Portal hypertension

Portal hypertension is the main complication of cirrhosis and is responsibl e for its most common complications: variceal hemorrhage, ascites, and port osystemic encephalopathy. Portal hypertension is the result of increased in trahepatic resistance and increased portal Venous inflow, which in turn is the result of splanchnic vasodilatation. Vasodilatation (splanchnic and sys temic) and hyperdynamic circulation are hemodynamic abnormalities typical o f cirrhosis and portal hypertension. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation con tributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodil atation and activation of neurohumoral systems. The hepatorenal syndrome re presents the result of extreme vasodilatation with an extreme decrease in e ffective blood volume that leads to maximal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure. Spontaneous bacterial p eritonitis is a potentially lethal infection of ascites that occurs in the absence of a local source of infection. Portosystemic encephalopathy is a c onsequence of both portal hypertension (shunting of blood through portosyst emic collaterals) and hepatic insufficiency that result in the accumulation of neurotoxins in the brain. This paper reviews the recent advances in the pathophysiology and management of the complications of portal hypertension . Curr Opin Gastroenterol 2001, 17:281-190 (C) 2001 Lippincott Williams & W ilkins, Inc.