COAGULOPATHY AND COVID-19: A REVIEW FOR MEDICAL PRACTICE.

In December 2019, an outbreak of a new coronavirus disease (formally known as COVID-19) was first reported in Wuhan, China, and soon spread around the world. On March 11, 2020, COVID-19 was declared as a pandemic by the World Health Organization (WHO). So far, COVID-19 has proven to be a disease with multiorgan involvement, affecting the hematological system as well. Patients with COVID-19, especially those with moderate to severe disease, frequently experience a coagulopathy associated with a high incidence of thrombotic events, which leads to poor outcomes. The pathogenesis of COVID-associated coagulopathy (CAC), is not fully understood yet, although the host inflammatory response to the infection appears to be a crucial element in the development of CAC. IL2, IL-6, IL7, G-CSF, PI10, MIP1, and TNF alpha, among other molecules, act as proinflammatory cytokines that stimulate endothelium damage and alter the coagulation homeostasis. CAC usually manifests as venous thromboembolisms (VTE). While bleeding can also occur, it is a rare form of presentation. Inpatients with COVID-19 must receive thromboprophylaxis, mainly with low-molecular-weight heparin (LMWH); unfractioned heparin can be accepted under certain circumstances. Patients with a diagnosis or high suspicion of VTE should receive the complete doses of anticoagulation treatment and must continue on it for at least three months. Recommendations regarding prophylaxis and treatment may vary among institutions and countries. There is not clear evidence for the regular use of antiplatelet therapy in patients with COVID-19. This review will provide key insights regarding the pathophysiology, clinical manifestations, diagnosis and treatment of COVID-19 and its associated coagulopathy.