Portal Vein Thrombosis in non cirrhotic patients

Extrahepatic portal vein thrombosis (EPVT) is the most common cause of portal hypertension in non- cirrhotic patients. EPVT has been defined as an obstruction of the extrahepatic portal vein with or without involvement of the intrahepatic portal veins. Although the portal vein accounts for two third of the total hepatic blood flow, interruption of the portal vein has few clinical consequences. This could be explained by two findings. First a compensatory mechanism so called arterial ’buffer’ response, which consists of immediate vasodilatation of the hepatic arterial bed in response to a decreased portal vein blood flow. This mechanism has been well demonstrated experimentally, but also in patients following portal vein clamping at hepatic surgery. The second compensatory mechanism is a rapid development of collateral veins bypassing the thrombosed portion of the portal vein. As a result of the arterial buffer response and development of collaterals, total hepatic blood flow is minimally reduced. Portal pressure, however is increased. This increase in portal pressure can be viewed as a compensatory mechanism allowing portal vein perfusion to be maintained through the collateral veins. So, portal perfusion is maintained at the expense of portal hypertension. The etiology of EPVT is diverse and can be divided into local risk factors such as cirrhosis, hepatobiliary malignancies and pancreatitis, and systemic risk factors such as inherited and acquired prothrombotic disorders. In at least one third of the patients a combination of thrombotic risk factors is demonstrated.

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