• K Almahmoud, A N Abboud, R A Namas, O Abdul-Malak, A Zaaqoq, R Zamora, J Sperry, A B Peitzman, H-C Pape, T R Billiar, and Y Vodovotz.
• 1Department of Orthopedic Trauma Surgery, University of Aachen Medical Center, Germany 2Department of Surgery, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
• Shock. 2015 Oct 1;44 Suppl 2:10.

IntroductionWe sought to examine the association between the clinical outcomes and the early, dynamic, systemic acute inflammatory response in the setting of major bone/soft tissue injury.MethodsFrom a cohort of 472 blunt trauma survivors, two stringently matched cohorts were derived: 32 patients who had a severe extremity injury (AIS ≥ 3) following blunt trauma (18 males and 14 females; age: 52.5 ± 3.1; ISS: 21.5 ± 1.5) and 30 trauma patients with mild/moderate extremity injury (AIS < 3; 15 males and 15 females; age: 53 ± 2.4; ISS: 22.4 ± 1.4). Serial blood samples (3 samples within the first 24 h and then from days 1 to 7 post- injury) were assayed for multiple inflammation mediators. Two-Way ANOVA was used to compare groups, and Dynamic Bayesian Network (DyBN) analysis to infer network connectivity.ResultsICU length of stay [LOS], total LOS, days on mechanical ventilation, Marshall MODScore, as well admission lactate and CPK were significantly altered in AIS ≥ 3 group. Plasma levels of IL-6, IL-8, MIG, IP-10, and MCP-1 were significantly elevated in the AIS ≥ 3 group, while plasma levels of IL-7, Eotaxin, and MIP- 1α were significantly elevated in the AIS < 3 group over the 7 days post-injury. DyBN inference suggested a different core chemokine-based network upstream of mediators including IL-6 and IL-10.ConclusionOur results suggest that severe extremity/soft tissue injury can drive a differential inflammation program including multiple chemokines that affect systemic IL-6 and IL-10, in a manner associated with worse clinical outcomes as compared to mild/moderate soft tissue injury.

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