Current Overview on Hypercoagulability in COVID-19

Abstract

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has brought many unique pathologies, such as coagulopathy, prompting a desperate need for effective management. COVID-19-associated coagulopathy (CAC) can cause various thromboembolic complications, especially in critically ill patients. The pathogenesis is likely due to endothelial injury, immobilization, and an increase in circulating prothrombotic factors. Data on treatment are limited, although prophylactic anticoagulation is advised in all hospitalized patients. Herein, we have comprehensively reviewed the current literature available on CAC and highlight the pathogenesis, clinical features, and management of CAC.

Fig. 1

Pathogenesis of coagulopathy in COVID-19. Endothelial injury (endotheliitis) is caused by direct invasion of endothelial cells by the SARS-CoV-2 virus via ACE-2 receptors, release of inflammatory cytokines such as IL-6, acute-phase reactants, complement activation, and direct injury from intravascular catheters. Stasis is due to immobilization in all hospitalized patients. The hypercoagulable state is due to elevated circulating prothrombotic factors such as elevated vWF activity, factor VIII, D-dimer, fibrinogen, neutrophil extracellular traps, prothrombotic microparticles, and anionic phospholipids. TEG findings showed shortened R (increased early thrombin burst), shortened K (increased fibrin generation), increased MA (greater clot strength), and reduced LY30 (reduced fibrinolysis). ACE-2 angiotensin-converting enzyme 2, C4d complement 4d, C5b-9 complement 5b-9, COVID-19 coronavirus disease 2019, IL interleukin, K clot formation time, LY30 clot lysis at 30 min, MA maximum amplitude, MAC membrane attack complex, MASP2 mannose-binding protein-associated serine protease 2, R reaction time, SARS-CoV-2 severe acute respiratory syndrome coronavirus 2, TEG thromboelastography, vWF von Willebrand factor