A. R. Macko1, L. J. Schaub1, J. J. Glaser1, H. B. Moore2,3, E. E. Moore2,3, F. R. Sheppard1 1Naval Medical Research Unit-San Antonio,Expeditionary Trauma And Medicine,Ft. Sam Houston, TX, USA 2Denver Health Medical Center,Aurora, CO, USA 3University Of Colorado Denver,Aurora, CO, USA
Introduction: The contribution of fluid resuscitation to the development of coagulopathy remains controversial. We hypothesize that resuscitation accentuates the Acute Coagulopathy of Trauma (ACOT).
Methods: NHPs (n=8) underwent poly-traumatic (soft tissue injury and femur fracture) severe hemorrhagic shock (MAP=20 mmHg). Resuscitation was accomplished via a combination of whole blood (WB) and normal saline (NS), with resuscitation volume determined by shed blood volume (SBV). Animals were randomized to receive one of two, 3-stage sequences of WB and NS: 1) NS-WB-NS or 2) WB-NS-NS. Blood samples were collected at baseline (BSLN), end-of-shock (EOS), end of first (R1), second (R2) and third (EOR) resuscitation phases, and 360 minutes after the initiation of shock (T360) for assessments of clinically-relevant indicators of coagulopathy including: viscoelastic clotting properties in response to extrinsic pathway activation (EXTEM®) via rotational thromboelastometry (ROTEM®): clotting time (CT), -angle, and maximal clot firmness (MCF). Data presented as mean ± SEM; statistical analysis via paired sample t-test and 2-way ANOVA; significance at p<0.05.
Results: Baseline lab values, blood pressure, percent blood loss, duration of shock, and survival were equivalent between groups. EXTEM CT, α-angle and MCF were minimally altered at EOS compared to BSLN; however in the NS-first group CT significantly increased, and -angle and MCF decreased significantly (p<0.05) at R1 (Table 1). CT, α-angle and MCF returned to baseline following WB.
Conclusion: In this model of traumatic hemorrhage, significant alterations in coagulation function consistent with clinically described ACOT did not manifest until saline resuscitation commenced. WB-first resuscitation was protective in maintaining coagulation function and effectively reversed the apparent acute coagulopathy induced by crystalloid resuscitation as determined by EXTEM. This data supports not only blood first but potentially blood only resuscitation with regards to prevention of full blown ACOT and supports the concept that an acute coagulopathy of resuscitation (ACOR) is the largest driver of ACOT.
