Esophageal varices develop in response to an increase in venous pressure in a location distal to the azygos vein and the right ventricle. The impedance to flow may be functional, as in a hyperdynamic circulatory state, or mechanical, as with a blood clot or tumor. Further vasodilation of the splanchnic venous system may also result from secondary changes in vascular circulatory mediators such as nitric oxide and vasoactive intestinal peptide. A variety of disorders, ranging from splenic, portal, or hepatic vein thrombosis (BuddChiari syndrome) to rightsided heart failure, may lead to esophageal varices. The most common cause of esophageal varices is portal hypertension secondary to intrahepatic causes, such as cirrhosis. In cirrhosis, there is fibrosis of the sinusoids and shunting that leads to portal vein backflow. As many as half of patients presenting with a new diagnosis of hepatic cirrhosis have esophageal varices on initial evaluation. The vast majority of patients with cirrhosis will also develop esophageal varices over the course of the disease if they do not undergo liver transplantation. If varices are present, there is a greater risk for bleeding with risk factors such as larger varices, increased portal hypertension, hepatic failure, and endoscopic signs of recent or impending bleeding (e.g., red wale signs). Bleeding from esophageal varices may be brisk and massive, and the risk of death is considerable.
Many treatments are available for esophageal varices and are used on the basis of whether they are needed for management of acute bleeding, prevention of recurrent bleeding. or prophylaxis in patients with diagnosed nonbleeding varices. Amongst these clinical scenarios, treatments are divided into the broad categories of variceal obliteration (endoscopic banding and sclerosis), pharmacologic reduction of portal venous pressure (betaantagonists, nitrates, somatostatin), and mechanical reduction of portal venous pressure (transhepatic intravascular portosystemic shunt [TIPS], surgical portacaval shunt, liver transplantation). Acute and chronic treatments may be a combination of obliterative and pharmacologic treatments. For example, acute bleeding may be managed by esophageal variceal banding and intravenous octreotide, whereas chronic prevention may rely on banding and use of betaantagonists. Prophylactic therapy tends to be pharmacologic, but obliterative techniques may be used in addition. Therapies such as TIPS and transplant are reserved for more severe and/or refractory cases of variceal bleeding.