COVID-19 infection presenting as massive, multi-organ thromboembolism

Abstract

The emergence of Coronavirus disease 2019 (COVID-19) has presented an unprecedented challenge for the healthcare community across the world. Based on the rapid increase in the rate of human infection, the World Health Organization (WHO) has classified the COVID-19 outbreak as a pandemic [1-3]. Respiratory involvement, presenting as mild flu-like illness to potentially lethal acute respiratory distress syndrome or fulminant pneumonia, is the dominant clinical manifestation of COVID-19 [4]. However, pre-existing cardiovascular disease (CVD) and CV risk factors may enhance vulnerability to COVID-19; further, COVID-19 can worsen underlying CVD and even precipitate new cardiac complications, due to possible endothelial dysfunction [5-6]. Furthermore, patients with COVID-19 pneumonia exhibit a number of coagulation abnormalities that have been associated with a higher mortality rate [7-8]; in particular, severe lung inflammation and impaired pulmonary gas exchange in COVID‐19 infected individuals has been suggested to be due to the up-regulation of pro‐inflammatory cytokines [9]. Further, it has been demonstrated that the activation of the coagulation system is relevant in the pathogenesis of acute respiratory distress syndrome (ARDS), one of the most common complications of COVID‐19 infection [10]. As a consequence, COVID-19 infection may predispose to both venous and arterial thromboembolic disease due to excessive inflammation, hypoxia, immobilization and diffuse intravascular coagulation (DIC).