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. 2020 Aug;46(8):1603-1606.
doi: 10.1007/s00134-020-06088-1. Epub 2020 May 15.

Understanding pathophysiology of hemostasis disorders in critically ill patients with COVID-19

Bérangère S Joly  1 , Virginie Siguret  2 , Agnès Veyradier  3
Affiliations

Understanding pathophysiology of hemostasis disorders in critically ill patients with COVID-19

Bérangère S Joly et al. Intensive Care Med. 2020 Aug.
No abstract available

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Conflict of interest statement

On behalf of all authors, the corresponding author states that there is no conflict of interest.

Figures

Fig. 1
Fig. 1
Pathophysiology for thrombosis in critically ill patients with COVID-19. The figure summarizes the steps of the thrombotic pathophysiological sequence that consecutively includes the aggression of the host cells by the SARS-CoV-2, the excessive immune response-induced cytokine storm, the local and systemic inflammatory response responsible for an endotheliopathy and a hypercoagulability state, leading to both systemic and macro- and micro-thrombosis. The exact pathophysiological mechanisms leading to severe pulmonary vascular dysfunction and ARDS have not been elucidated. SARS-CoV-2 severe acute respiratory syndrome coronavirus 2, ACE-2 angiotensin-converting enzyme 2, GI gastrointestinal, IL interleukin, G-CSF granulocyte colony stimulating factor, TNF tumor necrosis factor, IFN interferon, SIRS systemic inflammatory response syndrome, EC endothelial cells, TF tissue factor, ULVWF ultralarge von Willebrand factor multimers, FVIII factor VIII, ARDS acute respiratory distress syndrome
See this image and copyright information in PMC

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