Concomitant chest trauma and traumatic brain injury, biomarkers correlate with worse outcomes.

Abstract

Clinical data are lacking on the influence of chest trauma on the secondary injury process after traumatic brain injury (TBI), with some data suggesting that multiple trauma may worsens brain injury. Blunt chest trauma and TBI represent the two major single injury entities with the highest risk of complications and are potential biomarker targets. Trauma patients with severe TBI were enrolled. Serum biomarker levels were obtained every 6 hours for 72 hours. Baseline, 6 hours and 24 hours CT head scans were evaluated. Neurologic worsening was defined as increased contusions, ischemia, compression of basal cisterns, and/or midline shift. The TBI patients with chest injury (Abbreviated Injury Scale chest score ≥1) and those without chest injury were compared. Wilcoxon rank sum test, univariate logistic regression and receiver operating characteristic were reported. Fifty-seven patients. Mean age of 40.5 years. Median motor Glasgow Coma Scale score at admission and 24 hours was 3 (interquartile range, 1-5) and 5 (interquartile range, 3-5). Of the patients enrolled, 12.2% patients underwent craniotomy within 6 hours from the time of admission and 22.8% within 12 hours. Patients with chest trauma, 24.5% had a chest Abbreviated Injury Scale score of 3 or greater, and 73.6% sustained blunt chest trauma. Stratifying TBI patients with and without chest injury revealed higher mean levels of IL-4, IL-5, IL-8, and IL-10 and lower mean IFN-γ and IL-7 levels in patient with chest injury. IL-7 levels adjusted for chest injury predicted neurological worsening with area under the receiver operating characteristic of 0.59 (p value = 0.011). The TBI and chest trauma patients' IL-4 and neuron-specific enolase levels were predictive of mortality (area under the receiver operating characteristic of 0.67 and 0.63, p = 0.0001, 0.003), respectively. Utilizing biomarkers for early identification of patients with TBI and chest trauma has the capability of modifying adverse factors affecting morbidity and mortality in this subset of TBI patients. Level III.