From the R Adams Cowley Shock Trauma Center (A.M.C., P.L., T.M.S., D.M.S.), Baltimore, Maryland; Department of Anesthesiology, University of Maryland School of Medicine (S.Y., P.H., Y.I.), Baltimore, Maryland.
J Trauma Acute Care Surg. 2019 Jul;87(1S Suppl 1):S146-S151. doi: 10.1097/TA.0000000000002256.
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.
关于胸部创伤对创伤性脑损伤(TBI)后继发性损伤过程的影响,临床数据尚缺乏,一些数据表明多发伤可能使脑损伤恶化。钝性胸部创伤和 TBI 代表两种主要的单一损伤实体,具有最高的并发症风险,是潜在的生物标志物靶标。
纳入严重 TBI 的创伤患者。在 72 小时内每 6 小时采集血清生物标志物水平。评估基线、6 小时和 24 小时头部 CT 扫描。神经恶化定义为挫伤增加、缺血、基底池受压和/或中线移位。比较有胸部损伤(损伤严重程度评分胸部 1 分)和无胸部损伤的 TBI 患者。采用 Wilcoxon 秩和检验、单因素 logistic 回归和受试者工作特征进行报告。
共纳入 57 例患者,平均年龄 40.5 岁,入院和 24 小时时的平均运动格拉斯哥昏迷量表评分为 3(四分位距 1-5)和 5(四分位距 3-5)。纳入的患者中,12.2%的患者在入院后 6 小时内接受了开颅手术,22.8%的患者在 12 小时内接受了开颅手术。有胸部创伤的患者中,24.5%的患者胸部损伤严重程度评分(Abbreviated Injury Scale)为 3 或更高,73.6%的患者为钝性胸部创伤。对有和无胸部损伤的 TBI 患者进行分层,发现胸部损伤患者的 IL-4、IL-5、IL-8 和 IL-10 平均水平较高,IFN-γ 和 IL-7 平均水平较低。调整胸部损伤后,IL-7 水平对神经恶化有预测作用,受试者工作特征曲线下面积为 0.59(p 值=0.011)。TBI 和胸部创伤患者的 IL-4 和神经元特异性烯醇化酶水平分别对死亡率有预测作用(受试者工作特征曲线下面积为 0.67 和 0.63,p=0.0001、0.003)。
利用生物标志物早期识别 TBI 和胸部创伤患者,有可能改变影响这部分 TBI 患者发病率和死亡率的不利因素。
III 级。