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

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 oxy...

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Veröffentlicht in:Neurosurgery 1998-05, Vol.42 (5), p.1057-63; discussion 1063-4
Hauptverfasser: Brown, J I, Moulton, R J, Konasiewicz, S J, Baker, A J
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container_end_page 63; discussion 1063-4
container_issue 5
container_start_page 1057
container_title Neurosurgery
container_volume 42
creator Brown, J I
Moulton, R J
Konasiewicz, S J
Baker, A J
description 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. 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. 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. 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.
doi_str_mv 10.1097/00006123-199805000-00060
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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. Monitoring of 97 patients with severe traumatic brain injury (Glasgow Coma Scale scores of &lt; 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. 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. 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. 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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. 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. 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. 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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. Monitoring of 97 patients with severe traumatic brain injury (Glasgow Coma Scale scores of &lt; 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. 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. 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.</abstract><cop>United States</cop><pmid>9588550</pmid><doi>10.1097/00006123-199805000-00060</doi></addata></record>
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subjects Adult
Brain - metabolism
Brain Damage, Chronic - etiology
Brain Injuries - complications
Brain Injuries - metabolism
Brain Injuries - mortality
Brain Injuries - physiopathology
Brain Ischemia - etiology
Cerebrovascular Circulation
Energy Metabolism
Evoked Potentials, Somatosensory
Glasgow Coma Scale
Humans
Middle Aged
Oxygen - metabolism
Oxygen Consumption
Survival Analysis
title Cerebral oxidative metabolism and evoked potential deterioration after severe brain injury: new evidence of early posttraumatic ischemia
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