Introduction Covid -19 has become the latest pandemic that humanity had and still is facing. Due to unknown mechanisms and unorthodox course of illness, COVID-19 infected patients present with various unprecedented complications. Coagulopathies are of the most feared as they carry a high mortality rate. Most of the published data agree on the high incidence of deep venous thrombosis highlighting the fact that the pathophysiology of COVID-19 associated coagulopathy is complex and remains to be fully understood [1]. After extensive research, it has been found that the coronavirus can infect endothelial cells via the ACE2 which acts as a receptor for the SARS-CoV-2. The endothelial binding of the coronavirus limits the ACE2 ability to play its role in maintaining the coagulation factor balance with the vascular system. This leads to the exacerbation of the cellular damage with concomitant downregulation of the protein C anti-coagulation system, hence the frequent occurrence of thrombotic events [2].