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

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。本研究探讨了成人中度/重度 TBI 中PRx 和 PbtO ₂之间的关系。使用欧洲外伤性脑损伤协作性神经创伤有效性研究 (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高频数字颅内压 (ICP) 和 PbtO ₂监测数据的患者至少 6 小时的持续时间，并且存在 6 个月的格拉斯哥结局量表 - 扩展 (GOSE) 评分。ICP、PbtO ₂处理数字生理信号和 PRx，确定高于/低于定义阈值的时间百分比。表征了ICP、PbtO ₂和PRx 紊乱的持续时间。评估了与二分法 6 个月 GOSE（生/死，有利/不利结果；≤ 4 = 不利）的关联。共纳入 43 名患者。在升高的 ICP 和低 PbtO ₂发作期间观察到严重受损的脑血管反应性。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 升高或低 PbtO ₂发作。很少看到没有 PRx 损伤的低 PbtO ₂。当阈值为 0 时，高于 PRx 阈值的时间百分比与 6 个月时的死亡率相关（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，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。在 ICP 升高和 PbtO ₂低的同时发生期间，可以看到脑血管反应性的极度受损。然而，在急性 ICU 阶段所见的大多数脑生理机能紊乱是脑血管反应性受损，大多数受损发生在 PbtO ₂水平正常的情况下。与 ICP 和 PbtO ₂相比，脑血管反应性的测量似乎显示出与 TBI 总体结果最一致的关联。