The Clinical Management of Gastroesophageal Varices

Rowen K. Zetterman, MD


January 20, 2012

In This Article

Cirrhosis, Portal Hypertension, and Varices

Portal hypertension, a common complication of cirrhosis,[1] is associated with the development of ascites, hepatic encephalopathy, hepatorenal syndrome, and portosystemic shunts often involving superficial vessels of the stomach and esophagus. Portal hypertension develops from increased vascular resistance and enhanced blood flow within the portal system. Increased vascular resistance results from changes within the liver including hepatic fibrosis, regenerative nodules, collagenization of the space of Disse, hepatocyte enlargement, isolated vascular occlusion, or the effect of circulating neurohumoral vasoconstricting agents[2]and increased portal blood flow following vasodilation of splanchnic arterial vasculature. Gastroesophageal varices develop as collaterals to divert blood from the high-pressure portal circulation back to the heart.

Portal hypertension is typically progressive, with esophageal varices occurring in 5%-10% of patients with cirrhosis each year,[3] especially in patients with advanced or decompensated liver disease. Of those with compensated cirrhosis, 30% will have gastroesophageal varices compared with 60% of patients with decompensated cirrhosis.[4] Patients with decompensated cirrhosis and small varices should have more frequent subsequent screening because they are at high risk for progressive disease. Eventually, varices will develop in most patients with cirrhosis, gradually increasing in size and leading to gastrointestinal bleeding.[5]

Gastroesophageal variceal hemorrhage is a medical emergency that occurs in up to 10% of patients with cirrhosis each year.[6] Bleeding is more likely in patients with Child's B or C cirrhosis. Red coloration ("red wales") on varices is a marker of increased risk. Of all causes of gastrointestinal bleeding in cirrhosis, varices account for more than 70% of bleeding episodes. Gastric varices are less likely to bleed than esophageal varices, although bleeding is often more severe and more difficult to manage. Mortality from bleeding gastroesophageal varices remains at 15%-20%.[7]

This article will focus on screening and medical therapies for both primary prophylaxis and for treatment of initial variceal hemorrhage. The emphasis will be on pharmacotherapy and endoscopic therapy, with limited information on transvenous intrahepatic portosystemic shunts (TIPS) and surgical shunts.


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as: