Chemical and Histopathologic Effects of COVID-19 on Virchow’s Triad

Original Research

Abstract

Although COVID-19 is known primarily as a respiratory disease, infected patients have been known to experience COVID-19-associated coagulopathy from overactivation of immune response resulting in cytokine storm. As a fundamental principle of venous thromboembolism, Virchow’s triad – consisting of stasis, hypercoagulability, and endothelial injury – remains the foundation for increased clotting risk which can often precipitate life-threatening complications, such as pulmonary embolism, if left untreated. We conducted a literature search using PubMed for evidence to explain the increased coagulopathy in COVID- 19 positive patients in relation to the three pillars of Virchow’s triad. Hypercoagulability in COVID-19 patients is increased due to cytokine-induced fibrin clot formation. Infected patients also have decreased ADAMTS13, which leads to endothelial injury. Lastly, the increased blood viscosity combined with patient immobility promotes vascular stasis. These factors put COVID-19 patients at an increased risk of acquiring blood clots. In conclusion, we have defined a plausible mechanism by which COVID-19 may induce venous thrombosis using the three components of Virchow’s triad. Due to the fatal nature of vascular complications, it is important to consider prophylactically treating these patients with a low molecular weight heparin regimen in order to mitigate the effects of hypercoagulability.