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Portal vein thrombosis (PVT) is a clinical situation that usually begins at the extrahepatic portal vein and sometimes extends into the intrahepatic portal vein, or distally to the superior mesenteric and splenic veins. The clinical presentation (asymptomatic to fatal bowel ischemia) and etiology (liver cirrhosis, systemic cause such as hypercoagulable state and myeloproliferative diseases, local cause such as acute appendicitis) is so diverse that the clinical decision making is sometimes very difficult. When the thrombus extends into the superior mesenteric vein, bowel ischemia and infarction should be anticipated and prevented cautiously with immediate initiation of anticoagulant therapy. The most troublesome chronic sequelae of the portal vein thrombosis is portal vein hypertension, which deteriorates patients’ quality of life. The goal of treatment is to prevent ischemic bowel infarction and portal vein hypertension. Color Doppler sonography, computed tomography, and magnetic resonance imaging are convenient diagnostic tools to confirm PVT. The systemic thrombotic state or cause of infection must be determined through serologic studies. It is helpful to divide PVT patients into cirrhotic and non-cirrhotic, acute and chronic patients. In cases of non-cirrhotic acute PVT, rapid correction of the systemic and local cause of thrombosis and early initiation of anticoagulant therapy are considered the gold standard of treatment. In cases of cirrhotic and chronic PVT, the risk of bleeding and the efficiency of anticoagulation therapy should be measured and balanced for each patient. This article discusses the debated issue of the various treatment paradigms for PVT.
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