Coagulopathy in severe COVID-19 patients: causes, concerns and current treatment regimen

Abstract

Elevated D-dimer and fibrinogen level, mild thrombocytopenia, modest prolongation of prothrombin time, and activated partial thromboplastin time, are key indicators of coagulopathy, and have been consistently reported in severely ill COVID-19 patients. Coronavirus disease 2019 (COVID-19)-induced coagulopathy can develop serious venous and arterial thromboembolic complications. Endothelial dysfunction and hypercoagulability, triggered mostly by overproduction of inflammatory cytokines as an immune response to the infection, are the pivotal factors responsible for the above-mentioned coagulation disorder. Thus, low-molecular-weight heparin (LMWH), which has both anticoagulant and anti-inflammatory properties, has been reported to improve disease prognosis. However, there have been increasing reports of venous thromboembolic events for intensive care unit patients suffering from COVID-19 despite the use of prophylactic doses of LMWH. Alternative clinical approaches involve the use of other antithrombotic agents, antiplatelet therapy, tissue plasminogen activator, and non-pharmacological tools. Ample cohort studies and clinical trials are needed to justify all these approaches of treatment. Finally, the discovery of several COVID-19 vaccines has reduced fatality from the disease enormously. However, prudent clinical practice still requires a circumspect response in order to deal with any potentially deleterious effects of coagulopathy.