PORTAL VEIN THROMBOSIS – A STUDY OF RISK FACTORS, CLINICAL PROFILE, COMPLICATIONS AND MANAGEMENT

Background: The portal vein is formed by the conuence of the splenic and superior mesenteric veins. Occlusion of the portal vein by thrombus (portal vein thrombosis [PVT]) typically occurs in patients with cirrhosis and/or prothrombotic disorders/ pancreatitis. Patients with acute PVT have the sudden onset of portal venous occlusion due to thrombus. Patients with acute PVT have not yet developed features of chronic PVT, such as collateral circulation (e.g., cavernous portal transformation) or portal hypertension. Chronic PVT develops when acute doesn't resolve with formation of collaterals. In patients with suspected acute PVT, we typically obtain a contrast-enhanced abdominal computed tomography (CECT) to conrm the diagnosis, evaluate for predisposing conditions (eg, intra-abdominal infection), assess the extent of the thrombosis and the anatomy of collaterals, and detect evidence of intestinal infarction. Doppler and MRI are other alternative imaging modalities. The primary management of acute portal vein thrombosis (PVT) is anticoagulation and, when possible, treatment of predisposing condition. The goal of anticoagulation is to prevent extension of the clot and to allow for recanalization, so that intestinal infarction and portal hypertension do not develop. Unlike chronic PVT, where the role of anticoagulation in patients with cirrhosis is unclear, studies suggest anticoagulation for acute PVT is benecial for patients with cirrhosis. However, because patients with cirrhosis may have esophageal varices, we typically screen for varices prior to initiating anticoagulation. 60 cases of extrahepatic portal vein thrombosis or intrahepatic Methods: portal vein thrombosis were included. All registered diagnoses were based on either ultrasound with Doppler, CT-angiography or MRI. In our study, Ris Results: k factors were established in 24 cases (80%). When including all risk factors, 16 cases (53.3%) had local risk factor, and 8 cases (26.6%) had a systemic risk factor. Anatomical location was in 26 cases (86%)extrahepatic, (14%) intrahepatic. In addition, patients with extrahepatic PVT also had intrahepatic thrombosis (38%) and/or in the splenic vein (23%). 66% had oesophageal varices, 53% gastric varices, 46% portal hypertensive gastropathy, 26% variceal haemorrhage, and 40% ascites. Most patients had a combination of local and systemic risk Conclusion: factors for PVT. Partial/ complete recanalization is more in patients treated with anticoagulation therapy, and that regression of varices was more in patients who were treated with active endoscopy combined with beta blockers.