COVID-19 Associated Coagulopathy and Implications for its Treatment

Abstract

Abstract The SARS-CoV-2 coronavirus (COVID-19) pandemic is due to lack of prior immunity and there is no certain management, regarding the complications of this viral illness. The target organ for COVID-19 infection are the lungs. Patients may develop acute lung injury that can be complicated by acute respiratory failure, as well as multiorgan failure. The pathophysiology of COVID-19 infection is characterized with inflammatory changes, associated with coagulopathy. Recent data suggests diffuse bilateral pulmonary inflammation observed in COVID-19 infection that is related to a novel pulmonary-specific vasculopathy, defined as pulmonary intravascular coagulopathy (PIC), distinct from disseminated intravascular coagulopathy (DIC). The coagulopathy associated with COVID-19 is distinguished by initial elevation of D-dimer and fibrin/fibrinogen degradation products. Abnormalities in prothrombin time (PT), partial thromboplastin time (APTT) and platelet counts are not common in the early stages of the infection. This suggests the early screening measurement of D-dimer and fibrinogen. The implications for COVID-19-associated-coagulopathy is the established thromboembolic prophylaxis and standard management for sepsis-induced coagulopathy or DIC. High levels of D-dimer are a marker of higher mortality risk. However, current studies do not show the common use of full therapeutical doses of anticoagulants, unless there are other clinical indications. Bleeding in COVID-19 infection is uncommon, even when a laboratory constellation for DIC is present. However, if it occurs, standard guidelines for DIC management should be followed.