Abstract

The portal vein is formed by the confluence of the splenic and superior mesenteric veins. Portal vein thrombosis (PVT) is caused by the formation of a blood clot within the extra-hepatic portion of the portal vein. Occlusion of the portal vein by thrombus typically occurs in patients with cirrhosis and/or prothrombotic disorders including hepatocellular carcinoma, myeloproliferative disorder, inherited thrombophilia and abdominal trauma [1]. Chronic portal vein thrombosis (PVT) may have a myriad of presentations including worsening clinical symptoms of portal hypertension i.e. ascites, gastroesophageal variceal bleeding or even completely asymptomatic, detected in routine abdominal imaging [1]. The management of portal vein thrombosis (PVT) includes differentiating acute from chronic, cirrhotic from non-cirrhotic causes, considering risk of variceal bleeding from anticoagulation, risk of bowel ischemia from clot extension and possibility of liver transplant [2].

Highlights

  • Portal Vein Thrombosis in Cirrhotic Patients: Decision to Anticoagulate

  • A recent study on 56 chronic portal vein thrombosis (PVT) patients (35 received anticoagulation and 21 control), 36% recanalization rate was achieved with low molecular weight heparin for at least 6 months in the treatment group, compared with 5% in control group

  • Anticoagulation in PVT cases may be started with LMWH, followed by coumadin therapy for 3-6 months [4,6]

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Summary

Introduction

Portal Vein Thrombosis in Cirrhotic Patients: Decision to Anticoagulate *Corresponding author: Raktim Kumar Ghosh, Department of Internal Medicine, St. Vincent Charity Medical Center, An Affiliate of Case Western Reserve University, Cleveland, OH, USA, Tel: 216-363-2725; E-mail: raktimghoshmd@gmail.com Occlusion of the portal vein by thrombus typically occurs in patients with cirrhosis and/or prothrombotic disorders including hepatocellular carcinoma, myeloproliferative disorder, inherited thrombophilia and abdominal trauma [1]. Chronic portal vein thrombosis (PVT) may have a myriad of presentations including worsening clinical symptoms of portal hypertension i.e. ascites, gastroesophageal variceal bleeding or even completely asymptomatic, detected in routine abdominal imaging [1].

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