COVID-19-Associated Hyperviscosity: A Potential Link between Inflammation and Thrombophilia

Abstract

Although COVID-19 begins as a respiratory pneumonia, we are now discovering it causes an intense inflammatory response accompanied by systemic microangiopathy. In reflecting on Virchow’s triad, we considered the possibility that extreme elevation in acute phase response proteins like fibrinogen may result in hyperviscosity, a known cause of endothelial damage and resultant thrombosis. We found elevations in plasma viscosity in all 15 COVID-19 patients tested to date. Notably, the patients with the highest plasma viscosities experienced thrombotic complications despite receiving therapeutic anticoagulation. Plasma viscosity correlated strongly with illness severity (Pearson's r = 0.841, p <0.001). Given the growing evidence of thrombotic complications associated with COVID-19, the role of hyperviscosity in disease pathogenesis should be examined more widely. Therapeutic plasma exchange is a mainstay of treatment for immunoglobulin-related hyperviscosity, where symptomatic hyperviscosity is considered a medical emergency. Study of its use in critically ill patients with COVID-19 who have thrombotic complications despite therapeutic anticoagulation is urgently needed.