Portal hypertension

Abstract

Cirrhosis represents the end stage of any chronic liver disease. Two major syndromes result from cirrhosis: 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. Hyponatremia and the hepatorenal syndrome result from water retention and renal vasoconstriction, respectively, both of which are also consequences of peripheral vasodilatation. Vasodilatation that occurs in the pulmonary circulation leads to the hepatopulmonary syndrome. Another complication of cirrhosis, portosystemic encephalopathy, is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency. This paper reviews the recent advances in the pathophysiology and management of the complications of cirrhosis and portal hypertension.