Advances in G.I.T Related Mucosal Disease in I.C.U

Abstract

Gastrointestinal complications frequently occur in patients admitted to the intensive care unit. Of these, ulceration and bleeding related to stress-related mucosal disease (SRMD) could lengthen hospitalization and increase mortality. Risk factors for stress ulcer formations that have been identified are numerous and varied: • In critically ill medical patients with 2 or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, renal failure, stroke, hypertension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin. • In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy. The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastro duodenal mucosa. Stress results in splanchnic vasoconstriction leading to gastric mucosal ischemia and decreased delivery of oxygen and nutrients resulting in a deficit in aerobic metabolism and high-energy phosphate compounds. This leads to a drop in intramucosal PH from a deficit of systemic bicarbonate that normally buffers back diffusion of hydrogen ions. Suppressing acid production is fundamental to preventing stress related mucosal ulceration and clinically important gastrointestinal bleeding. Traditional prophylactic options for SRMD in critically ill patients include antacids, sucralfate, histamine2-receptor antagonists (H2RAs), and proton pump inhibitors. H2RAs act by decreasing gastric acid secretion through reversible, competitive inhibition of histamine-stimulated acid secretion and are effective in reducing basal acid production.