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.
Causes
Portal vein thrombosis may be caused by inherited prothrombotic disorders and acquired thrombophilic disorders. Less common causes of portal vein thrombosis include acquired conditions such as cirrhosis andhepatocellular carcinoma and procedures such as abdominal surgery or surgical injury of the portal vein axis and splenectomy.
Differentiating portal vein thrombosis from Other Diseases
- Portal vein thrombosis must be differentiated from other diseases that cause abdominal pain, diarrhea, nausea and vomiting , such as chronic pancreatitis, Pancreatic carcinoma, Dumping syndrome, Acute appendicitis, acute diverticulitis, Infective colitis, viral hepatitis, Liver abscess, Mesenteric ischemia, Acute ischemic colitis.
Epidemiology and Demographics
The incidence of portal vein thrombosis in cirrhotic patients is unknown. The prevalence of portal vein thrombosis is approximately 5000-10,000 per 100,000 in overall cases of portal hypertension in developed counties and 40,000 per 100,000 in developing countries. The overall mortality rate of portal vein thrombosis is less than 10% except for patients with malignancy or cirrhosis. Patients of all age groups may develop portal vein thrombosis. There is no racial predilection to portal vein thrombosis. Portal vein thrombosis affects men and women equally.
Risk Factors
Common risk factors in the development of portal vein thrombosis include cirrhosis, pancreatitis, duodenal ulcer, cholecystitis, Crohn’s disease, ulcerative colitis and cholecystectomy, diverticulitis and appendicitis . Less common risk factors in the development of portal vein thrombosis include oral contraceptives, pregnancy or puerperium, and hyperhomocysteinemia.