Abstract
The development of acute stress bleeding in intensive-care patients occurs on a multifactorial basis. The basic mechanism lies in the imbalance between aggressive and protective factors. Most intensive care patients show a reduced acid secretion, a reduction of the gastric mucosal blood flow, and a decreased mucus and bicarbonate secretion. Sucralfate enhances most of the defensive mechanisms. These actions are the pathophysiologic basis of the efficacy of sucralfate in the prevention of stress bleeding. Because sucralfate has only a minor influence on the gastric pH and at the same time has proven bactericidal effects, gastric and gut bacterial overgrowth is significantly reduced. These effects explain the observed differences in mortality between sucralfate and alkalinizing drugs like antacids or H2-antagonists. The indications and limits of sucralfate in stress bleeding prophylaxis are pointed out.