Duke University School of Medicine.
Biostatistics Research Center, Herbert Wertheim School of Public Health and Human Longevity Science, University of California, San Diego, San Diego.
J Neurosurg Anesthesiol. 2023 Jul 1;35(3):284-291. doi: 10.1097/ANA.0000000000000828. Epub 2021 Dec 30.
Early circulatory shock following traumatic brain injury (TBI) is a multifactorial process; however, the impact of brain injury biomarkers on the risk of shock has not been evaluated. We examined the association between neuronal injury biomarker levels and the development of circulatory shock following moderate-severe TBI.
In this retrospective cohort study, we examined adults with moderate-severe TBI (Glasgow Coma Scale score <13) enrolled in the TRACK-TBI study, an 18-center prospective TBI cohort study. The exposures were day-1 levels of neuronal injury biomarkers (glial fibrillary acidic protein, ubiquitin C-terminal hydrolase-L1 [UCH-L1], S100 calcium-binding protein B [S100B], neuron-specific enolase), and of an inflammatory biomarker (high-sensitivity C-reactive protein). The primary outcome was the development of circulatory shock, defined as cardiovascular Sequential Organ Failure Assessment Score ≥2 within 72 hours of admission. Association between day-1 biomarker levels and the development of circulatory shock was assessed with regression analysis.
The study included 392 subjects, with a mean age of 40 years; 314 (80%) were male and 165 (42%) developed circulatory shock. Median (interquartile range) day-1 levels of UCH-L1 (994.8 [518.7 to 1988.2] pg/mL vs. 548.1 [280.2 to 1151.9] pg/mL; P <0.0001) and S100B (0.47 μg/mL [0.25 to 0.88] vs. 0.27 [0.16 to 0.46] μg/mL; P <0.0001) were elevated in those who developed early circulatory shock compared with those who did not. In multivariable regression, there were associations between levels of both UCH-L1 (odds ratio, 1.63 [95% confidence interval, 1.25-2.12]; P <0.0005) and S100B (odds ratio, 1.73 [95% confidence interval 1.27-2.36]; P <0.0005) with the development of circulatory shock.
Neuronal injury biomarkers may provide the improved mechanistic understanding and possibly early identification of patients at risk for early circulatory shock following moderate-severe TBI.
创伤性脑损伤（TBI）后早期循环休克是一个多因素的过程；然而，尚未评估脑损伤生物标志物对休克风险的影响。我们研究了神经元损伤生物标志物水平与中重度 TBI 后循环休克发展之间的关系。
在这项回顾性队列研究中，我们研究了中度至重度 TBI（格拉斯哥昏迷量表评分<13）的成年患者，这些患者均参加了 TRACK-TBI 研究，这是一个 18 个中心的前瞻性 TBI 队列研究。暴露因素是第 1 天的神经元损伤生物标志物（胶质纤维酸性蛋白、泛素 C 端水解酶-L1[UCH-L1]、S100 钙结合蛋白 B[S100B]、神经元特异性烯醇化酶）和炎症生物标志物（高敏 C 反应蛋白）水平。主要结局是循环休克的发生，定义为入院后 72 小时内心血管序贯器官衰竭评估评分≥2。使用回归分析评估第 1 天生物标志物水平与循环休克发生之间的关系。
该研究纳入了 392 名受试者，平均年龄为 40 岁；314 名（80%）为男性，165 名（42%）发生循环休克。与未发生早期循环休克者相比，发生早期循环休克者的 UCH-L1（994.8[518.7 至 1988.2]pg/ml 比 548.1[280.2 至 1151.9]pg/ml；P<0.0001）和 S100B（0.47μg/ml[0.25 至 0.88]比 0.27μg/ml[0.16 至 0.46]；P<0.0001）水平升高。多变量回归分析显示，UCH-L1（比值比，1.63[95%置信区间，1.25-2.12]；P<0.0005）和 S100B（比值比，1.73[95%置信区间，1.27-2.36]；P<0.0005）水平与循环休克的发生均相关。
神经元损伤生物标志物可能为中重度 TBI 后早期循环休克提供更好的发病机制理解，并可能实现早期识别高危患者。
