Portal hypertension due to portal venous thrombosis: Etiology, clinical outcomes

Harmancı, Özgür; Bayraktar, Yusuf

doi:10.3748/wjg.v13.i18.2535

Cited by 55 publications

(57 citation statements)

References 43 publications

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“…173 Liver transplantation in PVT however has been associated with an increased operative time, transfusion requirements, reintervention and lower survival rate depending on PVT extension. 174 Surgical techniques like thrombectomy, thromboendovenectomy with venous reconstitution, interposition of vein graft, portocaval liver transposition have all been done including radiological endovascular interventions to overcome venous obstruction in the recipient. 175 The most frequent technique employed is thrombectomy/thromboendovenectomy with end to end donorrecipient portal anastomosis (75%).…”

Section: Liver Transplant (Lt) In Portal Vein Thrombosismentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion. ( J CLIN EXP HEPATOL 2015;5:22-40)

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Section: Liver Transplant (Lt) In Portal Vein Thrombosismentioning

confidence: 99%

Portal Vein Thrombosis

Chawla

Bodh

2015

Journal of Clinical and Experimental Hepatology

151

147

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“…Treatment options for ET include aspirin (or an equivalent therapy) and cytoreductive therapy to control the platelet count such as hydroxyurea, anagrelide and interferon, however, there is still a lot of controversy regarding the role of anticoagulation in patients with chronic PVT. The management of bleeding varices due to MPD is not different from cirrhotic or cancer patients, but the prognosis is unquestionably better in the former cases [8] . It seems that the mortality rate from variceal bleeding in patients without liver disease is primarily related to underlying diseases other than bleeding itself [9] .…”

Section: Discussionmentioning

confidence: 98%

A latent form of essential thrombocythemia presenting asportal cavernoma

Cai¹,

Zhou²,

Hong³

et al. 2009

WJG

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Essential thrombocythemia is frequently associated with abdominal thrombotic complications including portal cavernoma as a consequence of chronic portal vein thrombosis. Essential thrombocythemia in a latent form is difficult to identify at onset due to the absence of an overt disease phenotype. In the presented case report, the diagnosis of essential thrombocythemia was initially missed because the typical disease phenotype was masked by bleeding and hypersplenism. The correct diagnosis was only reached when the patient experienced persistent thrombocytosis and pseudohyperkalemia after a shunt operation.

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“…Gradual loss of hepatic mass because of chronically decreased blood flow is considered responsible for the ultimate functional decompensation that occurs in non-cirrhotic patients with portal vein thrombosis. 28 …”

Section: Discussionmentioning

confidence: 99%

Hepatic arterial buffer response: pathologic evidence in non-cirrhotic human liver with extrahepatic portal vein thrombosis

et al. 2016

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Increase in hepatic arterial flow in response to reduced portal flow (hepatic arterial buffer response) has been demonstrated experimentally and surgically. We provide pathologic evidence for hepatic arterial buffer response in non-cirrhotic patients with extrahepatic portal vein thrombosis and elucidate the histopathologic spectrum of non-cirrhotic portal vein thrombosis. Liver biopsies and resections from non-cirrhotic patients with extra-hepatic portal vein thrombosis were retrieved. Morphologic features, extent of CD34 staining, outer diameters, luminal diameters and wall thickness of hepatic arteries cut in cross-section and outer diameters of cross-sectioned paired bile ducts were compared with age-and gender-matched controls. There were 12 male and 9 female patients. Measurements of 280 and 193 arteries from patients and controls, respectively, demonstrated statistically significant (Po 0.05) arterial dilatation (increase in percentage of arterial lumen to outer diameter) and arterial wall thinning in resection specimens of non-cirrhotic patients with extra-hepatic portal vein thrombosis. Subtle and/or focal dilatation of central veins, portal veins and sinusoids; focal trabecular thinning/ thickening and mild ductular reaction were common findings in both the patient and control groups. Diffuse and obvious changes, and portal vein absence or attenuation were seen only in the patient group. Capillarization of sinusoids was not seen on CD34 stain. Two patients showed significant ductular reaction, one of who developed biliary strictures on follow-up. Hepatic arterial dilatation and wall thinning in non-cirrhotic patients with portal vein thrombosis provide pathologic evidence of hepatic arterial buffer response in the human liver. Obvious and diffuse sinusoidal dilatation and absence or attenuation of portal veins are highly suggestive of extrahepatic portal vein thrombosis in non-cirrhotic patients with portal hypertension. Periportal shunt vessels, hypervascular portal tracts, muscularized portal veins, large thick-walled or dilated arteries aid diagnosis but are rare findings. Normal or near-normal biopsies do not rule out portal vein thrombosis.

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Portal hypertension due to portal venous thrombosis: Etiology, clinical outcomes

Cited by 55 publications

References 43 publications

Portal Vein Thrombosis

Portal Vein Thrombosis

A latent form of essential thrombocythemia presenting asportal cavernoma

Hepatic arterial buffer response: pathologic evidence in non-cirrhotic human liver with extrahepatic portal vein thrombosis

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