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Paper reading: Portal vein thrombosis - New insight into aetiology and management Aliment Pharmacol Ther 2005; 21: 1-9 - A concise review The American Journal of Gastroenterology Vol. 97, No. 3, 2002. Ri è— å¡. Introduction.
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Paper reading:Portal vein thrombosis - New insight into aetiology and managementAliment Pharmacol Ther 2005; 21: 1-9- A concise review The American Journal of Gastroenterology Vol. 97, No. 3, 2002 Ri 藍 叡
Introduction • Portal vein thrombosis (PVT) is an cause of pre-hepatic portal hypertension • At time it is idiopathic, although several predisposing conditions are known to exist • The management of PVT has perceived risks of anticoagulant therapy
Aetiology • Voorhees et al. (1974), Webb et al. (1979): The majority of patients with PVT did not have underlying etiologies • Systemic thrombophilic factors • Inherited • Acquired • Local factors
Pathogenesis • Cirrhosis: • Portal blood flow • Liver synthetic activity of protein C, S and antithrombin III • High incidence of concomitant HCC • Cancer: • Tumor invasion • Compression or constriction effect from tumor mass • Prothrombogenic changes (cysteine protease)
Pocket Medicine the Massachusetts General Hospital Handbook of Internal Medicine, 2nd edition, 5-12
Multiple factors contributing to the development of venous thrombosis~ Rosendaal FR. Lancet 1999 • At least one mutated thrombophilic gene was detected in 69.5% of the cirrhotic patients with PVT (Amitrano et al. Hepatology 2000) • Infant with infection of the umbilical vein in the absence of prothrombotic disorders infrequently go on to develop PVT (Valla et al. J Hepatol 2000) • Blunt trauma and surgical procedures, generally, do not precipitate PVT unless there is an associated prothrombotic state. (Eguhi et al. Arch Surg 1991)
Clinical manifestations • No definitive time-frame distinguishes acute from chronic PVT (~ 60 days) • Acute PVT • Abdominal pain, N/V (Mesenteric veins involved) • Few clinical consequences : • Immediate vasodilation of the hepatic arterial system • Rapid development of tortuous collateral veins bypassing (cavernous transformation)
Chronic PVT • Portal hypertension • Hemorrhage of Gastroesophageal varices, splenomegaly, hypersplenism • Ascites, jaundice, hepatoencephalopathy • Outcome of the bleeding is far better than the patient with cirrhosis • 10-year-survival was 81% without cirrhosis, cancer or mesenteric vein thrombosis (Janssen et al. Gut 2001)
Investigation • Color doppler ultrasonography (CDUS) • Echogenic thrombus within portal vein lumen • Dilation proximal to the occlusion • Absence of an identifiable portal vein • Collateral vessels (cavernous transformation) • CT scan • Filling defect in contrast-enhanced lumen • Train track appearance when totally occluded • MR angiography • Portal venography • Endoscopic ultrasound
Management • Reverse or prevent the advancement of thrombosis • Treat the complications
Reverse or prevent the advancement of thrombosis • Acute/ recent-onset • Anticoagulation may result in recanalization in more than 80% of cases (Condat et al. Hepatology 2000) • High rates of recanalization with thrombolysis compared with consevative treatment (Malkowski et al. Hepatogastroenterology 2003) • Role of transjugular intrahepatic porto-systemic shunt (TIPSS) insertion • Anticoagulation fails • Endoscopic therapies are effective
Reverse or prevent the advancement of thrombosis • Chronic • the risk of thrombosis is currently as clinically significant as the risk of bleeding. The benefit-risk ratio favors anticoagulant therapy (Condat et al. Gastroenterology 2001) • Cohort study with 136 patients, 84 received anticoagulants, followed for median of 46 months.
Management • Reverse or prevent the advancement of thrombosis • Treat the complications • no studies about bleeding complications in patient with PVT • Primary prophylaxis: beta-blockade • Secondary prophylaxis: beta-blockade + endoscopic therapy
Take home message • Multiple risk factors are involved in the majority of cases • The prognosis from variceal bleeding in non-cirrhotic patients with PVT is good • In patients with acute PVT, the efficacy of thrombolytic therapy has been demonstrated • In patients with chronic PVT, risks of anticoagulation therapy may be overstated. Risk of thrombus extension, as mesenteric infarction is an important cause of death