Abstract

36th International Symposium on Intensive Care and Emergency Medicine : Brussels, Belgium. 15-18 March 2016.

Highlights

  • A hallmark of sepsis is early onset microvascular dysfunction

  • This loss of local microvascular control was partially off-set by increased capillary red blood cell (RBC) supply rate, which correlated with increased plasma NOx

  • The similarities in the phenotype induced by sepsis and suppression of A1R support our hypothesis that dysfunction/downregulation of the Gi-A1R at the onset of sepsis changes the effect of adenosine towards Gs-A2AR/A2BR-mediated leukopenia and immune paralysis

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Summary

Introduction

A hallmark of sepsis is early onset microvascular dysfunction. the mechanism responsible for maldistribution of capillary blood flow is not understood. Methods: We studied 212 patients [survival (S) group: 146; nonsurvival (NS) group: 66] in whom PMX-DHP was performed for severe sepsis and septic shock and who were admitted to the ICU. Methods: Histone H3 (H3) plasma levels of 43 sepsis patients who were admitted to the Intensive Care Unit were measured and we determined the correlation of H3 levels with disease severity, organ failure, mortality and coagulation- and tissue homeostasis parameters including LDH levels, thrombin potential (ETP), prothrombin levels, antithrombin levels and platelet counts. Results: For sepsis patients at the ICU we found that median H3 levels were significantly increased in non-survivors as compared to survivors with levels found being 3.15 μ g/ml versus 0.57 μg/ml respectively, P = 0.04. Our survey could contribute towards liberalizing visiting policies in Italian PICUs and promoting more attentive care for the patient and his/her family

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