Division of Neurocritical Care and Emergency, Department of Neurology, Yale University School of Medicine, 15 York St, LCI 1003, New Haven, CT, CT 06510, USA.
Department of Neurosurgery, Yale University School of Medicine, New Haven, CT, USA.
Neurocrit Care. 2024 Aug;41(1):91-99. doi: 10.1007/s12028-023-01896-x. Epub 2023 Dec 29.
The Brain Oxygen Optimization in Severe Traumatic Brain Injury Phase II randomized controlled trial used a tier-based management protocol based on brain tissue oxygen (PbtO) and intracranial pressure (ICP) monitoring to reduce brain tissue hypoxia after severe traumatic brain injury. We performed a secondary analysis to explore the relationship between brain tissue hypoxia, blood pressure (BP), and interventions to improve cerebral perfusion pressure (CPP). We hypothesized that BP management below the lower limit of autoregulation would lead to cerebral hypoperfusion and brain tissue hypoxia that could be improved with hemodynamic augmentation.
Of the 119 patients enrolled in the Brain Oxygen Optimization in Severe Traumatic Brain Injury Phase II trial, 55 patients had simultaneous recordings of arterial BP, ICP, and PbtO. Autoregulatory function was measured by interrogating changes in ICP and PbtO in response to fluctuations in CPP using time-correlation analysis. The resulting autoregulatory indices (pressure reactivity index and oxygen reactivity index) were used to identify the "optimal" CPP and limits of autoregulation for each patient. Autoregulatory function and percent time with CPP outside personalized limits of autoregulation were calculated before, during, and after all interventions directed to optimize CPP.
Individualized limits of autoregulation were computed in 55 patients (mean age 38 years, mean monitoring time 92 h). We identified 35 episodes of brain tissue hypoxia (PbtO < 20 mm Hg) treated with CPP augmentation. Following each intervention, mean CPP increased from 73 ± 14 mm Hg to 79 ± 17 mm Hg (p = 0.15), and mean PbtO improved from 18.4 ± 5.6 mm Hg to 21.9 ± 5.6 mm Hg (p = 0.01), whereas autoregulatory function trended toward improvement (oxygen reactivity index 0.42 vs. 0.37, p = 0.14; pressure reactivity index 0.25 vs. 0.21, p = 0.2). Although optimal CPP and limits remained relatively unchanged, there was a significant decrease in the percent time with CPP below the lower limit of autoregulation in the 60 min after compared with before an intervention (11% vs. 23%, p = 0.05).
Our analysis suggests that brain tissue hypoxia is associated with cerebral hypoperfusion characterized by increased time with CPP below the lower limit of autoregulation. Interventions to increase CPP appear to improve autoregulation. Further studies are needed to validate the importance of autoregulation as a modifiable variable with the potential to improve outcomes.
《严重颅脑创伤阶段 II 中脑氧优化》的随机对照试验采用了基于脑氧（PbtO）和颅内压（ICP）监测的分级管理方案，以减少严重颅脑创伤后的脑组织缺氧。我们进行了二次分析，以探讨脑组织缺氧、血压（BP）和改善脑灌注压（CPP）的干预措施之间的关系。我们假设血压管理低于自动调节下限会导致脑灌注不足和脑组织缺氧，可以通过血液动力学增强来改善。
在《严重颅脑创伤阶段 II 中脑氧优化》试验中，共有 119 名患者入组，其中 55 名患者同时记录了动脉 BP、ICP 和 PbtO。通过时间相关分析检查 CPP 波动时 ICP 和 PbtO 的变化来测量自动调节功能。根据每个患者的情况，使用所得的自动调节指数（压力反应指数和氧反应指数）来确定“最佳”CPP 和自动调节下限。在所有旨在优化 CPP 的干预措施之前、期间和之后，计算个性化自动调节下限的个体患者的自动调节功能和 CPP 超出个性化自动调节下限的时间百分比。
在 55 名患者（平均年龄 38 岁，平均监测时间 92 小时）中计算了个体化的自动调节下限。我们确定了 35 例脑组织缺氧（PbtO<20mmHg）患者，采用 CPP 增强治疗。每次干预后，平均 CPP 从 73±14mmHg 增加到 79±17mmHg（p=0.15），平均 PbtO 从 18.4±5.6mmHg 改善到 21.9±5.6mmHg（p=0.01），而自动调节功能呈改善趋势（氧反应指数 0.42 比 0.37，p=0.14；压力反应指数 0.25 比 0.21，p=0.2）。尽管最佳 CPP 和下限相对保持不变，但与干预前相比，干预后 60 分钟内 CPP 低于自动调节下限的时间百分比显著降低（11%比 23%，p=0.05）。
我们的分析表明，脑组织缺氧与以 CPP 低于自动调节下限时间增加为特征的脑灌注不足有关。增加 CPP 的干预措施似乎改善了自动调节。需要进一步的研究来验证自动调节作为一个可改变的变量的重要性，以及它改善结果的潜力。
