Acute Chylous Peritonitis

The extravasation of chyle into the peritoneal cavity is rarely associated with the sudden development of clinical signs and symptoms of peritonitis, and the natural history of the disease is spontaneous closure of the chyle leak with regression of the ascites.

Abstract

The cause of duodenal ulcer (DU) is unknown, but gastric acid and pepsin must be involved in the pathogenesis of the disorder: (1) Patients with massive acid hypersecretion due to gastrinoma almost develop peptic ulcer, usually duodenal; (2) ordinary DU patients, on the average, secrete much more acid basally and also have larger acid secretory capacities than healthy people; and (3) reduction of gastric acid secretion (e.g., with cimetidine) accelerates DU healing and prevents DU from recurring. Although factors responsible for increased basal acid secretion rates and for increased maximal secretory capacity (parietal cell mass) in many DU patients are not completely understood, it is likely that neural and hormonal factors are involved: The stomachs of some DU patients may be under increased vagal drive in the basal state. Parietal cells of DU patients are more sensitive to the hormone gastrin, which is released by food. In this review, evidence for abnormalities in vagal function and gastrin physiology in DU will be discussed, with emphasis on recent developments.