Portal Hypertension



The normal liver offers little resistance to portal venous blood flow (about 1 L/min), and portal pressure is normally less than 5 mm Hg above in­ferior vena caval pressure. The distortion of he­patic architecture in cirrhosis leads to a marked increase in resistance to portal venous flow, which in turn leads to an increase in portal venous pressure.

Although cirrhosis is the most important cause of portal hypertension, any process leading to in­creased resistance to portal blood flow into or through the liver or to hepatic venous outflow from the liver will result in portal hypertension . Since the pressure within any vas­cular system is proportional to both resistance and blood flow, a marked increase in blood flow will also result in portal hypertension, although such situations are rare.

Portal hypertension leads to the formation of venous collaterals between the portal and sys­temic circulations. Collaterals may form at several sites, the most important clinically being those connecting the portal to the azygos vein which form dilated, tortuous veins (varices) in the sub-mucosa of the gastric fundus and esophagus.

Variceal Hemorrhage. Hemorrhage occurs most frequently from varices in the esophagus and is a common and serious complication of portal hypertension, with a mortality rate of 30 to 60 per cent. What leads to variceal rupture is unknown, but reflux esophagitis and the presence of ascites do not appear to be important. Bleeding may pre­sent as hematemesis, hematochezia, melena, or any combination of these . Bleeding may lead to shock, stop spontaneously, or recur.





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