Pulmonary Embolism in Patients with COVID-19

Abstract

Infection with the novel severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) and the resulting syndrome, COVID-19, have been associated with inflammation and a prothrombotic state, with increases in fibrin, fibrinogen, fibrin degradation products and D-dimers. In some studies, elevations in these markers have been associated with worse clinical outcomes. Several studies have demonstrated a high prevalence of venous thromboembolism (VTE), and pulmonary embolism (PE), particularly in patients admitted to the intensive care unit (ICU), even in those receiving prophylactic anticoagulation. The high rate of thrombosis in COVID-19 is driven by at least two interrelated processes: a hypercoagulable state responsible for large-vessel thrombosis and thromboembolism and direct vascular and endothelial injury responsible for in situ microvascular thrombosis. The presence of PE and pulmonary thrombosis may explain why hypoxemia is out of proportion to impairment in lung compliance in some patients with COVID-19 pneumonia. Diagnosing PE in patients with COVID-19 pneumonia may be challenging, because the two pathologies share many signs and symptoms. It has been demonstrated that the administration of prophylactic anticoagulation within 24 h of admission in patients with COVID-19 was associated with decreased mortality when compared with no prophylactic anticoagulation. Given the antithrombotic, anti-inflammatory and possibly antiviral properties of heparins, it has been hypothesized that anticoagulation with heparin administered at doses higher than conventionally used for venous thromboprophylaxis may improve outcomes. In non-critically ill patients hospitalized with COVID-19, therapeutic-dose anticoagulants with heparin (most commonly, low-molecular-weight heparin) increased the probability of survival until hospital discharge with a reduced need for ICU-level organ support at 21 days as compared with usual-care thromboprophylaxis. In Critically ill patients with confirmed COVID-19, therapeutic-dose anticoagulation did not increase the probability of survival to hospital discharge or the number of days free of cardiovascular o respiratory organ support and had a 95% probability of being inferior to usual-care pharmacologic thromboprophylaxis. Currently, randomized trials evaluating the use of tissue plasminogen activator and Tenecteplase in patients with COVID-19 ARDS are underway.