A. Slaughter1,2, M. P. Chapman1,2, A. Banerjee1, E. Gonzalez1,2, H. B. Moore1,2, E. E. Moore1,2 1University Of Colorado Denver,Surgery,Aurora, CO, USA 2Denver Health Medical Center,Surgery,Aurora, CO, USA
Introduction: Despite the established effects of moderate, long-term ethanol consumption on platelet function, the impact of acute ethanol exposure based on homotypic platelet aggregometry remains contradictory. Thus the role of acute ethanol intoxication in the pathogenesis of trauma induced coagulopathy has not been elucidated. The development of recent whole blood viscoelastic assays however provides the opportunity to better evaluate the effect of acute ethanol exposure on the hemostatic capacity of platelets. We hypothesized that acute ethanol intoxication will impair platelet function in otherwise healthy individuals.
Methods: Healthy volunteers (n=7) participated in the study. Baseline venous blood samples for kaolin-activated whole blood thromboelastography (TEG) and platelet mapping (PM) were obtained at the beginning of the study. Additional blood samples were drawn and incubated with ethanol for 1 h (in vitro exposure). Participants then consumed ethanol to legal intoxication, a blood alcohol content of >0.1 g/dL, as monitored by repeated breathalyzer testing. Blood was drawn after 1h of sustained intoxication (in vivo exposure). We then repeated TEG and PM on the post-incubation and post-intoxication samples. Percentage platelet inhibition at the adenosine diphosphate (ADP) and thromboxane A2 (TxA2) receptors following ethanol exposure was calculated.
Results: The platelet TxA2 receptor, stimulated by arachidonic acid (AA), demonstrated a significant increase median (IQR) percentage inhibition from baseline following in vivo ethanol intoxication, 50.4% (27.9) vs. 75.2% (25.3) (p=0.018). Likewise, the TxA2 receptor demonstrated a significant increase percentage inhibition from baseline following in vitro ethanol incubation, 50.4% (27.9) vs. 75.6% (30.35) (p=0.046). Platelet ADP channel percentage inhibition comparing baseline and post-intoxication was 40.2% (35.7) vs. 61.3% (35.1) (p=0.398). ADP channel percentage inhibition comparing baseline and post-incubation was 40.2% (35.7) vs. 64.65 (42.6) (p=0.917).
Conclusion: Acute ethanol intoxication significantly impaired platelet function via the TxA2 receptor. Furthermore TxA2 receptor inhibition followed both in vivo and in vitro exposure. Our results therefore suggest that platelet dysfunction could exacerbate coagulopathy in intoxicated trauma victims.
