الفهرس 
EPIDEMIOLOGY AND RISK FACTORS OF STRESS RELATED MUCOSAL BLEEDING (SRMB) IN ICUOnly 14 pages are availabe for public view
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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) can lengthen hospitalization and increase mortality.
Risk factors for stress ulcer formation that have been identified are numerous and varied:
• Non-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 w+ith a coagulopathy.
SRMD is the most common cause of GI bleeding in patients receiving MV. Within a few hours of critical illness, macroscopic damage becomes evident as sub epithelial petechiae progress to lesions ranging from superficial erosions to true gastric ulcers. Overt bleeding because of SRMD occurs in up to 25% of critically ill patients who do not receive prophylactic therapy
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 gastroduodenal 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
PPIS block the final pathway for acid secretion by irreversibly inhibiting H+/K+ ATPase in gastric parietal cells. Sucralfate coats the early shallow mucosal lesions and protects them from further acid and pepsin damage without altering gastric PH.
Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid base balance, and treatment of other illnesses helps prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk. In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent rebleeding. In selected patients, either endoscopic therapy or selective infusion of vasopressin into the left gastric artery may help control the hemorrhage