4 research outputs found
Shock-Driven Endotheliopathy in Trauma Patients Is Associated with Leucocyte Derived Extracellular Vesicles
Endotheliopathy following trauma is associated with poor outcome, but the underlying mechanisms are unknown. This study hypothesized that an increased extracellular vesicle (EV) concentration is associated with endotheliopathy after trauma and that red blood cell (RBC) transfusion could further enhance endotheliopathy. In this post hoc sub study of a multicentre observational trial, 75 trauma patients were stratified into three groups based on injury severity score or shock. In patient plasma obtained at hospital admission and after transfusion of four RBC transfusions, markers for endotheliopathy were measured and EVs were labelled with anti CD41 (platelet EVs), anti CD235a (red blood cell EVs), anti CD45 (leucocyte EVs), anti CD144 (endothelial EVs) or anti CD62e (activated endothelial EVs) and EV concentrations were measured with flow cytometry. Statistical analysis was performed by a Kruskall Wallis test with Bonferroni correction or Wilcoxon rank test for paired data. In patients with shock, syndecan-1 and von Willebrand Factor (vWF) were increased compared to patients without shock. Additionally, patients with shock had increased red blood cell EV and leucocyte EV concentrations compared to patients without shock. Endotheliopathy markers correlated with leucocyte EVs (ρ = 0.263, p = 0.023), but not with EVs derived from other cells. Injury severity score had no relation with EV release. RBC transfusion increased circulating red blood cell EVs but did not impact endotheliopathy. In conclusion, shock is (weakly) associated with EVs from leucocytes, suggesting an immune driven pathway mediated (at least in part) by shock
The coagulopathy underlying rotational thromboelastometry derangements in trauma patients: a prospective observational multicenter study.
BACKGROUND: Viscoelastic hemostatic assays such as rotational thromboelastometry (ROTEM®) are used to guide treatment of trauma induced coagulopathy. We hypothesized that ROTEM derangements reflect specific coagulation factor deficiencies after trauma. METHODS: Secondary analysis of a prospective cohort study in six European trauma centers in patients presenting with full trauma team activation. Patients with dilutional coagulopathy and patients on anticoagulants were excluded. Blood was drawn on arrival for measurement of ROTEM®, coagulation factor levels and markers of fibrinolysis. ROTEM® cut-off values to define hypocoagulability were: EXTEM clotting time (CT) >80s, EXTEM clot amplitude after 5 minutes (CA5) 80s had no impact on mortality, all other ROTEM® derangements were associated with increased mortality. Also, coagulation factor levels in this group were similar to patients with a normal ROTEM®. Of coagulation factors, decrease was most apparent for fibrinogen (with a nadir of 0.78 g/L) and for factor V levels (with a nadir of 22.8%). In addition, increased fibrinolysis can be present when LI30 is normal but EXTEM and FIBTEM CA5 is decreased. CONCLUSION: Coagulation factor levels and mortality in the group with an isolated clotting time prolongation is similar to patients with a normal ROTEM ®. Other ROTEM ® derangements are associated with mortality and reflect a depletion of fibrinogen and factor V. Increased fibrinolysis can be present when lysis after 30 minutes is normal