Management of the thrombotic risk associated with COVID-19: guidance for the hemostasis laboratory
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REVIEW
Open Access
Management of the thrombotic risk associated with COVID-19: guidance for the hemostasis laboratory M. Hardy1,2, T. Lecompte3, J. Douxfils4,5, S. Lessire2, J. M. Dogné4, B. Chatelain1, S. Testa6, I. Gouin-Thibault7, Y. Gruel8, R. L. Medcalf9, H. ten Cate10, G. Lippi11 and F. Mullier1*
Abstract Coronavirus disease 2019 (COVID-19) is associated with extreme inflammatory response, disordered hemostasis and high thrombotic risk. A high incidence of thromboembolic events has been reported despite thromboprophylaxis, raising the question of a more effective anticoagulation. First-line hemostasis tests such as activated partial thromboplastin time, prothrombin time, fibrinogen and D-dimers are proposed for assessing thrombotic risk and monitoring hemostasis, but are vulnerable to many drawbacks affecting their reliability and clinical relevance. Specialized hemostasis-related tests (soluble fibrin complexes, tests assessing fibrinolytic capacity, viscoelastic tests, thrombin generation) may have an interest to assess the thrombotic risk associated with COVID-19. Another challenge for the hemostasis laboratory is the monitoring of heparin treatment, especially unfractionated heparin in the setting of an extreme inflammatory response. This review aimed at evaluating the role of hemostasis tests in the management of COVID-19 and discussing their main limitations. Keywords: Thrombosis, D-dimers, Anticoagulation, COVID-19, Coagulopathy, Hemostasis, Fibrinolysis, Heparin, Thrombin generation, Viscoelastic tests
Introduction Since the beginning of the coronavirus infectious disease 2019 (COVID-19) pandemic in December 2019, increasing data have supported a major thrombotic risk, which could explain a substantial part of morbidity and mortality associated with this infection. The first observations in China reported a marked increase in plasma Ddimers, associated with unfavorable prognosis and enhanced thrombotic risk [1, 2]. A recent meta-analysis demonstrated an association between several inflammatory biomarkers (such as C-reactive protein (CRP), procalcitonin, interleukin (IL-6) and ferritin) with COVID-19 severity [3]. There is a cross-talk between * Correspondence: [email protected] 1 Université catholique de Louvain, CHU UCL Namur, Namur Thrombosis and Hemostasis Center (NTHC), Hematology Laboratory, Yvoir, Belgium Full list of author information is available at the end of the article
inflammation and coagulation as inflammation leads to coagulation activation, and coagulation also affects inflammatory activity [4, 5]. Although heparin at prophylactic doses appears to be effective in reducing mortality in severe COVID-19 patients [6], several studies reported a considerably high incidence of venous and even arterial thromboembolic events (deep vein thrombosis, pulmonary embolism or in situ thrombosis in the pulmonary arteries; arterial thromboses in the systemic circulation) despite thromboprophylaxis, thus raising the issue of increasing anticoagulant doses [7–14]. This approach has been sug
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