COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation

The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other fact...

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Main Authors: Wolfgang Miesbach MD, Michael Makris MD
Format: Article
Language:English
Published: SAGE Publishing 2020-07-01
Series:Clinical and Applied Thrombosis/Hemostasis
Online Access:https://doi.org/10.1177/1076029620938149
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author Wolfgang Miesbach MD
Michael Makris MD
author_facet Wolfgang Miesbach MD
Michael Makris MD
author_sort Wolfgang Miesbach MD
collection DOAJ
description The novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d -dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d -dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.
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spelling doaj.art-9bf5648031f84ec3b3d736f49bfb0e5d2022-12-21T18:14:05ZengSAGE PublishingClinical and Applied Thrombosis/Hemostasis1938-27232020-07-012610.1177/1076029620938149COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for AnticoagulationWolfgang Miesbach MD0Michael Makris MD1 Department of Haemostaseology and Hemophilia Center, Medical Clinic 2, Institute of Transfusion Medicine, University Hospital Frankfurt, Germany Sheffield Haemophilia and Thrombosis Centre, Royal Hallamshire Hospital, Sheffield, United KingdomThe novel coronavirus infection (COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as adult respiratory syndrome, sepsis, coagulopathy, and death in a proportion of patients. Among other factors and direct viral effects, the increase in the vasoconstrictor angiotensin II, the decrease in the vasodilator angiotensin, and the sepsis-induced release of cytokines can trigger a coagulopathy in COVID-19. A coagulopathy has been reported in up to 50% of patients with severe COVID-19 manifestations. An increase in d -dimer is the most significant change in coagulation parameters in severe COVID-19 patients, and progressively increasing values can be used as a prognostic parameter indicating a worse outcome. Limited data suggest a high incidence of deep vein thrombosis and pulmonary embolism in up to 40% of patients, despite the use of a standard dose of low-molecular-weight heparin (LMWH) in most cases. In addition, pulmonary microvascular thrombosis has been reported and may play a role in progressive lung failure. Prophylactic LMWH has been recommended by the International Society on Thrombosis and Haemostasis (ISTH) and the American Society of Hematology (ASH), but the best effective dosage is uncertain. Adapted to the individual risk of thrombosis and the d -dimer value, higher doses can be considered, especially since bleeding events in COVID-19 are rare. Besides the anticoagulant effect of LMWH, nonanticoagulant properties such as the reduction in interleukin 6 release have been shown to improve the complex picture of coagulopathy in patients with COVID-19.https://doi.org/10.1177/1076029620938149
spellingShingle Wolfgang Miesbach MD
Michael Makris MD
COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation
Clinical and Applied Thrombosis/Hemostasis
title COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation
title_full COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation
title_fullStr COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation
title_full_unstemmed COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation
title_short COVID-19: Coagulopathy, Risk of Thrombosis, and the Rationale for Anticoagulation
title_sort covid 19 coagulopathy risk of thrombosis and the rationale for anticoagulation
url https://doi.org/10.1177/1076029620938149
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