• Edward P Sloan, Max D Koenigsberg, Nora B Philbin, Weihua Gao, DCLHb Traumatic Hemorrhagic Shock Study Group, and European HOST Investigators.
• Department of Emergency Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA. edsloan@uic.edu
• J Trauma. 2010 May 1;68(5):1158-71.

BackgroundDiaspirin cross-linked hemoglobin (DCLHb) has demonstrated a pressor effect that could adversely affect traumatic hemorrhagic shock patients through diminished perfusion to vital organs, causing base deficit (BD) and lactate abnormalities.MethodsData from two parallel, multicenter traumatic hemorrhagic shock clinical trials from 17 US Emergency Departments and 27 European Union prehospital services using DCLHb, a hemoglobin-based resuscitation fluid.ResultsIn the 219 patients, the mean age was 37.3 years, 64% of the patients sustained a blunt injury, 48% received DCLHb resuscitation, and the overall 28-day mortality rate was 36.5%. BD data did not differ by treatment group (DCLHb vs. normal saline [NS]) at any time point. Study entry BD was higher in patients who died when compared with survivors in both studies (US: -14.7 vs. -9.3 and European Union: -11.1 vs. -4.1 mEq/L, p < 0.003) and at the first three time points after resuscitation. No differences in BD based on treatment group were observed in either those who survived or those who died from the hemorrhagic shock. US lactate data did not differ by treatment group (DCLHb vs. NS) at any time point. Study entry lactates were higher in US patients who ultimately died when compared with survivors (82.4 vs. 56.1 mmol/L, p < 0.003) and at all five postresuscitation time points. No lactate differences were observed between DCLHb and NS survivors or in those who died based on treatment group.ConclusionsAlthough patients who died had more greatly altered perfusion than those who survived, DCLHb treatment of traumatic hemorrhagic shock patients was not associated with BD or lactate abnormalities that would indicate poor perfusion.

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