Portal vein thrombosis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Historical Perspective
Portal vein thrombosis was first discovered by Balfour and Stewart in 1868. In 1868, G201210A mutations were first implicated in the pathogenesis of portal vein thrombosis. In 1945, Allan Whipple, an American surgeon, reported treatment of some cases of the portal hypertension with shunts. He eventually tried shunts between different mesenteric veins. Finally, he found portocaval shunt as the best choice. In 1980s, researchers have observed that endoscopic sclerotherapy is more efficient than surgical shunting in preventing recurrent variceal bleeding.
Classification
Portal vein thrombosis may be classified according to the extension into 4 groups including confined to the portal vein beyond the confluence of the splenic vein, extended to the superior mesenteric vein, but with patent mesenteric vessels, extended to the whole splanchnic venous system, but with large collaterals, and extended to the whole splanchnic venous system with only fine collaterals. Based on the duration of symptoms, portal vein thrombosis may be classified as either acute or chronic.
Pathophysiology
It is thought that vein thrombosis is caused by Virchow's triad which includes reduced portal blood flow, hypercoagulable state, vascular endothelial injury. There are two mechanisms that contribute in loss of portal vein blood flow to liver, arterial rescue and venous rescue. It is a rapid process and takes a few days to start and 3-5 weeks to complete after portal vein obstruction. Collateral vessel joins to form cavernoma which connects the proximal and distal part of thrombosed portal vein. Finally, the portal vein becomes fibrosed, thin cord. All these events leads to low systemic vascular resistance and high cardiac output. These are the characterstic findings of hyperkinetic circulation.