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Inherited disorders of hypercoagulability may lead to thrombosis of the hepatic vein and Budd–Chiari syndrome. Factor V Leiden is responsible for 8% of cases. [ 2 ] Other less common inherited disorders leading to the condition include factor II mutation (3%), protein C deficiency (5%), protein S deficiency (4%), and antithrombin III ...
Portal vein thrombosis, incidental PM finding. Portal vein thrombosis (PVT) is a vascular disease of the liver that occurs when a blood clot occurs in the hepatic portal vein, which can lead to increased pressure in the portal vein system and reduced blood supply to the liver. The mortality rate is approximately 1 in 10. [1]
The treatment for recently developed or acute hepatic artery thrombosis include anticoagulant medications, fibrinolytic therapy to break up the blood clot, or surgical revascularization. [2] If acute hepatic artery thrombosis occurs after liver transplantation, then retransplantation with a new liver may be necessary. [2]
Budd-Chiari syndrome is the blockage of a hepatic vein or of the hepatic part of the inferior vena cava. This form of thrombosis presents with abdominal pain, ascites and enlarged liver. Treatment varies between therapy and surgical intervention by the use of shunts. [5]
Preoperative PVE is a very well tolerated procedure with extremely low mortality rates (0.1 percent) and technical failure rates (0.4 percent). [3] Complication rates from the procedure are low as well (2–3 percent) and include portal vein thrombosis, liver infarction, necrosis, infection, pneumothorax, and other risks as listed above. [3]
Portal hypertension is defined as increased portal venous pressure, with a hepatic venous pressure gradient greater than 5 mmHg. [3] [4] Normal portal pressure is 1–4 mmHg; clinically insignificant portal hypertension is present at portal pressures 5–9 mmHg; clinically significant portal hypertension is present at portal pressures greater than 10 mmHg. [5]
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