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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