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Ri 藍 叡

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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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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)
slide9
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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