Stress ulcer.

Abstract

Stress ulceration is a recognized cause of morbidity and mortality in the critically ill patient. These superficial lesions occur in both the stomach and duodenum within hours after admission to a critical care unit. Although the pathogenesis of stress ulcer is not well understood, it is now established that a decrease in mucosal pH below 6.5 is essential for the induction of stress ulceration. This drop in mucosal pH can result from high luminal hydrogen ion (H+) concentration, increased permeability of the mucosa for H+, or defective neutralizing ability of the mucosa. Local and systemic factors that modulate mucosal blood flow are also important in the development of stress ulceration. It is estimated that 20% to 30% of patients with stress ulcer develop significant gastrointestinal bleeding that requires blood transfusion. The routine administration of H2-receptor antagonists has become standard practice in most intensive care units to prevent the development of stress ulcer and gastrointestinal bleeding, although in many cases their efficacy is unproven. Antacids are clearly effective and remain the gold standard with which alternative therapies are compared. The best treatment for stress ulceration is identification of the patient at risk and institution of prophylaxis. For patients who bleed from stress ulceration, conservative measures should include aggressive treatment of the underlying medical problem and neutralization of acid.