Pressure reactivity index (PRx) and brain tissue oxygen (PbtO₂) are associated with outcome in traumatic brain injury (TBI). This study explores the relationship between PRx and PbtO₂ in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution intensive care unit (ICU) sub-study cohort, we evaluated those patients with archived high-frequency digital intraparenchymal intracranial pressure (ICP) and PbtO₂ monitoring data of, a minimum of 6 h in duration, and the presence of a 6 month Glasgow Outcome Scale –Extended (GOSE) score. Digital physiological signals were processed for ICP, PbtO₂, and PRx, with the % time above/below defined thresholds determined. The duration of ICP, PbtO₂, and PRx derangements was characterized. Associations with dichotomized 6-month GOSE (alive/dead, and favorable/unfavorable outcome; ≤ 4 = unfavorable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevated ICP and low PbtO₂ episodes. However, most of the acute ICU physiological derangements were impaired cerebrovascular reactivity, not ICP elevations or low PbtO₂ episodes. Low PbtO₂ without PRx impairment was rarely seen. % time spent above PRx threshold was associated with mortality at 6 months for thresholds of 0 (area under the curve [AUC] 0.734, p = 0.003), > +0.25 (AUC 0.747, p = 0.002) and > +0.35 (AUC 0.745, p = 0.002). Similar relationships were not seen for % time with ICP >20 mm Hg, and PbtO₂ < 20 mm Hg in this cohort. Extreme impairment in cerebrovascular reactivity is seen during concurrent episodes of elevated ICP and low PbtO₂. However, the majority of the deranged cerebral physiology seen during the acute ICU phase is impairment in cerebrovascular reactivity, with most impairment occurring in the presence of normal PbtO₂ levels. Measures of cerebrovascular reactivity appear to display the most consistent associations with global outcome in TBI, compared with ICP and PbtO₂.

中文翻译：

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创伤性脑损伤中的脑组织氧和脑血管反应性：欧洲神经创伤协作有效性研究对创伤性脑损伤侮辱负担的探索性分析。


压力反应指数（PRx）和脑组织氧（PbtO ₂ ）与创伤性脑损伤（TBI）的结果相关。本研究探讨成人中度/重度 TBI 中 PRx 和 PbtO ₂之间的关系。利用欧洲创伤性脑损伤神经创伤有效性合作研究 (CENTER-TBI) 高分辨率重症监护病房 (ICU) 子研究队列，我们​​评估了那些具有存档的高频数字脑实质颅内压 (ICP) 和 PbtO ₂监测数据的患者持续时间至少 6 小时，并且存在 6 个月的格拉斯哥结果量表 - 扩展 (GOSE) 评分。针对 ICP、PbtO ₂和 PRx 处理数字生理信号，并确定高于/低于定义阈值的时间百分比。对 ICP、PbtO ₂和 PRx 紊乱的持续时间进行了表征。评估了与二分 6 个月 GOSE（存活/死亡，以及有利/不利结果；≤ 4 = 不利）的关联。总共包括 43 名患者。在ICP升高和PbtO ₂降低期间观察到脑血管反应性严重受损。然而，大多数急性 ICU 生理紊乱是脑血管反应性受损，而不是 ICP 升高或 PbtO ₂过低。没有 PRx 损害的低 PbtO ₂很少见。高于 PRx 阈值的时间百分比与 6 个月时的死亡率相关，阈值为 0（曲线下面积 [AUC] 0.734， p = 0.003）、> +0.25（AUC 0.747， p = 0.002）和 > +0.35（ AUC 0.745， p = 0.002）。在该队列中，对于 ICP >20 mm Hg 和 PbtO ₂ < 20 mm Hg 的时间百分比，没有看到类似的关系。 ICP 升高和 PbtO ₂降低同时发生时，可观察到脑血管反应性的极度损害。然而，在急性ICU阶段出现的大部分脑生理紊乱是脑血管反应性损伤，其中大多数损伤发生在PbtO ₂水平正常的情况下。与 ICP 和 PbtO ₂相比，脑血管反应性测量似乎显示出与 TBI 总体结果最一致的关联。