Low‐molecular‐weight heparin in patients with advanced cirrhosis

Bechmann, Lars P.; Sichau, Matthias; Wichert, Marc; Gerken, Guido; Kröger, Knut; Hilgard, Philip

doi:10.1111/j.1478-3231.2010.02358.x

Cited by 125 publications

(128 citation statements)

References 32 publications

(38 reference statements)

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“…Enoxaparin appeared to delay the occurrence of hepatic decompensation and improve survival. However, an increased volume of distribution, such as that produced by ascites and edema, in patients with cirrhosis makes it difficult to determine the optimal dose of LMWH [82] . The administration of antithrombin Ⅲ (AT-Ⅲ) could be an attractive alternative to PVT in cirrhosis.…”

Section: Treatmentmentioning

confidence: 99%

Portal vein thrombosis in liver cirrhosis

Kinjo¹,

Kawanaka²,

Akahoshi³

et al. 2014

WJH

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Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis. However, unlike PVT in patients without cirrhosis, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions, such as gastroesophageal bleeding and acute intestinal ischemia. Moreover, no consensus regarding PVT in cirrhosis exists. Suggested causes of PVT in cirrhosis include reduced portal blood flow velocity, multiple congenital or acquired thrombophilic factors, inherited or acquired conditions, and derangement of liver architecture. However, the understanding of PVT in cirrhosis is incomplete. In addition, information on the management of PVT in cirrhosis is inadequate. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Portal vein thrombosis; Liver cirrhosis; Thrombophilic factors; Anticoagulation; Splenectomy Core tip: Portal vein thrombosis (PVT) is considered to be a frequent complication of liver cirrhosis; however, very few data are available on the natural history and management of PVT in cirrhosis, despite its association with potentially life-threatening conditions. The understanding and information on the management of PVT in cirrhosis are incomplete. The aims of this review are to: (1) assemble data on the physiopathological mechanism, clinical findings, diagnosis and management of PVT in cirrhosis; (2) describe the principal factors most frequently involved in PVT development; and (3) summarize the recent knowledge concerning diagnostic and therapeutic procedures.

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Section: Treatmentmentioning

confidence: 99%

Portal vein thrombosis in liver cirrhosis

Kinjo¹,

Kawanaka²,

Akahoshi³

et al. 2014

WJH

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“…Cirrhotic individuals often have an increased volume of distribution because of fluid overload and this makes it difficult to determine the optimal dose of LMWH. 61 LMWH is eliminated by the kidneys and since many patients with cirrhosis have renal insufficiency, the half-life of LMWH is increased. 61 Monitoring of anti-Xa activity to guide therapy is unreliable in cirrhosis.…”

Section: Choice Of Anticoagulationmentioning

confidence: 99%

“…61 LMWH is eliminated by the kidneys and since many patients with cirrhosis have renal insufficiency, the half-life of LMWH is increased. 61 Monitoring of anti-Xa activity to guide therapy is unreliable in cirrhosis. 59,61,62 The primary problem with VKA is determination of adequate anticoagulation in patient with cirrhosis who already have altered coagulation and abnormal prothrombin time.…”

Section: Choice Of Anticoagulationmentioning

confidence: 99%

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Portal Vein Thrombosis in Cirrhosis

Raja

Jacob

Asthana

2014

Journal of Clinical and Experimental Hepatology

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Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10-25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33-45% and 15-35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term. ( J CLIN EXP HEPATOL 2013;4:320-331)

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“…There is a potential risk of further lowering of protein C and they are associated with extensive drug interactions. [22][23][24][25] The aims of anticoagulation are to achieve recanalization of the portal vein and to prevent extension of the thrombus to the splenic and superior mesenteric vein. A recanalized portal vein allows a conventional end-to-end portal venous anastomosis without adding to the complexity of orthotopic liver transplantation (OLT).…”

Section: Correct Answers: C and Ementioning

confidence: 99%