TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy

An important component of severe COVID-19 disease is virus-induced endothelilitis. This leads to disruption of normal endothelial function, initiating a state of failing normal clotting physiology. Massively increased levels of von Willebrand Factor (VWF) lead to overwhelming platelet activation, as...

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Autores principales:	Gert Jacobus Laubscher, Petrus Johannes Lourens, Chantelle Venter, Douglas B Kell, Etheresia Pretorius
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	COVID-19 consumptive coagulopathy platelets blood clotting fibrinolysis von Willebrand factor Medicine R
Acceso en línea:	https://doaj.org/article/c61254e54a4541ca9ebaeba748245c52
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spelling	oai:doaj.org-article:c61254e54a4541ca9ebaeba748245c522021-11-25T18:02:16ZTEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy10.3390/jcm102253812077-0383https://doaj.org/article/c61254e54a4541ca9ebaeba748245c522021-11-01T00:00:00Zhttps://www.mdpi.com/2077-0383/10/22/5381https://doaj.org/toc/2077-0383An important component of severe COVID-19 disease is virus-induced endothelilitis. This leads to disruption of normal endothelial function, initiating a state of failing normal clotting physiology. Massively increased levels of von Willebrand Factor (VWF) lead to overwhelming platelet activation, as well as activation of the enzymatic (intrinsic) clotting pathway. In addition, there is an impaired fibrinolysis, caused by, amongst others, increased levels of alpha-(2) antiplasmin. The end result is hypercoagulation (proven by thromboelastography<sup>®</sup> (TEG<sup>®</sup>)) and reduced fibrinolysis, inevitably leading to a difficult-to-overcome hypercoagulated physiological state. Platelets in circulation also plays a significant role in clot formation, but they themselves may also drive hypercoagulation when they are overactivated due to the interactions of their receptors with the endothelium, immune cells or circulating inflammatory molecules. From the literature it is clear that the role of platelets in severely ill COVID-19 patients has been markedly underestimated or even ignored. We here highlight the value of early management of severe COVID-19 coagulopathy as guided by TEG<sup>®</sup>, microclot and platelet mapping. We also argue that the failure of clinical trials, where the efficacy of prophylactic versus therapeutic clexane (low molecular weight heparin (LMWH)) were not always successful, which may be because the significant role of platelet activation was not taken into account during the planning of the trial. We conclude that, because of the overwhelming alteration of clotting, the outcome of any trial evaluating an any single anticoagulant, including thrombolytic, would be negative. Here we suggest the use of the degree of platelet dysfunction and presence of microclots in circulation, together with TEG<sup>®</sup>, might be used as a guideline for disease severity. A multi-pronged approach, guided by TEG<sup>®</sup> and platelet mapping, would be required to maintain normal clotting physiology in severe COVID-19 disease.Gert Jacobus LaubscherPetrus Johannes LourensChantelle VenterDouglas B KellEtheresia PretoriusMDPI AGarticleCOVID-19consumptive coagulopathyplateletsblood clottingfibrinolysisvon Willebrand factorMedicineRENJournal of Clinical Medicine, Vol 10, Iss 5381, p 5381 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	COVID-19 consumptive coagulopathy platelets blood clotting fibrinolysis von Willebrand factor Medicine R
spellingShingle	COVID-19 consumptive coagulopathy platelets blood clotting fibrinolysis von Willebrand factor Medicine R Gert Jacobus Laubscher Petrus Johannes Lourens Chantelle Venter Douglas B Kell Etheresia Pretorius TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy
description	An important component of severe COVID-19 disease is virus-induced endothelilitis. This leads to disruption of normal endothelial function, initiating a state of failing normal clotting physiology. Massively increased levels of von Willebrand Factor (VWF) lead to overwhelming platelet activation, as well as activation of the enzymatic (intrinsic) clotting pathway. In addition, there is an impaired fibrinolysis, caused by, amongst others, increased levels of alpha-(2) antiplasmin. The end result is hypercoagulation (proven by thromboelastography<sup>®</sup> (TEG<sup>®</sup>)) and reduced fibrinolysis, inevitably leading to a difficult-to-overcome hypercoagulated physiological state. Platelets in circulation also plays a significant role in clot formation, but they themselves may also drive hypercoagulation when they are overactivated due to the interactions of their receptors with the endothelium, immune cells or circulating inflammatory molecules. From the literature it is clear that the role of platelets in severely ill COVID-19 patients has been markedly underestimated or even ignored. We here highlight the value of early management of severe COVID-19 coagulopathy as guided by TEG<sup>®</sup>, microclot and platelet mapping. We also argue that the failure of clinical trials, where the efficacy of prophylactic versus therapeutic clexane (low molecular weight heparin (LMWH)) were not always successful, which may be because the significant role of platelet activation was not taken into account during the planning of the trial. We conclude that, because of the overwhelming alteration of clotting, the outcome of any trial evaluating an any single anticoagulant, including thrombolytic, would be negative. Here we suggest the use of the degree of platelet dysfunction and presence of microclots in circulation, together with TEG<sup>®</sup>, might be used as a guideline for disease severity. A multi-pronged approach, guided by TEG<sup>®</sup> and platelet mapping, would be required to maintain normal clotting physiology in severe COVID-19 disease.
format	article
author	Gert Jacobus Laubscher Petrus Johannes Lourens Chantelle Venter Douglas B Kell Etheresia Pretorius
author_facet	Gert Jacobus Laubscher Petrus Johannes Lourens Chantelle Venter Douglas B Kell Etheresia Pretorius
author_sort	Gert Jacobus Laubscher
title	TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy
title_short	TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy
title_full	TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy
title_fullStr	TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy
title_full_unstemmed	TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy
title_sort	teg<sup>®</sup>, microclot and platelet mapping for guiding early management of severe covid-19 coagulopathy
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/c61254e54a4541ca9ebaeba748245c52
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TEG<sup>®</sup>, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy

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