Vascular disorders of the liver # †

DeLeve, Laurie D.; Valla, Dominique; García–Tsao, Guadalupe

doi:10.1002/hep.22772

Cited by 847 publications

(813 citation statements)

References 336 publications

(508 reference statements)

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“…28 While in non-cirrhotic patients, PVT is related to prothrombotic states (myeloproliferative diseases and/or inherited coagulation disorders) in a significant percentage of patients, in cirrhotic patients portal hemodynamics also plays an important role in the development of PVT. 29 Portal flow is reduced in cirrhotic livers due to increased intrahepatic vascular resistance and this phenomenon is further pronounced as liver disease progresses. 30,31 This may be another reason to explain the increased prevalence of PVT in advanced cirrhotics as compared to early cirrhotics with well compensated disease.…”

Section: Pathophysiologymentioning

confidence: 99%

“…8,12,33 Apart from gene mutations, it is actually difficult to detect underlying prothrombotic condition in these patients due to the non-specific decrease in both coagulation factors and inhibitors. 29 Among other factors that may increase the risk of PVT is endotoxemia. 34 Endotoxemia is common with worsening liver disease when PVT is also more common.…”

Section: Pathophysiologymentioning

confidence: 99%

“…29,63 The impact of PVT on the natural history of cirrhosis is still a matter of great debate and the clinical benefits of PV recanalization have been very well demonstrated. 60 Despite this, there is evidence that cirrhotic individuals with PVT on the waiting list for liver transplantation should be treated with anticoagulation therapy.…”

Section: Selection Of Patients For Anticoagulationmentioning

confidence: 99%

“…62 Other logical situations where anticoagulation is expected to be beneficial are cirrhotic patients with acute PVT with extension to the superior mesenteric vein. 29,63 However these situations are quite rare. Cirrhotic patients with documented to have a well characterized prothrombotic disorder (viz.…”

Section: Selection Of Patients For Anticoagulationmentioning

confidence: 99%

“…There has been a high incidence of major bleeding also. 29,72 There is no data to support this option in this setting.…”

Section: Tips and Thrombolysismentioning

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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Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

Section: Selection Of Patients For Anticoagulationmentioning

confidence: 99%

Section: Selection Of Patients For Anticoagulationmentioning

confidence: 99%

“…There has been a high incidence of major bleeding also. 29,72 There is no data to support this option in this setting.…”

Section: Tips and Thrombolysismentioning

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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Long-term Clinical Outcomes of Splanchnic Vein Thrombosis

et al. 2015

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IMPORTANCE Little information is available on the long-term clinical outcome of patients with splanchnic vein thrombosis (SVT).OBJECTIVE To assess the incidence rates of bleeding, thrombotic events, and mortality in a large international cohort of patients with SVT. DESIGN, SETTING, AND PARTICIPANTSA prospective cohort study was conducted beginning May 2, 2008, and completed January 30, 2014, at hospital-based centers specialized in the management of thromboembolic disorders; a 2-year follow-up period was completed January 30, 2014, and data analysis was conducted from July 1, 2014, to February 28, 2015. Participants included 604 consecutive patients with objectively diagnosed SVT; there were no exclusion critieria. Information was gathered on baseline characteristics, risk factors, and antithrombotic treatment. Clinical outcomes during the follow-up period were documented and reviewed by a central adjudication committee. MAIN OUTCOMES AND MEASURESMajor bleeding, defined according to the International Society on Thrombosis and Hemostasis; bleeding requiring hospitalization; thrombotic events, including venous and arterial thrombosis; and all-cause mortality. RESULTSOf the 604 patients (median age, 54 years; 62.6% males), 21 (3.5%) did not complete follow-up. The most common risk factors for SVT were liver cirrhosis (167 of 600 patients [27.8%]) and solid cancer (136 of 600 [22.7%]); the most common sites of thrombosis were the portal vein (465 of 604 [77.0%]) and the mesenteric veins (266 of 604 [44.0%]). Anticoagulation was administered to 465 patients in the entire cohort (77.0%) with a mean duration of 13.9 months; 175 of the anticoagulant group (37.6%) received parenteral treatment only, and 290 patients (62.4%) were receiving vitamin K antagonists. The incidence rates (reported with 95% CIs) were 3.8 per 100 patient-years (2.7-5.2) for major bleeding, 7.3 per 100 patient-years (5.8-9.3) for thrombotic events, and 10.3 per 100 patient-years (8.5-12.5) for all-cause mortality. During anticoagulant treatment, these rates were 3.9 per 100 patient-years (2.6-6.0) for major bleeding and 5.6 per 100 patient-years (3.9-8.0) for thrombotic events. After treatment discontinuation, rates were 1.0 per 100 patient-years (0.3-4.2) and 10.5 per 100 patient-years (6.8-16.3), respectively. The highest rates of major bleeding and thrombotic events during the whole study period were observed in patients with cirrhosis (10.0 per 100 patient-years [6.6-15.1] and 11.3 per 100 patient-years [7.7-16.8], respectively); the lowest rates were in patients with SVT secondary to transient risk factors (0.5 per 100 patient-years [0.1-3.7] and 3.2 per 100 patient-years [1.4-7.0], respectively). CONCLUSIONS AND RELEVANCEMost patients with SVT have a substantial long-term risk of thrombotic events. In patients with cirrhosis, this risk must be balanced against a similarly high risk of major bleeding. Anticoagulant treatment appears to be safe and effective in most patients with SVT.

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