COVID-19-induced coagulopathy: Experience, achievements, prospects

Cardiol J. 2023;30(3):453-461. doi: 10.5603/CJ.a2022.0123. Epub 2023 Jan 2.

Abstract

The presence of coagulopathy as part of the systemic inflammatory response syndrome is a characteristic feature of severe coronavirus disease 2019 (COVID-19). Hematological changes (increased D-dimer [DD], prolonged activated partial thromboplastin clotting time [APTT] and prothrombin time [PT], high fibrinogen levels) have been observed in hospitalized patients with COVID-19, which characterize the risk of thrombotic events. Against the background of COVID-19 there is endothelial dysfunction, hypoxia and pulmonary congestion, mediated by thrombosis and microvascular occlusion. Up to 71.4% of patients who died from COVID-19 had disseminated intravascular coagulation syndrome, compared with only 0.6% of survivors. The main manifestation of COVID-19-associated coagulopathy is a significant increase in DD without a decrease in platelet count or prolongation of APTT and PT, indicating increased thrombin formation and the development of local fibrinolysis. An increase in DD levels of more than 3-4 times was associated with higher in-hospital mortality. Therefore, COVID-19 requires assessment of the severity of the disease for further tactics of thromboprophylaxis. The need for continued thromboprophylaxis, or therapeutic anticoagulation, in patients after inpatient treatment for two weeks using imaging techniques to assess of thrombosis assessment.

Keywords: COVID-19-induced coagulopathy; SARS-CoV-2; coronavirus disease 2019 (COVID-19) infection.

MeSH terms

  • Anticoagulants / therapeutic use
  • Blood Coagulation Disorders* / diagnosis
  • Blood Coagulation Disorders* / drug therapy
  • Blood Coagulation Disorders* / etiology
  • COVID-19* / complications
  • Humans
  • SARS-CoV-2
  • Thrombosis* / drug therapy
  • Venous Thromboembolism* / drug therapy
  • Venous Thromboembolism* / prevention & control

Substances

  • Anticoagulants