COVID-19: opening a new paradigm in thromboprophylaxis for critically ill patients?
Raquel Ferrandis 1 , Juan V Llau 2 , Manuel Quintana 3 , Pilar Sierra 4 , Francisco Hidalgo 5 , Concepción Cassinello 6 , Aurelio Gómez-Luque 7
To the Editor:
The novel infection caused by coronavirus SARS-CoV-2 determining COVID-19 disease causes alterations mainly in the respiratory system. Many reports have postulated a procoagulant state accompanying the respiratory distress with thrombosis at both venous and arterial levels . The procoagulant pattern is characterized by hyperfibrinogenemia and elevated d-dimer levels, with mild thrombocytopenia and a moderately prolonged prothrombin time . Although d-dimers are not specific indicators of clot formation, in combination with the other parameters, its elevation may suggest a systemic coagulation activation with an increase of thrombin generation and fibrinolysis.
A complex physiopathology has been proposed trying to explain this profile. Coming from the thromboinflammation concept, thrombin generation appears to be the key determinant of the thromboinflammatory response extent. The damaged endothelium, many blood cellular elements, and other activated hemostatic components are involved in this prothrombotic picture . Microvascular thrombi impair the blood flow all over the body, with a vascular shunt due to capillary obstruction. This determines hypoxia and tissue dysfunction at several organs, being the lung the more affected one.