Chapter XXX: Front Matter (30)

In some cases of gastric ulcer pain is felt in regions at a distance from the stomach. The most frequent of these so-called radiation neuralgias are--neuralgia of the lower intercostal spaces, combined sometimes with {491} hyperæsthesia or with analgesia of the affected region, pain in the right shoulder (perhaps due to adhesions between the stomach and the liver or the diaphragm), pain in the left shoulder, and pain in the loins. In a case of ulcer reported by Traube terminating in perforation the sole complaint, besides loss of appetite and retching, had been difficulty in breathing and oppression in the chest. These symptoms, which may be combined with gastralgic paroxysms, are referred by Traube to transference of the irritation from the gastric to the pulmonary filaments of the pneumogastric nerve.[40]

[Footnote 40: _Deutsche Klinik_, 1861, No. 10. These symptoms evidently correspond to the vagus neurosis described by Rosenbach, in which, as the result of reflex irritation of the pneumogastric nerve in the stomach, occur difficulty in breathing, oppression in the chest, palpitation, arhythmical action of the heart, and epigastric pulsation (_Deutsche med. Wochenschr._, 1879, Nos. 42, 43).]

Sometimes the pain of gastric ulcer intermits for days or even weeks. When the intermission is of considerable duration it is probable that cicatrization has been in progress. It should, however, be remembered that gastralgic attacks may continue even after cicatrization of the ulcer is completed, probably in consequence of compression of nerve-filaments by the cicatricial tissue. Once in a while the pain exhibits a marked periodicity in its appearance. Thus in a case of ulcer ending fatally from hemorrhage the pain came on but once a day, and that with considerable regularity at the same hour. In this case the pain was relieved by taking food.[41] The pain of gastric ulcer may be temporarily relieved by hemorrhage from the stomach, and perhaps by division of the irritated nerve by sloughing (Habershon).

[Footnote 41: Case reported by Peacock, _Rep. of Proceedings of London Path. Soc._, vol. i. p. 253, 1847.]

The causes of the pain of gastric ulcer are not far to seek. Foremost is the irritation of nerve-filaments exposed by the ulcerative process. The irritation may be by mechanical, chemical, or thermic agencies. With our present imperfect knowledge it is profitless to discuss whether the pneumogastric or the sympathetic nerves are the chief carriers of the abnormal sensations.[42] In the next place, we may have radiation of the irritation from these nerves to neighboring and even to remote nerves. Furthermore, the extension of the inflammation to the peritoneum and the surrounding parts, and the formation of adhesions, are additional factors in some cases in causing pain. Finally, the great differences in susceptibility to pain manifested by different individuals is to be borne in mind.

[Footnote 42: Leven, without sufficient reason, distinguishes two kinds of gastralgic attacks--the one having its point of departure in the pneumogastric, the other in the sympathetic nerve; in the former the pain is associated with dyspnoea and palpitation of the heart; in the latter the pain is deeper, and is accompanied by vaso-motor (?) troubles on one side of the body.]

Next to pain, vomiting is the most frequent symptom of gastric ulcer. There is, however, little which is characteristic of ulcer in this symptom, unless the vomited material contains blood. In some cases of gastric ulcer vomiting is the most marked and most distressing symptom of the disease. It may, however, be absent during the whole course of gastric ulcer.

Vomiting occurs most frequently after taking food, and is greatly aggravated by an unregulated diet. Sometimes nearly everything which is taken into the stomach is vomited. The vomiting of mucus or of a {492} thin fluid unmixed with food is indicative only of chronic catarrhal gastritis. Alimentary vomiting, which is more indicative of gastric ulcer, usually occurs not immediately after taking food, but at the acme of a gastralgic attack caused by the food. Soon after the stomach is emptied by one or more acts of vomiting the pain is relieved. The act of vomiting is usually easy, and at times is hardly more than regurgitation of the food. Sometimes the patient experiences an excessively sour taste from the vomit.

Vomiting exhausts the patient by withdrawing nutriment, and when persistent may even cause death from inanition. But in some cases of gastric ulcer, especially in women, the vomiting seems to be mainly a nervous symptom, and even when long continued may be attended by little or no loss of flesh. Evidently, more food is retained in these cases than might be supposed.

There are two evident causes of vomiting in gastric ulcer--namely, chronic catarrhal gastritis, which is a frequent complication, and direct irritation of the nerves in the ulcer. Vomiting due to dilatation of the stomach is oftener a sequel than an immediate symptom of gastric ulcer.

For the diagnosis of gastric ulcer hemorrhage from the stomach is the most important symptom.

The frequency of only the larger hemorrhages can be determined with any degree of exactness. If the blood be effused in small quantity or slowly, it may be discharged solely with the stools and escape detection. Such slight hemorrhages doubtless occur in most cases of gastric ulcer. It is probable that easily-recognized hemorrhages from the stomach occur in about one-third of the cases of gastric ulcer.[43] Hemorrhage is absent as a rule in the acute perforating ulcer of the stomach.

[Footnote 43: In consequence of the uncertainty of the diagnosis in cases of gastric ulcer which recover without hemorrhage, the estimates of the frequency of this symptom have a very limited value, and will vary with different observers according to their standard of diagnosis of this disease. Lebert observed gastric hemorrhage in four-fifths of his carefully-studied cases, and in three-fifths of his cases there was profuse hæmatemesis. Brinton estimates that the larger hemorrhages occur in about one-third of the cases. Müller found them in one-fourth of the cases which he analyzed.]

In most cases hemorrhage from gastric ulcer is preceded by pain, vomiting, and disturbances of digestion. Antecedent symptoms may, however, be absent, or may be so obscure that no suspicion of ulcer exists until the hemorrhage occurs.

The hemorrhage may be slight, moderate, or excessive in amount (Cruveilhier). The larger hemorrhages are those which are most distinctive of gastric ulcer.

The blood may be vomited, or voided with the stools, or retained in the stomach and the intestines.

As has been remarked, when the hemorrhage is scanty all the blood may escape by the bowel. Sometimes, although much less frequently, blood effused in large quantity is entirely evacuated with the stools. After hæmatemesis more or less blood is discharged by the bowel, sometimes for several days after the vomiting of blood has ceased. Blood which has traversed the whole length of the intestinal canal acquires a tarry consistence and a black or brownish color in consequence of the production of dark-brown hæmatin by the action of the digestive juices {493} upon the hæmoglobin, and in consequence of the formation of black sulphide of iron by the union of hydrogen sulphide in the lower part of the intestine with the iron of the hæmatin. The passage of these black viscid stools is called melæna. Inasmuch as we cannot presume gastric hemorrhage to be absent simply because no blood has been vomited, it is evidently important to examine the stools for blood when the diagnosis of gastric ulcer is obscure, and also in cases of gastric ulcer where there are symptoms of internal hemorrhage not accounted for by blood vomited. It should be remembered that certain drugs, particularly iron and bismuth, may blacken the feces.

In very exceptional cases of gastric ulcer the effusion of a large volume of blood causes sudden death before any of the blood has been vomited. The autopsy shows the stomach and more or less of the small intestine distended with coagulated blood.

Hemorrhage from gastric ulcer is usually made manifest by the vomiting of blood. The quantity of the vomited blood varies from mere traces to several pounds. The color and the consistence of the blood depend upon the quantity effused and the length of time that the blood has remained in the stomach. Blood which has been acted upon by the gastric juice is coagulated, has a grumous consistence, and acquires by the formation of hæmatin out of hæmoglobin a dark-brown color, often compared to that of coffee-grounds. Blood effused in small quantity is usually vomited only with the food, and has usually the coffee-grounds appearance. The patient's condition is not appreciably influenced by this slight loss of blood. A little blood expelled after repeated acts of vomiting has no diagnostic importance. Vomiting usually occurs soon after a large gastric hemorrhage. It is the mechanical distension of the stomach rather than any irritating quality of the blood which causes the vomiting. Blood which is rejected immediately after a large gastric hemorrhage is alkaline, fluid, and of an arterial (rarely of a venous) hue. Often, however, even with large hemorrhages, the blood remains sufficiently long in the stomach to be partly coagulated and to be darkened in color. Ulcer more frequently than any other disease of the stomach causes the vomiting of unaltered blood in large quantity. But this kind of hæmatemesis is not peculiar to simple ulcer. It may occur in other diseases, such as gastric cancer, and coffee-ground vomiting may be associated with ulcer.

Copious hæmatemesis in cases of gastric ulcer appears usually without premonition, or it may be preceded for a day or two by increased pain. Its occurrence is somewhat more common during the digestion of food than in the intervals, but there have been cases of ulcer where the bleeding was favored by an empty stomach and was checked by the distension of the organ with food. The free use of stimulants and violent physical or mental exertion may excite hemorrhage. With the onset of the hemorrhage the patient experiences a sense of warmth and of oppression at the epigastrium, followed by faintness, nausea, and the vomiting of a large quantity of blood. An attack of syncope often causes, at least temporarily, cessation of the hemorrhage. But the thrombus which closes the eroded vessel may easily be washed away, so that the hemorrhage often recurs and continues at intervals for several days, thereby greatly increasing the danger to the patient. Thus, the tendency is for {494} the hemorrhage from gastric ulcer to appear in phases or periods occupying several days.

A single hemorrhage is rarely so profuse as to cause immediate death. More frequently the patient dies after successive hemorrhages. In the majority of cases the hemorrhage is not immediately dangerous to life, but is followed by symptoms of anæmia, more or less profound according to the strength of the patient and the amount of blood lost. Prostration and pallor follow the larger hemorrhages. Dizziness, ringing in the ears, and dimness of vision appear when the patient attempts to leave the recumbent posture. Thirst is often a marked symptom. The pulse is feeble and more frequent than normal. There is often a moderate elevation of temperature (anæmic fever) after profuse hemorrhage. The urine is pale, abundant, and sometimes contains albumen (Quincke). After a few days anæmic cardiac murmurs can often be heard. Under favorable circumstances these symptoms of anæmia disappear in the course of a few weeks.

The other symptoms of ulcer, particularly the pain, are sometimes notably relieved, and may even disappear, after an abundant hemorrhage. They usually, however, return sooner or later. After a variable interval one attack of hæmatemesis is likely to be followed by others. There is much diversity in different cases as regards the frequency of these attacks and the character of the symptoms in the intervals. In a few cases recovery follows a single attack of gastric hemorrhage; in other cases the hemorrhage recurs frequently after intervals of only a few days, weeks, or months; in still other cases hemorrhage recurs only after long intervals, perhaps of years, although other symptoms of ulcer continue. Sometimes the disappearance of symptoms indicates only an apparent cure, and later the patient dies suddenly while in apparent health by a profuse gastric hemorrhage. In the rare cases of this last variety Cruveilhier has found sometimes that the ulcer has cicatrized except just over the eroded blood-vessel.

The sources of the hemorrhage in gastric ulcer will be described in connection with the morbid anatomy.

The symptoms of gastric indigestion are commonly, although not constantly, present in gastric ulcer. They may constitute the sole symptoms, in which case the diagnosis of the lesion is impossible. The most important local symptoms of gastric dyspepsia are diminution, less frequently perversion or increase, of the appetite; increased thirst; during digestion, and sometimes independent of digestion, a feeling of discomfort merely or of painful oppression, or even of sharp pain, in the epigastrium; nausea; vomiting of undigested food, of mucus, and of bile; regurgitation of thin fluids; often acid, sometimes neutral or alkaline, flatulence, with belching of gas, and constipation. In many cases of gastric ulcer the appetite is not disturbed, but the patient refrains from eating on account of the pain caused by taking food. Among the so-called sympathetic symptoms of dyspepsia are headache, dizziness, depression of spirits, oppression in the chest, and irregularity of the heart's action. Dyspepsia contributes its share to the production of the anæmia and of the loss of flesh and strength which are present in some degree in most cases of chronic gastric ulcer.

{495} In many cases of acute perforating ulcer, as well as in some cases of chronic ulcer, the symptoms are either absent or they are but slightly marked. It has been demonstrated that in many cases of gastric ulcer the resorptive power of the mucous membrane of the stomach is unimpaired.[44]

[Footnote 44: This is shown by the experiments of Pentzoldt and Faber, who determined the length of time which elapsed between swallowing gelatin capsules containing iodide of potassium and the appearance of the iodide in the saliva (_Berl. klin. Wochenschr._, No. 21, 1882). Quetsch observed rapid absorption from the stomach in two cases of gastric ulcer (_ibid._, 1884, No. 23). It is believed that also the duration of the digestive process in the stomach is often within normal limits in cases of gastric ulcer, although exact experiments upon this point, as they require the use of the stomach-pump, have not been made in this disease (Leube).]

The most common cause of dyspepsia in gastric ulcer is the chronic catarrhal gastritis which usually accompanies this disease. It is probable that the movements of the stomach may be seriously interfered with by destruction of the muscular coat of the stomach when the ulcer is of considerable size and is seated in the pyloric region. Adhesions of the stomach to surrounding parts may likewise impair the normal movements of the stomach. It is possible that ulcers, especially those which are very painful, may cause reflex disturbance of the peristaltic movements of the stomach and alterations in the quality or the quantity of the gastric juice. The serious digestive disturbances which are caused by distortions and dilatation of the stomach resulting from cicatricial contraction of gastric ulcer are not considered in this article.

Although Niemeyer emphasized the frequency in gastric ulcer of a strikingly red tongue with smooth or furrowed surface, it does not appear that any especial importance is to be attached to this or to any other condition of the tongue as a symptom of the disease.

Increased flow of saliva is a rare symptom, which, when it occurs, is usually associated with dyspepsia.

Constipation is the rule in gastric ulcer. The most important of the various circumstances which combine to produce this condition is the small amount of solid food taken and retained by the patient. The restraint caused by gastric ulcer and gastric catarrh in the normal movements of the stomach may diminish by reflex action the peristalsis of the intestines (Traube and Radziejewski). The passage of large quantities of blood along the intestinal canal is often associated with colicky pains and diarrhoea.

Amenorrhoea is a symptom which was formerly thought to be characteristic of gastric ulcer, although there was much discussion as to whether it was the cause or the result of the ulcer. Amenorrhoea is indeed common in the gastric ulcer of young women, but there is nothing strange in this when one considers the frequency of amenorrhoea in general, and its causation by various debilitating and depressing influences such as are to be found in gastric ulcer. Notwithstanding a few striking cases which have been recorded, it has not been demonstrated that hemorrhages vicarious of menstruation take place from gastric ulcer.

Gastric ulcer is not a febrile disease. Temporary elevation of temperature may follow profuse gastrorrhagia and may attend various complications, of which the most important are gastritis and peritonitis. It has been recently claimed by Peter that the surface-temperature of the {496} epigastrium is elevated in gastric ulcer, but the observations upon this point are as yet too few for any positive conclusions.[45]

[Footnote 45: According to Peter, the normal surface-temperature of the epigastrium is from 95½° to 96° F. (35.3° to 35.5° C.), while in gastric ulcer the temperature may equal or even exceed by one or two degrees the axillary temperature. It is said to register the highest during attacks of pain and of vomiting and after hemorrhages (_Gaz. des Hôpitaux_, June 23 and 30, 1883). See also Beaurieux (_Essai sur la Pseudo-gastralgie, etc._, Thèse, Paris, 1879).]

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. Litten[46] 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.

[Footnote 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] Rosenbach[48] 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.

[Footnote 47: A. Beer, _Wiener med. Wochenschrift_, No. 26, 1857.]

[Footnote 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.

{497} 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]

[Footnote 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]

[Footnote 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]

[Footnote 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.

{498} 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.

[Footnote 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).]

[Footnote 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).]

[Footnote 54: Other symptoms which have been thought to be diagnostic of pneumo-peritoneum in {499} 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.

[Footnote 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 {500} 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]

[Footnote 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.]

[Footnote 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]

[Footnote 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.

{501} 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 Lebert[59] 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.

[Footnote 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, {502} 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.

[Footnote 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 3-1/3.]

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 {503} associated with ulcer in a case under my observation. In a case of ulcer under the care of Owen Rees[61] 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.

[Footnote 61: _Med. Times and Gaz._, April 24, 1869.]

[Footnote 62: _Berlin. klin. Wochenschrift_, 1883, No. 51.]

[Footnote 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]

[Footnote 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).]

[Footnote 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] {504}

Lesser curvature 288 (36.3 per cent.)
Posterior wall 235 (29.6 " )
Pylorus 95 (12 " )
Anterior wall 69 ( 8.7 " )
Cardia 50 ( 6.3 " )
Fundus 29 ( 3.7 " )
Greater curvature 27 ( 3.4 " )

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.

[Footnote 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]

[Footnote 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]

[Footnote 68: Murchison, _Trans. of the Path. Soc._, vol. xxi. p. 162, London, 1870.]

[Footnote 69: In one of Cruveilhier's cases the ulcer was 6½ inches long and 3-1/3 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 {505} 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.

[Footnote 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 {506} 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]

[Footnote 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.]