicions should be aroused by the advanced age of the patient, cachexia, swelling of the left supraclavicular glands and oedema. Ulcer of the stomach often affects anaemic or chlorotic individuals, the pain is more violent and localized than in simple gastritis, and fol- lows more closely on the ingestion of food. Haematemesis would at once decide in favor of ulcer. Y. Prognosis.—The prognosis is bad when the gastritis is secondary to some incurable affection. In the primary variety, recovery can be looked for only when the patients can break their bad habits and adhere strictly to the prescribed diet. YI. Treatment.—Prophylactic measures possess no slight impor- tance. We refer to proper mastication of the food, proper intervals between meals, intact condition of the teeth, etc. Individuals who are liable to gastritis from cold should wear a warm belly band. 63 DISEASES OF THE STOMACH. Dietetic measures constitute the chief feature in treatment. Leube’s dietary contains four groups, arranged, according to their digestibility, in the following order: a. Meat soup, Leube-R,osenthal*s meat solution, milk, raw and very soft boiled eggs. b. Stewed calves* brain, thymus gland of the calf, chicken, pigeon, calves* feet, in addition glutinous, soup at dinner, and porridge at supper, c. Boiled scraped beef and raw ham. d. Boiled chicken, pigeon, rare roast beef, veal, hare, pike, trout (with caution), macaroni, bouillon with rice, and small amounts of old white or red wine, or Bavarian beer. We should carefully prescribe the amount of food to be taken, and the hours of eating; the patient should eat slowly, and masticate thoroughly. Fresh bread must be forbidden. It should be toasted, or we may order zwieback or English crackers (Albert). Fatty articles, fresh vegetables, and amylaceous articles are tabooed. Krukenberg recommended a milk or butter-milk cure, but in some patients this produces disgust or violent heart-burn. The latter may sometimes be prevented by the addition of lime-water or bicarbonate of soda. Some patients suffer less from a diet of more spicy articles, for exam- ple, smoked tongue or beef, pork sausage. In chlorotic and anaemic patients, the careful use of hydrochloric acid is often serviceable. It is sufficient to give five drops in half a wine- glassful of lukewarm water half an hour after dinner. Its action is some- times increased by the addition of a little pepsin. When fermentation of the contents of the stomach occurs to a slight degree, we may resort to the internal administration of salicylic acid (gr. vij. t. i. d., half hour after meals), resorcin (gr. iss. t. i. d.), creasote (gtt. v. in 15 pills, one pill t. i. d.), or benzolum (twenty drops twice a day). There are two indications for the use of the stomach-pump in chronic gastritis, viz., excessive fermentation of the gastric contents, and inabil- ity of the organ to propel its contents. The pump should then be used every morning until the symptoms of fermentation and stasis are no longer demonstrable. The stomach should be washed with lukewarm water (30 to 35° C.) until it runs out perfectly clear. It is advisable to follow this up with a weak solution (1 to 2 per cent) of natrium salicyli- cum, or resorcin, aqua creasoti (1 : 2 of water), benzolum (4- per oent). If there is an excessive formation of acid, a solution of sodium bicar- bonate (1 to 2 per cent) or Carlsbad salts (1 to 2 per cent) is indi- cated. If we have reason to suspect impaired muscular tonus of the organ, we may order bitters, for example, strychnia (gr. ss., pulv. althaeae, q.s. ut f. pil. No. 15. D. S. 1 pill t. i. d.), tinct. amara (25 to 30 drops t. i. d.), tinct. gentian, 25 to 30 drops t. i. d., tinct. quassiae, cortex condurango, tinct. quiniae comp., etc. Cold baths and rubbings, sea baths, and cold- water cures are often useful under such circumstances. Electrical applications are also said to be attended with good results. One elec- trode of a strong faradic current is placed upon the back, the other is passed slowly across the epigastrium from left to right, or a flexible stomach electrode is introduced into the stomach, and the other one placed upon the epigastrium. Bismuth, nitrate of silver, or opium must be administered with caution, as they sometimes aggravate the symptoms. Certain symptoms may require special treatment. If the pain is very 64 DISEASES OF THE STOMACH. severe, we may order: R Aq. amvgdal. amar. 3iij., morphin. hydro- chlor. gr. iss. M. D. S. 10 drops t. i. d.; extract, belladonn. gr. £t. i. d.; morphin. hydrochlor. gr. -fa t. i. d.; or R Chloral.. hydrat. gr. lxxv., pulv. althoeae et tragacanth. q. s. ut f. pil. No. xx. D. S. One pill t. i. d. before meals. Heartburn may be relieved by magnesia usta, natrium bicarbonate, aq. calcis, or the previously mentioned antifermentatives. Constipation may be combated by : 11 Aloes, ext. rhei co., jalapae aa gr. xv.,'pulv. et sue. liq. q. s. ut f. pil. No. 30. D. S. 2 to 4 pills at night, etc. When the gastritis is secondary to diseases of the circulatory or re- spiratory apparatus or liver, our chief attention should be directed to the primary disease. Special repute in the treatment of chronic gastritis is enjoyed by mineral waters, particularly the alkaline acidulous waters (chief constit- uents: carbonic acid and natrium carbonate), alkaline-muriatic waters (chief constituents: carbonic acid, sodium carbonate, and sodium chloride), alkaline-saline waters (large amount of sodium sulphate) and salt water. a. The alkaline acidulous wells are preferable when the patients suffer frequently from eructations, heartburn, and gastric pain. b. The alkaline-muriatic‘waters are indicated when there is marked nausea, with a flat taste in the mouth, and lively secretion of tough mucus, c. The alkaline-saline waters are best in obstinate constipation (Carlsbad is par- ticularly indicated if the stomach is very sensitive to pressure and spicy articles are poorly tolerated, while Marienbad is useful in obese individ- uals and drunkards), d. Salt waters are specially useful in very feeble individuals. Ferruginous waters are indicated when the patients are anaemic. 4. Purulent Gastritis. (Gastritis phlegmonosa s. submucosa.) I. Anatomical Changes.—Purulent gastritis involves exclusively or mainly the submucous cellular tissue, either as a diffuse infiltration or circumscribed abscess. In diffuse purulent infiltration the submucosa may attain a thickness of one cm. The tissue often has a gelatinous look, and is infiltrated with puriform fluid, which may contain an excess of serum or fibrin, or be purely purulent. The infiltration may sometimes be squeezed out of the tissue. The pus sometimes perforates the mucous membrane in many places. The openings vary in size from that of a pin’s head to that of a bean. The larger ones are irregular in shape, the small ones are round. Upon the introduction of a sound, the mucous membrane is often found to be separated from the submucosa over a considerable area. As a rule, these changes are most marked near the pylorus. In Chvostek’s case, they extended to the oesophagus. The mucous membrane is unchanged in some cases, and is even very pale in color. In a case reported by Glax, it formed a fluctuating mass, which could be moved to and fro upon its base. In some cases it is injected in patches, in others diffusely inflamed. Rokitansky reported one case in which the mucous membrane was converted into a jDulpy, blackish-brown necrotic mass. From the submucosa the pus passes along the intermuscular connect DISEASES OF THE STOMACH. 65 live tissue septa into the muscular coat and subserous cellular tisssue. The muscular coat may be almost entirely destroyed. Peritonitis is ob- served in almost all cases of phlegmonous gastritis. Key and Malmsten observed marked distention and sinuosity of the subperitoneal lymphatics. The stomach is generally distended with gas, and contains a bile-stained or brownish, flocculent, opaque fluid. The following lesions have also been observed occasionally: ulceration, cancer, enlargement of the spleen, acute and chronic nephritis, diphtheria of the large intestine, gall-stones, gangrene, and perforation of the gall-bladder, pleurisy, mediastinitis, pericarditis. Abscess of the stomach is a circumscribed accumulation of pus in the submucosa, and may attain the size of a fist. Several abscesses are some- times present. The pus may burst into the cavity of the stomach, the peritoneum or adjacent organs. II. Etiology.—The disease may be primary or secondary. The causes of primary phlegmonous gastritis cannot always be deter- mined. Cold, injury, errors of diet have been mentioned, but a certain predisposition seems to be necessary to its development. This may be the result of the abuse of alcohol. Secondary phlegmonous gastritis develops during certain infectious diseases, especially typhoid fever, variola, pyaemia, puerperal fever, peri- tonitis, and splenic fever. It may also follow the ingestion of caustic poisons. It is more frequent in men than in women (among 45 cases, 38 oc- curred in men, 7 in women). As a rule, it develops in middle life. The youngest patient was 17 years old, the oldest 76 years. III. Symptoms.—The disease either begins suddenly, or is preceded for a few days by anorexia, vomiting, and a feeling of pressure in the epigastrium. In secondary gastritis, symptoms may be entirely absent, or, at least, overlooked on account of the severity of the primary dis- ease. The patients usually complain of pain in the gastric region, some- times extending to the right or left hypochondrium. There is often no increase of pain on pressure. Vomiting or eructation is almost always present. The vomited matters consist of the contents of the stomach, or are biliary or brownish; pus is rarely vomited. There is usually com- plete anorexia with almost unquenchable thirst. The bowels are some- times constipated, sometimes the passages are diarrhceal, occasionally bloody; in Key and Malmstens* case, they were dysenteric in character. In this case, the urine was bloody and contained casts; it is generally scanty and concentrated. Physical examination is negative in many cases, in others a circumscribed abscess can be felt as a tumor. The general condition is seriously affected in the majority of cases. The temperature may reach 41° C., and a typhoid condition is often ob- served, and may be mistaken for typhoid fever or meningitis. In other cases, the abdomen is distended and sensitive, and the signs of peritonitis develop. Apyrexial cases are rare, but death sometimes occurs unexpectedly without any noteworthy previous symptoms. The disease usually runs an acute course. As a rule, death occurs inside of two weeks, not infrequently in a few hours or days. The dis- ease rarely extends over several weeks or even months. IV. Diagnosis.—This is hardly possible unless pus is vomited. In 66 DISEASES OF TIIE STOMACH. such cases, we must endeavor to satisfy ourselves that the pus has not perforated the stomach from the pleura, pericardium, liver, spleen, kid- neys, peritoneum, or spinal column. The vomited matters should also be examined with the microscope, since the pus may not be visible to the naked eye. The disease may be mistaken for typhoid fever, meningitis, or peritonitis; in other cases, it remains latent during life. Y. Prognosis.—The prognosis is usually unfavorable. Brand and Dittrich showed that recovery is possible, since they found cicatricial tissue in parts of the submucosa, which had produced stenosis in the pyloric region. Cases have been reported of recovery from abscess of the stomach after the vomiting of pus. VI. Treatment.—This is purely symptomatic. Vomiting and pain are combated by subcutaneous injections of morphine, an ice-bag to the stomach, and ingestion of pieces of ice. Rectal alimentation should be resorted to (vide page 32). Fever is treated with antipyrin ( 3 i. to iss. in | ij. of lukewarm water per rectum). In collapse, stimulants are administered, preferably camphor gr. xv., ol. amygdal. 3 iij., one syringe- ful three or four times a day. 5. Toxic Gastritis. (Gastritis venenata.) I. Etiology.—This is generally the result of the ingestion of acids- or alkalies, but may also be produced by any other irritating substance, and*by certain vegetable poisons. II. Anatomical Changes.—These depend mainly on the amount and concentration of the poison which has entered the stomach. The most extensive lesions are generally found in cases of suicide. When the poison is taken accidentally, the patient soon discovers the mistake, and attempts to get rid of the poison as soon as possible. Under such cir- cumstances, the changes may be confined to the mouth and oesophagus. The nature of the poison often exerts an influence on the character of the gastric lesions. In sulphuric-acid poisoning, the scurf upon the mucous membrane is grayish-black; in nitric-acid poisoning, it is yel- lowish (xanthoprotein); in poisoning with alkalies, it is brownish; in copper-poisoning, it has a blue or green color (the latter changing to dark-blue on the addition of ammonia); in silver-poisoning, it is deep- black. In cases of phosphorus-poisoning, the mucous membrane not infrequently has a milky, opaque, or yellowish appearance. The glands of the mucous membrane are in a state of marked fatty degeneration (so- called gastritis parenchymatosa, s. glandularis, s. gastro-adenitis). The lesions are most marked in those places with which the poison has been longest in contact (fundus and posterior wall). In mild cases, branching stripes are sometimes seen running along the posterior wall from the cardiac end to the fundus, where they attain greater dimensions. According to the intensity of the irritant action, we will find super- ficial excoriations, removal of the epithelial layer, simple or hemorrhagic catarrh (rarely croupous inflammation in ammonia-poisoning, or the formation of pustules in poisoning with tartar emetic), or the formation of a scurf, while the other coats are infiltrated with serum, or all the layers of the stomach are seriously implicated. In the most severe cases, the stomach forms a black, sloughy mass, which tears on the slightest touch, or has ruptured spontaneously, and has poured its brownish or DISEASES OF THE STOMACH. 67 hemorrhagic contents into the abdominal cavity. The vessels of the stomach contain firm clots, or dark, fluid, tar-like blood. The lesions sometimes extend, in a less marked degree, to the mucous membrane of the intestines. Lesions which atfect chiefly the mucous membrane may recover. After suppuration, the slough is thrown off, and cicatricial connec- tive tissue develops. Large pieces of the mucous membrane are some- times vomited. Cicatrization may give rise to new dangers by causing stenosis of the entire gastric cavity, or of the orifices. It is said that the organ some- times contracts to the dimensions of a hen’s egg. III. Symptoms.—The first symptom is burning, agonizing pain in the region of the stomach, which is increased on the slightest pressure. The patients toss to and fro restlessly and anxiously. As a rule, pain is also felt along the spine (oesophagitis) and in the mouth and pharynx. Singultus develops, with occasional vomiting, usually of bloody masses. The thirst is unquenchable. The passages are often diarrhceal and mixed with blood. If peritonitis develops, the abdomen becomes tympanitic, tender on pressure, and presents abnormal areas of dulness. In perforation-peri- tonitis, the hepatic dulness disappears, because the air which escapes from the stomach pushes the liver away from the wall of the thorax. As a rule, there are very grave disturbances of the general condition. The sensorium is often clouded. The pulse is small and unusually fre- quent. The skin is cold and covered with clammy sweat. Bamberger observed two deaths from shock, although the stomach did not present any marked lesions. Death may occur within a few hours. In other cases, cicatrization occurs, but recovery is sometimes only temporary, and the patient dies from inanition. Profuse and occasionally fatal hemorrhage may occur when the slough is thrown off. IV. Diagnosis.—That we have to deal with poisoning must be concluded from the usually sudden illness. The nature of the poison is determined, as a rule, by the history of the case. Whether we have to deal, in doubtful cases, with poisoning with alkalies or acids is shown by the reaction of the buccal mucous membrane to litmus paper. V. Prognosis.—The prognosis is always grave, and should be guarded for a long time, in view of the possibility of hemorrhage or re- traction of the cicatricial tissue VI. Treatment.—In recent cases of poisoning with acids, an alkali should be administered, such as magnesia usta (gr. lxxv. to a glass of milk with ice, a tablespoonful every ten minutes), or, in case of necessity, powdered chalk or lime. In poisoning with alkalies, dilute vinegar may be administered. In other cases, the stomach should be washed out through a soft tube, and then the ordinary antidotes given. Pieces of ice, ice and milk, or an ice-bag to the epigastrium may be ordered for the gastritis. Violent pain should be relieved by subcutane- ous injections of morphine. 6. Round Ulcer of the Stomach. (Ulcus ventriculi simplex s. chronicum s. perforans, s. pepticum.) I. Anatomical Changes.—The round gastric ulcer (either recent 68 DISEASES OF THE STOMACH. or cicatrized) is found with remarkable frequency (in about five per cent of all autopsies). As a rule, the ulcer forms a perfectly round or elongated, oval loss of substance. This is particularly true of small ulcers. Large ones are irregular, either because the ulcer has spread in different directions with varying rapidity, or because adjacent losses of substance have coalesced with one another. In some cases the diameter of the ulcer is hardly one centimetre, in others it may attain the size of the palm of the hand. Cruveilhier described a case in which the ulceration extended along the lesser curvature from the pylorus to the cardiac extremity. It is situated most frequently in the pyloric portion upon the posterior wall near the lesser curvature, most infrequently at the fundus. Brinton collated the following statistics : Posterior wall, . . . . . 86 (42 per cent). Lesser curvature, . . . . . 55 (26.8 “ ). Pylorus, ...... 32(15.6 “ ). Anterior and posterior walls, . . .13(6.3 “ ). Anterior wall, . . . . . 10 ( 4.9 “ ). Greater curvature, . . . . . 5 ( 2.4 “ ). Cardia, . . . . . . 4 ( 2.0 “ ). 205 There is usually but one ulcer, more rarely several: even as many as eight have been observed in different parts of the organ. As a rule, they present various stages of development. The round ulcer has also been found in the duodenum and oesophagus. The ulcer has such sharply defined borders that it very often looks as if it had been punched out. At first the loss of substance affects only the mucous membrane, then it spreads to the muscular coat, and finally to the serous layer. It is always funnel-shaped, the small end being situ- ated at the serous layer. But the centre of the loss of substance in the mucous membrane and the tip of the funnel are not situated directly above one another. In ulcers of the upper half of the stomach the tip is usually directed upwards, in those of the lower half, downwards, corre- sponding to the mode of ramification of the gastric vessels. The edges of the ulcer are rarely thickened, and an inflammatory zone is almost always absent. The edges are terrace-shaped, their slope being steeper in the cardiac region than near the pylorus. The base of the ulcer is remarkably clean in many cases. In others it has a brownish, hemorrhagic coating. In many cases perforation of the stomach is prevented by adhesive peritonitis which binds the stomach to adjacent organs. In most cases we find adhesions to the pancreas and adjacent lymphatic glands, to the left lobe of the liver or the omentum, more rarely to the spleen, colon, small intestine, diaphragm or anterior abdominal wall. Saccu- lated peritonitis sometimes develops at the site of threatened perfo- ration, and the rupture occurs into the sacculated peritoneal space. The round ulcer may give rise to subphrenic pyopneumothorax (Vol. I., page 375). If the base of the ulcer is formed by the adherent pancreas, liver, or spleen, the mucous membrane, as a rule, projects over the muscular coat and forms the transition from the cavity of the stomach to the base of the ulcer. The adherent organs are sometimes involved in the destructive process, so that the latter may produce large cavities filled with pus or 69 DISEASES OF THE STOMACH. ichor. In this manner the stomach may connect with other cavities and organs (internal gastric fistula), such as the duodenum, colon, pleural or pericardial cavities, left ventricle, or through the lungs into the bronchi, gall-bladder. If adhesions to the anterior abdominal wall have formed, an external gastric fistula may develop, the complete formation of which may be preceded by emphysema of the skin. Perforation into the peritoneal cavity depends chiefly on two factors: the rapidity with which the ulcer forms, and the more or less favorable opportunity for the production of adhesions. Ulcers of the anterior wall are especially apt to lead to perforation because the mobility of this part is not favorable to the production of adhesions. Among 75 ulcers of the anterior wall, perforation occurred 64 times; among 30 cases of the cardiac extremity, it occurred twelve times. The development of the ulcer within the walls of the stomach and its extension to adjacent organs afford the possibility for hemorrhage. On account of its course along the posterior wall of the stomach (the most frequent site of ulceration) the arteria lienalis is most frequently eroded. The bleeding artery is sometimes found in a condition of aneurismal dilatation. Audral observed a fatal hemorrhage from varicose veins near the ulcer. In order to detect the bleeding vessel, the main trunk should be injected with water; this will escape from the erosion. Cicatrization of gastric ulcers is not uncommon. If the loss of sub- stance is slight and affects only the mucous membrane, the cicatrization may be so complete as to be readily overlooked on autopsy. If the ulcer is deeper and larger, the adjacent mucous membrane is involved in the cicatricial process. Thick, fibrous callosities sometimes form, and their retraction may impart an unusual shape to the organ. Ulcers upon the posterior wall may spread in a girdle around the stomach, and their sub- sequent cicatrization may divide the organ into abnormal cavities (hour- glass shape). These are most marked if the curvatures of the stomach are specially involved in the retracting process. Cases have been ob- served in which the anterior division was alone employed in digestion, and was connected by a fistula with the colon or duodenum. Another mode of recovery is the formation of numerous fibrous ad- hesions: the stomach is sometimes adherent to all the adjacent organs. The adhesions may also be the cause of death. In one case the adhe- sions between the stomach and gall-bladder ruptured and produced fatal hemorrhage. II. Etiology.—The disease is extremely rare before the age of 14 years, but cases have been reported at the age of 3, 3U and 4 years. Vergely observed a recent gastric ulcer in a woman set. 83 years. Clini- cal observation teaches that the disease is most common from the 15th to the 30th years. Women are attacked more frequently than men. Brinton found a proportion of 2 :1; With of 7.3 :1. Starcke observed the disease more frequently in men. A marked predisposition is offered by certain general diseases, such as chlorosis. This is also true of phthisis, arterio-sclerosis, and syphilis. According to Rokitansky it may be associated with intermittent fever. London reported a case which he attributed to pigment embolism of the gastric vessels in protracted intermittent fever. Among other causes may be mentioned abuse of alcohol, indigestible food, inordinate inges- tion of vegetables, and imperfect mastication. Bamberger noticed the disease frequently in cooks. Speck attributes 70 DISEASES OF THE STOMACH. its extraordinary frequency in Eastern Siberia to the almost exclusive diet of fatty fish. Violent vomiting, severe gastritis, injury of the mucous membrane by a blow or fall, or by poisonous or foreign bodies, may give rise to hemorrhage into the mucous membrane and then to ulceration. After extensive cutaneous burns, ulceration of the stomach and duodenum has been observed. This is probably the result of destruction of red blood-globules and occlusion of the vessels of the mucous membrane by the products of corpuscular degeneration. Certain trades exert an influence on the development of round gastric ulcer. Bernutz calls attention to its frequency in potters and glass workers, and explains it by the ingestion of sharp particles of dust. I have observed the disease frequently in metal workers. The shape of the ulcers resembles the mode of ramification of the gastric vessels, and it often seems as if the subdivisions of the smaller arteries were to a certain extent punched out of the mucous membrane. In addition, the round ulcer develops under circumstances which warrant us in assuming changes in the walls of the vessels and circulatory disturbances in general. It is known that chlorosis leads to fatty degeneration of the vessels. This is also true of pulmonary phthisis which, in addition, may give rise, like syphilis, to waxy degeneration of the vessels. Atheromatous changes in the vessels have also been observed. The influence of the acid gastric juice is evident from the fact that round ulcers are found only in those parts of the digestive tract in which its digestive effect is present. Under normal conditions, the gastric juice does not digest the wall of the stom- ach because it is neutralized by the alkaline blood. Self-digestion is possible if the gastric juice is excessively acid, and is no longer completely neutralized by the blood, or if the circulation in the mucous membrane is so feeble that neutrali- zation is impossible. The former view is not plausible because the ulcer would then extend over large surfaces. As a matter of course, various circulatory disturbances may give rise to a gastric ulcer; there must simply be a disproportion in the process of neutralization. The more marked this is, the more rapidly will the ulcer develop. It may result from embolism, thrombosis, simple stenosis following arterio-sclerosis, deep-spreading ecchymoses. It is doubtful, however, whether mere spasm of the arteries leads to the formation of an ulcer. Axel Key believes that spasm of the muscular coat of the stomach causes disturbance of the venous circulation, and thus may give j ise to an ulcer. Boettcher attributes gastric ulcers to the action of scliizomy- cetes Ulcers have been produced experimentally by ligature or embolism of the gastric vessels, ligature of the portal vein, by injuries of the central nervous sys- tem which caused hemorrhages into the mucous membrane of the stomach. III. Symptoms.—In a few cases the development of gastric nicer is entirely latent. Individuals who were previously healthy, or had merely suffered for a few days from trifling gastric symptoms, are suddenly seized with a profuse gastric hemorrhage, or suddenly fall down, com- plain of intolerable pain in the abdomen or that something has burst, and die in a few hours or in one to three days, with symptoms of per- foration-peritonitis. In the large majority of cases, annoying symptoms develop, among which pain in the stomach is most constant. As a rule, it begins after eating, either immediately or withioi one to two hours. It is so much more severe, the larger the meal and the more imperfect the mastication of the food. In rare cases the pain occurs in the morning or while fasting, and disappears after eating. It is usually described as boring, gnawing, burning, more rarely as lancinating. It is sometimes so intolerable that the patients groan aloud, are covered with perspiration, and fall into convulsions. DISEASES OF THE STOMACH. 71 As a rule, the pain is located immediately beneath the ensiform car- tilage ; in addition to diffuse tenderness, a circumscribed spot is specially painful. In other cases, the pain is situated under the sternum, in one of the hypochondriac spaces, lower part of the dorsal spine, or between the scapulae. If the pain is especially severe in dorsal decubitus, the ulcer may be assumed to be situated on the posterior wall of the stomach, and the pa- tients often assume a crouching position, bent over forwards. An ulcer on the anterior wall is associated with violent pain in abdominal decubi- tus. Left lateral decubitus is often assumed in ulcers of the pyloric por- tion, the opposite position in ulcers of the fundus and cardiac end. It is not true that the occurrence of pain one to two hours after meals indicates that the ulcer is situated at the pylorus, nor that small ulcers cause slight pain. The pain is sometimes produced by direct irritation of the ulcer by the ingesta (when it develops immediately after eating). In other cases the movements of the stomach affect the surface of the ulcer. If the pain is independent of the meals, it must be attributed to the further development of the ulcer and the injury of nerves in the walls of the stomach. Finally, severe pains may result from inflammation of the serous layer or adhesion of the stomach to adjacent organs. Pains sometimes radiate into other nerve tracts (intercostal neuralgia and oppressed breathing, neuralgia of the left brochial plexus, pain in the shoulder). Vomiting occurs with remarkable frequency, sometimes early in the morning or when the stomach is empty. The usually watery, mucous mass is generally alkaline and consists of saliva (it turns red on the ad- dition of chloride of iron) which has been secreted in increased quanti- ties and swallowed during the night. In other cases the ingestion of food produces vomiting, sometimes despite the utmost caution in diet. The food is vomited in an unchanged or slightly modified condition, and sometimes contains sarcina ventriculi. Bilious matter may also be vom- ited. The vomited matters will be tinged with blood if emesis constantly recurs and gives rise to small extravasations of blood upon the gastric mucous membrane, or if capillaries have been opened by the ulcerative process. In some cases the vomiting is so obstinate thpt the patients waste away to a skeleton. Haematemesis is a very valuable sign from a diagnostic standpoint. It occurs spontaneously, after bodily or mental exertion, a heavy meal, or as the result of a blow on the epigastrium. It is apt to occur in women at the time of menstruation. Among 120 cases of round ulcer collected by L. Muller, haematemesis was observed in 35. The patients occasionally state that something warm is trickling in the stomach, they have a peculiar taste of blood in the mouth, nausea occurs, and then bloody masses are vomited. If the hemorrhage is very profuse, the signs of sudden cerebral anaemia develop (dizziness, syncope, tinnitus aurium, small pulse, etc.). The amount of blood varies, but may reach several pounds. It is sometimes pure, sometimes mixed with food. It consists generally of dark, blackish-red, acid clots, which are not frothy. If a large arterial vessel has been opened, the blood is bright-red. The more profuse and sudden the hemorrhage, the earlier will vomiting occur and the less changed will'be the blood. If the hemorrhage occurs gradually, the 72 DISEASES OF THE STOMACH. coloring matter of the blood will be changed by the gastric juice and pe- culiar “ coffee grounds” masses will make their appearance. The hemorrhage is rarely the immediate cause of death. The patients generally recover gradually, and many suffer from repeated attacks. If it is very profuse, it may enter the air-passages and be coughed up, so that patients who have suffered little from gastric symptoms may think that they have had an attack of hsemoptysis. The appetite is sometimes unaffected, occasionally even increased, but many patients dread to satisfy it, because their discomforts are thereby increased. Thirst is often increased. Some patients suffer from pro- found depression, and occasionally from obstinate insomnia. The general nutrition is sometimes so good that the patients present a blooming appearance. Rapid emaciation may occur when the nutri- tion suffers in consequence of the vomiting and violent pains. The tongue is sometimes clear, sometimes coated. In many cases it has an extremely red, smooth or fissured surface, which has been attrib- uted to partial desquamation of the epithelium from contact (during vomiting) with the acid contents of the stomach. The epigastrium is occasionally distended. As a rule, it is tender on pressure, especially over a spot which corresponds to the situation of the ulcer. The lower dorsal or upper lumbar vertebrae are especially sensi- tive in ulceration of the lesser curvature and posterior wall of the stomach. Pain at the level of the umbilicus corresponds to ulceration of the greater curvature; pain in the right or left hypochondrium to ulcer- ation of the pylorus or fundus. If inanition threatens, the abdominal walls are sunken, the aorta is seen pulsating vigorously, and the spine and aorta are readily reached on palpation. The bowels are usually constipated. Gastric hemorrhage is some- times manifested solely by bloody, tarry, or black passages. But even when hsematemesis is produced, the stools are almost always stained with blood. The quantity of urine is generally diminished; the urine is concen- trated and often very acid. Slight temporary albuminuria may develop after profuse haematemesis. The duration of the disease is extremely variable. Brinton reports a case which lasted thirty-five years. Relapses occur very frequently, even at the end of years. Rapid and permanent recovery is not very frequent. Even under favorable circumstances, a striking tenderness of the stomach often re- mains, and is manifested after every indiscretion in diet by a feeling of pressure, fulness in the epigastrium, severe gastric pains, and frequent emesis. Among the sequelae may be mentioned very violent gastric pains, which not infrequently continue for years, appear in paroxysms for a few days or weeks, and then disappear for a long time. In other cases, the symptoms of gastro-intestinal catarrh continue. If cicatrices have formed at the pylorus, stenosis of the pylorus and dilatation of the stomach (gas- trectasia) will develop. Symptoms of pyloric insufficiency (inconti- nentia pylori) may be expected if the muscular coat has suffered serious, injury. In many cases in which the shape of the stomach has been materially changed by cicatrices, and constrictions of the cavity have formed, sud- den symptoms of ileus may develop as soon as the communication be- 73 DISEASES OF THE STOMACH. tween the anterior and posterior divisions of the stomach is inter- rupted. If one of these divisions communicates with the colon by means of a a fistula, lientery has been observed, i. e., the food passes with great rapidity and very little changed into the colon, and very soon appears in the evacuations. Haematemesis forms a transition between the symptoms proper and the complications. A very grave complication is cancer of the stomach, which develops not infrequently, at an advanced age, on the base of a round ulcer. If signs of perforation appear, the situation becomes very grave. The patients usually complain of unspeakable pain, a feeling of annihilation, and sometimes of a sensation as if something had burst in the belly. The abdomen is tympanitic and extremely tender. Circumscribed and unu- sual areas of dulness, corresponding to exudation beneath the abdominal walls, make their appearance. If the liver and spleen are not bound down by old adhesions, the areas of dulness of these organs disappear, because the gas which escapes from the stomach separates these organs from the thoracic walls. Grave collapse is manifested by cool skin, small pulse, and sunken features. Vomiting is more frequently absent than present in perforation of the stomach. The sensonum is usually un- clouded to the last moment. Death occurs with symptoms of increasing exhaustion or disturbances of respiration and circulation, as the dia- phragm is pushed into the thoracic space to an extreme degree. Cases of recovery have been reported, but are extremely exceptional. If the ulcer perforates through the anterior abdominal wall, cuta- neous emphysema may develop from the passage of the gases of the stomach into the subcutaneous cellular tissue. The signs of pneumo- pericardium or pneumothorax (usually hydropneumopericardium or hydropneumothorax) rapidly develop after perforation into the pleural or pericardial cavities. Perforation into the lungs is recognized by the acid reaction of the sputum or the appearance of particles of food in it. A gastric ulcer sometimes causes thrombosis of the portal vein and thus gives rise to the formation of numerous metastatic abscesses in vari- ous organs. IV. Diagnosis.—This is usually as easy in the majority of cases as it is impossible in rarer cases. The development of pain in the stomach, vomiting and haematemesis in a young, pale individual is almost always associated with a round ulcer of the stomach. The diagnosis is difficult if it must be made from single symptoms. The disease may be mistaken for the following: a. Chronic gastritis.—Errors of diet can usually be demonstrated as the cause; the tenderness is slighter but more diffuse; haematemesis is absent; a cure is more readily effected. h. Pure nervous gastritis.—The pains are not closely associated with the meals, and are sometimes diminished by pressure in the epigastrium: haematemesis is absent; there are usually other nervous disturbances (in- tercostal neuralgia, clavus, etc.). c. Cancer of the stomach.—The age of the patient is significant ; cachexia soon develops; the left supraclavicular glands may be enlarged; the course of the disease is rapid; a tumor can be felt in the gastric re- gion (cicatrices following ulcers are also perceptible to the touch). d. Biliary colic.—The pains are confined chiefly to the region of the gall-bladder (outer border of the right rectus abdominis immediately be- 74 DISEASES OF THE STOMACH. neath the right thorax); vomiting and chill often occur during the pains; scleral and even cutaneous jaundice develop not infrequently; the passages should be carefully examined for gall-stones. Y. Prognosis.—A guarded prognosis should always be given. Even under favorable circumstances disturbances of digestion may persist for life, and on the other hand, hemorrhage or perforation may unexpect- edly place the patient in great jeopardy. The prognosis is especially grave when we may assume that the ulcer is situated on the anterior wall of the stomach, since perforation is frequent in this locality. VI. Treatment.—The patient should be kept quiet in bed until all acute inflammatory symptoms have subsided. A warm poultice should be applied constantly to the epigastrium. The chief importance should be attached to dietetic measures. If the ulcer is recent, solid food should be entirely avoided. If the patient tolerates milk, this should form the sole article of diet for weeks, and may be taken boiled, warm or cold, as the patient desires. It should be taken often but in small quantities. If it is immaterial to the patient, the milk should be thoroughly boiled. If this gives rise to an excessive formation of acid in the stomach, sodium bicarbonate or lime-water should be added. When this proves ineffectual, a little flour may be added. I have recently obtained good results by mix- ing the milk with an equal quantity of soup. When milk produces a tendency to nausea or vomiting, Debove administers it through the oesophageal sound. When it is converted in the stomach into thick cheesy lumps, buttermilk should be given. But if milk is not tolerated in any shape, we should order weak tea, meat soup, raw or soft boiled eggs (the latter taken in wine or bouillon, or seasoned with salt or sugar), and Leube-RosenthaTs meat solution. Rectal alimentation may also be resorted to. Solid food may only he taken after acute symptoms have disappeared (vide Yol. II., page 63). Among medicinal agents the Carlsbad waters enjoy the greatest re- pute. As a rule, the cooler wells (Schlossbrunnen, Marktbrunnen, Theresienbrunnen) are employed because the others are apt to produce gastric hemorrhage. If the treatment is to be carried out at home, one to three teaspoonfuls of Carlsbad salts dissolved in one-half litre water (50-55’ C. should be taken early in the morning (in three portions, one every ten minutes). Within two hours afterwards, the patient should have one or two thin, profuse evacuations. Breakfast may be taken half an hour after the last dose of the salts. Acetate of lead (gr. £ every two hours) and nitrate of silver (gr. | in pill t. i. d.) have been recommended to produce cicatrization, but much may not be expected from these agents. If the pain is violent, we may order bismuth, subnitrat. gr. vij., mor- phin. hydrochloric, gr. fa, ext. belladonna gr. £, sacch. alb. gr. v., one powder t. i. d. Subcutaneous injections of morphine in the epigastrium, chloral hydrate (gr.lxxv., tragaeanthaa et pulv. althaaae, q. s. u. f. pil.No x. D. S. One pill t. i. d.), and warm compresses to the epigastrium may also be employed. Gerhardt extols liq. ferri sesquichlorat. (three or four drops in a wineglassful of water, several times a day). In cases of obstinate vomiting, we may order the ingestion of small pieces of ice, subcutaneous injections of morphine, creasote (gtt. vij., aq. destil. I iij. D. S. One tablespoonful every two hours), or tincture of iodine (gtt. vij., aq. destil. 3 v. M. D. S. One tablespoonful every two hours). DISEASES OF THE STOMACH. 75 Concerning the treatment of gastric hemorrhage, vid Yol. II., page 55. In recurring hemorrhages, Ejdgier recommended the operative removal of the ulcer, and this was successfully performed by Kleef. If signs of perforation-peritonitis develop, we may give large doses of opium, and cover the abdomen with light warm poultices. When the acute symptoms have subsided, and anaemia is left over, preparations of iron may be cauciously administered. Appendix. Two other forms of ulceration occur upon the mucous membrane of the stomach, viz., the hemorrhagic erosion and the follicular ulcer. a. The hemorrhagic erosions are very often found at autopsies. They consist of reddish, brownish, or blackish spots, which are sometimes round, sometimes elongated, and are situated at the top of the folds of the mucous membrane. They are sometimes so numerous that the mucous membrane presents a speckled appearance. They are found mainly or exclusively in the pyloric portion of the stomach. Upon the application of a stream of water, a superficial loss of sub- stance appears which rarely extends to the submucosa. The base is often villous, the edges slightly elevated and pulpy. Hemorrhagic infarcts are found not infrequently in the immediate vicinity, and there are often gradual transitions between these, and more or less distinct losses of substance. In all probability, the hemorrhagic infarctions are converted into erosions, inasmuch as the extravasated blood interferes with the circulation, and thus exposes the affected part to the digestive action of the gastric juice. Hence gradual transitions are possible between erosion and round gastric ulcer. Hemorrhagic erosions are more frequent in adults than in children. They result from all conditions which impede the circulation in the mu- cous membrane, or, in which the walls of the vessels have become abnor- mally permeable to red blood-globules. This includes emesis, gastric catarrh, ulcer and cancer, cough, pointed or irritating particles of food, disturbances in the portal circulation (diseases of the portal vein, liver, heart, and lungs), severe infections, febrile, exhausting diseases, scurvy, morbus maculosus Werlhofii, haemophilia, etc. The lesion sometimes seems to develop during the agony, as the result of violent contractions of the stomach. This condition is not recognizable during life. In rare cases, it may give rise to violent hemorrhage which may prove fatal. b. Follicular ulcers are the result of inflammatory swelling and sup- puration of the lymphatic follicles. They may follow gastritis, but can- not be diagnosed during life. 7. Cancer of the Stomach. I. Etiology.—Cancer of the stomach is rarer than round ulcer, for while the latter is found in five per cent of all autopsies, the former is found in only two per cent. Nothing is known positively concerning its etiology, except that it is almost always a disease of advanced age. It is observed most frequently from the fortieth to the seventieth years of life, and is extremely rare before the age of thirty years. Two cases of congenital cancer of the stomach have been observed, and one in a child set. five weeks. 76 DISEASES OF THE STOMACH. The male sex is said to be affected more frequently, but this state- ment has been disputed. The poorer classes are affected somewhat more frequently than the well-to-do, probably because the excessive ingestion of vegetables by the former tasks the activity of the stomach, and often produces chronic gastric disorders. > There is no doubt that patients who suffer from chronic diseases of the stomach, particularly chronic gastritis and round ulcers, are pre- disposed in later years to cancer of the stomach. The disease has been associated, by many writers, with alcoholic excesses and injuries in the epigastrium. Pulmonary phthisis is also said to constitute a predispos- ing cause. r The statement that psychical causes exercise an etiological influence is entirely unfounded. According to some reports, climate exercisejra.,certain influence. Thus, Griesinger observed no cases in Egypt, although gastrp-intestinal diseases are very common. Heineman makes a similar statement concerning Yera Cruz. Autenrieth states that the disease is extremely frequent in JJpper Suabia and the Black Forest, and attributes this fact to the excessive ing’esEion of farinaceous articles, potatoes, and sour articles of food. Cloquet makes £ similar statement concerning Normandy, and explains it by the excessive drinking of cider. II. Anatomical Changes.—Cancer occurs more,-frequently in the' stomach than in any other organ. In the large majority of cases, it is primary. Secondary gastric cancer is remarkably rare; eight cases have been collected by Grawitz, four of which were secondary to oesophageal cancer, two to cancer of the rectum, one to cancer of the testicle, and one to cancer of the calf of the leg. Five additional cases have been since reported '({flimary site in the oesophagus, omentum, suprarenal capsules, and pelvis). One of three varieties is usually observed: a. scirrhus; b. medullary or alveolar cancer; c. colloid cancer. The most frequent form is scirrhus (this is firm, fibrous, and rela- tively dry); alveolar cancer is rarer (this is soft and juicy). The most infrequent form is colloid cancer. This is composed of a connective- tissue stroma forming cavities which are filled with yellowish or brown- ish gelatinous contents. Scirrhus presents the most protracted course; alveolar cancer is characterized by a tendency to degeneration and the formation of meta- stases; and colloid cancer is apt to spread to the peritoneum. Hard and soft cancer masses are observed not infrequently in the same case, and indeed a single cancerous nodule may present transitions from scirrhus to medullary cancer. Waldeyer applied the term carci- noma simplex to the transition stage between these two forms. If cylin- drical cells predominate in medullary cancer, it is known as cylindrical epithelioma. Very vascular growths are called fungus htematodes. Waldeyer teaches that cancer of the stomach is always of epithelial origin. It starts in a circumscribed proliferation of the principal cells of the tubular gastric glands, and these rupture through the muscular stratum of the mucosa. As soon as the proliferated cells reach the submucosa, they find a very suitable place for further growth, so that the submucosa often appears to be the starting- point of the tumor. Cancer develops most frequently at the pylorus, not infrequently in the shape of a ring. Next in order of frequency are the lesser curvature and anterior wall of the stomach, then the posterior wall, cardia, and DISEASES OF THE STOMACH. 77 greater curvature. It is observed only exceptionally at the fundus, even if almost the entire remainder of the organ is infiltrated. Cancer of the cardiac end may spread to the oesophagus, that of the pylorus to the duodenum. The cancer may form a circumscribed tumor or diffuse infiltration. In the former event, it may project into the cavity of the stomach like a fungus, sometimes with a smooth, sometimes with a villous surface (car- cinoma villosum), which is often depressed in the centre (umbilication). The surface is not infrequently ulcerated, and the deep, crater-like loss of substance has a bloody, blackish, or discolored base. This should be attributed to the digestive action of the gastric juice. Circumscribed tumors are usually single, but multiple ones are not extremely rare. Diffuse cancerous infiltration is most marked in the submucosa, and the latter is sometimes thickened three to five fold. The walls of the stomach are rigid, collapse very little or not at all, when the organ is opened, and present an unusual resistance to the knife. The surface of the mucous membrane is uneven and nodular, and is ulcerated whenever it is involved in the cancerous process. Ulceration and gangrene of can- cerous tissue hardly ever occur in cancer of the stomach, probably be- cause the gastric juice is strongly antiseptic. The cancerous proliferation may extend to the muscular coat and even beneath the serous layer. In the former, it spreads particularly within the fibrous septa, the majority of which extend vertically through the muscular coat. The lymph channels also offer a favorable road for the growth, the endothelium of the lymphatics undergoing active prolif- eration. The bundles of muscular fibres, which are surrounded by the cancer- ous septa, generally undergo hyperplasia, and their rosy color contrasts strongly with the white bands of cancerous tissue. Atrophic conditions of the muscular coat have also been observed in some cases. From the connective-tissue strands of the muscular coat the cancer- ous new-formation extends to the subserous tissue, and there often spreads farther. The part played by the lymphatic vessels is recognized from the fact that the lymph-vessels of the serous layer are filled with firm cancer masses, thickened in places and dilated into the shape of a rosary. At times circumscribed fungoid tumors form which project above the serous layer into the peritoneal cavity. In those places at which the tumor touches neighboring organs, the abdominal walls or the diaphragm, are found similar tumors which depend upon local infection. Serious danger arises from the tendency of the cancer to spread and to ulcerate. The more it extends the more the stomach loses its digestive function and inanition threatens. Marked implication of the muscular coat of the stomach interferes with the movements of the organ which are so important in digestion. The progressive ulceration causes frequent hemorrhages, which are sometimes scanty and gradual, some- times profuse. In addition, perforation may occur and be followed by peritonitis. Perforation may be prevented by preceding perito- nitis and peritonitic adhesions to adjacent organs. But this only obviates the danger temporarily. The ulceration finally extends to the adherent organs, where it not infrequently gives rise to gangrenous changes. Abnormal communications may develop between the stomach and the colon, more rarely with the small intestine, anterior abdominal wall, pleural or pericardial cavities, lungs, and air passages. Hence manifold complications, such as pneumopericardium, hydropneumoperi- 78 DISEASES OF THE STOMACH. dium, pneumothorax, hydropneumothorax, pneumonia, abscess and gan- grene of the lungs. An external gastric fistula may be preceded by emphysema of the skin. In some cases, the ulceration extends to the spine, and finally causes changes in the spinal membranes, substance of the spinal cord, and nerves. In a few cases, the stage of ulceration is followed by the formation of a cicatrix. But the destruction generally proceeds further in other places, so that the occurrence of complete recovery by cicatricial formation has not been proven. Cicatrizing can- cers with slightly prominent proliferations may be mistaken for granu- lating round ulcers. Vertical sections should then be made through the edges of the ulcers as far as the serous layer, and we should note whether cancerous proliferations can be detected in the muscular and subserous layers. Even the microscopical diagnosis may be difficult in firm can- cers which are poor in cells. We should then look for cancerous degen- eration of the epigastric glands. Hauser, who recently investigated the relations between gastric cancer and round ulcer, emphasizes the fact that at the edges of cicatrizing ulcers lively proliferation occurs into the stomach glands, and is apt to lead to cancer. Cancer not infre- quently changes the shape and position of the organ. If situated at the pylorus, the stomach is often dilated, while it is exceedingly small if located at the cardiac extremity. Changes in shape are also produced by retraction of cancerous or cicatrizing masses. The weight of the tumor occasionally pulls the stomach downwards, so that the pylorus has been found in the iliac fossa, and even in the pelvis. The remain- der of the mucous membrane of the stomach is often in a condition of chronic catarrh, and covered with ecchymoses or hemorrhagic erosions. Secondary cancer occurs not infrequently in other organs, sometimes from a direct spread of the growth, sometimes from metastasis. The latter may be produced by the agency of the lymphatic vessels and veins. Can- cer elements which have been loosened from the mother tumor enter the circulatory channels, and are carried to other organs, where they remain and incite further proliferation. The retroperitoneal glands are usually in a condition of cancerous degeneration, thence the process spreads to the glands in the thorax and even to the peripheral glands (inguinal, supra- clavicular). Cancerous growth has also been observed a number of times in the thoracic duct. Hepatic cancer or cancerous thrombosis of the portal vein occurs very often. The peritoneum, omentum, pancreas, spleen, kidney, pelvic organs, male sexual organs, pleura, lungs, bi.xin or bones may also be affected. Among other organic changes, we may mention brown atrophy of the heart muscle, fatty degeneration of the heart and kidney, waxy degeneration, lymphoid medulla of the bones, and marantic thrombosis. Phthisical changes are often found in the lungs. III. Symptoms.—The most important symptom is the demonstra- tion of gastric tumor. If we remember that in the healthy stomach the pylorus and lesser curvature are covered by the liver, and that the cardiac end is not in direct contact with the abdominal walls, it is evi- dent that, as a general thing, gastric tumors will only become evident to the hand or eye when they have reached a very large size, or the stomach has been dislocated downwards so that the parts which are usually cov- ered are in direct contact with the anterior abdominal walls. If a gas- tric tumor is evident to the eye, we generally find a round or elongated, occasionally nodular prominence, which does not move with the respira- tory movements. We must avoid mistaking the respiratory sliding of DISEASES OF THE STOMACH. 79 the abdominal walls over the tumor with a respiratory dislocation of the tumor itself. The growth sometimes changes its position with the posi- tion of the body. It is generally situated so much higher the more the stomach is filled with food, and it may even disappear beneath the liver. Prominences of less size are better seen on oblique illumination of the abdominal walls. The tumor is found most frequently in the epigas- trium, the larger portion being situated to the right of the median line; it is also seen in the umbilical region and lower down, and more rarely in the hypochondrium. On palpation we not infrequently recognize a tumor which is not visible to the eye. Sometimes we must remain satis- fied with the demonstration of increased resistance in the region of the stomach. The tumor is often uneven, nodular, and sensitive on pressure. It may sometimes be moved to a certain extent in the abdominal cavity. Sometimes it can be felt only at -times and disappears, particularly when the stomach is full. A tumor may sometimes be reached more readily in the knee-elbow position. It has often been found to increase in size during protracted observation, or sometimes to grow smaller. To demon- strate the connection of the tumor with the stomach, the latter may be distended with carbonic acid gas, according to Frerich’s method. A tea- spoonful of tartaric acid in a little water is given to the patient and then an equal amount of sodium bicarbonate. As the position of the stomach changes with its distention, the tumor will be more or less distinctly dis- located. If the patient is very greatly emaciated, pulsation of the tumor will be seen occasionally and felt even more frequently. The pulsa- tions are conveyed from the aorta and are never diffusely pulsating in character. Respiratory displacement of a gastric tumor will occur when the latter is adhe- rent to the liver or spleen, and the dislocation is conveyed from these organs, or when the tumor is very large, so that the walls of the stomach are diffusely infil- trated with cancer, and therefore cannot yield to the respiratory compression produced by the diaphragm. As a rule, percussion shows a dull tympanitic note over the tumor and the tympanitic quality is rarely absent. Auscultation of the stom- ach gives no decisive results ; but if the aorta is compressed, a systolic murmur of stenosis may be heard. The diagnosis is generally more or less doubtful if a tumor cannot be demonstrated. Hemorrhage from the stomach is practically important in diagnosis. The vomiting of dark, clotted blood is more rare than in gastric ulcer. In the majority of cases smaller hemorrhages occur, the blood remains for some time in the stomach and is changed by the gastric juice, and coffee grounds, choco- late, or inky masses are vomited. Under the microscope these are found to consist of constituents of the food and discolored, more or less changed red blood-globules. (Vide Vol. II., fig. 9.) This form of vomiting occurs not only in cancer of the stomach; it also takes place, though much more rarely, in gastric ulcers. In suspicious cases, the stools should be carefully examined, since vomiting may be absent in slight hemorrhages, and the blood passes through the intestines. In other cases, the hemorrhage is so profuse that death is the immediate result. Vomiting of mucoid, biliary matter or of articles of food occurs very often, and is especially significant of cancer when advanced age, increasing emaciation, cachexia, and cancerous degeneration of peripheral glands, especially the left clavicular glands, are associated with one another. According to Bamberger, sarcina ventriculi occurs more frequently in the vomited matter than in other diseases of the stomach. Obstinate vomiting sometimes ceases suddenly. This 80 DISEASES OF THE STOMACn. occurs in pyloric cancer when the increasing destruction of the tumor ren- ders free an existing narrowing, or when the stomach is diffusely degenerated and no longer produces vigorous muscular contractions. Sometimes this is a symptom of exhaustion. Riegel, who found that free hydrochloric acid was very generally absent in the gastric juice in cancer, recently observed that the cancer proliferation can give rise to rapid disappearance of hydrochloric acid when present. Wolff and Quetsch agree that the absorption of potassium iodide is delayed. Methyl violet is the most practical test of the presence of free hydro- chloric acid in the gastric juice or contents. If to a solution of 0.05 : 200 a fluid is added which contains minimum amounts of hydrochloric acid, the violet color is changed to a dark blue at the point of contact of the fluids. Other free acids give a similar, though not so decided reaction, so that a negative result alone proves the absence of hydrochloric acid. To study the absorption, 0.2 of potas- sium iodide in a gelatin capsule should be given to the patient and the saliva examined for iodine every five to ten minutes. A piece of starch paper moist- ened with saliva is touched with a trace of pure nitric acid, and the presence of iodine is shown by the yellowish-red color of the paper. The statements with re- gard to the normal rapidity of absorption differ very widely. Among the other symptoms of cancer, the signs of marasmus and dis- turbed digestion are the most important. The patients often attract our attention by rapid emaciation, a sallow or greenish complexion, loss of strength, and oedema of the ankles. The skin is usually lean, thin, ex- tremely dry, desquamating, and itching. Indeed, violent pruritus in cachectic individuals points to latent cancer, if albumin and sugar are not present in the urine. If local changes are absent, the history may be very similar to that of progressive pernicious anaemia, especially as the blood is often very pale, almost serous, and poor in red blood-globules. The latter may be irregular and unequal in size (poikilocytosis). The majority of patients complain of loss of appetite, rarely the desire for food is unchanged, or boulimia is present (especially in stenosing can- cers of the cardiac portion). Increased thirst has been observed a number of times. The weight of the body diminishes constantly, but in rare exceptions a temporary increase of weight is observed. Elevation of bodily temperature occurs at times, probably as the result of septic fever from absorption of degenerating masses of cancer. The patients often suffer from obstinate insomnia. Many are tortured by boring, burning pain in the stomach. It is almost constant, increases after meals, and sometimes becomes excessive at night. The pain may radiate into adjacent nerve tracts and give rise to asthmatic and stenocardiac dis- turbances. The epigastrium is sensitive on pressure, sometimes over a localized spot corresponding to the tumor. As a general thing, however, the pains are not so violent as in round ulcers. The tongue sometimes has a grayish-white or brownish coating, some- times is very red, clean, fissured, the latter especially when very sour masses are vomited. Increased secretion of saliva has also been ob- served. Ebstein noticed spasm of the pharynx, which interfered with deglutition and appeared to be reflex. Frerichs noticed eructation of inflammable gases. At first the bowels are almost always constipated. Later obstinate diarrhoea sometimes occurs and has been attributed to intestinal catarrh resulting from decomposition of the food by ulcerated portions of the cancer. Dysenteric symptoms (tenesmus, bloody and purulent stools) are observed occasionally. The urine is generally scanty, high-colored, and occasionally contains a very large amount of indican. The color becomes a reddish-blue or deep blue, if a test tube is half filled with urine, the other half with pure hydrochloric acid, and one to three drops of a fresh concentrated solution of chloride of lime are cautiously added. Jaksch DISEASES OF THE STOMAOH. 81 observed acetone in a few eases (Burgundy color of the urine on the addition of a very dilute solution of chloride of iron). Maixner found peptone in the urine in a number of cases. Special symptoms develop not infrequently when the cancer narrows the pyloric or cardiac orifices. In the former event, the signs of dila- tation of the stomach gradually develop. But if the cancer destroys the pyloric muscle in places and thus makes it incapable of function, the symptoms of incontinence of the pylorus may be produced. Cancer of the cardiac orifice occasionally gives rise to symptoms of stenosis of the oesophagus. The patients cannot swallow the food, and after a while it regurgitates in a macerated condition. On auscultation of the oesophagus, the murmur of deglutition diminishes or ceases at the level of the eleventh dorsal vertebra. The introduction of the oesophageal sound meets with an obstruction at the same locality, and particles of cancer occasionally remain in the fenestra of the sound. (Vide Yol. II., Fig. 7.) The patients emaciate with extreme rapidity, and generally complain of a feeling of hunger. The duration of gastric cancer is determined with difficulty, because the duration of the latent stage is unknown. In some cases death is said to have oc- curred at the end of the first month, in others not until the third year. A year may be regarded as the average duration. In many cases death follows with the signs of increasing marasmus. The patients waste away to a skeleton, and become more apathetic with each succeeding day.. (Edema of the subcutaneous tissue and serous cavities often occurs and finally death ensues. Slight albuminuria or marantic thrombosis of a lower extremity is observed in some cases. Inanition delirium may pre- cede death. In some cases death is the result of intercurrent diseases, such as pneumonia. Sometimes it occurs unexpectedly as the result of complications, for example, profuse hemorrhage, perforation-peritonitis, or rupture into other organs; but fistulse may be tolerated for a long time. This includes stomach-colon fistula, the chief characteristics of which have been considered in the description of the round gastric ulcer. Williams reports a case in which perforation of the stomach, occurring upon sitting up, was accompanied by a slight noise. Sometimes the symptoms of secondary cancer in other organs, especially the liver, predominate to such an extent that the primary gastric cancer is over- looked. IY. Diagnosis.—The diagnosis is not easy, and we often find nothing during life, although the autopsy reveals a cancerous tumor of able size in the stomach. If a tumor is visible or palpable during life, it should be remembered, in differentiating it from tumors of the liver and spleen, that it does not move on respiration, apart from the exceptions mentioned on page 79. We must also avoid mistaking it for coprosta- sis, intestinal tumors, tumors of the omentum and pancreas, diseases of the lymphatic glands, tumors of the uterus and ovaries, aneurisms of the aorta and coeliac axis, or encapsulated peritonitic exudations. Apart from other symptoms, we must lay special stress upon the fact that gastric tumors change their position more or less with the disten- tion of the stomach. But not every tumor of the stomach is cancerous, and hypertrophy of the muscular coat, cicatrices following round ulcer, or foreign bodies may be mistaken for it. Advanced age and very marked cachexia testify in favor of cancer, and these factors are also im portant in the differential diagnosis from ulcer, cardialgia, and chronic gastritis. Cancerous tumors of the lymphatic glands above the left 82 DISEASES OF THE STOMACH. clavicle, although they are by no means constantly present, are very im- portant in diagnosis. But these should not be mistaken for tubercular glands, and it must be remembered that the swelling affects only the glands on the left side, that is, those which are adjacent to the point of entrance of the thoracic duct. These cancerous glands are also very important from a diagnostic standpoint, in cases of general marasmus whose origin we must investi- gate. The demonstration of dilatation of the stomach or incontinence of the pylorus may also be important, provided that other causes for these conditions may be excluded. The condition is suspicious when the patients suffer from pruritus of the skin and when free hydrochloric acid cannot be found in the gastric juice or contents, and when absorp- tion can be shown to be slower than normal. V. Prognosis. —The prognosis is bad. Permanent recovery is hardly possible, even when the tumor is removed by operation. VI. Treatment.—The use of condurango is said to have produced recovery. Although this drug will not cure cancer, it is, nevertheless, an excellent stomachic which often increases the appetite, stops the vomiting, and diminishes the pain. The following prescription may be given. B Corticis condurango, . . . . § ss. Macera horas xii. c. aq., . . § xij. Dein coq. ad remanent col., ... 3 vi. D. S. One tablespoonful two to three times a day. In addition we should order light, nutritious food, according to the principles laid down on page 63, improve digestion by the adminis- tration of hydrochloric acid and, if stenosis of the cardiac extremity is present, maintain life by nutritive enemata (vide Vol. II., page 33). In addition, symptomatic treatment must be adopted (narcotics against pain, etc.). Billroth has recently resected the cancerous stomach. Among seven of his cases three died, while Czerny had two deaths in four operations. The patient to be operated on should still be in pos- session of a certain amount of vigor, the cancerous degeneration should not be too extensive and, if possible, adhesion to adjacent organs and metastases should be absent. The success of the operation depends in great part upon the period at which it is performed. According to Czerny, thirty-six operations had been performed up to the beginning of 1884, among which twenty-seven ended fatally; eighteen of these died within the first twenty-four hours after the operation, so that this was probably performed too late, but it is probable that recovery will be tem- porary even in the most favorable cases. Appendix. The other neoplasms of the stomach hardly possess more than an anatomical interest, not that they are destitute of symptoms, but on the demonstration of a tumor, we will always be led to diagnose a gastric can- cer. We may make brief mention of the following tumors: a. Gastric polypi are usually the result of chronic gastritis. They may be single or multiple, of very unequal size, and are sometimes the product of a proliferation of the mucous membrane, sometimes of that of the submucous tissue. In one case Cruveilhier observed stenosis of the pylorus by a polypus. DISEASES OF THE STOMACH. 83 b. Sarcoma. Myosarcoma has been found a number of times, and in one case smooth muscular fibres were found in the secondary sarcoma nodules of the liver. Papilloma, myoma, adenoma, cysts, teleangiectesia, lymphangioma, lipoma, and gumma, have also been described. 1. Dilatation of the Stomach. (Gastroectasia. Dilatatio ventriculi.) I. Etiology.—The conditions necessary to dilatation of the stom- ach are always furnished when the forces necessary to propel the gastric contents are insufficient. Such conditions may develop either because unusual obstacles are situated at the pylorus or because the muscular coat of the stomach is paralyzed, or finally because the amount of ingesta is unusually large. As a matter of course, some of these factors have only a temporary effect, so that we may differentiate an acute and chronic dilatation of the stomach. For example, an unusually heavy meal may produce an acute dilatation. Chronic conditions of gastric dilata- tion have a special clinical interest, and the following remarks will refer chiefly to them. Stenosis at the pylorus is the most frequent and im- portant of all the causes. It may affect either the pylorus directly, or the first part of the duodenum. The most frequent lesion is a cicatrix at the pyloric ring, usually the result of a preceding ulcer, more rarely of poisoning by caustics, finally of cancerous degenera- tion. But benign hypertrophy of the pylorus, such as occurs in chronic gastritis, or when polypi have entered the pylorus, may also give rise to stenosis. In some cases cicatrices or tumors are situated in the first part of the small intestine, but produce the same effect as pure stenosis of the pylorus. Tumors of the adjacent organs may also compress and narrow the pylorus or duodenum. Bartels and Mueller-Warneck first called attention to the association of dilata- tion of the stomach with floating kidney (right side). Two cases of this kind have recently come under my observation. Landerer recently called attention to the not infrequent occurrence of congenital stenosis of the pylorus which is followed by dilatation of the stomach. Sometimes twists occur at the pylorus or duodenum and are followed by gastroectasia. In one case Kussmaul observed that on the filling of the stomach the cancerous pylorus, with the remainder of the stomach, turned around the long axis of the organ, at the same time pushed from before backwards, against the entrance to the small intes- tine and occluded it like a valve. In other cases the twist occurs be- tween the first horizontal and vertical sections of the duodenum. Dilatation of the stomach also occurs not infrequently from disease of the muscular coat, either as the result of local or general causes. Among the local causes is chronic gastritis; the same effect is also produced by destruction of the muscular coat by extensive ulcers or cancerous infiltration, especially if the points of insertion of the circular muscular bundles are destroyed. Traube showed that in many cases of ulcer the gastric branches of the vagus are destroyed, thus giving rise to a diminution in the tonus of the organ. The muscular power of the stomach is occasionally interfered with by peritonitic adhesions to the anterior abdominal walls or adjacent organs, or because the organ is pulled upon by the transverse colon which has entered a hernia. Gastric dilatation has also been observed as the result of injury in the region of the stomach. Among the general causes which may weaken the muscular coat of the stomach we may mention chlorosis, anaemia, phthisis, typhoid fever, pyaemia, diseases of the brain and spinal cord, hysteria, and hypochondria (atonic gastroectasia.) 84 DISEASES OF THE STOMACH. It should also be mentioned that the stomach sometimes assumes a vertical position, either as a congenital condition or as the result of tight corseting or of tumors in the abdominal cavity. This condition also predisposes to gastric dilatation, especially of the pyloric portion, be- cause the propulsion of the gastric contents is impeded. It may also develop when the abdominal walls are very flaccid and the recti abdo- minis are separated from one another. Finally dilatation of the stomach develops when an excessive demand is made upon its energy. It is remarkably frequent in heavy feeders, and also in countrymen who live on a chiefly vegetable diet. It is often observed in diabetics and in them is attributed to the excessive in- gestion of food and drink. The ingestion of indigestible articles also gives rise to gastroectasia. Neuwark reports a case in which in a girl, set. 23 years, the signs of acute stenosis of the pylorus developed after eating cherries. Dilatation of thq stomach occurred later, and at the autopsy, three months afterwards, ten cherry pits were found in the stomach. Dilatation of the stomach is not a very rare disease. It is not so in- frequent even in childhood. According to Comby it is relatively com- mon in rachitic children. It develops most frequently from the fortieth to the fiftieth years, and is more frequent in males than in females. II. Anatomical Changes.—Dilatation of the stomach may attain a. remarkable size. Cases are known in which, upon opening the abdomen, very little but the stomach was visible and the greater curvature ex- tended into the pelvis. In Jadon’s case the cavity of the organ is said to have contained ninety pounds of fluid. The spleen and liver are usually found pushed upwards, the small intestines downwards and to the sides, the heart is also pushed upwards; atrophic changes are occa- sionally noticed in the displaced organs. If the dilatation is in the first stages of development, it is found, as a rule, to be most marked at the fundus. Circumscribed and diverticulum-like sacculations of the stomach are observed very rarely, and are generally produced by foreign bodies or peritoneal adhesions. If the dilatation is the result of pyloric or duodenal stenosis, the oesophagus sometimes takes part in the dilata- tion. The mucous membrane of the dilated organ is generally in a condition of chronic catarrh. The muscular coat is sometimes thick- ened three or four fold, sometimes thin and atrophic, sometimes thick- ened and thinned in places. As a matter of course, the condition of the muscular coat depends upon the causes of the disease. Thickening, to a certain extent of a compensatory character, is to be expected in stenosis of the pylorus, while atrophic conditions are apt to develop in direct affections of the muscular coat, especially in conditions of general weak- ness. Fatty and colloid degeneration of the muscular fibres are often, though not constantly, found on microscopical examination. III. Symptoms.—Two groups of symptoms must be sharply differen- tiated from each other, viz., the chemical and physical changes. The former are the result of the stasis of the gastric contents and of abnormal fermentation, and even gangrenous decomposition, while the physical changes depend entirely on the increased size of the organ. As a rule, medical aid is sought on account of the chemical changes. In the beginning, the disturbances of gastric digestion are so slight that the condition is apt to be regarded as catarrh of the stomach. As the disease progresses, disturbances of nutrition are not long delayed. The patients emaciate, the complexion grows pale, the skin thin and dry,. DISEASES OF THE STOMACH. 85 +he muscles become soft, and sometimes the bones appear under the skin ike those of a skeleton. The face usually has an ashen and wrinkled appearance. The appetite is diminished in many cases, in others boulimia is present. The latter is especially true when the dilatation is the result of marked stenosis of the pylorus, so that very little food passes into the duodenum, while the chief mass of food remains in the stomach and is vomited from time to time. Furthermore, Fader and Penzoldt have shown that absorption is rendered slower in the dilated stomach. Thirst is often increased because fluid is absorbed with difficulty, and very often little passes into the intestines. Many patients complain of eructa- tions. heart-burn, and pyrosis. Sometimes odorless gases are eruc- tated. sometimes they have the foul odor of sulphuretted hydrogen, even a gangrenous odor has been noticed. Eructation of inflammable gases has been described in a number of cases. In Frerichs’ case the patient noticed that, upon eructating while lighting a cigar, the gas caught fire so that his moustache was burned. In a case reported by Friedreich, in which the flame was occasionally one-third meter in length, marsh gas was found in the eructated gases. The chief constituents are oxygen and nitrogen in the same proportions as in atmospheric air (probably swallowed air), hydrogen and carbonic acid (from fermentation of carbo- hydrates), in a few cases marsh gas, and in one case an oil-producing gas. The following are the results of the chemical analysis of the gases: Frerichs. Popoff. Schultze. Carbonic acid, . 20.57 per cent. 12.82 per cent. 26.56 per cent. Hydrogen, 20.57 << 32.32 32.30 Marsh gas, . . 10.75 U 0.34 Oil-producing gas, . 0.20 a Oxygen, . 6.52 u 7.9 0.36 Nitrogen, 41.38 u 46.5 33.44 “ Vomiting is an almost constant symptom. It is especially early and profuse when the disease is caused by stenosis of the pylorus. If the stomach gradually increases in size, the vomiting again becomes more infrequent and often occurs only at intervals, perhaps every three or four days. Astonishing amounts are sometimes vomited, in some cases as much as sixteen pounds at one time. The vomited matters almost always have a strongly acid reaction. Many patients complain that the teeth feel extremely blunt after the vomiting, and a rapidly progressing affection of the teeth is often notice- able. The smell of the vomited matters is often intensely sour; in other cases, rancid and sweetish. In rare cases the odor is gangrenous. This occurs, it appears, with relative frequency in carcinoma. The reaction should always be tested with litmus paper, because a sour smell is not positive evidence of an acid reaction. The vomited matter is sometimes fluid, sometimes like porridge, depending chiefly upon the character of the food. This is also true of its color. If the dilatation is due to cancerous degeneration, the vomited matters may be colored like choco- late, coffee grounds, or ink. It usually separates very quickly into three layers; the uppermost consisting chiefly of frothy masses, the middle one of fluid, and the lowermost of a crumbly sediment. If kept for a few hours, it often continues to ferment. Lactic, butyric, and acetic acids have been repeatedly demonstrated in 86 DISEASES OF TIIE STOMACH. the vomited matter; peptone, undigested albumen, starch, and sugar have also been found. On microscopical examination, we find more or less changed debris of food, sarcina ventriculi, yeast cells, and schizomycetes (vide Fig. 10). In two cases Naunyn found mould fungi. Vomiting often occurs with extreme facility. As the disease ap- proaches a fatal termination, it may cease completely. A very note- worthy feature is the unusually long stay of food in the stomach. In washing out the healthy stomach, in a fasting condition early in the day, the fluid flows out clear, while the dilated stomach always contains more or less considerable remains of the food taken on the preceding day. Faver and Penzoldt showed that absorption in the stomach is delayed in gastroectasia. Fig. 10. Sarcina ventriculi (sc) from the vomited matters in gastric dilatation following a stenosing pyloric cicatrix after round ulcer. On the right a few yeast cells (hf). At the edges three swollen vegetable cells from the food. Enlarged 275 diameters. Frequent and profuse vomiting exercises a great effect upon the stools and the urine. The bowels are usually constipated, the patient often going from one to two weeks without an evacuation. The urine is often alkaline. This reaction is explained by the fact that the blood becomes poor in acids on account of the profuse and very acid vomiting. Ebstein, Stein, and Scherf showed that the alkaline reaction of the urine results in the formation of unusual sediments (triple phosphates and crystals of phos- phate of magnesia, vide Fig. 11.) If a twenty-per-cent solution of ammonium carbonate is added to the latter, the ci'ystals undergo disintegration at once. If triple phosphates or phosphate of lime are also present in the sediment, the reagent produces no change in the former, while the phosphate of lime is grad- ually destroyed after a long time. DISEASES OF THE STOMACH. 87 The profuse vomiting also diminishes the amount of urine, and many cases have been observed in which the daily amount fell to 400-300 Fig. 11. Crystals of phosphate of magnesia from the alkaline urine in dilatation of the stomach. After Ebstein and Scherf. ccm. As a matter of course, its chemical constitution changes. Scherf obtained the following results in two cases : Daily amount in ccm. Specific grav- ity. Daily amount of urea ia gms. Daily amount of chlorides in gms. Daily amount of phosphoric acid in gms. Case 1. Average 1030 1022 14.8 8.11 1.19 Maximum 2220 1027 22.7 14.3 1.69 Minimum 500 1013 8.5 3.0 0.75 Case 2. Average 1350 1018 22.7 11.9 1.16 Maximum 2200 1025 35,0 16.6 1.48 Minimum 600 1012 17.1 8.5 0.54 There are not a few subjective symptoms in this disease. The pa- tients are particularly annoyed by emesis, heartburn, a feeling of fulness 88 and pressure in the stomach, and increasing loss of strength. Attacks of dyspnoea and palpitation may occur if the development of gas in the stomach is very considerable and interferes with the mobility of the dia- phragm. But these symptoms merely result from abnormal fermentation of the gastric contents, and the demonstration of dilatation of the stomach can only be determined by physical examination. On inspection, we notice not infrequently an unusual prominence of the gastric region. In advanced cases, this extends below the umbilicus. The greater curvature of the stomach can often be followed with the eye, and occasionally the lesser curvature is also visible at a little distance be- low the ensiform cartilage. As a matter of course, the entire organ is situated abnormally low in such cases, since under normal conditions the lesser curvature lies behind the liver. The peristaltic movements of the stomach may be very active, partic- ularly when the gastric dilatation is the result of pyloric stenosis. The waves of contraction generally run from the cardiac to the pyloric ex- tremities, rarely in the opposite direction. Bamberger reported a case in which a deep constriction formed at about the middle of the stomach, whence the peristaltic contractions travelled in both directions. These movements may often be provoked by pinching or faradization of the abdominal walls, or douching with cold water. The occurrence of these contractions below the umbilicus is especially important in the diagnosis of gastroectasia, because the greater curvature of the healthy stomach is generally situated above the navel. Kussmaul states that unusually active peristalsis of the stomach may give rise to a disagreeable feeling of movement in the abdomen (peristaltic restlessness of the stomach). The waves of contraction require about a minute to travel from the cardiac to the pyloric extremity. They are particularly apt to occur in cica- tricial stenosis of the pylorus or first part of the duodenum. Palpation reveals a peculiar feeling of resistance which is recognized on short, quick strokes of palpation. A sensation is felt as if we were touching a distended air bag. If palpation, or rather immediate percus- sion, is carried out from above downwards, we can often recognize the lower border of the stomach with great distinctness. If the peculiar feeling of resistance extends below the umbilicus, the diagnosis of gastric dilatation can usually be made with certainty. If the stomach contains gas and fluid, as is generally the case, vigor- ous shaking movements will give rise to very loud splashing sounds. These are sometimes heard throughout the entire room. These sounds may also be heard in the healthy stomach when the lat- ter contains gas and fluid. In gastroectasia, however, the sounds are unusually frequent and loud. The splashing sounds can sometimes be felt as fluctuation. If the patient sits up, the fluid in the stomach will accumulate in the greater curvature, and the lower border of the organ can sometimes be deter- mined by the feeling of fluctuation. If fluctuation is recognizable below the umbilicus, the diagnosis of dilatation of the stomach may be made. Examination with the oesophageal sound may furnish extremely important results (vide p. 30). Leube showed that the sound, when introduced into the dead body, may push that portion of the wall of the stomach which is situated opposite the cardiac extremity to a line con- necting the anterior superior spinous processes of the ilea. In individuals DISEASES OF THE STOMACH. DISEASES OF THE STOMACH. 89 with thin abdominal walls, the tip of the sound may be felt from the outside during life, indeed, in combined examination from the abdominal walls and rectum, the sound may sometimes be felt between the examining fingers. Leube concludes, therefore, that dilatation of the stomach may be diagnosed if the tip of the sound can be felt below the above-men- tioned horizontal line. But this mode of examination is not devoid of danger, particularly if recent ulcers are situated on the gastric mucous membrane. Penzoldt employs another method of examination. He found that in the healthy individual the sound maybe introduced about 60 centimetres before meeting with the resistance of the wall of the stomach which is situated opposite the cardiac extremity. In three cases of gastric dila- tation this distance amounted to 70 centimetres. Purgecz fastened a manometer to the posterior extremity of the oesophageal sound. So long as the sound remained in the oesophagus, the manometer showed negative pressure, but this became positive as soon as it entered the cavity of the stomach. From this point Purgecz could advance the sound (in healthy individuals) from 27 to 30 centi- metres before meeting with the resistance of the lower border of the stomach. In gastroectasia this distance was considerably greater. Oser calls attention to the fact that in both these methods of exam- ination the sound may perhaps glide along the greater curvature to the pylorus, where it first causes a feeling of resistance, i. e., a stomach appears to be dilated, although in reality it possesses normal dimensions. The symptoms obtained on percussion are extremely important in diagnosis. Percussion of the dilated stomach almost always gives a deep, tympanitic sound, which not infrequently possesses a metallic quality. If the stomach contains fluid, a dull percussion sound will be heard over the corresponding region, and this will vary with the position of the body. If the stomach contains but little fluid, it may accumulate, in dorsal decubitus, along the posterior wall, while in the vertical position it is situated along the greater curvature. Hence the entire gastric region will give a tympanitic sound during dorsal decubitus, but in the erect position a strip of dulness makes its appearance, corresponding to the greater curvature. Gastroectasia is present if this strip of dulness is situated below the umbilicus. If dulness has been detected in the region of the greater curvature, and the fluid contained in the organ is then removed by means of the stomach-pump, the previously dull region will become tympanitic. It has been shown that if one litre of fluid is drunk in a fasting con- dition, a strip of dulness as broad as a finger will make its appearance along the greater curvature of the stomach, while the patient is in an erect position. In healthy individuals this area of dulness is situated above the umbilicus. Frenchs* method, which we described above, is the most rapid and certain for percussing the distended stomach. This makes the contours of the stomach more distinct, so that they are appreciable to the hand, the eye, and the percussion hammer with great facility. Mannkopf and Wagner showed that the lower curvature of the healthy stomach never lies beneath the umbilicus, and dilatation of tho stomach is thus readily recognized. (Vide Fig. 12.) In percussion of the stomach when dis- tended with carbonic acid, we should not be satisfied with determining a .single point of the lower border of the organ, because dilatation can only be diagnosed if, in addition to abnormal depression of the lower 90 DISEASES OF THE STOMACH. border, the lateral boundaries of the percussion figure of the stomach extend at least to the normal borders, that is, on the left side to the anterior axillary line, on the right to the parasternal line. If the lateral borders approach closer to one another, the depression of the lower bor- der of the stomach must be attributed to congenital or acquired vertical position of the non-dilated organ. Distention of the stomach sometimes remains absent after the devel- opment of carbonic acid gas, and acute intestinal tympanites develops in its stead. This is an evidence of incontinence of the pylorus. Recently, in employing this method, I have not been satisfied with percussion alone, but have also resorted to auscultation. Auscultation of the stomach shows an extremely fine crackling, which results from a development of fine bubbles of carbonic acid. This ceases abruptly at Fig. 12. The percussion boundary of the dilated stomach (which has been distended with carbonic acid), in a woman set. 37 years. the boundary of the greater curvature of the stomach. Bamberger aus- cultated the stomach during drinking. This produces 1he impression as if a drop of water is dropping into a large empty cavity. It is said that this falling of drops cannot be heard beyond the greater curvature. In some cases a crackling murmur in the region of the stomach can be heard without previous artificial distention with carbonic acid, but in my experience the former is coarser than the murmur described above, and is owing to the development of gas produced by fermentation of the gastric contents. Sometimes it is difficult to demonstrate gastroectasia despite all the methods mentioned. It is difficult, particularly, to distinguish the lower DISEASES OF THE STOMACH. 91 border of the stomach from the transverse colon. Under such circum- stances we may inject fluid or air into the transverse colon through the rectum. The injection of water is best effected by means of a funnel and rubber tube, through which water is allowed to flow into the intes- tine. To inject air we may employ a flexible tube, which is connected with the balloon of the Richardson ether spray apparatus. Naunyn recently emphasizes the fact that microscopical examination of the vomited matter or of the contents of the stomach which have been removed by the stomach-pump is important in diagnosis, because yeast fungus and schiozomycetes indicate abnormal fermentation of the gastric contents, and this occurs with greatest frequency in gastroectasia. The dilated stomach may displace adjacent organs. The apex beat Fig. 13. Stomach pump. of the heart is often found in the fourth intercostal space. The move- ments of the heart are sometimes extremely distinct, because the organ is pressed forcibly against the anterior chest-walls. Metallic resonance of the heart-sounds in the dilated cavity of the stomach is observed occasionally, and this may increase the intensity of the sounds to such an extent that they may be heard at some distance from the patient. Thmore the heart is pushed upwards the larger Trauhe’s semilunar space oecomes. The liver and spleen are also often pushed upwards. The disease is almost always chronic. If it is incurable on account of the primary affection, the strength of the patient diminishes more and more, cedema develops, and the patient finally dies with symptoms of inanition and marasmus. Bamberger observed a sort of spontaneous 92 recovery in pyloric stenosis, inasmuch as unchanged portions of the pylorus yielded and thus eliminated the constricting action of the cica- tricial tissue. IV. Diagnosis.—The recognition of dilatation of the stomach will generally present no special difficulties when the methods of examination described above are properly employed. But the diagnosis is only com- plete when the cause of the dilatation is recognized. For this purpose the clinical history must be relied upon. V. Prognosis.—This is is unfavorable in many cases, because we are unable to relieve the primary affection. This is especially true of many cases which are the result of pyloric stenosis, hut the tendency to relapse is also marked under other conditions, and we must therefore be very cautious in giving a favorable prognosis. VI. Treatment.—The object of local treatment is to relieve the stomach of its excessive and decomposing contents, and thus to prevent further fermentation of the food. The removal of the gastric contents is best effected by means of a stomach pump or stomach siphon. The stomach pump (vide Fig. 13) is an aspiration syringe, which possesses two outlets at its anterior extremity. By means of a valvular arrangement at the side of the syringe, it is possible, when the valve is untouched, to have only one opening in communication with the interior of the syringe, so that when this is con- nected with a sound which is introduced into the stomach, and the pis- ton of the syringe is withdrawn, the contents of the stomach will be sucked into the interior of the syringe. After the syringe is filled, the valvular apparatus is pressed downwards. The opening which connects with the stomacli-tube is thus closed, while the other, previously closed opening now communicates with the cavity of the syringe. If the piston is now driven home, the contents of the syringe can be expelled. This procedure may be repeated until the stomach is empty. Force must be avoided, since otherwise pieces of the mucous mem- brane of the stomach may be aspirated and torn off. This accident hitherto has been unattended with any special danger. This danger is lessened by the employment of the stomach siphon. The following is the simplest arrangement of this apparatus: A rubber tube, one metre in length, is fastened to an oesophageal sound (this should be made of soft rubber) by means of a glass tube, about fifteen cm. in length (vide Fig. 14). The free end of the tube is now provided with a glass funnel. The sound is introduced into the stomach and fluid is poured into the funnel. Before all of the fluid has escaped from the funnel, the tube is firmly pressed between the thumb and index ■finger, and the funnel is bent downwards and placed in a vessel. The fluid which has been poured in and the contents of the stomach will now escape spontaneously. If the fenestra of the sound is choked up by un- dissolved fragments of food, the patient should be allowed cautiously to cough or to bear dowm, or the region of the stomach may be compressed. Sudden and repeated compression of the rubber tube is often sufficient to remove the obstacle. If this does not prove successful, wrater should again be poured into the funnel, and the entire procedure be repeated. When the contents of the stomach have the consistence of a thick por- ridge. it is best to dilute them by large amounts of water. But we should carefully measure the quantity removed in order to prevent over- loading of the stomach. The first manipulations with the instrument are apt to be attended with difficulty, because they produce nausea and diseases of the stomach. 93 perhaps attacks of dyspnoea and palpitation of the part. The operation is best performed in the morning in a fasting condition, the water being at a temperature of 30°. After the stomach is empty, it should be washed with a solution of Carlsbad salts (one teaspoonful of the salt to one litre of water at 30° R.), until the outflowing water is alkaline. We may then inject to advantage anti-fermentative remedies, such as resorcin (one per cent), natrium salicylicum (one per cent), creasote, benzol, carbolic acid, permanganate of potash. The patient should take no food for several hours after the operation. It should be repeated daily, and the intervals should be increased only after the symptoms of fermentation of the food have disappeared. Double sounds have been employed by some writers, but in our opinion they are unnecessary. Some physicians make use of an ordinary rubber tube. As a rule, the patients feel marked relief after artificial emptying of the stomach. In others, dizziness, ringing in the ears, twitching in in- DISEASES OF THE STOMACH. Fig. 14. Stomach siphon of soft rubber. dividual muscles, and even extensive muscular spasms have been pro- duced; but these symptoms usually possess no serious significance. One case, however, has been reported in which the patient employed this method himself in an irrational manner, and died in an attack of tetany. After the stomach is emptied, the patient is allowed to rest for several hours, during which an ice-bag is applied to the region of the stomach. I have often obtained very good results from subcutaneous injections of ergotinum Bombelon or strychnine (gr. iss. : 3 iij., 2 to 3 minims), faradi- zation of the stomach—measures which should be employed immediately after the stomach is empty. The patient should wear a tight abdominal bandage while walking about. The faradic current should be employed by placing one electrode on the left hypochondrium, while the other is slowly passed over the region 94 DISEASES OF THE STOMACH. of the stomach from the cardiac to the pyloric extremity; strong current, moist electrodes; duration of the sitting, five minutes. Scanty meals should be frequently taken, perhaps every two hours. Fluids, carbohydrates, and fats should be avoided as much as possible, the diet consisting chiefly of animal food (vide Vol. II., page 63). Milk, and milk mixed with pieces of ice, are especially indicated when the vomiting is very violent, but small quantities only should be taken at one time. Digestion may be improved by giving a few drops of hydrochloric acid (five drops to a wineglassful of lukewarm water) half an hour after the principal meal. Two or three hours later we may give resorcin (gr. v.). or carbolic acid (gr. xxx., pulv. althseae, q. s. ut f. pil. No. 25. D. S. 1 pill t. i. d.). As a rule, favorable effects soon follow the local treatment of dilatation of the stomach; the patients become more cheerful, their appearance improves, and the weight of the body increases. Vomiting, pyrosis, and eructations disappear; the urine becomes more abundant and acid; evacuations from the bowels are more frequent, and the boun- daries of the stomach approach the normal. General treatment must also be adopted. We must pay especial attention to anaemic and nervous conditions (preparations of iron, nervines, cold-water treatment, sea-bathing, etc.). As a rule, treatment must be continued for a long time. Indeed, if stenosis of the pylorus is present, it must be continued for life. The patients soon learn to introduce the stomach tube, and to empty and wash out the stomach without the aid of the physician. This may be done two or three times a week, but should be intrusted only to intelli- gent patients. Eesection of the pylorus (pylorectomy) has been performed a number of times with success. Loreta attempted dilatation of the pylorus in two men suffering from cicatricial stenosis, the stomach being laid free, and both index fingers being introduced into the pylorus through the exter- nal wall of the stomach. 9. Incontinence of the Pylorus. 1. This condition is recognized by the fact that the stomach can be distended only temporarily or not at all by Frerichs’ method. In its stead we notice acute tympanites of the intestines, because the gas rapidly passes through the open pylorus. The entire abdominal walls become distended within a few minutes, and the ascending and descending colon are especially apt to project as prominences which are as thick as a man’s arm. 2. It is produced by interference with the muscular layer of the pyloric ring, either of an anatomical or purely functional character. The former may be produced by round ulcer, or cancerous infiltration and ulceration. The latter is generally produced by cerebral or peripheral disturbances of innervation. The latter category probably includes attacks of acute tympanites iri hysterical individuals. Ebstein also found incontinence of the pylorus in a woman suffering from softening of the spinal cord, while the walls of the stomach were anatomically in- tact. I have repeatedly observed transitory incontinence of the pylorus. It occurred in individuals suffering from acute or chronic gastritis, with violent exacerbations, and the incontinence disappeared as soon as the gastric affection was relieved. Perhaps it resulted from paralysis of the DISEASES OF THE STOMACH. 95 muscular fibres of the pylorus in consequence of inflammatory, serous in- filtration. According to Kussmaul, the signs of incontinence of the pylorus are presented by healthy individuals who are in a fasting con- dition. 3. Incontinence of the pylorus may produce injurious effects. The very acid contents of the stomach may give rise to diarrhoea by the un- usual irritation of the intestinal mucous membrane. On the other hand, the occurrence of the incontinence may improve or entirely relieve previous vomiting. Stenosis and incontinence of the pylorus may exist side by side. If the pyloric ring is converted by cancer into a narrow rigid fissure, which is incapable of contraction, the conditions are furnished both for stenosis and incontinence. 4. The treatment must be directed against the primary affection. 10. Degenerative Changes in the Stomach. Degenerative changes in the walls of the stomach hardly possess more than an anatomical interest; fatty degeneration (especially after phos- phorus poisoning and anaemic conditions), calcification (in carious and other processes associated with the destruction of bone) and waxy de- generation have been described. Occlusion of the blood-vessels by waxy degeneration may cause ulceration of the mucous membrane. In several cases of waxy degeneration, Edinger was unable to detect free hydrochloric acid in the gastric juice. It is therefore possible to reeognize this change, if, under conditions in which waxy degeneration is apt to develop, free hydrochloric acid cannot be found in the gastric juice, provided cancer may be excluded. Edinger obtained the gastric juice by allowing the patient to swallow small sponges which were fastened to a thread and which after a time were withdrawn from the stomach and compressed. If free hydrochloric acid is present, a yellow solution of tropaeolin (gr. f : § vij.) turns red, and methyl aniline violet (gr. viiss. : § vij.) dark blue. 11. Atrophic Changes in the Stomach. Fenwick has recently shown that disappearance of the glands may produce very dangerous conditions. In some cases this disease is inde- pendent. In others it is associated with other gastric affections or fol- lows cancerous disease in other organs, and marantic conditions in general. The peptic glands disappear in places and are replaced by connec- tive tissue; some of them have become cystic. The process seems to be the result of an interstitial interglandular proliferation of connective tissue. In other respects the condition of the stomach depends upon the primary disease; sometimes it is small and thin, sometimes dilated or thickened. A few cases run their course with the symptoms of progressive per- nicious anaemia. The condition cannot be diagnosed with certainty. 12. Softening of the Stomach. (Gastromalacia.) 1. Softening of the stomach is most frequent in children until the end of the second year, especially after artificial feeding and diseases of the stomach. In adults it has been observed in sudden death after a 96 DISEASES OF THE STOMACH. heavy meal, or after diseases of the brain, of the spinal cord, typhoid fever, pyaemia, dysentery, etc. 2. The condition is easily recognized anatomically. In the milder grades, the mucous membrane is found softened in places, swollen, easily removed with a knife, and sometimes even by a stream of water. In advanced cases the softening extends to the muscular coat, so that the stomach is only held together by thin serous membrane. The latter often ruptures on contact, and the contents of the stomach pass into the peritoneal cavity. In many cases the rupture of the stomach occurs before the abdominal cavity is opened, especially if the corpse has not been carried with great care. The lower third of the oesophagus may also show softening, and if this organ is perforated, the contents of the stomach enter the pleural cavity. The adjacent portions of the dia- phragm may also be softened and destroyed. Although other organs may be affected, the softening is always most marked in the stomach. The color of the softened tissue is not always the same, so that we are accustomed to speak of white, brown, and black softening. In white softening, the swollen tissue is gray or milky white, and in a few places we recognize brownish streaks and lines which correspond to the larger distended blood-vessels. The other coats of the organ are usually very anaemic. In brown or black softening, we have to deal with a brown- ish or blackish pulpy mass, the color of which is dependent on the dis- tention of the veins of the mucous membrane. Occasionally the softened tissue may assume some other color corre- sponding to that of the food taken just before death. Under the micro- scope, the epithelium and connective tissue are found more or less, dissolved and destroyed, while the smooth muscular fibres and elastic tissue are intact, and can thus be readily separated from one another. 3. Elsaesser stoutly maintains that all these changes are post-mortem. His principal reasons for holding this position were the following: a. the absence of all symptoms of inflammation, even after perforation of the stomach; b. the influence of age and diet. The softening is especially frequent in children, because in them the tissue possesses very little resist- ance, and the contents of the stomach have a special tendency to acid fermentation, c. The softening only extends as far as the contents of the stomach are in contact with its walls, d. It can be produced in other portions of the stomach, in addition to the fundus, by changing the position of the body. e. It is found especially in the summer months, because the stomach then undergoes cooling very slowly, and the gastric juice exercises its solvent action for a long time. In recent times, however, a number of cases have again been reported in which brown softening is said to have occurred at the close of life. The question cannot, however, be settled with positiveness. At all events, the lesions belong more to pathological anatomy than to clinical observation. 13. Rupture of the Stomach. (Gastrorhexis.) 1. Rupture of the stomach may occur from without inwards or in the opposite direction. Traumatic rupture is infrequent. Buyst has re- cently described a case in which a fall, without external injury of the abdominal wall, produced rupture of the pylorus, duodenum, and spleen. Perforations sometimes occur into the stomach from adjacent organs, for example, in abscesses of the liver, spleen, or peritoneum, purulent DISEASES OF THE STOMACn. 97 pleurisy and pericarditis, tuberculosis of the spine and ribs, etc. Dis- eases of the walls of the stomach, especially ulcer, cancer, and toxic gas- tritis, are a frequent cause of perforation. It is occasionally produced by the ingestion of sharp, hard, or insoluble foreign bodies. It has also been maintained that an excessively heavy meal or abundant development of gas may produce spontaneous rupture of the stomach, despite the fact that the walls of the organ are healthy. The reported cases are not reliable. 2. Sudden pain, signs of grave collapse, extensive tympanites, and symptoms of perforation-peritonitis (pain, disappearance of hepatic and splenic dulness) are mentioned as the chief symptoms of rupture of the stomach. Vomiting may be absent. A rupture is sometimes said to be attended with a loud noise. Emphysema of the skin developed in a case reported by Newman, probably as the result of injury of the parietal peritoneum. 3. The prognosis is bad. The treatment consists of the administra- tion of opium and stimulants. 14. Animal and Vegetable Parasites in the Stomach. 1. Among the animal parasites may be mentioned trichina spiralis, ascaris lumbricoides, and tape worms. These not infrequently produce intolerable gastralgia, which ceases abruptly when the worms are vom- ited. It may also be mentioned that ecchinococci may enter the stomach from the liver, spleen, omentum. Meschede observed a very violent gas- tritis in a boy after eating cheese. This disappeared after living cheese mites were vomited. Gerhardt also observed acute gastritis, which dis- appeared after the vomiting of larvae of diptera. The diagnosis can only be made during life after the worms have been vomited. Caution must be exercised, particularly in hysterical females who sometimes bring living frogs, snails, etc., to the physician, with the claim that these had been ejected from the stomach. 2. The vegetable parasites include sarcina ventriculi, yeast fungus, sprue, mould fungus, and bacteria. Sarcina ventriculi is often found. Its peculiar shape (vide Figs. 9 and 10) renders a mistake hardly possible. It may occur in the gastric con- tents of healthy individuals. Bamberger believes that its abundant development is characteristic of gastric cancer. Its mode of develop- ment is unknown. Its power of resistance is very great; for example, Duckworth kept it for three years in closed tubes. Yeast fungus is very intimately connected with fermentative processes in the gastric contents, but scattered yeast cells are found very often in vomited matters without justifying us in assuming abnormal fermentation. Their shape is easily recognized (vide Yol. II., Fig. 10). Oidium albicans (sprue) does not occur often in the stomach. Its appearance is shown in Fig. 2. Masses of sprue sometimes spread directly from the oesophagus to the mucous membrane of the stomach. In other cases the sprue develops in the stomach, although the oesophagus is intact. In a woman who died of cholera, Rudenew found pcnicillium glaucum, the fungus infiltrating two small tumors situated near the pylorus. Naunyn also observed mould fungus, in two cases, in the gastric contents. Schizomycetes are always found in the contents of the stomach. Their relation to the digestive processes still remains to be explained. They increase very markedly in number in abnormal fermentation of the gastric contents. Klebs re- 98 DISEASES OF TAE STOMACH. cently described brown spots upon the mucous membrane of the stomach, which consisted of colonies of bacteria, situated partly free in the lumen of the glands, partly between the epithelium and the membrana propria. In addition there was an inflammatory accumulation of round cells be- tween the glands. He called the bacterium bacillus polystorus brevis s. gastricus (5.9-11.56 p in leugth and 11.47 p in width.) 15. Foreign Bodies in the Stomach. Foreign bodies are rarely swrallowed with suicidal intent; they are sometimes found in the stomach of the insane ; thus Baillarger reported a case in which a lunatic swallowed a fork 14 cm. in length. Six years later, at the autopsy, the fork (blackened and covered in places with a reddish coating) was found in the stomach. Mountebanks sometimes suf- fer from this accident. Gussenbauer recently reported a case in which a sword swallower, who had introduced the sword into the stomach, broke the weapon by an incautious movement of the head, and a piece 20 cm. in length and 2 cm. in width entered the stomach. Bussell and others have described cases in which women had acquired the habit of swallowing the hairs which remained in the comb after their toilet. Gradually the stomach became filled with a large mass of hair which could be felt during life, and was regarded as a tumor. A case of this kind recently came under my own observation, but in this instance the hair was discharged through the rectum. Foreign bodies, even when they possess very large dimensions, may be tolerated by the stomach for a long time. In some cases they produce the symptoms of pyloric stenosis or in- flammation of the walls of the stomach which may even lead to perfora- tion. On the other hand, the foreign body may pass through the stom- ach and give rise to disease of the intestines, for example, typhlitis. A large proportion of the foreign bodies pass off with the stool without giv- ing rise to any symptoms. This is true even of pointed objects such as needles. Expectant measures must be adopted. Porridge, mashed potatoes, and similar articles of food may be given, and, if necessary, gastrotomy must be performed. 16. Changes in the Shape and Position of the Stomach. 1. Changes in the shape of the stomach are congenital or acquired. Stokes recently described a deep constriction at the middle of the stom- ach, which produced no symptoms during life. We have previously re- ferred to the constrictions which are occasionally produced by ulcerative and cicatrizing processes in the wall of the organ. These changes can sometimes be recognized during life, by the employment of Frerichs’ method. Buhl has also described an excellent example of congenital oc- clusion of the pylorus. 2. Among the changes of position we may mention transposition of the viscera. This generally affects all the other abdominal and thoracic organs. The stomach is situated on the right side, the liver on the left, the cardiac extremity is directed towards the right, the pylorus toward the left. This condition is generally recognized with facility, particu- larly if the stomach is dilated with carbonic acid, because Traube's semi- 99 lunar space will be present to the right in the hepatic region instead of a dull percussion sound. Not very infrequently we notice an abnormal vertical position of the stomach so that the pylorus is situated lower and is nearer to the median line. This condition may be congenital or acquired. The latter partic- ularly in women who wear tight stays, and in large tumors of the liver or spleen. This is easily recognized on distention of the stomach with carbonic acid. The lower border of the stomach is beneath the umbilicus, but the percussion figure of the organ is smaller from the right to the left, and extends very little or not at all beyond the median line of the abdomen. (Vide Figs. 15 and 12.) We have previously mentioned that a vertical position of the stomach predisposes to gastroectasia, and abnormally low position of the stom- DISEASES OF THE STOMACH. Fig. 15. Outline of the stomach on percussion in vertical position of the organ. ach is found when tumors of the organ have dragged it downward. Per- itoneal adhesions may also give rise to an unusual position of the organ. The stomach is sometimes found to be abnormally high, so that the upper border of the semilunar space extends to the fourth left intercostal space, and also possesses unusual dimensions in the left side of the thorax. In cases of diaphragmatic hernia the stomach may be situated in the left pleural cavity. Appendix. Changes in the gastric vessels are not very infrequent, but they rarely constitute an independent affection. Ponfick described aneurism of the 100 DISEASES OF THE STOMACH. right gastro-epiploic artery in a woman who suffered from repeated at- tacks of pain around the gall-bladder and epigastrium, and suddenly died from rupture of the aneurism. Aneurism of the right coronary artery of the stomach has also been observed. b. Embolism and thrombosis of the gastric arteries play an important part, as we have previously mentioned, in the development of the round gastric ulcer. Infectious emboli may produce abscess of the stomach. B. FUNCTIONAL DISEASES OF TIIE STOMACH. NEUROSES OF THE STOMACH. 1. Rumination (Merycismus). I. Etiology. Rumination in man is a rare phenomenon. Bourneville and Seglas were able to collate only forty-six cases. It must not be forgotten, how- ever, that many patients conceal the disease. It is more frequent in men than in women, and almost always before the age of twenty years. It sometimes seems to be inherited by the children of the patients, but this apparent heredity may perhaps be explained as the result of imitation, which undoubtedly plays a great part in the etiology of rumination. In somo cases the disease seems to be the result of congenital weakness of the muscular coat of the stomach. These individuals are generally able to force food from the stomach into the buccal cavity by slight pressure upon the epigastrium, deep in- spirations, laughing or vigorous muscular exertion. This perhaps occurs sponta- neously at first, is continued out of sport, and finally becomes pronounced rumi- nation. The condition has sometimes been attributed to errors of diet (imperfect mas- tication, excess of vegetables, etc.). Occasionally it results from gastro-intesti- nal diseases (chronic gastritis, obstinate constipation, a blow upon the stomach). Cold and mental excitement have also been mentioned among the causes. A predisposition to the disease is furnished by anaemia, hypochondria, hys- teria, epilepsy, idiocy, insanity, chorea, onanism. In one case it was preceded by an attack of whooping-cough. II. Symptoms.—Some time after eating,the patients regurgitate the food into the mouth (at first voluntarily, then involuntarily), and then expectorate it, swallow it forthwith, or masticate it again and then swallow it. Rumination may begin five to ten minutes after the meal and last five to six hours or more. Somo patients ruminate after each meal, others only after they have eaten rapidly or have partaken excessively of vegetables, or after obstinate constipation, etc. Rumination may be repressed by some patients, in others this is no longer pos- sible. In many cases the general condition is unaffected. In others, gradual emaci- ation occurs, and finally a dangerous condition of exhaustion, particularly when the ruminated food is at once expectorated. Other patients present symptoms of gastric catarrh, especially if the regurgitated food is immediately swallowed in an imperfectly masticated condition, and irritates the gastric mucous membrane. According to Canstatt, emesis is produced with difficulty in these patients. The disease often lasts for life. In others it ceases abruptly after marriage or after recovery from a previous gastro-intestinal affection. III. Anatomical Changes.—A dilatation (the so-called prgestomach) is some- times observed at the transition of the oesophagus into the stomach, sometimes above, sometimes below the diaphragm. But this condition is sometimes acci- dental, sometimes secondary to the rumination. IY. Diagnosis, Prognosis, Treatment.—The absence of oesophageal disease or over-distention of the stomach distinguishes rumination from the regurgitation observed in such conditions. The disease is rarely attended with serious danger,, and recovery generally follows if the co-operation of the patient is secured. The diet should be carefully regulated. Fluid food in small quantities should be given every two hours, a daily evacuation from the bowels should be secured, and any primary affection which may be present should receive suitable treat- ment. At the same time the patients should endeavor to repress the act of rumi- nation by all the power of their will. Koerner has recently recommended verv highly the ingestion of pieces of ice immediately after meals. Perhaps the cold stimulates the cardia to more vigorous contractions. DISEASES OF THE STOMACH. 101 2. Peristaltic Restlessness of the Stomach. (Tormina ventriculi nervosa.) 1. Under the term peristaltic restlessness of the stomach, Kussmaul has described conditions of unusually vigorous movements of the stom- ach. The muscular contractions are visible under the abdominal walls, moving slowly from right to left, the walls of the stomach occasionally rise very high in places. In addition, there is a feeling of restlessness and moving to and fro in the gastric region. The most varied splashing noises are often heard on auscultation of the stomach. The intestines may also take part in the peristaltic restlessness, although constipation is sometimes present because the large intestine is unaffected. These phe- nomena appear particularly after meals, but may also occur while fast- ing, or even at night. 2. Such conditions may be the result of mechanical causes, and occur in stenosis of the pylorus (vide page 88), but they also occur as an independent neurosis, and are produced by mental excitement, sexual excesses, anaemia, and general nervousness. Stiller regards them as the result of spastic closure of the pylorus. 3. Treatment consists in careful regulation of the diet and stools. In addition, rest in bed, warm poultices, and treatment of the primary disease. 3. Hypersecretion of the Gastric Mucous Membrane. Reichmann describes a case of idiopathic hypersecretion of the gastric mucous membrane in a man aet. 27 years, who was annoyed during the night by spasm of the stomach, heart-burn, and increased thirst. In addition, increased appetite, no signs of an anatomically demonstrable dis- ease of the stomach, and constipation. If the stomach-pump was used early in the morning, after fasting for some time, 180-300 ccm. of a fluid, which was colored green with bile, could be removed from the stomach. This had an acid reaction, and digested’fibrin completely in seven minutes at 40° C. It contained no diastatic ferment, and therefore did not consist of swallowed saliva (vide p. 60). The patient was cured by restriction of the amount of fluids, meat diet, washing out of the stomach morning and evening, poultices to the abdomen, and enemata to relieve thirst. 4. Nervous Pain in the Stomach. Gastralgia. (Cardialgia. Gastroclynia.) I. Etiology. —Pain in the stomach is sometimes produced by anatom- ical changes, sometimes it occurs as an independent nervous affection. The latter alone will now be considered. This is found not infrequently in chlorosis and conditions of conva- lescence and exhaustion. Glastralgia seems to be a neuralgia of the sensory nerves of the stomach, perhaps as the result of perverse processes of nutrition. It occurs not infrequently in onanists and those who indulge in sexual and alcoholic excesses. It is also very frequent in phthisis and Bright’s dis- ease, even in the early stages. Certain general diseases may also give rise to attacks of spasm of the 102 DISEASES OF THE STOMACH. stomach. Thus gastralgia may take the place of or precede an attack of gout. It develops occasionally as the result of malaria, occurring in periodical attacks which are only relieved by quinine or arsenic. In some cases the disease is the result of an affection of the brain, spinal cord, or peripheral nerves. Attacks may occur during the course of locomotor ataxia (Crises gastriques). They have also been observed in softening of the brain and tumors of the pneumogastric and sympa- thetic. Furthermore, they occur not infrequently in hysteria, neuras- thenia, and hypochondria. Sometimes we have.to deal with a reflex disease, provoked by affections of other abdominal organs. This is observed most frequently in women who suffer from diseases of the uterus or ovaries. The gastralgia occurs occasionally at the period of menstruation. It may also develop in the course of diseases of the bladder, kidneys, liver, pancreas, spleen, and intestines. In many cases no cause is demonstrable. Gastralgia is much more frequent in women than in men, and occurs generally from the fifteenth to the fortieth years. It is rare in childhood, more frequent in old age. II. Symptoms.—The chief symptom of the disease is pain in the- stomach, which begins suddenly or is preceded by prodromata (feeling of fulness in the stomach, frequent eructations, nausea, vomiting, mental depression, pain in the head, etc.). The pain may be intolerable. It is described as boring, burning, sticking, spasmodic, and is located chiefly in the epigastric region. But it often extends into the back between the scapulae, into the umbilical region and the hypochondrium. It is often increased by gentle pressure, while it is usually relieved by more vigorous pressure. Hence many patients firmly press the hands into the epigastrium, or assume the abdominal position, or are bent over forwards. The epigastrium is often sunken. The abdominal walls are hard and contracted, and we can often recognize the pulsation of the aorta. In other cases the epigastrium is distended, and the stomach itself tense and prominent. The attacks of pain often occur without an exciting cause. In other cases they are preceded by mental or bodily exertion. They appear very frequently in the fasting condition, and are often relieved by eating. Many patients complain of boulimia, or desire unusual, often very indi- gestible articles of food. The duration of the pain is extremely variable. Sometimes it lasts a few minutes, sometimes several hours. Only a single attack may occur, or they may be repeated daily and even several times a day for weeks, months, or years. The gastralgia of intermittent fever occurs at definite inter- vals at certain hours of the day. In women gastralgia sometimes occurs only at the period of menstruation, or it is produced by certain manipu- lations upon the sexual organs. (In Memeyer’s case it occured whenever leeches were applied to the os uteri.) At the height of a paroxysm many patients are terrified by a feeling of annihilation ; the face is pale, the skin cool; the pulse is small and irregular, sometimes slow, sometimes rapid; perspiration breaks out over the body. In some cases we notice syncope, and partial muscular spasms or general convulsions. The end of the attack is often announced by special symptoms, such as eructations, vomiting, yawning, etc. Constipation is generally present DISEASES OF THE STOMACH. 103 at the period of the attacks. The urine is often scanty, and shows an abundant brick-red sediment. In hysterical patients, on the other hand, a very clear and pale urine (urina spastica) is often discharged at the close of the attack. Fischl has observed albuminuria which sometimes lasted for several days. Hyaline casts also were found in the urine. The albuminuria is said to be owing to the fact that the pain diminishes the pressure of blood in the renal artery. Gastralgia sometimes alternates with other neuralgias. In rarer cases it is present at the same time. III. Diagnosis.—The recognition of gastralgia is not always easy, and we must differentiate it from the following diseases: (a) Rheumatism of the abdominal muscles. In this disease the pain is less paroxysmal; it is increased on pressure, and not infrequently jumps from one place to another. (b) Neuralgia of the lower intercostal nerves. The pain can be traced along a single intercostal space; Valleix’s painful points can gen- erally be demonstrated; gastric symptoms are absent. (c) Circumscribed peritonitis. There is great tenderness on gentle pressure, and true paroxysms of pain are absent; the etiology should also be taken into consideration. (d) Biliary colic. The pain is generally confined to the region of the gall-bladder (external border of the right rectus muscle, immediately below the edge of the thorax); signs of jaundice; passage of gall-stones in the stools. (e) Intestinal colic. The pains change their situation more rapidly, and signs of accumulation of gas in the intestines are noticeable. (/) Radiated pains. Pains in the epigastrium occur in renal colic, pleurisy, and pericarditis, but careful examination of the organs will establish the diagnosis. In addition we should endeavor to determine from the clinical history whether the gastralgia is a purely nervous affection or the result of ana- tomical changes in the walls of the stomach. IV. Prognosis.—This is favorable, in so far as death from gastralgia is unknown. Recovery will not occur unless tliecause can be re- moved. In some cases the disease continues for years. V. Treatment.—The first indication is the treatment of the primary affection. To combat the gastralgia itself, we may apply a warm poultice to the region of the stomach, after a subcutaneous injection of morphine has been made. If syncope occur, the patient should inhale ammonia or eau de cologne, and five drops of ether or twenty drops tincture of valerian may be given internally. An immense number of other remedies have been recommended, of which we may mention: narcotics (opium, chloral hydrate, belladonna, chloroform, etc.), nervines (bismuth, nitrate of silver, FowleFs solution), sinapisms, irritating inunctions. Kussmaul and Marlfranc report very good results from washing out the stomach. Two to three litres of a carbonated fluid at 38° are injected into the stomach every morning by means of the ordinary siphon apparatus, and then removed. Electricity is often serviceable. Indeed Leube maintains that, when it is ineffective, the gastralgia is the result of anatomical changes in the stomach. Leube applied the anode of the constant current to the painful part 104 DISEASES OF THE STOMACH. in the region of the stomach, the cathode to the axillary region, or to the spine. (Strong stabile current of five to ten minutes’ duration.) Others recommend the faradic current, either both poles to the abdomi- nal walls, or one electrode is passed into the stomach through a rubber tube, the other is applied externally. 5. Nervous Dyspepsia. (Neurasthenia Gastrica.) I. Symptoms.—Dyspepsia implies difficult digestion, especially in the stomach. It may accompany various gastric affections, or appear as an independent neurosis. The latter will alone be considered. In nervous dyspepsia the mechanical and chemical digestion in the stomach does not appear to be changed, but nevertheless the digestive process is attended with local disturbances and general nervous symp- toms. The latter must be regarded as reflex. The symptoms occur after a heavy meal, generally after dinner, and gradually subside toward the end of digestion, i. e., in five or six hours. The patients have a disagreeable sensation of fulness and pressure in the region of the stomach despite careful regulation of the diet. Sometimes there is decided pain which is usually lessened by pressure on the stomach. Eructation is a frequent symptom. The patients complain of heartburn, sometimes of nausea and vomiting. There is usually ano- rexia, more rarely boulimia. Thirst is occasionally increased, the tongue is not coated, sometimes a bad or perverse taste in the mouth is noticed. Some patients have a feeling of constriction along the oesopha- gus; the bowels are usually constipated. General nervous symptoms are very common. The patients com- plain of a rush of blood to the head, dulness, ringing in the ears, spots before the eyes, pain in the head, and dizziness. They are depressed and moody. Sleep is disturbed, but sometimes there is marked drowsiness and constant yawning after a hearty meal. Asthmatic attacks or palpi- tation of the heart may be prominent symptoms. The patients grow pale and gradually emaciate. II. Etiology.—The disease is more frequent in men than in women, and begins generally between the ages of thirty and forty years. It often accompanies other neuroses, for example, hysteria, hypochondria, neurasthenia, and insanity. In other cases it is associated with anaemia and conditions of weakness (chlorosis, phthisis, Bright’s disease, syphilis, lactation, etc.). It sometimes seems to be the result of toxic causes (excessive use of alcohol or tobacco, uraemia, and malaria). Nervous dyspepsia is sometimes a sequel of other diseases of the stomach, for example, chronic gastritis and round ulcer. Finally, it may develop in a reflex way in diseases of the intestines, uterus, ovaries, and kidneys. III. —Diagnosis and Prognosis.—The diagnosis cannot be made with certainty unless we are able to exclude anatomical diseases. Leube attaches great importance to the fact that the chemical digestion in the stomach is properly performed. The prognosis should be given with caution, because complete and permanent recovery is not frequent. IV. Treatment.—The improvement of the general condition is much more important than regulation of the diet. We may resort to sea baths, cold-water cures, a trip to the mountains, and, in anaemic in- DISEASES OF THE INTESTINES. 105 dividuals, to mild iron waters; in addition, quinine, arsenic, and bella- donna. Local galvanization of the stomach, or the application of elec- tricity to the central nervous system, may be attended with excellent results. Appendix. Leyden has called attention to the occurrence of periodical vomiting associated with pain, which occurs as a pure neurosis in ancemic and nervous individuals. Under the term nervous gastroxynsis, Rossbach describes a symptom complex which occurs chiefly in individuals suffering from nervous exhaustion. It occurs every week or month in attacks of one to three days’ duration. There is usually an excessive formation of acid in the stomach, nausea, and vomiting. The patients suffer from a feeling of dulness in the head and severe headache. Considerable lactic and hydrochloric acid can be demonstrated in the oontents of the stomach. The attack subsides rapidly after the stomach is relieved of its contents, and is often aborted if lukewarm water is taken at the beginning. In addition to general treatment, we should order one to two glasses of luke- warm water or weak tea, since the disease seems to be the result of irri- tation of the sensory nerves of the stomach by an excessively acid gastric juice. PART IV. DISEASES OF THE INTESTINES. 1. Acute Intestinal Catarrh. Enteritis Catarrhalis Acuta. I. Etiology.—Acute intestinal catarrh is an extremely frequent dis- ease. It is sometimes independent and primary; sometimes it is sec- ondary, and develops during the course of other diseases. Errors of diet constitute the most frequent cause of the primary form of the dis- ease. We see every day that excessive meals give rise to acute enteritis. The secretions of the digestive tract are evidently unable to properly digest the food, so that the latter undergoes abnormal decomposition, irritates the mucous membrane of the intestines, and gives rise to in- flammation. In other cases, it is the result of poor quality of the food. Enteritis is produced not infrequently by bad drinking water. Sometimes it is the result of the ingestion of spoiled food, such as spoiled meat, sour milk, unripe fruit, etc. In the summer months, a sort of epidemic may occur as the result of causes of this character. A cold which may act either generally or locally not infrequently gives rise to intestinal catarrh. Sudden wetting when the body is heated, or a cold bath, is often mentioned as the cause of acute enteritis. Among the local causes of this character, we may mention the drinking of cold water when the body is heated. In not a few cases, I have seen diarrhoea develop from the application of an ice-bag to the abdominal walls. In rare cases, the disease is the result of injury, such as a fall, or blow upon the abdomen. Those cases in which a sort of internal injury has been sustained are much more frequent (ingested foreign 106 DISEASES OF TIIE INTESTINES. bodies, concretions in the intestines, worms, or foreign bodies which have been pushed into the rectum through the anus). Obstinate con- stipation gives rise not infrequently to enteritis, because the exces- sively hard masses of faeces mechanically irritate the mucous membrane of the intestine. Finally, we must mention toxic enteritis, which may be produced by various drastics, tartar emetic, arsenic, acids, alkalies, or caustics in general. Acute enteritis occasionally develops epidemically, without our being able to demonstrate any of the previously mentioned causes. This occurs almost always in the hot summer months, especially if there has been a long heated term or marked changes of temperature. Such epi- demics are observed occasionally as the forerunners of Asiatic cholera and dysentery. In secondary acute enteritis, the inflammation is often propagated from adjacent parts. Thus, gastritis extends not infrequently to the mucous membrane of the small intestine. In other cases, the connec- tion between acute gastritis and enteritis is somewhat different, inas- much as decomposed, or imperfectly prepared food is conveyed to the intestines, and there produces irritation. Acute enteritis also occurs with extreme frequency in peritonitis from the spread of the tion from the serous membrane to the mucous membrane of the intes- tine. Inflammation of the rectum occasionally occurs in women who suffer from gonorrhoea, because the infectious secretion enters the anus. Sodomy may also give rise to inflammation of the rectum. In some cases, eczema around the anus extends to the rectum, and there pro- duces catarrh of the mucous membrane. In many cases, acute enteritis is the result of other diseases of the intestinal canal, such as ulcerative processes, invagination or volvu- lus, etc. The disease is often the result of disturbances of circulation, espe- cially of obstruction in the portal system. Tumors of the abdominal organs will produce a similar effect if the mesenteric veins are com- pressed. The obstruction to circulation is sometimes situated above the diaphragm (chronic diseases of the respiratory or circulatory organs). General diseases occasionally give rise to acute enteritis. This is observed in cachectic conditions, for example, phthisis, Bright's disease, syphilis, etc. Or it occurs during infectious diseases. It is well known that acute enteritis plays a prominent part in typhoid fever, cholera, and dysentery. It is also observed in fibrinous pneumonia, pyaemia, septicae- mia, etc. The septicaemic intestinal catarrhs include those which are observed in patients suffering from pulmonary gangrene and putrid bronchitis, as the result of swallowing the ichorous sputum. Some cases depend upon malaria. This is shown by their periodical and paroxysmal development and by their disappearance after the use of quinine. In a number of cases, the symptoms of acute enteritis have been observed after extensive burns of the skin. The connection between the two affections is still obscure. II. Anatomical Changes.—When the anatomical changes are very marked, the mucous membrane of the intestine is very red and swollen. The redness is usually most marked upon the villi and the folds; some- times it is uniform, sometimes in streaks or patches; extravasations of blood may be observed in some parts. The swelling of the mucous DISEASES OF THE I]SrTESTI]SrES. 107 membrane generally extends to the submucous tissue, where it is the re- sult of an inflammatory, serous infiltration. As a rule, the solitary and agminated lymph follicles are enlarged. They project to a more marked extent above the mucous membrane, and appear as gray, transparent granules or nodules. On being punc- tured, they discharge a little drop of almost clear fluid, and then usually collapse. When the acute enteritis has lasted for some time, no fluid may escape, and the follicle may not collapse after puncture. Hence the enlargement of the follicle depends at first upon inflammatory oedema, while later it is the result of inflammatory hyperplasia of the cellular elements. These follicles are surrounded by an areola of enlarged blood-vessels. The mesenteric lymphatic glands are almost always enlarged, streaked with blood, injected, and very succulent. The muscular and serous coats are unchanged as a rule, except in secondary enteritis when affected by the primary disease. Sometimes unusual congestion is found in various portions of the serous layer. In extremely rare cases, acute enteritis gives rise to losses of substances in the mucous membrane. These are sometimes superficial, so-called catarrhal erosions, sometimes more deeply spreading catarrhal ulcers. If the latter is the result of ulceration of the lymph follicle, it is known as a catarrhal follicular ulcer; if produced by destruction of the mucous membrane proper, as catarrhal ulcer of the mucous membrane. The latter begin generally as erosions. Desquamation of the epithelial covering of the mucous membrane is found not infrequently in the dead body, but a part of these changes may be of a cadaverous character, probably from post-mortem macera- tion. A part of the lesion disappears not infrequently in the dead body. This is particularly true of the congestion and swelling of the mucous membrane. Under such circumstances we must pay attention to the enlargement of the lymph follicles, the congested zone around them, the enlargement and injection of the mesenteric glands, and the character of the intestinal contents. III. Symptoms.—The symptoms are not always alike, and depend upon the part of the intestines in which the inflammation is situated. We therefore distinguish duodenitis, jejunitis, ileitis, typhlitis, colitis, and proctitis. The inflammation almost always spreads from one part of the intes- tines to the adjacent part. Inflammation of the ileum and colon is most frequent, and this will first be considered. The most constant symptom is diarrhoea. The patient must go ta stool more often than normally, and discharges thin unformed masses. The number of evacuations may far exceed twenty in the twenty-four hours. In many cases the amount passed is greater than we would be led to expect from the qiiantity of food ingested. Hence the evacuations are not only the result of unusually active per- istalsis, but there is an excessive secretion of the mucous membrane in consequence of the inflammation. The appearance of the stools is very often abnormal. They may be bright yellow, greenish, tinged with blood, and sometimes contain an unusual amount of mucus. Their color sometimes changes after exposure to the air. If the evacuations follow one another very rapidly, they may not be stained by bile, and colorless, grayish fluid masses make their appearance in which float de- 108 squamated shreds of epithelium (rice-water stools). The faecal odor then diminishes, and the stools have a peculiar sickish odor which has also been compared to that of semen. The patients sometimes pass very frothy and foul-smelling masses, in which decomposition and fermenta- tion continue outside of the body. The consistence of the stools may be like that of thick or thin porridge, or they may be watery. The reaction is usually alkaline. The stools sometimes contain undigested particles of food, worms, or particles of faeces of extreme hardness ; the latter indi- cate previous constipation. Under the microscope they are found to contain muscular fibres, starch granules, vegetable cells, and drops of fat. Bacteria form an important constituent, but pathogenic schizomy- cetes have not hitherto been discovered. In addition, we find desqua- mated epithelium cells, also round cells and a few red blood-globules. We often find crystals of the triple phosphates, the neutral phosphate of lime, tablets of cholestearin, Charcot-Neumann crystals (vide Vol. I., page 233, fig. 58), and needles of the fatty acids. Diarrhoea is sometimes the sole symptom of acute enteritis. It is often preceded by borborygmus, a feeling of distress, and cutting pain. Physical examination of the abdomen may reveal extremely slight changes. The unusually vigorous peristaltic movements are sometimes recognized through the abdominal walls, loops of intestines rising and falling in places, to reappear in other parts. In other cases we find dis- tention of the abdomen. This is the result of abnormally active devel- opment of gas in the intestines. The abdomen is often as tense as a a drumhead, the diaphragm is pushed high up in the thorax, compressing the lungs and interfering with their mobility, and the apex of the heart is sometimes pushed into the fourth intercostal space. It is not astonish- ing, therefore, that many patients complain of palpitation, dyspnoea, and asthmatic disturbances. Flatus is often passed in abundance, after which the patient feels relieved. At the same time small quantities of a thin stool may be voided. On palpation we not infrequently notice a purring murmur, gargouillement, produced by pressure upon the intes- tinal fluid which is mixed with air. If pain is present, it is not infre- quently ameliorated by increasing pressure upon the abdominal walls. The results of percussion vary, according as we percuss intestines which contain gas or are filled with non-aerated contents. (In the former event a tympanitic or metallo-tympanitic note, in the latter a dull per- cussion note is heard.) The rumbling intestinal noises may often be heard at a distance of several paces. The excretion of urine is generally very scanty, and if the diarrhoea is very violent, almost complete anuria may result. The urine is concen- trated, very acid, and on cooling, deposits urates; micturition is some- times attended with burning pains in the urethra, Fischl found casts in the urine not infrequently, and occasionally in very large numbers. They were usually hyaline, sometimes covered with epithelium and round cells, rarely with red blood-globules. The casts sometimes appeared very soon after the beginning of the diarrhoea, particularly in old persons, and if the evacuations were very copious. They soon disappeared from the urine. Albumin was sometimes present, sometimes absent. Fischl attributes the albuminuria to an aborted nephritis, the result, in great part, of diminished arterial pressure in the kidneys. This writer has also called attention to enlargement of the spleen. Fever may be absent, but in some cases the temperature rises beyond DISEASES OF THE INTESTINES. DISEASES OF THE INTESTINES. 109 39° 0. If the rise of temperature continues for several days, the diagno- sis between simple acute enteritis and typhoid fever maybe doubtful. In children and very excitable individuals, the fever may give rise to de- lirium and convulsions. At times it begins with a chill or chilly feeling. Thirst is almost always increased. The appetite may be retained, particularly when the inflammation affects chiefly the large intestine. As a rule, however, the appetite is diminished or entirely abolished. The signs of collapse are sometimes prominent. The skin becomes cool, and is covered with a cold, clammy sweat; the pulse is small and frequent; the eyes are sunken, and the voice becomes muffled. This is observed particularly in old individuals, or when the pains in the abdo- men attain a certain severity, because some patients are extremely sus- ceptible to them. Each attack of pain may be attended with syncope and symptoms of collapse. The disease often lasts only one to two days, sometimes a week or more. The patients often feel very weak for a few days after recovery. The symptoms described are observed particularly in ileo-colitis, the most frequent form of intestinal catarrh. When the acute catarrh is confined to the small intestines, diarrhoea is sometimes absent. The pa- tients complain of rumbling and pain in the belly, but no changes are noticed in the evacuations. Catarrhal inflammation of the duodenum is often attended with jaundice, because the opening of the ductus choledochus is occluded by secretion or by swelling of the mucous membrane, or the catarrh spreads directly from the mucous membrane of the duodenum to that of the ductus choledochus. Jejunitis and ileitis cannot be differentiated during life; moreover, the jejunum and ileum are usually affected at the same time. Isolated inflammation of the caecum and vermiform appendix (typhli- tis) occurs not infrequently. The most frequent causes are faecal stasis and foreign bodies. The chief symptoms are pain in the right iliac fossa, the demonstration of a tumor in this region, and dulness on per- cussion. Acute colitis is the most frequent form of intestinal catarrh, but is generally associated with ileitis. If the rectum is inflamed (proctitis), violent tenesmus is usually pro- duced. The patients feel the necessity of going frequently to stool, but very small quantities are evacuated. Shortly before the evacuation, cutting pain is felt in the left iliac region, and the evacuation itself is apt to be accompanied by the most violent pain. The left iliac fossa and pelvis are sensitive to pressure, and a dull or dull tympanitic note is heard on percussion. As a rule, the stools contain a very large amount of mucus, and often specks of blood, or even larger accumulations of blood. The anus is often seen to undergo spasmodic contractions, and some- times it is strongly retracted. Digital examination often produces an unusually severe pain. The finger is grasped spasmodically by the sphincter, and at the same time twitching movements can be felt. The mucous membrane of the rectum is often very warm, appears loosened, and unusually slippery. By means of the rectal speculum, we can detect redness, swelling, and excessive secretion of the mucous membrane. If proctitis has lasted for some time, the sphincter may undergo a sort of paralysis. Fluid constantly trickles from the anus, irritates the exter- nal integument, and produces an eczema intertrigo; prolapsus recti occurs not infrequently. The inflammation sometimes spreads to the 110 DISEASES OF THE INTESTINES. surrounding connective tissue, and gives rise to periproctitis and its sequela?, especially fistula. Extensive enteritis may be associated with gastritis. IV. Diagnosis.—As a rule, the diagnosis of acute enteritis is not difficult. If it occurs during an epidemic of Asiatic cholera, and we must decide whether the diarrhoea is the result of a simple intestinal catarrh, or of mild cholera infection, the stool should be examined for KoclTs comma bacillus (vide Vol. IV., sec. Cholera). V. Prognosis.—The prognosis is almost always good. As a rule, there is no danger unless the disease occurs in exhausted individuals. But the prognosis also depends upon the causation. If it is the result of disease of the liver, respiratory or circulatory organs, the individual at- tack may be relieved, but there is danger of relapse and the gradual development of chronic intestinal catarrh. VI. Treatment.—If fever is present, the patients should remain in bed. If they complain of pain, a warm poultice may be applied to the abdomen. They should be permitted to take nothing but soup (strained •oatmeal or barley soup). Bouillon is also allowed. The patient may drink claret, either pure or diluted with water. Brandy and water may also be recommended. If the water is impure, it should be boiled for a little while in order to de- stroy the organisms and noxious substances contained in it. These measures sometimes prove sufficient. Laxatives are indicated if the disease has been preceded by over-feed- ing or constipation, or the intestine contains foreign bodies or worms, or is filled with fermenting and decomposed masses. The simplest remedy is castor oil, of which one to two tablespoonfuls may be taken, mixed with the froth of beer to disguise the taste. A single large dose of calomel is also effective (B Hvdrarg. chlorid. mite, pulv. jalap., sach. alb., aa gr. iij.). If the development of acute enteritis is dependent on worms, the calomel may be mixed with an anti-helminthic. After the administration of a laxative, the patient usually passes a few thin stools, and then the disease often recovers spontaneously. If the diarrhoea continues, we may order the following: B Pulv. ipecacuanh. opiat., Sacch. alb aa gr. ivss. One powder every three hours. B Tinct. opii, Tinct. valerian, aether aa 3 i. M. D. S. 15 drops t. i. d. B Bismuth subnitrat gr. viij. Opii gr. ss. Sacch. alb gr. v. One powder every three hours. We may also mention the following astringents: Acetate of lead (gr. £ every two hours); tannic acid (gr. iss. every two hours); nitrate of silver (gr. iss. : f iss,; glycerin, 3 iij.; one tablespoonful every three hours); alumen (gr. iss. every two hours); alumina acetica (gr. iss. : § iij. every two hours), etc. In catarrhal inflammation of the caecum, colon, and rectum, local DISEASES OF THE INTESTINES. 111 applications may be made. For this purpose, we employ a rectal tube, the posterior extremity of which is fitted with a rubber tube, about one to two metres in length, while the free end is provided with a glass fun- nel (vide Fig. 16). By means of this apparatus, large amounts of fluid Can be poured into the large intestine when the patient is lying on hia back; indeed, the fluid may pass the ileo-csecal valve and enter the small intestine. The pressure of the fluid can be varied at will by raising or lowering the funnel. It should be remembered that in the beginning, as a rule, no water flows from the funnel into the rectum; the flow be- gins only when rapid pressure has been made a number of times upon the rubber tube, in order to remove air from the rectum. Fig. 16. Fig. 17. Tunnel apparatus for intestinal infusion. After Hegar. Apparatus for intestinal infusion. After Korup. Korup recently constructed an apparatus which is shown in Fig. 17. It consists of an irrigator, the tube of which can be closed by a stop- cock. The tube enters a rectal bougie. A glass tube, which is con- nected with the inside of the irrigator, shows the amount of fluid in the latter. It is, perhaps, best to simply wash the rectum and then to follow with a weak solution of nitrate of silver (gr. iss. to viiss. : If pint of distilled water). Certain prominent symptoms require special treatment. If the pains are very severe, we may make a subcutaneous injection of morphine. This often relieves the diarrhoea, especially if peristalsis has been very vigorous. Other narcotics have also been recommended to relieve 112 unusually active peristalsis, viz., chloral hydrate, potassium bromide, and strychnine. In violent tenesmus and spasm of the anus, we may employ suppositories of morphine or belladonna. (J£ Morphin. hydrochloric., gr. ss.; 01. Cacao, q. s. ut fiant suppositoria No. iij. D. S. One supposi- tory two or three times a day. I£ Ext. Belladonnae, gr. f; 01. Cacao, q. s. ut f. suppositoria No. iij.) The etiology must also be taken into consideration. When the diar- rhoea is produced by malaria, it is rapidly cured by quinine (gr. xv.-xxx. every day in a single dose). Suitable treatment must also be adopted when the disease is associated with affections of the heart, the lungs, liver, etc. As a rule the patients must be carefully watched during convalescence. Strict diet should be maintained for a considerable time, and sometimes a woollen abdominal bandage should be worn to prevent catching cold. Appendix. a. Cholera morbus (Cholera nostras, G-astro-enteritis catarrhalis acu- tissima). 1. This term is applied to an acute gastro-intestinal catarrh of extreme intensity, whose symptoms are very like those of Asiatic cholera. As a rule, the disease begins in the latter part of summer (July, still more frequently in August and September), when the oppressive heat during the day is followed by cooler temperature at night. Isolated or sporadic cases are sometimes observed, but the disease also occurs in a sort of epidemic. Its causes are cold, errors of diet, ingestion of impure drinking water, spoiled meat or unripe vegetables. It is very probable that a certain part is played by infection with low organisms, but this has not been determined with certainty. 2. The first symptoms sometimes develop with extreme suddenness; sometimes there are prodromata, such as anorexia, nausea, and general malaise. The first symptoms often occur at night. The patients awake, com- plain of a feeling of pressure in the epigastrium, feel anxious, then ex- perience nausea and repeated vomiting. At first this expels the contents of the stomach, later biliary, yellowish-greenish, finally almost watery masses are vomited. At first tiie vomiting is usually easy. It occasion- ally occurs with such frequency that the patients vomit twenty to forty times within a few hours. At the same time or soon afterwards, the patients feel a rumbling and pain in the belly, and diarrhoea begins. At first the stools contain masses of the consistence of thick porridge, but the faecal character is soon lost. The stools become colorless, contain slireds of desquamated epithelium, lose the faecal odor—in short, they acquire the characteristics of the dreaded rice-water stools, such as are observed in the course of Asiatic cholera. The diarrhoea sometimes is so frequent that the patients use the vessel almost constantly. It is often extremely copious, so that we must assume an unusually vigorous transudation of fluid from the blood-vessels and a hyper-secretion of the intestinal mucous mem- brane. The clinical history acquires an almost specific character, from the symptoms of severe collapse which soon make their appearance. The skin is cool, sometimes covered with cold, clammy sweat, appears flaccid, DISEASES OF THE INTESTINES. DISEASES OF THE INTESTINES. 113 and occasionally can be lifted into permanent folds. The features are sunken, so that after a short time they are hardly recognizable. The nose becomes pointed, the eyes are situated deep in their sockets, and usually surrounded by a grayish ring, the expression is dull and apathetic, the eyelids are often half closed and the globe rolled upwards. The pulse is strong and extremely frequent, the heart sounds are very feeble. The patients speak in a feeble muffled tone, and the voice may some- times become falsetto. They complain of unquenchable thirst, throw themselves restlessly about, and often cry out suddenly on account of painful muscular spasms. These are observed most frequently in the calves, more rarely in the thighs, arms or abdominal muscles. Involuntary contractions of the muscles occur during the cramps. Diuresis is very much diminished or almost abolished. The urine often contains hyaline casts and albumin, and an extremely large amount of indican. As a rule, the disease does not last more than one to two days. The vomiting and diarrhoea diminish and finally cease, the skin becomes warm, the pulse stronger, the muscular pains disappear, the voice re' sumes its former timbre, a profuse excretion of urine occurs, and recov- ery ensues. Great feebleness often remains for days and weeks. A fata] termination hardly ever occurs except in children, old people, or other exhausted individuals. If the disease takes a fatal turn, the vomiting and diarrhoea usually cease, but the patients complain of distressing singultus, collapse in- creases, the pulse and heart sounds become imperceptible, and finally death occurs. 3. The diagnosis is usually easy; since Koch showed that the comma bacillus is always found in the stools in true Asiatic cholera, we can readily make the differential diagnosis between this and cholera morbus by the aid of the microscope. (For further particulars vide Yol. IV., Asiatic Cholera.) The symptoms of cholera morbus may sometimes be produced by poisoning by tartar emetic, arsenic, and corrosive sublimate, so that in suspicious cases the gastro-intestinal contents may be subjected to a chemical examination. 4. The preparations of opium enjoy great repute in the treatment of this disease: 1$ Opii, gr. ss.; sacch. alb., gr. v. M. f. p., d. t. d. No. x., one powder every two or three hours. ljf Tinct. Opii, Tinct. Valerian., ./Ether, aa f ss.; fifteen drops t. i. d. B Pulv. Ipecacuanh. co., Sacch. alb., aa gr. v.; one powder every two to three hours. In addition, the abdomen should be covered with a warm poultice, and hot bottles applied to the side of the body, if the skin feels cool and the patient complains of cold. The bottle should be covered with cloth, and not be so hot as to produce burns. Violent vomiting may be re- lieved by a subcutaneous injection of morphine in the epigastrium. In addition, pieces of ice may be given to diminish the thirst and vomiting. The muscular spasms can also be relieved most effectually by injections of morphine. In addition, the parts may be rubbed with cloths or spirits of camphor. To combat the collapse we may order brandy, port wine, champagne, in teaspoonful doses, or inject camphor subcutaneously (Camphor, gr. xv.; 01. amygdal., 3iij.; one syringeful t. i. d.). Bouillon is the only food which may be allowed, and even after re- covery the patient must exercise great care in diet for some time. 114 DISEASES OF THE INTESTINES. b. Acute gastro-intestinal catarrh of infants. I. Etiology.—The great mortality in children, particularly in large cities and during the summer months, is almost entirely owing to this disease. It seems to be the result of errors in nutrition, of certain develop- mental processes, or of certain miasmatic influences. Milk, the most natural article of food for infants, is very apt to undergo changes and to give rise to gastro-enteritis. In addition, the in- testinal tract of nursing infants is extremely sensitive. This hypersensi- bility is recognized by the fact that acute gastro-enteritis may be produced in infants at the breast as the result of mental excitement in the mother, although no change in the milk can be discovered in such cases. It should not be forgotten that the organization of the digestive apparatus in infants constitutes a predisposition to disease. Very little saliva is secreted, the fundus ventriculi is still imperfectly developed, and the muscular coat of the stomach does not possess much power. The principal cells of the stomach glands are but little developed, so that the gastric juice is poor in pepsin. Furthermore, the pancreas furnishes no glycogenic ferment until the end of the third month of life. Experience teaches that certain processes of development in infancy favor the development of acute gastro-enteritis. This category includes teething and weaning. In very many children the symptoms of acute gastro-enteritis occur with the eruption of each tooth. Diarrhoea is most apt to occur at the period of weaning, if the transition to mixed diet is undertaken too suddenly. Another very important form of acute gastro- enteritis is that which occurs in the hot summer months in the form of an epidemic, and is known as cholera infantum or summer diarrhoea. It is most frequent in August and September, more rare in July and October. If we bear in mind that the disease is found principally in badly ventilated and overcrowded houses, we will be inclined to assume the existence of miasmatic influences in this disease. II. Anatomical Changes.—The anatomical changes differ in no respect from those observed in acute gastro-enteritis of adults. In cholera infantum we often notice softening of the stomach (vide page 96). If the children have perished with choleriform symptoms, the blood often has a dark color and increased consistence, and the serous membranes are peculiarly dry, or present a soapy appearance. III. Symptoms.—The chief symptoms consist of vomiting and diar- rhoea. Sometimes one, sometimes the other begins first. At first the milk is vomited in caseous lumps. Later, it is thin and uncoagulated, because the stomach no longer produces sufficient acid to coagulate it. As collapse increases, the vomiting subsides, and singultus takes its place. The diarrhoea is sometimes so frequent that more than forty evacua- tions occur within the twenty-four hours. The yellow color of the normal stool is mixed with greenish parts, or the stools are entirely greenish, or they are yellow at first and become green after exposure to the air. Later they are apt to lose the biliary coloring, so that we find chiefly a watery fluid, at the most a few grayish, yellowish, or greenish specks and masses. Sometimes the stools become more consistent for a while, and occasionally have a brownish color, but often a very foetid smell. So long as the stools are not watery, they usually contain whitish or grayish-white shreds, which have been regarded as undigested frag- diseases of the intestines. 115 ments of casein, but Uffelmann showed that these are composed of drops of fat, or of bacteria, or of crystals of a combination of fatty acids and lime. The reaction of the faeces is almost always acid. The evacuations are often preceded by colicky pain; the children cry out aloud, and draw their legs upon the abdomen. The pains are not infrequently relieved by pressure on the belly. The abdomen is sometimes sunken, sometimes distended by gas in the intestines. Palpation sometimes reveals a peculiar sensation of fluctuation which corresponds to distention of the intestine with fluid. If the anus and thighs are soiled by the faeces, eczema intertrigo is often produced. Prolapsus of the rectum is occasionally observed. The appetite is often undisturbed, but the patients soon vomit the ingested food. Thirst is increased to an extreme degree. The excretion of urine often ceases. The mucous membrane of the mouth may be dry and hot, and covered with masses of sprue or with aphthae. If the disease, which occasionally ceases in one or two days, lasts for several days, the symptoms of severe collapse make their appearance. The extremities become extremely cold, while the trunk feels very hot. The fontanelles are depressed, the eyes are sunken in, and deep wrinkles appear in the face, which looks like that of an old man. The child becomes apathetic, and often lies with half-closed eyes; the eyelids are partly adherent by dry mucus, the cornea dries, may ulcerate, and even undergo perforation. (Edema sometimes develops, and extravasations of blood may occur into the skin and mucous membranes. Sometimes we notice the signs of objective dyspnoea, which have been attributed usually to thickening of the blood, but which Gerhardt explains by anaemia of the medulla oblongata. Death sometimes occurs after cerebral symptoms, convul- sions, muscular twitchings, delirium. This symptom-complex has also been called hydrocephaloid, because it is similar to the symptoms of acute hydrocephalus. Among the complications may be mentioned atelectasis of the lungs, broncho-pneumonia, and thrombosis of the sinuses. In favorable cases the rapidity of recovery is often astonishing. Children who to-day are struggling with death, to-morrow appear almost well. IV. Diagnosis.—The diagnosis of the disease is easy, but is only completed when the etiology is recognized. The physician should inves- tigate in detail the mode of nourishment, and should himself examine the various articles of food. V. Prognosis.—The prognosis is always serious, but of all the forma of gastro-enteritis, summer diarrhoea is the most dangerous. VI. Treatment.—We will first give a brief resume of the principles of rational nutrition of infancy. Nursing at the breast is the most natural and the best form of nutrition, but mothers who have not reached the age of eighteen years should not be allowed to nurse their children at the breast. We know from experience that their milk is not sufficiently nutritious and that lactation in very young mothers threatens the production of chlorosis and phthisis. Nor should nursing at the breast be carried on by mothers who present an hereditary family history of phthisis, cancer, or neuroses of all kinds. This is also true of mothers who suffer from chlorosis or infectious diseases. A syphilitic mother should not be allowed to nurse her healthy infant because the latter may be infected in this manner (vide Vol. IV., Congenital Syphilis). Nursing 116 DISEASES OF THE INTESTINES. is sometimes prevented by purely mechanical factors, for example, a poorly developed nipple which cannot be grasped by the child. As a matter of course, nursing must cease if the milk is produced in insuffi- cient quantities. During the first few months of life, the child should be nursed every two hours, later every three hours, the breast being first offered about six o’clock a.m., and not later than ten o’clock p.m. After each nursing the mouth should be carefully washed with a piece of linen which has been dipped in cold water, in order to prevent the retention and decom- position of the particles of milk in the mouth. During the period of nursing the mother should avoid excitement and also coitus, because these are apt to be followed by symptoms of gastro-enteritis in the infant. The mother should avoid fresh vegetables and acids as much as possible. Beer, eggs, milk, and farinaceous articles may be especially recommended. When pregnancy occurs, nursing should be discontinued because the mother’s milk becomes poorer, and in addition the maternal organism is incapable of properly fulfilling both functions. It is some- times found that the children do not thrive, although nothing abnormal can be detected in the mother. Some other mode of nourishment must be then adopted. However, the growth of the child cannot always be determined with the eye, and we must resort to the use of the scales. The child should be weighed once a week under exactly similar condi- tions. Immediately after birth the average weight of the healthy new born infant is 3,250 gm. Boys weigh about 120 gm. more than girls, and the children of a multipara 60 to 120 gm. more than those of a primipara. During the first three days after birth the weight diminishes about 300 gm. on account of the losses in the meconium, desquamation of the skin, and res- piration. The weight then slowly increases, and on the tenth day reaches the same figures as immediately after birth. During the first five months the infant increases 20 to 30 grammes daily, later from 10 to 15 grammes. The following table indicates the weight of the infant during the first year: Weight at hirtli, 3,250 grammes. Age. Daily increase in weight in gm. Monthly increase. Weight. 1st month 25 750 4,000 2d “ 23 700 4,700 3d “ 22 650 5,350 4th “ 20 600 5,950 5th “ 18 550 6,500 6 th “ 17 500 7,000 7th “ 15 450 7,450 8th “ 13 400 7,850 9th “ ... 12 350 8,200 10th “ 10 300 8,500 11th “ 8 250 8,750 12th “ 6 200 8,950 If for any reason the mother is unable to nurse the child, a wet-nurse fur- nishes the best substitute. In selecting a wet-nurse, we should be guided by the same principles as in determining whether the mother should be permitted to nurse her child. The difference in age between the mother’s child and that of the wet-nurse should not exceed two months. 117 DISEASES OE THE INTESTINES. When nursing at the breast is impracticable, we must resort to nutrition with animal milk or substitutes for milk. The chemical constitution of mother’s milk is compared with that of animals in the following table: Mother’s milk. Asses’ milk. Cow’s milk. Goat’s milk. Water 889.08 890.12 864.06 844.90 Solid matters 110.92 109.88 135.94 155.10 Casein 89.24 35.65 55.15 55.14 Fat 26.66 18.53 36.12 56.87 Milk sugar 48.64 50.46 38.03 36.91 Salts 1.38 5.24 6.64 6.18 Asses’ milk resembles mother’s milk more closely than other varieties, but practically we may only choose between cow’s milk and goat’s milk. The former is preferable, but water and sugar should be added to it, in order to make it re- semble mother’s milk more closely. It is important that those who superintend the feeding of the infant, should know that red litmus paper is quickly turned blue by mother’s milk, and that lime-water should be added to cow’s milk, until the reaction produced by it upon litmus paper approximates that pi’oduced *by mother’s milk. Cow’s milk sometimes'has an acid reaction, even when taken di- rectly from the udder. The milk should be boiled as soon as received, and then one to two tablespoonfuls of lime-water added, particularly in summer, in order to avoid acidification. It should always be given to the infant at the temperature of the body. It may be warmed by placing a bottle of milk in a vessel of hot water. When it has reached the proper temperature, a sufficient amount of lime-water should be added, and then enough water to dilute the milk by half (during the first month). The dilution should be gradually diminished so that the child takes pure milk after the fifth month. In addition, the milk should be well sweetened with sugar. The milk should be given in the same way, with regard to quantity and time of administration, as has been recommended witli regard to nursing at the breast. After being used, the bottle and nipple should be carefully washed in salt and water, and then kept in pure water until again required. The children should not be' permitted to keep the nipple in the mouth as a “ soothing measure.” But despite all these precautions, the digestion of cow’s milk is often difficult, as is shown by the fact that the faeces of children who are fed with cow’s milk have a cheesy, whitish-yellow appearance, while in children who are nursed at the breast, the faeces have a uniform yellow color. This difference is still more marked when the infant is fed with goat’s milk. Artificial feeding with substitutes for milk is only indicated when good milk cannot be obtained, since it favors the development of diarrhoea and rachitis. These substitutes may also be employed temporarily in gastro-enteritis. We may recommend Nestle’s food, Biedert’s cream mixture, Swiss condensed milk, Lie- big’s infant’s food, Lcefiund’s food, and Beneke’s leguminous soup. Healthy children should be gradually weaned at the age of nine months. Weaning should be delayed if the child is teething, or if infantile diarrhoea is rife in the neighborhood, or during the hot summer months. The milk should be gradually mixed with weak bouillon, later bouillon mixed with egg may be given at mid-day, and a very soft boiled egg may be given in the morning or after- noon; also cocoa, crackers, or wine. Finally, we may give raw scraped meat or ham. If gastro-enteritis has developed, no milk should be given to the child for twelve to twenty-four hours. In its stead we may order water which has first been boiled, and then allowed to cool, mixed with claret or brandy. The milk should be permanently withheld, if it was not well tolerated previously or if the symptoms do not diminish in three to four days despite proper treatment. In its stead, we may give Nestled or Faust’s food, barley-water, sago, or arrow-root. Raw scraped meat or mutton, and beef-tea are often very useful. Beef-tea is prepared in the 118 DISEASES OF TIIE INTESTINES. following manner: Fresh lamb or beef is cut into small pieces, eight times the quantity of water is added and allowed to stand for a half an hour. It is then covered, placed in a bottle in hot water and the latter allowed to boil. The meat is then squeezed, the fluid strained through a cloth, and a little salt or sugar added. It should be prepared fresh three times a day. Among medicinal agents, antifermentatives produce the best effect. We prefer calomel (gr. } every two hours); in violent vomiting creasote (gr. f, spirit dilut. gtt. x., decoct, rad. salep. 3 iiiss., one teaspoonful every two hours). Carbolic acid (gr. iss. to gr. viiss.: 3 ij., one teaspoonful every two hours), resorcin (gr. viiss : § iiiss., one teaspoonful every two hours), and benzolum have also been recommended. If the diarrhoea is very violent, the administration of astringents must be resorted to. The best in our opinion is nitrate of silver (gr. viss., aq. destil. 3 iij., glycerin fss., one teaspoonful every two hours). With regard to other remedies we refer to page 110. Preparations of opium should not be given to nursing infants. This is often done perhaps without bad effects, until finally poisoning is produced despite every pre- caution, as we have observed in a number of cases. •We may also recommend treatment with eneinata of nitrate of silver (gr. iij. to gr. viiss. at a dose). Hydropathic compresses to the abdo- men are often employed, if the temperature of the trunk is very much increased. Small doses of hydrochloric acid (gtt. viij. : 3 iijss., one teaspoonful every two hours) are occasionally indicated when the vomit- ing of uncoagulated milk indicates a deficiency of acid in the stomach. Threatening collapse may be combated by subcutaneous injections of camphor (gr. xv.; 01. amygdal. 3 iij. M. D. S. One-quarter of a syr- ingeful), champagne and port wine. 2. Chronic Intestinal Catarrh. Enteritis Catarrhalis Chronica. I. Etiology.—Chronic enteritis either develops as such from the start, or it follows acute enteritis if attacks of the latter recur with unusual frequency, or appear before the previous attack has entirely sub- sided. In the latter cases the etiology of chronic enteritis is the same as that of the acute form. But even that form which runs a chronic course from the start is hardly ever the result of other causes, unless cer- tain etiological factors have a tendency to favor the development of chronic rather than of an acute intestinal catarrh. These include partic- ularly conditions of stasis (diseases of the portal vein, hepatic diseases, chronic affections of the respiratory or circulatory organs) and general diseases (pulmonary phthisis, malaria, and cachectic diseases), it must also be mentioned that the presence of infusoria in large numbers in the large intestines keeps up, if it does not give rise to, a chronic catarrh. II. Anatomical Changes.—As a rule, the color of the mucous membrane is livid or reddish-brown, and the large veins are generally unusually full. If the catarrh has lasted for a long time, the mucous membrane not infrequently has a slate-gray color, owing to the fact that the blood pigment in previous extravasations of blood is converted into melanin. This is generally most abundant at the apices of the villi and around the lymph follicles. The mucous membrane and submucous tissue are often thickened, and many of the lymph .follicles are enlarged. In some cases the in- creased thickness is the result of hyperplasia of the connective tissue. DISEASES OF THE INTESTINES. 119 The muscular coat may also take part in the hyperplastic process. It is thickened three to four fold, and traversed by fan-like bands of con- nective tissue. The serous layer in places presents tendon-like thicken- ings and opacities. The tissue of the mucous membrane sometimes un- dergoes hyperplasia to such an extent as to give rise to the formation of polypi (enteritis polyposa). Lebert describes a case in which numerous polypi were present throughout the entire large intestine. Occlusion and cystic dilatation of the glands are sometimes observed, and are associated occasionally with the formation of polypi (enteritis polyposa cystica). Hyperplasia of the muscular coat sometimes produces stenosis. This is observed most frequently near the ileo-coecal valve, but also at the sig- moid flexure and at the outlet of the rectum. In the chronic enteritis of children, however, the mucous membrane is not infrequently pale, and the intestinal walls are remarkably thin and atrophic. Atrophic changes in the glandular apparatus may also be observed under the microscope. The hypersecretion of the mucous membrane gives rise to the forma- tion of a serous, sometimes of a mucoid or pus-like fluid, which is found upon the inner surface of the membrane. Among the sequelae of chronic enteritis the most important are ulcerative processes of the mucous membrane. One form is the result of direct ulceration, the other is produced by suppuration of the lymph follicles. The former may be called catarrhal ulcers of the intestine, the latter follicular ulcers. In catarrhal ulceration the changes generally begin with superficial epithelial losses of substance. These are originally round or lentil-shaped and gradually spread in depth and circumference. On account of the coalescence of adjacent ulcerations the ulcer finally becomes irregularly jagged. The adjacent mucous membrane is often undermined. Strips of mucous membrane sometimes extend into the ulcer from its edges, and occasionally isolated islets of mucous membrane remain within the ulcer. Polypoid proliferations are sometimes noticeable at the edges. There are numerous terminations and complications of catarrhal intes- tinal ulcers. The least important is the formation of pus which attends the development of the ulcer. More serious dangers arise when larger vessels are involved in the destructive process, since violent hemorrhage may then be produced. In other cases the destructive process spreads deeper and deeper and gives rise to perforation and perforation-peritonitis ; or if this occurs in parts of the intestines which are destitute of a peritoneal cover- ing, faecal abscesses develop. Under certain circumstances these may ex- tend to the cervical region, and death occurs after symptoms of pyae- mia. Perforation is prevented not infrequently by the formation of adhesions to adjacent loops of intestine or to other organs ; or an encap- sulated peritonitis is produced, into which the perforation first occurs. If perforation of intestine finally occurs, despite previous adhesions, abnormal communications are formed, for example, with other loops of intestine, the bladder, vagina, stomach, or gall-bladder, or large abdom- inal vessels may be eroded (aorta, vena cava, portal vein, etc.). If the adhesion has formed between the intestine and the anterior abdominal wall, an external intestinal fistula may be produced. Ulcers in the rectum may give rise to inflammation of the surrounding cellular tissue (peri- proctitis). The most favorable termination is cicatrization. The cicatricial tissue is often pigmented and retracted to such an extent that the edges of the ulcer are almost in contact with one another. As a matter of course, 120 DISEASES OF THE INTESTINES. the lumen of the intestine is thus narrowed, and serious symptoms of intestinal stenosis may be produced. Follicular intestinal ulcers are situated chiefly in the colon. They are sometimes so numerous that the mucous membrane appears to Ixj perforated almost like a sieve; they may also be very numerous in the rectum. We have previously stated that the lymph-follicles become enlarged in enteritis. This enlargement is the result, at first, of an inflammatory serous infiltration, but later of a cellular proliferation. The mutual pressure of the cells first gives rise, in the middle of the follicles, to necrosis and cheesy degeneration, then to softening and rupture externally. The middle of the follicle at first appears opaque, yellowish and cheesy. Later we find a sharply-defined, crater-like ulcer with raised edges. The ulcerative degeneration continues to spread, soon passes beyond the solitary follicles and extends to the mucous mem- brane. The coalescence of adjacent ulcers gives rise to irregular but sharply-defined losses of substance, whose edges are undermined over considerable areas. The edge of the mucous membrane is often bent into the base of the ulcer. Vitreous, gelatinous masses are found not infrequently in the ulcers, similar to those which are observed in the stools during life. The complications are the same as those of simple ulcers of the mucous membrane. III. Symptoms.—Changes in the stool constitute the most important symptoms of chronic intestinal catarrh. As a rule, we notice constipation, or there is irregularity in the evacuations, so that constipation alternates with diarrhcea. Chronic diarrhoea is rarely observed, although cases are known in which it has lasted twenty years. Sometimes several thin stools are passed only in the morning, and many patients experience the desire to go to stool while still in bed. The evacuation sometimes con- tains undigested articles of food, not infrequently a large amount of pus and mucus. Indeed, at times, faecal matter is entirely absent in the passages, and these consist solely of mucus and pus. This is especially true of catarrh of the large intestine, particularly the rectum. A slight admixture of blood is sometimes observed. The mucus sometimes forms cylindrical moulds of the intestine. These may be more than one-half metre in length, or they have a flat- tened, tape-like shape (enteritis membranacea). This sometimes occurs only at times, perhaps at intervals of months or years. Occasionally it continues for a long time; it is most frequent in middle life, rare in old people or children. In these moulds Da Costa found •mucin and some- times traces of albumin. Alcohol and carbolic acid produce retraction of the masses. Bjoernstroem found that they were composed of a structureless substance, which contained a few free nuclei, epithelium, and small drops of fat. This form of disease is found especially in hysterical and hypochondriacal individuals. The passage of the membranes is often preceded by violent pains and loud rumbling in the abdomen. Chronic intestinal catarrh of childhood is sometimes associated with stools which contain fat (diarrhcea adiposa.) The stools have a fatty gloss, smell strongly of fatty acids, and are grayish-yellow or reddish-gray in color. Under the microscope they are found to contain numerous large drops of fat. In healthy faeces the fat drops are scanty and small in size. Biedert found from 3.8-20.3 per cent of fat in the faeces of healthy infants, and 41.17-67 per cent in fatty diarrhoea. The latter seems to develop when the duodenum is affected to a marked degree and interferes with the passage of bile and pancreatic juice into the intestines, since these fluids cause DISEASES OF THE INTESTINES. 121 an absorption of fats in the intestine. Demme also found parenchyma- tous and interstitial inflammation of the pancreas. Fatty diarrhoea of children, however, should not be regarded as a special disease. The microscopical examination of the fasces should not be neglected in chronic intestinal catarrhs. A good idea of the impairment of diges- tion is easily obtained from the greater or lesser abundance of particles of food in the evacuation. The patients complain not infrequently of borborygmus and cutting pains in the abdomen, which appear sometimes after meals or shortly before an evacuation. Many patients also suffer from flatulence, which may be so severe as to produce disturbance of breathing, palpitation of the heart, and a rush of blood to the head. These symptoms are partly reflex, partly the result of mechanical inter- ference with the movements of the diaphragm. The discharge of flatus usually produces great relief. In many cases my attention has been attracted by slowness of the pulse. If the inflammation extends to the •stomach we also find coated tongue, a bad taste in the mouth, anorexia, singultus, etc. Emaciation and pallor of the skin soon make their appearance. In addition, the patients are greatly worried about their condition, become dissatisfied with themselves and those about them, and fall into a condi- tion of hypochondria and melancholy. The latter may become intensi- fied into insanity. Chronic enteritis may affect the entire intestine or single parts. In the latter event the colon and ileum are most frequently affected at the same time. Chronic duodenitis is generally associated with chronic gastritis, and is recognized only by the accompanying jaundice. Isolated ileitis cannot be recognized during life. The symptomatology given above holds good for the combination of ileitis and colitis. Inflammation of the rectum (proctitis) not infrequently gives rise to tenesmus, though not so severe as in acute enteritis. The stools may be also entirely purulent (proctitis blenorrhoica). It may be associated with inflammation of the surrounding connective tissue, and sometimes gives rise to prolapse and eczema around the anus. Dilatation of the haemorrhoidal veins is often observed. Proctitis chronica and haemorrhoids may be the results of the same primary disease, for example, cirrhosis of the liver; or the catarrh causes looseness of the mucous membrane, and thus favors the development of haemorrhoids; or,* finally, the dilatation of the rectal veins gives rise to proctitis. Chronic enteritis lasts months and years; sometimes a lifetime. The disease is dangerous to life in children and old people, rarely in vigorous adults. Children grow weak, emaciate, and finally die from dropsy and marasmus, sometimes from intercurrent bronchitis, broncho- pneumonia or thrombosis of cerebral sinuses. In old people, death occurs with signs of increasing exhaustion. (Edema of cachectic char- acter, or unilateral oedema from marantic thrombosis, sometimes appears as the precursor of death. Catarrhal ulcers of the intestines are often latent during life. ISToth- nagel attaches great importance to the presence of pus in the stools. Great significance has also been attached to the appearance of swollen sago-like grains in the stools. These were regarded as an accumulation of intestinal secretion in the follicular ulcers. But, apart from the fact that these little lumps are also observed in simple enteritis, Virchow 122 diseases of the intestines. showed that they are composed of swollen starchy matters from the food. The presence of shreds of the mucous membrane in the stools is a positive indication of intestinal ulceration, but this is a very rare event. Atten- tion should also be paid to localized pain, circumscribed peritonitis, hemorrhages, and symptoms of perforation of the intestine. In rectal ulceration, mucus, pus, and blood will often adhere to the examining finger, and the fasces are not infrequently surrounded by these products. It should be remembered that diarrhoea is by no means present in all cases of ulceration of the intestines. IV. Diagnosis.—This is not difficult, except with regard to accurate localization. The diagnosis is not complete until the etiology has been recognized. V. Prognosis.—Chronic enteritis is often a very obstinate affection. Profound mental depression is an especially grave complication. The disease produces direct danger to life in children and old people. The prognosis is also unfavorable when the primary disease cannot be re- lieved. VI. Treatment.—If constipation is present, we should order mild laxatives: R Aloes, Ext. rhei comp aa gr. xxiiss. Pulv. et succ. liq q. s. ut fiant pil. No. xxx. D. S. Two to four pills to be taken at night. R Aloes, Ext. rhei comp., Jalapse aa gr. xv. Pulv. et succ. liq q. s. ut fiant pil. No. xxx. D. S. Two to four pills at night. R Pulv. liq. comp § i. D. S. One to two teaspoonfuls at night. Numerous other laxatives have been recommended, which it is un- necessary to mention. Many patients resort to household remedies: a glass of cold water every morning before breakfast, smoking a cigar early in the morning, stewed fruit, etc. Many resort to the use of bitter waters, for example, Ofener (Hunyadi- Janos, Franz Josef, or Victoria), Pullnaer, Saidschuetzer, Friedrichs- liall, and Sedlitzer bitter waters. One to two wdneglassfuls may be taken early in the morning; and half an hour later, a glass of cold water. In marked atony of the muscular coat of the intestines, I have seen good results, in a number of cases, from massage of the abdomen. Not in- frequently obstinate constipation is relieved by faradization of the intes- tines (vigorous current, one electrode upon the lumbar spine, the other firmly pressed upon the abdomen, and applied labile for three or ten minutes; or one electrode is introduced five to ten cm. into the rectum, the other as before upon the abdomen; daily sittings). If diarrhoea is present, we may order the preparations mentioned on page 110. A strict milk diet has produced recovery in a number of cases of diarrhoea which had lasted for years. Mineral waters may be very useful in chronic intestinal catarrh. When obstinate constipation is present, we may recommend the alkaline saline waters (Marienbad, Franzensbad, Rohitsch, Steiermark, Tarasp). The salt waters of Kissingen and Homburg also merit favorable men- 123 tion. If there is a tendency to chronic diarrhoea, we may resort to the alkaline saline waters of Carlsbad, Ems, or Vichy, or the warm sodium chloride wells of Wiesbaden and Baden-Baden. In such cases, good results are sometimes obtained from the earthy mineral waters (Wildun- gen, Waldeck, Lippspringe). Many patients are improved or cured by cold-water treatment, a trip to the mountains, or a sea voyage. The grape cure is not without benefit in many cases. Due attention should be paid in treatment to the etiology. If infusoria are found in the stools we should make daily intestinal infu- sions with lukewarm water, and then inject a dilute solution of bi- chloride of mercury (gr. iss. : 3 x.).' Appehdix. Phlegmonous inflammation of the intestine (enteritis phlegmonosa, s. submucosa, s. purulenta) possesses merely an anatomical interest. It gives rise to diffuse purulent infiltration, or to the formation of abscesses in the submucosa, sometimes in the muscular coat. In Bellfrage’s case, in which the jejunum was affected, the diseased part was 18 cm. in length. Rupture externally results in peritonitis. If the process is situated in the rectum, it may be followed by periproctitis. The disease is usually secondary to typhoid, tubercular, dysenteric, or cancerous ulcers. 3. Inflammation of the Caecum and Vermiform Appendix and Sur- rounding Parts. Typhlitis, Perityphlitis, and Paratyphlitis. I. Etiology.—Inflammation of the caecum and vermiform appendix is known as typhlitis, inflammation of the peritoneal coat, as peri- typhilitis and inflammation of the retrocaecal (retroperitoneal) cellular tissue, as paratyphlitis. Inflammation of the caecum is produced most frequently by faecal stasis (coprostasis). The faeces act as an irritant and give rise to inflam- mation. More rarely this is the result of the ingestion of sharp foreign bodies, or of ulcerative changes in the mucous membrane. Faecal stasis is more apt to develop in the caecum, because the small intestine enters it almost at a right angle, and because in this part the faeces first undergo a marked increase in consistence. In addition, the faeces must pass directly upwards along the ascending colon. The danger becomes greater if the muscular coat of the intestine is enfeebled by previous catarrhal or other disease of the caecum. In many cases, also, we notice errors of diet and irrational habits of life. Individuals who pursue sedentary occupations are predisposed to stasis of faeces in the caecum. Injury to the right iliac fossa sometimes seems to produce the disease by giving rise to a paralytic condition of the muscular coat of the intestines. Inflammation of the vermiform appendix is due to the same causes as inflammation of the caecum. The retention of foreign bodies and faeces in the vermiform appendix may be aided by its abnormal anatomical structure, or by previous dis- ease. The entrance to the appendix is surrounded by a valve-like pro- jection, the excessive development of which may prevent the exit of substances which have entered it. Biermer and Bossard found that catarrhal inflammation of the vermiform process is not infrequent If DISEASES OF THE INTESTINES. 124 DISEASES OF THE INTESTINES. this affects the muscular coat, it interferes with the discharge of its con- tents and favors stasis. The pieces of faeces contained in the appendix are sometimes ex- tremely hard (enteroliths). Enteroliths are divided into two classes, true and false, according as we have to deal with very hard masses of faeces or with earthy deposits (carbonate and phosphate of lime and magnesia). True enteroliths are often laminated, and not infrequently contain a foreign body. They should not be mistaken for gallstones, which may also enter the csecum and vermiform appendix. Enteroliths are usually round or elongated in sh;ipe. The following are the results of chemical analysis by Aberle and Schuberg: Aberle. Schuberg. Water, ..... . 22 57.3 Ammonia magnesia phosphate, 4.3 24.4 Calcium phosphate, o . 60.5 6.7 Calcium sulphate, . . . , 1.1 1.3 Alcohol-ether extract, . 0.3 0.8 Other organic substances, . 11.3 9.2 It may finally be mentioned that typhoid, phthisical, and catarrhal ulcers may be restricted to the vermiform appendix. As a rule, paratyphlitis is a secondary disease. The primary form has been attributed to cold, and I have seen a number of cases which re- sulted from violent bodily exertion. According to Kraussold, walking the tight rope is a frequent cause of perityphlitis and paratyphlitis in children. Secondary paratyphlitis generally follows inflammation of the caecum; but the inflammation may extend from more remote parts, since the cellular tissue extends to the kidneys, into the pelvis, the abdo- minal wall, and inguinal ring. Thus, paranephritis and parametritis may give rise to paratyphlitis. The latter may also be secondary to psoitis, diseases of the pelvic bones, and even to spinal caries. In some cases the disease isa metastatic inflammation. This is observed in pyaemia and puerperal fever, more rarely in certain infectious diseases, such as typhoid fever, articular rheumatism, and measles. Perityphlitis is like- wise secondary to inflammation of the caecum and vermiform appendix in the majority of cases. The disease rarely extends from adjacent or- gans, for example, in oophoritis, salpingitis, and perimetritis. Primary perityphlitis after cold or injury does not often occur. These forms of inflammation are often associated with one another. They are observed much more frequently in men than in women, and usually from the ages of fifteen to twenty-five years. II. Symptoms.—Typhlitis, paratyphlitis, and perityphlitis give rise to pain and swelling in the right iliac fossa, and to disturbances of diges- tion. Typhlitis—we choose typhlitis stercoralis as an illustration—some- times begins slowly, sometimes suddenly. In the former event, it is sometimes preceded for days by signs of disturbed digestion, constipa- tion alternating with diarrhoea, cutting pains in the right iliac region, eructations, nausea, and loss of appetite. If the disease begins suddenly,, the immediate causes can often not be demonstrated. The patients complain of intolerable pain in the right iliac region, which is increased on the slightest movement or pressure. In order to relieve the tension of the abdominal walls and to diminish the violence of the pain, the patient assumes a passive position of the body (upon the right side, with the body bent forwards and the right thigh drawn upwards). 125 DISEASES OF THE INTESTINES. The fever sometimes exceeds 39° C., the pulse is correspondingly accel- erated, usually small and hard. The features express pain, and, after the disease has lasted for a few days, the eyes are sunken; the tongue may be clean or coated; speech is often whispering, as in peritonitis. The patients often suffer from annoying singultus; vomiting occurs in many cases, sometimes of the contents of the stomach, sometimes of biliary matter, sometimes of masses which have a faecal appearance and odor. Such cases are especially grave, since they indicate impermeability of the intestines. While anorexia is complete, thirst is usually increased. Sleep is almost always restless and disturbed. The right iliac region is generally more prominent than the left, and not infrequently forms a distinct tumor beneath the abdominal walls. Palpation reveals an increased feeling of resistance, and usually a more or less distinctly circumscribed tumor. This is generally elongated, ex- tends diagonally upwards above Poupart’s ligament, is sometimes smooth, sometimes nodular, and may occasionally be indented. It is very sen- sitive on pressure. There is dulness on percussion over the tumor. The abdomen is often tympanitic, and the diaphragm is pushed up- wards. The upper border of the liver is unusually high, and the apex of the heart is situated in the third and even in the fourth intercostal space, often to the outside of the right nipple line. The urine is gene- rally scanty and concentrated. It contains an increased amount of indi- can (vide page 80). The bowels are constipated, or a few thin passages first occur, and then obstinate constipation follows. Recovery often occurs with great rapidity if the masses of faeces can be removed from the intestines. If this does not happen, ulcerative processes develop in the caecum, and may give rise to paratyphlitis or perityphlitis, more rarely to perforation-peritonitis. Death may also occur from ileus or from rupture of the intestines, as the result of exces- sive distention by faecal masses and gas. Ulceration of the caecum may be followed by the formation of cica- trices, the retraction of which may give rise to stricture. Inflammation of the vermiform process produces almost the same symptoms as that of the caecum, but it usually begins more suddenly and violently. The tumor is less extensive, oris altogether absent. Vomiting of faeces is not observed in uncomplicated cases, and meteorism is usually absent. The percussion sound over the iliac fossa remains tym- panitic. The disease gives rise to perityphlitis more frequently than to paratvphilitis. Not infrequently we find perforation of the appendix and signs of perforation-peritonitis. The perforation is sometimes pre- vented for a time by peritonitic adhesions to the omentum or adjacent loops of intestines. The destruction of the vermiform process is some ■ times annular; indeed, the outer part may be entirely separated and fall into the abdominal cavity. The inflammation-producing foreign body then enters the peritoneal cavity, so that it is often difficult on autopsy to discover the corpus delicti. In some cases the ulcers cicatrize. If they are very numerous, the entire organ may obliterate. If only a few are present, occlusion may occur only at the entrance of the appendix. This may result in the gradual accumulation of a serous fluid, which may distend the organ to the size of a fist. In paratyphlitis, we find a very painful tumor in the right iliac fossa which appears to lie dee.p down, because it is surrounded by air-contain- ing loops of intestines. On gentle percussion over the region of the caecum a tympanitic note is heard. Dulness is only produced when the 126 DISEASES OF THE INTESTINES. finger is pressed in deeply. The pains often radiate into the back, shoulders, right hand, or leg. The right testicle is sometimes drawn spasmodically upwards, and some patients complain of dysuria. At times obstinate erections are observed. The patients complain not in- frequently of formication and coldness of the right leg, and weakness of this limb sometimes remains long after the other symptoms have disap- peared. This is evidently the result of pressure of the exudation upon the nerves of the lower extremity. (Edema of the right leg must be explained in a similar manner. In the most favorable event, the exudation is entirely' absorbed. Under less favorable circumstances, the inflammation extends to the pararenal connective tissue, to the cellular tissue of the pelvis, rectum, or groin, and the pus finally perforates externally, or into the bladder, uterus, rectum, or vagina, or appears beneath the groin. The pus may also break through the abdominal walls, the perforation being preceded occasionally by erysipelas, or extensive gangrene of the skin. If there is a communication at the same time with the caecum, an intestinal fistula is produced. Cases have been reported in which the pus perfo- rated the pleural or pericardial cavities. In some of these cases the paratyphlitis subsides, and the sequelae alone remain. In some cases the abscess ruptures into the caecum, colon, or abdom- inal cavity. This is followed by symptoms of gangrene and pyaemia, or perforation-peritonitis. In perityphlitis, the peritonitic symptoms predominate. The tumor in the right iliac fossa is extremely sensitive, and very superficial. Gentle percussion reveals dulness, but this is mixed with a tympanitic sound, on account of the subjacent colon and caecum. Gerhardt noticed peritonitic friction murmurs (Beath-Bright friction murmur) on auscul- tation and percussion. The dangers include rupture of the pus ex- ternally, or into internal organs, erosion of the vessels and internal hemorrhage, thrombosis of the mesenteric veins with subsequent pylephlebitis, hepatic abscess, pyaemia. Encapsulated exudations in the right iliac fossa sometimes persist for months, even for years, and on slight provocation may suddenly give rise to an acute exacerbation. The duration of typhlitis, paratyphlitis, and perityphlitis is extremely Variable. Typhlitis stercoralis not infrequently terminates in a few days, while paratyphlitis and peritypliilitis may extend over months. Improvement is sometimes followed by unexpected relapse, perhaps from very trifling causes, such as incautious movement of the body, straining at stool, etc. The disease exhibits a marked tendency to re- lapse. In one patient I observed the symptoms of perityphlitis five times within one and a half years. III. Diagnosis.—These three affections often pass into one another and their differential diagnosis may be impossible. They should be distinguished from the following conditions : a. Simple coprostasis in the caecum in which inflammatory symptoms are absent, b. Intestinal cancer. This affects older individuals and runs a slow, chronic course, c. Invagination. Muco-bloody evacuations are here observed, d. Floating kidney, when situated in the right iliac fossa. This is determined by the shape of the kidney, its mobility, and sometimes by the perceptible pulsation of the renal artery, e. Biliary and renal colic. Jaundice or haematuria is present, the pains are inter- mittent and situated higher up. /. Cold abscess in caries of the spine and pelvic bones. Changes are found in the spinal column or the pelvis. DISEASES OF THE INTESTINES. 127 g. Psoitis. Disturbances of digestion are absent, h. Tuberculosis and cancer of the mesenteric and retro-peritoneal glands. Nodular and mov- able tumors are found. IV. Prognosis.—The prognosis in inflammation of the caecum is much more favorable than in that of the vermiform process, paratyph- litis, and perityphlitis. The three latter affections always present a very grave prognosis, and we must be prepared to find that the disease runs a very slow course. V. Treatment.—Prophylactic measures must be directed towards securing regular evacuations from the bowels, especially in individuals who have already suffered from these diseases. In typhlitis stercoralis, we should employ intestinal infusion in order to remove the contents of the gut. At first the infusion should be repeated every hour until a copious discharge of faeces results. As much water should be injected each time as the intestines are capable of holding. Even after copious evacuations, a tumor not infrequently remains for a time in the right iliac fossa, dependent in part upon an inflammatory, serous infiltration of the intestinal walls. We place less reliance on the internal use of laxatives, especially in cases which have lasted for some time, because intestinal peristalsis is thereby made excessive. This may prove injurious in advanced inflam- mation. In paratyphlitis and perityphlitis, and in inflammation of the vermi- form process, we should order absolute rest, fluid food, and give large doses of opium (0.03 every hour or two) until the tenderness is distinctly less; in addition, light warm poultices to the right iliac fossa. If the opium produces constipation, the bowels should be evacuated every other day by means of intestinal infusion. If a circumscribed and fluctuating tumor is demonstrable, it should be opened and treated according to surgical principles. Willard Parker recommended the fifth to twelfth day of the disease as the most suitable for operation. If the infiltration is diffuse and not fluctuating, an incision should not be made. We should then endeavor to produce resolution by warm poultices, iodine applica- tions, potassium iodide, iodoform (gr. 45, vaseline § iss.) ointment, or blue ointment. The inunction should be made very gently, in order to avoid starting up fresh inflammation. It is better to apply the ointment constantly to the part by means of a strip of flannel. Repeated blisters have also been recommended. 4. Stenosis and Occlusion of the Intestines. Enterostenosis and Ileus. I. Etiology.—The symptoms of intestinal occlusion are sometimes preceded by those of stenosis. The causes of both conditions depend upon changes in the intestinal contents, the intestinal walls, or adjacent organs. Occasionally the symptoms are produced by simple stasis of faeces (coprostasis). This may occur in habitual constipation, or may develop acutely after errors in diet, for example, after an excessive meal of grapes, etc. In some cases, the disease results from foreign bodies in the intes- tines, particularly gall-stones and enteroliths. Whether occlusion may be produced by coils of round worms has, to say the least, not been positively proven. Occlusion by gall-stones is more frequent than is generally believed. The obstruction is sometimes the result of the size of the stone, sometimes of its unfavorable position. Calculi which have 128 DISEASES OF TIIE INTESTINES. passed through the biliary passages will not necessarily pass unimpeded through the much wider intestinal canal. In the first place, the biliary passages are capable of very marked dilatation, and, in addition, a large stone may pass directly into the intestines, through a fistula between the gall-bladder and colon, more rarely between the gall-bladder and duodenum. Finally, several gall-stones may be united into a large mass by means of the faeces. Enteroliths may attain a weight of four pounds and a diameter of twenty-three cm. In one case, Niemeyer found thirty-two stones, which weighed two and a half pounds. Friedlaender described a case in which the foreign body, which had given rise to intestinal occlusion, was com- posed of shellac, and similar concretions were found in the stomach. Their entire weight was thirty-two ounces. The patient was a drunkard, and had been in the habit of drinking an alcoholic solution of shellac. Foreign bodies which have passed through the anus into the rectum, may also give rise to intestinal occlusion. Changes in the intestinal walls which give rise to stenosis or oc- clusion may be the result of structural changes, disturbances of inner- vation or displacement (torsion, invagination, internal and external hernia). Among the structural changes may be mentioned neoplasms which either proliferate into the lumen of the canal or interfere with the dilatability of the intestinal wall. Even hemorrhoids, particularly inter- nal ones, may give rise to symptoms of intestinal stenosis. Cicatrices are not infrequently the cause of stricture of the intestines. This is par- ticularly true of dysenteric cicatrices, while it is extremely rare after typhoid ulcers. A similar condition may also follow catarrhal, follicu- lar, and tubercular ulcers. In the rectum, it is occasionally observed as the result of syphilis. Disturbances of innervation of the intestinal wall, followed by symp- toms of stenosis or occlusion, are sometimes central, sometimes periph- eral in their origin. Obstinate constipation, followed by enterostenosis and ileus, occurs occasionally in diseases of the brain and spinal cord. Symptoms of ileus, which can only be explained by partial paralysis of the muscular coat of the intestines, have been observed after injury of the abdomen, the reposition of external hernia, and in peritonitis. Among the dislocations of the intestines, the most important is invagination or intussusception. This is the most frequent cause of ileus in childhood, and about one-fourth of the cases occur between the third and twelfth months. The lumen of the intestine is not infrequently occluded by torsion upon its own long axis or around the axis of its mesentery, or by the knotting of one loop of intestine around another loop, thus inter- fering with the lumen of the latter. In addition, a loop of intestine sometimes enters an opening or abnormal fissure, where it becomes incar- cerated and impermeable (internal hernia). This is observed in abnormal fissures in the omentum, suspensory ligament of the liver, round ligament of the uterus, fissures in the blad- der or uterus, perforation of the intestine itself, operative injury of the peritoneum. In this cateory are also included so-called internal hernia in the strict sense of the term (hernia diaphragmatica, duodemo-jejunalis, re- troperitonealis anterior, caecales, iliaco-subfascialis, etc.). External hernia3 also give rise to occlusion of the intestines as soon as they become incarcerated. DISEASES OF THE INTESTINES. 129 Dislocation of the intestine sometimes occurs as the result of abnor- mal torsion in consequence of previous peritonitic adhesions. Abnormal ligaments may also act in the same way, most frequently after peritonitis. A loop of intestine sometimes slips beneath a ligament, and is con- ctricted, sometimes the ligament first forms a loop into which the intes- tine falls; finally, a free ligament may surround the intestines like a bandage. In the latter way, intestinal occlusion is sometimes prod need by the normal vermiform appendix, or by diverticula of the intestines. Finally, intestinal occlusion is produced by diseases of adjacent organs, such as tumors of the pelvis, uterus, ovaries, bladder, and other abdom- inal viscera, by peritonitic exudations, and movable abdominal organs. A loop of intestines, which is distended by faeces, sometimes presses so strongly upon an adjacent loop that the latter becomes occluded. This may also be the result of a very fat mesentery. Uterine pessaries have also been known to give rise to occlusion of the intestine. Intestinal stenosis and occlusion occur at every age, but the period of life exercises a certain influence on the character of the obstruction. In children, we have to deal chiefly with invagination, or at the most, with stenosis from torsion on the axis, or intestinal polypi, while certain other forms, for example, occlusion by gall stones, have never been ob- served in childhood. Coprostasis plays a prominent part at an advanced age. As a general thing, men are more frequently affected than women, and the disease is more often found among the laboring classes than in those who pursue sedentary occupations. According to Lingen, torsion of the axis of the intestine is frequent in St. Petersburg. He explains this on the ground that the Russians have an especially long intestine, on account of the abundant ingestion of vegetables. According to Leichten- stern, there is one case of intestinal occlusion among three hundred to five hundred cases of death from all causes. According to Fagge, the percentage is 1.4. II. Anatomical Changes.—If the lumen of the intestines is inter- rupted at any point, the part above the site of occlusion becomes dis- tended from the accumulation of intestinal contents, and is also unusually convoluted, while the portion beneath the site of occlusion is empty and contracted. If the obstruction is situated in the duodenum, the stomach and oesophagus may take part in the dilatation. Immediately above the occlusion, we find firm or semi-solid masses; higher up, fluid and gas. The intestinal walls may be so tense as to rupture. If the occlusion occur acutely, the intestinal walls appear transpar- ent, thin, and pale ; if the changes are chronic, the muscular coat of the upper portions of the intestine are hyperplastic. This is a compensatory process which develops because the passage of faeces through the nar- rowed part requires unusual force. If the power of the muscular coat is paralyzed, there is danger of complete occlusion as the result of faecal stasis. Necrotic and ulcerative changes may be found in the intestinal mucous membrane above the stenosis, as the result of mechanical irrita- tion by firm scybala. Bloody suffusion of the mucous membrane and serous layer is often found in the immediate vicinity of the site of occlu- sion. Signs of circumscribed or diffuse peritonitis are often present. Per- foration-peritonitis, furthermore, is not infrequent, and renders it very difficult to unravel the mechanical processes connected with the occlu- sion. Among the changes in the other organs we may mention the frequent 130 occurrence of foreign-body pneumonia, as the result of entrance of vom- ited matters into the air passages. The organs are often extremely dry, as the result of the abundant losses of water in the vomited matters. In invagination (intussusception), one portion of the intestine is found shoved into another. Two varieties of intestinal invagination are recog- nized—the agonal and vital. The former presents no clinical interest. It is observed most frequently in children who have suffered from intes- tinal catarrh and cerebral diseases. It is generally multiple, can usually be replaced with readiness by pulling upon both ends of the intestines, and inflammatory symptoms are entirely absent. This form is probably owing to the fact that towards the end of life the various sections of the intestines die with varying rapidity, so that a portion which is still in active motion can readily force itself into an adja- cent motionless one which has already perished. It is almost always observed in the small intestine, and may be ascending or descending. Vital invagination is almost always descending. Indeed, the occur- rence of ascending invagination has been altogether denied, but Jones describes a case in which the descending colon passed into the transverse colon. At the point of transition of the entering portion into the emerging portion of the intestine, is formed the lower or inner angle of flexion, while the transition of the emerging portion and of the sheath (envelop- ing portion of the intestine) is known as the upper or outer angle of flexion. This forms the so-called neck of the invagination. It is readily understood that not only the intestine, but also the mesentery is invagi- nated. The latter is compressed by the sheath and tjms exercises a cer- tain traction upon the invaginated intestine, so that the latter is curved within the sheath, with its concavity towards the mesentery. The invag- nation acts injuriously in two ways: by narrowing or occluding the lumen of the intestine, and by producing circulatory disturbances in its walls. Thus the invaginated portion may become necrotic, and be evacuated with the fseces. This sometimes results in natural recovery. In other cases it is followed by dangerous hemorrhage; or perforation occurs, because the peritonitic adhesions at the neck of the invagination are not sufficiently firm ; or a portion of the intestine is cast off beyond the region of intussusception. Finally stenosis may again develop on account of increasing cicatricial contraction at the site of lesion. In incomplete intestinal invagination, only a small portion of the circumference of the intestine is implicated. Invagination has a tendency to increase. For if stasis of fseces de- velops above the site of occlusion, the weight of the faeces will favor an increase of the invagination. The increase always takes place at the ex- pense of the sheath. This is rolled inwards to a greater and greater extent so that the parts which are situated next to the neck are converted into emergent intestine, and the outer angle of flexion is moved down- wards. The invaginated portion of the intestine sometimes pro- trudes from the anus. Cases have been reported in which the prolapsed portion was one-half metre in length. Multiple invagination is very rare. A double or even a triple invagination is sometimes found at the site of the lesion. It is occasionally found that a portion of the intes- tine forces itself from below between the sheath and outer part of the invaginated gut, so that there is, to a certain extent, a combination of descending and ascending invagination. The following table is furnished by Leichtenstern: DISEASES OF THE INTESTINES. DISEASES OF THE INTESTINES. 131 479 invaginations : Ileo-caecal invaginations, . 212 (44 per cent) Ileum invaginations, 142 (30 “ ) Colon invaginations, . . 86 (18 “ ) Ileo-colon invaginations, . 39 ( 8 “ ) 479 Occlusion of the intestine by twisting on its axis around the mes- entery develops most frequently at the sigmoid flexure, because the mesentery is here extremely narrow and at the same time very long and movable. Much more rarely we find twisting of the axis of the entire small intestine with the exception of the duodenum or a few loops of intestines. Among seventy-six cases of torsion of the axis Leichtenstern found At the sigmoid flexure, . . 45 cases (59 per cent) At individual loops of the ileum, 23 “ (30 “ ) At the entire small intestine, . 8 “ (11 “ ) Occlusion of the intestine, bv the development of a knot between the loops, is found most frequently at the sigmoid flexure which twists around the loops of the ileum. Torsion on its own axis occurs most frequently in the ascending colon. III. vSymptoms.—The chief symptoms in stenosis and occlusion of the intestines are disturbances in the passages from the bowels; in the former they are impeded, in the latter they cease entirely. In many cases the sole symptom of stenosis is unusual constipation. Even this may be absent, if the patients take only easily digested food and eschew vegetables, bread, and other feculent articles of food. Any error of diet may give rise to great danger and convert the stenosis into complete occlusion. Some cases are associated with chronic diarrhoea. This is observed not infrequently in syphilitic or cancerous stricture of the rectum. The faeces not infrequently assume a peculiar shape, particularly when the stenosis is situated at the end of the large intestine. They are flat, ribbon-shaped, or broken off short, or resemble the fseces of goats or sheep. A furrow may be found in one part, particularly in cases of polypi. It should be remembered, however, that faeceg of this character are observed occasionally in other conditions, particularly in inanition. In some cases, constipation is associated with pain, the result of me- chanical irritation of the site of stenosis by the faeces. This is especially true of stenosis of the large intestine. If the lesion is situated at the outlet of the rectum, the act of defecation is apt to be attended with great pain. Hemorrhoids often develop in such cases as the result of venous stasis in the hemorrhoidal veins. On examination of the abdomen, we sometimes find it markedly dis- tended as the result of accumulation of faeces and gas in the intestines. Vigorous peristalsis is not infrequently visible, and the intestinal move- ments are often accompanied by borborvgmus. The faeces which are accumulated above the stenosis can often be felt through the abdominal walls. The obstruction itself is sometimes felt as a prominence, hard- ness, or circumscribed site of tenderness. Examination through the rectum and vagina should never be omitted. 132 DISEASES OF THE INTESTINES. Stenosis of the rectum is often felt directly on palpation, or by means of the sound. Sometimes, however, stenosis is simulated from the fact that the tip of the sound catches in a fold of mucous membrane or in the promontory of the sacrum. Less reliable results are obtained by ex- amination with the speculum or intestinal infusion. The capacity of the rectum is so variable that no reliable conclusions can be drawn from the amount of water which may be injected. In some cases it is advisable to examine the rectum by the introduction of the entire hand and fore- arm. This requires the administration of chloroform, and a careful introduction of the hand, in order to prevent rupture of the rectum. The combined method of examination may be employed in resorting to vaginal examination, the fingers of the outer hand being placed upon the abdominal walls. We have already remarked that the signs of stenosis sometimes pass suddenly into those of intestinal occlusion (ileus). There are three prominent symptoms of ileus, viz., the absence of evacuation from the bowels, or of the passage of flatus, and vomiting o*f faeces. It is readily understood that defecation does not occur in occlusion of the intestines. Evacuation of faeces, occasionally even diarrhoeal in character, may be observed in the beginning, before the intestinal con- tents, which are situated below the site of occlusion, have been entirely evacuated. For this reason we must be cautious in giving a prognosis, even if the enema produces an evacuation of fasces after the previous absence of defecation. But if flatus is again discharged, we can usually feel certain that the intestine is again permeable, unless considerable air has been pumped into the lower part of the intestine during the intro- duction of the enema. Vomiting is an almost constant symptom of in- testinal occlusion. The vomited matter consists at first of the contents of the stomach, and finally assumes a faecaloid or faecal character. On microscopical examination of the vomited matter, we find debris of food, granular detritus, desquamated epithelium cells; according to Betz, the greenish vomited matter contains algse. It is erroneously held by some that faecal vomiting occurs only in occlusion of the large intestine, but this can be readily disproved. Faecal vomiting sometimes ceases after the disease has lasted for a long time, and the vomited matters then consist of rice-water like masses mixed with flocculi; this is evidently owing to the fact that all the faecal masses situated above the occlusion have been removed. Towards the end of life, vomiting sometimes ceases entirely and gives way to sin- gultus. The objective abdominal changes are similar to those described in stenosis, but as a rule they are more marked. The palpation of any tumor which may be present is accompanied by pain. In addition, we often notice colicky pains which may be associated with vigorous peri- staltic movements. Diuresis is very scanty and occasionally almost entirely abolished. Great importance must be attached to the amount of indican in the urine. It is increased in occlusion of the small intestines, unchanged in occlu- sion of the large intestines (in the absence of peritonitis which in itself increases the amount of indican). This is owing to the fact that indi- can is derived chiefly from indol, which forms during the pancreatic digestion of the albuminoids in the intestine and passes off in great part with the fasces. If the small intestine is impermeable, almost all of the DISEASES OF THE INTESTINES. 133 indol is absorbed by the blood, and the indican is then excreted in the urine (vide page 80). As a rule, the severity of the disease is soon shown in the general condition. Collapse occurs with great rapidity, the face becomes cool, the eyes are sunken and surrounded with blue rings, the nose becomes peaked, the patients exhibit a peculiar restlessness, the temperature may be normal or irregularly increased, sometimes almost subnormal. The pulse is usually small but regular, more often accelerated than slowed. If the vomiting is very profuse, eholeriform symptoms develop. The skin loses its roundness, the extremities feel as cold as ice, even cramps in the calves may be produced. The sensorium is often unclouded until the end of life. A fiecal odor is sometimes emitted from the mouth of the patient. Death sometimes occurs in a very short time (to a certain extent, as in cases of shock), probably as the result of anaemia of the brain. In rarer cases, the disease lasts for several weeks, until death occurs from exhaus- tion. Death may also be the result of suffocation, if the excessive accum- ulation of gas in the intestines pushes upwards the diaphragm, lungs, and heart to an extreme degree. In a third series of cases, intercurrent accidents terminate the scene; for example, rupture of the intestine above the stenosis and perforation-peritonitis or general peritonitis start- ing at the site of stenosis. If the loop of intestine becomes adherent to the abdominal walls, perforation may occur through the latter with the formation of an artificial anus. Two loops of intestines sometimes be- come adherent, and communicate with one another by means of a fistula, and in this way restore the permeability of the intestinal canal. A fis- tula sometimes forms between the intestine and uterus, bladder, etc. Finally, intestinal occlusion may be attended with the symptoms of pyaemia. The gut ruptures into an encapsulated peritonitic exudation (faecal abscess); through the agency of the mesenteric veins this gives rise to metastatic abscesses in the liver, occasionally to emboli in the lungs. Recovery is not frequent. It may occur spontaneously or as the re- sult of treatment. It is recognized by the reappearance of flatus and defecation, the cessation of vomiting, and gradual restoration of strength. At the same time tumors, concretions, foreign bodies, and unusually large faecal masses are sometimes found in the stool. The symptoms of intestinal invagination require special consideration. The disease not infrequently begins with a sudden colicky pain in the ab- domen. This is soon followed by thin mucous, and particularly bloody stools. We not infrequently feel an elongated, smooth, firmly elastic tumor, which is most frequent near the right iliac fossa, because ileo-caecal invagination is the most frequent form of the disease. The patency of the anus has often been regarded as a very valuable sign of invagination. Bloody, mucous masses sometimes trickle constantly from the anus. The finger is readily introduced into the rectum, thus showing that we have to deal with paralysis of the sphincter. Not infrequently, however, the patient complains of tenesmus. Hirschsprung attaches importance to the fact that the rectal folds are smooth or drawn upwards. The invaginated part can sometimes be reached by digital examination of the rectum. The originally muco-bloody diarrhoea is very often followed in a short time by symptoms of occlusion, and these prove fatal as in occlu- sion from other causes. Muscular spasms and convulsions occur not infrequently towards the end of life. A sort of natural recovery occurs 134 DISEASES OF THE INTESTINES. in rare cases from spontaneous exfoliation of the invaginated part of the intestine. Sometimes the exfoliated portion passes off in small shreds, in other cases in the shape of the larger part of the intestine (three metres in length in Cruveilhier’s case). Spontaneous exfoliation occurs most frequently from the eleventh to the twenty-first days. It is often preceded by stinking, bloody stools. In the most favorable cases it is followed immediately by recovery. In others, intestinal hemorrhage, rupture or perforation-peritonitis develops, or renewed symptoms of stenosis occur after apparent recovery. The duration of the disease depends upon the degree of stenosis. If the occlusion is complete, life will only be prolonged for a few days, although Kussmaul reports a case in which the symptoms of ileus lasted twenty-three days. In intestinal stenosis, life may be prolonged for months, even for years. Exfoliation of the invagination sometimes does not occur until after the lapse of months. Invagination presents a great tendency to relapse. (In Senator’s case a replaced invagination recurred nine times in seven- teen days.) IV. Diagnosis.—With regard to the location of the lesion special attention should be paid to the results of the external and internal ex- amination of the abdomen. Great importance should also be attached to the amount of indican in the urine (increased in occlusion of the small intestine, unchanged in occlusion of the large intestine), but in such cases we should be able to exclude peritonitis, since this in itself may increase the amount of indican in the urine. It is also said that in occlusion of the small intestines the symptoms run a more rapid course. The vomiting and pain are more violent, the meteorism is slighter or entirely absent, the nervous symptoms predominate, and diuresis is diminished or abolished. With regard to the character of the obstruction, the diagnosis is easy if the lesion can be reached from the rectum or vagina, or if we have to deal with incarcerated external hernia. The diagnosis can also be made post hoc, if tumors, foreign bodies, etc., appear in the stools, and at the same time the signs of occlusion cease. Invagination is often recognized with facility. It occurs usually in children in whom muco-bloody stools are passed, and the anus is patent. The previous history will enable us to determine whether the occlusion is the result of coprostasis. But we will rarely be able to ascertain with certainty whether an ileus is the result of internal incarceration or vol- vulus of the intestine. The signs of ileus (vomiting of faeces, constipation, and absence of flatus) are sometimes observed, although stenosis of the intestine is not found on autopsy. The symptoms of occlusion may be mistaken for: a, the action of certain poisons, for example, arsenic. The diagnosis depends on the history, examination of the vomited matter, and the objective abdomi- nal symptoms, h, Cholera, c, Peritonitis, in which the causes of the inflammation are only revealed on autopsy. V. Prognosis.—As a matter of course, this is much more favorable in stenosis than in occlusion of the intestines; in the latter disease it is very grave The bad prognosis should not, however, lead us to fold our hands and leave the patient to his fate. VI. Treatment.—In the treatment of intestinal stenosis, the chief weight should be attached to dietetic measures. The food should be of such a nature as to be readily digested and absorbed (milk, eggs, bouillon, meat, brandy, beer, wine). In addition, care should be taken DISEASES OF THE INTESTINES. 135 in the mastication of the food. A daily evacuation from the bowels should be secured (vide p. 122). Certain forms of stenosis may be relieved by operation, for example, in cancer of the rectum and polypi by removal of the obstruction, or in stricture of the rectum by gradual dilatation. If the signs of occlusion follow coprostasis, as large an amount of water as the intestine will hold should be injected (at first every two hours) until a copious evacuation follows. Then this should be repeated two or three times a day, and in addition cathartics should be given internally. For example: R Inf. sennse comp., §vi.; Natri sulph., 3 vi. M. D. S. One tablespoonful every two hours. 3 01. croton., gtt. iij.; 01. ricini, §i.; Gummi arab., 3 ij-; ft. c. aq. destil., q. s., emulsio, fvi.; Syr. Sennae, 3 vi. M. I). S. One tablespoonful every two hours. The first injections are often ineffective because a certain length of time elapses before the lowermost masses of faeces are softened. Hard masses, which are felt above the anus, can often be removed by the finger. In some cases it is advisable to push the rectal tube through the masses of faeces. In invagination, the intestine should be quieted as quickly as possible by large doses of opium (gr. ss. every hour in adults until the pupils are distinctly contracted), and then large amounts of water should be in- jected into the rectum to relieve the invagination. The infusion may be repeated three or four times a day. Distention of the large intestine with gas may also be attempted. This is done most readily by means of a rectal*bougie which is connected with the bulb of a Richardson ether spray, care being taken that the bougie is introduced as far as possible into the rectum. Ziemssen recommended distention of the large intestine by means of carbonic acid gas, which is produced by the combination of tartaric acid and sodium bicarbonate. This required about 3 vi. sodium bicarbonate and 3 v. tartaric acid. These substances, dissolved in water, should be introduced into the rectum in small portions in order to prevent sudden distention. If the invagination has extended to the lower part of the large intes- tine, we may attempt to replace it by means of an oiled flexible sound. As relapses occur not infrequently, it may be necessary to retain the sound for some time in the anus. If the invagination cannot be re- placed, abdominal section may be resorted to, but the operation only offers chances of success if it is performed as early as possible, and peritonitic adhesions are not present. Among twenty cases of lapa- rotomy in intestinal invagination of children, there were six recoveries. In all forms of intestinal occlusion, the sites of external hernia should be carefully examined, and in cases of incarceration of external hernia, these should be replaced or relieved by operation. If we have reason to assume torsion of the intestine or internal strangulation as the cause of an existing intestinal occlusion, the greatest chances of success are afforded by the operation of laparotomy at as early a period as possible. Instead of laparotomy, some authors recommend the formation of an artificial anus, enterotomy, above the site of occlusion. This operation seems to be preferable when peritonitis—which interferes very materially, if it does not render impossible, our search for the obstruction—may be assumed to be present. The artificial anus should not be made too large, so that it may be readily closed by an obturator. 136 Schramm collected the statistics of 199 laparotomies which were performed for intestinal occlusion from various causes, and in which 122 cases proved fatal (61 per cent). Since the introduction of Lister’s method of treatment, there were 65 deaths (53 per cent), among 122 laparotomies. In the majority of cases, however, the cause of the occlusion remains undiscovered during life, or the patients do not consent to an operation. With the aid of the antiseptic mode of treatment, the surgeon is often tempted, even when the cause of occlusion is unknown, to perform lapa- rotomy and to search for the obstruction to the intestine, but the difficulty of the undertaking should not be underestimated. It is usually extremely difficult to unravel the mass of distended and twisted loops of intestines; at all events, laparotomy should not be performed if peritonitic symp- toms are present. When we are restricted to purely internal measures of treatment, we should recommend chiefly the administration of large doses of opium, while the administration of cathartics, which is recommended by some writers, is, in our opinion, very dangerous. Calm has recently claimed that he repeatedly succeeded in relieving the symptoms of ileus after copious injection of the stomach with water, and thus removing the con- tents of the stomach and intestines above the stenosis. The stomach should be washed out from three to four times a day. The patient should not be allowed to drink much water, and thirst should be relieved by the ingestion of pieces of ice. Even in recent times, reliable physicians have recommended the ad- ministration of large amounts of mercury (five to ten ounces, »even as much as two lbs.), and in desperate cases this may be employed as a dernier ressort. We should not fail to attempt to relieve the obstruction in the in- testine by repeated infusions of water and enemata of air into the rectum. I may also mention that in one case in which all methods of treatment had been adopted for almost a week without success, so that the patient was about to be sent to the operating-room, faradization of the intestine produced a copious evacuation from the bowels at the end of three min- utes (one pole in the rectum, the other, labile, upon the abdominal walls, particularly near the caecum and colon); recovery was permanent. In less favorable cases, faradization should be repeated three or four times a day. At all events, in the treatment of ileus no plan of treatment should be left untried. 5. Round Ulcer of the Duodenum (Ulcus Duodeni Pepticum). I. Etiology.—The round duodenal ulcer has the same origin as the round gastric ulcer, that is, the mucous membrane is digested by the digestive juices, after circulatory disturbances in the tissues. The ulcers are almost always found above the entrance of the ductus choledochus and ductus pancreaticus. This is explained on the ground that the gastric juice which has entered the intestinal canal with the food re- tains its acid reaction and digestive power, only until it reaches the parts mentioned, while lower down it becomes inactive. In one case, Merkel observed embolism as the cause of the circulatory disturbance. Billroth calls attention to the development of duodenal ulcer in septicaemia, and is inclined to attribute such ulcers to the same cause as the duodenal ulcers, which occur not infrequently after burns of the external integu- DISEASES OF THE INTESTINES. DISEASES OF THE INTESTINES. 137 ment. The latter occur usually from the seventh to seventeenth days, occasionally on the second day, after the accident. Very slight burns are sometimes sufficient to produce duodenal ulceration. Congelation is also said to be an occasional cause of duodenal ulcers. Some writers have also associated them with erysipelas, pemphigus, and waxy degeneration of the intestinal vessels. Ulcerative changes of an embolic character are observed even in the new-born, and explain certain cases of melaena neonatorum. The male sex is affected more frequently than the female. II. Anatomical Changes.—In the mucous membrane we find sharply-circumscribed losses of substance, the edges of which are terrace- shaped and free from inflammation. The ulcers are situated generally in the upper horizontal, rarely in the descending part of the duodenum. They sometimes extend from the duodenum to the mucous membrane of the pylorus. They are usually single, more rarely multiple. Peptic ulcers are very rarely found in other parts of the intestine, and then must also be attributed to interference with the circulation which per- mits the action of the digestive ferments upon the mucous membrane. Duodenal ulcers are characterized by a tendency to perforation or fatal hemorrhage. The erosion may affect the pancreatico-duodenalis, gastro- epiploica or hepatic arteries, the portal vein and vena cava. Sticli de- scribed perforation into the aorta, and abnormal communication with the gall-bladder has also been observed. Cicatrization results quite often in stenosis of the duodenum, followed by dilatation of the stomach and oesophagus. Cicatricial occlusion of the ductus choledochus and ductus pancreaticus with chronic jaundice have been observed when the ulcer was situated at the point of entrance of the ducts. HI. Symptoms and Diagnosis.—The symptoms may be so similar to those of round gastric ulcer that it is hardly possible to differentiate them during life. The most prominent symptoms are pains in the epi- gastric region, especially on the right side, tenderness of the abdominal walls, vomiting, hsematemesis and enterorrhagia. The ulcer occasionally develops in a latent manner, and death results quickly after sudden symp- toms of perforation-peritonitis, or intestinal hemorrhage. In making a differential diagnosis between round gastric and duodenal ulcers we should notice whether the pain is most marked on the right side, and whether intestinal hemorrhage occurs repeatedly, but hsematemesis not at all. Some attach great importance to the fact that in round gastric ulcer the pain develops very soon after meals, while not infrequently three to four hours elapse before the occurrence of pain in duodenal ulcers. IY. The prognosis and treatment are the same as in round gastric ulcer. (Vide p. 73.) 6. Intestinal Cancer. I. Anatomical Changes.—Cancer of the intestines is generally primary. It is less frequently secondary to cancer of adjacent organs, extending to the intestinal walls by contiguity ; in very rare cases it is metastatic. Primary cancer of the intestine has a tendency to spread in a ring shape, giving rise to stenosis or stricture, which is sometimes so marked that a lead pencil cannot be passed through the narrow portion. In rare cases we find isolated nodules. The cancer may be scirrhus, medullary, or colloid. Colloid is relatively frequent in the rectum, in which pigment cancer (melanocarcinoma) is also observed in rare cases. The gross appearances depend in great part on the microscopical 138 DISEASES OF THE INTESTINES. structure. Sometimes we find white, dry, and crumbling, or more juicy masses; sometimes a tumor which is infiltrated with a yellowish or brownish colloid fluid ; sometimes, finally, the cancer forms a callus- like, firm, almost cartilaginous thickening of the intestinal walls. Me- lanocarcinoma has a coal-black appearance. The cancerous changes sometimes extend to the muscular coat and serous membrane. The mus- cular coat is thickened, infiltrated with a meshed connective tissue; it also contains white bands of cancer. If the cancer lias given rise to stricture of the intestines, the gut above the stenosis is found dilated and filled with fseces and its walls are thickened. Below the stenosis the gut is empty and its walls thin. The intestinal walls may rupture if the tension has been excessive. Cancerous stenosis may disappear on account of partial degeneration of the growth, which passes olf iu the evacua- tions. In such places cicatricial tissue may form and, according to Kokitansky, a sort of spontaneous recovery may occur in this way. The degeneration of the tumor is associated not infrequently with considera- ble danger. Sometimes it gives rise to very violent hemorrhage, or per- foration of the intestine occurs, or the adjacent organs become adherent by peritonitic adhesions and perforation then occui*s into such organs. In this way the intestine may communicate with the bladder, vagina, and uterus, or, in rare cases, an external faecal fistula forms. Sometimes the perforation occurs into the retroperitoneal cellular tissue, giving rise to a faecal abscess and then to pyaemia. Primary cancer may be confined to the intestine ; in other cases it spreads to adjacent organs, especially those situated in the pelvis, or finally metastases form in the lymphatic glands. Cancer is most frequent in the rectum, particularly at the transition into the sigmoid flexure; next in the flexure itself and the points of flexion of the colon. It is rare in the small intestine, relatively frequent in the duodenum, partic- ularly at the point of entrance of the ductus choledochus or at the origin of the duodenum, into which it usually extends from the pylorus. Among 34 cases of intestinal cancer (exclusive of cancer of the rec- tum) collected by Koehler, 22 were situated in the large intestine, and 12 in the small intestine. II. Etiology.—Intestinal cancer is more frequent in males than in females, and as a rule, develops after the age of forty years. In rare cases it is observed in childhood. (Wiederhofer reports two cases in in- fants of three and sixteen days respectively.) III. Symptoms.—These are sometimes so indefinite that a diagnosis is impossible during life. The patients complain of pain in the abdomen, often in a circumscribed spot. They suffer from irregular evacuations, usually constipation, more rarely diarrhoea. Emaciation and marasmus develop, but the cause of the disease is only discovered on autopsy. In other cases ileus suddenly develops, errors of diet occasionally being the immediate cause. In cancer of the lower part of the large intestine, the first symptom is intolerable pain in the sacral region, radiating into the genitals and the distribution of the sciatic nerves. The chief symptoms are demon- stration of a tumor and changes in the stools. If the cancerous tumor can be reached through the abdominal walls, it is usually found as a nodular, elongated, roundish tumor. In some cases this attains the size of a fist, or even more. It is generally sensitive on pressure, but, unlike coprostasis, it cannot be indented on pressure. It may be either mova- ble or immovable. DISEASES OF THE INTESTINES. 139 Its mobility sometimes depends upon the part to which it is attached, or upon the development of peritonitic adhesions. When situated in the small intestine or transverse colon, it occasionally presents an extraordi- nary degree of mobility. Since these parts of the intestine are rendered heavier by the tumor, they often sink very deep in the abdominal cavity. Hence the majority of intestinal cancers are found below the umbilicus. Very great variations are sometimes found, at brief intervals, in the distinctness with which the tumor is felt. Furthermore, in examinations at different times, we often notice a remarkable change in the size of the growth as the result of varying distention and position of other loops of intestine. The tumor gives a dull tympanitic percussion sound, but the pleximeter must be firmly pushed into the abdominal walls. Rectal cancer is particularly accessible to examination through the rectum. Sometimes we find an annular, usually smooth stenosis of the rectum, sometimes ulcerated nodulated surfaces. On combined exami- nation (one hand upon the abdominal walls), the changes are often recognized more distinctly. The finger, on its withdrawal, is usually found covered with foul-smelling muco-purulent, and often bloody fluid. Suspicious debris may also be examined under the microscope (vide page In rare cases, prolapse of the rectum occurs. When the cancer is situated very low down, it may become visible to the eye. In other cases, the rectal speculum may be employed, although this usually gives rise to great pain. The stools may be changed with regard to amount, shape, and consti- tution. In the majority of cases there is obstinate constipation. Cooper Foster reported a case of constipation lasting eighty-eight days in colloid cancer of the descending colon. The constipation sometimes ceases quite suddenly, and is followed by frequent evacuations. This must be attrib- uted to ulceration of the cancer and relief of the stenosis, or to the for- mation of a fistulous communication between the stenotic part of the intestine and lower parts. The faeces sometimes become flattened and tape-like, or are voided in small round lumps like the faeces of a sheep. Violent intestinal hemorrhage is observed in some cases. In others, the stools contain ichorous, mucous, muco-purulent, or bloody masses, in which particles of cancer are occasionally seen. All other symptoms are unreliable (pain, emaciation, and increasing cachexia). Special symptoms, dependent upon the situation of a cancer, are ob- served in not a few cases. In duodenal cancer, which is situated near the papilla of the ductus choledochus, obstinate jaundice is produced, while in cancer of the first part of the duodenum, the signs of stenosis of the pylorus become evident. In rectal cancer, the general condition remains good for a very long time. The evacuations may be followed by the most violent pains, so that many patients retain the stool as long as possible. Obstinate diar- rhoea occurs not infrequently. Thin, ichorous masses, mixed with blood, may trickle constantly from the anus. There is often very marked dila- tation of the hsemorrhoidal veins, and indeed we must be on our guard against mistaking the disease for bleeding piles. The duration of the disease may extend to four years. In one of my cases death occurred at the end of the fifth year. Some patients die from increasing marasmus. Occasionally, secondary cancer in the liver or other organs is the real cause of death. In some cases, the symptoms of intes- tinal stenosis and ileus give rise to the fatal termination. This may also 140 DISEASES OF THE INTESTINES. result from perforation of the intestine, the development of faecal ab-> scesses, with pyaemia, or abnormal communication with other organs. IV. Diagnosis.—In not a few cases the diagnosis is impossible; in many others, extremely difficult. Cancer of the rectum and sigmoid flexure alone is easily recognized if a digital examination of the rectum is performed. If the tumor can be felt through the abdominal walls, it may be mis- taken for faecal stasis (which does not always disappear after the admin- istration of cathartics, especially if they are not repeated daily for a number of days), tumors of the stomach, pancreas, liver, lymphatic glands, kidneys, omentum, or encapsulated peritonitic exudations, etc. The diagnosis is rendered positive by the discovery of elements of cancer in the stools, but this occurs very rarely. Fig. 18. Microscopic appearance of a spontaneously desquamated, intestinal polypus, in a girl set. 10 years Enlarged 275 times. Y. Prognosis.—The prognosis is bad, although it has been improved by modern surgery. VI. Treatment.—The treatment of intestinal cancer belongs to surgery rather than to internal medicine. Internal remedies are indi- cated only when secondary deposits in other organs render an operation useless. We should order a nutritious diet, which will give rise to the minimum amount of faeces; milk, eggs, meat, beer, wine, soup. If con- stipation is present, we may give mild laxatives or enemata; if the pain is violent, subcutaneous injections of morphine, or, in rectal cancer, sup- positories of morphine or belladonna. If there is an ichorous discharge from the rectum, the large intestine should be washed daily with an in- fusion of water, to which is added kalium hypermanganicum (one per cent), or liq. alum, acetic. ( 3 i. : 1 iij. One teaspoonful to a glass of water). DISEASES OF THE INTESTINES. 141 Appendix. The other neoplasms of the intestines are interesting to the anatomist or surgeon rather than to the physician. a. Polypi.—We may find pedunculated fibromata, which start from the submucosa, or mucous polypi, dependent chiefly on proliferation of the mucous glands. They are situated most frequently in the rectum, immediately above the sphincter, are single or multiple, and are found particularly in children, in whom they produce diarrhoea and muco- purulent discharges. The polypi sometimes protrude from the anus during evacuation. The faeces sometimes present a furrow, which has been produced by the tumor. The polypi are occasionally separated from the pedicle during defecation, and are then voided, giving rise to slight hemorrhage. Large growths sometimes give rise to intestinal in- vagination, or to sudden stenosis. b. Lipomata may give rise to the same symptoms as polypi, but are much rarer. c. Angiomata, myomata, sarcomata, and cystomata of the intestines have also been observed. 7. Animal Parasites of the Intestines. Helminthiasis. Animal parasites in the intestines are included either among the pro- tozoa or the worms. Among the former, we distinguish rhizopods and infusoria, among the latter flat worms (platodes) and round worms (ne- matodes). ■ The following list includes those parasites which possess a practical interest: First Group. Protozoa. Rhizopods. Amoeba coli. Infusoria. Cercomonas intestinalis. Trichomonas intestinalis. Balantidium coli. Second Group. Worms. Flat worms. Platodes. Taenia solium. Taenia saginata. Bothriocephalus latus. Round worms. Nematodes. Ascaris lumbricoides. Oxyuris vermicularis. Trichocephalus dispar. Anchylostomum duodenale. Trichina spiralis. PROTOZOA IN THE INTESTINES. There are hardly any differences in the clinical symptoms produced by the various forms of protozoa in the intestine. They are almost always found in individuals who suffer from chronic diarrhoea, more frequently in typhoid fever patients. The relation of protozoa to the diarrhoea has not been positively 142 DISEASES OF THE INTESTINES. determined. In some cases, the diarrhoea ceases afiier the protozoa have been removed from the intestine by the use of enemata, but this may have been the effect of the enemata themselves. In individuals who suffer from obstinate chronic diarrhoea, the faeces Fig. 19. Fig. 30. Amceba coli. After Loesch. Cercomonas intestinalis. After Lambl. should be examined fresh under the microscope, since the parasites be- come immovable after a time, assume a spherical shape, and thus escape observation. According to Nothnagel, the occurrence of protozoa in the intestines is almost a normal condition. Fig. 21. Fig. 22. Balantidium s. Paramecium coli. a, peristoma; b, anus; c, row of cilia; d, contractile vesicles; e, nucleus; /, ingested granules of starch flour. Trichomonas intestinalis. After Zunker. We will add the chief morphological characteristics of the individual forms: a. Amoeba Coli.—This was observed once by Loesch in a Russian peasant, who suffered from chronic dysenteric attacks. The amoeba ap- pears in the shape of round, granular structures, 0.02-0.35 mm. in size, DISEASES OF THE INTESTINES. 143 with a nucleus and nucleolus and a number of vacuoles (Fig. 19). It is capable of changing its locality. b. Cercomonas Intestinalis.—The animal is pear-shaped, with a short prolongation posteriorly; anteriorly is a long whip by means of which locomotion is mainly effected (length of body, 0.008-0.01 mm.). The parasite has been observed in mucous evacuations of children, in the stools of cholera, typhoid fever (Fig, 20). Attention has been called to the foul odor of the stools. c. Trichomonas Intestinalis.—The animals are almond-shaped, 0.01- 0.015 mm. long, and 0.007-0.01 mm. wide (Fig. 21). The anterior portion of the body possesses a fringe of cilia in active motion. The parasite lias been observed in acute and chronic diarrhoea, the stools of typhoid fever, and the tartar of the teeth. d. Balantidium s. Paramcecium Coli.—This animal has been ob- served in man only in the vicinity of Stockholm, Upsala, and Dorpat. Leuckliart showed that it is always present in the large intestine of the pig. The animal is pear-shaped, and 0.07-0.1 mm. in length (vide Fig. 22). The interior is granular, and usually contains two vacuolae, to- gether with particles of food, debris of plants, red and white blood- globules. Henschen and Waldenstroem recommended the destruction of the parasite by intestinal infusion of a can of water, 3 iss. vinegar and 3 iss. tannic acid (at a temperature of 37° 0.). PLAT WORMS IM THE IXTESTINES. Platodes. Tape Worms. I. Symptoms.—Among the various forms of tape-worm, three pos- sess practical importance, viz., Taenia solium, Taenia saginata (medio- canellata), and Bothriocephalus latus. The patients sometimes enjoy the best of health, and the presence of a tape-worm in the intestine only becomes evident after the passage of pieces in the faeces or the acci- dental discovery of the ova under the microscope. In another series of cases, purely local disturbances of the stomach and intestines are observed, and may last for years before their cause is discovered. Many patients complain of a feeling of pressure in the ab- domen which is sometimes constantly present in one place, sometimes passes from one part to another. Colicky pains are observed not infre- quently. Some patients state that they experience a peculiar sensation in the intestine, as if a long worm were moving about; but this is proba- bly the result of a preconceived notion. These local symptoms are often produced or increased by the ingestion of certain articles of food. This is particularly true of herring, onions, garlic; while milk, eggs, and oily substances relieve the symptoms. Many patients complain of frequent vomiting, particularly in the morning. Among the frequent symptoms are disturbances of the appetite and digestion. Some patients present an almost insatiable appetite, but continue to emaciate despite the as- tonishing amount of food ingested. Others suffer from obstinate loss of appetite. The bowels are sometimes constipated, sometimes diarrhoea is noticed. General symptoms may be superadded to the local disturbances. 144 DISEASES OF THE INTESTINES. Indeed, there is scarcely an organ in which the morbid symptoms have not been observed. As a matter of course, purely accidental com- plications may be regarded as the reflex symptoms of the presence of the tape-worm. The proof of the connection between the two is afforded only by the immediate disappearance of the symptoms after the removal of the parasite. Among the general symptoms may be mentioned obstinate singultus, dizziness, pain m the head, syncope, delirium, mania, spasms, chorea, paralysis, difference in the pupils, disturbances of sight and hearing, etc. From time to time, mature links of the tape-worm are spontaneously evac- uated in the faeces. This occurs most frequently in spring or autumn, because the tape-worm requires a certain time before its development is completed. Sometimes the tape-worm is cast off in toto. I have re- peatedly observed this in children or adults who were subjected to treat- ment with cathartic mineral waters. Certain articles of diet, which are disagreeable and injurious to the tape-worm, or the administration of Fig. 23. Proglottides from a, Taenia solium; b, Bothriocephalus latus; c, Taenia saginata. Lower row natural size; upper row, enlarged 3 times. laxatives, may also cause their spontaneous evacuation. This is some- times observed during febrile diseases, particularly typhoid fever. In certain cases, it is the result of an affection of the tape-worm itself, as is often shown by certain malformations of the individual links. Peroncito found that cysticerci and tape-worms exhibited lively movements at a temperature of 30° to 35° C., which continued up to 48° C. and at 50° C. were permanently lost. Spontaneous evacuation of pieces of the tape-worm occurs most fre- quently, though not always, through the anus. In rare cases, they may be vomited. The appearance of links of the tape-worm in the faeces not alone ren- ders the diagnosis certain, but also enables us to determine the variety of tape worm. In Bothriocephalus, the individual links are broader than they are long, and at the middle present a dark, often pigmented DISEASES OF THE INTESTINES. 145 spot, corresponding to the sexual opening. In the two varieties of taenia, the links are longer than they are broad, and the sexual opening is indicated by a slight prominence to one side. In taenia solium the uterus, which is situated in the middle, sends out seven to twelve thicker and less branching lateral shoots, while in taenia saginata the ramifica- tions are much more abundant (fifteen to twenty). In taenia solium these ramifications are shaped like the branches of a tree, in taenia saginata they are simply fork-shaped. The examination of the members is best effected by slightly compress- ing them between two object glasses. In examination with transmitted light the sexual parts then appear distinctly; when still alive the parts not infrequently present vermicular contractions. In Bothriocephalus latus the links are usually cast off in the shape of small chains, the taenia are cast off in single pieces or very few are joined together. On microscopical examination the difference between the ova of Bothriocephalus latus and Taenia is easily recognized. The egg of Bothri- ocephalus (vide Fig. 24, a) is oval and from 0.06-0.07 mm. in length. It has a brown shell of waxy consistence, on the posterior end of which is a removable cover; the interior of the egg has a cellular structure. The ova of Taenia sodium and Taenia saginata differ from one another Fig. 24. only in size. The former are smaller, being 0.032 mm. in width and 0.036 mm. in length, while the ova of taenia saginata are 0.035 mm. wide and 0.039 mm. long. They are oval and have a thick shell composed of radiating rods. Their interior consists of granular protoplasm in which six small booklets of chitin are visible. II. Anatomical Changes.—Tape worms are located in the small intestine. They adhere to the mucous membrane by means of suction apparatus, in part by means of hooklets located in the head; then there are usually a few loose turns round the neck, while the rest of the body ex- tends towards the large intestine, and occasionally reaches into the colon. Not infrequently the worm is found rolled up into a knotted mass. In the majority of cases only one tape-worm is present, but Berenger-Feraud observed twelve taeniae and Kleefeld forty-one in one individual. As a rule, tape-worms in the intestine belong to the same variety, but both kinds of taeniae maybe present, less frequently taenia and bothriocephalus. Not infrequently we find other parasites, such as ascaris, oxyuris, tri- chocephalus, or anchylostomum. a. Bothriocephalus latus (vide Fig. 25). This worm is 5 to 8 metres in length. The number of its links may reach 4,000. The head is club-shaped or almond-shaped, about two mm. in length and one mm. at its widest part. Under the microscope a deep elongated suction-groove is found on each side of the head (vide Fig. 25, B). The head is followed by a thread-shaped, thin, cervical portion, 3 to 5 mm. in length. This is followed by the individual members or proglottides, Ova of a, Bothriocephalus latus; b, Taenia solium; c, Taenia saginata. Enlarged 300-350 times. 146 DISEASES OF THE INTESTINES. Fig. 25. The first ones are considerably broader than they are long, the last have a more quadrilateral shape. The first sexually mature proglottides occur about at the six hundredth link. These are about 5 mm. in width and 2 mm. in length. The quadrilateral ones are about 5 mm. in width and length. b. Taenia solium (vide Fig. 26). The length of the mature worm varies from two to two and a half metres. The head is round, about as large as the head of a pin, and its tip is not infrequently of a smoky gray or blackish color. Under forty to fifty magnifying powers, we find upon the top of the head a projection (rostellum) which is surrounded by a row of hooklets. The hooklets vary in size, a larger one alternating with a smaller one. To a certain extent two rows are formed, the outer one by smaller, Fig. 25. Fig. 25. Bothriocephalus latus. A, head and anterior portion (natural size); B, enlarged head with the two lateral suction grooves. C, Impreg- nated links. 1, lateral stripes; 2, middle stripe. the inner one by the larger hooklets. They vary from twenty-six to fifty in number. On the sides of the head are four suction-cups, and under the microscope these may be seen to pro- trude and retract. The head is followed by the thick cervical portion which is 5 to 10 mm. in length. In mature worms, there are about 850 proglottides, of which only 80 to 100 are sexually matured. The latter are 9 to 12 mm. in length, 5 to 10 mm. in width. c. Taenia saginata (mediocanellata). This at- tains a length of 7 to 8 metres, and is distinguished from taenia solium by the greater development of DISEASES OF THE INTESTINES. 147 the individual links. The head is larger than that of taenia solium (about 2.5 mm. wide, in taenia solium 1.3 mm. wide), but possesses no rostellum or hooklets. It is also often pigmented at the apex, and has four suction cups. The neck is only 1 to 1.5 mm. in length. The body is composed of 1,200 to 1,300 links. The sexually mature proglottides begin at about the 600th. The most mature ones have the Fig. 26. b Fig. 27a. Fig. 276. Fig. 26.—Taenia solium, a, natural size; 6, head enlarged 450 times. After Leuckart. Fig. 27.—Taenia saginata. a, natural size; 6, head enlarged. shape of pumpkin seeds, and are 15 to 20 mm. in length, 5 to 7 mm. in width. Any hemorrhages, erosions, or other lesions which may be found in the intestines must be regarded as accidental complications. According to some statements, a worm may live for thirty years in the individual. III. Etiology.—Tape worms are not conveyed directly from one individual to another, because the ova undergo development outside of 148 DISEASES OF TIIE INTESTINES. the human organism, and must develop into cysticerci before the latter can develop further into tapeworm in the human intestines. Sexually ripe proglottides are cast off by the tapeworm in the human intestine, and either these or the ova alone are devoured by animals. In the lat- ter the ova develop into cysticerci, and these are eaten by human beings in whose intestines they develop into tape worms. Tfenia solium is developed from the cysticercus cellulosae of swine, but this is also found in the dog, deer, monkey, bear, and, according to some, in the sheep. Taenia saginata develops from the cysticercus of beef ; the latter has also been found in the giraffe. The developmental history of Botli- riocepalus latus is still partly unknown. It is assumed that the eggs enter the water, and then are either swallowed and developed in the in- Fig. 28. Fig. 29. Fig. 28.—Cysticerci. a, in pork; b, in lamb. After Leuckart. Fig. 29.—Cysticercus cellulosae. «, with retracted; b, with protruded, head elevation. After Leuckart. Enlarged 1 diameter. testine into a tape worm, or this occurs after they have previously been partly developed in fishes or aquatic birds. Braun has recently main- tained that the scolex of bothriocephalus latus is especially frequent in the muscles and intestines of the pike and turbot. It seems, however, that these fishes are particularly apt to be affected when living in the Russian East Sea Provinces, while none are found in those caught in Switzerland. Zaesslein has explained the occurrence of bothriocephalus on the shores of the lakes in west Switzerland from the ingestion of let- tuce, which grows in ditches which are irrigated by the lakes. Certain habits exert an influence on the development of tape worms in the human body. Uncleanliness, the defecation of ffeces loaded with the ova of tape worm in open places, so that the fasces may be eaten by swine, or the ova may mingle with the drinking water and fodder and 149 DISEASES OF THE INTESTINES. thus be conveyed into the stomach of the animal, which serve as inter- mediaries; the eating of raw meat, etc., are especially favorable to the spread of tape worms. Individuals are apt to suffer from tape worms in places in which it is customary to eat raw meat; certain occupations also furnish a large contingent; for example, butchers, cooks, etc. Bothriocephalus latus is found in the western parts of Russia, Poland, East Prussia, Pommerania, Holland, Belgium, North Sweden, Finland, and the wrestern cantons of Switzerland. Zaesslein recently showed that several zones can be distinguished at the Swiss lakes ; one at the shore of the lake, in which one person out of five to ten is affected ; then a second zone, in which the parasite is found less frequently, finally a zone of immunity, at a distance of four to five miles from the shore. Taenia saginata is most widely diffused, because beef is everywhere eaten. Taenia solium is much rarer. Some races (Jews, Orientals) if they abstain from eating pork, remain free from the worms. IV. Treatment.—Prophylactic treatment is very important. In the first place, the receptacle for faeces should be inclosed, so that the excrement cannot be eaten by pigs. In addition, there should be a compulsory examination of meat by sanitary officers. We add here two plates of cysticerci in pork and lamb. They are situated in the intermuscular connective tissue, are elongated yellow vesicles 8 to 10 mm. in length, and running in the direction of the muscular fibers. The situation of the so-called head elevation is shown by a bright, usually somewhat retracted and firmer portion which appears in the plates as the clear centre. Butcher stores should be kept extremely clean. The various kinds of meat should be separated from one another, and a separate knife em- ployed for each. We should caution patients against the ingestion of raw meat. Moreover, the meat should be well done. Active treatment should not be begun until the presence of the tape- worm is shown by the evacuation of its links in the faeces. If the state- ments of the patients cannot be trusted, we should attempt to produce evacuation of proglottides by the administration of small doses of laxa- tives or vermifuges. For example : B Hydrarg. Chlorid. mite, J alapae, Sacch alb., . . . . . aa gr. ivss. M. f. p. One powder morning and evening. B Extract. Filicis, Khizomat. Filicis, ... aa gr. xxx. Ft. pil. No. xx. D. S. Ten pills to be taken morning and evening. The treatment proper may be divided into three parts : The object of preparatory treatment is to empty the intestine as thoroughly as possible, in order to facilitate the discharge of the tape-worm. For three days the diet should consist chiefly of milk, soup, and eggs, and several passages a day should be secured by mild laxatives. At night we may give a con- siderable amount of herring salad, mixed with onions and garlic. Ver- mifuges proper usually do not kill the parasite, but merely benumb it. Among the numerous remedies of this class, we give the preference to filix mas : B Extract Filicis, Khizomat. Filicis, . . . aa gr. 75. Ft. pil. No. xxx. D. S, Fifteen pills should betaken about 7 a.m., and again at 7:30 a.m. The patient should remain in bed and may take only coffee, or in 150 DISEASES OF THE INTESTINES. case of nausea, lemonade or a little brandy. Sometimes the tape-worm is passed in toto at the end of two to three hours, in other cases it is removed in pieces. We should avoid pulling upon ends which hang Fig. 30. Fig. 31. Fig. 33. Taenia flavopunctattt. After Weinland. Natural size. Tig. 32. Fig. 30.—Taenia liana. Enlarged 18 times. After Leuckart. Fig. 31.—Taenia cucumerina s. elliptica. Natural size. After Leuckart. Fig. 32.—a, Bothriocephalus cordatus. Natural size. After Leuckart. b, Heart-shaped head, enlarged, c, Mature links. out of the anus, since the tape-worm may thus be torn and the success of the treatment destroyed. Treatment with cathartics is employed if the tape-worm cannot he evacuated in toto at the end of an hour. It is also useful even after DISEASES OF THE INTESTINES. 151 the worm is removed, in order to clear the intestine as quickly as pos- sible of the remedies which have been administered. Within three hours after taking the pills which have been recommended above, one tablespoonful of castor-oil should be given every hour until the tape- worm is discharged. In addition, an infusion of pure water in the large intestine should be made four times a day. Or if the tape-worm has not made its appearance, we may order : IJ Decoct, rhizom. filic., 3 ij. : § xx. The treatment can only be regarded as successful if the head of the par- asite is discharged. If the worm has been evacuated in pieces, the faeces should be carefully stirred in water and thoroughly examined. If the head is not found, the result remains uncertain ; but the patient may usually be regarded as cured if no new links have been evacuated within ten to fifteen weeks. We may also mention the following remedies : a. Flores kousso, 3 vi. to be taken in two portions in the morning, in sugar water, lemonade, or red wine. b. Koussinum, 3 i. to be taken in the morning, in two portions, c. Oamala, § ss. to be taken in coffee, in the morning, in two portions, d. B Cort. rad. granat. 3 xiij., aq. frigida § x., macerate for twelve hours, then boil down to § viij., add syr. zingib. | i. D. S. to be taken in the morning in two portions, e. 01. terebin- thin., 3 xiij. in two portions. /. 01. Chaberti or benzolum, 60-200 drops in capsules, etc. The patient should be kept under observation for some time after treatment. I have seen a number of cases of chronic catarrh of the large intestine and serious exhaustion in which the patients asserted that their disease was the result of treatment adopted against the tape worm. Appendix. A few examples of other forms of tape-worm have been found in the human intestines. We will mention : a. Taenia nana in large numbers was observed by Billharz in the duodenum of a child who had died from meningitis. This tape-worm does not exceed 15 mm. in length, has a round head with rostellum, and four suction cups. The rostellum is sur- rounded by twenty-two to twenty-four hooklets. It has one hundred and fifty to one hundred and seventy links, the last twenty to thirty con- taining matura ova. (Vide Fig. 30.) b. Taenia flavo-punctata was ob- served in one case by Weinland. It attained a length of three hundred mm. The structure of the head is unknown. The anterior half of the tape-worm consists of immature links, each of which contains a yellow patch, while the posterior links present a profuse brownish discoloration, the result of an accumulation of ova (vide Fig. 31). c. Taenia cucume- rina s. elliptica has been found a number of times in children. This parasite is the tape-worm of dogs and cats. It attains a length of one hundred and fifty to two hundred mm. The head possesses a rostel- lum which can be protruded, and beneath which are sixty hooklets, arranged in four irregular rows. The anterior end of the body is very thin. At the posterior end the sexually ripe links again diminish in size. The number of links may exceed one hundred. The color of the sexually mature ones is reddish. (Vide Fig. 32.) d. Tasnia madagascar- iensis has been observed twice on an island near the coast of Madagascar. e. Bothriocephalus cordatus was described by Leuckart (vide Fig. 33). It is found, in Greenland, in the small intestine of men and in the dog. It may attain a length of one hundred and fifteen cm,, has a short heart- 152 DISEASES OF THE INTESTINES. shaped head, which passes directly into the broad belly. The number of links varies from four hundred to six hundred. A longitudinal furrow is visible on the ventral surface, still more distinctly upon the dorsal sur- face. The mature proglottides are quadrilateral in shape, with a diam- eter of from five to six mm. The uterus rosette has from six to eight lateral horns. 0 Round Worms in the Intestines. Nematodes. Round Worm. Ascaris Lumbricoides. I. Anatomical Changes.—This animal is a round long worm of whitish or pale rose, sometimes brownish-red color. The female is longer (thirty to forty cm.) than the male (twenty cm.). The latter is also more slender and its caudal extremity is usually curved or rolled in towards the ventral surface (vide Fig. 34, B). Transverse furrows in close proxim- ity to one another are readily recognized, and without great diffi- culty we can also see four longitudinal stripes which run from the head to the tail. Two of these are situated upon the ventral and dorsal sur- faces, and the other two run along each side. The head sits like a but- ton upon the rest of the body. At the posterior caudal extremity in the male is found the cloaca, from which the spicula often protrudes. This opening must be looked for in the previously-mentioned ventral stripe (vide Fig. 34, B). The sexual opening in the female is also found in the abdominal line, at the boundary of the anterior and the middle thirds of the body. A small excretion-pore is found upon the abdominal line, in both sexes, not far from the head. The ova are easily recognized. They have an elongated, founded shape, and are about 0.05 to 0.06 mm. in length. Their contents are granular, and surrounded by a firm, dark membrane, which in turn possesses an albuminoid covering. The latter presents nodular projections. Leuckart and Eschricht estimate the number of ova in the genital canal of a female at sixty millions. The parasite inhabits the small intestine and is found exceptionally in the large intes- tine. It is often present in very large numbers. II. Etiology.—The developmental history of Ascaris lumbricoides is unknown. Attempts to produce ascaris in the intestines by ingestion of ova have been attended with negative results. It is therefore supposed either that a go-between is necessary, or that worms which have partly devel- oped outside of the human body enter the intestinal tract. Vegetables, fruits, and drinking water have been regarded as the sources of infection. The worm is found very frequently in women and children. It is especially frequent among the insane and in the Orient. III. Symptoms and Diagnosis.—The local symptoms include loss of appetite, boulimia, perverse sensations of taste, foetor ex ore, tender- ness of the abdomen, colicky pains, and irregularity of the bowels. The patients, particularly children, grow very pale, change color quickly, and grayish and bluish-gray rings appear around the eyes. Among the general symptoms may be mentioned a tickling sensation in the nose, so that the patient often introduces the finger into the nostrils, irregularity of the pupils, dizziness, syncope, spasms, epilepsy, chorea, meningitic symptoms, paralysis, disturbances of sight and hearing, etc. Huber also found that ascarides seem to produce an irritation in a chemical (toxic) wray, for after handling them he experienced itching DISEASES OF THE INTESTINES. 153 around the head and neck; then wheals made their appearance, the ear became swollen,the external auditory canal began to secrete, conjunctivitis and chemosis developed, together with an annoying throbbing in the head. The diagnosis may be made either when the worms are passed in the. Fig. 34. Fig. 34. Fig. 35. Fig. 34.—Ascaris lumbricoides. a, female; b, male, natural size. 1, cephalic end; -2, abdominal stripe; 3, left lateral stripe; 4, right lateral stripe; 5, porus excretorius; 6, female genital opening; 7, caudal end of the female with anal opening; 8, caudal end of the male with, opening of cloaca and spicula. Fig. 35.—Ovum of Ascaris lumbricoides with membrane and albuminous covering. stools or are vomited, or if the ova can be detected in the faeces. If the ascaris is vomited, the patients often complain of very violent pain in the 154 DISEASES OF THE INTESTINES. stomach. The number of worms vomited may be very considerable. Fauconneau-Dufresne reported a case in which a boy vomited 103 ascar- ides in the morning and 22 the same night. Very dangerous conditions may be produced by the migration of the parasites. They sometimes enter the ductus choledochus, give rise to incurable and fatal jaundice, even pass into the hepatic ducts and pro- duce hepatic abscess. They sometimes form the nucleus of gall-stones. They have also been found in the ductus Wirsungianus. A number of cases have been reported in which the ascaris entered the larnyx and produced suffoca- tion. They may also pass into the bronchi and may give rise to gangrene and pulmonary abscess. Ascarides have been removed from the nose, the lachrymal canal, and the external auditory canal. As a matter of course, the latter is only possible if the drum membrane has been previ- ously perforated. If perforating ulcers are found in the intestines, ascarides are often Fig. 36 Ascaris mystax. A, female; B, male; C, ovum. 1, cephalic end; 2, abdominal stripe; 3, right lateral stripe; 4, porus excretorius; 5, female genital opening; 6, anus; 7, rolled-in caudal end with cloaca and spicula. found in the peritoneal cavity on autopsy. In cases of intestinal fistula the worms are occasionally found in the uterus, vagina, or urethra, also in the pleural and pericardial cavities. If a peritonitic abscess communicate with the intestines and also through the abdominal walls with the exterior, the round worms may pass externally through the fistula. They are sometimes found in the intestines in astonishing numbers. Fauconneau-Dufresne counted 5,126 which were passed by a boy of twelve within three months, although many evacuated by him were not counted. IV. Prognosis.—Complications produced by the migration of a para- site are so rare that the prognosis is not thereby rendered appreciably worse. V. Treatment.—Ascarides are removed most effectually by the use of santonine: I£ Trochisci santonini, .... aa gr. f D. t. d. No. x. S. Take one troche t. i. d. It should be remembered, however, that certain individuals are apt 155 DISEASES OF THE INTESTINES. to suffer very readily from santonine poisoning (xanthopsia, yellow color of the skin, yellow urine, delirium, and even convulsions). Among other remedies we may mention the following: a. Flores cinae gr. 75, jalapae gr. viiss. syr. simp. 3 viss. M. D. S. To be taken in three portions, h. Natrium santonicum gr. viiss. c. Inf. flor. tanaceti 3 iij. : 3 iiiss. cl. 01. tanaceti. e. 01. terebinthinae. Appendix. . Ascaris mystax (round worm of the cat) has been found in man in a few cases. It is smaller than ascaris lumbricoides. The cephalic end presents a wing-like projection (vide Fig. 36). Thread Worm. Oxyuris vermicular is. I. Anatomical Changes.—The length of the mature female is twelve mm., that of the male five mm. The caudal end of the male is rolled in towards the abdominal surface, Fig. 37. Fig. 38. Oxyuris vermicularis. On the left, the female; on the right, the male. Natural size. Ova of Oxyuris vermicularis, obtained from the faeces. Enlarged 275 times. and runs out into a fine end in both sexes, while at the anterior extremity the head is recognized as a very fine button. The ova are 0.052 mm. in length and 0.024 mm. in width. They are oval, curved more on one side than on the other, contain granular con- tents with a distinct nucleus and nucleolus, and have a clear membrane. Their habitat is the entire large intestine. The rectum contains chiefly impregnated females in extremely large numbers. II. Etiology.—If ova enter the stomach of the human being, the membrane is dissolved by the gastric juice, and gives exit to the embryo, which first remains in the small intestine and continues to develop. Here impregnation of the fully developed parasite takes place. Hence, uncleanliness mav give rise to self-infection or infection of others. It is not true, however, that infection may take place by the migration of the oxyuris from the rectum to another individual sleeping in the same bed. Infection does not occur through the agency of drinking water because this rapidly destroys the ova. Children and women are most frequently affected. The worm is also 156 DISEASES OF THE INTESTINES. found often in filthy insane. Some persons suffer during their whole life, but the life of the individual thread-worm is very brief, so that in such cases self-infection must constantly be produced. In a number of cases Zenker found the worms beneath the tips of the nails of human beings. III. Symptoms.—The local and general symptoms are similar to those produced by ascarides (vide page 152), but there are certain local peculiarities. Violent itching at the anus is very often produced. Diarrhoea may Fig. 39. Integument infiltrated with ova of oxyuris. After Michelson. occur occasionally. The parasites present a tendency to migrate; they leave the rectum and crawl across the perineum to the vagina, more rarely beneath the prepuce. In this manner they may produce leucor- rhcea, balano-posthitis, and thus may give rise to onanism, even to nym- phomania, spermatorrhoea, or prostatorrhcea. Michelson described an eruption like eczema in the genito-crural fold, pro- duced by inoculation with the ova of oxyuris (vide Fig. 39), but we must add that this was the result perhaps of an accidental infection with the ova. IV. Diagnosis.—The diagnosis is easy. In the faeces we notice parasites in motion, often of a lively char- acter. If they are not visible, the faeces should be examined microscopi- cally for the ova. DISEASES OF THE INTESTINES. 157 Y. Prognosis.—The prognosis is good, but it seems as if certain in- dividuals are especially apt to suffer infection. YI. Treatment.—The object of treatment by the mouth is to remove the parasite from the small intestine. This is effected by the use of santonin lozenges, aa gr. f three times a day, or the anthelmintics men- tioned on page . Treatment per rectum consists of intestinal in- fusions to remove the parasites from the rectum. We may recommend an infusion of garlic, dilute vinegar, or soap and water. The infusion should be repeated daily for a number of days. The migration of para- sites across the perineum may be prevented bv smearing the vicinity of the anus with unguent, hydrargyri. Whip Worm. Trichocephalus Dispar. This is found in the caecum, usually in small numbers. Its thick caudal extremity resembles the handle of a whip, while the thin cephalic ■extremity corresponds to the lash. Fig. 40. The female is about fifty mm. in length, the male forty to forty-five mm. The caudal extremity in the male is rolled in towards the dorsal Tricocephalus dispar. The male above, the female below. Natural size. Fig. 41. Ova of tricocephalus dispar. Enlarged 275 times. surface. The ova are oval in shape, 0.05-054 mm. in length, have a brownish color and a button-shaped projection at both poles. The mode of infection is unknown. The parasite is found in almost 158 all countries. Copious discharge of the parasites has been observed in typhoid fever. Nothing is known regarding the symptoms to which they give rise. Anchylostomum Duodenale. (.Dochmius s. Strongylus cluodenalis.) This is observed most frequently in the Orient and in the Tropics; it has also been found in northern Italy. Menche observed a case in the vicinity of Bonn, and a number of cases have also been reported in other localities. The parasite is cylindrical in shape, the female ten to eighteen mm. long, the male six to ten mm. The cephalic end is curved towards the dorsal surface, and terminates with an oblique surface; the ova are oval, 0.05 mm. long, and 0.1023 mm. wide. They have granular contents and a clear membrane, but are often found in the faeces in a condition of begin- ning fission. With high powers the mouth is found to be armed with teeth. The parasite is probably ingested in the immature form in impure water. Its habitat is the small intestine. The buccal opening surrounds DISEASES OF THE INTESTINES. Fig. 42. Fig. 43. Fig. 44. Fig. 42. -Anchylostomum duodenale. Male to the left, female to the right. Natural size. Fig. 43.—Ova of Anchylostomum duodenale from human faeces. After Bugnion. Fig. 44.—Buccal opening, armed with teeth, of Anchylostomum duodenale. the intestinal villi, whence it draws blood. When the parasite seeks another part of the mucous membrane, the previous site continues to bleed. Hence the clinical symptoms of increasing anaemia. The pas- sages from the bowels also contain blood. The entire symptom-complex has been termed anchylostomiasis. Griesinger first recognized the an- chylostomum as the cause of tropical chlorosis. Perroncito attributes the anaemia of certain classes of workingmen (miners, brickburners, etc.), to the development of anchylostomum in the intestine. The diag- nosis is possible if the parasite or ova are recognized in the stools. The prognosis is serious on account of the profound anaemia to which the disease gives rise. The treatment is the same in general as that of tape- worm, but it has been found that large doses of filix mas are the most effective. Treatment must sometimes be repeated a number of times. Anguillula Intestinalis et Stercoralis. Individuals living in the tropics sometimes suffer from dyspeptic conditions, diarrhoea, increasing emaciation, and anaemia. In 1876 Normand found anguillula in the stools of such patients. Perroncito also found them in the stools of the workingmen who suffered from the DISEASES OF THE INTESTINES. 159 Gotthard-tunnel anaemia. Seifert found the parasites in the vomited matters, so that they seem to be situated in the upper part of the intes- tine. This writer found that the best remedy is thymol, of which gr. xv. Fig. 45. Anguillula intestinalis. Enlarged 100 times. After Seifert. was given every hour until twelve doses had been taken daily. The parasites have a lively movement in the faeces, and in Seifert’s case were Fig. 46. Fig. 47. Distomum crassum. Natural size. After Leuckart. Distomum heterophyes. 0.27 mm. long, and 0.016 mm. wide. The cephalic end was round, the caudal end pointed, the sexual opening was round. Appendix. Trichina spiralis will be discussed in Yol. IY. Echinorhjnchus gigas was observed by Lambert in a child, by Welch in an Indian soldier, and by Lindmann in several individuals living on the Yolga. In a few cases, trematodes have also been observed in the intestinal tract of human beings, for example, Distomum crassum (Fig. 46) and Distomum heterophyes (Fig. 47). Distomum haematobium has also been observed, and may give rise to serious ulceration of the mucous mem- brane. 8. Intestinal Hemorrhage. Enterorrhagia. I. Etiology.—Intestinal hemorrhage is the result of anomalies of the intestinal contents, of local diseases of the intestinal wall, or of gen- eral diseases. Obstinate constipation may give rise to hemorrhage if the excessively hardened faeces mechanically injure the mucous membrane. 160 DISEASES OF THE INTESTINES. The hemorrhage is usually insignificant, and appears in the shape of bloody dots and streaks, which are found upon the surface of the hard lumps of faeces. Ingested foreign bodies may act in a similar manner. Intestinal hemorrhage may also be the result of poisoning, and it should be remembered, that the immoderate use of cathartics acts in a similar manner. Finally, it maybe produced by parasites (Anchylostomum duo- denale and Distomum haematobium). Among the local diseases the most important are the ulcerative changes of the intestinal mucous membrane. The comparative infre- quency of hemorrhage in intestinal ulcers is owing to the fact that, if the ulceration progresses slowly, thrombi may form in the affected vessels. Injuries are sometimes the cause of intestinal hemorrhage. Rectal hem- orrhages are not infrequently traumatic in character. Hemorrhage, though slight in extent, occurs not infrequently in enteritis. It is relatively frequent in those forms which follow cutaneous burns. Bayer described a case in which it occurred in fatal erysipelas. Tumors of the intestinal mucous membrane are also causes of enterorrhagia. Furthermore, it is an important symptom in invagination, where it is the result of circulatory disturbances. Cases of a similar nature are observed in occlusion of the portal vein, and in hepatic, respiratory, and circula- tory diseases. Intestinal hemorrhages may also be the result of waxy degeneration of the vessels, embolism of the superior or inferior mesenteric arteries, or aneurisms of adjacent arteries which have ruptured into the lumen of the intestine. Among general diseases, typhoid fever, dysentery and syphilis give rise to intestinal hemorrhage by ulceration of the mucous membrane. In intermittent fever, intermittent hemorrhages have been observed as the result of embolic occlusion of branches of the portal vein by mela- nine. Intestinal hemorrhages have been observed in typhus fever, though no ulcerations were present in the intestinal mucous membrane. Hemorrhage is rare in Asiatic cholera, frequent in yellow fever. It is observed occasionally in pygemia and in septicaemia ; also in the new- born as the result of puerperal infection. It is also observed in acute exanthemata of a hemorrhagic character, in haemophilia, morbus maculo- sus Werlhofii, scurvy, purpura haemorrhagica, and uraemia. Vicarious intestinal hemorrhage, i. e., in the place of menstruation, has also been described. Intestinal hemorrhage occurs most commonly in middle life. It is more frequent in males than in females. II. Anatomical Changes.—Bloody contents are found in the intes- tine, which is either distended with blackish-red clots or with tarry, foul-smelling masses. Sometimes the masses of faeces are hard and black, or the intestinal contents have the color of meat juice, and are partly mucous or muco-purulent. In some cases the intestinal wall is extremely pale, in others the mucous membrane is suffused in places with blood or presents ulcera- tions. If the latter are the cause of hemorrhage, their blood-vessels contain thrombi, or water which is injected into the mesenteric artery will escape at the base of the ulcer. Ulcers, degenerating tumors, and foreign bodies may open directly into arterial or venous vessels, sometimes of considerable size. In inflammations and circulatory stasis, the chief factor is the increased blood pressure, which cannot be resisted by the perhaps very DISEASES OF THE INTESTINES. 161 slightly changed wall of the blood-vessel. In conditions of blood disso- lution we must assume changes in the walls of the vessels, which become unusually permeable. The hemorrhage may be arterial, venous, or capillary; even the latter may be very profuse and indeed fatal. The other organs are usually very pale. If extensive previous hemorrhages have occurred, we not infrequently find fatty degeneration of the heart, liver, kidneys, pancreas, and glandular cells of the stomach and intestines. III. Symptoms.—Only those symptoms will be considered which are independent of the primary disease. Intestinal hemorrhage sometimes gives rise to no other signs than those of internal hemorrhage. The patients grow exceedingly pale, the features are peaked, the skin cool, the pulse accelerated or scarcely perceptible, the heart sounds feeble ; they complain of spots before the eyes and ringing in the ears, nausea, vomiting, dizziness, and fainting spells. Finally, death may occur, although not a drop of blood has escaped externally. An abnormal area of dulness, corresponding to the accumulation of blood, is occasionally found in the abdomen. The chief manifest symptom is the evacuation of bloody stools. Sometimes these are purely bloody, forming loose blackish clots, more rarely fluid and bright red. In other cases the blood and faeces are intimately mixed, and the evacuations form blackish, tarry masses, often emitting an intolerable stench. The bloody masses are sometimes hard and intensely black. In hemorrhages from the rectum the blood appears on the surface of the faeces, while the inside of the mass of faeces is free from blood. In dysentery, the stools have the color of meat juice and contain muco-purulent or purulent masses. The evacuations are sometimes attended with tenesmus. I have also observed obstinate constipation associated with fever ; the administration of cathartics led to the evacuation of astonishingly large masses of bloody faeces, and the tenesmus and fever soon ceased. On microscopical examination of the stools, the red blood-globules are sometimes found unchanged, sometimes swollen, sometimes discol- ored and in a condition of degeneration. Nothnagel showed that microscopical examinations of the faeces sometimes reveals premonitory signs. In cases of typhoid fever, he found small amounts of. blood in the faeces twelve to thirty-six hours before an extensive internal hemorrhage. Hematemesis may be expected in those cases alone in which the hemorrhage takes place in the duodenum. Physical examination of the abdomen must be performed very cau- tiously, in order to avoid an exacerbation of the hemorrhage. We should pay attention to dulness, increase in the area of dulness, and increased feeling of resistance. Some patients state that they experience the sensation as if a warm fluid were flowing into the abdomen. If the hemorrhage cannot be checked, or if it is too extensive, death will ensue. Under other circumstances oedema may develop and some- times even mild albuminuria. In one case Traube observed death from oedema of the glottis, but this was complicated by laryngeal ulcerations. IV. Diagnosis.—The diagnosis involves an answer to the following four questions : a. Is blood present in the stools ? b. Is the blood de- 162 DISEASES OF THE INTESTINES. rived from the intestine ? c. Does it come from the small or large intestine ? d. What are the special causes of the hemorrhage ? a. In very obstinate constipation the faeces may assume a brown- ish-black color ; if there is a copious admixture with bile the stools may also have a blackisli-green color, which is mistaken for blood. A similar mistake may be made after the use of iron preparations and bismuth, or the passage of undigested red fruit. In doubtful cases the microscope maybe resorted to; finally, we may resort to spectrum analy- sis and the formation of Teichmann’s blood crystals. b. Bloody stools indicate intestinal hemorrhage only when hemor- rhages from the nose, pharynx, oesophagus, or stomach may be excluded. Bloody stools are also observed in the new-born after the operation for hare-lip, or the ingestion of blood during delivery or as the result of lesion of the nipples of the mother. Fig. 48.» Changed red blood-globules from enterorrhagia, five days after the beginning of the hemorrhage. Enlarged 275 times. c. Inspection and palpation occasionally suffice to decide the location of the hemorrhage (lower part of the rectum). The causes should also be taken into consideration. For example, intestinal hemorrhages after burns always originate in the duodenum; dysenteric hemorrhages in the large intestine, etc. If the blood is situated only upon the surface of the faeces, the hemorrhage must be referred to the large intestines. In some cases, the occurrence of abdominal dulness is useful in diagnosis. d. The etiology depends upon the clinical history and associated symptoms. In latent intestinal hemorrhage, the diagnosis depends upon the symptoms of internal hemorrhage and the exclusion of a lesion of other organs. V. Prognosis.—The prognosis depends upon the causes and the pro- fuseness of the hemorrhage. In many cases, the prognosis is unfavora- ble on account of the primary disease. Occasionally a favorable influ- diseases of the intestines. 163 ence is attributed to the hemorrhage; this is especially true of typhoid fever. If the hemorrhage exceeds a certain amount, however, it cannot pos- sibly be regarded as a favorable event. VI. Treatment.—Prophylactic measures must be taken into con- sideration in ulceration of the intestines. The diet and stools must be carefully regulated in order to avoid irritation of the surface of the ulcers. When the hemorrhage occurs, the treatment should be the same in general as in hemorrhage from the stomach (vide page 55). The patient should be kept absolutely quiet, and receive only fluid, cool food, for example, milk and ice, red wine and ice, etc. An ice-bag should be applied to the abdominal walls, a subcutaneous injection of ergotinum Bombelon (one-half syringeful mixed with an equal amount of water) should be made, and liquor ferri sesquichlorati given inter- nally. If the intestinal movements are vigorous, we should give several large doses of opium in rapid succession. In rectal hemorrhage, we may inject ice-water, which may be mixed with astringents, for example, tan- nic acid (gr. xxx.); nitrate of silver (gr. viiss.); liquor ferri sesquichlo- rati (10 drops). In. collapse, we should give strong wine, brandy, musk (gr. ivss. every hour), or subcutaneous injections of camphor (gr. xv., 01. Amygdal., 3 iij., one syringeful three times a day). Appendix. Melania Neonatorum. {Apoplexia Neonatorum Intestinalis.) I. Etiology.—The term melsena is now applied only to haemateme- sis and enterorrhagia in the new-born. In melaena vera the blood is de- rived from the stomach or intestine; in melaena spuria the blood has been ingested. We will now discuss only melaena vera. In a few cases gastric ulcers have been observed in the stomach and duodenum. Henoch described one case in Avhich the ulcer was situated in the oeso- phagus immediately above the stomach. In some cases, we find merely congestions of the intestinal mucous membrane. In another group, there are signs of general dissolution of the blood. Opinions differ in regard to the ulcerative forms of melaena, whether we have to deal with the results of embolism or of hemorrhagic infiltration of the mucous membrane. According to Bohn, the ulcers are the result of occlusion and suppuration of the gastro-duodenal glands. Steiner claims to have noticed fatty degeneration of the vessels of the mucous membrane. In many cases, no cause whatever could be discovered, the disease attacking well-developed children of healthy parents. In some cases, difficult labor had been regarded as the cause of melaena, and it is said to be ob- served with special frequency in asphyxiated children. Finally Kiwisch and Landau attach great importance to the too early ligature of the funis. The disease is not frequent. Hecker observed it once amongst five hundred births, Genrich only once in one thousand births. II. Anatomical Changes.—The anatomical changes, in so far as they affect the wall of the intestine, have been previously mentioned. The lymph follicles of the intestinal mucous membrane have been found swollen, and even follicular ulcers have been described. Enlargement of the spleen has been observed a number of times, and likewise changes in the liver. 164 diseases of the intestines. III. Symptoms.—The symptoms sometimes develop suddenly, or are preceded by prodromata (pallor of the skin, low temperature, disappear- ance of the pulse, increasing apathy), which must be attributed to an internal hemorrhage. The first manifest symptoms often appear a few hours after birth, but generally on the second day. In rare cases, they have been observed in the second week, and even the beginning of the third week. As a rule, the first manifest symptom is the passage of bloody stools, and then haematemesis soon occurs. Silbermann collected forty-two cases, with the following results: Hemorrhage from the stomach and intestines, . 25 times. “ “ “ intestines alone, . 10 “ “ “ “ stomach alone, . . 7 “ The blood is sometimes dark and sometimes bright-red. Occasion- ally only one or a few bloody stools are passed; in other cases, the hem- orrhages are repeated, and may even continue for several days. Symp toms of increasing anaemia develop and prove fatal. Even in favorable cases, dangerous weakness may persist for months, and in some cases a tendency to gastric and intestinal diseases continues for the remainder of life. IV. Diagnosis.—The symptoms of melaena neonatorum are so sharply defined that it is scarcely possible to mistake it for other con- ditions. V. Prognosis.—The prognosis is always grave, and, on the average, fifty per cent of the cases prove fatal. If the hemorrhage has lasted longer than thirty-six hours, recovery is exceptional. VI. Treatment.—The funis should not be tied until pulsation is no longer felt and respiration is regularly performed. During an epi- demic of puerperal fever, the infant should be removed from the mother in order to avoid as much as possible the danger of infection. After melaena has developed, we may apply compresses to the abdo- men, give Ergotinum Bombelon (one-quarter syringeful) subcutaneously, and internally give a few drops of wine. 1. Hcemorrlioids, Phlebectasia licemorrlioidalis. (Hcemorrhoidal disease. Piles.) I. Etiology.—Haemorrhoids are a dilatation of the hemorrhoidal veins, and sometimes occur in a diffuse manner, sometimes in the shape of individual varices. The causes may be purely local and confined to the rectum. For example, in individuals who suffer from obstinate con- stipation, it is generally assumed that the retained faeces impede the circulation in the lower part of the rectum, but Duret attaches chief importance to excessive straining during defecation. Haemorrhoids are s imetimesthe result of protracted proctitis, inasmuch as the submucous tissue becomes more yielding, and the veins contained in it undergo dila- tation. Not infrequently haemorrhoids and proctitis are the result of the same cause, and, in addition, haemorrhoids may give rise to secondary proctitis. Cancer and stricture of the rectum are often followed by the development of haemorrhoids. They are occasionally the result of affec- tions of the uterus, ovaries, or prostate, when these organs press upon surrounding parts and interfere with the circulation. The obstruction to the circulation is sometimes situated higher, as in stasis of the portal circulation, whether the result of portal thrombosis, compression of the 165 DISEASES OF THE INTESTINES. portal vein, or diseases of the liver itself. Affections of the circulatory and respiratory apparatus act in the same manner as soon as they give rise to stasis in the inferior vena cava. Haemorrhoids are of tea found in plethoric individuals, who are fond of the pleasures of the table and averse to bodily exercise. In these cases circulatory disturbances in the portal vein are usually regarded as the cause of the disease. As a rule, haemorrhoids develop between the thirtieth and fiftieth years of life. They are very exceptional in child- hood, but Lannelongue reported a case in which they developed a few days after birth. They are more frequent in men than in women. Their development is favored by sedentary occupations; excesses in venery, constant sitting on benches, abuse of alcohol, constant horse-back riding, are also predisposing factors, partly because they produce congestion of the pelvic organs and partly because they favor stasis in the rectal veins. I have often observed the disease in old musicians who play on wind in- struments. The facility with which the rectal veins yield to obstructions in the circulation is owing particularly to the fact that they are destitute of valves. The portal vein also is destitute of valves, so that all disturb- ances of the portal circulation are very readily propagated to the haem- orrhoidal veins. In addition, we must take into consideration the action of the force of gravity. II. Anatomical Changes.—We distinguish between external and internal haemorrhoids. The former are situated outside of the sphincter ani, while the latter are situated above this muscle, and are only recog- nized by digital examination or by means of the speculum. In some cases, a portion of the varix is situated outside of the anus, the other part within. There may be a diffuse dilatation of the rectal veins, so that in the case of external haemorrhoids the rectum is surrounded by a bluish prominent ring; in other cases we find circumscribed dilatations, which vary considerably in number and size (from that of a lentil to that of a pigeon’s egg, and even an apple). They may be round, flattened, or irregularly angular. Internal and external piles may be associated with one another. As a rule, internal haemorrhoids are also situated near the sphincter ani, but Petit described a case in which they extended to the sigmoid flexure. Secondary changes may develop in the haemorrhoids themselves or in their vicinity. A relatively favorable process is the formation of thrombi, which become organized, and thus produce spontaneous occlusion of the dilated portion of the veins. This may also result in calcification and the formation of venous calculi (phleboliths). If the varices are extensive and closely aggregated, the septum between the adjacent ones sometimes disappears, so that several large spaces partly coalesce, and thus constitute a sort of cavernous tumor. A frequent complication is thickening of the submucosa of the rectum and chronic proctitis, which is generally manifested by a profuse puriform secretion. Not infrequently there is inflammatory hyperplasia of the periproctal connective tissue. Some- times an acute inflammation develops, and results in the formation of an abscess. This may rupture externally into the rectum, or in both directions, thus giving rise to external, internal, or complete rectal fistula. In external haemorrhoids the covering of skin is sometimes as thin as paper, sometimes abnormally thickened. Internal haemorrhoids are oc- 166 DISEASES OF THE INTESTINES. easionally pedunculated, particularly if they have been extruded from the anus. III. Symptoms.—Dilatation of the haemorrhoidal veins not infre- quently exists without giving rise to symptoms; the latter are not produced until the piles have reached a certain size, and thus give rise to mechanical disturbances. On the other hand, patients sometimes complain that they have suffered for years from haemorrhoids, although nothing is discovered on the most careful examination. Many patients complain of an annoying sensation of itching, burning pain, or increased heat at the anus. These symptoms increase after a heavy meal, constant sitting or riding, and excesses in Bacchoet Venere. Not infrequently the patients are annoyed by the sensation of a foreign body in the region of the anus. The symptoms become more severe when the piles narrow the exit from the rectum, and thus interfere with the stools. The patients are often tortured by the most violent pains during defecation, and in sensi- tive individuals this may give rise to syncope and convulsions. Many patients delay the passages as long as possible. This may result in dis- tention of the abdomen, singultus, nausea, vomiting, difficulty of breath- ing, palpitation of the heart, rush of blood to the head, etc. Haemorrhoids are sometimes manifested by nothing beyond chronic blennorrhoea of the rectal mucous membrane. The patients must often go to stool, and pass muco-purulent or almost purely purulent masses, which may or may not be mixed with faeces. Dots and streaks of blood are occasionally noticeable, and the disease may be mistaken for dysen- tery. Hemorrhages are very often observed in these patients. The are not always the result of rupture of the varix, but in the majority of cases are of capillary origin. Hemorrhage very rarely occurs without the previous existence of other symptoms. It is usually preceded by the so-called molimina hsemorrhoidalis, which consist of a feeling of increased tension and pain in the anus, a rush of blood to the head, palpitation of the heart, etc. The amount of blood discharged may vary from a few table- spoonfuls to several pounds. Sometimes a single hemorrhage occurs, sometimes the hemorrhages are repeated for days. In many patients this is followed by a feeling of great relief. As the blood is derived from the lower part of the rectum it is usually but little changed. It merely coats the faeces, and not infrequently is discharged m an unmixed condition. The loss of blood is rarely so considerable as to threaten life, but if the hemorrhages last for a long time, or are re- peated in rapid succession, they may give rise to serious conditions of anaemia. The patients are pale, short of breath, feeble, suffer from oedema, and occasionally from slight albuminuria. Dilatation of the right ventricle sometimes occurs, and we may find anaemic cardiac murmurs, the bruit de diable in the jugular veins, and the arterial sounds, in smaller peripheral arteries. Very painful conditions are produced by prolapse and incarceration of internal haemorrhoids. After violent straining, internal piles may be forced through the sphinc- ter to the outside. If the sphincter ani now undergoes spasmodic con- traction, the prolapsed haemorrhoids are prevented from returning. Such conditions cause extremely violent pain. The patients groan aloud, the brow is covered with perspiration, the pulse becomes small and frequent, and in some cases syncope and convulsions make their appearance. If the haemorrhoids cannot be replaced, inflammation and DISEASES OF THE INTESTINES. 167 gangrene set in. and this may be followed by serious conditions, for example, pyaemia. The duration of haemorrhoids is usually short if their causes are tran- sitory in character, as for example, in pregnancy. In the majority of cases, however, the disease is chronic, and usually lasts for life. Pyschi- cal depression often develops, but is the result of the associated gastric and intestinal affection rather than of the haBmorrhoids. IV. Diagnosis.—External haemorrhoids are readily recognized on inspection, internal ones by digital examination and the use of the spec- ulum. The following mistakes in diagnosis may be made: a. With folds of skin at the anus (the bluish appearance, tension, and spherical shape of haemorrhoids are wanting); h. With condylomata (other signs of syph- ilis are usually present upon the genitals, or mucous membranes); c. Rectal cancer (cachexia present in these cases). V. Prognosis.—Prognosis as regards life is good, but, as a rule, we cannot hope for the permanent disappearance of the disease. VI. Treatment.—Prophylactic measures must not be omitted. The remedies recommended on page 122 should be given to individuals who suffer from constipation. Gourmands should be restricted in diet, should eat less meat and more vegetables, and should avoid rye bread, strong wine, coffee, or tea. Stasis should be prevented as long as possi- ble in diseases of the respiratory organs, heart, liver, or portal vein. After haemorrhoids have developed, care should be taken to secure an easy and soft evacuation from the bowels. The following prescriptions enjoy special repute: RPulv. liquirit. comp., . . . . f i. 1). S. One or two teaspoonfuls to be taken at night. R Sulphur. depurat., Kali bitartrat., ..... aa 3 vi. Rhizomat. zingiber., Rhizomat. calami, . . . . aa 3 i. M. D. S. One teaspoonful to be taken at night. As a matter of course, the dietetic measures previously referred to must rIso be adopted. Good results are obtained in many cases from the use of the waters of Carlsbad, Kissingen, Homburg, Marienbad, Rohitsch, Tarasp, etc. In very plethoric patients excellent results are often secured by the sulphur waters of Weilbach, Neuendorf, Eilsen, Baden near Vienna, Schinznach. In anaemic individuals we may employ mild acidulous iron springs, for example, Elster, Franzenbad, Cudowa, or the alkaline-muri- atic acidulous waters, for example, Ems, Soden, Cannstatt, Baden-Baden, •etc. Whey cures and grape cures are indicated in cases of obstinate constipation and marked mental depression. Specially prominent symptoms not infrequently require treatment. In order to prevent irritation of large external piles, they may be anointed with o. amygdalar., ol. cacao, etc. If there is violent pain in the region of the anus, we may order suppositories of opium, morphine, belladonna (vide page 112). Relief is also afforded, as a rule, by com- presses of ice-water, lead wash, or liq. alumin. acetic, (one per cent). In rectal blennorrhoea, intestinal infusions should be made with cold water and astringents, for example, nitrate of silver (gr. iss.-viiss. at each infusion), tannicacid (gr. iiiss.-xv.), etc. Hemorrhages require treatment only when they are unusually severe. We may inject ice-water, pure or mixed with astringents, or the rectum may be tamponed with cotton and Ergotinum Bombelon injected subcutaneously (one-half syringeful). Lan- 168 DISEASES OF THE INTESTINES. dowski recently extols repeated hot sitz-baths (to 40°) and rectal injec- tions of hot water. If the hsemorrhoids are prolapsed, the patient should be placed in the knee-elbow or lateral position, and an attempt made to replace the piles with the oiled finger, or a piece of linen dipped in oil. After reposition of the piles, renewed prolapse should be prevented by a light bandage to the anus. If this is associated with severe pain, the bandage may be sprinkled with laudanum, or smeared with an ointment of morphine or belladonna. If the piles cannot be replaced, they may be punctured or incised, and the attempt at reposition then renewed. If gangrene sets in, we may apply moist, warm poultices to facilitate the removal of the necrotic portions. In cases of violent molimina haem- orrhoidalis, five to ten leeches may be applied to the anus, and the hem- orrhage kept up by allowing the patient to use a vessel in which hot water has been placed. Eadical relief can only be effected by surgical operation, but for the discussion of the subject we must refer the reader to text-books on surgery. 10. Nervous Intestinal Pain. Enteralgia (Colic. Enterodynia. Neur- algia mesenterica). I. Etiology.—The term colic is applied only to those cases of intes- tinal pains which are independent of anatomical changes in the intestinal walls. The disease is a neurosis which sometimes occurs from peculiar changes in the intestinal contents, sometimes as an independent neurosis. The following changes in the intestinal contents must be taken into consideration: a. Coprostasis.—The process is here chiefly mechanical, inasmuch as the hard masses of faeces irritate the mucous membrane; in addition, the intestine is markedly distended. A special form is colica meconialisof the new-born, which occurs when the meconium is retained for some time after birth, b. Foreign bodies in the intestines sometimes give rise to colic (a coil of ascarides, tape-worm, ingested sharp bodies, faecal calculi, and gall-stones, which pass through the intestines), c. De- composing food, for example, sour beer, unripe fruit, fermented milk. d. In some cases, certain physical characteristics of the food are injurious; in others, there are peculiar idiosyncrasies. Thus a cold drink may be the cause of colic, and some individuals suffer whenever they partake of fish, oysters, certain vegetables, or fruits, etc. e. A frequent form is wind colic (flatulent colic), which is the result of the excessive develop- ment of gas and distention of the intestinal walls. It is found particu- larly in children, f. Toxic colic is observed after the use of certain cathartics, for example, senna, castor oil, etc. This is also noticed in lead and copper poisoning. Colic is observed as a neurosis, in the stricter sense, in hypochondria and hysteria, and also in organic diseases of the nervous system. It develops not infrequently as a reflex symptom in disease of the uterus, ovaries, liver, or kidneys. It has been observed immediately before an attack of gout, or instead of the seizure. In many cases, it is the result of a cold. II. Symptoms.—The chief symptom of colic is intestinal pain. This is referred usually to the region of the umbilicus, but often radiates into the back, chest, testicles, and thighs. It often remains in one locality. In other cases, it moves from place to place, and is associated with bor- borygmus, or with perceptible protrusion of individual parts of the intes- tines. The pain gradually assumes greater and greater intensity, and then DISEASES OF THE INTESTINES. 169 gradually subsides. More rarely the pains are lightning-like in char- acter. They are described as cutting, twisting, sticking, or as if the in- testine were violently stretched. The patients groan aloud, the face grows pale, the skin becomes cool and often covered with perspiration, the pulse is usually slow and hard. Sometimes the pains last a few sec- onds, and at other times many minutes. Many patients assume peculiar positions of the body. The thighs are drawn up on the abdomen, or the hands are pressed against this region, or the abdomen is pressed against a firm object, or the patient assumes abdominal decubitus. The abdomen is sometimes hard or sunken, sometimes it is tym- panitic. In certain cases, peristaltic movements of distended loops of the in- testines can be seen beneath the abdominal walls. Pressure often, though not constantly, relieves the pain; indeed, in some patients the sensitiveness of the abdominal walls is so great that a suspicion of peri- tonitis may be aroused. Reflex symptoms are often noticed in other organs, for example, sin- gultus, vomiting, asthmatic symptoms, palpitation of the heart, strangury, tenesmus, etc. The testicles are not infrequently drawn strongly up- wards, and the levator ani is spasmodically contracted. Priapism and pollutions are observed in rare cases, cramps in the calves, fainting-spells, and general convulsions develop in others. In many cases, the colic ceases suddenly after vomiting, eructations, or the discharge of flatus or faeces. Death occurs only in exceptional instances. Oppolzer observed it as the result of rupture of the intestine from excessive distention by the gas, and Wertheimber noticed death in convulsions in another case. III. Diagnosis.—The disease may be mistaken for: a. Rheumatism of the abdominal muscles. In this disease, the pain often changes its locality, lasts for a longer time, and presents no distinct exacerbations and remissions. The pain is situated nearer the surface, and is produced on slight contact with the abdominal walls, b. Lumbo-abdominal neur- algia. Valleix’s pressure points are present in this disease, c. Nervous pain in the integument of the abdominal muscles in hysterical patients. According to Briquet, this is rapidly relieved by the faradic current. d. Circumscribed peritonitis. Dulness on percussion and fever are present in this affection. IV. Prognosis.—The prognosis is almost always good, but relapses occur very frequently. V. Treatment.—The Colic itself may be treated by the subcutaneous injection of morphine, or the internal administration of chloral hydrate or opium (gr. ss., three powders at intervals of half an hour). Constipa- tion does not contraindicate the administration of opium. The abdo- men should be covered with a warm poultice (flaxseed), and one or more cups of warm carminative tea given. Among numerous other remedies which have been recommended we may mention belladonna and its preparations. Good results have also been obtained from the use of electricity: a vigorous faradic current, one pole in the rectum, the other labile upon the abdominal walls for five to ten minutes. Appendix. 1. Trousseau called attention to disturbances in the motor activity of 170 DISEASES OF THE INTESTINES. the intestinal nerves. Nervous constipation or diarrhoea ma»y be pro- duced according as the activity is diminished or increased. In some individuals fright or bashfulness exerts a laxative effect. In others certain articles of diet give rise almost immediately to diarrhoea, so that this can hardly be explained except as the result of increased peristalsis from purely nervous causes. Such cases are observed par- ticularly in neurasthenic, hysterical, and hypochondriacal individuals, but occasionally as reflex symptoms of diseases of the female sexual organs. The intestinal affection can only be relieved by treatment of the primary disease. 2. A few words with regard to embolism of the mesenteric artery. Scattered emboli in the smaller branches often produce no serious results, because the numerous collateral vessels compensate the obstruction to circulation. But if the main trunk or several adjacent branches are oc- cluded, that portion of the intestine whose circulation is interfered with undergoes hemorrhagic infarction, and even becomes necrotic. Extra- vasation also occurs between the layers of the mesentery. Peritonitic symptoms are not infrequent. The emboli are derived generally from vegetations of the valves of the leftside of the heart, more rarely from aortic aneurisms. The patients are suddenly seized with violent colicky pains, they grow pale and collapse occurs. The signs of peritonitis develop, occasionally the extravasation in the mesentery is felt as a tumor. In addition, blood is evacuated from the bowels. The prognosis is grave, although two cases of recovery have been reported. Treatment: Stimulants, morphine in violent pain, and intestinal infusion of ice-water against the hemor- rhage, if this appears in the stools as fresh blood, and therefore indicates embolism of the inferior mesenteric artery; otherwise Ergotinum Bom- belon should be given subcutaneously. DISEASES OF THE LIVEK. 171 SECTION Y. DISEASES OF THE LIVER. a. Diseases of the Biliary Passages. 1. Stenosis and Occlusion of the Bileducts. (Obstructive Jaundice. Absorption Jaundice. Icterus Hepaticus s. Mechanicus). I. Etiology.—In stenosis or occlusion of the bile-ducts the bile must accumulate above the obstruction. As it is secreted under very slight pressure, insignificant disturbances in the bile-ducts will produce stasis. The bile is then absorbed in greater part by the lymphatic vessels of the liver, to a less extent by the blood-vessels, and is thus carried into the general circulation. The biliary coloring matter in the blood then gives rise to jaundice (icterus). As a rule, occlusion of the bile-ducts can be recognized only by the existing jaundice. The causes of the stenoses of the bile-ducts may be situated within or without the liver. In the first event they affect chiefly the finer ducts within the hepatic parenchyma, not infrequently the intralobular biliary capillaries, while extra-hepatic causes affect the large excretory ducts (ductus hepaticus, choledochus, cysticus). Absorption jaundice is a frequent symptom of many hepatic diseases. It is absent in uncomplicated fatty and waxy liver. In one and the same disease icterus is sometimes absent, sometimes very marked, according to the degree of implication of the biliary passages. If only small amounts of bile are absorbed it will be excreted by the kidneys with suf- ficient rapidity to prevent its accumulation in the blood. Absorption jaundice sometimes depends indirectly upon diseases of the liver, for example, in hepatic cancer when the periportal glands are enlarged and compress the excretory ducts. Diseases of the biliary passages themselves not infrequently give rise to stenosis and occlusion, and thus to jaundice. One of the most fre- quent causes is catarrh of the bile-ducts, in which a profuse accumula- tion of secretion constitutes the obstruction. Ebstein showed that the catarrhal affection may be confined under certain circumstances to the intra-hepatic biliary passages, so that the origin of the jaundice can only be determined by microscopical examina- tion of the finer ducts. Yirchow showed that not infrequently marked inflammatory swelling of the walls of the bile-ducts may disappear after death. Croupous inflammation of the bile-ducts rarely gives rise to ab- sorption jaundice because the former disease is in itself infrequent. The bile-ducts are often obstructed by foreign bodies, usually gall- stones, in other cases parasites. Eor example, echinococcus vesicles may rupture into the biliary passages, or multilocular echinococci may take their origin in this locality. Distomum of the bile-ducts may also give rise to stenosis. Occlusion of the ductus choledochus may also be produced by ascarides, cherry-stones, etc. Whether occlusion may be produced by inspissated bile, has not been positively decided. 172 DISEASES OF THE LIVEK. Cicatricial strictures (usually the result of ulceration by gall-stones) occasionally produce stenosis, sometimes even obliteration of the bile- ducts. Similar conditions have been observed after catarrh of the biliary passages attended by epithelial desquamation, and after infectious diseases. In a few cases, cancer, lipoma, or polypi of the walls of the bile-ducts are the cause of the obstruction to the flow of bile. According to Schueppel, chronic inflammation of the excretory ducts and surrounding connective tissue may also produce stenosis. Congenital obliteration of the bile-ducts from foetal inflammation has been observed in several cases. In not a few cases the stenosis is the result of an affection of adjacent organs. Thus, catarrh of the duodenum very often gives rise to occlu- sion at the point of entrance of the ductus choledochus, either by a plug of catarrhal secretion and desquamated epithelium, or by catarrhal swelling of the mucous membrane itself. Cancer and cicatrizing ulcer in the duodenum may act in a similar manner. The bile-ducts some- times undergo compression in consequence of cancer of the stomach, and similar changes may be produced by distention of the colon with fseces, cancer of the colon, the pregnant uterus, large tumors of the uterus or ovaries, of the pancreas, omentum, mesentery, retroperitoneal glands, aneurism of the hepatic or mesenteric arteries, renal tumors, and floating kidney. In some cases the obstruction is the result of chronic perito- nitis which has given rise to the formation of retracting callosities. Obstructive jaundice has also been observed in right diaphragmatic pleurisy and acute peri-hepatitis. As is well known, the movements of the diaphragm exercise a very material influence upon the flow of bile, inasmuch as the inspiratory movements increase the pressure to which the liver is subjected, and thus facilitate the flow of bile into the intes- tine. But since the movements of the diaphragm are diminished or abolished in the diseases mentioned, the bile may accumulate in the in- tra-hepatic ducts, and thus pass into the general circulation. II. Symptoms.—If sufficient amounts of the biliary coloring matter enter the blood, the skin will assume a yellow color; this may vary from bright sulphur or orange-yellow to saffron-yellow, greenish-yellow, bronze and even blackish-yellow. Apart from the intensity of the stasis of bile, the color of the skin, as a rule, is so much darker, the older the patient, the thicker the epidermis, and the longer the jaundice has lasted. The mucous membrane also assumes a yellow color. The white color of the sclera disappears, and gives place to yellow. On the mucous membrane of the lips, tongue, and buccal cadty. pressure with the fingers must first be exercised in order to squeeze out the blood before the icteric color makes its appearance. If the mouth is widely opened, two icteric stripes will be seen on the soft palate and the posterior part of the hard palate, because the tension produced by opening the mouth has caused anaemia of these localities. If sudden, complete occlusion of the ductus choledochus or liepaticus has occurred, three days generally elapse before the first icteric changes become visible in the integument. The first indication generally ap- pears in the sclerotic conjunctiva, although in some cases this remains unchanged despite marked jaundice of the skin. The yellow color then appears in those parts of the skin which possess a thin epidermis and abundant vessels (naso-labial folds and lips, forehead, chest, abdomen, and back). The yellow color at first depends upon the presence of the DISEASES OF THE LIVES. 173 biliary coloring matter in the plasma of the blood, but later, this is de- posited in the deeper layers of the rete Malpighi. Very annoying itching of the skin (pruritus cutaneus) is observed in not a few cases. It generally appears after the jaundice has lasted for some time, more rarely at the beginning of the disease (Graves reported a case in which it even preceded the jaundice). This symptom may sometimes almost drive the patient to distraction. It occasionally occurs only at night, and indeed, as a rule, it is intermittent. It usually occurs only in circumscribed spots, particularly in the palms of the hands and soles of the feet, or between the fingers and toes. Scratch marks are generally present upon the skin. The pruritus sometimes disappears unexpectedly, although the jaundice continues unchanged. It has been attributed to irritation of the cutaneous nerves by the biliary pigment which has accumulated in the epidermis. A well-known physicist who suffered from intense jaundice assured me that, shortly before the begin- ning of the itching, he experienced in the affected parts a sensation of cold; on a number of occasions this was also recognized objectively. This will suggest the idea that the symptom is the result of vaso-motor dis- turbances. Eruptions may make their appearance upon the skin, some- times of an erythematous character, sometimes similar to urticaria. English authors call attention to the occasional development of xanthelasma which is confined not alone to the skin, but may also ex- tend to the mucous membrane of the buccal cavity. The perspiration very often presents an icteric color. Andral even reports that he ob- served icteric perspiration in a patient, although the integument and conjunctivae appeared to be unaffected. According to some authors urinary changes precede the cutaneous symptoms, but in our experience this is exceptional. The kidneys serve to remove from the body the biliary coloring matter which has accumu- lated in the blood. Its presence in the urine causes the latter to assume an unusually dark, reddish-brown appearance resembling that of porter. It is distinctly dichroitic, i. e., it glitters in reflected light, especially at the sides; after standing for some time it not infrequently assumes a greenish color throughout. When shaken, a yellow froth makes its ap- pearance, and remains for an unusually long time. Traces of albumin are sometimes present and casts are constantly found in the urine. The latter are hyaline, not infrequently covered with fat granules, and occasionally bile-stained epithelium cells from the urinary tubes. The presence of bile pigment in the urine may be shown by MarechaFs nr GmelnFs test. a. In carrying out the former, the urine is poured into a tube, and a few drops of tincture of iodine are added. If the urine is shaken, it assumes a beautiful emerald green color when bile pigment is present, b. Gmelin’s test is employed in the following manner: Com- mercial nitric acid is poured into a test-tube, and the urine is then allowed to flow slowly upon its surface. If the urine contains bile pigment a series of colored rings will appear at the layer of contact, the uppermost green, then blue, then violet-red, then orange, and finally yellow. The green color alone is conclusive, since a brown ring is obtained in many concentrated urines. 0. Rosenbach has made the following modification of Gmelin’s test. White blotting paper is dipped into the urine, and the excess allowed to drip off; it is then spread upon a white plate, and touched with a glass rod which has previously been dipped in impure nitric acid. Very distinct rings of color (yellow, violet-brown, and a 174 DISEASES OF THE LIVER. peripheral green) form at the point of contact. In a number of cases, I have noticed that Marechal’s test alone gave positive results. It is well known that Gmelin’s test particularly gives negative results, in febrile conditions. Frerichs found that some samples of icteric urine furnished no reaction unless exposed to the air for a certain length of time. On the other hand, too long exposure may cause the disappear- ance of Gmelin’s reaction, because the bile pigment undergoes further changes. The biliary acids are not always found in the urine owing to the fact that they are occasionally changed very rapidly in the blood. They are readily recognized by means of Pettenkofer’s test; their aqueous solution assumes a purple-violet color on the addition of a solution of cane sugar, and concentrated sulphuric acid, if it is not heated above 70° C. modification of this test is readily made. A piece of cane sugar is dissolved in the urine, a piece of filtering paper dipped therein, and then dried. If the dried paper is then touched with a glass rod which has been dipped in pure concentrated sulphuric acid, a dis- tinct carmine or purple-violet spot forms at the end of a few minutes at the point of contact. If the passage of bile into the intestines is entirely abolished, the faeces assume an ashen gray color. At the same time the evacuations are retarded and the faeces dry. They have a nauseous odor, and not in- frequently contain unusual amounts of fat. In some cases, true stear- rhcea, i. e., the discharge mainly of masses of fat, has been observed. These changes are readily explained by the fact that the bile pigment colors the faeces, that the bile stimulates peristalsis and exercises an anti- fermentative action on the contents of the intestines, and that it aids the absorption of fat. If the icterus is the result of intra-hepatic causes, the stools are not entirely destitute of bile. They usually have a clayey appearance, but occasionally bile-stained stools alternate with unstained evacuations. Gerhardt often observed numerous needle-shaped crystals of magnesia soaps in the faeces. The interference with the functions of the liver exercises injurious influences upon a number of other organs. Changes are observed most constantly in the digestive apparatus. The tongue usually presents a whitish, grayish, yellow or brownish coating. There is often foetor ex ore. The patients complain not infrequently of a bitter taste in the mouth, and eructations and vomiting may be observed. As a rule, there is marked anorexia; in rarer cases, the appetite is unchanged or bulimia is noticeable. There is often a feeling of distention of the stomach, and frequent complaints of borborygmus and colicky pains. In many patients there is a feeling of tension and tenderness in the region of the liver. The organ increases in size after a time, but later this symptom disappears while an increase of consistence becomes noticeable. If the obstruction is situated in the ductus choledochus, the gall-bladder is unusually distended with bile. It appears under the abdominal walls as a round, smooth tumor, which moves with respiration or, in other cases, is only accessible to the palpating finger. Increase in the size of the gall-bladder is also observed in occlusion of the cystic duct. Indeed, the organ may then attain the dimensions of a child’s head. In such cases, the bile, which was originally present in the gall-bladder, is ab- sorbed, and the organ becomes filled with a colorless secretion which con- tains mucus (hydrops cystidis felleae). 175 DISEASES OF THE LIVER. The pulse is sometimes extremely slow (twenty-one beats a minute in a case observed by Frerichs). In my own experience, however, this symptom is by no means constant. It has been attributed to irritation of the intra-cardiac ganglia by the biliary acids in the blood. In cases of fever, the pulse is not accelerated in proportion to the increase of the bodily temperature. Changes in the bodily temperature are not the result of jaundice itself. The disposition of the patients changes very early. They become moody, capricious, and unusually irritable. Many complain of a con- stant insomnia. Yellow vision (xanthopsia) is observed in rare cases. This must be regarded as a purely nervous symptom; in the first place, because it does not correspond to the intensity of the jaundice, and, furthermore, be- cause it is usually intermittent. Day-blindness (nyctalopia) has been observed in some cases. Other writers have noticed night-blindness (hemeralopia). Bamberger is inclined to attach an unfavorable signi- ficance to these symptoms. Retinal hemorrhages have been repeatedly observed on ophthalmoscopic examination. Signs of emaciation and feebleness not infrequently develop with sur- prising rapidity. Apart from disturbance of the functions of the liver, these symptoms are partly the result of a diminished supply of food and imperfect digestion. It has been assumed by some that the biliary acids which are absorbed by the blood partly dissolve the red blood-globules, but these acids are in part very rapidly destroyed in the blood, and, on the other hand, are soon excreted in the urine, so that they do not attain the degree of con- centration necessary to dissolve the red blood-globules. This disposes of the theory that every obstruction jaundice is associated with haematog- enous jaundice, in which the coloring matter of the red blood-globules, which are supposed to be dissolved, is converted within the vessels into bile pigment. Leucin and tyrosin and an unusual amount of fat have been repeatedly observed in the blood. The bile pigment is sometimes excreted in the milk of nursing wo- men, and during pregnancy the foetus becomes jaundiced if the icterus of the mother has lasted more than two weeks. The duration of obstruction-jaundice depends upon its causes. In some cases the disease lasts a few days, in others a few months, and even years. As a rule, the icterus which lasts more than one to two months, or even increases in intensity, is usually due to something more serious than gall-stones or catarrh of the biliary passages. Van Swieten reports a case, however, in which recovery occurred after the jaundice had lasted eleven years. The occurrence of recovery is first recognized by the bile- staining of the faeces. A tumor of the gall-bladder, which had previously existed, disappears. When the biliary passages are suddenly freed from obstruction, bile may enter the intestines in such large quantities that thin blackish-green stools are evacuated. Next, the urine loses its dark color, and the bile-pigment reaction becomes more and more distinct. The return of the normal color appears last in the skin, since this re- quires a gradual desquamation of the deeper cell layers of the rete Mal- pighi* If recovery does not occur, the jaundice itself may prove a source of danger. Death may occur with symptoms of increasing marasmus. Emaciation and loss of power increase, and are followed by hemorrhages 176 DISEASES OF THE LIVER. upon the skin and mucous membranes, uncontrollable diarrhoea, gastric and intestinal hemorrhages. In other cases, severe nervous symptoms develop (cholaemia). The patients usually become apathetic, and delirium ensues; they toss rest- lessly to and fro, moan, and breathe irregularly. Cheyne-Stokes respir- ation is observed in some cases. Finally death ensues. The delirium rarely assumes a furibund character. Death sometimes occurs suddenly, with symptoms of perforation- peritonitis, as the result of rupture of the distended bile-ducts. In other cases, rupture of the biliary canals takes place within the liver. The signs of hepatic abscess then develop, and finally prove fatal. III. Anatomical Changes.—A yellow color is observed in the skin, conjunctiva, subcutaneous adipose tissue, the fat about the heart and on the mesentery, and in the muscles of the body. Effusions into the serous cavities have a yellowish-brown color. Icterus has also been ob- served in the fasciae, cartilages,bones, intima of the vessels, aqueous humor, occasionally in the cornea and sclerotica. Icterus is always absent ip the nerve tissues, although if considerable oedema of the brain develops as the result of infiltration with serum of an icteric color, a section of the brain may present a yellowish appearance. In the liver, the biliary pas- sages above the stenosis are dilated. If the obstruction is situated at the extremity of the ductus choledochus, all the bile-ducts may attain the circumference of the finger. At the same time, they appear elongated and sinuous. Similar changes are observed if the bile-ducts are followed into the parenchyma of the liver; indeed, sacculated diverticula are here aggregated still more closely than in the ducts. In some portions of the surface of the liver they project like cysts, which are filled with biliary contents. The gall-bladder also takes part in general dilatation of the bile-ducts. The walls of the bile-ducts are often thickened, in other cases, ex- tremely thin. At first, their contents consist of unchanged bile, but if the obstruction persists for a long time, and the liver loses its bile-pro- ducing function, the bile is absorbed and replaced by a more serous, mucous fluid, which is furnished by the mucous membrane of the biliary passages. At the beginning of general biliary stasis, the liver increases in size, but later it becomes smaller. Its consistence often changes; sometimes it is unusually flabby, sometimes extremely hard and firm. In recent cases, its color is golden or saffron-yellow; in older ones, greenish or greenish-black. The immediate vicinity of the central veins is most in- tensely colored, so that the liver not infrequently presents a nutmeg appearance. Under the microscope, the hepatic cells, particularly near the central veins, are in part diffusely infiltrated with bile, in part filled with gran- ular bile pigment. This first accumulates near the nuclei of the cells, sometimes in the shape of fine granules, sometimes as irregular jagged dots, sometimes as small delicate rods. Later, some of the hepatic cells undergo granular degeneration; not infrequently the interlobular con- nective tissue undergoes proliferation (cirrhosis). The interlobular biliary passages are not infrequently filled with thickened, blackish-green bile. Frerichs noticed that the cylindrical epithelium is gradually flattened, and assumes more and more the appearance of pavement epithelium. Fat granules are observed here and there in these cells. After prolonged obstruction jaundice, important anatomical changes DISEASES OE THE LIVER. 177 develop in the kidneys. Externally they appear greenish; in old cases, the cut section is also greenish; in recent cases it presents an intense saffron color. The consistence is often extremely soft and flabby. At first, the epithelium cells of the convoluted tubes and Henle’s loops are diffusely covered with bile pigment; later they contain a de- posit of granular bile pigment. The yellow color is least intense in the Malpighian capsules. At a still later period, there is a deposit of gran- ular pigment in the lumen of the tubes, in which we find pigment casts, especially in the straight tubes of the pyramids. Under such circum- stances, flakes, granules, and cylindrical casts of bile pigment are found in the sediment of the urine. These lesions may obstruct the renal tubules, and thus render impossible the excretion of the constituents of the bile which have been taken up from the blood. The development of cholaemic symptoms is favored in this manner. In addition, fatty de- generation, desquamation, and destruction of epithelium of the tubes are sometimes observed. IV. Diagnosis.—The diagnosis of obstruction jaundice is easy, but it should be remembered that daylight is requisite to recognize the icteric color of the skin. In anaemic and cachectic individuals, we should avoid mistaking an excessive development of subconjunctival adipose tissue for conjunctival jaundice. It is not always easy to dis- tinguish obstruction jaundice from haematogenous icterus, i. e., that form which develops from the dissolution of red blood-globules within the vessels and their conversion into bile pigment. In the latter, biliary acids will always be absent in the urine; but, on the other hand, they cannot always be demonstrated in this fluid in undoubted cases of ob- struction jaundice. On the other hand, biliary acids have been detected in the urine of healthy individuals. In addition, the stools retain the normal color in haematogenous icterus, since the flow of bile has not been interrupted; bile-stained stools may also occur in obstruction jaundice, if it is the result of intra-hepatic causes, and not of complete closure of the ductus hepaticus or choledochus. In order to determine whether an obstruc- tion jaundice is the result of diseases of the hepatic parenchyma or of causes situated outside of the liver, careful examination should be made of all the organs in question, and, in addition, attention should be paid to the character of the stools. These are rarely constantly destitute of bile when the jaundice is the result of intra-hepatic causes. It is only in affections of the ductus choledochus that an increase in the size of the gall-bladder may be expected. Y. Prognosis.—The prognosis depends upon the causes in each individual case. It is unfavorable when symptoms of dissolution of the blood occur, since these indicate an advanced stage of marasmus. Cholaemic symptoms also have an unfavorable significance. VI. Treatment.—The chief importance must be attached to the diet; fats must be particularly avoided. We may recommend skimmed milk, coffee, tea, soup, lean meat, stewed vegetables, and fruit, soft boiled eggs, and white wine. If the thirst is increased, we may give lemonade or water, Selters water, etc. If the patients complain of a bitter taste in the mouth, the tongue is coated, and nausea is present, we may order acids, for example: § Sol. acid, hydrochloric., TTtxij. : § vi. D. S. One tablespoonful every three hours. Acid, hydrochloric., acid, nitric., aa Tflviij.; aq. destil. ad § viss. M. D. S. One tablespoonful every three hours, etc. 178 DISEASES OF THE LIVER. Constipation necessitates the administration of laxatives, especially the vegetable ones (I£ Inf. rad. rliei, 3 ss. : 3 vi. One tablespoonful every three hours. 1$ Inf. sennae comp., | v. One tablespoonful t. i. d. B Pulv. liq. comp., | i. D. S. One to two teaspoonfuls at night. B Aloes, ext. rhei comp., ail gr. xxij., pulv. et succ. liq., q. s. ut ft. pil. No. xxx., three to four pills at night). Calomel may be given in a single dose of gr. iv.-vij. If organic changes in the liver can be excluded, and we have to deal merely with chronic absorption jaundice, we may make use of mineral waters. If the jaundice is associated with obstinate jaundice, we may order waters containing Glauber’s salts and sodium chloride—in plethoric individuals Marienbad, Kissingen or Homburg, in feeble individuals Carlsbad, Soden or Kronthal. In addition, the alkaline and alkaline- muriatic wells, such as Ems, Vichy, Selters, Bilin, etc. When necessary, diuresis should be stimulated by the administration of carbonated waters (for example, Selters), acetate or bitartrate of pot- ash, etc. I have relieved several cases of annoying pruritus by large doses of potassium bromide (gr. xxx. morning and evening). The surface may also be washed with a solution of carbolic acid (2$), corrosive sublimate, vinegar, warm baths, etc. Warm baths are agreeable to the majority of patients. Their efficacy is increased by the addition of about fifteen ounces of soda to each bath. In my experience, chloral hydrate (gr. xxx. to xlv. in a wineglassful of sugar-water) gives the best results in obstinate insomnia. The development of cholaemic symptoms requires stimulant measures, for example: B Acid, benzoic., gr. ivss.; camphor., gr. i.; sacch. albi, gr. viiss. M. f. p. No. x. S. One powder every two hours; strong wine, mustard poultices to the nape of the neck, ice-bag to the head, cups to the neck, etc. 2. Catarrh of the Bile-ducts. Cholangitis et Cholecystitis Catarrhalis. {Catarrhal or Simple Jaundice. Gastro-duodenal Jaundice.) I. Etiology.—Catarrh of the bile-ducts occurs in rare cases as a primary affection following a cold. It is almost always the result of secondary changes, most frequently of the extension of inflammation to the ductus choledochus and often higher up from previous gastro-duo- denal catarrh (vide page 105). Concretions or parasites in the bile-ducts sometim esgive rise to catarrh of the mucous membrane by their purely mechanical irritation. According to some authors, this catarrh may be the result of anomalies in the chemical constitution of the bile. According to Frerichs, pro- longed fasting causes stasis of bile within the gall-bladder, favors de- composition of the accumulated bile, and may thus produce catarrh which is confined to the gall-bladder and cystic duct. Catarrh of the intra-hepatic biliary canals is not infrequently pro- duced by diseases of the hepatic parenchyma (cancer, abscess, echinococ- cus, and cirrhosis). The diagnosis of catarrh, instead of compression of the biliary passages, may be made in these conditions, if jaundice occurs transitorily despite the continued advance of the affections mentioned. The disease is sometimes the result of disturbance of circulation 179 DISEASES OF THE LIVER. (valvular disease of the heart, emphysema of the lungs, chronic bron- chitis, and other chronic diseases of the respiratory tract). Cases have been described in which signs of catarrh of the bile-ducts repeatedly occurred during menstruation, probably as the result of vicari- ous congestion of the liver. In those cases in which the symptoms follow mental excitement, we are inclined to attribute the disease to vaso-motor disturbances, and anom- alies in the distribution of the blood to the liver. Toxic catarrh of the bile-ducts may be the result of poisoning with phosphorus, lead, and chloral hydrate. This category also probably includes those forms which are observed during infectious disease (fibrinous pneumonia, typhoid fever, cholera, malaria, and the beginning of the so-called secondary stage of syphilis). The epidemic occurrence of catarrh of the bile-ducts has been de- scribed by a number of writers. In some cases it is the result of colds, and hence is observed during periods of marked changes of tem- perature. Koehnhorn attributes some epidemics which have occurred in barracks to the monotony of the diet. Certain epidemics are undoubtedly the result of miasmatic influences. Rehn described an epidemic in Iianau in which children alone were affected; in other cases, adults alone suffered from the disease. Catarrh of the bile-ducts occurs with equal frequency in both sexes. The disease is rare in old age. Fig. 49. Pulsus trigeminus in catarrhal jaundice in a man set. 32 years; right brachial artery. II. Symptoms.—Catarrh of the bile-ducts cannot he recognized un- less occlusion, and therefore stasis of bile, takes place as the result of swelling of the inflamed mucous membrane, excessive secretion of mucus, and active desquamation of epithelium. The symptoms are then the same as those of the obstruction jaundice just described, so that we need not again enter upon their description. It may here be mentioned, how- ever, that slowness of the pulse is especially frequent in catarrhal jaun- dice, and that allorythm of the pulse is not infrequently observed (vide Fig. 49). As a rule, the occurrence of jaundice is preceded by the symptoms of gastro-duodenal catarrh (coated tongue, flat taste in the mouth, anorexia, eructations, nausea, vomiting, tenderness in the gastric region, etc.) Febrile movement is observed not infrequently. These prodromata sometimes last two weeks, but in some cases they are so slight as to be almost overlooked. After the appearance of jaundice the gastro-ente- ritic symptoms sometimes diminish entirely; in other cases they increase in severity. The duration of the jaundice, on the average, is two to six weeks, but under certain circumstances it may last for several months. The disease almost always ends in recovery. In rare cases, cholaemic symptoms develop and terminate fatally. Adhesion of the bile-ducts sometimes occurs in those places at which active desquamation of the epithelium has occurred, and this results in chronic jaundice. In equally 180 DISEASES OF THE LIVER. rare cases, the catarrh is followed by ulceration and hepatic abscess. Catarrh of the bile-ducts may also give rise to the formation of gall- stones. III. Anatomical Changes.—The changes in this disease can rarely be observed in the dead body. In addition, a part of the symptoms (congestion and swelling of the mucous membrane) disappear in the cadaver. Nevertheless, we are justified in assuming congestion, swelling, and unusual succulence of the mucous membrane in this condition. An accumulation of mucus and desquamated epithelium cells remains in the ducts as signs of a previous inflammation. Occasionally we find that their consistence is increased, so that they float to and fro in water. In older cases, they are not infrequently of a puriform character. Stenosis apd occlusion are especially apt to occur at the entrance of the ductus choledochus into the duodenum. Pressure along this duct in the direction towards the intestine often discharges a plug of mucus and epithelium. In other cases, the stenosis is rather the result of swelling of the mucous membrane which has disappeared in the cadaver, so that the mechanical conditions are explained with difficulty. Under such circumstances, it should be remembered that the mucous membrane is pale in that portion of the duct which was occluded, while it appears yellow above on account of the stasis of bile. The bili- ary passages are dilated and filled with bile above the site of occlusion. If the catarrh was confined chiefly to the gall-bladder, its contents con- tain an unusual amount of mucus. This inflammation is sometimes fol- lowed by thickening or calcification of the wall of the gall-bladder, adhesion, inflammation of the serous surface, the formation of concre- tions, or dropsy of the organ. The liver is icteric, and may present the changes described in the previous section. IV. Diagnosis.—The recognition of catarrh of the bile-ducts is gen- erally easy if obstruction jaundice is present. Careful examination of the liver and adjacent organs and an accurate history of the case will generally enable us without special difficulty to determine the cause of the disease. We should be careful, however, not to make too positive a diagnosis. We recently had under treatment a man, aet. 75 years, who suddenly suffered from constipation and jaundice, presumably catarrhal in charac- ter. At first the liver appeared unchanged. Three weeks later, it in- creased in size; at the end of another month, prominences appeared upon its lower surface, and in the thirteenth week death occurred from cancerous cachexia. Our suspicions should always be aroused if .jaun- dice occurs in old age, and its intensity does not diminish at the end of four weeks. Catarrhal jaundice may be mistaken for gall-stones which have ob- structed the ducts; but in the latter, colicky pains are usually present, the jaundice generally disappears more rapidly, and finally the gall-stones should be looked for in the stools. V. Prognosis.—This is almost always favorable. VI. Treatment.—The causal indications should be first considered. If the patient suffers from gastro-duodenitis, he should be placed on fluid diet (milk, soup, tea, lemonade) and acids given internally (acid hydrochloric, nxxxx. : f viss., one tablespoonful every two hours, etc). If the stomach is overloaded, an emetic may be ordered. The vigorous contractions of the abdominal walls sometimes dislodge the plug in the DISEASES OF THE LIVEE. 181 bile-ducts. These remedies, however, should be used with caution, since it is known that they not infrequently give rise to jaundice. Gerhardt recommended compression and faradization of the gall- bladder in order to remove, mechanically, the plug in the bile-duct. This writer found that, in compression of the gall-bladder, the en- trance of bile into the duodenum could sometimes be felt as a fine r&le. The stools then usually assume a biliary color on the second day ; the ap- petite improves at once, and the pruritus which is produced by jaun- dice also ceases. in faradization of the gall-bladder Gerhardt applies one pole to the region of the organ, the other posteriorly along the spine. A strong current should be used. This method should be employed when the gall-bladder cannot be reached with the fingers. If the application is successful, the urine soon becomes lighter in color and its specific gravity diminishes. Krull has repeatedly obtained very rapid results from the infusion of large amounts of water (one to two litres at 12° R.; later, at 18°) into the large intestine. The patient should endeavor to retain the water as long as possible. 3. Purulent Inflammation of the Bile-ducts. Suppurative Cholangitis and Cholecystitis. I. This is observed most frequently in gall-stones, parasites, or foreign bodies in the bile-ducts. The inflammation in the beginning is generally catarrhal, then becomes purulent, and, in some cases, even diphtheritic and croupous. The sup- purative inflammation is sometimes the result of stasis of bile, the latter under- going decomposition and irritating the mucous membrane to an intense degree. In other cases the inflammation extends from the liver (abscess, inflammation of branches of the portal vein, etc.) Purulent inflammation sometimes develops from catarrh of the bile-duct. In some cases the disease is the result of infectious diseases (typhoid fever, pyaemia, etc.). Cases have also been reported in which no cause could be discovered. II. The inflammation is sometimes confined to the gall-bladder, sometimes to the excretory ducts, sometimes to the intra-hepatic canals, or finally, it may ex- tend over the entire system of the biliary passages. The contents of the biliary passages contain an admixture of pus, sometimes they are almost entirely puru- lent, occasionally ichorous. The mucous membrane is loosened, injected, sometimes ecchymotic, or if the condition has lasted for a long time, it is pig- mented in spots. Losses of substance may occur and give rise to perforation either into the abdominal cavity or, after peritonitic adhesions have formed, into the stomach, duodenum, colon, portal vein, external abdominal walls, etc. In purulent inflammation of the intra-hepatic ducts, the inflammation sometimes extends to the parenchyma, inasmuch as ulcerations of the canals cause partial destruction of the walls, and thus inflammation and abcess formation in adjacent parts of the liver. The abscesses are generally multiple and small in size, more rarely they are single and attain large dimensions. III. A diagnosis can hardly be made with certainty during life. All symptoms may be absent, particularly in infectious diseases in which the primary disease occupies the foreground. Jaundice, chill, fever, enlargement of the liver, and perhaps painful swelling of the gall-bladder are occasionally observed. The dis- ease sometimes ends fatally in a few days, or it is more protracted and ends in recovery. For example, gall-stones may be discharged and the retained masses of pus may then find their way into the intestines. The prognosis is always grave. The treatment is symptomatic. 4. Gall-Stones. Cholelithiasis. I. Etiolgy.—The disease is observed most frequently in women after the age of forty years. Among three hundred and ninety-five cases, Hein found only three below the age of twenty years. 182 DISEASES OF THE LIVER. In a few cases, however, the calculi have been found in still-born children, infants, and during the first decade. Compared with men, women are affected in the proportion of 5-3 : 1. The predisposition of females has been attributed to tight lacing, which interferes with the flow of bile, and to the relations between the liver and the sexual organs of the female. It has been noticed that the development of gall-stoues is favored by previous pregnancy, that it develops most frequently at the menopause, or that the first symptoms become noticeable at the beginning of the period of puberty. According to some writers, sedentary habits predispose to the develop- ment of gall-stones. Similar statements are made with regard to high living. Local and climatic influences are considered important by some writers. In some regions this has been attributed to the abundance of lime in the drinking-water. Gall-stones are extremely rare in the tropics in which abscess of the liver and hepatic enlargement are usually fre- quent. Beneke has called attention to the fact that the disease is often associated with atheroma of the arteries. In some cases the gall-stones form around foreign bodies, such as clots of blood, parasites, etc. Met- tenheimer believed that fatty and calcified cells of the mucous mem- brane of the gall-bladder, when they had been separated from the latter, may become the nuclei of the gall-stones. II. Anatomical Changes.—Gall-stones form most frequently in the gall-bladder, much more rarely in the intra-hepatic ducts, while they are never found in the ductus cysticus, hepaticus, choledochus, unless they have migrated from other parts. Bile gravel is a finely granular mass, which sometimes looks inspissated; it is usually greenish, blackish, more rarely brown, or even whitish in color. It is sometimes found alone, sometimes in combination with gall-stones. It is most frequent in the gall-bladder, in which its development is favored by the physiological stagnation of the bile. The size of gall-stones varies from that of a grain of sand to that of a egg. Those situated in the gall-bladder are usually larger than those found in the narrow intra-hepatic ducts. Meckel described one which was fifteen cm. in length and twelve cm. in circumference. Their number is extremely variable. Sometimes but a single one is found, in other cases they are almost innumerable. On the average, the gall-bladder contains ten to fifteen; in one case Otto counted seven thousand eight hundred and two. Chopart reports a case in which the intra-hepatic ducts were distended with gall-stones to such an extent that the liver could hardly be cut with a scalpel. The shape of the stones depends partly on the place of development. In the intra-hepatic canals they are often cylindrical, not infrequently with lateral projections (cast of the branches of the ducts). Such gall- stones are sometimes hollow, and the lumen may be filled with inspis- sated bile. Stones in the gall-bladder may be round, elongated, or angular. Sometimes they reproduce the pear shape of the gall-bladder, especially if only one calculus is present which completely fills the organ. In not a few cases the shape resembles that of a nutmeg. Sometimes we find regular stereometric bodies, for example, tetrahedra, octahedra, etc. More frequently, the calculi are irregular in shape, and their surfaces often fit into one another (vide Fig. 50). It was formerly supposed that the many angles of the gall-stones were the result of the friction of the calculi against one another; but this view is incorrect. Their shape is at first round, and spaces are thus left be- tween adjacent stones. Hence, the further growth of the calculi must deviate from the spherical shape. DISEASES OF THE LIVER. 183 The surface the calculus may be entirely smooth. In other cases it presents numerous nodules (mulberry stones). The color may be black, greenish-brown, white, yellow, or gray, and depends particularly upon their chemical constitution. Calculi Fig. 50. Fig. 51. Fig. 50.—Facetted gall-stones; the one to the left has been sawn through. Natural size. Fig. 51.—Gall-stones of cholestearin; the one to the left has been sawn through. Natural size. composed of cholestearin are white as alabaster, appear transparent when fresh, and only lose this appearance after they have been exposed to the air. The brownish, greenish, or blackish color becomes more marked the greater the amount of bile pigment which is present. Calculi of calcium carbonate have a chalky whiteness. In very rare cases, bluish gall-stones have been observed. In the fresh condition, they can usually be compressed between the fingers. Their surfaces often have a Fig. 52. Fig. 53, Tig. 52.—Cholestearin calculus with cortex of bilirubin-lime. On the right side the surface liaa been sawn through. Natural size. Fig. 53.—Laminated calculus of bilirubin-lime. This stone was crushed during evacuation. peculiar fatty or soapy feel. Fragments of the calculi are occasionally found in the gall-bladder or excretory ducts. The surface of fracture of cholestearin calculi is radiating and crystalline (vide Fig. 51). In those which are composed chiefly of bilirubin-lime, the surface of fracture is often very irregular; more rarely the stone consists of con- centric layers (vide Fig. 53). The weight depends upon the size and •..chemical constitution. Those formed of cholestearin are especially 184 light. Ritter reports a case in which a single gall-stone weighed 4f ounces. The specific gravity is always greater than that of water, in one case it was 1.580, in another 1.966. After the calculi have been exposed to the air for a long time, and have become desiccated, they may float on water. After they have re-absorbed water they again sink. The following substances have been found in gall-stones: Cholestearin, bile- pigments, especially bilirubin, which, in combination with lime, is found in most calculi, smaller quantities of the biliary acids, fatty acids, mucin, and epi- thelium. The inorganic substances include carbonate, phosphate, and sulphate of lime, phosphate and carbonate of magnesia, traces of iron, copper, and man- ganese. Mercury is sometimes found if the patients have been subjected to mercurial inunctious. In some gall-stones, cholestearin is the chief constituent (ninety- eight per cent), and it is only in rare cases that this substance is entirely absent. Ritter found, as the result of numerous analyses, that the ma- jority of the calculi contained: Cholestearin, . . . . . 70.6 Organic substances, . . . 22.9 Inorganic substances, . . . . 6.5 Ritter also furnishes the following detailed analysis of a gall-stone: Cholestearin, . . . . . 0.4 Bilirubin and bilifuscin, . . . 0.6 Biliprasin, . . . . . 0.8 Bilihumin, . . . . . .12.8 Biliary constituents, soluble in water, . . 2.3 Calcium carbonate, . . . . .64.6 Calcium phosphate, . . . . 12.3 Ammonium-magnesia phosphate, . . .3.4 Mucus, . . . . . . 2.8 Biliary calculi are either homogeneous or conglomerate. The former have the same physical and chemical constitution throughout. In the centre of the latter we find a nucleus and the peripheral layers often present a special cortex. Thus Fig. 51 represents a cholestearin calcu- lus, with a simple nucleus, while in Fig. 52 we notice a nucleus, a body composed of cholestearin, and a cortex composed, in the main, of bili- rubin-lime. The nucleus of gall-stones usually consists of mucin, epithelium cells, and bilirubin-lime, in some cases of foreign bodies. The nucleus is sometimes situated eccentrically. This is always the case when more than one is present (as many as five have been observed). Multinuclear gall-stones usually result from the conglomeration of single ones. With regard to their chemical constitution, we may distinguish: a. pure cholestearin stones; b. pure pigment stones; c. pure lime stones; d. cholestearin pigment stones. a. Pure cholestearin calculi are transparent in transmitted light when in a fresh condition; but when dry, become opaque. They usually have a crystalline, glistening surface of fracture, and a radiating structure. The surface is sometimes smooth, sometimes nodular. They have a peculiar fatty structure, and are usually light. The specific gravity is also very low, though always higher than that of water. They are com- bustible, and burn with a bright flame, b. Pure pigment stones are much rarer than cholestearin calculi. They may be of a rusty brown, greenish or blackish color, are often homogeneous and not infrequently DISEASES OF THE LIVER. 185 very brittle, c. Pure lime stones (composed of carbonate of lime) are very rare. They are white or grayish-white, very hard and heavy. d. Oholestearin pigment stones form the most frequent variety. Their structure is not infrequently laminated, or the body consists chiefly of oholestearin, the cortex contains bilirubin-lime or carbonate of lime. If a number of calculi are contained in the gall-bladder, they almost always present the same physical constitution. The surface of gall-stones is sometimes eroded and more or less de- stroyed (vide Fig. 54). It has been supposed, therefore, that the bile itself is capable of dissolving gall-stones. Schueppel has recently suggested that this is the result of the proliferation of bacteria. The calculi often exert a noxious influence on the integrity of the biliary passages. They sometimes distend the gall-bladder to such an extent that it is unable to receive fluid bile. In other cases, it contains also a mucous or purulent fluid and indications of catarrhal inflamma- tion of the mucous membrane. This fluid is sometimes converted into a mortar-like mass. The mucous membrane is sometimes very smooth, like a serous membrane; sometimes its normal recesses are distended into diverticula, which may also contain gall-stones; the latter may be- come encapsulated. Fatty degeneration of the muscular coat, calcifica- tion, hypertrophy, and atrophy of the walls are not infrequent Similar anatomical changes may occur in the intra-hepatic ducts. The parenchyma of the liver itself may be implicated, and hepatic abscess, the formation of cicatrices, or inflammation of the portal vein may be the result. The real causes of the formation of biliary calculi are not known with certainty. In the majority of cases, it seems that their development is preceded by catarrh of the biliary passages. The abundant mucus which is thus produced decomposes the bile, particularly the salts of the biliary acids. Inasmuch as the biliary acids retain oholestearin and bile pigment in solution, changes in the former may render possible the deposit of the hitherto dissolved substances. It is also probable that the car- bonate of lime is derived from deposits in the bile, although it is pos- sibly at times a direct product of the inflamed mucous membrane. In a number of cases, the formation of gall-stones has been observed in the glands of the mucous membrane. III. Symptoms.—In many cases, the presence of gall-stones remains entirely latent during life. In others, they give rise to no annoyance, but can be positively diagnosed, for example, if the gall-bladder is dis- tended with calculi, and can be felt as a hard, tense tumor. If the gall- bladder contains several stones, we are sometimes able to rub these against one another, thus giving rise to a peculiar hard friction. Upon the application of the stethoscope, this is heard as a metallic clattering. In a case in which it was doubtful whether the enlargement of the gall- bladder was due to cancer or to an accumulation of gall-stones, Whitaker employed puncture, and attempted to base the diagnosis of gall-stones upon the hard scratching of the instrument employed in puncture. Gall-stones are sometimes found accidentally in the faeces, although they have given rise to no symptoms. This is observed in old people in whom the symptoms remain absent on account of flaccidity and unusual dilatation of the biliary passages and the diminished sensibility of the mucous membrane. DISEASES OF THE LIYEK. Fig. 54. Bile pigment calcu- lus with numerous erosions and de- pressions. 186 DISEASES OF TIIE LIVER. In some cases, the calculi are concealed by the symptoms of other dis- eases, for example, inflammatory changes in the intra-hepatic ducts, and abscess of the liver. The typical clinical history by which the presence of gall-stones is revealed is that of biliary colic. But this occurs only when the gall- stones have a tendency to migrate, and meet with obstructions in their passage. The attacks of colic sometimes occur spontaneously, some- times follow bodily exertion, occasionally mental emotion. Asa rule, the colic appears some time after a hearty meal. The most prominent symp- tom is the atrocious pain, of a boring, burning, lancinating character, and situated in the right hypochondrium. It generally radiates into the right thigh and testicle, the back, the right, more rarely the left, shoul- der, and the right arm. The face expresses pain and terror, the fore- head is covered with perspiration, and the features are pale, or, in rare cases, unusually red. The patients often toss to and fro in bed, press the fists into the region of the liver, and are bent over forwards. The ab- dominal walls are tense and contracted; sometimes this is found only on the right side. The region of the liver is unusually sensitive to pressure, and in many cases the patients cry out aloud, as soon as the regio»of the gall-bladder is touched (outer border of the right rectus abdominis, im- mediately below the eighth rib). A chill occurs not infrequently at the beginning of the attack. The temperature may gradually rise beyond 40 C. in other cases, it re- mains normal, or even subnormal. The pulse is not infrequently inter- mittent or irregular, sometimes rapid and small, sometimes slow and full; the respirations are interrupted and deep. In many cases, vomiting occurs, at first of the contents of the stomach, then of bilious, and finally of muco-watery masses. Obstinate singultus is not an infrequent symptom. The bowels are generally constipated, but in some cases diarrhoea is noticed (muco-bloody or rice-water dis- charges). The urine is scanty, dark, and loaded with urates. The violent pains occasionally cause severe disturbance of conscious- ness. The patients become delirious, and general convulsions and un- consciousness may be produced. As a rule, the average duration of an attack of pain is three to five hours; then a pause follows, after which the pains again occur. Finally they may cease quite suddenly. The pains must be attributed to the irritation of the mucous mem- brane of the excretory ducts by the gall-stones. After the calculus has left the ductus cysticus, the pains generally cease for some time, because the ductus choledochus is much wider than the former. The pains re- appear as soon as the stone passes through the narrow outlet into the intestine. The calculi of the intra-hepatic canals generally pass along without special mechanical difficulty, and therefore without pain until they reach the point of outlet of the ductus choledochus. An attack of biliary colic not infrequently ceases because the gall-stone which has passed from the gall-bladder into the ductus cysticus is again pushed into the former. In not a few cases, the symptoms mentioned are associated with jaundice; sometimes only the conjunctiva is affected, sometimes the skin and urine. The symptoms vary according as the calculus, when it passes the ductus hepaticus or choledochus, merely slows or entirely abolishes the flow of bile. Whether the gall-stone is present in the ductus hepaticus ■or choledochus may be determined by the fact that in the latter event the DISEASES OF THE LIVEK. 187 gall-bladder increases in size, and becomes accessible to palpation. The icterus develops some time after the beginning of biliary colic, since stasis of bile and the accumulation of bile pigment in the blood must attain a certain intensity before distinct jaundice is produced. The evacuations should be dissolved under a vigorous stream of water in a coarse sieve, so that the latter may retain any calculi which have entered the intestine. The stools should be examined daily for a week after the beginning of an attack, since the calculi are often retained in the intestine for a number of days. In the majority of cases biliary colic terminates in recovery, but there is danger of relapse, particularly if we find only a single facetted calculus in the stools. In rare cases, violent biliary colic may result in death. The intensity of the pain may give rise to rapid collapse, and the patients die, as in shock, from paralysis of the heart. Hemorrhage into the brain has been observed occasionally in old people during an attack of biliary colic. Incarceration of the gall-stone in the biliary passages occasionally occurs. This is followed by the symptoms of total obstruction of the bile-ducts; marked jaundice, enlargement of the liver, later atrophy of the liver, death with cholaemic symptoms, or, if the ductus cysticus is alone occluded, hydrops cystidis fellese. In some cases this is preceded by rupture of the bile-ducts with sud- den symptoms of exhaustion and perforation-peritonitis to which the patients rapidly succumb. In other cases, the incarcerated gall-stones give rise to inflammatory and ulcerative processes. The gall-bladder or bile-ducts become adherent to adjacent organs, enter into communication with them, and empty into them their calculous contents. Thus, communication has been observed with the stomach, so that in some cases the gall-stones are vomited. The fistula may also open into the transverse colon, duode- num, more rarely the ileum. As a rule, gall-stones cannot pass through the normal bile-ducts if their diameter exceeds one cm. Largei gall- stones in the stools can hardly have entered the intestinal tract except by means of abnormal communications. The formation of a fistula and the rupture of gall-stones into the kidneys and bladder have also been observed. Sometimes the gall-baldder becomes adherent to the abdominal walls, and an external fistula forms through which gall-stones and bile are discharged. Not infrequently the perforation does not occur until a sort of cavity has been developed in the vicinity of the gall- bladder by circumscribed peritonitis, and this then gives rise to the external fistula. The opening of the fistula is sometimes a considerable distance from the liver, for example, at the umbilicus, or a little above Poupart’s ligament. Such conditions are sometimes well tolerated for an extremely long time. Philipson reports a case in which pregnancy and delivery occurred despite the existence of an external fistula. If, at the same time, the ductus choledochus is occluded by a calcu- lus, almost all the bile may escape through the external fistula. If the cystic duct is also occluded, the escaping fluid soon loses its biliary char- acter, assumes a more colorless and mucous appearance, like that of the secretion of the mucous membrane of the gall-bladder. Calculi in the intra-hepatic canals may also perforate through the diaphragm, lungs, and bronchi, in rare cases into the portal veins. After the gall-stones have entered the intestines, the danger is usually, though not always, past. In some cases the calculus is so large, or is 188 DISEASES OF THE LIVER. situated in such a peculiar manner, that it occludes the intestine and gives rise to the symptom of ileus. Cases have also been reported in which numerous gall-stones became adherent to one another through the agency of the faeces, and thus caused intestinal occlusion. Sometimes a gall-stone remains immediately above the anus, and must be removed bv the finger; smaller ones may enter the vermiform process, and give rise to typhlitis, perityphlitis, and paratyphlitis. It may also be men- tioned that the symptoms of pyloric stenosis have occasionally been observed as the result of gall-stones (compression of the pylorus by the distended bile-ducts). Obliteration of the bile-ducts may also be owing to the fact that the gall-stones, in their passage, have injured the mucous membrane, and subsequent cicatrization has given rise to adhesion of the opposite walls. We cannot enter into all the symptoms which may be the result of biliary calculi, but will merely refer to a few changes in the liver: abscess, cirrhosis, and even cancer. Among the complications may be mentioned renal calculi (in six per cent of Kraus’ cases), gout (two per cent), diabetes mellitus (four per cent), and glycosuria (seven per cent). IV. Diagnosis.—Biliary calculi may be mistaken for the following diseases: A. Gastralgia. In gastralgia, the pain is more associated with the ingestion of food; it is confined to the gastric region proper, is pre- ceded by gastric symptoms, and jaundice is absent. B. Colic and Lead Colic. Flatulence often present in colic, and, as a rule, the pain diminishes in intensity upon pressure over the painful spot. In lead colic, the previous history and the blue line on the gums must be taken into consideration. C. Hepatic Neuralgia. ' Many writers believe that attacks of pain in the hepatic region may be the result of purely nervous causes. These alternate occasionally with neuralgia in other nerve tracts. Treatment which is directed against gall-stones is entirely useless in such cases. D. Typhlitis, perityphlitis, and paratyphlitis. The pain is chiefly confined to the right iliac fossa, and in addition we should search for a tumor in this region. E. Renal colic. Attention should be paid to the passage of gravel in the urine, blood in the urine, and pains in the region of the kidneys. F. Internal incarceration. This is associated with vomiting, obstinate constipation, and vomiting of faeces. G. Psoas abscess. Fiedler saw a case of this kind in which large gall-stones had been retained in the sigmoid flexure. H. Aneurisms of the coeliac axis or abdominal aorta. We should search for abnormal pulsation and murmurs in the vessels. I. Intermittent fever. A mistake is possible if the pains are not severe, and chill and fever occur daily; but quinine is useless in biliary colic, and in addition, the chill and elevation of temperature in the latter usually occur, not in the morning but in the afternoon. K. Cholera. During a cholera epidemic mistakes may arise if obsti- nate vomiting and watery stools occur in biliary colic. L. Poisoning. If biliary colic proves rapidly fatal, the suspicion of poisoning may arise. V. Prognosis. As a rule, the prognosis is good, but it should be given with caution since there is a possibility of unexpected accidents. On the other hand, the hope of recovery should not be given up too soon. Frerichs observed recovery after the ductus choledochus had been 189 occluded several months. There is always great danger, however, of a recurrence of the attacks. V. Treatment. Biliary colic should be treated by large doses of nar- cotics. We give the preference to chloral hydrate (gr. xlv. in a wineglass of sugar water) or morphine. In addition, rest in bed and warm poultices, no solid food, and Selters, Vichy, or Ems waters as drinks. The narcotics not alone relieve the pain, but also relax the spasmodic muscular fibres of the biliary passages. If we have reason to believe that the cal- culus has entered the intestine, a mild laxative may be given. The administration of emetics during an attack is very dangerous, since the biliary passages may be ruptured during the act of vomiting. In DISEASES OF THE LIVER. Fig. 55. Fig. 56. Fig. 58. Distomum hepaticum. Natural size. Fig. 57. Distomum lanceolatum. En- larged 10 times. After Leuckart. Fig. 59. Ovum of Distomum hepati- cum. Enlarged 400 times. Distomum hepaticum. Enlarged 10 times. After Leuckart. Ova of Distomum lanceola- tum. Enlarged 400 times. very obstinate cases it may be necessary to give chloroform for hours. Chloroform has also been given internally as a solvent. According to Kennedy, § vi. olive oil taken internally, favors the passage of the gall- stones. To prevent a relapse, the patient should live regularly, take exer- cise, and avoid the excessive ingestion of meats and alcoholics. I am inclined to believe that I have obtained good effects in a number of cases by the prolonged administration of salicylic acid (gr. viiss. t. i. d.). We should order alkaline wells (Carlsbad, Ems, Vichy), but the patient should be told that a violent attack of colic may occur at the springs. The cure should be repeated for several years in succession. During 190 DISEASES OF THE LIY*EE. the winter the patients may take alkaline acidulous waters. In cases in which attacks of biliary colic recur constantly, Langenbuch has success- fully performed extirpation of the gall-bladder (cholecystotomy). 5. Parasites of the Biliary Passages. The animal parasites found in the biliary passages are the ascaris lumbricoides, echinococcus, and distomum. a. Ascaris lumbricoides is never found in the biliary passages unless it migrates from the intestines through the ductus choledochus, or abnormal communica- tions exist between the biliary passages and the intestines. In many cases the migration occurs post-mortem, in others it happens during life, the worms passing into the gall-bladder or the larger branches of the intra-hepatic canals. They may give rise to occlusion of the bile-ducts and hepatic abscess, or may form the nu- cleus of gall-stones after they have died. A diagnosis is impossible, unless an ab- scess of the liver is discharged externally and an ascaris is discharged at the same time. b. Echinococci either enter the bile-ducts from the liver (and then give rise to the symptoms of biliary colic in their passage to the intestine) or they develop within the biliary canals. c. Distomum hepaticum and distomum lanceolatum occur most frequently in the sheep, but are found, in rare cases, in the human being. In the majority of cases they were found accidentally at the autopsy; in others, variable symptoms were produced (jaundice, enlargement of the liver, cachexia, hemorrhage, etc.). The diagnosis is only possible if the parasite or its ova are vomited or discharged in the faeces. Distomum hepaticum has a flat, elongated, oval shape, and is 2.5 to 4 cm. long (Fig. 55). The ova are easily recognizable (Fig. 57). Distomum lanceolatum is smaller and more slender (Fig. 58), and its ova have a different shape (Fig. 5i»). These parasites probably enter the intestines in the form of cercariae in drinking- water or imperfectly cleaned vegetables. 6. Dropsy of the Gall-Bladder. Hydrops Cystidis Fellece. 1. This term is applied to distention of the gall-bladder with a serous or mucin- containing fluid. The disease is the result of occlusion of the neck of the gall- bladder or the cystic duct by gall-stones, adhesion of the mucous membrane, or cancer. The bile retained in the gall-bladder is gradually absorbed and is replaced by a mucin-containing fluid secreted by the mucous membrane of the gall-bladder or a serous fluid from the blood-vessels. The amount of fluid may be remarkably large (sixty to eighty pounds in Erdmann’s case). The gall-bladder, filled with synovia-like fluid, is transparent, its walls are not infrequently calcified in places, the mucous membrane is smooth and shiny like a serous membrane, the mucous glands are atrophic or have disappeared ; the muscular coat is also atro- phied. The organ is sometimes adherent to adjacent organs. Frerichs found the following substances in the contents of the gall-bladder: Water Organic matters (mucus, etc.) Alkalies Earthy matters .... 1.6 .. .. 0.06 • 100.00 2. The chief symptom is the demonstration of a smooth, tense, usually fluctu- ating tumor in the region of the gall-bladder. The tumor is generally as large as the fist, but occasionally attains the size of the head, and then extends to the pelvis. If the gall-bladder is very tense, fluctuation may be absent. In one case, circular fibres produced a deep constriction at the middle of the tumor, so that it simulated the shape of the kidney. The tumor often presents considerable lateral motion, and accompanies the respiratory movements of the liver. In one of my cases, the transverse colon was permanently situated between the anterior tip of the tumor and the lower border of the liver, so that it was separated from the liver by a tympanitic note on percussion. If the abdominal walls are very thin and the tumor sufficiently large, prominence and respiratory displacemen 191 DISEASES OF THE LIVEE. may become visible to the eye. Subjective symptoms are often absent, some- times there is a slight feeling of pressure or tenderness in the region of the gall- bladder. 3. The diagnosis is usually easy, although the disease has been mistaken for ascites. In empyema of the gall-bladder, there is usually fever and cachexia; in cancer of the organ, we find a harder, usually nodular tumor; in distention with gall-stones, there is a feeling of stony resistance and palpable or audible friction of the calculi against one another; distention with bile is usually a more acute condition, and jaundice is generally present; in cancer of the lower surface of the liver, the palpable prominences are hard and nodular, and have a broad base; fever and hectic symptoms are present in abscess of the liver. 4. As a rule, the prognosis is good. Rupture of the gall-bladder rarely occurs from excessive distention, more frequently from injury. 5. Treatment is hardly necessary. Puncture may be performed if the absence of respiratory movements of the tumor or the immobility of the abdominal walls over it, indicates adhesion of the tumor to the abdomen. In the other event, adhesion to the abdominal walls should first be secured as in operations for hepatic abscess. 7. Accumulation of Pus in the Gall-Bladder. Empycema Cystidis Fellece. The accumulation of pus in the gall-bladder is generally the effect of gall- stones, more rarely of occlusion of the ductus choledochus. If the cystic duct is also obstructed, the pus may distend the gall-bladder into a tumor as large as a man’s head. The physical signs are the same as those of dropsy of the gall-bladder, but severe pain, chili, fever, and emaciation are also present in the former affection. The prognosis is grave. If adhesions to the abdominal walls have formed, the treatment consists of cholecystotomy and removal of the contents of the tumor; in other cases, adhesion to the abdominal walls should first be secured. 8. New Growths in the Biliary Passages. Fibroma and myxoma have been observed in these organs, but a diagnosis is impossible during life. Cancer alone possesses clinical interest. The tumor may be primary or sec- ondary, the latter either spreading from adjacent organs or developing as metastases. Primary cancer of the biliary passages is rare, but is more frequent in the gall- bladder than in the ducts. In the former region, it forms a nodular tumor which may attain the size of a child’s head. The interior of the gall-bladder contains bile or ichorous masses, and often gall-stones. The other symptoms are: Pain over the tumor, jaundice, vomiting, haematemesis, diarrhoea, enterorrhagia, and marasmus. Perforation sometimes takes place into the abdominal cavity, duo- denum, or colon. The disease generally develops after the age of forty years. Primary cancer of the bile-ducts causes occlusion, the causes of which cannot be discovered during life. B. DISEASES OF THE PAKEHCHYMA OF THE LIVEE. 1. Hypercemia of the Liver. I. Etiology.—Hyperaemia of the liver maybe the result of impeded flow of blood from the organ or of an increased supply of blood. The former is called mechanical or stasis (passive) hyperaemia, the latter con- gestive (active) hyperaemia. The causes of passive congestion are: Diseases of the circulatory and respiratory apparatus, diseases in the mediastinum and peritoneal cavity which compress the inferior vena cava, and diseases of the hepatic veins themselves. 192 DISEASES OF THE LIVER. Congestion of the liver is often found in uncompensated valvular diseases of the heart. The stasis readily extends to the hepatic veins, because these enter the vena cava in the immediate vicinity of the heart, and also because the blood pressure in the hepatic veins is normally low. Hepatic congestion is especially frequent in mitral and tricuspid lesions, rarer in aortic lesions. Congestion of the liver is also an inevitable result of diseases of the heart muscle and pericar- dium (myocarditis, fatty heart, pericarditis, synechia pericardii) when these give rise to stasis in the right side of the heart; it is also the result of insufficiency of the heart’s action in old age and marantic conditions. Among respiratory dis- eases, hepatic congestion is especially frequent in pulmonary emphysema, chronic bronchitis, asthma, interstitial pneumonia, pleurisy, and obliteration of the pleura. These diseases entail increased work on the right heart; when the power of this organ fails, stasis is the result. Deformities of the spine and thorax not infrequently produce hepatic congestion by displacing the lungs and heart, and interfering with the function of the latter organ. It is an almost constant effect of asphyxia in the new-born. Aortic aneurism, mediastinal tumors, and cancer of the retro-peritoneal glands give rise to the disease when they compress the inferior vena cava. In very rare cases, the hepatic vein itself undergoes com- pression. Frerichs observed the formation of valves in the hepatic veins. Ste- nosis of the hepatic veins is an occasional result of periphlebitis or of thickening and retraction (as the result of chronic perihepatitis) near the entrance of the hepatic veins into the inferior vena cava. Local congestion of the liver may de- velop in tiglit-laced fissures, if the circulation below the latter is impeded. Active congestion of the liver is sometimes physiological, for ex- ample, during the period of digestion. This physiological process be- comes morbid and permanent, if the ingestion of food is constantly excessive, and sufficient bodily exercise, which aids the circulation in the portal vein, is not taken. In some cases hepatic congestion is the result of the introduction of irritating substances in the food (condiments, alcoholics), which are con- veyed into the portal circulation. The affection is more frequent in the tropics than in temperate zones. It is not uncommon as the result of infectious diseases, for example, malaria, typhoid and typhus fevers, relapsing fever, pneumonia, ery- sipelas, scurvy, dysentery, etc. In some cases it develops (locally or generally) as the result of injury. In some of these cases the congestion passes into inflammation and abscess. Partial congestion is observed not infrequently around foci of disease in the hepatic parenchyma (abscess, tumors, parasites). Finally, we must mention vicarious congestion which seems to be produced m a reflex manner through the agency of the vaso-motor nerves. Thus, hepatic congestion may take the place of menstruation, or it develops shortly before the menses appear; it is not infrequent at the menopause. It is often associated with uterine and ovarian diseases, and sometimes takes the place of an hemorrhoidal flux. Ilypersemia of the liver is almost exclusively a disease of adult life. The male sex predominates in some forms, the female sex in others. II. Anatomical Changes.—In passive congestion of the liver the organ is enlarged, sometimes in all directions, sometimes particularly in thickness. The capsule is very tense, and is either entirely smooth or thickened in places. Its free edge is often blunt and round, its notches abnormally deep. The consistence is increased; on pressure, serous fluid sometimes escapes from the cut surface. The organ contains an unusual amount of blood, and sometimes lias a deep blackish-red or steel-blue color. The central veins of the lobules are particularly dilated, and contrast strongly with the pale periphery of 193 DISEASES OF THE LIVER. the acini, particularly if the cells in the latter are fatty or pigmented (nutmeg or cyanotic nutmeg liver). If passive congestion has lasted for a long time, atrophic processes gradually develop (red atrophy of Virchow). The liver, which is still enlarged, has an uneven and nodular surface, and increased firmness. In a few of these cases Frerichs found that the bile contained albumin. In the simple cyanotic nutmeg liver the central veins of the lobules and the adjacent intralobular capillaries are unusually wide. The dilatation diminishes towards the periphery of the lobules. The enlargement of the vessels causes compression of the cells; they undergo fatty degeneration, become infiltrated with bile pigment, diminish in size and finally disappear, leaving flakes of pig- ment behind. Connective tissue proliferation develops around the dilated capil- laries. The atrophic, cyanotic nutmeg liver develops when retraction takes place in the newly formed connective tissue. In exceptional cases, this occurs also in the intra- lobular connective tissue. Brieger noticed the new-formation of biliary capil- laries. The atrophic nutmeg liver is often mistaken for true cirrhosis of the liver; the former does not possess a yeast-like color, the irregularities in it are less marked and distributed more irregularly, and enlargement of the spleen is usu- ally absent. The mucous membrane of the stomach and intestines is often in a condition of stasis-catarrh, and ecchymoses are observed not infrequently. The hemorrhoidal veins are often dilated. The trabecular tissue of the spleen generally undergoes hyperplasia. The pancreas is often very hyperaemic, and unusually firm as the result of interstitial development of connective tissue. The appearances of passive congestion are presented by the kidneys and pelvic organs. Active hepatic congestion is either partial or diffuse. The liver ia uniformly red, peculiarly succulent, and an unusual amount of blood exudes upon pressure. III. Symptoms.—Passive congestion of the liver is not distinguished clinically until the organ increases in size. This enlargement is not often sufficient to produce prominence of the right hypochondrium. The lower border of the liver is occasionally found unusually low, and the lower ribs on the right side are raised upward. The lower edge of the liver is often felt distinctly on palpation. It is unusu- ally firm and round, and extends lower than normal. It is sometimes felt below the umbilicus, or even as low as the anterior superior spinous process of the ilium. Both fissures at the lower edge of the liver can sometimes be distinctly felt. Percussion reveals increase of the greater (relative) and lesser (absolute) hepatic dulness, especially inferiorly (absolute hepatic dulness normally extends upwards, in the right nipple line, to the lower border of the sixth rib, inferiorly in the median line midway between the ensiform cartilage and the umbilicus). Palpatory percussion often furnishes more certain results. Physical examination may prove useless if the abdomen is distended by ascites. Palpation may then furnish positive results, if it is performed vigorously and interruptedly with the tips of the fingers, and the fluid between the abdomi- nal walls and anterior surface of the liver is thus pushed aside. Examination in the knee-elbow position may also be useful. The conditions often become very clear if puncture of the abdomen is performed and the fluid removed. Jaundice is frequent in passive congestion of the liver. It is observed usually in the conjunctiva, sometimes in the face and on the trunk. If the patient is suffering from cardiac disease the face often has a peculiar greenish color. The jaundice is the result of stenosis of the finer biliary passages by the di- lated vessels and of catarrh of the bile-ducts. Severe jaundice is the result of gastro-duodenal catarrh. 194 diseases of the liver. The stasis gives rise to gastro-intestinal catarrh (anorexia, vomiting, eructations, constipation, more rarely diarrhoea). Haemorrhoidal haem- orrhages also occur from stasis in the haemorrhoidal veins. (Edema, albuminuria, etc., depend upon the primary affection. But ascites is the direct result of the passive congestion of the liver, inas- much as the atrophic changes narrow the domain of the portal circula- tion. If ascites exists alone, or is more marked than oedema of the sub- cutaneous tissue, it is evidence of the face that atrophy has begun in the passively congested liver. In addition, it will be found that a previous enlargement of the liver begins to diminish. In many cases the subjective symptoms are extremely slight (tender- ness in the hepatic region, increased in the sitting position and m right lateral decubitus). Many patients also experience pain when they assume left lateral decubitus. There is often shortness of breath, some- times severe pains, which may shoot into the right shoulder and arm. The size of the liver often undergoes rapid changes, sometimes even within twenty-four to forty-eight hours. In active, diffuse hepatic congestion the local symptoms are similar to those described above; in local congestion they hardly form an object of clinical observation. IV. Diagnosis.—The diagnosis is easy if we can determine the three following factors: (a) The demonstration of the causes of hepatic con- gestion; (b) The presence of hepatic enlargement; (c) Rapid changes in the size of the organ. V. Prognosis.—Hepatic congestion per se rarely gives rise to any danger, but the primary disease may render the prognosis unfavorable. VI. Treatment.—The treatment must be chiefly causal. When the disease is the result of insufficiency of the heart’s action, digitalis should be administered; in addition, nourishing diet. Four to six leeches may be applied to the anus to relieve the portal circulation. Mild laxa- tives may also be given for the same purpose (rhubarb, senna., colocynth, aloes). If the patient is not too weak, he may be sent to Kissingen, Homburg, Marienbad, Carlsbad, Tarasp. In marked ascites, as the result of the atrophic nutmeg liver, puncture of the abdomen may become necessary. Diuretics may also be employed, but diaphoretics are contra- indicated. Faradization of the abdominal walls has been successful in some cases. In active hepatic congestion following an injury, the region of the liver should be covered with ice-compresses, leeches applied to the anus, leeches and cups over the liver, and mild laxatives administered inter- nally. High livers should be restricted as to the amount of food, should avoid spiced articles and alcoholics, exercise a good deal in the open air, and drink the above-mentioned mineral waters. Grape cures and whey cures are also indicated. If the hepatic congestion is the result of disturbances of menstrua- tion, a few leeches may be applied to the upper inner surface of the thighs or the portio vaginalis, and a warm mustard foot-batli taken at night. 2. Perihepatitis. I. Etiology.—Perihepatitis is rarely primary, and in almost all such cases is the result of injury. This includes the pressure of the corset. The affection is more often secondary to hepatic diseases (congestion, DISEASES OF THE LIVER. 195 cirrhosis, abscess, cancer, echinococcus). In other cases it forms a part of general peritonitis. Diseases of the stomach, duodenum, colon, and even the kidneys may also give rise to hepatitis, the inflammatory process extending along the ligaments of the liver to its hilus. Perihepatitis may also be associated with right pleurisy. Syphilis sometimes acts as a cause. II. Anatomical Changes.—Perihepatitis may be acute or chronic, circumscribed or diffuse. In chronic perihepatitis we find opacity and thickening of the capsule, frequently fibrous adhesions between the liver and adjacent organs. The capsule is sometimes so thick as to form a tendon-like, almost cartilaginous covering of the organ. In some cases retraction of the capsule causes slight depressions upon the surface, in others retrac- tion at the hilus causes stenosis or occlusion of the portal vein or excretory ducts, or similar processes near the suspensory ligament produce stenosis of the inferior vena cava and hepatic veins. The shape of the liver is sometimes changed; it becomes smaller and more spherical. At the beginning of the chronic inflammation, the lymphatics of the capsule are often very widely dilated (perilymphangoitis chronica). Acute perihepatitis presents the same appearances as acute peritoni- tis. The capsule is sometimes lifted up from the parenchyma by a circumscribed abscess. Small abscesses have also been observed in the fibrous bands which extend inward from the hilus. III. Symptoms and Diagnosis.—In many cases chronic perihepa- titis is attended with hardly any symptoms. In others, the disease is recognized by the absence of respiratory movements of the lower border of the liver, on account of adhesions to adjacent organs. Peritonitic friction murmurs are sometimes heard and felt, either with every inspi- ration or only when the abdominal walls are purposely moved over the surface of the liver. In some cases, finally, the disease gives rise to the symptoms of occlusion of the portal vein, incurable jaundice, congestion or cirrhosis of the liver. Hambursin has called attention to the fact that, as the result of perihepatitic adhesions between the liver and diaphragm, pericardial adhesions may form over the corresponding parts of the upper surface of the diaphragm, and may gradu- ally prove fatal with the signs of insufficiency of the heart’s action. Acute perihepatitis begins occasionally with a chill and fever. The patients complain of pain and tenderness in the hepatic region, and this may give rise to dyspnoea by interference with the respiratory movements. Slight jaundice sometimes develops, also vomiting, anorexia, indigestion. Friction murmurs are less frequent than in chronic perihepatitis. IV. Prognosis.—In acute perihepatitis, the prognosis depends upon the primary disease; in the chronic form, the prognosis is usually good, V. Treatment.—In the acute form, the patient should keep to bed, a warm poultice applied over the liver, and morphine injected sub- cutaneously if the pains are very severe. The following measures have also been recommended: cups and leeches over the liver, blisters, tinc- ture of iodine, ice-bags, calomel internally, etc. Chronic perihepatitis, as a rule, does not require special treatment. 3. Suppurative Hepatitis. (Abscess of the Liver.) I. Etiology.-—This disease is rare in our climate, but much more frequent in the tropics. It is more frequent in men than in women 196 DISEASES OF THE LIVEK. (30 :1), and occurs chiefly in adult life. During childhood it occurs principally in the new-born (from inflammation of the umbilical vein). Suppurative hepatitis is rarely primary, and then is always the result of injury. The disease is almost always secondary, usually metastatic in character. It often follows inflammations in the domain of the portal vein (operations on the rectum, diseases of the uterus and ovaries, gastro-intestinal ulcerations, puru- lent inflammation of the trunk of the portal vein itself). This can only be explained by the conveyance of inflammation-producers from the primary focus througli the portal circulation into the liver. This occurs much more rarely through the medium of the hepatic artery, for example, in acute septic endocar- ditis, gangrene of the lungs, and putrid bronchitis. In very rare cases the inflammation-producers reach the liver through the hepatic veins, the substances in question passing through the inferior vena cava into the hepatic veins by the action of gravity. This is favored by unusually low pressure in the inferior vena cava. Hepatic abscesses may develop in the manner mentioned if the primary site of inflammation is situated at the periphery of the body (panaritium, venesection wounds, injuries to the bones). The latter are especially dangerous, because the veins in the spongy substance are incapable of collapse, and therefore present a special tendency to the formation of thrombi. Hence, abscesses of the liver occur with relative frequency after injuries to the skull. In peripheral inflammations, the inflammation-producers may also reach the liver through the vascular system of the lungs. The inflammatory products pass from the periphery to the right heart and then to the lungs, where they give rise to secondary changes. From the latter particles are dislodged, which pass to the left heart, and then through the hepatic artery to the liver. This mode of genesis is only probable if pulmonary and hepatic abscesses are both present. If the former are absent, it is hardly plausible that the inflammation-producers have passed through the pulmonary capillaries and lodged in the hepatic capillaries. In rare cases, perhaps, these elements may pass from the right to the left side of the heart through direct communications between small pulmonary arteries and veins. Virchow showed that in some cases of peripheral suppuration marantic thrombi form in the vesical, prostatic or uterine plexuses, that these assume malignant properties, and that dislodged particles pass into the liver and produce secondary inflammations. Suppurative hepatitis may also take its origin in the biliary passages. Thus, gall-stones or ascarides which are incarcerated in the bile-ducts may produce inflammation and suppuration in their walls, and subse- quently in the adjacent parenchyma of the liver. According to some writers, this may be the result of simple stasis of bile following catarrh of the bile-ducts. Suppurative hepatitis may also follow ulcerative pro- cesses in the walls of the ducts through the agency of the blood-vessels. Abscess of the liver may also complicate other hepatic diseases (tubercles, echinococci). In other cases, the disease is propagated from adjacent organs (ulcer and cancer of the stomach, which extend to the liver after the formation of adhesions.) Finally, a series of cases remains in which the mode of origin cannot be discovered. Europeans are especially apt to be attacked in the tropics. This has been at- tributed to the fact that the European in the tropics continues to partake largely of meat and stimulants. Sachs thought that alcohol directly produces, in the tropics, an acute hepatitis. At all events, the influence of climate cannot be denied. Telluric influences are also demonstrable, since certain regions in the tropics are notorious for the frequency of abscess in the liver. Perhaps malaria exercises a certain etiological influence. 197 DISEASES OF THE LIVEE. II. Anatomical Changes.—An abscess of the liver may be situated in any part of the organ, and is either single or multiple. It is more frequent in the right lobe than in the left. As many as forty abscesses have been observed in some cases. On the average, the size, of the ab- scess varies from that of a hazelnut to that of a walnut. In not a few cases it attained the size of a child’s head (in Toman’s case it contained eighteen pounds of pus). The cavity generally contains laudable pus. If the abscess has lasted a long time, it sometimes acquires an ammo- niacal, more rarely a foetid odor, and the pus may assume a brownish- yellow or chocolate color, from admixture with bile. In rare cases, the pus has a bloody color from rupture of a blood-vessel into the abscess. The pus usually contains an unusually large number of drops of fat. Its chief constituents are the pus-corpuscles, many of which are in a condition of fatty degeneration ; in addition, granular detritus, part of which is composed of bac- teria. A few fatty hepatic cells are found occasionally ; in one case I observed tablets of cholestearin. The walls of a recent abscess are irregular and jagged, and occasion- ally present a creamy, cheesy coating. In older cases the abscess is encapsulated, evidently from proliferation of the interstitial tissue. The capsule is often laminated, and sometimes acquires a cartilaginous con- sistence. The adjacent blood-vessels are usually obliterated, but a case has been reported in which an aneurism situated on the wall of an ab- scess gave rise to violent hemorrhage. The hepatic parenchyma adjacent to the abscess is usually very livid and brittle. In Lepido-Chioli’s case the entire organ was waxy. The size of the liver may be nearly doubled. The biliary passages are not infrequently dilated, and sometimes con- tain a fibrinous exudation in places. An abscess near the lower surface of the liver may cause general dilatation of the biliary passages by com- pressing the ductus choledochus and hepaticus. The portal vein may be similarly affected. In superficial abscesses, the capsule is generally inflamed, and hence adhesions to adjacent organs are formed. In the absence of these, rupture of the abscess would be followed by perforation-peritonitis. If adhesions are present, the perforation may occur into other viscera (stomach, colon, duodenum, rarely into the pelvis of the right kidney, or through the diaphragm into the pleural and pericardial cavities). Adhesions form not infrequently between the pulmonary and parietal pleura, and the abscess may then rupture into the lungs and bronchial tubes. The ab- scess may also rupture into the portal vein, inferior vena cava, and hepatic veins. It opens occasionally into the large biliary ducts, or the gall-bladder, and then passes into the intestines. Finally, the pus may break through the abdominal walls, either directly or through long fis- tulae which may open in the axilla, groin, etc. In rare cases, the pus follows the round ligament to the umbilicus. If perforation does not occur, the abscess may undergo various changes. These include encapsulation, which may be followed by thick- ening, caseation, or calcification of the pus. Smaller abscesses are sometimes converted into a retracted cicatrix which contains a calcified nucleus. In rare cases, a cystoid degeneration takes place, the pus as- suming a thin, colloid quality. Kecovery after perforation is often rendered difficult from the fact that the walls of the abscess do not approach one another on account of 198 DISEASES OF THE LIVER. their rigidity. In very rare cases, gangrenous changes develop when the air enters the abscess. If the disease is the result of pyaemic or septicaemic infection, abscesses are often found in other organs, particularly the lungs. The first changes in pyaemic abscesses of the liver consist of distention of the capillaries of the hepatic lobules with bacteria. These proliferate very rapidly, thrombose the vessel, and affect the adjacent cells by pressure and by exerting a chemical influence. The hepatic cells undergo coagulation-necrosis and are finally destroyed. This is followed by the formation of pus. According to some writers, the pus-corpuscles are derived, apart from diapedesis, from the hepatic cells them- selves, and from the connective tissue cells of the interstitial tissue. The original focus is lobular ; larger abscesses are produced by the coalescence of smaller ones. Symptoms.—In not very rare cases, abscess of the liver is found ac- cidentally in the dead-house, the patients never having presented any hepatic symptoms. In other cases, the abscess produces the symptoms of intermittent fever, usually of the type (periodical chill, fever, and sweat). A mistake is apt to arise if the spleen is enlarged by previous malaria or pyaemic infection. Some patients present the symptoms of severe typhoid fever: high fever, clouded sensorium, tympanites, roseola, enlargement of the spleen, delirium, perhaps convulsions or spasms of individual muscles towards the close of life. A few cases run the course of pulmonary phthisis: gradual emacia- tion and pallor, night sweats, hectic symptoms. In another series of cases, the suspicion of hepatic abscess is aroused by suddenly developing symptoms; sudden vomiting of pus, passage of pus in the stools or urine, purulent expectoration, unexpected empyema, or pericarditis, etc. Cases in which the symptoms are well developed present the follow- ing clinical history: The liver is enlarged, generally in an upward direction (sometimes as high as the second rib). As a rule, this enlargement is not uniform, and percussion of the anterior surface of the thorax reveals convex prominences with the convexity directed upwards. In other cases the enlargement is chiefly or exclusively in a downward direction. If the liver is much enlarged, the right hypochondrium is more or less prominent. The right lower intercostal spaces are narrowed, the lower ribs raised upwards. In a few cases the epigastric veins are con- siderably dilated. An important diagnostic point is the recognition of prominences in the intercostal spaces or beneath the abdominal walls, which undergo re- spiratory movements so long as no adhesions have formed to the walls of the abdomen. Palpation reveals the lower border of the liver, which is sometimes remarkably distinct, sometimes is recognized only by the increased feel- ing of resistance. There is sometimes circumscribed tenderness in the hepatic region. The entire organ is occasionally tender, but this is more marked in cir- cumscribed regions. Pressure on the liver sometimes causes pain in the right shoulder or gives rise to cough. One of the most important signs is the demonstration of a fluctuating tumor. This is found to move with respiration so long as no adhesions are present. 199 DISEASES OF THE LIVER. If perihepatitis is present, friction murmurs may be heard and felt. There is sometimes unusual tension of the right rectus abdominis, either as a reflex symptom of the pam or as the result of the enlargement of the liver. Jaundice is absent in the majority of cases, and usually does not ap- pear until the development of the abscess has ceased. It may be the result of pressure on adjacent biliary ducts, catarrh or fibrinous inflam- mation of the ducts or, in pyaemia, it may be a sign of general infection (haematogenous icterus). Subjective symptoms may be entirely absent. In other cases there is a feeling of fulness and tension in the hepatic region, sometimes intensi- fied into pain, which is situated either superficially or deeply. The pain radiates not infrequently into the right shoulder and arm (through the medium of the phrenic nerve which supplies the liver and also gives off shoulder branches in the distribution of the fourth cervical nerve). In one case the pain in the shoulder was followed by atrophy of the deltoid. According to Annesley, pain in the shoulder occurs only in abscesses of the convexity of the liver. Pain in the left shoulder has been observed in abscesses of the left lobe. Insomnia and anorexia are not infrequent; mental depression is sometimes observed. Many patients complain of dyspnoea, the result of interference with the movements of the diaphragm and compression of the lungs by the enlarged liver. The disease is sometimes entirely apyrexial, in other cases there is a continuous or remittent, hectic or intermittent fever, which may rise above 41° C. Chills often occur, likewise sweats with their sequlas upon the skin (miliaria, pityriasis tabescentium, defluvium capillorum). The pulse is usually very frequent, small, and soft. Considerable emaciation is generally noticeable and, together with the pale or yellowish, waxy complexion, gives the patient a cachectic appearance. According to older writers, abscess of the liver is accompanied not infrequently by cough, vomiting, and eractations. The bowels are often constipated, though diarrhoea, even of a bloody character, has been ob- served in a few cases. The patients sometimes lie upon the right side, with the trunk bent over forwards and the right thigh flexed, evidently in order to relieve the liver from pressure. If the abscess ruptures externally, the skin becomes red, cedematous, and hot, gradually grows thin and bursts. The perforation is sometimes preceded by the formation of vesicles on the integument. The suppura- tion may continue for a long time, even for years. The fistula some- times closes completely and re-opens at a later period. When the abscess ruptures into the stomach, the sudden vomiting of pus is observed, preceded sometimes for days by ordinary vomiting. In 1 rvine’s case haematemesis was produced as the result of rupture of an aneurism of the hepatic artery situated in the wall of the abscess. Purulent evacuations from the bowels indicate rupture into the in- testines, either directly into the colon or through the bile-ducts into the duodenum. Rupture into the pelvis of the right kidney is manifested by pain in the region of the kidney, and by a purulent sediment in the iirine. In Huet’s case the urine contained numerous liver cells. 200 DISEASES OF THE LIVER. Rupture into the inferior vena cava, portal or hepatic veins, gives rise to the signs of internal hemorrhage or metastatic abscess-formation in other organs. Rupture into the peritoneal cavity is followed by signs o| diffuse, rarely of circumscribed, peritonitis. Rupture into the pericardium is followed by pericarditis which usu- ally proves rapidly fatal. Rupture into the pleura is followed by the signs of empyema, rup- ture into the lungs by expectoration of pus. The latter often becomes putrid within the lungs and assumes a brownish-yellow or chocolate color. The sputum is sometimes mucous, but contains a larger or smaller number of balls of pus. In a number of cases, the expectoration of pus has been followed by the expectoration of almost pure bile. It should not be forgotten that pleurisy and pericarditis are sometimes the result of a direct spread of the inflammation without perforation, but the inflam- mation is then of a serous character. The duration of the disease is extremely variable. The symptoms sometimes terminate fatally at the end of a few days; in other cases, they may last many years. IV. Diagnosis.—Despite the exercise of the greatest care, the recog- nition of abscess of the liver may be impossible. The best means of differentiation from intermittent fever is the use- lessness of the administration of quinine. It is distinguished from pul- monary phthisis by the absence of changes in the lungs, and of elastic fibres and bacilli in the sputum. If fluctuating prominences are felt on the surface of the liver, they must be distinguished from echinococci, soft, pseudo-fluctuatiug sar- comas and cystic distention of the gall-bladder. In echinococci, we must look for the hyatid thrill, in sarcoma for umbilication of the prominences; in dilatation of the gall-bladder, the tumor is pear-shaped and very tense. In addition, puncture should be made with a very fine trocar. Fluctuating prominences in the hepatic region may also depend on tuberculosis of the ribs or spine, or abscess of the abdominal walls. In these conditions, there is no respiratory movement of the tumor. In the two former conditions pain is felt along the ribs or spine. To distin- guish hepatic abscess from one situated in the abdominal walls, Sachs recommended the introduction of a long Carlsbad needle. In the former disease, the head of the needle will present respiratory movements; in the latter, these are absent. The disease may be mistaken for pleurisy if the upper border of the liver is unusually high, but in abscess of the liver the dulness is irregu- lar, and is usually higher anteriorly. If pus is suddenly evacuated, we must attempt to convince ourselves of the absence of purulent inflammation in the organ through which the abscess has opened. On microscopical examination, the pus will usu- ally be found to contain liver cells or bile-pigment. V. Prognosis.—The mortality in abscess of the liver is about eighty per cent. Spontaneous recovery occurs in exceptional cases. Early operative interference has reduced the mortality to forty per cent. VI. Treatment.—The treatment belongs to surgery, not to internal medicine. As soon as the diagnosis has been made with certainty, the pus should be removed. Concerning the methods of operation, we must refer the reader to the text-books on surgery. DISEASES OE THE LIVER. 201 4. Chronic Interstitial Inflammation of the Liver. [Cirrhosis of the Liver. Chronic Interstitial Hepatitis.) I. Etiology.—The disease is generally the result of the excessive ingestion of alcohol (hence the term whiskey liver). The alcohol is probably conveyed to the liver through the portal vein, and there sets up an inflammatory process in the interstitial tissue. Some authors believe that, as the result of chronic gastro-enteritis produced by the alcohol, abnormal products of decomposition of the food are conveyed to the liver, where they give rise to inflammatory changes. It has also been assumed that the inflammation may spread from the gastro-intestinal tract to the liver along the sheaths of the portal vein. The more undiluted the alcohol the greater is the danger of cirrhosis. The disease rarely results from drinking beer or wine. The disease is more frequent in males, particularly from the ages of thirty to sixty years. A number of cases have been reported in which cirrhosis of the liver was ob- served in children who had been in the habit of drinking brandy from an early age. Wilkes reported a case in a girl set. 8 years. Budd believed that other irritating substances in the food may act in the same way as alcohol in producing the disease. He attributes its frequency in India to the habitual use of strong spices (curry, etc.). Cirrhosis of the liver sometimes appears to be produced by infectious diseases.' Thus, it is relatively frequent after intermittent fever, and, according to Ererichs, it is sometimes the result of constitutional syphi- lis. Proliferation of the interstitial connective tissue of the liver, which is usually recognized only with the aid of the microscope, is observed almost constantly in the course of miliary tuberculosis. Whether the disease may be the result of typhoid fever, cholera, or gout, is still a matter of dispute. In some cases, it seems to start from the biliary passages, and de- velops after occlusion of the bile-ducts by gall-stones or tumors, but the cases hitherto reported are not entirely free from doubt. Botkin and Salowieff have attributed cirrhosis of the liver to occlusion of the portal vein. In some cases, it is the result of the extension of chronic perihepatitis. Bamberger noticed the development of the disease after menstrual disturb- ances, Murchison after hemorrhoidal hemorrhages. Weber and Virchow reported two cases of foetal cirrhosis, but these were probably the result of syphilitic changes. Typical cirrhosis has been produced experimentally in animals by the pro- longed administration of phosphorus (toxic cirrhosis). In not a few cases, the etiology remains unknown. In a number of cases, I have noticed that the disease developed apparently spontaneously beyond the age of forty-five years, terminated unfavorably quite rapidly, and, at the autopsy, was found to be associated with proliferation of the interstitial connective tissue of the kidneys, and with signs of endarte- ritis obliterans and arteriosclerosis in the vessels of many organs. I am inclined, therefore, to assume a senile (arteriosclerotic) cirrhosis of the liver, which appears to depend on senile changes in the vessels. II. Anatomical Changes.—The inflammatory process in this dis- ease begins in the interlobular connective tissue, in the majority of cases 202 DISEASES OF THE LIVER. in the immediate vicinity of the medium-sized and smaller branches of the portal vein. The connective tissue increases in amount, encircles single or, more frequently, several lobules, and causes fatty degeneration and dis- appearance of the liver cells by the increasing pressure. On sec- tion, the abnormally broad bands of connective tissue are readily recognized, and between them the remains of the parenchyma project above the surface, so that the latter assumes a nodular and granular appearance. This appearance is also presented by fatty liver, atrophic nutmeg liver, and pylephlebitis adhesiva. There are two stages of cirrhosis of the liver. In the first, the organ is enlarged; in the second, it is small and retracted. The latter is the result of retraction of the newly-formed connective tissue. But the processes of hyperplasia and retraction are associated with one another to such a degree that we may long remain in doubt whether the disease should be considered to be in the first or second stage. In some cases, indeed, the organ never grows smaller (hypertrophic cirrhosis). In the so-called second stage the liver presents the following changes: It is diminished in size, and not infrequently is only one-third the normal dimensions. The weight may be diminished from 50-65 ounces to 35 ounces. The retraction affects the left lobe to the most marked extent. The liver is not infrequently adherent to adjacent organs (stomach, colon, duodenum, diaphragm, etc.). Its surface is uneven and nodular, the individual prominences varying from the size of a pea to that of a hazelnut. Some prominences may be almost entirely sepa- rated from the rest of the organ. The capsule is thickened in places, especially where the prominences coalesce. Upon section, the capsule is often found to send firm bands of connective tissue into the interior of the liver. The gall-bladder usually contains but little bile, and this is generally very light, almost straw-yellow in color. The liver is increased in consistence, and'not infrequently creaks when cut with the knife. It has a bright reddish-yellow color, partly from fatty degeneration, partly from the marked amount of pigment in the hepatic cells. In rare cases portions of the organ have a blackish- gray or greenish-black color. The lower border of the liver is blunt and rolled upwards, more rarely downwards. Injection of the liver with colored substances will produce different effects, according as the injection-canula is inserted into the portal vein or hepatic artery. In the former event the fluid soon ceases to flow, whence it may be inferred that the fibrous retraction has led to occlusion of branches of the portal vein within the parenchyma; while, in the latter event, the injection-fluid readily enters the branches of the hepatic artery. The biliary passages may be readily injected, in almost all cases, through the hepatic duct. The liver almost always presents the various stages of development of the chronic inflammatory process. In parts which have been recently affected, the interlob- ular connective tissue is broad and infiltrated with numerous round cells, partic- ularly around the branches of the portal vein. These are probably derived partly from the blood, partly from division of pre-existing connective-tissue cells. It is even believed by some that the liver cells may be converted into connective- tissue cells. At a later period this cellular infiltration is converted into connective tissue. In the beginning, the connective-tissue hyperplasia usually encircles several lobules, but later it extends into the lobules themselves. Round cells continue to emigrate from the capillaries between the liver cells, compress the latter, and cause them to disappear, are finally converted into connective tissue, and thus replace the destroyed parenchyma. DISEASES OF THE LIVER. 203 The liver cells are thus compressed from the periphery and from the interior of the lobules. In addition, some of the branches of the portal vein are occluded by the interlobular proliferation of connective tissue, and hence the hepatic cells are partly deprived of their supply of blood. The most marked changes are ob- served at the periphery of the lobules, where the cells are filled with drops of fat and bile pigment, in yellowish or brownish granules or in fine needles. The individual cell gradually disappears, and leaves only a little bile pigment. In this way many lobules may be entirely destroyed. The vascular system of the liver, particularly that of the portal vein, also undergoes changes. Numerous branches are narrowed and finally occluded as the result of endophlebitis obliterans. The same process may take place in the intralobular capillaries. In the distribution of the hepatic artery, on the other hand, numerous capillaries may develop, and may form communications with the remains of the branches of the portal vein. The biliary canals also undergo proliferation. The interlobular connective tissue is traversed by numerous biliary canals; the epithelium of these new- formed vessels is said to develop from rows of hepatic cells. The occlusion of the branches of the portal vein explains the symptoms of stasis (splenic enlargement, ascites, gastro-intestinal catarrh, etc.), the non-affec- tion of the biliary canals explains the frequent absence of jaundice. In rare cases the hepatic veins, and even the inferior vena cava may be nar- rowed, inasmuch as the inflammatory proliferation extends to the walls of these vessels. Among the complications of this disease we may mention waxy degeneration, in rare cases, cancer, abscess, or echinococcus. In two cases Bamberger ob- served acute atrophy of the liver in places in a cirrhotic liver. According to Ackermann, the process begins in the liver cells, and is followed at a later period by increase of the interstitial connective tissue. Charcot and Gombault distinguished three forms of cirrhosis : a. Cirrhosis starting from the veins. b. Cirrhosis starting from the biliary passages. c. Monocellular cirrhosis. That form which starts from the veins corresponds to that described above. In that variety which starts from the biliary passage the new-formed connective tissue forms scattered foci, and from the beginning involves each lobule sepa- rately. It is said that this form of the disease may be produced experimentally in animals by ligature of the bile-ducts, occurs in man as the result of occlusion of the ducts, and that in some cases it occurs as an independent disease. Olivier and Hayem called this disease hypertrophic cirrhosis, because the organ is en- larged and presents no tendency to subsequent atrophy. The liver and spleen undergo considerable increase in size ; icterus is a prominent symptom, and the disease is very protracted. Monocellular cirrhosis begins with intralobular and extralobular proliferation of connective tissue, which surrounds single hepatic cells. This form includes many cases of syphilitic changes in the liver. English and German authors have protested against the strict acceptance of these views. To a certain extent they are founded on truth, but there are so many transitions between the different forms that they cannot be regarded as distinctly separate. In fatty hypertrophic cirrhosis, the accumulation of fat in the hepatic cells is so extensive that the organ is increased in size. Simple induration of the liver is the term applied to a chronic process of pro- liferation of the connective tissue, in which large foci of hepatic tissue are entirely destroyed and replaced by connective tissue. In this condition many branches of the portal vein undergo obliteration. The disease cannot be distinguished dur- ing life from cirrhosis of the liver. The initial changes in cirrhosis are not often observed on autopsy. The liver is enlarged one to three fold, is unusually firm, and on section we notice numerous broad, gray bands of connective tissue, which traverse the parenchyma. The abdominal cavity usually contains a considerable quantity of a serous, more rarely of a hemorrhagic transudation. Extravasations of blood not infrequently are found here and there upon the peritoneum. In places the peritoneum is 204 DISEASES OF THE LIVER. thickened, opaque, and even oedematous. The portal vein sometimes contains adherent thrombi. The spleen is usually enlarged, firm, and its capsule thickened in places ; on section the trabecular tissue is found to be abnormally developed. The gastro-intestinal mucous membrane presents evidences of chronic catarrh, not infrequently extravasations of blood. In several cases Fraentzel observed phlegmonous gastritis. The kidneys are often congested, not infrequently cir- rhotic or in a condition of parenchymatous inflammation. Fatty degeneration, the formation of callosities, and endocarditic changes are found in the heart. Hydrothorax and hydropericardium are found not very infrequently. The lungs present evidences of bronchitis, emphysema, oedema, and inflammation. III. Symptoms.—The first symptoms are usually masked by those of obstinate gastro-intestinal catarrh (anorexia, eructations, coated tongue, feeling of pressure in the stomach, etc.). An affection of the liver is not recognized until the organ has under- gone changes in size. The liver is at first enlarged ; later it grows smaller. The increase in size is usually most marked in the downward direction, so that the lower border of the organ can be seen and felt far below the umbilicus. Atro- phy of the liver is especially marked in the left lobe, whose dulness is absent or very much diminished in extent, and is replaced by the tym- panitic note of the stomach. If perihepatitis is present, peritonitic friction murmurs are sometimes felt and heard. The nodules on the surfaces are sometimes felt on pal- pation in lean individuals, but we should avoid mistaking the nodules for the panniculus adiposus. It should be remembered that the former move with respiration. The development of ascites, without oedema of the lower limbs, is a very important symptom in cirrhosis, although it only indicates ob- struction to the circulation in the portal vein. We' must therefore exclude diseases of the portal vein itself (pylephlebitis, compression by tumors, exudations, fibrous cicatrices) or of the peritoneum (cancer, tuberculosis, serous peritonitis). It is said that ascites is usually absent in hypertrophic cirrhosis. When the patient, at the first examination, presents marked ascites, the diag- nosis is rendei'ed difficult on account of our inability to determine the size of the liver. This can sometimes be done by placing the patient on the left side or in the knee-elbow position, and thus displacing the fluid which is situated in front of the liver. After puncture of the abdomen and discharge of the fluid, the out- lines of the organ usually become extremely distinct, but at the end of a few hours or days the fluid has often accumulated to such an extent that the organ is again submerged. The amount of fluid is often astonishing ; its color varies from an amber-yel- low to a bile-stained, sanguinolent, or distinctly bloody color. The blood-corpuscles contained in it may be entirely The specific gravity varies from 1010 to 1015 ; the fluid contains 2 to 3 per cent*of solid constituents. Enlargement of the spleen is the third one of the cardinal symptoms in cirrhosis of the liver. It may be absent if the capsule has been pre- viously thickened and calcified. The dimensions of the organ may be increased four to six fold. The splenic enlargement is chiefly the result of stasis in the portal circulation. In some cases, however, the connective-tissue proliferation in the spleen seems to result from the same causes as that in the liver. In a few cases, abscess and infarctions have been found in the organ. Jaundice may be absent during the entire course of the disease, be- cause the biliary canals are not affected in such a manner as to encroach 205 DISEASES OF THE LIVER. materially upon their lumen. Early and marked jaundice will occur only in those rare cases in which the hepatic affection is the result of stenosis of the bile-ducts. In the majority of cases, the jaundice is con- fined to the sclera. Icterus should be distinguished from the grayish-yellow, sallow com- plexion observed in most of the patients. The integument is generally lean, thin, and dry. Marked emaciation generally develops at an early period. (Edema of the skin may be entirely absent, but at a late period in the disease slight oedema is usually observed in the lower limbs as the result of marasmus, pressure of the ascites on the inferior vena cava, or implication of this vein (as the vessel passes across the posterior border of the liver) in the process of retraction. The abdominal walls often present abnormal dilatation and sinuosity of the cutaneous veins. The inferior epigastric veins ascend from about the middle of Poupart’s ligament, and uniteat the level of the umbilicus with the superior epigastric veins; the latter unite near the thorax with the mammary veins. The dilatation is the result of compression of the inferior vena cava, so that a portion of the blood from the lower limbs reaches the heart by circuitous routes. Unusual vascular channels are sometimes opened as the result of occlusion of branches of the portal vein (caput Medusae s. cirsom- phalos). Under such conditions, a portion of the blood in the portal vein flows through the open umbilical vein, which is generally unused, passes externally at the middle of the umbilicus, and there communicates with the adjacent epigastric veins. The umbilical vein and its external ramifications undergo varicose dilatations and sometimes give rise to a purring thrill and an almost continuous venous hum. Various other collateral communications may be formed between the portal vein and the right heart, for example, a. Left coronary vein of the stomach—in- ferior oesophageal veins—vena azygos. The oesophageal veins may also undergo varicose dilatation, and thus be the source of dangerous hemorrhage, b. Veins of the capsule of the liver or gall-bladder—diaphragmatic veins, c. New-formed veins in the fibrous adhesions—diaphragmatic veins, d. Sappey’s accessory veins, which run from the surface of the liver along the round ligament to the ab- dominal walls—epigastric, mammary, and superficial abdominal veins, e. Mesen- teric veins—veins of the abdominal walls. /. Mesenteric veins—spermatio veins. g. Internal hemorrhoidal vein—hypogastric vein. Abnormal communications may also develop. Virchow reported a case in which an anastomosing varix developed between the splenic vein and vena azygos. The patients usually suffer from anorexia, and often from increased thirst. The tongue has a grayish-white, or brownish-yellow coating. Singultus and vomiting are observed not infrequently. Very marked disturbances of respiration are often produced by meteorism associated with ascites. As a rule, there is constipation, more rarely diarrhoea. Hemorrhoids are found only in rare cases. If the symptoms of stasis increase, hemorrhages are sometimes pro- duced (hsematemesis, hemorrhoidal hemorrhages). Ileiller reported a case in which haematemesis was the first symptom of the disease. In Rollet’s case, this symptom occurred at almost regular intervals of four to five weeks’ duration. Schilling reported a case in which fatal hemat- emesis was the first and only symptom of cirrhosis of the liver. Ascites and enlargement of the spleen are apt to diminish after hemorrhages. The urine is almost always diminished in amount; its specific gravity is increased, its reaction very acid, and on cooling it very often deposits 206 DISEASES OF THE LIVER. a red sediment of urates. If jaundice is present, biliary coloring matter and biliary acids are found in the urine. Langenbeck observed hem- orrhage from the bladder in two cases. A small amount of albumin in the urine must be attributed to cachexia and stasis produced by ascites, a large amount of albumin to nephritis. In the latter event, the pres- ence of casts is important. In cases of jaundice, a few hyaline casts may be present, despite the absence of nephritis. According to Andiguer, the amount of urea in the urine is diminished; Debove claims that, when the urea is diminished in the urine, it is increased in the blood. The chlorides in the urine have also been found diminished, the am- monia increased. The urine sometimes contains sugar. French writers claim that the abundant ingestion of sugar in cirrhosis of the liver gives rise to glycosuria, and explain this on the theory that a portion of the sugar is not converted into glycogen within the liver, on account of the occlusion of branches of the portal vein, and destruction of liver-cells. Respiration may be seriously interfered with as the result of extensive ascites; bronchitis and pneumonia develop quite frequently. Gee and Galliard observed haemoptysis; the latter writer also observed haematoma of the pleura. The heart is not infrequently displaced as the result of ascites. Signs of dilatation of the heart, particularly of the right side, cardiac insuffi- ciency, and valvular lesions may be noticed. The peripheral arteries are often in a condition of arteriosclerosis. The following ocular symptoms have also been observed: retinal hemorrhages, retinitis pigmentosa, xanthopsia. The average duration of the disease is one to three years, though it occasionally lasts five years, or even more. The disease is usually apyrexial, but Riva described intermittent attacks of fever, which ho attributes to disturbances in the function of the liver. Fever often de- velops towards the close of life. Death occurs not infrequently from increasing marasmus, sometimes preceded by the signs of dissolution of the blood. It is sometimes hastened bv violent diarrhoea or gastro-intestinal hemorrhage. Towards the close of life the lower limbs usually become cedematous. In other cases the ascites becomes excessive, and proves fatal by interfering with circulation and respiration. Intercurrent bronchitis, pneumonia, or heart failure is sometimes the immediate cause of death. in rare cases death occurs with symptoms of cholaemia. The patients become comatose, restless, delirious, are attacked by general convulsions or twitchings, the temperature often rises, and a typhoid condition de- velops which terminates in death. When intense jaundice is present, cholasmia appears to be due to blood-poisoning with the constituents of the bile. It may also be the result of acholia, the liver ceasing to secrete bile, and injurious excre- mentitious substances being thus retained in the blood. In rare cases the scene terminates with the symptoms of acute yellow atrophy of the liver. IV." Diagnosis.—The diagnosis can only be made with certainty if it is favored by the etiology (alcoholism, etc.), if an enlarged liver gradu- ally grows smaller, and if ascites and splenic enlargement are demon- strable. Demonstrable atrophy generally does not occur until after the lapse of weeks. In one case Strieker observed a diminution of eleven DISEASES OF THE LIVER. 207 cm. in the area of hepatic dulness within four weeks. Ascites must often be relieved by puncture of the abdomen, before a diagnosis can be made. The disease is most frequently mistaken for the following affections : a. Waxy liver. Enlargement of the liver and spleen, and ascites are also present in this affection, but the etiology is different (suppuration, cachexia, etc.); the liver is smooth and very tense; the urine contains a large amount of albumin; there is marked oedema of the limbs, often of the face; jaundice is absent unless the excretory ducts are compressed by degenerated glands. b. Cancer of the liver. Enlargement of the liver and ascites are often present, but splenic enlargement is rarely observed; in addition, rapidly increasing cachexia, cancer in other organs, advanced age of the patient. c. Syphilis of the liver. This is distinguished by the history and the presence of syphilitic changes in the skin, mucous membrane, and bones. d. Pylephlebitis adhmiva. Symptoms of stasis develop rapidly, and the etiology is different. e. Congestion of the liver, vide page 191. f. Chronic peritonitis; usually attended with diffuse, marked ten- derness of the abdomen. V. Prognosis. —This is always unfavorable. VI. Treatment.—If we suspect the beginning of cirrhosis in drunk- ards, we should warn them against the abuse of alcohol, prescribe easily digested, unirritating food; and a cure in Carlsbad, Kissingen, Horn- burg, etc. Mercury internally and by inunctions, leeches and cups over the liver, leeches around the anus, blisters, warm and cold compresses over the liver have also been recommended. If the disease is at its height, the diet should be nutritious, but the patient should not be deprived entirely of alcohol, in order to avoid col- lapse. The milk-cure is said to have produced improvement, and even recovery in some cases. In the treatment of ascites too much should not be expected from the administration of diuretics, diaphoretics, and drastics. Puncture of the abdomen should not be looked upon as a last resort. The operation should be performed relatively early, and, if necessary, should be repeated. In one case Bamberger repeated the operation eleven times in two and a half months, and thus removed three hundred and fifty pounds of fluid. £. Acute Yellow Atrophy of the Liver. {Acute, diffuse parenchymatous hepatitis. Hepatitis cytophthora.) I. Etiology.—The disease is probably the result, in many cases, of infection with bacteria. The affection is extremely rare. It may be primary or secondary, the former variety occurring as an independent disease, the latter being secondary to another hepatic affection, or to diseases of the entire organ- ism. The primary form is more frequent in women than in men (1.6 :1). As a rule, it affects individuals from the twenty-fifth to the fortieth years, but occasionally beyond the age of sixty years or in childhood (earliest case in an infant aet. four days). No cases have been observed between the ages of five and nine years. It is especially frequent during pregnancy (fifth to eighth months), rarer after parturition. It is hardly ever observed during the first three months of pregnancy. 208 DISEASES OF THE LIVEK. A sort of epidemic spread has sometimes been noticed. Arnould ■observed it in ten soldiers who lived in the same wing of the barracks. Mental emotions and sexual excesses have been regarded as the excit- ing cause in certain cases. In the large majority of cases no exciting cause is ascertainable. Some authors believe that phosphorus poisoning may give rise to acute yellow atrophy of the liver, but it is at least questionable whether the changes in these two affections are identical with one another. Secondary yellow atrophy may be associated with cirrhosis and fatty liver, but it only affects parts of the organ. It has also been observed after certain infectious diseases (typhoid and relapsing fever, pyaemia, etc.). In one case it followed pharyngeal diphtheria, and the hepatic affection was, perhaps, secondary to diphtheria of the stomach. Syphi- lis and mercurialism are also said to favor the development of the dis- ease. II. Anatomical Changes.—The liver is diminished in size, its tis- sue is flaccid, and it has an ochre, saffron, or rhubarb color. The organ may be diminished to one-half or two-thirds, in some cases to one-fourth of the normal size; its thickness is especially affected. It has usually fallen backwards upon the spinal column, so that the anterior surface is covered by the intestines. The capsule is wrinkled because its dimensions are comparatively too large. The liver is peculiarly flaccid and almost fluctuates on being moved to and fro. In some cases it presents an almost uniform ochre yellow color, in others more or less yellowish-brown or reddish-brown parts alternate with one another. The red portions constitute a later stage of the disease. Since the changes are most marked in the left lobe, this portion sometimes has a reddish-brown color, while the right lobe is yellow. The yellow portions project above the cut surface, the red ones are depressed ; the former are brittle, the latter tough and leathery. The gall-bladder is sometimes almost empty. In other cases it has mucoid, faintly yellow, more rarely greenish contents. In the yellow portions the liver cells are in a condition of more or less marked fatty degeneration and destruction, particularly at the periphery of the lobules. Finally, nothing remains but a detritus of larger and smaller drops of fat. In places we notice bilirubin crystals, occasionally fine needles of tyrosin. In places in which the disease was beginning, Frerichs found an exudation between the liver-cells. It is also said that the degeneration of the cells is pre- ceded by cloudy swelling. The vessels contain small amounts of blood. Injection of the hepatic veins is unsuccessful because the injection mass at once extravasates. Frei'ichs found needles of tyrosin in these veins. The reddish-brown spots are developed from the yellow ones by the gradual absorption of the fatty detritus. Finally a basement substance remains contain- ing a few cells and fatty granules. The latter are occasionally found within the intra-acinous blood-vessels and lymphatics, and the walls of the latter may also present fatty degeneration. The biliary canals may present processes of proliferation. Nuclear prolifera- tion has been observed often in the interlobular tissue, particularly near the branches of the portal vein. Bacteria have been repeatedly found in the diseased parts. If the liver re- mains in the open air for several days it becomes covered with a whitish coating of leucin and tyrosin. In the fresh liver Salkowski found 2.51 per cent peptone and 0.36 per cent hemi- albumose, while the spleen contained 2.39 per cent peptone, and 0.58 per cent liemialbumose, and the kidneys 1.8 percent peptone, and 0.2 per cent hemialbu- mosc. DISEASES OF THE LIVER. 209 The blood is usually thin, of a tarry, black color, small in quantity, and occasionally contains a large amount of urea and tyrosin. Extravasations of blood are found in many organs. The periportal, retroperitoneal, and mesenteric glands are sometimes swollen and con- gested. The lymph-follicles of the intestines are rarely atfected. The spleen is usually large, soft, and flaccid. The gastro-intestinal tract presents signs of catarrh ; the ductus choledochus is sometimes occluded by a plug of mucus. The epithelium cells of the renal tubules are in a condition of fatty degeneration, and sometimes contain hsematoidin crystals, leucin, and tyrosin. The heart muscle is in a condition of fatty degeneration. Dropsy of the pleura and pericardium has been repeatedly observed. (Edema and inflammation have been observed in the lungs and oedematous changes in the brain. Finally, the voluntary muscles may undergo fatty degeneration. III. Symptoms.—The prodromal stage of the disease consists of the symptoms of gastro-intestinal catarrh (anorexia, nausea, vomiting, malaise, occasionally slight abdominal tenderness). After a while jaundice usually develops, at first in the face and neck, and gradually extends over the rest of the body. This stage lasts from a few days to several weeks. Then the patients become restless, begin to grow delirious and violent, the sensorium becomes more and more clouded ; grinding of the teeth, attacks of trismus, twitchings in the muscles, or general convulsions make their appearance. The somnolence increases to coma, respiration becomes irregular and stertorous, and the patients finally die in complete coma. In addition to the nervous system, many other organs are also affected. The liver undergoes a rapid diminution in size. As the anatomical changes begin earliest in the left lobe, dulness first disappears in the epigastrium, and gives place to a tympanitic note. Then the lower border of the liver gradually extends upwards, and, in marked cases, the hepatic dulness is confined to a nar- row strip in the right axillary line. The hepatic region may even be depressed. The atrophy of the liver is sometimes preceded by enlargement of the organ. In rare cases the atrophy is very slight or entirely absent, especially if the liver had been very fatty or exhibited considerable interstitial proliferation of con- nective tissue. Pain in the liver was absent in none of my cases. Despite the impairment of consciousness, the patient manifested pain when pressure was exercised upon the liver. Some authors believe that this is the result of general liypersesthesia of the skin. Enlargement of the spleen is a very frequent, though not a constant symptom. It remains absent if the capsule is thickened or calcified. In some cases it is prevented by hemorrhages from the stomach and intestines. The splenic enlarge- ment is the result in part of the disturbances of circulation in the portal vein, in part of the general infection. Changes in the integument are almost always present. Jaundice is not a necessary symptom in this disease, and its intensity does not always correspond to the severity of the nervous symptoms. A roseolar eruption has been repeatedly observed. Petechise and larger extravasations of blood are sometimes present, and are usually associated with hemorrhages in other regions. Very important changes are found in the urine. It is greatly diminished in amount, and anuria may occur towards the end of life. The reaction is acid; the specific gravity varies from 1.012 to 1.080. The urine has an icteric color, and also contains biliary acids. It usually deposits a fiocculent, brownish or green- 210 DISEASES OF THE LIVEK. ish sediment, and the presence of leucin or tyrosin in it is almost pathognomonic (vide Fig. 60). These substances can usually be extracted if a drop of urine is placed on an object glass, a little acetic acid added, and then allowed to evapo- rate. The sediment also contains casts (hyaline or fatty) and fatty, often icteric epithelium from the renal tubules. The urea is absent or greatly diminished. Frerichs noticed an increase of kreatin, absence of phosphate of lime, and con- siderable increase of extractive matters. Schmeisser noticed the absence of soda salts and a large amount of lime. Riess and Schultzen found lactic acid and peptonoid bodies in the urine. Albumin is found not infrequently, but usually in small amounts. The disease is almost always accompanied by gastro-intestinal symp- toms. The patients often vomit coffee-ground-like, bloody masses. Towards the end of life, this symptom is superseded by obstinate singul- tus. The tongue has a whitish-gray or brownish-yellow coating; the lips and gums are often covered with sordes. Fig. 60. Leucin drops ana tyrosin needles from the urinary sediment in acute yellow atrophy of the liver. Enlarged 275 times. The stools are dry and deficient in bile. Dissolution of the blood is often shown by hemorrhages into the va- rious organs (stomach, intestines, nose, respiratory tract, skin, etc.). Riess and Schultzen found tyrosin in the blood. Rosenstein noticed increase of the white blood-globules, amceboid movements and even con- strictions of the red globules, and a great tendency to the formation of “raspberry” prominences. The pupils are usually dilated, and their reaction is slow. Xanthop- sia and bilateral amaurosis have been observed. Fever may be absent, and occasionally the temperature is subnormal towards the end. In other cases, there is an elevation of temperature towards the close of life, occasionally even liyperpyretic temperature (above 41° C.). 211 DISEASES OF THE LIVER. At first the pulse is often slow; later it becomes frequent, small, and finally barely perceptible. The disease is almost always acute, and sometimes lasts only a few days. Death occurs, in the majority of cases, within the first two weeks. In a few cases, death ensued as late as the eighth week, in one case in the fourteenth week. Those writers who regard acute yellow atrophy of the liver as a general dis- ease lay stress on its occasional epidemic development, the implication of other organs, and the disproportion which may exist between the relatively slight local changes and the severe general symptoms. We regard the disease as a local affection of the liver. Its epidemic occurrence may be explained on the ground that the noxious agent affects several persons at the same time. In other affec- tions of the liver, we also find that other organs are implicated (probably from poisoning with biliary acids). Numerous theories have been advanced with regard to the real cause of the disease, but none possesses any solid foundation. The anatomical changes in the liver we regard as inflammatory in character, not as a simple degeneration. This view is favored by the fact that the atrophy of the organ is often preceded by enlargement, by the occurrence of nuclear and cellular proliferation in the interlobular tissue, etc. The jaundice may be explained by the occlusion of the biliary capillaries by the fatty and granular detritus of the liver cells. The severe nervous symptoms are the result of the accumulation in the blood of excrementitious matters which are normally excreted by the liver and kidneys. IV. Diagnosis.—The diagnosis is usually easy. In grave icterus from other causes, a mistake may arise if the transverse colon, distended with gas, is situated between the anterior surface of the liver and the abdominal walls, and thus artificially diminishes the hepatic dulness. But this condition is usually not permanent; in addition, vigorous percussion will enable us to hear the hepatic dulness. The differential diagnosis from phosphorus poisoning may be difficult; we must rely upon the history and the demonstration of phosphorus in the contents of the stomach, or, after death, in the other organs. V. Prognosis.—It is doubtful whether recovery from this disease ever takes place. VI. Treatment.—This must be confined to symptomatic measures. 6. Fatty Liver. I. Etiology.—An unusual amount of fat in the liver may be the result either of an excessive supply in the portal vein or of unusually vigorous metamorphosis of albuminoids in the liver cells, one part of which is converted into urea, the non-nitrogenous part into fat. The former constitutes fatty infiltration, the latter fatty degeneration of the liver. Fatty infiltration of the liver is found in individuals who eat largely, particularly of starchy and saccharine food and alcoholics, and take but little exercise. Fatty liver is also one of the alcoholic diseases. It is usually associated with other signs of obesity. In recent times, the views concerning the formation of fat have been mate- rially changed. It has been shown that it may be formed of albuminoids, which are converted into nitrogenous and non-nitrogenous components. It has been rendered doubtful whether the fats are produced by the carbohydrates. The fatty liver of drunkards is explained on the theory that the alco- 212 DISEASES OF THE LIVER. hoi diminishes oxidation, so that less fat is oxidized, and an unusually large amount remains in the liver. Fatty degeneration of the liver results if a poverty of oxygen is pro- duced by general or local causes and the hepatic cells are also involved. Their albuminoid constituents then undergo the changes mentioned above and the fat then remains in the cells because, on account of the deficiency of oxygen, it does not undergo further oxidation. This is observed in anaemic and cachectic conditions and after exten- sive hemorrhages, because the blood is poor in red blood-globules, which act as carriers of oxygen. Fatty liver is especially frequent in phthisis, particularly in females. The ac- cumulation of fat in the liver cells of phthisical individuals is evidently favored by the slight oxidation of fat in this disease. Fatty liver is also observed in cancer, chronic diarrhoea, rachitis, scrofula, per- nicious anaemia, chlorosis, leukaemia, spinal cord diseases attended with bed-sores, bone suppui’ation, malarial and syphilitic cachexia. This category also includes the fatty liver of pregnant and purperal women, the so-called acute fatty degen- eration of the new-born, etc. Abnormally high temperature of the body is sometimes the cause of fatty degeneration of the liver cells. This change is often preceded by cloudy swelling. The process of infection itself predisposes to the disease so that it is sometimes found in infectious diseases which run an apyrexial course. Marked fatty degeneration of the liver is found after poisoning with phosphorus, arsenic, antimony, etc., because these substances interfere with the absorption of oxygen. The disease also is produced by stasis in the hepatic veins, since this interferes with tissue respiration. In a case of this kind Frerichs found the first accumulation of fat in the immediate vicinity of the central veins. Finally, it may be produced by local diseases of the liver (cirrhosis, abscess, etc.). II. Anatomical Changes.—Slight grades of fatty liver can only be recognized with the aid of the microscope. The organ may increase to double the normal size, the edges are usually thickened and blunted. In the fresh condition the liver is soft and compressible; it has a pale or sallow yellow color. The capsule is smooth and tense, and its vessels may be dilated. The gall-bladder sometimes contains only a small quantity of a slightly bile-stained fluid, which may be chiefly mucoid. The organ is pale on section. The markings are often wiped out, in other cases the centre of the lobules is deeply stained with bile. If the disease is the result of stasis, the centre of the lobules has a blood-red or brownish-red color. The fatty changes are occasionally pronounced only in places. The right lobe is sometimes chiefly affected. After cutting the liver, the blade of the knife is found covered with an emulsion-like fluid which contains numerous drops of fat. In well marked cases the liver burns with a bright flame. The weight of the liver is increased, but its specific gravity is dimin- ished, sometimes even to that of water. Fatty changes are often found in other organs. In slight grades of the disease the hepatic cells are often filled with more oi less numerous fatty granules. In marked cases the cell is filled by a single shin- ing drop of fat; it is round and increased in size, and appears to‘be destitute of DISEASES OF THE LIVER. 213 membrane and nucleus. After sections are placed in turpentine or Canada bal- sam, the membrane and nucleus make their appearance. A few of the cells may contain crystals of fat. The fatty degeneration generally begins at the periphery of the lobules. It was formerly held that in fatty infiltration an accumulation of large drops of fat occurred in the individual liver cells, but that these were filled with very fine fat granules in fatty degeneration. But this distinction is not real. Fatty infiltration may begin with an accumulation of fine fat granules, and the latter sometimes coalesce into a single drop of fat in fatty degeneration. In fatty infiltration Peris found a deposit of fat in the intercellular biliary capillaries. Platen observed an accumulation of fat in the stellate cells which are scattered between the capillaries and liver cells. The hepatic cells contain drops of fat even under normal conditions, so that the transition from the physiological to the pathological fatty liver occasionally occurs very gradually. In one case Frerichs found 78.07 per cent fat in the dried hepatic tissue. Leucin and tyrosin were also found in large quantities. In one case Frerichs found a peculiar yellow coloring matter, which differed essentially from ordinary bile pigment. Frerichs and Peris have attempted to distinguish by chemical means the dif- ference between fatty infiltration and degeneration. In the former the fat accu- mulates chiefly at the expense of the water in the hepatic cells, so that the organ becomes rich in fat, poor in water, and unchanged with regard to albuminoids. In fatty degeneration the fat forms at the expense of the albuminoids, so that the organ is rich in fat, poor in albumin, water unchanged. Rokitansky described tlie so-called wax liver as a special form of fatty liver. It presents unusual firmness and brittleness and a waxy color; it is probably richer in the firmer fats (palmitin and stearin). III. Symptoms.—In many cases no symptoms are produced during life. In others we notice the mechanical symptoms arising from en- largement of the liver fa feeling of pressure and tension in the hypo- chondrium, perhaps real pain in the liver). Concerning enlargement of the organ we refer to the previous section. It may be mentioned here that the lower border of the soft liver can rarely be felt distinctly. These symptoms may be associated with functional disturbances (anorexia, eructations, vomiting, a tendency to diarrhoea and often to hemorrhoids). IV. Diagnosis.—This is not always easy. The existence of fatty liver must be assumed in “high livers” and obese individuals, even if a thick panniculus adiposus prevents the recognition of the size of the organ. It is distinguished from cirrhosis by the less resistance of the organ to the feel, and the absence of ascites and enlargement of the spleen. In waxy liver, the resistance is greater, and the lower border can be mapped out distinctly; there is often enlargement of the spleen or oedema and albuminuria, if the kidneys are waxy. V. Prognosis.—This depends upon the causation. The disease may hasten death by interfering with digestion and nutrition. VI. Treatment.—This depends upon the etiology of each individual case. Otherwise, purely symptomatic treatment is indicated. 7. Waxy Liver. (.Amyloidosis hepatis.) I. Etiology.—Waxy liver is always secondary to cachectic condi- tions (chronic suppuration and ulceration, chronic diseases, syphilis, and intermittent fever). 214 DISEASES OF THE LIVER. Among the suppurations, tubercular affections of the bones and joints are the most important. Waxy liver, also, is not infrequently the result of abscesses of the soft parts, whether they are encapsulated or have perforated externally. Among the chronic ulcerative processes, pulmonary phthisis is the most import- ant etiological factor. Waxy liver may be the result of the following chronic diseases: Rickets, osteomalacia, pseudoleukaemia, Bright’s disease, gout, tumors (cancer, sarcoma, lymphosarcoma, fibromyoma, ovarian cysts, etc.). Nothing positive is known concerning the connection between waxy liver and cachexia. Dickinson found that the liver was poor in alkalies; since the organism loses alkalies in suppuration, etc., he assumed that the amyloid substance is fibrin which has been deprived of alkalies (?). The disease is almost always acquired; it may be congenital in hered- itary syphilis. It is much more frequent in men than in women, and from the tenth to the fiftieth years of life. 11. Anatomical Changes.—In well-marked cases the liver may in- crease to double its normal size, and its lower border is often thickened and blunted. It has been known to extend from the third rib to the crest of the ilium. The weight of the organ is increased. The capsule is usually smooth, tense, and free from adhesions. The organ presents an increased resistance when cut through. The cut surface has a peculiar lardaceous appearance. A thin section appears transparent in trans- mitted light. The surface looks anaemic and brownish-red; the lobular markings are indistinct. The liver is brittle and doughy, and pressure produces permanent depressions. If to the cut surface is applied a solu- tion of iodine (potass, iodid.. gr. xxx.; iodin. pur., gr. xv.; aquae, | iiiss.), and this is washed off after a time, we will notice a deep, red- dish-brown, mahogany color of the affected parts, while the unaffected parts are light yellow or unstained. This appearance is often seen best in thin sections. The gall-bladder is often empty, or contains a mucoid fluid, more rarely greenish, inspissated bile. When the waxy degeneration is less diffusely developed, it will be found to be confined to about the middle third of the lobules. This part is grayish, transparent, is stained of a mahogany color by iodine, while the peripheral zone is opaque (fatty changes in the cells) and the central portion deep yellow or brownish-yellow (bile staining of the cells). In the incipient stages of waxy degeneration the diagnosis can only be made with the microscope. In addition to waxy changes, we not infrequently find fatty degenera- tion of the liver cells. Amyloidosis may also develop in cirrhotic or syphilitic livers, and in the cyanotic nutmeg liver. In all such cases the waxy changes may not appear on superficial observation. They sometimes occur in small, scattered foci, for example in syphilitic cica- trices. On microscopical examination, the amyloid parts have a peculiar, waxy gloss, are increased in size, and appear homogeneous. If microscopical sections are placed in a weak solution of iodine, the waxy parts assume a reddish-brown or mahogany color. If the section is then placed in a weak solution of sulphuric acid, hydrochloric acid, chloride of lime or zinc, the waxy parts will turn dirty violet, violet-blue, or pure blue. Boettcher recommends the following solutions: (a) gr. 3| iodine, gr. 7£ potass, iodid., § iiiss. water; (b) 2.7 ccm. sulphuric acid to 100 water. Various aniline colors have been recently found to form valuable reagents. (a) Methyl violet (1%) stains the waxy parts bright red, the non-waxy parts assume a blue color; (b) Saffranin stains amyloid orange yellow, non-amyloid parts rose-red. The first changes in this disease are observed in the finest branches of the hepatic artery, then in the communicating intralobular capillaries. Since the DISEASES OF THE LITER. 215 points of communication are situated in the middle zone of the lobules, this re- gion is affected very early. The process then spreads toward the hepatic vein, next toward the periphery of the acinus. The interlobular branches of the portal vein are finally involved. Freriehs found waxy changes even in the vessels of the capsule and the mucous membrane of the gall-bladder. In the capillaries, the amyloid change appears as a deposit of the waxy mate- rial. The endothelium remains intact, but the lumen of the vessels is narrowed, and even occluded in places. In other places the waxy deposits are separated in the shape of shining clumps, and are converted into a sort of cellular structures, which are readily mistaken for waxy liver cells. The adjacent hepatic cells are compressed and atrophied by the waxy deposits. At the periphery of the lobules we find fatty degeneration of the cells, in their centre an unusual staining with bile pigment. We can confirm the statements of those writers who believe that a few of the liver cells sometimes take part in the waxy change. It has been shown that amyloid is a nitrogenous, albuminoid substance, and that leucin and tyrosin may be derived from it. It is distinguished from other albuminoids by insolubility in an acid solution of pepsin and its long resistance to decomposition. The question as to the site of origin of the amyloid material—whether it develops in the liver or has been carried thither in the blood—is not definitely settled, although it is more probable that it is a true degeneration of the affected parts. Waxy changes are generally found in other organs, usually in the spleen, next in the kidneys and intestines. The liver is rarely affected alone. III. Symptoms.—Waxy changes are not infrequently present in the liver without giving rise to striking symptoms. They often produce merely the mechanical disturbances observed in other forms of hepatic enlargement. Physical examination shows that the liver is enlarged, very smooth and firm, and has a sharp lower border. The spleen is also usually found enlarged. In other cases the patients complain of functional disturbances (ano- rexia, eructations, vomiting, etc.), but the origin of these symptoms is determined with difficulty. If the kidneys are implicated, the urine not infrequently contains albumin, and pallor, ascites, and oedema develop. Jaundice does not occur in this disease unless the ductus choledochus is compressed by swollen and degenerated glands at the hilus. Amyloid degeneration does not follow fully developed cachexia at once, but there has been a tendency to over-estimate the duration of the intervening stage. Cohnheim showed that the disease may develop in three months after gunshot injuries, and in Bull's case amyloid degenera- tion, at least in the kidneys, developed in eighteen days after an acute psoas abscess. The disease may last for years. Death may occur from marasmus, general dropsy, oedema or inflammation of the lungs, etc. IV. Diagnosis.—In advanced cases the diagnosis is easy. Apart from the etiology we must rely upon the tense, firm consistence of the enlarged organ, which often assumes remarkable dimensions. In some cases the demonstration of waxy kidneys and spleen may be useful in differential diagnosis. V. Prognosis.—This is almost always unfavorable, although reliable authors think that recovery is possible. VI. Treatment.—The prophylaxis belongs to the domain of surgery. In other respects treatment must be directed to the primary disease (phthisis, rickets, syphilis, etc.). 216 DISEASES OF THE LIVEE. 8. Cancer of the Liver. I. Etiology.—Age exerts a certain influence. The disease is most frequent from the fortieth to the sixtieth years, especially in women at the menopause. It is rare in the first two decennia, but Siebold reported a case in a new-born infant. Cancer of the liver is more frequent in women, because it is often secondary to cancer of the breast, uterus, or ovaries. A few observations indicate that heredity is an occasional etiological factor. The disease is rarely observed in the tropics. Injury is sometimes mentioned as a cause. Reliable authors include gall-stones among the traumatic factors. At all events gall-stones are often found in cancerous livers,.but this may perhaps be explained as an accidental complication or as a secondary development of the calculi on account of occlusion of the bile-ducts by the cancer. Cancer of the liver may be primary or secondary. In rare cases primary cancer gives rise to secondary development of cancer in other organs. Secondary cancer of the liver usually follows the development of tumors in organs which are connected with the portal vein either directly or by means of collateral branches (uterus, rectum, stomach, etc.). Cancer of remote parts (eye, brain, etc.), may also give rise to secondary deposits in the liver. In some cases the growth spreads to the liver by contiguity, for example, from the stomach. Secondary cancer of the liver is much more frequent than the pri- mary form. .III. Anatomical Changes.—Cancer of the liver may be circum- scribed or infiltrated. In the former variety we find sharply defined tumors, in the latter a diffuse infiltration which often passes very gradu- ally into the healthy tissues. The nodules of cancer may vary from the size of a pin’s head to that of a child’s head. In primary cancer a single growth or a small number is usually present, in secondary cancer we find a large number of tumors, sometimes more than one hundred. If but a single tumor is present, it generally involves the right lobe. The liver sometimes increases more than sixfold in weight. It may extend from the third or even the second rib to beneath the anterior superior spinous process of the ilium. The hepatic substance proper diminishes as the cancerous masses increase. Small nodules within the liver will only be recognized on section. If they extend to the capsule, they often project beneath it above the sur- face of the liver, and the prominences frequently present a plate-shaped depression (umbilication). Cancerous nodules are sometimes found on the opposite side of the diaphragm or abdominal wall,.to a certain extent as the expression of a local infection. Virchow regards the umbilication as the result of fatty degeneration of the cancer cells and of cicatricial formation in the central, oldest portion of the tumor. Cicatrization of the entire nodule is prevented by the new formation of cancerous tissue at the periphery of the cancer. Frerichs observed umbilication in young nodules, and attributes it to the fact that the connective tissue at the centre of the nodule is more contractile than that at the periphery and the amount of cancer juice is less. Primary circumscribed cancer forms a rounded tumor which usually projects somewhat above the cut surface, has a creamy cancer juice, and contains fatty, occasionally cheesy or hemorrhagic foci. Its periphery DISEASES OF THE LIVES. 217 may be sharply defined, or in places it may pass gradually into the healthy tissue. The adjacent hepatic tissue is compressed, and has a , pale or brownish-red color. The tumor sometimes breaks into adjacent vessels, such as the hepatic veins, portal veins, finally into the biliary canals. Metastases are rarely found in remote organs. In primary infiltrated cancer of the liver the appearances are some- what like those of cirrhosis. The liver is traversed by broad bands of connective tissue, and its surface is nodular. Within the connective- tissue bands are little islets of cancer cells. No retrogressive metamor- phoses occur except fatty degeneration. The infiltration sometimes ex- tends to the wall of the gall-bladder, but proliferation into the vessels or metastases to other organs are not observed. In both forms, the portal glands are often implicated and may pro- duce serious symptoms by pressure on the excretory ducts or portai vein. Naunyn showed that the cancer develops from a proliferation of the epithelium cells in the biliary canals and that these dilate, in places, into alveoli. Some writers believe that the liver cells are also converted into cancer cells, or that both modes are combined. The tumor is nourished by the hepatic artery. In secondary cancer of the liver, the tumor is almost always circum- scribed. Its histological character depends upon that of the primary growth (alveolar, scirrhus, colloid, cystic cancer, fungus haematoides, cylindrical and pavement cell cancer). The cancer germs may be transported to the liver through the portal vein, hepatic artery, or the lymphatics. In some cases, corpuscular elements are probably carried to the liver as emboli, proliferate and affect the adjacent tissue. Secondary cancer may also proliferate into the biliary canals, portal and hepatic veins, and the gall-bladder. Secondary cancer of the liver is also an epithelial new-formation. Its cells are derivatives of hepatic cells, its stroma is derived from the capillaries and sur- rounding connective tissue ; it is nourished by the hepatic artery. Cancer of the liver is a frequent disease. In the Vienna General Hospital one case occurred to three hundred and twenty-two cases of other internal diseases. III. Symptoms.—In not a small number of cases, cancer of the liver is unrecognized, because the tumor, on account of its small size and localization, produces neither mechanical nor functional disturbances. In other cases, the symptoms are concealed by those furnished by other organs (cancer of the stomach, rectum, etc.). In some cases there is marked ascites, whose cause is unrecognized until the autopsy. Or the patients may die with symptoms of ichorous or hemorrhagic pleurisy, and the autopsy reveals cancer of the liver and secondary deposits on the pleura. Finally, the symptoms may consist of undefined malaise and increasing marasmus. The chief symptoms consist of mechanical and functional disturb- ances of the liver (enlargement, nodular surface and tenderness of the liver, and jaundice). The liver may attain remarkable dimensions in this disease. An important feature is the increase in size under observation. In Farre’s case the organ increased five pounds in weight within ten days. It pre- sents respiratory displacement until it has become so large as to be im- pacted and immovable in the abdomen. In rare cases, atrophy and diminution of the size of the liver are observed (three times in thirty-one of Frerichs’ cases). 218 DISEASES OF THE LIVER. An important symptom is the recognition of prominences on the surface of the liver. Special attention should be paid to the lower bor- der of the organ. Ererichs also recommends careful examination along the inner border of the rectus abdominis. The tendinous insertions along the belly of the muscle may be mistaken for nodules on the liver. The prominences are sometimes visible to the eye. They are usually hard, very rarely fluctuating. In a very emaciated patient, I was able to detect the umbilication of the nodules, but this is very excep- tional. The nodules also present respiratory displacement (unless adhe- sions to the diaphragm or anterior abdominal walls have formed), and sometimes cannot be felt except after deep inspirations. Peritonitio friction murmurs can sometimes be felt and heard (perihepatitis). The enlarged liver sometimes presents pulsating movements, which are evi- dently conveyed from the aorta. These movements consist of a simple lifting and falling of the organ. Pain is rarely absent; it is sometimes spontaneous, sometimes pro- duced only on pressure. It is sometimes limited to the hepatic region, or it may radiate to the sacrum, right shoulder, or arm. In some cases there is merely a feeling of pressure or tension in the right hypochon-