Background: The incidence of venous thromboembolism (VTE) in chronic liver disease (CLD) patients has been reported to be 0.5% to 6.3%. Studies report the use of thromboprophylaxis in CLD patients as suboptimal, with at least 75% of patients receiving no prophylaxis.
Objective: To describe the use of VTE prophylaxis in CLD patients.
Design: A retrospective review.
Setting: Tertiary-care academic medical center.
Patients: Inpatient admissions from August 2009 through July 2011 with CLD diagnosis.
Intervention: None.
Measurements: Initiation and type of thromboprophylaxis, incidence of VTE, bleeding events, hospital length of stay, in-hospital mortality, 30-day readmission for VTE.
Results: Of the 410 patients included, 225 (55%) patients received thromboprophylaxis. For patients with international normalized ratio (INR) >2.0, a significant decrease in overall thromboprophylaxis use and pharmacologic prophylaxis use was seen compared to those with INR 1.4 to 2.0 (P = 0.013 and P < 0.001, respectively). Overall incidence of VTE was 0.7%. Fifteen bleeding events occurred (3.7%): 9 on mechanical prophylaxis, 1 on pharmacologic, 3 on combination, and 2 with no prophylaxis. The majority of patients experiencing a bleeding event had an INR >2.0 (P = 0.001).
Conclusion: The use of thromboprophylaxis in CLD patients is higher in our study than previous reports but remains suboptimal. Use of VTE pharmacologic prophylaxis does not appear to increase bleeding in CLD patients with INR ≤2.0. Further studies are needed to provide additional safety data.
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http://dx.doi.org/10.1002/jhm.2086 | DOI Listing |
Hip Int
January 2025
Department of Orthopaedics and Traumatology, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
Background: A population-based study delineating the epidemiologic, clinical, and treatment characteristics of femoral neck fractures (FNFs) in elderly patients has not yet been conducted in Turkey. In this nationwide study, the epidemiologic, clinical, and treatment characteristics of patients aged ⩾65 years with FNFs who underwent osteosynthesis, hemiarthroplasty (HA), or total hip arthroplasty (THA) were examined.
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Ann Med
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Department of Internal Medicine, Hallym Medical Center, Hallym University College of Medicine, Chuncheon, Republic of Korea.
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View Article and Find Full Text PDFCells
January 2025
Department for Life Quality Studies, University of Bologna, Corso d'Augusto 237, 47921 Rimini, Italy.
Hepatocellular carcinoma (HCC) is a heterogeneous tumor associated with several risk factors, with non-alcoholic fatty liver disease (NAFLD) emerging as an important cause of liver tumorigenesis. Due to the obesity epidemics, the occurrence of NAFLD has significantly increased with nearly 30% prevalence worldwide. HCC often arises in the background of chronic liver disease (CLD), such as nonalcoholic steatohepatitis (NASH) and cirrhosis.
View Article and Find Full Text PDFAim And Background: This study aimed to evaluate the efficacy of silymarin in improving liver function and reducing liver stiffness in chronic liver disease (CLD) patients. Silymarin, a hepatoprotective agent, has shown potential benefits in non-alcoholic fatty liver disease (NAFLD) and liver fibrosis, but evidence in CLD with varied etiologies remains limited. This study addresses the gap by assessing its impact across diverse etiological subgroups.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Hepato-Neuro Laboratory, Centre Hospitalier de l'Université de Montréal (CRCHUM), Université de Montréal, 900, Rue Saint-Denis - Pavillon R, R08.422, Montréal (Québec), H2X 0A9, Canada.
Sarcopenia and hepatic encephalopathy (HE) are complications of chronic liver disease (CLD), which negatively impact clinical outcomes. Hyperammonemia is considered to be the central component in the pathogenesis of HE, however ammonia's toxic effects have also been shown to impinge on extracerebral organs including the muscle. Our aim was to investigate the effect of attenuating hyperammonemia with ornithine phenylacetate (OP) on muscle mass loss and associated molecular mechanisms in rats with CLD.
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