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The treatment of portal vein thrombosis is performed based on a symptomatic acute clot or an asymptomatic chronic clot and further depends on whether the underlying disease is cirrhosis or not. In all cirrhotic cases, attention should be paid to hemorrhagic complications. In particular, it is necessary to perform appropriate prophylactic endoscopic injection sclerotherapy/endoscopic variceal ligation in complicated case of esophagogastric varices. In recent years the use of antithrombin-III (AT-III) preparations and danaparoid sodium have increased in place of heparin, urokinase, and warfarin for the treatment of portal vein thrombosis. Based on the fact that antithrombotic action (fibrinolysis) has been reported even with AT-III alone, and that AT-III doesn’t affect the bleeding tendency, it is safe and effective to use it for portal vein thrombosis with esophagogastric varices. And danaparoid sodium has higher anti-factor Xa activity than heparin. In addition, the usefulness of danaparoid with less risk of bleeding has also been reported.

Portal vein thrombosis is considered to develop from portal venous vascular wall disorder, abnormal portal venous flow, and abnormalities of the blood coagulation system as the thrombogenic origins. Portal vein thrombosis can easily occur in patients with hepatic cirrhosis due to three additional factors. The first factor is the hyperpermeability of the gastrointestinal mucous membrane. Cirrhosis creates an environment susceptible to bacterial translocation, and loads to the flow of lipopolysaccharide into a portal vein, resulting in sinusoid wall injury. The second factor is clot formation promoted by portal venous congestion (sluggish blood flow) due to portal hypertension. The third factor is a decrease of antithrombin-III synthesis in liver cirrhosis. Among the underlying diseases of 539 cases of portal vein thrombosis in Japan in 2014, there were 434 cases (80.5%) of portal hypertension, whose breakdown consisted of 406 cases (75.3%) of liver cirrhosis, 25 cases of idiopathic portal hypertension, 8 cases of extrahepatic obstruction, and 7 cases of others, while 105 cases (19.5%) were not associated with portal hypertension. Secondary portal vein thrombus accounted for 69 (12.8%) of the total, if it is defined as that developed within 30 days after an operation or interventional radiology.