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Introduction: The liver has many haemostatic functions, including the synthesis of most coagulation factors and inhibitors as well as fibrinolytic factors . The balance between procoagulant and anticoagulant factors is essential to avoid excessive thrombin generation under physiological conditions. Therefore, advanced liver disease results in a complex pattern of defects in haemostatic functions in the form of reduced synthesis of coagulation factors, inhibitors, and abnormal clotting factors, abnormalities of fibrinolytic activity, disseminated intravascular coagulation and platelet function defects. Development of portal vein thrombosis (PVT) is asignificant milestone in the natural history of cirrhosis. It is associated with worsening liver function, ascites, and the occurrence of gastroesophageal variceal bleeding. It is clear that PVT increases morbidity and mortality associated with liver transplant and may even contraindicate it and. Thus, taken together, these data suggest that PVT is a major index of poor prognosis in patients with cirrhosis. Although spontaneous resolution of PVT has been reported in the literature specific therapeutic management is mandatory to resolve portal vein obstruction and avoid serious complications. The goal of treatment is similar correction of causal factors, prevention of thrombosis extension, and achievement of portal vein patency Objective: the aim of the work was to clarify the risk factors , clinical presentation and complications of portal vein thrombosis in patients with liver cirrhosis and to study the out come after short term follow up. Subject and methods :- A total number of 80 patients with cirrhosis were included and were classified into two main groups. Group I ( 50 ) cirrhotic patients with portal vein thrombosis. Group II ( 30 ) cirrhotic patients without portal vein thrombosis. Each group was divided in two sub groups A and B a ccording to prescence or absence of HCC respectively.The 2 groups were compared as regard risk factors and clinical presentation and out come. Result: PVT developed as result of combination of both local and systemic risk factors. HCC and abdominal infection specially spontaneous bacterial peritonitis and intervention to the portal system ,were the most important local risk factors . Protein C and S defficincy were amog systemic risk factors. Most of cases were asymptomatic and accidentally discovered , other patients presented with upper GIT bleeding or other complications of liver cell failure .Anticoagulant administration was associated with increased incidence of partial or complete recanalization without increased risk of bleeding. Conclusion and Recommendations:- Portal vein thrombosis occurs mostly in a cirrhotic patient with advanced liver disease. Patients with advanced liver cirrhosis and not so prolonged coagulation parameters might be at particular risk of developing PVT. So regular monitoring using Doppler-ultrasound should be carried out in these patients. Development of varices is a time dependent phenomenon, so it is advisable to screen all PVT patients endoscopically.Early administration of anticoagulation was associated with increased incidence of partial or complete recanalization. Keywords :Portal vein ,Thrombosis, risk factors, cirrhosis |
