Treatment of acute variceal bleeding: general management and prevention of infections

Abstract

Ruptured esophageal varices cause 60–80% of all upper gastrointestinal bleeding episodes in cirrhosis. Variceal bleeding ceases spontaneously in 40–50% of patients; however, a small percentage of patients (∼5%) die from uncontrolled bleeding. Even in patients in whom bleeding stops, rebleeding occurs within the first 6 weeks in ∼20%. A poor outcome, either failure to control bleeding, early recurrent bleeding or death, occurs in 15–30% of cases. Several factors predictive of a poor outcome have been identified in various studies. Some of them, such as hypovolemia, renal dysfunction and bacterial infection, apply to cirrhotic patients with any gastrointestinal hemorrhage, independent of etiology. Other predictive factors, such as active variceal bleeding at the time of diagnostic endoscopy and an hepatic venous pressure gradient >20 mmHg, apply to cirrhotic patients with variceal hemorrhage and are factors that can be prevented or treated by using pharmacologic or other portal pressure-reducing methods. A third group of predictive factors are intrinsic to the cirrhotic patient, as is the case of an alcoholic etiology of cirrhosis, the degree of liver dysfunction (albumin, bilirubin levels and the presence of hepatic encephalopathy) and the presence of hepatocellular carcinoma.