K. Wolf1, L. J. Schaub2, C. G. Morgan2, P. Hemond2, J. J. Glaser2 1Wake Forest University School Of Medicine,Winston-Salem, NC, USA 2Naval Medical Research Unit San Antonio,Fort Sam Houston, TX, USA
Introduction: Acute traumatic coagulopathy is a major contributor to mortality within the first 24 hours of injury. The use of Hextend® as a pre-hospital fluid per military clinical practice guidelines amplifies this life threatening coagulopathy. ALM is a cardioplegic agent that has been shown to mitigate coagulopathy in animal models of traumatic shock. We hypothesized that ALM, as an adjunct to whole blood resuscitation, would improve coagulopathy as compared to whole blood resuscitation alone in a swine model of shock.
Methods: Swine (N=18) were randomized to three treatment groups: (1) Whole blood alone, (2) Whole blood + 30 mL of ALM bolus (A:1mg/kg; L:2 mg/kg; M:0.5 mg/kg) infused at 5 mL/min, or (3) Whole + 30 mL of vehicle control (VC) (0.9% NaCl bolus) infused at 5 mL/min. Animals underwent a pressure controlled hemorrhage to MAP of 30 mmHg. At T= 0, 60 min of simulated prehospital care was initiated per TCCC guidelines (Hextend®), followed by 4 hours of ‘hospital care’ resuscitation with varying adjunct treatments above. Physiologic variables were recorded; arterial blood gas and viscoelastometry analyses were performed at specified time points.
Results: Lactate levels were significantly lower in the WB+ALM group compared to the WB+VC groups during shock and resuscitation (T= 0 through T= 120). WB+VC group base deficit was significantly worsened as compared to WB and WB+ALM when treatment began (T= 60). MAP was equivalent between groups except at T= 65, when WB+ALM MAP dropped, and at T=75/85 when WB+ALM MAP increased. All values were equivalent at T= 300. After treatment, T= 60, all groups showed comparable viscoelastometry parameters with the exception of ExTEM MCF at T=180.
Conclusion: In this model, ALM as an adjunct to WB resuscitation demonstrated no advantage to WB alone. While lactate and BD showed improvement during shock and initial resuscitation with ALM, these values were equivalent between WB and WB+ALM at all other time points after resuscitation. No differences were noted in coagulopathy. Previous reports of correction of coagulopathy, in similar animal models, were not reproduced here. Further investigation into the interactions of ALM and whole blood may be warranted to clarify ALM’s effects on coagulopathy.
