COVID-19 and Hypercoagulability

Daniel I Spratt and Rachel J Buchsbaum
Endocrinology, Volume 161, Issue 12, December 2020, bqaa121
https://doi.org/10.1210/endocr/bqaa121

Abstract

The novel coronavirus, SARS-CoV-2, has proven unusual with respect to the spectrum of its pathological effects. In addition to damage inflicted on the lungs, kidneys, heart, and other organ systems, reports have emerged of hypercoagulable states in patients hospitalized with COVID-19. Macro- and micro-vascular thrombosis in venous and arterial beds along with venous thromboembolic events (VTEs) occur with a troublesome frequency. A recent study found increased platelet activation and aggregation in patients infected with SARS-CoV-2, with increased expression of platelet adhesion protein P-selectin along with altered gene expression in multiple pathways, which may underlie platelet hyperreactivity contributing to thromboinflammation in COVID-19 disease. Although all of the underlying mechanisms of COVID-associated hypercoagulability are not clear, multiple laboratory abnormalities related to coagulation occur commonly in hospitalized COVID-19 patients including increased levels of D-dimer, fibrinogen, fibrin, fibrinogen degradation products, and cytokines. as well as decreased antithrombin,variable platelet counts over the course of disease, and platelet-fibrin microthrombi in the pulmonary arterial vasculature on early autopsy studies. With this initial information regarding hypercoagulability, several groups have suggested routine coagulation prophylaxis with low-molecular-weight heparin or unfractionated heparin in patients upon hospitalization with COVID-19, with consideration of escalation to intermediate and/or full therapeutic anticoagulation in the event of clinical disease progression according to established institutional risk algorithms. Our medical centers and others across the United States are implementing this strategy.

You may also like...