Coagulopathy in COVID-19

Abstract

Hemostatic disorders play an important role in the pathogenesis and clinical manifestations of COVID-19. The purpose of the research was a detailed consideration of the pathogenesis, clinical manifestations, and methods of diagnosing and treatment of coronavirus-induced coagulopathy (CIC). At the onset of COVID-19, hypercoagulability is detected, and consumption coagulopathy and disseminated intravascular coagulation (DIC) syndrome are usually observed at later stages of the disease. In the pathogenesis of hypercoagulation in patients with COVID-19, pro-inflammatory cytokines, hyperfibrinogenemia, increased blood levels of von Willebrand factor, factor VIII, neutrophilic extracellular traps, platelet activation, production of antiphospholipid antibodies, microvesicles are of importance. Laboratory findings show increased plasma concentrations of D-dimer, fibrinogen, a longer prothrombin time and a decrease in the number of platelets. The cumulative incidence of thrombotic complications ranges from 21 to 31%. Thrombosis risk factors are intensive care unit stay, leukocytosis, and a high plasma D-dimer concentration. Differential diagnosing of CIC should be carried out with disseminated intravascular coagulation, sepsis-induced coagulopathy, antiphospholipid, hemophagocytic syndromes, thrombotic microangiopathy, and heparin-induced thromocytopenia. CIC may be complicated by sepsis, antiphospholipid syndrome, hemophagocytic syndrome, thrombotic microangiopathy, and heparin-induced thrombocytopenia. The main therapy is low molecular weight heparins treatment. Treatment recommendations are provided.