Cirrhosis represents the end-stage of any chronic liver disease. Two major syndromes result from cirrhosismdash;portal hypertension and hepatic insufficiency. Additionally, vasodilatation and the hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Complications of cirrhosis occur as a consequence of a combination of these factors. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. Hepatorenal syndrome also results from severe peripheral vasodilatation that leads to renal vasoconstriction. Another complication of cirrhosis, portosystemic encephalopathy, is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency. In this article, recent advances in pathophysiology and management of the complications of cirrhosis and portal hypertension are reviewed.
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