Portal hypertension has been treated surgically by diversion of blood from the portal system, by interruption of the flow of blood to esophageal varices, or by direct obliteration of the varices. At the beginning of the twentieth century, portal diversion was achieved by omentopexy and, in a few patients, by the creation of a portacaval shunt. The latter operation was abandoned because of high mortality and morbidity rates, including shunt encephalopathy. In the 1940's, interest was renewed in the portacaval shunt. Improved understanding of hepatic physiology and the establishment of precise criteria for selection of cases for surgery resulted in a low operative mortality rate. The operation was highly successful in the control of hemorrhage from esophageal varices but was associated with an undesirable incidence of impairment of hepatic function. Currently, selective decompression of varices by the distal splenorenal shunt is under evaluation as a method of preventing variceal hemorrhage, while preserving hepatic function. Elimination of the threat of hemorrhage from varices by arterial ligation, sclerotherapy, or direct suture has been practiced for almost a century. The result remains one of temporary control with recurrent hemorrhage in the majority of cases.Ascites was formerly considered the dominant manifestation of portal hypertension. Currently, it is usually well controlled by diuretics. Surgery is reserved for the rare case of intractable ascites, often with hepatorenal syndrome. In such cases, a shunt is established between the peritoneal cavity and the systemic venous system, a procedure first performed early in this century.