The critically ill liver patient: the variceal bleeder.

Abstract

Esophageal varices develop in patients with cirrhosis once portal pressure, measured by hepatic venous pressure gradient, and exceeds 10 mm Hg. At a portal pressure of 12 mm Hg, variceal bleeding may develop that is associated with a mortality of 30% to 50% per episode. In addition to an elevated portal pressure, other risk factors for the development of variceal hemorrhage include: variceal size, endoscopic features on the variceal wall (i.e., red wales), and Child-Pugh class. In patients with suspected variceal hemorrhage, the treatment of the acute episode includes intravascular volume expansion, hemostasis through the use of pharmacological agents and endoscopy, and the prevention and treatment of potential complications associated with variceal hemorrhage such as aspiration pneumonia, spontaneous bacterial peritonitis and hepatic encephalopathy. Given a high rate of rebleeding, long-term prevention through secondary prophylaxis should be instituted in all patients who have survived an episode of variceal bleeding. Current prophylactic options include: non-selective beta-blockers alone (first line) or in combination with long-acting nitrates (isosorbide mononitrate) and/or endoscopic variceal obliteration achieved through sclerotherapy or preferably, band ligation.