Alcohol and oesophageal varices

Abstract

Oesophageal varices are abnormally dilated veins that develop beneath the mucosa of the lower oesophagus and upper stomach and cause profound gastrointestinal haemorrhage associated with a high mortality. Varices develop in the presence of protal hypertension, which, in Europe and the USA, is most commonly due to alcoholic cirrhosis of the liver. Alcoholic cirrhosis develops in 10-20% of chronic ethanol abusers as a result of prolonged hepatocyte damage, leading to centrilobular inflammation and fibrosis. The net effect on the portal venous system is an elevation of resistance, and/or increase of inflow, producing portal hypertension, and the development of collateral channels in the form of varices. Such parenchymal liver disease also causes ascites, clotting deficiencies, secondary malnutrition and hepatic encephalopathy, all of which contribute to the high mortality associated with variceal haemorrhage. Variceal bleeding is more likely to occur when the varices are large, long and numerous, with surface red markings, and may be precipitated to respiratory tract infection, non-steroidal anti-inflammatory drugs, alcohol, or may occur spontaneously. Once identified by endoscopy, the aims of management are to control the haemorrhage, to prevent recurrent haemorrhage, and to treat the underlying cause of portal hypertension. Attention to nutrition and long-term rehabilitation are particularly important in those alcoholic cirrhotic patients who survive.