Chapter XXXI: Front Matter (31)

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. Hauser[72] 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.

[Footnote 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 {507} 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, {508} as into the general peritoneal cavity, into the pleural cavity, into the retro-peritoneal tissue, through the abdominal or thoracic walls, etc.

[Footnote 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]

[Footnote 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).]

[Footnote 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).]

[Footnote 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).]

[Footnote 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 {509} passed through a hole in the transverse meso-colon which had been caused by a gastric ulcer.

[Footnote 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).]

[Footnote 79: Oser, _Wiener med. Blätter_, 1880, No. 52; Brenner, _Wiener med. Wochenschr._, 1881, No. 47.]

[Footnote 80: Müller, _Memorabilien_, xvii., Oct., 1872.]

[Footnote 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. Chiari[83] 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.

[Footnote 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."]

[Footnote 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]

[Footnote 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; {510} 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]

[Footnote 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 {511} of the duodenum.[87] The arch of the aorta was atheromatous and contained a thrombus. Patches of hemorrhagic infiltration existed in the stomach.

[Footnote 86: _Trans. of the N.Y. Path. Soc._, vol. ii. p. 1.]

[Footnote 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]

[Footnote 88: For cases in point see Norman Moore, _Trans. of the Path. Soc. of London_, vol. xxxiv. p. 94.]

[Footnote 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 Powell[90] found a small aneurism of the coronary artery in an ulcer of the lesser curvature of the stomach. Hauser[91] 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]

[Footnote 90: _Trans. of the Path. Soc. of London_, vol. xxix.]

[Footnote 91: _Das chronische Magengeschwür, etc._, p. 11, Leipzig, 1883.]

[Footnote 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.

[Footnote 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 {512} 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.

[Footnote 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]

[Footnote 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).]

The view which has met with the greatest favor is that which attributes the origin of gastric ulcer to impairment or arrest of the circulation in a circumscribed part of the wall of the stomach, and to a subsequent solution by the gastric juice of the part thus affected. Rokitansky first suggested this view by assigning hemorrhagic necrosis of the mucous membrane as the first step in the formation of the ulcer; but it is Virchow who has most fully developed this view and has given it its main support. The first cause of gastric ulcer, according to Virchow, is a hemorrhagic infiltration of the coats of the stomach induced by local disturbances in the circulation. The part the nutrition of which is thus impaired or destroyed is dissolved by the gastric juice.

{513} The affections of the gastric blood-vessels to which importance has been attached are (_a_) embolism and thrombosis; (_b_) diseases of the coats of the vessels, as atheroma, obliterating endarteritis, fatty degeneration, amyloid degeneration, and aneurismal and varicose dilatations; (_c_) compression of the veins by spasm of the muscular coats of the stomach in vomiting and in gastralgia; (_d_) passive congestion of the stomach by obstruction in the portal circulation.

In support of this view are urged the following facts: First, it has been proven by the experiments of Pavy that parts of the gastric wall from which the circulation has been shut off undergo digestion; second, hemorrhagic infarctions have been observed in the stomach, both alone (Von Recklinghausen, Hedenius) and associated with gastric ulcer (Key, Rindfleisch); third, the hemorrhagic infiltration in the walls of recently-formed ulcers indicates a hemorrhagic origin; fourth, the funnel-like shape of the ulcer resembles the funnel-shaped area of distribution of an artery; fifth, gastric ulcers have been experimentally produced by injecting emboli into the gastric arteries (Panum, Cohnheim).[96]

[Footnote 96: Pavy, _Philosoph. Trans._, 1763, p. 161; V. Recklinghausen, _Virchow's Archiv_, Bd. 30, p. 368; Axel Key, _Virchow und Hirsch's Jahresb._, 1870, Bd. ii. p. 155; Rindfleisch, _Lehrb. d. path. Gewebelehre_, 5te Aufl., Leipzig, 1878; Panum, _Virchow's Archiv_, Bd. 25, p. 491; Cohnheim, _Vorles. über allgem. Path._, Bd. ii. p. 53, Berlin, 1880.]

The main objections to this view are the infrequency with which the assumed changes in the blood-vessels have been demonstrated, the common occurrence of gastric ulcer at an age earlier than that at which diseases of the blood-vessels are usually present, and the absence of gastric ulcer in the vast majority of cases of heart disease, with widespread embolism of different organs of the body. To meet some of these objections, Klebs[97] presupposes in many cases a local spasmodic contraction of the gastric arteries, causing temporary interruption of the circulation; Rindfleisch and Axel Key, compression of the gastric veins, with resulting hemorrhagic infiltration by spasm of the muscular coat of the stomach in vomiting and in gastralgic attacks. But these are pure hypotheses.

[Footnote 97: _Handb. d. path. Anat._, Bd. i. p. 185, Berlin, 1869.]

What is actually known concerning diseases of the gastric blood-vessels in ulcer of the stomach has already been stated under the morbid anatomy. From this it may be inferred that the origin of gastric ulcer in diseased conditions of the blood-vessels has been established only for a comparatively small group of cases.

Böttcher's[98] view that gastric ulcer is of mycotic origin, being produced by micrococci, has thus far met with no confirmation.

[Footnote 98: _Dorpater med. Zeitschr._, Bd. v. p. 148, 1874.]

There are those who hold an eclectic view concerning the origin of gastric ulcer. They believe that ulcer of the stomach may be produced by a variety of causes, such as inflammation, circulatory disturbances, irritating substances introduced into the stomach, traumatism, etc. The peculiarities of the ulcer are due not to any specific cause, but to the solvent action of the gastric juice, which keeps clean the floor and the sides of the ulcer. These clean edges and floor, which are incident to all ulcers of the stomach, justify no conclusion as to the cause of the ulcer. Engel[99] over thirty years ago held that gastric ulcer might {514} originate in various ways--that there was nothing specific about it. Brinton was also of similar opinion.

[Footnote 99: _Prager Vierteljahrschr._, 1853, ii.]

Gastric ulcers have been produced experimentally in animals in a variety of ways, but these experiments have not materially elucidated the pathenogenesis of ulcer in man. Schiff by lesions of various parts of the brain, and later Ebstein by lesions of many parts of the central and peripheral nervous system by injections of strychnine--in fact, apparently by any means which greatly increased the blood-pressure--produced in the stomachs of animals ecchymoses and ulcers. Müller by ligation of the portal vein, Pavy by ligation of arteries supplying the stomach, likewise produced hemorrhages and ulcers. The results of Pavy could not be confirmed by Roth and others. Panum, and afterward Cohnheim, produced gastric ulcers by introducing multiple emboli into the gastric arteries. Daettwyler under Quincke's direction caused, in dogs with gastric fistulæ, ulcers of the stomach by various mechanical, chemical, and thermic irritants applied to the inner surface of the stomach. Aufrecht observed hemorrhages and ulcers in the stomachs of rabbits after subcutaneous injections of cantharidin.[100]

[Footnote 100: Schiff, _De vi motorea baseos encephali_, 1845, p. 41; Ebstein, _Arch f. exp. Path. u. Pharm._, 1874, p. 183; Müller, _Das corrosive Geschwür im Magen, etc._, p. 273, Erlangen, 1860; Pavy, _Guy's Hosp. Rep._, vol. xiii., 1867; Roth, _Virchow's Archiv_, Bd. 45, p. 300, 1869; Panum, _loc. cit._; Cohnheim, _op. cit._; Daettwyler, Quincke, _Deutsche med. Wochenschr._, 1882, p. 79; Aufrecht, _Centralbl. f. d. med. Wiss._, 1882, No. 31.]

The most interesting of these experiments are those of Cohnheim and of Daettwyler, who demonstrated that in one essential point all of these experimental ulcers differ from simple gastric ulcer in man--namely, in the readiness with which they heal. To this ready healing the gastric juice, much as it has been accused of causing the spread of gastric ulcers in man, seems to have offered no obstacle. We know that similar losses of substance in the human stomach heal equally well.[101] Hence it has been maintained throughout this article that it is unjustifiable to regard all of the scars found in the human stomach as the result of simple ulcer.

[Footnote 101: Portions of the mucous membrane of the stomach, sometimes with some of the submucous coat, have been in several instances removed with the stomach-pump, but thus far no bad effects have followed.]

It appears from these experiments, as well as from observations on man, that it is more difficult to explain why ulcers in the stomach do not heal than it is to understand how they may be produced. From this point of view the observation of Daettwyler is of interest, that in dogs which had been rendered anæmic by repeated abstraction of blood not only did slighter irritants suffice to produce ulcers of the stomach, but the ulcers healed much more slowly. Practically, it is important to learn what are the obstacles to the repair of gastric ulcers, but our positive knowledge of these is slight. It is probable that such obstacles are to be found in constitutional causes, such as anæmia and chlorosis, in abnormal states of the blood-vessels around the ulcer, in catarrhal affections of the stomach, in irritating articles of food, in improper modes of living, and in increased acidity of the gastric juice.

DIAGNOSIS.--In many cases the diagnosis of gastric ulcer can be made with reasonable certainty; in other cases the diagnosis amounts only to a suspicion more or less strong, and in still other cases the diagnosis is impossible.

{515} The diagnostic symptoms are epigastric pain, vomiting, and gastric hemorrhage. The characteristics of the pain which aid in the diagnosis are its fixation in one spot in the epigastric region, its onset soon after eating, its dependence upon the quantity and the quality of the food, its relief upon the complete expulsion of the contents of the stomach, its alleviation by changes in posture, and its increase by pressure. That the pain of gastric ulcer has not always these characteristics has been mentioned under the Symptomatology. Vomiting without hæmatemesis is the least characteristic of these symptoms. It aids in the diagnosis when it occurs after eating at the acme of a gastralgic attack and is followed by the relief of pain. Hæmatemesis is the most valuable symptom in diagnosis. The more profuse the hemorrhage and the younger the individual in whom it occurs, the greater is the probability of gastric ulcer. It should not be forgotten that the blood is sometimes discharged solely by the stools.

The simultaneous occurrence of all these symptoms renders the diagnosis of gastric ulcer easy.[102] In all cases in which gastrorrhagia is absent the diagnosis is uncertain; but gastric ulcer should be suspected whenever the ingestion of food is followed persistently by severe epigastric pain and other causes of the pain have not been positively determined. When the course of the ulcer is latent and when the symptoms are only those of dyspepsia, the diagnosis is of course impossible. In cases previously obscure a diagnosis in extremis is sometimes made possible by the occurrence of perforation of the stomach.

[Footnote 102: That even under the most favorable circumstances absolute certainty in the diagnosis of gastric ulcer is not reached is illustrated by a case reported with great precision and fulness by Banti: A female servant, twenty-one years old, had every symptom of gastric ulcer, including repeated hæmatemesis and the characteristic epigastric pain. She was nourished by enemata. She died from an ulcerative proctitis four days after the last hemorrhage from the stomach. Only a slight catarrhal inflammation of the stomach was found at the autopsy, without trace of ulcer, cicatrix, or ecchymosis ("Di un Caso d'Ematemesi," _La Sperimentale_, Feb., 1880, p. 168). It would seem as if there must have been an ulcer which had healed so completely as to leave no recognizable scar.]

In making a differential diagnosis of gastric ulcer, as well as of any disease, reliance should be placed more upon the whole complexion of the case than upon any fancied pathognomonic symptoms.

The diseases which are most difficult to distinguish from gastric ulcer are nervous affections of the stomach. Like gastric ulcer, most of these are more common in women than in men, and especially in chlorotic women with disordered menstruation and with hysterical manifestations. These nervous affections are manifold and their leading characteristics are not yet well defined. The most important of these affections are nervous dyspepsia, nervous vomiting, nervous gastralgia, and gastric crises.

The leading symptoms of nervous dyspepsia, as described by Leube,[103] are the ordinary symptoms of dyspepsia without evidence of anatomical alteration of the stomach, and with the proof by washing out the stomach that the process of digestion is not delayed. Nervous dyspepsia is often associated with other nervous affections, and is caused especially by influences which depress the nervous system. Epigastric pain, and especially tenderness on pressure over the stomach, are not common symptoms in nervous dyspepsia. Only those rare cases of gastric ulcer in which hemorrhage from the stomach is absent and epigastric pain is not prominent {516} are likely to be confounded with nervous dyspepsia. In such cases, although the diagnosis of nervous dyspepsia is by far the most probable, the patient may be confined to bed and put upon the strict regimen for gastric ulcer. If in the course of ten days or two weeks essential relief is not obtained, ulcer may be excluded, and the proper treatment for nervous dyspepsia with tonics and electricity may be adopted (Leube).

[Footnote 103: _Deutches Arch. f. klin. Med._, Dec. 18, 1878.]

In nervous vomiting, which occurs most frequently in hysterical women, other nervous manifestations are present; there are usually less epigastric pain and tenderness than in ulcer; the nutrition is better preserved; the vomiting is less dependent upon the ingestion of food and more dependent on mental states; and there are longer intervals of relief than in ulcer. Still, it may be necessary to resort to the therapeutical diagnosis as in the preceding instance.

In this connection attention may be called to the importance of searching for reflex causes of vomiting, such as beginning phthisis, ovarian or uterine disease, cerebral disease, and pregnancy; also to certain cases of chronic Bright's disease in which gastric disturbances are the main symptoms.

Of all the nervous affections of the stomach, nervous gastralgia is the one which presents the greatest similarity to gastric ulcer. Its diagnosis from gastric ulcer is often extremely difficult, and may be impossible. The points of difference given in the following table may aid in the diagnosis:

NERVOUS GASTRALGIA. | ULCER OF THE STOMACH.
|
1. Pain is often independent of | 1. Pain is mostly dependent upon
the ingestion of food, and may | taking food, and its intensity
even be relieved by taking food.| varies with the quality and the
| quantity of the food.
|
2. Pain is often relieved by | 2. Pain is increased by pressure.
firm pressure. |
|
3. Pain is rarely relieved by | 3. Pain after a meal is usually
vomiting. | relieved by vomiting.
|
4. Fixed point of tenderness and| 4. These are often present.
of subjective pain not generally|
present. |
|
5. Relief is usually complete | 5. Some pain often continues
between the paroxysms. | between the paroxysms.
|
6. Nutrition frequently well | 6. Nutrition usually affected.
preserved. |
|
7. Usually associated with other| 7. Neuropathic states less
nervous affections, such as | constantly present.
hysteria, neuralgia in other |
places, ovarian tenderness, etc.|
|
8. Benefited less by regulation | 8. Benefited not by electricity,
of diet than by electricity and | but by regulation of diet.
tonic treatment. |
|
9. Not followed by dilatation of| 9. Dilatation of stomach may
stomach. | supervene.

According to Peter,[104] the surface temperature of the epigastrium is elevated in gastric ulcer, but not in nervous gastralgia.

[Footnote 104: _Gaz. des Hôp._, June, 1883.]

Probably not a single one of the points mentioned in the table is without exception. Nervous gastralgia may be associated with gastric ulcer, and if the ulcer is otherwise latent the diagnosis is manifestly impossible. A diagnosis of purely functional gastralgia has been repeatedly overthrown by the occurrence of profuse hæmatemesis. There is no symptom {517} upon which it is more unsatisfactory to base a diagnosis than upon pain. There is much difference among physicians as regards the frequency with which they diagnose gastric ulcer in the class of cases here described. It is probable that the error is oftenest a too frequent diagnosis of gastric ulcer than the reverse. Nevertheless, when there is doubt it is well to submit the patient for a time to the proper treatment for gastric ulcer.

In several instances gastric crises have been mistaken for gastric ulcer. These gastric or gastralgic crises, as they are called by Charcot, by whom they have been best described,[105] are most frequently associated with locomotor ataxia, but they may occur in connection with other diseases of the spinal cord (subacute myelitis, general spinal paralysis, and disseminated sclerosis), and an analogous affection has been described by Leyden[106] as an independent disease under the name of periodical vomiting with severe gastralgic attacks. Gastric crises have been most carefully studied as a symptom in the prodromic stage of locomotor ataxia. The distinguishing features of these crises are the sudden onset and the atrocious severity of the gastric pain; the simultaneous occurrence of almost incessant vomiting; the habitual continuance of the paroxysms, almost without remission, for two or three days; the normal performance of the gastric functions in the intervals between the paroxysms, which may be months apart; the frequent association with other prodromic symptoms of locomotor ataxia, such as ocular disorders and fulgurating pains in the extremities; and the development after a time of ataxia. Leyden has observed during the attacks retraction of the abdomen without tension of the abdominal walls, obstinate constipation, scanty, dark-colored urine, even anuria for twenty-four hours, and increased frequency of the pulse (also noted by Charcot). Vulpian[107] mentions a case in which there was vomiting of dark-colored blood, and in which naturally the diagnosis of gastric ulcer had been made. In the autopsies of Leyden and of Charcot no lesions of the stomach have been found.

[Footnote 105: _Leç. sur les Maladies du Syst. nerveux_, t. ii. p. 32, Paris, 1877.]

[Footnote 106: _Zeitschr. f. klin. Med._, iv. p. 605, 1882.]

[Footnote 107: _Maladies du Syst. nerveux_, p. 273, Paris, 1879.]

The differential diagnosis of gastric ulcer from gastric cancer will be considered in the article on GASTRIC CANCER.

It has already been said that a part of the symptoms of gastric ulcer are due to an associated chronic catarrhal gastritis. Usually other symptoms are present which render possible the diagnosis of the ulcer. There is usually some apparent external or internal cause of chronic catarrhal gastritis, whereas the etiology of ulcer is obscure; in chronic gastritis gastralgic paroxysms and the peculiar fixed epigastric pain of gastric ulcer are usually absent; in chronic gastritis profuse hæmatemesis is a rare occurrence; and in gastritis the relief obtained by rest and proper regulation of the diet, although manifest, is usually less immediate and striking than in most cases of gastric ulcer.

The passage of gall-stones is usually sufficiently distinguished from gastric ulcer by the sudden onset and the sudden termination of the pain, by the situation of the pain to the right of the median line, by the complete relief in the intervals between the attacks, by the occurrence of jaundice, by the recognition sometimes of enlargement of the liver and of the gall-bladder, and by the detection of gall-stones in the feces.

{518} There is not much danger of confounding abdominal aneurism and lead colic with gastric ulcer, and the points in their differential diagnosis are sufficiently apparent to require no description here. The diagnosis of duodenal ulcer from gastric ulcer will be discussed elsewhere. The different causes of gastric hemorrhage, a knowledge of which is essential to the diagnosis of gastric ulcer, will be considered in the article on HEMORRHAGE FROM THE STOMACH.

PROGNOSIS.--Although a decided majority of simple ulcers of the stomach cicatrize, nevertheless, in view of the frequently insidious course of the disease, the sudden perforations, the grave hemorrhages, the relapses, and the sequels of the disease, the prognosis must be pronounced serious.

The earlier the ulcer comes under treatment the better the prognosis. Old ulcers with thickened indurated margins containing altered blood-vessels naturally heal with greater difficulty than recently-formed ulcers.

Profuse hemorrhage adds to the gravity of the diagnosis. It usually indicates that the ulcer has penetrated to the serous coat of the stomach. A hemorrhage may exert a favorable influence, in so far as to convince the patient of the necessity of submitting to the repose and the strict dietetic regimen which the physician prescribes.

The severity of the pain is of little value as a prognostic sign. Vomiting and dyspepsia, if uncontrolled by regulation of the diet, lead to a cachectic state which often ends in death.

Little basis as there is to hope for recovery after perforation into the general peritoneal cavity, there nevertheless have been a very few cases in which there is reason to believe that recovery has actually taken place after this occurrence.[108]

[Footnote 108: The most convincing case of recovery after perforation of gastric ulcer is one reported by Hughes, Ray, and Hilton in _Guy's Hosp. Rep._, 1846, p. 332. A servant-girl was suddenly seized with all of the symptoms of perforation. Fortunately, she had eaten nothing for four hours before the attack, and then only gruel. She was placed at once under the influence of opium, was kept in the recumbent posture, and was fed by the rectum. She was discharged apparently cured after fifty-two days. Two months afterward she was again suddenly seized with the same symptoms, and she died in fourteen hours. Shortly before the second perforation she had eaten cherries, strawberries, and gooseberries, which were found in the peritoneal cavity. The autopsy showed, in addition to a recent peritonitis, evidences of an old peritonitis. There were adhesions of the coils of the intestines with each other and between the stomach and adjacent viscera. In the stomach were found a cicatrix and two open ulcers, one of which had perforated.

Other cases in which recovery followed after all of the symptoms of perforation of gastric ulcer were present, but in which no subsequent autopsy proved the correctness of the diagnosis, have been reported by Redwood (_Lancet_, May 7, 1870); Ross (_ibid._, Jan. 21, 1871); Tinley (_ibid._, April 15, 1871); Mancini (_La Sperimentale_, 1876, pp. 551, 665); and G. Johnson (_Brit. Med. Journ._, March 26, 1870).

Frazer's two cases, reported in the _Dublin Hosp. Gaz._, April 15, 1861, are not convincing. The case reported by Aufrecht (_Berl. kl. Wochenschr._, 1870, No. 21) and the one by Starcke (_Deutsche Klinik_, 1870, No. 39), which are sometimes quoted as examples of recovery, were cases of circumscribed peritonitis following perforation.

In an interesting case from Nothnägel's clinic reported by Lüderitz, the patient lived sixteen days after perforation into the peritoneal cavity, followed by all of the symptoms of diffuse perforative peritonitis. Death resulted from pneumonia secondary to the peritonitis. At the autopsy were found adhesions over the whole peritoneal surface and streaks of thickened pus between the coils of intestine. The perforation in the stomach was closed by the left lobe of the liver (_Berl. kl. Wochenschr._, 1879, No. 33).]

In estimating the prognosis one should bear in mind the possibility of relapses; of a continuance of gastric disorders, particularly of gastralgia, after cicatrization; of the formation of cicatricial stenosis of {519} the orifices of the stomach; and of the development of dilatation of the stomach.

After the worst has been said concerning the unfavorable issues of gastric ulcer, it yet remains true that the essential tendency of the ulcer when placed under favorable conditions is toward recovery, and that in many cases the treatment of the disease affords most excellent results, and is therefore a thankful undertaking for the physician.

TREATMENT.--In the absence of any agent which exerts a direct curative influence upon gastric ulcer the main indication for treatment is the removal of all sources of irritation from the ulcer, so that the process of repair may be impeded as little as possible.

Theoretically, this is best accomplished by giving to the stomach complete rest and by nourishing the patient by rectal alimentation. Practically, this method of administering food is attended with many difficulties, and, moreover, the nutrition of the patient eventually suffers by persistence in its employment. In most cases the patient can be more satisfactorily nourished by the stomach, and by proper selection of the diet, without causing injurious irritation of the ulcer.

At the beginning of the course of treatment it is often well to withhold for two or three days all food from the stomach and to resort to exclusive rectal feeding. In some cases with uncontrollable vomiting and after-hemorrhage from the stomach it is necessary to feed the patient exclusively by the rectum.

The substances best adapted for nutritive enemata are artificially-digested foods, such as Leube's pancreatic meat-emulsion, his beef-solution, and peptonized milk-gruel as recommended by Roberts.[109] Beef-tea and eggs, which are often used for this purpose, are not to be recommended, as the former has very little nutritive value, and egg albumen is absorbed in but slight amount from the rectum. Expressed beef-juice may also be used for rectal alimentation. The peptones, although physiologically best adapted for nutritive enemata, often irritate the mucous membrane of the rectum, so that they cannot be retained. It has been proven that it is impossible to completely nourish a human being by the rectum.[110] Rectal alimentation can sometimes be advantageously combined with feeding by the mouth.

[Footnote 109: Leube's pancreatic meat-emulsion is prepared by adding to 4-8 ounces of scraped and finely-chopped beef l-2½ ounces of fresh finely-chopped oxen's or pig's pancreas freed from fat. To the mixture is added a little lukewarm water until the consistence after stirring is that of thick gruel. The syringe used to inject this mixture should have a wide opening in the nozzle; Leube has constructed one for the purpose (Leube, _Deutsches Arch. f. klin. Med._, Bd. x. p. 11).

The milk-gruel is prepared by adding a thick, well-boiled gruel made from wheaten flour, arrowroot, or some other farinaceous article to an equal quantity of milk. Just before administration a dessertspoonful of liquor pancreaticus (Benger) or 5 grains of extractum pancreatis (Fairchild Bros.), with 20 grains of bicarbonate of soda, are added to the enema. This may be combined with peptonized beef-tea made according to Roberts's formula (Roberts, _On the Digestive Ferments_, p. 74, London, 1881).

Preparatory to beginning the treatment the bowels should be emptied by a clyster, and this should be occasionally repeated. About three to six ounces of the tepid nutritive fluid should be slowly injected into the rectum. The injections may be repeated at intervals of from three to six hours. If necessary, a few drops of laudanum may be occasionally added to the enema.]

[Footnote 110: Voit u. Bauer, _Zeitschrift f. Biologie_, Bd. v.]

There is universal agreement that the dietetic treatment of gastric ulcer is of much greater importance than the medicinal treatment. There is {520} hardly another disease in which the beneficial effects of proper regulation of the diet are so apparent as in gastric ulcer. Those articles of food are most suitable which call into action least vigorously the secretion of gastric juice and the peristaltic movements of the stomach, which do not cause abnormal fermentations, which do not remain a long time in the stomach, and which do not mechanically irritate the surface of the ulcer. These requirements are met only by a fluid diet, and are met most satisfactorily by milk and by Leube's beef-solution.

The efficacy of a milk diet in this disease has been attested by long and manifold experience. By its adoption in many cases the pain and the vomiting are relieved, and finally disappear, and the ulcer heals. In general, fresh milk is well borne. If not, skimmed milk may be employed. If the digestion of the milk causes acidity, then a small quantity of bicarbonate of soda or some lime-water (one-fourth to one-half in bulk) may be added to the milk. Large quantities should not be taken at once. Four ounces of milk taken every two hours are generally well borne. Sometimes not more than a tablespoonful can be taken at a time without causing vomiting, and then of course the milk should be given at shorter intervals. It is desirable that the patient should receive at least a quart, and if possible two quarts, during the twenty-four hours. The milk should be slightly warmed, but in some cases cold milk may be better retained. In some instances buttermilk agrees with the patient better than sweet milk. Although many suppose that they have some idiosyncrasy as regards the digestion of milk, this idiosyncrasy is more frequently imaginary than real. Still, there are cases in which milk cannot be retained, even in small quantity.

For such cases peptonized milk often proves serviceable.[111] The artificial digestion of milk as well as of other articles of food is a method generally applicable to the treatment of gastric ulcer. The main objection to peptonized milk is the aversion to it that many patients acquire on account of its bitter taste. The peptonization should not be carried beyond a slightly bitter taste. The disagreeable taste may be improved by the addition of a little Vichy or soda-water. Peptonized milk has proved to be most valuable in the treatment of gastric ulcer.

[Footnote 111: Milk may be peptonized by adding to a pint of fresh milk, warmed to a temperature of 100° F., 5 grs. of extract pancreatis (Fairchild Bros. and Foster) and 20 grs. of bicarb. sodii dissolved in 4 ounces of tepid water. The mixture is allowed to digest for about an hour at a temperature of 100° F., which may be conveniently done by placing the milk in a bowl in a pan of water maintained at this temperature. It is then boiled, strained, and placed on ice, or when the milk is to be taken immediately it is better not to boil it, in order that the partial digestion may continue for a while under the influence of the pancreatic ferment in the stomach. The milk without boiling may be kept on ice without further digestion; and this procedure has the advantage that the pancreatic ferments, although inactive at a temperature near that of ice, are not destroyed. The degree of digestion aimed at is indicated by the production of a slightly, but not unpleasantly, bitter taste. When the digestion is carried to completion, milk has a very bitter and disagreeable flavor. Peptonized milk-gruel, mentioned on page 519, may also be employed.]