Thrombosis is a serious medical condition, which causes blood clot inside the blood vessel resulting in obstruction through the circulatory system. Portal vein thrombosis refers to venous thrombosis that progress in the trunk part of the portal vein particularly at the right and left intrahepatic branches. It may also extend to the spleen or superior mesenteric veins (small intestine) or towards the liver involving intrahepatic portal branches. Portal vein thrombosis occurs in association with cirrhosis and rarely with malignancy of liver. It is an important cause of non-cirrhotic pre-hepatic portal hypertension all over the world.
Some Statistics of Portal Vein Thrombosis
The prevalence of portal vein thrombosis in compensated liver disease has been reported to be 0.6–16%; 15% in patients awaiting liver transplantation and up to 36% in explanted liver on histopathology. It is seen in up to 35% of cirrhotic patients with hepatocellular carcinoma. The lifetime risk of portal vein thrombosis in general population is reported to be 1%.
What Are The Portal Vein Thrombosis Complications?
The pathophysiology of portal vein thrombosis is often referred to as ‘Virchow’s triad’, which describes the three broad categories of factors such as venous stasis, endothelial injury, and hypercoagulopathy. These three conditions are the fundamental cause of portal vein thrombosis which is also the reason for malignancy, chronic liver diseases, local inflammatory processes, systemic disorders including myeloproliferative disorders, and thrombophilia.
The blood clot in the portal vein can able to cause a serious adverse reaction, which may be short or long-term events in the affected individuals. The interference makes complications in the extrahepatic portal and splenic vein. The obstruction of mesenteric vein also shows a high percentage of complications, which result in death due to intestinal infarction.
Portal hypertension is the main reason for a prolonged period of portal vein thrombosis in patients. It could also result in dilated and twisted veins which are referred to as varicose. It also happens in the esophagus and more frequently in the stomach. These conditions are called as esophageal varices and gastric varices where veins can bleed profusely. Bleeding occurs because of portal vein thrombosis in most of the patients with cirrhosis. When compared to cirrhotic patients without portal vein thrombosis, 10% higher bleeding rate occurs in cirrhotic patients with portal vein thrombosis. Cirrhotic portal hypertension is one of the most important risk factors for bleeding and portal vein thrombosis in cirrhotic patients significantly worsens the disease. This collateralization of the portal vein sometimes can lead to the progression of the condition so-called portal cavernoma.
Portal vein thrombosis also occurs rarely in the newborn and children. Infection of the umbilical cord stump (at the navel) and appendicitis are the two-factor triggers the formation of blood clots. Another complication that occurs less frequently in patients due to collateral vessel formation is hepatic encephalopathy.
To prevent thrombosis and bleeding in cirrhosis patients, low-molecular-weight heparin enoxaparin was very useful. It is effectively involved in decreasing the rate of bleeding, bacterial translocation, and liver decompensation.
Patient selection for anticoagulation remains contentious. Anticoagulation is significantly essential for liver transplantation to prevent the progress of portal vein thrombosis and to reduce post-transplant morbidity and mortality. Vitamin K antagonists, low-molecular-weight heparins, direct-acting oral anticoagulants are some of the anticoagulant currently available for the treatment of portal vein thrombosis.
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