Recent data has demonstrated that the pathophysiology of severe COVID-19 infection is associated with a significant pulmonary coagulopathy. Thrombotic complications have been reported in approximately 35-45% of patients with severe COVID-19. Entry of SARS-CoV-2 into the host cells leads to dysregulation in inflammatory signalling pathways, disrupting the normal coagulation mechanism. The hypercoagulability with abnormal clot formation is attributed to the inappropriately elevated immune response, culminating in a ‘cytokine storm’ with high levels of pro-inflammatory cytokines and subsequent thrombosis. The coagulopathy in COVID-19 affects many coagulation parameters such as D-dimer levels, fibrinogen levels, platelet count and prothrombin time. Coagulation parameters must be carefully monitored as they may indicate the requirement for clinical intervention. This suggests prophylactic anticoagulant treatment may be considered for COVID-19 patients with a predisposition to thrombosis. Current research indicates that immunomodulatory therapy may be beneficial to limit the propagation of the immune response. However, retrospective well-controlled studies are required to ensure that adverse effects do not outweigh therapeutic benefits. Despite the worldwide collaborative effort to elucidate COVID-19 pathophysiology, it is clear that further research and data analysis is required to uncover the immune mechanism causing the ‘cytokine storm’ in COVID-19 patients as well as therapeutic regimes to enable correct patient management and treatment of COVID-19 associated coagulopathies.
"Coagulopathy in COVID-19: A Review,"
International Undergraduate Journal of Health Sciences: Vol. 1:
1, Article 2.
Available at: https://sword.cit.ie/iujhs/vol1/iss1/2