Perforation and its temporary or permanent cure, demands a more minute exposition.

If it takes place at a portion of the stomach, which, like the greater part of the anterior gastric parietes, but rarely enters into a protective adhesion with neighboring tissues, perforation allows the contents of the stomach to pass freely into the peritoneal cavity, and fatal peritonitis follows.

This result is frequently prevented. Whilst we find the tolerably uniform irritation within, giving rise to hypertrophy of the mucous membrane and to callosity of the base of the ulcer and its circumference, we see at the corresponding points of the peritoneal surface, cellular adhesions, or a more intimate union between the stomach and the reverted omentum, the left hepatic lobe, or the pancreas, produced by repeated, circumscribed, inflammatory attacks. The cellular adhesions which have been effected between the stomach and the omentum, and are sometimes found to unite the former with the left lobe of the liver, are not sufficient to prevent a fatal issue when perforation occurs, for as soon as this event has taken place, the adhesions inflame, - this, and the forcible expulsion of the gastric contents, loosens and tears them, and thus the inflammation spreads to the peritoneum, both by continuity of tissue, and by direct contact. The perforation will be rendered more permanently innocuous by intimate adhesion, viz., by the agglutination of a fibro-carti-laginous exudation; as this tissue offers to the contents of the stomach, both from its density and its thickness, a sufficiently firm resistance. This frequently occurs between the small curvature, or the anterior surface of the stomach, and the concavity of the left lobe of the liver, and very frequently between the posterior gastric surface, the pancreas, and the adjoining lymphatic glands; but very rarely between the posterior surface of the stomach and the spleen, after the latter has been dragged into that position, or between the stomach and the diaphragm (Aber-crombie, Chardel). In such cases, after the external membranous layers have been destroyed to an extent proportionate to the loss of substance, the mucous membrane is invariably doubled back over the edge of the perforating ulcer, and impinges upon the pseudo-membranous agglutinating tissue external to the stomach; thus the orifice in the gastric parietes is never filled up by the superimposed tissue in such a manner as to be flush with the inner surface of the stomach, or even to project beyond it into the cavity of the latter.

In favorable but rare cases the pseudo-membranous tissue contracts and draws the edges of the orifices together, so as to produce a firm, callous cicatrix.

In other instances this does not occur; the cavity, though covered in as described, remains, and particularly when adjoining the pylorus, in consequence of the vis a tergo of the gastric contents, enlarges into a lateral sinus, which is lined by the false membrane.

Although in the majority of cases a free opening of the stomach is thus prevented, we may even here find exceptions; the soldering tissue may itself gradually be consumed, the adjoining organ is laid bare, and becomes exposed to an extension of the process. Thus we have seen one case in which the adjacent diaphragm, which had formed a plug, was perforated from the stomach, and the base of the adhering lung was attacked.

In the progress of the perforating gastric ulcer a very important occurrence frequently supervenes, viz., hemorrhage, which often kills on the first, but more frequently after repeated attacks. So long as the ulcer has not perforated the walls of the stomach, the loss of blood is inconsiderable, as the process involves only the small vessels of the membranes, which are easily plugged up. But as soon as the ulcer has penetrated through the gastric parietes, it meets with larger vessels in and beyond the pseudo-membranous layer, or with the vascular system of the obturating organ. Thus, the trunks of the splenic, the coronary, the pyloric, the gastro-epiploic, the gastro-duodenal arteries and their branches, and more especially those going to the pancreas, are corroded and opened, and exhausting and fatal hemorrhages ensue.

Bloodvessels are not alone involved in the destructive process, but other canals also, and we instance the pancreatic ducts, which, in the case to which we allude, open upon the base of the ulcer, and by forming pancreatic fistula, oppose the complete consolidation of the imperfect cicatrix.

The ulcer not only proves fatal by perforation, with consequent peritonitis and hemorrhage, but also, though rarely, by exhaustion from dyspepsia and harassing cardialgia. It is invariably accompanied by chronic catarrh and blennorrhcea of the gastric mucous membrane; it heals as we have remarked, very frequently, but it as often recurs. The cure of large ulcers is followed by considerable deformities of the stomach, and more especially by shortening of the posterior wall and the lesser curvature, or by annular structures. The disease occurs chiefly at the period of puberty, and very often, particularly in the female sex, as early as the 15th year.

The perforating gastric ulcer is in no way connected with gastritis and cancer, though it is often mistaken for these affections; but it is important to know, though it be for the mere cadaveric diagnosis, that in rare cases it may be complicated with cancer; yet it always retains its peculiar characters so as to be distinguishable in the midst of the cancerous growth and devastation.