Hyper-coagulopathy state in COVID-19: a pivotal challenge

The novel SARS-CoV-2 has caused a global pandemic. COVID-19 infection is described by the adverse impact on the population’s health and economy. Coagulopathy is associated with various thrombotic complications and disease severity. Therefore, this review aims to elucidate the pathophysiology of this coagulopathy. Relevant English language literature was searched and retrieved from the Google Scholar search engine and PubMed database. We used “COVID-19”, “SARS-CoV-2”, “Coagulopathy,” “Thrombosis,” “Anticoagulation,” and “ARDS” as keywords. Several studies showed that the primary targets of SARS-CoV-2 are pneumocytes, immune cells, and vascular endothelial cells. Coagulopathy appears to induce more thrombotic complications than hemorrhagic events. The critically ill patients stimulate the coagulopathy state and thrombosis complication through cytokine storm, systemic inflammation, complement cascade, and platelets. Accordingly, thromboembolic complications cause mortality among COVID-19-infected patients and can negatively affect disease management outcomes and treatment. A pivotal clinical feature of acute COVID-19 infection is coagulopathy and prothrombotic events, which are associated with excessive arterial and venous thrombosis, microvascular thrombosis, and adverse clinical outcomes. Therefore, adopting an approach for preventing, treating, and reducing thrombotic and bleeding events in these patients is necessary.