The pathophysiology of stress ulcer disease

Stress ulcers are superficial mucosal lesions located predominantly in the fundus of the stomach. They occur mainly in the victims of severe trauma and sepsis and are to be clearly distinguished from Cushing's ulcers, ulcers induced by drugs and from activation of a preexistent ulcer. It is generally agreed that mucosal ischemia is the major inciting event in the pathogenesis of acute stress ulceration of the stomach and that the presence of luminal acid and pepsin are required for overt ulceration to develop. Back‐diffusion of acid occurs in the absence of overt disruption of the gastric mucosal barrier, is closely related to the formation of ulcers, and may be enhanced by reflux of duodenal content into the stomach and by diffusion of blood urea into the stomach. Severe acidosis and base deficit together with depression of acid secretion and consequent lowering of alkaline tide are important contributing factors. A differential energy deficit in fundic mucosa as a result of ischemia probably contributes to mucosa damage by interfering with anion exchange (HCO 3 − for Cl − ). The exact role of steroids and prostaglandins is controversial.