Elevated Admission Base Deficit Is Associated with a Complex Dynamic Network of Systemic Inflammation Which Drives Clinical Trajectories in Blunt Trauma Patients.

Othman Abdul-Malak,Jesse Guardado,Andrew B Peitzman,Jinling Yin,Khalid Almahmoud,Jason Sperry,Akram Zaaqoq,Brian Zuckerbraun,Timothy R Billiar,Rami A Namas,Yoram Vodovotz

doi:10.1155/2016/7950374

Othman Abdul-Malak, Jesse Guardado + Show 9 more

Open Access

https://doi.org/10.1155/2016/7950374

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Abstract

We hypothesized that elevated base deficit (BD) ≥ 4 mEq/L upon admission could be associated with an altered inflammatory response, which in turn may impact differential clinical trajectories. Using clinical and biobank data from 472 blunt trauma survivors, 154 patients were identified after excluding patients who received prehospital IV fluids or had alcohol intoxication. From this subcohort, 84 patients had a BD ≥ 4 mEq/L and 70 patients with BD < 4 mEq/L. Three samples within the first 24 h were obtained from all patients and then daily up to day 7 after injury. Twenty-two cytokines and chemokines were assayed using Luminex™ and were analyzed using two-way ANOVA and dynamic network analysis (DyNA). Multiple mediators of the innate and lymphoid immune responses in the BD ≥ 4 group were elevated differentially upon admission and up to 16 h after injury. DyNA revealed a higher, sustained degree of interconnectivity of the inflammatory response in the BD ≥ 4 patients during the initial 16 h after injury. These results suggest that elevated admission BD is associated with differential immune/inflammatory pathways, which subsequently could predispose patients to follow a complicated clinical course.

Highlights

Traumatic injury can result in sudden metabolic and physiological alterations that are frequently proportionate to the degree and magnitude of the injury sustained [1,2,3]
The overall study cohort consisted of 472 blunt trauma survivors who were admitted to the Intensive Care Unit (ICU) after being resuscitated, which was described recently [17]
Of these patients and based on selection criteria, we identified 70 patients with an admission base deficit (BD) < 4 mEq/L and 84 patients with an admission BD ≥ 4 mEq/L

Summary

Introduction

Traumatic injury can result in sudden metabolic and physiological alterations that are frequently proportionate to the degree and magnitude of the injury sustained [1,2,3]. The host’s homeostatic mechanisms—often driven or accompanied by a broad systemic inflammatory response—attempt to correct for these metabolic perturbations and restore normal body functions [4, 5]. Further complicating the clinical scenario is the extent of the perpetuated metabolic derangement that could propagate the trauma-induced inflammatory response [4, 8,9,10]. This results in a positive self-feedback loop of inflammation driving damage or dysfunction, which in turn stimulates further inflammation [11,12,13]. We and others have hypothesized that the outcome of this vicious cycle eventually leads to immune dysregulation, which predispose trauma patients to develop complications such as multiple organ failure and nosocomial infections [14,15,16,17]

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