Abstract
Esophageal varices are the major complication of portal hypertension. It is detected in about 50% of cirrhosis patients. Portal hypertensionis associated with both increased portal inflow and increased intrahepatic vascular resistance. Intrahepatic vascular resistance is caused by the architectural distortion of the liver resulting from fibrosis and by increased sinusoidal tone. Portal venous inflow results from a combination of ahyperdynamic circulatory state and increased plasma volume. In response to the increased portal pressure, collateral circulation develops by the opening of preexisting vascular channels. Esophagogastric varices are the most important collateral vessels: they tend to increase in size with the increase of portal pressure and rupture when wall tension exceeds a critical value.
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