COVID-19 and Hypercoagulability: A Review. Clin Appl Thromb Hemost 2020;26:1076029620962853
Date
10/20/2020Pubmed ID
33074732Pubmed Central ID
PMC7592310DOI
10.1177/1076029620962853Scopus ID
2-s2.0-85092940768 (requires institutional sign-in at Scopus site) 114 CitationsAbstract
Thrombotic complications of the novel coronavirus (COVID-19) are a concerning aspect of the disease, due to the high incidence in critically ill patients and poor clinical outcomes. COVID-19 predisposes patients to a hypercoagulable state, however, the pathophysiology behind the thrombotic complications seen in this disease is not well understood. Several mechanisms have been proposed and the pathogenesis likely involves a host immune response contributing to vascular endothelial cell injury, inflammation, activation of the coagulation cascade via tissue factor expression, and shutdown of fibrinolysis. Treatments targeting these pathways may need to be considered to improve clinical outcomes and decrease overall mortality due to thrombotic complications. In this review, we will discuss the proposed pathophysiologic mechanisms for thrombotic complications in COVID-19, as well as treatment strategies for these complications based on the current literature available.
Author List
Kichloo A, Dettloff K, Aljadah M, Albosta M, Jamal S, Singh J, Wani F, Kumar A, Vallabhaneni S, Khan MZAuthor
Michael M. Aljadah MD Instructor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
BetacoronavirusBlood Coagulation
Coronavirus Infections
Global Health
Humans
Incidence
Pandemics
Pneumonia, Viral
Thrombophilia
