sults were obtained by cutting through one half of the medulla oblongata. Circulatory disturbance due to injury of the vasomotor tracts is offered as an explanation for these observations.

Extensive burns of the skin are frequently followed by the formation of one or more gastric ulcers.

Ulcer is usually single. There may be as many as five or more. Most frequently it is situated in the region of the lesser curvature, usually nearer the pylorus than the cardia. The ulcer has a punched-out appearance in acute cases; chronic cases show thickening of the edges with a funnel-shaped base. It is usually circular in outline, but by confluence of two or more ulcers irregular shapes may result, sometimes encircling the stomach. The base of the ulcer may be formed by the various layers of the stomach from the submucosa outward, or by some of the adjacent organs to which the stomach has become attached.

Healed ulcer with scar formation is found, as compared to open ulcer, as about 3 to 1. Probably a small ulcer may leave no scar when the base of the ulcer was not fixed and thus allowing the mucosa to close.

Healing usually results in a stellate scar, which is depressed and which is surrounded by puckered mucous membrane.

As the ulceration approaches the serous coat local peritonitis, with adhesion formation, occurs. The majority of the ulcers occupy the posterior wall. The ulcer usually becomes fixed to the pancreas or to the left lobe of the liver; more rarely fixation to other organs is seen. Cicatrization, with contraction of the alimentary tube, often leads to deformity, the character of which depends on the size, situation, and depth of the ulcer.

Pyloric stenosis, with dilatation of the stomach, and the so-called hour-glass contraction, resulting from a series of ulcers extending around the stomach, are the most common deformities.

Cardiac stenosis with dilatation of the esophagus oc

curs more rarely. Gastric ulcer, when followed by stenosis of the pylorus and dilatation of the stomach, especially where perigastric adhesions have produced a mass of considerable size, may so closely simulate carcinoma that a microscopical examination may be needed to identify the condition. This is most apt to occur where repeated, severe hemorrhages and constant vomiting have caused pronounced emaciation of the subject.

Perforation may pursue a chronic course, adhesions resisting and limiting the extent of the ulceration. Some solid organ may form a barrier. Perforation may occur into some of the hollow viscera.

Large abscesses may form in the lesser peritoneal cavity or beneath the diaphragm. Gastric ulcer or complicating abscesses may perforate the diaphragm into the pleura or the pericardium. Gastrocutaneous fistulæ are rare occurrences. Pylephlebitis and abscesses of the liver may occur without perforation of the ulcer. Often the condition is very complicated. Open and healed ulcers with contraction of the scars, deformities of the stomach, perforation communicating with one of the hollow viscera, with abscess cavities or with the stomach itself, may occur in a single case.

Fatal hemorrhage occurs in from 3 to 5 per cent of all cases. It is most frequent in men over 40. Fatal hemorrhage may occur from the erosion of small submucous vessels, but usually profuse bleeding signifies a deep chronic ulcer. The splenic artery and the artery of the lesser curvature are the usual seat of profuse hemorrhages.

Anemia following repeated hemorrhages may prove fatal from exhaustion, fatty degeneration of the heart, or thrombosis of the cerebral vessels.

ULCUS VENTRICULI-ROUND, GASTRIC ULCER OR PEPTIC ULCER

CHARLES F. NOOTNAGLE, M. D.

Minneapolis

SYMPTOMATOLOGY AND DIAGNOSIS

A good description of this disease was first published by Cruveilhier in 1829, hence it is also known as Cruveilhier's disease. From this time on, especially during the last twenty years of the 19th century, new facts were elucidated, especially in its diagnosis and treatment.

The symptoms of peptic ulcer may be so pronounced that an absolutely correct diagnosis may be made from these alone. In illustration I will cite a case from my practice:

Mrs. R, aged 30, well-nourished, good color, mother of one healthy child, doing light housework.

Family history was negative.

Personal history: always enjoyed the best of health with the exception of a mild attack of diphtheria at the age of 11. During the first part of Oct., 1901, she noticed that hot or cold ingesta caused pain in the epigastrium a little to the right of the median line. About ten days later a sensation of distress in the same spot commenced one-half to threequarters of an hour after meals and continuing for three or four hours. Within a few days vomiting occurred at times, producing an immediate cessation of the gastric distress. Pain was also marked in the back in the region of the 9th and roth dorsal vertebræ. At times a peculiar burning sensation and a feeling of pressure, extending along the esophagus into the throat, were associated with the gastric distress. Appetite was always good. A few times the vomitus and also the feces contained a very small amount of

blood. About three weeks after the beginning of the disease the vomitus (three hours after a mixed meal eaten against strict orders to the contrary) contained 0.38 of one per cent of free and combined hydrochloric acid.

The above leaves no room for doubt in regard to the diagnosis of peptic ulcer.

Again, the existence of the disease may be suddenly revealed in an apparently healthy person by symptoms of perforation or by a slight or pronounced hematemesis or by blood in the stools, or as is usually the case, blood appears in both vomitus and stools. To illustrate this I shall cite the following case:

Mrs K——, aged 33, mother of three healthy children, the youngest four months old, always enjoying good health, was suddenly attacked by a feeling of faintness during the afternoon of Dec. 11, 1902. In the evening of the same day she fainted, and I was hurriedly called. I found her suffering with all the symptoms of a severe internal hemorrhage, although consciousness had returned. While I was still at the bedside she vomited a large amount of blood, and the following day tarry stools appeared. The patient was kept absolutely at rest and without food of any kind for a number of days, and no hemorrhage recurred. Later on liquid diet was instituted and continued for about a month, without gastric distress of any kind during this entire period being manifested, but on permitting a more substantial diet all the classical symptoms of gastric ulcer, with pain in the epigastrium shooting through into the back shortly after meals, cessation of pains after vomiting, etc., developed. After a strict course of rectal feeding and absolute rest the patient recovered.

It may also be necessary to observe a case for a long time before having even a suspicion of the existence of a gastric ulcer.

To illustrate this I shall give you the following history from my case book:

May 10, 1899, Mr. B-, aged 45, married, healthy children, teacher in public school, weight 150 lb., which

one and one-half years ago was 180 lb., always lived in nonmalarial country.

Family history was negative.

Personal history: always enjoyed good health, except had measles in childhood, no venereal diseases of any kind. Present malady commenced one and one-half years ago with "gastric fever," was ill with severe pains in epigastrium, vomiting incessantly and the temperature at times was as high as 102° F., pulse rapid, 120 beats per minute. At the end of three weeks he gradually improved, regaining part of weight lost during illness, but stomach continued to cause discomfort. At the end of February, 1899, this discomfort in epigastrium increased; appetite disappeared; bowels became costive; the epigastric pain was increased by the ingestion of food, especially cabbage, sweets, onions, etc.; at times feels dizzy without reference to eating; sleeps well; weight 150 lb.; has slight daily headaches; does not vomit, nor feel nauseated; urine normal in every respect; entire tongue covered with a thick white coating, is flabby, and shows indentations of teeth.

Diagnosis, doubtful, but probably chronic gastritis. I proposed test-meal, but was refused.

Treatment: Restriction of diet, hot water night and morning with sodium phosphate, and the following prescription:

Ꭱ Tr. nucis vom., 10.

Sig. meals.

Tr. cinchon., 10.

Ext. M. condurango, fl., 40.

Teaspoonful three times daily ten minutes before

May 24, 1899. Improved and felt better until the past few days, when he contracted a cold, causing coryza, cough and return of old symptoms, except that bowels remained regular. This treatment, with slight changes, was continued, but without much success until patient went out fishing for four weeks when he improved remarkably, only to relapse after returning and resuming his old occupation. I