Abstract

Background: Emerging data suggest a complex role for immuno-thrombosis in the thrombotic complications in COVID-19. We report the case of a fatal mesenteric ischemia to illustrate the mechanisms of endothelial dysfunction in the gut, and the resulting hypercoagulability. Case Report: A 58-year-old woman was admitted in Intensive Care Unit, with initial severe acute respiratory distress syndrome due to SARS-CoV-2 pneumonia. Her respiratory status worsened, with a septic shock thirteen days after symptoms onset. The blood culture was positive with Pseudomonas aeruginosa and Candida. A rapid consecutive deterioration leading to multiorgan failure revealed colic perforation complicated with secondary peritonitis. Histopathological findings revealed small vein occlusions. Surprisingly, no SARS-CoV-2 viral particles could be detected in the bowel. We found intense endothelial dysfunction, contrasting with only mild neutrophil activation. A major increase in von Willebrand factor and resistance to fibrinolysis were the main hemostatic abnormalities. Discussion: This case highlights that COVID-19-associated hypercoagulability can lead to early primitive thrombotic events in small vessels, and adds new evidence concerning a potential role for immuno-thrombosis. Close monitoring of endothelial dysfunction, and further consideration of new targets to prevent thrombosis by adjunctive therapies may thus appear fundamental.

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