Coagulopathy Does Not Protect Against Venous Thromboembolism in Hospitalized Patients With Chronic Liver Disease

Dabbagh, Ousama; Oza, Aabha; Prakash, Sumi; Sunna, Ramez; Saettele, Timothy

doi:10.1378/chest.09-2177

Cited by 171 publications

(146 citation statements)

References 9 publications

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“…Similarly, medical patients with liver insufficiency and alterations in laboratory coagulation values have been shown to have a higher incidence of thrombotic complications than the general hospital population, leading to the routine use of chemoprophylaxis in these patients. 17–21 In the current study, we noted that nearly one in seven patients who underwent an extended hepatectomy developed a VTE (Fig. 3).…”

Section: Discussionsupporting

confidence: 51%

Defining Incidence and Risk Factors of Venous Thromboemolism after Hepatectomy

Ejaz

Spolverato

Kim

et al. 2014

Journal of Gastrointestinal Surgery

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Background The incidence of venous thromboembolism (VTE) among patients undergoing hepatic surgery is poorly defined, leading to varied use of VTE prophylaxis among surgeons. We sought to define the incidence of VTE after liver surgery and identify risk factors associated with VTE. Methods Incidence of VTE and associated risk factors within 90 days of hepatic resection between 2006 and 2012 at a major academic center was analyzed. Risk factors for VTE were identified using univariate and multivariate analyses. Results A total of 599 patients were included in the study cohort; 30 (5.0 %) had a prior history of VTE. The indications for surgery were malignant (90.8 %) and benign lesions (9.2 %). The majority of patients underwent a minor hepatectomy (<3 Couinaud segments; n =402, 67.1 %) while 195 (32.6 %) patients underwent a major hepatectomy (≥3 Couinaud segments). Three hundred seven (51.3 %) patients were started on VTE chemoprophylaxis preoperatively with 407 (67.8 %) patients receiving VTE chemoprophylaxis within 24 h of surgery. Twenty-eight (4.7 %) patients developed VTE; 20 (3.3 %) had deep venous thrombosis (DVT), 11 (1.8 %) had pulmonary embolism (PE), and three (0.5 %) developed both DVTand PE. Among the VTE patients, 23 (82.1 %) had received VTE chemoprophylaxis. On multivariate analyses, history of VTE (odds ratio [OR] 4.51, 95 % confidence interval [CI] 1.81–17.22, P =0.03), prolonged operative time (OR 1.17 per additional hour, 95 % CI 1.04–1.32, P =0.009), and increased length of stay (LOS) (OR 1.07, 95 % CI 1.02–1.12, P =0.01) were independent risk factors for VTE. Conclusion VTE within 90 days of hepatic resection is common, occurring in nearly one in 20 patients. Most VTE events occurred among patients who received current best practice prophylaxis for VTE. More aggressive strategies to identify and reduce the risk of VTE in patients at highest risk of VTE, including those with a history of VTE, extended operative time, and prolonged LOS, are warranted.

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Section: Discussionsupporting

confidence: 51%

Defining Incidence and Risk Factors of Venous Thromboemolism after Hepatectomy

Ejaz

Spolverato

Kim

et al. 2014

Journal of Gastrointestinal Surgery

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“…5 A more recent study by Dabbagh et al stratifying the severity of coagulopathy in cirrhosis using INR quartiles of 1.4/1.7/2.2 did not demonstrate significant difference in VTE incidence. 8 These results are supported by the knowledge that despite impaired synthesis of clotting factors involved in the forward reactions of coagulation, liver synthetic impairment also leads to reduced generation of the natural inhibitors of these same reactions (e.g. proteins C, S and antithrombin).…”

Section: Predictors Of Vte In Cirrhosismentioning

confidence: 77%

“…The incidence of VTE in hospitalized patients with cirrhosis is estimated to be 0.5–1.9% but has been reported to be as high as 6.3%. 4–8 Hospitalized cirrhosis patients without predisposing co-morbidities (e.g. neoplasm, congestive heart disease and chronic renal failure) have similar risks for VTE as compared to patients without cirrhosis.…”

Section: Incidence Of Vte In Cirrhosismentioning

confidence: 99%

“…The prevalence of non-prophylaxis in hospitalized cirrhosis patients has been quoted to be as high as 75%. 8, 43 The efficacy of VTE prophylaxis in cirrhosis has been poorly characterized, but the previously introduced study by Northup et al (with 113 cases of VTE) reported that 7% and 14% of patients experienced VTE while receiving either anticoagulation or mechanical prophylaxis respectively. 4 The combination of the low incidence of VTE and the large proportion of patients with cirrhosis who do not receive pharmacologic prophylaxis in published studies have posed difficulties in evaluating the efficacy of VTE prophylaxis.…”

Section: Vte Prophylaxis / Treatment In Cirrhosismentioning

confidence: 99%

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Venous Thromboembolism in Cirrhosis

Yang

Costa

Novelli

et al. 2012

Clin Appl Thromb Hemost

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The cirrhosis population represents a unique subset of patients who are at risk for both bleeding and developing venous thrombotic embolic events (VTE). It has been commonly misunderstood that these patients are naturally protected from thrombosis by deficiencies in coagulation factors. As a result, the cirrhosis population is often falsely perceived to be ‘autoanticoagulated’. However, the concept of ‘autoanticoagulation’ conferring protection from thrombosis is a misnomer. While patients with cirrhosis may have a bleeding predisposition, not uncommonly they also experience thrombotic events. The concern for this increased bleeding risk often makes anticoagulation a difficult choice. Prophylactic and therapeutic management of VTE in patients with cirrhosis is a difficult clinical problem with the lack of clear established guidelines. The elucidation of laboratory and/or clinical predictors of VTE will be useful in this setting. This review serves to examine VTE, and the use of anticoagulation in the cirrhosis population.

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“…Prevalence of deep vein thrombosis and venous thromboembolism in patients with liver disease are reported to be lower [7] or not significantly different [8] or higher [9,10] than in a comparable population of hospitalized patients with non-hepatic conditions. A large-scale, population-based, case-control study involving almost 100,000 cases showed that liver diseases increased the relative risk of venous thromboembolism with a marked tendency to deep vein thrombosis rather than pulmonary embolism and affects both hospitalized and outpatients [11].…”

Section: Thrombotic Complications In Liver Diseasementioning

confidence: 99%

Coagulopathy in Liver Diseases: Complication or Therapy?

Bianchini¹,

Pietri

Villa³

2014

Dig Dis

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Coagulopathy in cirrhosis is a composite condition where liver synthetic deficit rebalances coagulation to a parallel reduction of both pro- and anticoagulant factors. Cirrhosis is therefore no longer considered a hypocoagulable state but rather a more unstable hemostatic balance with a lower threshold for tipping toward thrombosis or bleeding. Tendency to bleeding in cirrhosis is due to the reduction in the synthesis of procoagulants and a low platelet count as well as hyperfibrinolysis. Variceal hemorrhage is a frequent bleeding complication in decompensated cirrhosis. However, the possible contribution of coagulopathy as a precipitant or an aggravating factor is poorly documented and further data are required to clarify its real contributing role. Moreover, apart from the gastrointestinal tract, the occurrence of spontaneous and procedure-related bleeding elsewhere in the body, whilst not uncommon, is less than would be expected. By contrast, a large-scale population-based study has shown the propensity towards venous thrombosis in patients with liver diseases. Portal vein thrombosis (PVT) is a critical but frequent event occurring in up to 40% of patients with liver cirrhosis. PVT causes deterioration of the clinical course, the complications of portal hypertension and an increase in post-transplant mortality. The pathogenesis of PVT includes both local alterations, like blood flow reduction and endothelial activation, and systemic derangement. Systemic prohemostatic alterations include high von Willebrand factor, low ADAMTS-13, low levels of anticoagulants (antithrombin, proteins C and S) and increases in procoagulants like factor VIII. Low-molecular-weight heparin such as enoxaparin has proven to be safe and effective in both the treatment and prevention of PVT. In addition, patients in prophylaxis with enoxaparin showed a lower rate of decompensation and a better survival without bleeding complications. In such patients, circulating bacterial DNA, endotoxemia and markers of inflammation were attenuated compared to controls. These results therefore suggest a possible connection between enoxaparin, decrease of endotoxemia and reduction of portal hypertension. The approach to the coagulopathy in patients with liver diseases is changing: while the main goal for clinicians so far has been to reduce the risk of bleeding, the results of these new studies highlight the importance of preventing or treating thrombophilic disorders like PVT to avoid microcirculatory damage and eventually liver decompensation.

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Coagulopathy Does Not Protect Against Venous Thromboembolism in Hospitalized Patients With Chronic Liver Disease

Cited by 171 publications

References 9 publications

Defining Incidence and Risk Factors of Venous Thromboemolism after Hepatectomy

Defining Incidence and Risk Factors of Venous Thromboemolism after Hepatectomy

Venous Thromboembolism in Cirrhosis

Coagulopathy in Liver Diseases: Complication or Therapy?

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