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Head-to-Head Comparison of Cytokines Storm-induced Coagulopathy in Septic Shock and Covid-19

1Université catholique de Louvain, Institut de Recherche Expérimentale et Clinique (IREC), Brussels, Belgium, 2Cliniques Universitaires St Luc, Cardiovascular Intensive Care, Brussels, Belgium, 3Cliniques Universitaires St Luc, Intensive Care, Brussels, Belgium, 4Cliniques Universitaires St Luc, Clinical Biology, Brussels, Belgium, 5University of Namur, Namur Research Institute for Life Sciences (Narilis), Department of Pharmacy, Namur, Belgium, 6Inotrem SA, Vandoeuvre-les-Nancy, France, 7Université catholique de Louvain, Institut de Duve (DDUV), Brussels, Belgium, 8Cliniques Universitaires St Luc, Cardiology, Brussels, Belgium

Abstract Number: PB0286

Meeting: ISTH 2021 Congress

Theme: COVID and Coagulation » COVID and Coagulation, Clinical

Background: Since December 2019, the coronavirus disease 2019 (Covid-19) is the main health concern around the world. Host immune response to the virus is variable and can induce a dysregulated inflammatory response associated with venous and arterial thrombosis called Covid-19 associated coagulopathy (CAC). During septic shock, inflammatory reaction generates endothelial activation and procoagulant state with microvascular thrombi inducing disseminated intravascular coagulation (DIC). Although CAC and DIC induce altered coagulation and fibrinolytic responses, their clinical outcomes are different.

Aims: We investigated and compared coagulopathy between septic shock and critical Covid-19 patients.

Methods: Septic shock patients were diagnosed following the Survival Sepsis Campaign guidelines. They were admitted in intensive care unit (ICU) and included in the study within 2 days after admission. Covid-19 patients were admitted in ICU for severe Acute Respiratory Distress Syndrome (ARDS) due to SARS-Cov2 infection and included within 2 days after admission. Patient’s plasma was isolated and used to measure circulating biomarkers by ELISA.

Results: We observed an increase in vWF and TFPI in both septic and Covid-19 patients compared to controls, highlighting endothelial damage. Interestingly, circulating TF was only elevated in Covid-19 patients. Platelet activation differed between the two cohorts of patients. P-selectin and Trem-like transcript 1 were specifically heightened in septic shock whereas CD40L was only augmented in Covid-19. Coagulation markers were increased in a disease-dependent way, with PAI-1, tPA and D-Dimers higher in septic shock and fibrinogen level, higher in Covid-19.

Conclusions: Covid-19 patients had longer length-of-stay with more pronounced respiratory failure. This strong lung disruption overtime induced plasmatic tissue factor release with sustained inflammatory response characterized by sCD40L and fibrinogen secretion. Given the similarities between Covid-19 and septic shock regarding fibrinolysis and coagulation, but not platelet activation, endothelium seems to play a central role in Covid-19 and might explain the differences between CAC and DIC.

To cite this abstract in AMA style:

De Poortere J, Dechamps M, Laterre P-, Octave M, Gigion A, Robaux V, Pirotton L, Bodart J, Gerard L, Gruson D, van Dievoet M-, Douxfils J, Derive M, Gatto L, Bouzin C, Castanares-Zapatero D, Bertrand L, Horman S, Beauloye C. Head-to-Head Comparison of Cytokines Storm-induced Coagulopathy in Septic Shock and Covid-19 [abstract]. Res Pract Thromb Haemost. 2021; 5 (Suppl 2). https://abstracts.isth.org/abstract/head-to-head-comparison-of-cytokines-storm-induced-coagulopathy-in-septic-shock-and-covid-19/. Accessed September 24, 2023.

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