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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 藍 叡. Introduction.

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Ri

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

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

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

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

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

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

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)


Ri

  • 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

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

Management

  • Reverse or prevent the advancement of thrombosis

  • Treat the complications


Reverse or prevent the advancement of thrombosis

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 thrombosis1

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.


Management1

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

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


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