[Thrombotic Risk and Covid-19: Review of Current Evidence for a Better Diagnostic and Therapeutic Approach]

Abstract

The new SARS-CoV-2 coronavirus has created an unprecedented global health problem, resulting in more than 250,000 confirmed deaths. The disease produced by this virus, called Covid-19, presents with variable clinical manifestations, from practically asymptomatic patients with catarrhal processes to severe pneumonias that rapidly evolve to acute respiratory distress syndrome (ARDS) and multiorgan failure. In recent weeks, papers have been published describing coagulation disorders and arterial and venous thrombotic complications in these patients, mainly among those admitted to intensive care units. The infection triggers an immune response, which causes different inflammatory mediators to be released into the blood. These include cytokines, which interact with platelets and different coagulation proteins, and promote thrombogenesis. One of the most widely studied coagulation markers in Covid-19 is D-dimer (DD), raised levels of which have prognostic implications, although the best cut-off point for the diagnosis of venous thromboembolism (VTE) in this population has not been clarified, nor has its usefulness in determining the intensity of thromboprophylaxis required in these patients. Until sufficiently robust information (preferably from well-designed clinical trials) is available, the recommendations of clinical practice guidelines for the prophylaxis, diagnosis and treatment of VTE should be followed in Covid-19 patients.

Keywords: Anticoagulation; Covid-19; Pulmonary embolism; Thrombosis.

Figura 1

Fisiopatología de la activación de la coagulación en situación de sepsis. Los patógenos y sus componentes estimulan a los monocitos a través de receptores específicos situados en su superficie celular. Los monocitos activados producen una respuesta hiperinmune con liberación de distintas citocinas y otros mediadores inflamatorios, que activan plaquetas, neutrófilos y células endoteliales. Se produce un estado de hipercoagulabilidad y daño endotelial que modifica las propiedades del endotelio de un estado anticoagulante a uno procoagulante a través de la interrupción del glicocalix y la expresión del factor de von Willebrand (FVW). Por su parte, los neutrófilos expresan factor tisular y liberan proteínas granuladas y otros mediadores procoagulantes, como las trampas extracelulares de neutrófilos (NETs), compuestas de ADN procoagulante, histonas y otros patrones moleculares asociados al daño celular. Todo lo anterior lleva al desarrollo de los fenómenos micro y macrotrombóticos. FEC-G: factor estimulante de colonias de granulocitos; FNT-α: factor de necrosis tumoral alfa; IFN-γ: interferón gamma; IL: inteleucina; NETs: trampas extracelulares de neutrófilos.