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严重脑损伤后脑氧化代谢及诱发电位恶化:创伤后早期缺血的新证据

Cerebral oxidative metabolism and evoked potential deterioration after severe brain injury: new evidence of early posttraumatic ischemia.

作者信息

Brown J I, Moulton R J, Konasiewicz S J, Baker A J

机构信息

Division of Neurosurgery, Saint Michael's Hospital, University of Toronto, Ontario, Canada.

出版信息

Neurosurgery. 1998 May;42(5):1057-63; discussion 1063-4. doi: 10.1097/00006123-199805000-00060.

Abstract

BACKGROUND

We commonly observe progressive deterioration in somatosensory evoked potentials (SSEPs) after severe head injury. We had previously been unable to relate this deterioration to raised intracranial pressure but had noted a relationship with decreasing transcranial oxygen extraction (arteriovenous oxygen difference [AVDO2]). The purpose of this study was twofold: to prove the hypothesis that deterioration in SSEP values is associated with decreasing AVDO2 and to test the subsidiary hypotheses that deteriorating SSEPs were the result of either ischemia/reperfusion injury or failure of oxygen extraction/utilization.

METHODS

Monitoring of 97 patients with severe traumatic brain injury (Glasgow Coma Scale scores of < or = 8 after resuscitation) included twice daily AVDO2 measurement and hourly SSEP recording for an average of 5 days. The last 51 patients also underwent 12-hourly measurement of cerebral blood flow (CBF), with calculation of the cerebral metabolic rate of oxygen. Cluster analysis was used to classify patients based on initial AVDO2 values and subsequent SSEP trends. The time courses of CBF, SSEPs, AVDO2, and cerebral metabolic rate of oxygen were examined in the groups defined by the cluster analysis. The clinical outcomes considered were survival or nonsurvival and the Glasgow Outcome Scale scores obtained at 3 months or more after injury.

RESULTS

Cluster analysis confirmed the association between high initial AVDO2 values and subsequent SSEP deterioration. Patients in this category initially had significantly higher AVDO2, lower CBF, and higher cerebral metabolic rates of oxygen but recovered to adequate levels within 24 to 36 hours after injury. SSEP values were initially identical in the patients with normal AVDO2 values and those with elevated AVDO2 but differed significantly at 60 hours after injury and beyond.

CONCLUSION

The findings of increased oxygen utilization and lowered CBF in the patients with deteriorating SSEPs strongly imply that early ischemia rather than failure of O2 extraction or utilization is responsible for the associated SSEP deterioration. This issue of defining thresholds for ischemia based on AVDO2 is confounded by the dependency of CBF and AVDO2 values on the time after injury.

摘要

背景

我们通常观察到严重颅脑损伤后体感诱发电位(SSEPs)会逐渐恶化。我们之前无法将这种恶化与颅内压升高联系起来,但注意到其与经颅氧摄取减少(动静脉氧差[AVDO2])有关。本研究的目的有两个:证明SSEP值恶化与AVDO2降低相关的假设,并检验SSEP恶化是缺血/再灌注损伤或氧摄取/利用失败的结果这两个辅助假设。

方法

对97例重型颅脑损伤患者(复苏后格拉斯哥昏迷量表评分≤8分)进行监测,包括每天两次测量AVDO2以及每小时记录SSEP,平均持续5天。最后51例患者还每12小时测量一次脑血流量(CBF),并计算脑氧代谢率。采用聚类分析根据初始AVDO2值和随后的SSEP趋势对患者进行分类。在聚类分析定义的组中检查CBF、SSEPs、AVDO2和脑氧代谢率的时间进程。所考虑的临床结局为存活或未存活以及伤后3个月或更长时间获得的格拉斯哥预后量表评分。

结果

聚类分析证实了初始AVDO2值高与随后SSEP恶化之间的关联。此类患者最初的AVDO2显著更高、CBF更低且脑氧代谢率更高,但在伤后24至36小时内恢复到适当水平。AVDO2值正常的患者和AVDO2升高的患者最初的SSEP值相同,但在伤后60小时及以后有显著差异。

结论

SSEP恶化患者氧利用增加和CBF降低的发现强烈表明,早期缺血而非氧摄取或利用失败是相关SSEP恶化的原因。基于AVDO2定义缺血阈值的问题因CBF和AVDO2值对伤后时间的依赖性而变得复杂。

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