Pathophysiological and laboratory aspects of hemostatic disorders in patients with COVID-19

Hemostatic disorders in patients with COVID-19

Abstract

Although coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily affects the respiratory system, the possibility of multisystem tissue and organ damage is not excluded. In severe forms of the disease, hematological disorders with the accompanying laboratory derangements often occur. The pathophysiological basis of COVID-19 coagulopathy has been insufficiently elucidated so far, and it has been related to virus-associated endothelial dysfunction, hypoxia-induced activation of coagulation cascade as well as the action of certain inflammatory mediators. Clinical manifestations of hemostasis disorders vary a lot: from subclinical, unrecognized, microthrombosis to thromboembolic events, but also bleeding diathesis due to consumptive coagulopathy. Recognizable laboratory findings of these disorders include an increase in the concentration of D-dimer values, prolonged prothrombin time with or without slight changes in the activated partial thromboplastin time, changes in the number of platelets according to thrombocytopenia or thrombocytosis (rarely), as well as an increase in the concentration of fibrinogen, usually in the initial stages of the disease. The importance of COVID-19 coagulopathy is reflected in an increased mortality rate due to the high frequency of thromboembolic episodes, which can be the reason for multiorgan dysfunction syndrome.