As has already been explained, ulcers of the anterior wall are the ones most liable to perforate into the general peritoneal cavity,82 but on account of their comparative infrequency perforation occurs oftener in other situations, particularly in the lesser curvature and near the pylorus. Except on the anterior wall the perforation is often brought about by the rupture of adhesions which for a time had prevented this accident. In a considerable number of cases, particularly of ulcers on the anterior wall, the ulcer looks as if recently formed (acute perforating ulcer); in other cases its thickened and indurated margins indicate long duration. Chiari83 describes a case in which rupture into the peritoneal cavity took place through the cicatrix of an old ulcer, probably in consequence of the distension of the stomach with gas. The hole in the peritoneum is usually circular, smaller than the inner surface of the ulcer, and has sharp, well-defined edges. Less frequently the edges are ragged. Post-mortem digestion may, however, so change the borders of the opening as to make it difficult or impossible to tell from their post-mortem appearances alone whether perforation has occurred before or after death. The peritoneal cavity after death from perforation is found to contain gas and substances from the stomach. Usually within a few hours after perforation septic peritonitis is excited, but in exceptional cases no inflammation of the peritoneum has occurred even when life has been prolonged twenty-four hours after perforation.
82 According to Brinton, "the proportion of perforations to ulcers is such that of every 100 ulcers in each of the following situations, the numbers which perforate are—on the posterior surface, about 2; the pyloric sac, 10; the middle of the organ, 13; the lesser curvature, 18; the anterior and posterior surface at once, 28; the cardiac extremity, 40; and the anterior surface, 85."
83 Wiener med. Blätter, 1881, No. 3.
Emphysema of the subcutaneous, subperitoneal, and other loose areolar tissue of the body is a rare but remarkable result of the perforation of gastric ulcer. The emphysema is sometimes observed shortly before death, but it attains its maximum development after death, when it may spread rapidly over the greater part of the body. The gas consists in part of hydrogen, as it burns with a blue flame. It is generated, at least in great part, by fermentation of the contents of the stomach. The gas may enter the subserous tissue at the edges of the ulcer and thence spread, or, after perforation of the stomach, it may make its way from the peritoneal cavity into the loose subserous connective tissue through some place in the parietal peritoneum which has been macerated, perhaps by the digestive action of the gastric juice.84
84 Roger (Arch. gén. de Méd., 1862) and Demarquay (Essai de Pneumatologie médicale, Paris, 1866) deserve the credit of first calling general attention to the occurrence of subcutaneous emphysema after rupture of the digestive tract. The following writers have each reported a case of emphysema following the perforation of gastric ulcers: Cruveilhier, Anat. Path., t. i. livr. xx.; Bell, Edinb. Med. Journ., vol. vi. p. 783; Thierfelder, Deutsches Arch. f. klin. Med., iv., 1868, p. 33; Newman, The Lancet, 1868, vol. ii. p. 728; Poensgen, Das subcutane Emphysem nach continuitätstrennungen des Digestionstractus, etc., Inaug. Diss., Strassburg, 1879, p. 40; Korach, Deutsche med. Wochenschr., 1880 p. 275; Jürgensen, Deutsches Arch. f. klin. Med., Bd. 31, p. 441, 1882. Doubtful cases are reported by Lefèvre, W. Mayer, and Burggraeve. The fullest consideration of the subject is to be found in the dissertation of Poensgen.
In two cases of sudden death from gastric ulcer Jürgensen found gas in the veins and arteries of various parts of the body. He believes that this gas, which certainly was not the result of putrefaction after death, was derived from the stomach, and that it entered during life the circulation through vessels exposed in the borders of the ulcer, thus causing death. In one of the cases a profuse hemorrhage preceded death, and in the other the ulcer had perforated into the peritoneal cavity.85
85 Jürgensen does not consider whether this gas may not have made its way into the blood-vessels after death in a manner similar to its extension through the cellular tissue of the body in the cases of emphysema just mentioned. In the case which he has reported in full interstitial and subserous emphysema could be traced from the ulcer ("Luft im Blute," Deutsches Arch. f. klin. Med., Bd. 31, p. 441, 1882).
The source of hemorrhage from gastric ulcer is from blood-vessels either in the stomach itself or in the neighborhood of the stomach. Hemorrhages slight or of moderate severity occur from the capillaries and small arteries and veins in the mucous and submucous coats. Sometimes profuse and even fatal hemorrhage comes from arteries or from veins in the submucous coat, especially when these vessels are dilated. Quickly-fatal hemorrhages take place from the large vessels between the muscular and the serous coats, particularly from the main trunks on the curvatures. After the formation of adhesions, followed by the perforation of all of the coats of the stomach, profuse bleeding may proceed from the erosion of large vessels near the stomach, such as the splenic, the hepatic, the pancreatico-duodenal arteries, the portal and the splenic veins, and the mesenteric vessels. Bleeding may also occur from vessels in the parenchyma of organs invaded by the ulcer. The most common source of fatal hemorrhage is from the splenic artery, which from its position is peculiarly exposed to invasion by ulcers of the posterior wall of the stomach. The hemorrhage is usually arterial in origin. It may come from miliary aneurisms of the gastric arteries or from varicose veins in the wall of the stomach. As Cruveilhier has pointed out, an ulcer may cicatrize except over one spot corresponding to an artery from which fatal hemorrhage may occur. Ulcers which give rise to large hemorrhages are usually chronic in their course. Those seated on the middle of the anterior wall, although peculiarly liable to perforate, are comparatively exempt from hemorrhage on account of the small size of the blood-vessels there.
Changes in the blood-vessels of the stomach have been seen in a considerable number of cases of gastric ulcer. Instances have been recorded of the association with gastric ulcer of most of the diseases to which blood-vessels are subject. An example in all respects convincing of embolism of the artery supplying the ulcerated region of the stomach has not been published. Probably the best case belonging here is one of perforating ulcer of the stomach with hemorrhagic infiltration in its walls, presented by Janeway to the New York Pathological Society in 1871.86 In this case there was in the gastro-epiploic artery an ante-mortem fibrinous plug which was continued into the nutrient artery of the ulcerated piece of the stomach. No source for an embolus could be found. In one case Merkel found an embolus in a small artery leading to an ulcer of the duodenum.87 The arch of the aorta was atheromatous and contained a thrombus. Patches of hemorrhagic infiltration existed in the stomach.
86 Trans. of the N.Y. Path. Soc., vol. ii. p. 1.