The general health of the patient remains sometimes surprisingly good, even in cases of gastric ulcer with symptoms sufficiently marked to establish the diagnosis. But in most cases of chronic gastric ulcer the general nutrition sooner or later becomes impaired. This cannot well be otherwise when dyspepsia, vomiting, paroxysms of severe pain, and hemorrhage are present, separately or in combination, for any great length of time. In proportion to the severity and the continuance of these symptoms the patient becomes pale, weak, and emaciated. The face, thin, anxious, of a grayish-white color, and marked with sharp lines of suffering, presents the appearance which the older writers called facies abdominalis, to which even so recent an author as Brinton attaches exaggerated diagnostic importance. A little cachectic dropsy may appear about the ankles. While it is true that the general nutrition is less rapidly, less continuously, and, as a rule, less deeply, impaired in gastric ulcer than in gastric cancer, nevertheless sometimes a cachexia develops in the former which is not to be distinguished from that of cancer. Litten⁴⁶ relates a case of gastric ulcer which simulated for a time pernicious anæmia. In this case the profound anæmia could not be explained by vomiting, hemorrhage, or other symptoms of ulcer.

⁴⁶ Berliner klin. Wochenschrift, Dec. 6, 1880.

Beyond determining the existence of a fixed point of epigastric tenderness, physical examination of the region of the stomach is usually only of negative value in the diagnosis of gastric ulcer. In some cases of ulcer of the stomach epigastric pulsation is very marked, and sometimes most marked during gastralgic attacks. In these cases there may be dilatation of the aorta from paralysis of vaso-motor nerves analogous to the dilatation of the carotid and temporal arteries in certain forms of migraine (Rosenbach). When the diagnosis lies between gastric ulcer and gastric cancer, the presence of epigastric tumor is justly considered to weigh against ulcer; but it is important to know that tumor may be associated with ulcer. Thickening of the tissues around old ulcers and the presence of adhesions may give rise to a tumor. A thickened portion of omentum which had become adherent over an old gastric ulcer produced a tumor which led to a mistake in the diagnosis.⁴⁷ Rosenbach⁴⁸ calls attention to the occasional production of false tumors by spasm of the muscular coat of the stomach around a gastric ulcer. These tumors disappear spontaneously or yield to the artificial distension of the stomach by Seidlitz powders—a procedure which one would not venture to adopt if he suspected gastric ulcer. Fenwick thinks that in some cases of gastric ulcer fixation of the stomach by adhesions can be made out by physical exploration.

⁴⁷ A. Beer, Wiener med. Wochenschrift, No. 26, 1857.

⁴⁸ Deutsche med. Wochenschrift, 1882, p. 22.

The gravest symptom which can occur in gastric ulcer is the perforation of the ulcer into the general peritoneal cavity.

Only rough estimates can be made of the frequency of this symptom. These estimates vary from 2 to 25 per cent. From the data which I have collected I infer that perforation into the general peritoneal cavity occurs in about 6½ per cent. of all cases of gastric ulcer.⁴⁹

⁴⁹ Miquel (Schmidt's Jahrb., Bd. 125, p. 65, 1864) reckons the frequency of perforation at 2 per cent. Brinton's estimate of 13½ per cent. is the one generally accepted. He found 69 cases of perforation in 257 open ulcers collected from various sources. He doubles the number of open ulcers, as he considers cicatrized ulcers twice as frequent as the open. The statistics of some of the authors to whom he refers should not be used in this computation, either because they do not give accurately the number of cases of perforation, or because they include under perforation all cases of ulcer which have penetrated all of the coats of the stomach, whereas of course only perforation into the general peritoneal cavity should be here included. Valuable and laborious as are Brinton's researches, his statistics upon this point, as upon many others, are inaccurate.

In 249 fatal cases of open ulcer taken from the statistics of Jaksch, Dittrich, Willigk, Wrany (Prager Vierteljahr., vols. xcv. and xcix.), Eppinger, Starcke, Chambers, Moore, and Lebert (loc. cit.), I find 50 cases of perforation into the peritoneal cavity. This makes the percentage of perforations 6½ if the open ulcers be multiplied by 3, the number of cicatrized ulcers being taken as three times that of open ulcers (p. 482). This method of computation, which is adopted by Brinton, is defective on account of the uncertainty as to the proper proportion between cicatrized and open ulcers.

Lebert observed 9 cases of perforation with fatal peritonitis in his 252 cases studied clinically. He places the frequency of perforation with peritonitis at 3 to 5 per cent., which corresponds to Engel's estimate of 5½ per cent. (Prager Vierteljahrschrift, 1853, ii.).

As regards sex, perforation occurs two to three times oftener in the female than in the male. This increased liability is referable mainly to the preponderance of the acute perforating ulcer in young women.⁵⁰

⁵⁰ The liability to perforation in females seems to be not only absolutely, but also relatively, to the number of ulcers greater than in males, although, on the contrary, Brinton holds that the excess of perforations in females is not greater than that of ulcers. Berthold found perforation in 3.1 per cent. of the cases of gastric ulcer in males, and in 9.7 per cent. of the cases in females (op. cit., p. 28).

In the female the liability to perforation of gastric ulcer is greatest between fourteen and thirty years of age. In the male there seems to be no greater liability to perforation at one age than at another.⁵¹

⁵¹ Of 139 cases of perforated ulcer in females, Brinton found that four-fifths occurred before the age of thirty-five. He calculates the average age at which perforation occurs in the female as twenty-seven, and in the male as forty-two. He thinks that the average liability to perforation in both sexes decreases as life advances, although he holds that the liability to ulcer itself constantly increases with age.

As will be explained in considering the morbid anatomy, ulcers of the anterior wall of the stomach perforate more frequently than those in other situations.

As regards the symptoms which may have preceded perforation three groups of cases can be distinguished:

In the first there has been no complaint of gastric disturbance. In the midst of apparent health perforation may occur and cause death within a few hours. This is the ulcère foudroyante of French writers. It is met with more commonly in chlorotic young women than in any other class.

In the second group of cases, which are more frequent, gastric symptoms have been present for a longer or shorter time, but have been so ambiguous that the diagnosis of gastric ulcer is not clear until perforation occurs. Then, unfortunately, the diagnosis is of little more than retrospective interest.

In the third group of cases perforation takes place in the course of gastric ulcer, the existence of which has been made evident by characteristic symptoms, such as localized pain and profuse hemorrhage.

The immediate cause of perforation of gastric ulcer is often some agency which produces mechanical tension of the stomach, such as distension of the organ with food or with gas, vomiting, straining at stool, coughing, sneezing, pressure on the epigastrium, violent exertion, and jolting of the body.

With the escape of the solid, the fluid, and the gaseous contents of the stomach into the peritoneal cavity at the moment of perforation, an agonizing pain is felt, beginning in the epigastrium and extending rapidly over the abdomen, which becomes very sensitive to pressure. The pain sometimes radiates to the shoulders. Symptoms of collapse often appear immediately or they may develop gradually. The pulse becomes small, rapid, and feeble. The face is pale, anxious, and drawn (facies hippocratica). The surface of the body, particularly of the extremities, is cold and covered with clammy sweat. The internal temperature may be subnormal, normal, or elevated; after the development of peritonitis it is usually, but not always, elevated. Consciousness is usually retained to the last, although the patient is apathetic. Vomiting is sometimes absent—a circumstance which may be of value in diagnosis, and which Traube attributes to the readiness with which the contents of the stomach can be discharged through the abnormal opening into the peritoneal cavity. There is usually constipation. The respirations become more and more frequent and costal in type. Thirst is often urgent. Suppression of urine is not an uncommon symptom, although there may be frequent and painful attempts at micturition. Albumen and casts may appear temporarily in the urine. Retraction of one testicle, like that in renal colic, has been observed (Blomfield). The patient usually lies on his back with the knees drawn up. The abdomen is often at first hard and retracted from spasmodic contraction of the abdominal muscles, but later it usually becomes tympanitic, sometimes to an extreme degree. The presence of tympanitic resonance replacing hepatic dulness in front is usually considered the most important physical sign of gas free in the peritoneal cavity, but this sign is equivocal. On the one hand, the presence of adhesions over the anterior surface of the liver may prevent the gas from getting between the liver and the diaphragm;⁵² and on the other hand, in cases of meteorism coils of intestine may make their way between the liver and the diaphragm, or the liver may be pushed upward and backward, so that its anterior surface becomes superior and the hepatic dulness in front disappears. Physical examination may reveal in the dependent parts of the peritoneal cavity an accumulation of fluid partly escaped from the stomach and partly an inflammatory exudate.⁵³ For humane reasons one should not submit the patient to the pain of movement in order to elicit a succussion sound or to determine change in the position of the fluid upon changing the position of the patient.⁵⁴ There is sometimes relief from pain for some hours before death.

⁵² Even without these adhesions liver dulness may persist after perforation of the stomach, as in a case of Nothnägel's in which for twenty-four hours after a large perforation from gastric ulcer the abdomen was retracted and hepatic dulness was well marked (Garmise, Ulcus Ventriculi cum peritonitide perforativa, Inaug. Diss., Jena, 1879).

⁵³ In a case of peritonitis resulting from perforation of a latent ulcer of the duodenum, Concato found in the acid fluid withdrawn by aspiration from the peritoneal cavity Sarcina ventriculi (Giorn. internaz. delle Scienze Med., 1879, No. 9).

⁵⁴ Other symptoms which have been thought to be diagnostic of pneumo-peritoneum in distinction from meteorism, but the value of which is doubtful, are these: In pneumo-peritoneum the respiratory murmur can be heard by auscultation over the entire abdomen, while in meteorism it does not extend beyond the region of the stomach (Cantani); in the former amphoric sounds synchronous with respiration can sometimes be heard over the abdomen (Larghi); borborygmi are heard, if at all, distantly and feebly; the percussion note of gas free over the liver is different from that of tympanitic intestine (Traube); the percussion note is of the same character over the whole anterior wall of the abdomen; the epigastric region is more elastic to the feel than in tympanites; the distension of the abdomen is more uniform than in tympanites; and coils of distended intestine, sometimes showing peristaltic movement, cannot be seen or felt as in some cases of meteorism (Howitz).

There are exceptional cases of perforation in which some of the most important of the enumerated symptoms, such as pain, tenderness of the abdomen on pressure, tympanites, and the symptoms of collapse, are absent.

Death sometimes occurs from shock within six or eight hours after perforation. More frequently life is prolonged from eighteen to thirty-six hours, it may be even for three or four days, and, very rarely, even longer.⁵⁵ When life is prolonged more than twelve hours an acute diffuse peritonitis is usually but not always developed.

⁵⁵ In the Descriptive Catalogue of the Warren Anatomical Museum, by Dr. J. B. S. Jackson, p. 448, Boston, 1870, is described a case of gastric ulcer in which, so far as can be judged by the symptoms and the post-mortem appearances, the patient lived nineteen days after perforation.

The contents of the stomach, instead of being diffused throughout the peritoneal cavity, may be confined by a rapidly-developed circumscribed peritonitis to a space near the stomach, or perforation may occur into a space previously shut off from the general peritoneal sac by adhesions. In this way circumscribed peritoneal abscesses form in the neighborhood of the stomach. Diffuse peritonitis may be caused either by an extension of the inflammation or by the rupture of these abscesses into the general peritoneal cavity. The cases of circumscribed peritonitis following perforation of gastric ulcer, with escape of the contents of the stomach, although more protracted than those in which the whole peritoneal surface is at once involved, generally terminate fatally sooner or later. The symptoms are often very obscure.

The most interesting of these peritoneal abscesses is the variety to which Leyden has given the name of pyo-pneumothorax subphrenicus (false pneumothorax of Cossy), the diagnostic features of which first were recognized by G. W. Barlow and Wilks in 1845.⁵⁶ Here there is a cavity, circumscribed by adhesions, just beneath the diaphragm, containing pus and gas and communicating with either the stomach or the intestine. By the encroachment of this cavity upon the thoracic space the symptoms and signs of pyo-pneumothorax are simulated. Barlow and Leyden have diagnosed during life this affection when resulting from perforated gastric ulcer. The points in diagnosis from genuine pyo-pneumothorax are the presence of respiratory murmur from the clavicle to the third rib, the extension of the respiratory murmur downward by deep inspiration, history of preceding gastric disturbance with circumscribed peritonitis, absence of preceding pulmonary symptoms, rapid variations in the limits of dulness with changes in the position of the body, absence or only slight evidence of increased intrapleural pressure (such as bulging of the thorax as a whole, and of the intercostal spaces), displacement of the heart, displacement of the liver downward, and, if necessary, the determination by means of a manometer that the pressure in the abscess cavity rises during inspiration and falls during expiration, the reverse being true in genuine pneumothorax.⁵⁷

⁵⁶ Barlow and Wilks, London Med. Gazette, May, 1845; Leyden, Zeitschr. f. klin. Med., i. Heft 2; Cossy, Arch. gén. de Méd., Nov., 1879; Tillmanns, Arch. f. klin. Chirurg., Bd. 27, p. 103, 1881.

⁵⁷ Schreiber has shown that this last diagnostic point, which was given by Leyden, is not without exceptions, for the pressure in the peritoneal cavity may sink during inspiration and rise during expiration (as in the pleural cavity), especially when the diaphragm takes little or no part in respiration ("Ueber Pleural- und Peritonealdruck," Deutsches Arch. f. klin. Med., July 31, 1883).

Through the medium of subphrenic abscess, or directly through adhesions between the stomach and the diaphragm, gastric ulcer may perforate into one of the pleural cavities (generally the left) and cause empyema or pneumo-pyothorax. Adhesions may form between the diaphragm and the pulmonary pleura, so that the ulcer perforates directly into the lung; in which case pulmonary gangrene or pulmonary abscess is usually developed. The diagnosis of the perforation into the lung has been made by recognizing a sour odor and sour reaction of the expectoration, and by finding in the sputum particles of food derived from the stomach. Sudden death from suffocation has followed perforation of the stomach into the lung.⁵⁸

⁵⁸ Tillmanns (loc. cit.) has collected 12 cases of communication between the stomach and the thoracic cavity from perforation of gastric ulcer; all proved fatal. In Sturges's case of recovery from pneumothorax supposed to be produced by perforation of a gastric ulcer the diagnosis of the cause of the pneumothorax was very doubtful (The Lancet, Feb. 7, 1874).

Perforation of gastric ulcer into the transverse colon has been followed by the vomiting of formed feces and by the passage of undigested food by the bowel (Abercrombie). Enemata may be vomited, so that, as suggested by Murchison, the introduction of colored enemata may aid in the diagnosis.

Gastro-cutaneous fistulæ are among the rare results of perforation of gastric ulcer. In these cases food, sometimes only in liquid form, escapes through the fistula.

The opening of gastric ulcer into the pericardium is one of the rare causes of pneumo-pericardium.

Other varieties of perforation which are of pathological rather than of clinical interest will be mentioned under the morbid anatomy of gastric ulcer.

COURSE.—Few diseases are more variable in their course and duration than is simple gastric ulcer. It is customary to distinguish between acute and chronic forms of gastric ulcer, but this is a distinction which cannot be sharply drawn. Those cases are called acute in which, with absence or short duration of antecedent gastric symptoms, perforation or gastrorrhagia suddenly causes death. But in some of these cases the thickened and indurated margins of the ulcer found at the autopsy show that the disease has been of much longer duration than the clinical history would indicate. Still, there is reason to believe that within the course of a few days ulcers may form and perforate all of the coats of the stomach.

In the great majority of cases of gastric ulcer the tendency is to assume a chronic course, so that the often-used term chronic gastric ulcer is generally applicable.

The great diversity of the symptoms in different cases makes it impossible to give a generally applicable description of the course of gastric ulcer. It is, however, useful to designate the main clinical forms of the disease. Thus we may distinguish—

1. Latent ulcers, with entire absence of symptoms, and revealed as open ulcers or as cicatrices at the autopsy.

2. Acute perforating ulcers. With or without a period of brief gastric disturbance perforation occurs and causes speedy death.

3. Acute hemorrhagic form of gastric ulcer. After a latent or a brief course of the ulcer profuse gastrorrhagia occurs, which may terminate fatally or may be followed by the symptoms of chronic ulcer.

4. Gastralgic-dyspeptic form. In this, which is the most common form of gastric ulcer gastralgia, dyspepsia and vomiting are the symptoms. Sometimes one of the symptoms predominates greatly over the others, so that Lebert distinguishes separately a gastralgic, a dyspeptic, and a vomitive variety. Gastralgia is the most frequent symptom.

5. Chronic hemorrhagic form. Gastrorrhagia is a marked symptom, and occurs usually in combination with the symptoms just mentioned.

6. Cachectic form. This usually corresponds only to the final stage of one of the preceding forms, but the cachexia may develop so rapidly and become so marked that the course of the disease closely resembles that of gastric cancer.

7. Recurrent form. In this the symptoms of gastric ulcer disappear, and then follow intervals, often of considerable duration, in which there is apparent cure, but the symptoms return, especially after some indiscretion in the mode of living. This intermittent course may continue for many years. In these cases it is probable either that fresh ulcers form or that the cicatrix of an old ulcer becomes ulcerated.

8. Stenotic form. By the formation of cicatricial tissue in and around the ulcer the pyloric orifice becomes obstructed and the symptoms of dilatation of the stomach develop.

DURATION.—The average duration of gastric ulcer may be said to be from three to five years, but this estimate is not of great value, on account of the absence of any regularity in the course and duration of the disease. In cases of very protracted duration, such as forty years in a case of Habershon's and thirty-five in one of Brinton's, it is uncertain whether the symptoms are referable to the persistence of one ulcer or to the formation of new ulcers, or to sequels resulting from cicatrization.

In 110 cases (44 fatal) analyzed by Lebert⁵⁹ the course was latent until the occurrence of perforation or of profuse hemorrhage in 15 per cent., the duration was less than one year in 18 per cent., from one to six years in 46½ per cent., from six to twenty years in 18 per cent., from twenty to thirty-five years in 2½ per cent.

⁵⁹ Op. cit., p. 235.

TERMINATIONS.—In the majority of cases gastric ulcer terminates in recovery. The recovery is often complete. Various gastric disturbances may, however, follow the cicatrization of gastric ulcer, especially if the ulcer was large and of long duration. These sequential disturbances are due to the contraction of the cicatrix, to adhesions between the stomach and surrounding parts, to deformity of the stomach, and especially to dilatation of the stomach by cicatricial stenosis of the pylorus. Hence, gastralgia, dyspepsia, and vomiting may continue after the ulcer has healed, so that anatomical cure of the ulcer is not always recovery in the clinical sense. Relapses may occur after recovery, as those who have once had gastric ulcer are more prone to the disease than are others. Not infrequently the patient recovers so far as to be able to attend to the active duties of life, but to avoid renewed attacks he is always obliged to be very careful as regards his mode of living.

How often gastric ulcer ends in death it is impossible to say. It is certain that Brinton under-estimates the number of recoveries when he computes that only one-half of the ulcers cicatrize. Lebert reckons the mortality from gastric ulcer as 10 per cent., which appears to be too low an estimate. Perhaps 15 per cent. would be a more correct estimate of the mortality.

The causes of death are perforation, hemorrhage, exhaustion, and complicating diseases.

About 6½ per cent. of the cases of gastric ulcer terminate fatally by perforation into the peritoneal cavity. Although this estimate can be considered only approximative, there is little doubt but that the much larger percentages given by most writers are excessive, and are referable to the undue frequency with which cases of perforation of gastric ulcer have been published. Such cases naturally make a strong impression upon the observer, and are more likely to be published than those which terminate in other ways.

Death from hemorrhage occurs probably in from 3 to 5 per cent. of the cases of gastric ulcer.⁶⁰ In many more cases hemorrhage is an indirect cause of death by inducing anæmia. Unlike perforation, fatal hemorrhage from gastric ulcer is more common in males than in females—more common after than before forty years of age. The average age at which fatal hemorrhage occurs is given by Brinton as forty-three and a half years both for males and females.

⁶⁰ In 270 fatal cases of open ulcer from the statistics of Jaksch, Dittrich, Eppinger, Starcke, Chambers, Habershon, Moore, and Lebert, I find 27 deaths by hemorrhage. Reckoning three cicatrices to one ulcer, this would give a percentage of 3¹/3.

In a considerable proportion of the fatal cases exhaustion is the cause of death. According to Lebert, death from exhaustion occurs in about 4 per cent. of the cases of gastric ulcer. The causes of exhaustion are the pain, hemorrhage, dyspepsia, and vomiting which constitute the leading symptoms of the disease.

Finally, death may be due to some of the complications or sequels of gastric ulcer.

COMPLICATIONS.—Some of the complications of gastric ulcer are directly referable to the ulcer, others are only remotely related to it, and others are merely accidental.

Pylephlebitis is among the most important of the complications directly referable to the ulcer. This pylephlebitis is usually of the infectious variety, and leads to abscesses in the liver, sometimes to abscesses in the spleen and other organs.

As has already been mentioned, chronic catarrhal gastritis stands in close relationship to gastric ulcer. Chronic peritonitis is a rare complication of gastric ulcer (Moore, Vierordt). Chronic interstitial gastritis, with contraction of the stomach and thickening of its walls, was associated with ulcer in a case under my observation. In a case of ulcer under the care of Owen Rees⁶¹ this condition of the stomach was associated with chronic deforming peritonitis (thickening, induration, and contraction of the peritoneum) and ascites, so that the symptoms during life and the gross appearances after death resembled cancerous diseases of the peritoneum. Simple ulcer and cancer may occur together in the same stomach, or cancer may develop in an ulcer or its cicatrix. Glässer reports a case of phlegmonous gastritis with gastric ulcer.⁶² Extension of inflammation to the pleura without perforation of the diaphragm sometimes occurs. Fatty degeneration of the heart may be the result of profound anæmia induced by gastric ulcer.⁶³ Embolic pneumonia and broncho-pneumonia are occasional complications. A moderate degree of cachectic dropsy is not very infrequent in the late stages of gastric ulcer.

⁶¹ Med. Times and Gaz., April 24, 1869.

⁶² Berlin. klin. Wochenschrift, 1883, No. 51.

⁶³ Shattuck, Boston Med. and Surg. Journ., June, 1880, vol. ciii.

Other complications, such as pulmonary tuberculosis, valvular disease of the heart, general atheroma of the arteries, cirrhosis of the liver, syphilis, chronic Bright's disease, waxy degenerations, and malaria, have been considered under the Etiology, and some of them will be referred to again in connection with the Pathology, of gastric ulcer. In most instances when ulcer is associated with these diseases the ulcer is secondary.

SEQUELÆ.—The most important sequelæ of gastric ulcer are changes in the form of the stomach in consequence of adhesions and in consequence of the formation and contraction of cicatrices. These lesions are most conveniently described under the Morbid Anatomy. The symptoms of the most important of these sequels—namely, stenosis of the pylorus with dilatation of the stomach—will be described in another article.

MORBID ANATOMY.—As regards number, simple ulcer of the stomach is usually single, but occasionally two or more ulcers are present. It is not uncommon to meet in the same stomach open ulcers and the scars of healed ulcers. According to Brinton, multiple ulcers are found in about one-fifth of the cases. In one case O'Rorke found six ulcers on the anterior wall of the stomach.⁶⁴ Berthold mentions a case in which thirty-four ulcers were found in the same stomach.⁶⁵

⁶⁴ Trans. of the New York Path. Soc., vol. i. p. 241. Wollmann mentions the occurrence of over eight simple ulcers in the same stomach (Virchow und Hirsch's Jahresb., 1868, Bd. ii. p. 126).

⁶⁵ Op. cit., p. 21. It is expressly stated that these were not hemorrhagic erosions, but deep corrosive ulcers.

The usual position of simple gastric ulcer is the posterior wall of the pyloric portion of the stomach on or near the lesser curvature. Ulcers of the anterior wall are rare, but they carry a special danger from their liability to perforate without protective adhesions. The least frequent seats of ulcer are the greater curvature and the fundus.

The table on page 504 gives the situation of 793 ulcers recorded in hospital statistics:⁶⁶

From this table it is apparent that ulcers occupy the lesser curvature, the posterior wall, and the pyloric region three and a half times more frequently than they do the remaining larger segment of the stomach.

⁶⁶ These statistics are collected from the previously-cited works of Rokitansky, Jaksch, Wrany, Eppinger, Chambers, Habershon, Steiner, Wollmann, Berthold, Starcke, Lebert, and Moore. They represent 566 cases. So far as noted, most of the ulcers on the posterior wall were nearer to the lesser curvature than to the greater; those on the lesser curvature extended more frequently to the posterior than to the anterior wall. Although not apparent from the table, most of the ulcers of the lesser curvature and of the posterior wall were in the pyloric region. So far as possible, cicatrices were excluded. Pylorus and cardia in the table indicate on or near those parts.

Occasionally two ulcers are seated directly opposite to each other, the one on the anterior, the other on the posterior, wall of the stomach. The most plausible explanation of this is that the ulcers are caused by a simultaneous affection of corresponding branches which are given off symmetrically from the same arterial trunk as it runs along one of the curvatures of the stomach (Virchow).⁶⁷

⁶⁷ A. Beer, "Aus dem path. Anatom. Curse et. Prof. R. Virchow, etc.," Wiener med. Wochenschr., Nos. 26, 27, 1857.

The ordinary size of the ulcer varies from a half inch to two inches in diameter. The ulcer may be very minute, as in two cases reported by Murchison, in each of which a pore-like hole was found leading into a perforated artery from which fatal hemorrhage had occurred.⁶⁸ On the other hand, the ulcer may attain an enormous size, extending sometimes from the cardiac to the pyloric orifice and measuring five or six inches in diameter.⁶⁹

⁶⁸ Murchison, Trans. of the Path. Soc., vol. xxi. p. 162, London, 1870.

⁶⁹ In one of Cruveilhier's cases the ulcer was 6½ inches long and 3¹/3 inches wide. Law describes an ulcer measuring 6 inches by 3 inches (Dublin Hosp. Gaz., ii. p. 51).

The ulcer is usually round or oval in shape. The outline of the ulcer may become irregular by unequal extension in the periphery, or by the coalescence of two or more ulcers, or by partial cicatrization. Simple ulcers, especially when seated near the lesser curvature, have a tendency to extend transversely to the long axis of the stomach, thus following the course of the blood-vessels. By this mode of extension, or more frequently by the coalescence of several ulcers, are formed girdle ulcers, which more or less completely surround the circumference of the stomach, oftener in the pyloric region than elsewhere.

As the ulcer extends in depth it often destroys each successive layer of the stomach in less extent than the preceding one, so that the form of the ulcer is conical or funnel-shaped, with a terrace-like appearance in its sloping edges. The apex of the truncated cone, which is directed toward the peritoneum, is often not directly opposite to the centre of the base or superior surface which occupies the mucous membrane, so that one side of the cone may be vertical and the other sloping. In the half of the stomach nearer the lesser curvature the cone slopes upward, and in the lower half of the stomach it slopes downward. The usual explanation of its conical shape is that the ulcer exactly corresponds to the territory supplied by an artery with its branches. Virchow finds an explanation for the oblique direction of the funnel in the arrangement of the arteries of the stomach. These, coming from different sources, run along the curvatures of the stomach, and there give off symmetrically branches which run obliquely toward the mucous membrane, so that one of these branches with its distributive twigs (arterial tree) would supply a part shaped like an oblique funnel. One of the chief supports of the theory which refers the origin of simple gastric ulcer to an arrest of the circulation is this correspondence in shape of the ulcer to the area of distribution of the branches of the arteries supplying the stomach.

All ulcers do not present the conical form and terraced edges which have been described. These appearances are far from constant in fresh ulcers, and they are usually absent in those of long duration.

The most characteristic anatomical feature of simple ulcer of the stomach is the appearance of the edges and of the floor of the ulcer. The edges of recently-formed ulcers (acute ulcers) are clean-cut, smooth, and not swollen. To use Rokitansky's well-known comparison, the hole in the mucous coat looks as if it had been punched out by an instrument. The floor of the ulcer may be smooth and firm or soft and pulpy. The floor and edges of fresh ulcers are often infiltrated with blood, but they may be of a pale-grayish color. Usually no granulations and no pus are to be seen on the surface of the ulcer.⁷⁰ In ulcers of longer duration the margins become thickened, indurated, and abrupt; the floor acquires a dense fibrous structure.

⁷⁰ In rare instances granulations may be present, as in a case of W. Müller's, in which their presence rendered difficult the diagnosis of simple ulcer from carcinoma (Jenaische Zeitschrift, v., 1870). The microscope may also be required to distinguish the irregularly thickened margins of old ulcers from scirrhous cancer.

The floor of the ulcer may be the submucous, the muscular, or the serous coat, or, if the whole thickness of the stomach be perforated, it may be some adjacent organ to which the stomach has become adherent, this organ being usually the pancreas or the left lobe of the liver or neighboring lymphatic glands.

The microscopic examination of recently-formed ulcers shows that the tissue immediately surrounding the ulcer is composed of granular material, disintegrated red blood-corpuscles, pale and swollen fragments of connective-tissue fibres, and cells unaffected by nuclear-staining dyes. The red blood-corpuscles are sometimes broken into fragments of various sizes in about the same way as by the action of heat. The gastric tubules are separated from each other and compressed by infiltrated blood, and contain cells which do not stain. Around this margin of molecular disintegration, which has evidently been produced by the action of the gastric juice, there is often, although not constantly, a zone of infiltration with small round cells, probably emigrated white blood-corpuscles. These cells are most abundant near the muscularis mucosæ and in the submucosa. Extravasated red blood-corpuscles extend a variable distance around the ulcer, farthest as a rule in the submucous coat. Many of the blood-vessels in the immediate neighborhood of the ulcer appear normal; others, particularly the arterioles and the capillaries, may be filled with hyaline thrombi. Clumps of hyaline material may also be seen in the meshes of the tissue around the ulcer. Fine fatty granules may be seen in the tissue near the ulcer. The interstices of the loose submucous tissue and the lymphatic vessels are often filled with fibrillated fibrin and scattered blood-corpuscles for a considerable distance around the ulcer.

In the margins of old gastric ulcers there is also a zone of molecular necrosis. The induration and the thickening of the edges of these ulcers are caused by a new growth of fibrillated connective tissue, which blends together all of the coats invaded by the ulcer. This new tissue is usually rich in lymphoid cells, which are often most abundant in the lymphatic channels. In the fibrous edges and base of old ulcers are arteries which are the seat of an obliterating endarteritis, and which may be completely obliterated by this process. An interstitial neuritis may affect the nerve-trunks involved in the fibrous growth. Blood-pigment may be present as an evidence of an old hemorrhagic infiltration.⁷¹

⁷¹ The histological changes here described are based upon the examination of typical specimens both of recent and of old gastric ulcers which have come under my observation.

Cicatrization is accomplished by the development of fibrous tissue in the floor and borders of the ulcer. By the contraction of this new-formed tissue the edges of the mucous membrane are united to the floor of the ulcer, and may be drawn together so as to close completely the defect in the mucous membrane. The result is a white stellate cicatrix, which is usually somewhat depressed and surrounded by puckered mucous membrane. It is probable that small, superficial ulcers may be closed so that the scar cannot be detected. The mucous membrane which has been drawn over the cicatrix is intimately blended with the fibrous substratum, and is usually itself invaded by fibrous tissue which compresses and distorts the gastric tubules. Hauser⁷² has shown that the tubular glands grow down into the cicatricial tissue, where they may branch in all directions. These new-formed tubules are lined by clear cylindrical or cutical epithelial cells, and may undergo cystic dilatation. Very irregular cicatrices may result from the healing of large and irregular ulcers. When the ulcer is large and deep and the stomach is adherent to surrounding parts, the edges of the mucous membrane making the border of the ulcer cannot be united by the contraction of the fibrous tissue in the floor of the ulcer. The cicatrix of such ulcers consists of fibrous tissue uncovered by mucous membrane. The closure of the ulcer is incomplete. Such cicatrices are liable to be the seat of renewed ulceration.

⁷² Das chronische Magengeschwür, etc., Leipzig, 1883. In the rare instances of carcinoma developing in the borders or in the cicatrix of gastric ulcer, Hauser believes that the cancerous growth starts from these glandular growths, which in general have only the significance of Friedländer's atypical proliferation of epithelial cells.

The formation and contraction of the cicatrix may cause various deformities of the stomach. The character of these deformities depends upon the situation, the size, and the depth of the ulcer which is cicatrized. Among the most important of these distortions are stenosis of the pyloric orifice, followed by dilatation of the stomach, more rarely stenosis of the cardiac orifice, with contraction of the stomach, approximation of the cardiac and of the pyloric orifices by the healing of ulcers on the lesser curvature, and an hour-glass form of the stomach, produced by the cicatrization of girdle ulcers or of a series of ulcers extending around the stomach. These abnormalities in form of the stomach, particularly the constriction of the orifices, may be attended by more serious symptoms than the original ulcer.

As the ulcer extends in depth a circumscribed peritonitis, resulting in the formation of adhesions between the stomach and surrounding parts, is usually excited before the serous coat is perforated, so that the gravest of all possible accidents in the course of gastric ulcer—namely, perforation into the peritoneal sac—is permanently or temporarily averted. It has been estimated that adhesions form in about two-fifths of all cases of gastric ulcer (Jaksch). On account of the usual position of the ulcer on the lesser curvature or on the posterior wall of the stomach, the adhesions are most frequently with the pancreas (in about one-half of all cases of adhesion); next in frequency with the left lobe of the liver; rarely with other parts, such as the lymphatic glands, the diaphragm, the spleen, the kidney, the suprarenal capsule, the omentum, the colon, and other parts of the intestine, the gall-bladder, the sternum, and the anterior abdominal wall. Adhesions cannot readily form between the anterior surface of the stomach and the anterior abdominal wall, on account of the constant movement of these parts, so that ulcers of the anterior gastric wall are those most liable to perforate into the peritoneal cavity.

It is difficult to include in any description all of the various and complicated lesions which may result from perforation by gastric ulcer of all of the coats of the stomach. The consequences of perforation may be conveniently classified as follows:

1. Some solid organ, usually the pancreas, the liver, or the lymphatic glands, may close the hole in the stomach.

2. An intra-peritoneal sac shut in by adhesions may communicate through the ulcer with the cavity of the stomach.

3. A fistulous communication may form either between the stomach and the exterior (external gastric fistula) or between the stomach and some hollow viscus (internal gastric fistula).

4. The ulcer may perforate into the general peritoneal cavity.

These lesions may be variously combined with each other. It is to be noted that in the first three varieties protective adhesions are present, and that in the last these adhesions are either absent or ruptured.

When the pancreas, the liver, or the spleen form the floor of the ulcer, they may be protected from extension of the ulcerative process by a new growth of fibrous tissue extending from the floor of the ulcer a variable depth into these organs. Sometimes, however, the ulcerative process, aided doubtless by the corroding action of the gastric juice, eats out large excavations in these organs. These excavations communicate with the cavity of the stomach, and are usually filled with ichorous pus. The pancreas, unlike the spleen and the liver, possesses comparative immunity against this invasion by the ulcerative process.

The situation, the form, and the extent of circumscribed peritoneal abscesses resulting from perforation of gastric ulcer depend upon the parts with which the stomach has contracted adhesions. Should an ulcer on the posterior wall of the stomach perforate before the formation of adhesions, the perforation would of course be directly into the lesser peritoneal cavity. An interesting example of this rare occurrence has been communicated by Chiari.⁷³ In this case, the foramen of Winslow being closed by adhesions, the lesser peritoneal cavity which communicated with a gastric ulcer was filled with ichorous pus, and in this floated the pancreas, which had necrosed in mass and had separated as a sequestrum. That form of intra-peritoneal abscess known as subphrenic pneumo-pyothorax has been already described under Symptomatology. Peritoneal abscesses communicating with the stomach may open into various places, as into the general peritoneal cavity, into the pleural cavity, into the retro-peritoneal tissue, through the abdominal or thoracic walls, etc.

⁷³ Wiener med. Wochenschr., 1876, No. 13.

Gastro-cutaneous fistulæ are a rare result of the perforation of gastric ulcer.⁷⁴ The external opening is most frequently in the umbilical region, but it may be in the epigastric or in the left hypochondriac region or between the ribs. Fistulous communications resulting from the perforation of gastric ulcer have been formed between the stomach and one or more of the following hollow viscera or cavities: the colon, the duodenum and other parts of the small intestine, the gall-bladder, the common bile-duct, the pancreatic duct, the pleura, the lung, the left bronchus, the pericardium, and the left ventricle. Gastro-colic fistulæ, in contrast to gastro-cutaneous fistulæ, are more frequently produced by cancer than by ulcer of the stomach.⁷⁵ In rare instances the peritoneum over ulcers of the lesser curvature has contracted adhesions with the pyloric portion of the stomach or with the first part of the duodenum. To accomplish this it is necessary that a sharp bend in the lesser curvature should take place. By extension of the ulcerative process abnormal communication is established between the left and the right half of the stomach or between the stomach and the duodenum. In either case the right half of the stomach is often converted into a large blind diverticulum, the digested food passing through the abnormal opening.⁷⁶ Gastro-duodenal fistulæ are more frequently with the third than with the first part of the duodenum. In one of Starcke's cases the stomach communicated with the colon and through the medium of a subphrenic abscess with the left lung.⁷⁷

⁷⁴ Of the 25 cases of gastro-cutaneous fistula collected by Murchison, 18 were the result of disease. In 12 of these cases the probable cause was simple gastric ulcer (Med.-Chir. Trans., vol. xli. p. 11, London, 1858). Middeldorpf says that among the internal causes of the 47 cases of external gastric fistula which he tabulated, simple ulcer of the stomach played an important rôle (Wiener med. Wochenschr., 1860).

⁷⁵ Of 33 cases of gastro-colic fistula collected by Murchison, 21 were from gastric cancer and 9 or 10 probably from simple ulcer. On the other hand, gastro-cutaneous fistulæ are twice as frequently the result of simple ulcer as of cancer (Edinb. Med. Journ., vol. iii. 1857).

⁷⁶ Thierfelder has made the best study of the complicated relations existing in these cases (Deutsches Arch. f. klin. Med., Bd. iv. p. 33, 1868).

⁷⁷ Deutsche Klinik, 1870, No. 39. Habershon also reports a case in which a subphrenic abscess communicated with the lung, the stomach, and the colon, but he believes that the ulceration was primary in the colon (Guy's Hosp. Rep., Ser. 3, vol. i. p. 109).

Four cases of perforation of gastric ulcer into the pericardium,⁷⁸ with the production of pneumo-pericardium, have been reported, and two cases of perforation into the left ventricle.⁷⁹ Müller found lumbricoid worms in a pleural cavity which had been perforated by gastric ulcer.⁸⁰ Diaphragmatic hernia may result from perforation of the pleural cavity by gastric ulcer.⁸¹ In one instance the greater part of the small intestines passed through a hole in the transverse meso-colon which had been caused by a gastric ulcer.

⁷⁸ Hallin, Schmidt's Jahrb., cxix. S. 37; Säxinger, Prager med. Wochenschr., 1865; Guttmann, Berl. klin. Wochenschr., 1880, No. 23. Murchison mentions a specimen in the museum of King's College, London, of a simple gastric ulcer opening into the pericardium (Edinb. Med. Journ., vol. iii. p. 6). In a case reported by Graves a liver abscess burst into the stomach and into the pericardium (Clin. Lect., ii. p. 237, Dublin, 1848).

⁷⁹ Oser, Wiener med. Blätter, 1880, No. 52; Brenner, Wiener med. Wochenschr., 1881, No. 47.

⁸⁰ Müller, Memorabilien, xvii., Oct., 1872.

⁸¹ Needon, Wiener med. Presse, 1869, No. 42. In a case of Günsburg's the hole in the diaphragm was as large as the hand, and the left pleural cavity contained the upper half of the stomach and the spleen (Arch. f. phys. Heilk., xi. 3, 1852).

The various fistulæ which have been mentioned may be either direct or through the medium of an abscess. While some of them are only pathological curiosities, others, particularly the communications of the stomach with the pleural cavity and with the lung, are sufficiently frequent to be of practical clinical interest.

As has already been explained, ulcers of the anterior wall are the ones most liable to perforate into the general peritoneal cavity,⁸² but on account of their comparative infrequency perforation occurs oftener in other situations, particularly in the lesser curvature and near the pylorus. Except on the anterior wall the perforation is often brought about by the rupture of adhesions which for a time had prevented this accident. In a considerable number of cases, particularly of ulcers on the anterior wall, the ulcer looks as if recently formed (acute perforating ulcer); in other cases its thickened and indurated margins indicate long duration. Chiari⁸³ describes a case in which rupture into the peritoneal cavity took place through the cicatrix of an old ulcer, probably in consequence of the distension of the stomach with gas. The hole in the peritoneum is usually circular, smaller than the inner surface of the ulcer, and has sharp, well-defined edges. Less frequently the edges are ragged. Post-mortem digestion may, however, so change the borders of the opening as to make it difficult or impossible to tell from their post-mortem appearances alone whether perforation has occurred before or after death. The peritoneal cavity after death from perforation is found to contain gas and substances from the stomach. Usually within a few hours after perforation septic peritonitis is excited, but in exceptional cases no inflammation of the peritoneum has occurred even when life has been prolonged twenty-four hours after perforation.

⁸² According to Brinton, "the proportion of perforations to ulcers is such that of every 100 ulcers in each of the following situations, the numbers which perforate are—on the posterior surface, about 2; the pyloric sac, 10; the middle of the organ, 13; the lesser curvature, 18; the anterior and posterior surface at once, 28; the cardiac extremity, 40; and the anterior surface, 85."

⁸³ Wiener med. Blätter, 1881, No. 3.

Emphysema of the subcutaneous, subperitoneal, and other loose areolar tissue of the body is a rare but remarkable result of the perforation of gastric ulcer. The emphysema is sometimes observed shortly before death, but it attains its maximum development after death, when it may spread rapidly over the greater part of the body. The gas consists in part of hydrogen, as it burns with a blue flame. It is generated, at least in great part, by fermentation of the contents of the stomach. The gas may enter the subserous tissue at the edges of the ulcer and thence spread, or, after perforation of the stomach, it may make its way from the peritoneal cavity into the loose subserous connective tissue through some place in the parietal peritoneum which has been macerated, perhaps by the digestive action of the gastric juice.⁸⁴

⁸⁴ Roger (Arch. gén. de Méd., 1862) and Demarquay (Essai de Pneumatologie médicale, Paris, 1866) deserve the credit of first calling general attention to the occurrence of subcutaneous emphysema after rupture of the digestive tract. The following writers have each reported a case of emphysema following the perforation of gastric ulcers: Cruveilhier, Anat. Path., t. i. livr. xx.; Bell, Edinb. Med. Journ., vol. vi. p. 783; Thierfelder, Deutsches Arch. f. klin. Med., iv., 1868, p. 33; Newman, The Lancet, 1868, vol. ii. p. 728; Poensgen, Das subcutane Emphysem nach continuitätstrennungen des Digestionstractus, etc., Inaug. Diss., Strassburg, 1879, p. 40; Korach, Deutsche med. Wochenschr., 1880 p. 275; Jürgensen, Deutsches Arch. f. klin. Med., Bd. 31, p. 441, 1882. Doubtful cases are reported by Lefèvre, W. Mayer, and Burggraeve. The fullest consideration of the subject is to be found in the dissertation of Poensgen.

In two cases of sudden death from gastric ulcer Jürgensen found gas in the veins and arteries of various parts of the body. He believes that this gas, which certainly was not the result of putrefaction after death, was derived from the stomach, and that it entered during life the circulation through vessels exposed in the borders of the ulcer, thus causing death. In one of the cases a profuse hemorrhage preceded death, and in the other the ulcer had perforated into the peritoneal cavity.⁸⁵

⁸⁵ Jürgensen does not consider whether this gas may not have made its way into the blood-vessels after death in a manner similar to its extension through the cellular tissue of the body in the cases of emphysema just mentioned. In the case which he has reported in full interstitial and subserous emphysema could be traced from the ulcer ("Luft im Blute," Deutsches Arch. f. klin. Med., Bd. 31, p. 441, 1882).

The source of hemorrhage from gastric ulcer is from blood-vessels either in the stomach itself or in the neighborhood of the stomach. Hemorrhages slight or of moderate severity occur from the capillaries and small arteries and veins in the mucous and submucous coats. Sometimes profuse and even fatal hemorrhage comes from arteries or from veins in the submucous coat, especially when these vessels are dilated. Quickly-fatal hemorrhages take place from the large vessels between the muscular and the serous coats, particularly from the main trunks on the curvatures. After the formation of adhesions, followed by the perforation of all of the coats of the stomach, profuse bleeding may proceed from the erosion of large vessels near the stomach, such as the splenic, the hepatic, the pancreatico-duodenal arteries, the portal and the splenic veins, and the mesenteric vessels. Bleeding may also occur from vessels in the parenchyma of organs invaded by the ulcer. The most common source of fatal hemorrhage is from the splenic artery, which from its position is peculiarly exposed to invasion by ulcers of the posterior wall of the stomach. The hemorrhage is usually arterial in origin. It may come from miliary aneurisms of the gastric arteries or from varicose veins in the wall of the stomach. As Cruveilhier has pointed out, an ulcer may cicatrize except over one spot corresponding to an artery from which fatal hemorrhage may occur. Ulcers which give rise to large hemorrhages are usually chronic in their course. Those seated on the middle of the anterior wall, although peculiarly liable to perforate, are comparatively exempt from hemorrhage on account of the small size of the blood-vessels there.

Changes in the blood-vessels of the stomach have been seen in a considerable number of cases of gastric ulcer. Instances have been recorded of the association with gastric ulcer of most of the diseases to which blood-vessels are subject. An example in all respects convincing of embolism of the artery supplying the ulcerated region of the stomach has not been published. Probably the best case belonging here is one of perforating ulcer of the stomach with hemorrhagic infiltration in its walls, presented by Janeway to the New York Pathological Society in 1871.⁸⁶ In this case there was in the gastro-epiploic artery an ante-mortem fibrinous plug which was continued into the nutrient artery of the ulcerated piece of the stomach. No source for an embolus could be found. In one case Merkel found an embolus in a small artery leading to an ulcer of the duodenum.⁸⁷ The arch of the aorta was atheromatous and contained a thrombus. Patches of hemorrhagic infiltration existed in the stomach.

⁸⁶ Trans. of the N.Y. Path. Soc., vol. ii. p. 1.

⁸⁷ Wiener med. Presse, vii. p. 30, 1866.

In many cases thrombosis of the arteries, and especially of the veins involved in the diseased tissue around an ulcer, has been observed, and in some the thrombus was prolonged in the vessels for a considerable distance from the ulcer. It is probable that in most of these cases the thrombus was secondary to the ulcer. Hyaline thrombosis of the capillaries near the ulcer is also to be mentioned.

In a certain, but not large, number of cases atheroma with calcification or with fatty degeneration of the arteries of the stomach has been found associated with gastric ulcer.⁸⁸ Reference has already been made to the occurrence of obliterating endarteritis in the thickened edges and floor of gastric ulcer, where it is doubtless secondary. In one case of gastric ulcer I found a widespread obliterating endarteritis affecting small and medium-sized arteries in many parts of the body, including the stomach.⁸⁹

⁸⁸ For cases in point see Norman Moore, Trans. of the Path. Soc. of London, vol. xxxiv. p. 94.

⁸⁹ On the posterior wall of the stomach, midway between the greater and the lesser curvature and five inches to the right of the cardiac orifice, was a round ulcer half an inch in diameter, with smooth, sharp edges. In the floor of the ulcer, which extended to the muscular coat, was a small perforated aneurism of a branch of the coronary artery. In addition there were small, granular kidneys, hypertrophied heart without valvular lesion, and chronic interstitial splenitis. Small and medium-sized arteries in the kidneys, spleen, heart, lymphatic glands, and stomach were the seat of a typical endarteritis obliterans, resulting in some instances in complete closure of the lumen of the vessel. The patient, who was attended by Sassdorf, was seized during the night with vomiting of blood, which continued at intervals for twenty-four hours until his death. The patient was a man about fifty years of age, without previous history of gastric ulcer or of syphilis.

In one case Powell⁹⁰ found a small aneurism of the coronary artery in an ulcer of the lesser curvature of the stomach. Hauser⁹¹ found an aneurismal dilatation of an atheromatous and thrombosed arterial twig in the floor of a recent ulcer. In my case of obliterating endarteritis just referred to there was a small aneurism in the floor of the ulcer. These miliary aneurisms in the floor of gastric ulcers seem to be analogous to those in the walls of phthisical cavities. Miliary aneurisms occur in the stomach independently of gastric ulcer, and may give rise to fatal hæmatemesis, as in four cases reported by Galliard.⁹²

⁹⁰ Trans. of the Path. Soc. of London, vol. xxix.

⁹¹ Das chronische Magengeschwür, etc., p. 11, Leipzig, 1883.

⁹² L'Union méd., Feb. 26, 1884. Curtis reported a case of fatal hæmatemesis from an aneurism, not larger than a small pea, seated in the cicatrix of an old ulcer (Med. Annals of Albany, Aug., 1880).

Gastric ulcer is occasionally associated with waxy degeneration of the arteries of the stomach.⁹³ In most of these cases there were multiple shallow ulcers. Hæmatemesis is generally absent in gastric ulcer resulting from waxy disease of the gastric blood-vessels. As is well known, the amyloid material itself resists the action of the gastric juice.

⁹³ Hauser (op. cit.) alludes to a case in which, with waxy degeneration of the stomach, over one hundred small ulcers were found in different stages of development, from hemorrhagic infiltrations to complete ulcers. Cases belonging here are reported by Fehr, Ueber die Amyloide Degeneration, Inaug. Diss., Bern, 1866; Merkel, Wiener med. Presse, 1869; Edinger, Deutsches Arch. f. klin. Med., Bd. 29, p. 568; Marchiafava, Atti del Accad. Med. di Roma, iii. p. 114; and Mattei, Deutsche med. Zeitung, July 5, 1883.

Finally, varicosities of the veins of the stomach have been once in a while found with gastric ulcer. In a large number, probably in the majority, of cases of gastric ulcer no changes have been found in the blood-vessels of the stomach except such as were manifestly secondary to the ulcer.

That gastric ulcer is frequently complicated with chronic catarrhal gastritis has been repeatedly mentioned in the course of this article.

PATHOGENESIS.—Without doubt, the most obscure chapter in the history of gastric ulcer is that relating to its origin and to its persistence. Notwithstanding a vast amount of investigation and of discussion, unanimity of opinion upon these subjects has not been reached. In view of this uncertainty it is desirable in this article to do little more than to summarize the leading theories as to the development of gastric ulcer.

Most observers are agreed that the digestive action of the gastric juice has some share in the development and the progress of the ulcer, but as to the first cause of the ulcer there are various hypotheses.

The earliest theory refers the origin of simple ulcer of the stomach to inflammation. Since its advocacy by Abercrombie and by Cruveilhier this theory has always had its adherents, particularly among French writers. It is true that in stomachs which are the seat of simple ulcer evidences of inflammation can often be found both in the neighborhood of the ulcer and elsewhere. In recent times the supporters of the inflammatory origin of gastric ulcer lay especial stress upon the presence of foci of infiltration with small round cells in the mucous and the submucous coats.⁹⁴ But it is difficult to explain by the inflammatory theory the usually solitary occurrence and the funnel-like shape of gastric ulcer.

⁹⁴ Laveran, Arch. de Phys. norm. et path., 1876, p. 443; Galliard, Essai sur la Pathogenie de l'Ulcère simple de l'Estomac, Thèse de Paris, 1882; Colombo, Annali univ. di Med., 1877.

The theory that gastric ulcer is of neurotic origin has also been advocated. Some refer the origin to the secretion of an excessively acid gastric juice under abnormal nervous influence (Günsburg), others to vaso-motor disturbances, and others to trophic disturbances. Wilks and Moxon compare simple gastric ulcer to ulcers of the cornea resulting from paralysis of the trigeminus. The neurotic theory of the origin of gastric ulcer is altogether speculative and has never gained wide acceptance.⁹⁵

⁹⁵ The first to attribute gastric ulcer to nervous influence was Siebert (Casper's Wochenschr. f. d. Heilk., 1842, No. 29, and Deutsche Klinik, 1852). Cf. also Günsburg, Arch. f. phys. Heilk., xi., 1852; Wilks and Moxon, Lect. on Path. Anat., 2d ed., Philada., 1875, p. 386. Osborne in 1845 attributed gastric ulcer to the secretion of an abnormally acid juice by a circular group of the gastric glands (Dublin Journ. of Med. Sci., vol. xxvii. p. 357).