The Impact of COVID-19 Disease on Platelets and Coagulation

Pathobiology. 2021;88(1):15-27. doi: 10.1159/000512007. Epub 2020 Oct 13.

Abstract

Coronavirus disease 2019 (COVID-19) causes a spectrum of disease; some patients develop a severe proinflammatory state which can be associated with a unique coagulopathy and procoagulant endothelial phenotype. Initially, COVID-19 infection produces a prominent elevation of fibrinogen and D-dimer/fibrin(ogen) degradation products. This is associated with systemic hypercoagulability and frequent venous thromboembolic events. The degree of D-dimer elevation positively correlates with mortality in COVID-19 patients. COVID-19 also leads to arterial thrombotic events (including strokes and ischemic limbs) as well as microvascular thrombotic disorders (as frequently documented at autopsy in the pulmonary vascular beds). COVID-19 patients often have mild thrombocytopenia and appear to have increased platelet consumption, together with a corresponding increase in platelet production. Disseminated intravascular coagulopathy (DIC) and severe bleeding events are uncommon in COVID-19 patients. Here, we review the current state of knowledge of COVID-19 and hemostasis.

Keywords: COVID-19; Coagulopathy; D-dimer; Thrombocytopenia; Thrombosis.

Publication types

  • Review

MeSH terms

  • Blood Coagulation Disorders / complications*
  • Blood Coagulation Disorders / etiology
  • Blood Coagulation Disorders / virology
  • Blood Platelets / virology*
  • COVID-19 / complications
  • COVID-19 / virology*
  • Fibrin Fibrinogen Degradation Products / metabolism
  • Humans
  • SARS-CoV-2 / pathogenicity*
  • Thrombosis / complications

Substances

  • Fibrin Fibrinogen Degradation Products
  • fibrin fragment D