Coagulopathies, Prothrombotic State, Thromboembolism, Bleeding, and COVID-19

Abstract

COVID-19 is known to trigger a prothrombotic state, causing thromboses and thromboembolic events (TTEE) in patients with COVID-19. Both bleeding and thrombosis can result in significant morbidity in COVID-19. The entity paves the way to arterial TTEE (i.e., stroke and/or extremity ischemia) as well as small vessel thrombosis, which are commonly recorded at autopsy in the pulmonary vasculature. Elevated D-dimer is associated with a higher risk for TTEE, hemorrhage, critical illness, and mortality. Likewise, levels of fibrinogen, ferritin, procalcitonin are also higher in patients with thrombosis. There is also a propensity to develop pulmonary thromboembolism (PTE) in cases with COVID-19. Treatment with anticoagulant prophylaxis (i.e., heparin and/or aspirin) is recommended in many researches, but robust evidence is still warranted to draw firm conclusions on the benefit-to-harm ratio of the agents in most patients.

Keywords: Anticoagulant prophylaxis, Cardiovascular disease, Coagulopathy, COVID-19, D-dimer, Thromboembolic events, Thrombosis.

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