title: Base deficit as a marker of survival after traumatic injury: consistent across changing patient populations and resuscitation paradigms.
abstract: BACKGROUND
  Damage control resuscitation (DCR) has improved outcomes in severely injured patients. In civilian centers, massive transfusion protocols (MTPs) represent the most formal application of DCR principles, ensuring early, accurate delivery of high fixed ratios of blood components. Recent data suggest that DCR may also help address early trauma-induced coagulopathy. Finally, base deficit (BD) is a long-recognized and simple early prognostic marker of survival after injury.
  
  
  METHODS
  Outcomes of patients with admission BD data resuscitated during the DCR era (2007-2010) were compared with previously published data (1995-2003) of patients cared for before the DCR era (pre-DCR). Patients were considered to have no hypoperfusion (BD, >-6), mild (BD, -6 to -14.9), moderate (BD, -15 to -23.9), or severe hypoperfusion (BD, <-24).
  
  
  RESULTS
  Of 6,767 patients, 4,561 were treated in the pre-DCR era and 2,206 in the DCR era. Of the latter, 218 (9.8%) represented activations of the MTP. DCR patients tended to be slightly older, more likely victims of penetrating trauma, and slightly more severely injured as measured by trauma scores and BD. Despite these differences, overall survival was unchanged in the two eras (86.4% vs. 85.7%, p = 0.67), and survival curves stratified by mechanism of injury were nearly identical. Patients with severe BD who were resuscitated using the MTP, however, experienced a substantial increase in survival compared with pre-DCR counterparts.
  
  
  CONCLUSIONS
  Despite limited adoption of formal DCR, overall survival after injury, stratified by BD, is identical in the modern era. Patients with severely deranged physiology, however, experience better outcomes. BD remains a consistent predictor of mortality after traumatic injury. Predicted survival depends more on the energy level of the injury (stab wound vs. nonstab wound) than the mechanism of injury (blunt vs. penetrating).
authors.affiliation: Department of Surgery, Emory University School Medicine, Grady Memorial Hospital, Atlanta, Georgia 30303, USA.
authors.forename: Erica I
authors.initials: EI
authors.lastname: Hodgman
authors.forename: Bryan C
authors.initials: BC
authors.lastname: Morse
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Dente
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Mina
authors.forename: Beth H
authors.initials: BH
authors.lastname: Shaz
authors.forename: Jeffrey M
authors.initials: JM
authors.lastname: Nicholas
authors.forename: Amy D
authors.initials: AD
authors.lastname: Wyrzykowski
authors.forename: Jeffrey P
authors.initials: JP
authors.lastname: Salomone
authors.forename: Grace S
authors.initials: GS
authors.lastname: Rozycki
authors.forename: David V
authors.initials: DV
authors.lastname: Feliciano
mesh_terms: D000140:Acidosis, Lactic / Q000097:blood / Q000209:etiology* / Q000401:mortality; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001803:Blood Transfusion / Q000379:methods; D005260:Female; D006801:Humans; D015601:Injury Severity Score; D008297:Male; D011379:Prognosis; D012151:Resuscitation / Q000379:methods* / Q000401:mortality; D012189:Retrospective Studies; D016019:Survival Analysis; D016896:Treatment Outcome; D014947:Wounds and Injuries / Q000097:blood / Q000175:diagnosis / Q000401:mortality* / Q000628:therapy
chemical_list: D015415:Biomarkers