Esophageal varices are collateral veins that develop as a result of portal hypertension and are seen commonly in patients with cirrhosis of the liver. These collateral vessels grow and have a high risk of rupture that can result in life-threatening bleeding.

The primary risk factors for the development of esophageal varices are the risk factors for developing cirrhosis of the liver, although portal vein thrombosis, schistosomiasis, and Budd-Chiari syndrome are other risk factors for portal hypertension and subsequent variceal development. Cirrhosis of the liver is associated with excessive alcohol consumption, nonalcoholic fatty liver disease, and chronic hepatitis (primarily hepatitis C virus or hepatitis B virus), although there are a number of etiologies that can cause cirrhosis.

Esophageal varices are common in patients with cirrhosis, and approximately 50% of cirrhotics have evidence of varices (either esophageal or gastric) at the time of diagnosis. The natural tendency of varices is to grow, with a predilection toward rupture and bleeding. In the absence of an acute gastrointestinal bleed from ruptured varices, esophageal varices are asymptomatic. Symptoms of bleeding varices include hematemesis, melena, bright red blood per rectum, and signs of hypovolemic shock due to acute blood loss anemia.

The main goal of treatment is to prevent the potentially life-threatening complication of bleeding esophageal varices with the use of portal vein pressure-reducing medications such as nonselective beta blockers (nadolol or propranolol), splanchnic vasoconstrictors (octreotide), and variceal band ligation (endoscopic intervention).

In the event that an esophageal variceal bleed does occur, urgent endoscopy for banding and treatment with nonselective beta blockers and splanchnic vasoconstrictors are recommended. If bleeding persists refractory to these interventions, a transjugular intrahepatic portosystemic shunt should be considered, as well as evaluation for liver transplantation.