Brain tissue guided treatment supplementing ICP/CPP therapy after traumatic brain injury
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《神经病学神经外科学杂志》
Correspondence to:
Dr D Zygun
University Department of Anaesthesia, University of Cambridge, Box 93, Level 4, E block, Hills Road, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK; dzygun@ucalgary.ca
Keywords: brain tissue oxygen; cerebral perfusion pressure; head injury; outcome
The recent article by Meixensberger and colleagues comparing a brain tissue oxygen guided treatment protocol with a ICP/CPP protocol1 presents insufficient evidence to support the conclusion that PtiO2 guided cerebral perfusion management reduced cerebral hypoxic events following traumatic brain injury. Brain tissue oxygen levels can easily be modified through changes in FiO2.2,3 Although the authors indicated that changes in FiO2 were not used to raise the PtiO2, no data were presented to support this assertion. What was the FiO2 before and after cerebral hypoxic episodes in each group? Furthermore, despite no significant difference in CPP, PtiO2 was significantly higher on days 1, 2, 5, and 6. This could be explained by higher PaO2 levels in the PtiO2 guided group, yet no data on PaO2 were presented. To assess the influence of the PtiO2 guided cerebral perfusion management accurately, the patient’s PaO2 and incidence of systemic hypoxaemia must be known, because of the strong correlation between PaO2 and PtiO2. These data are essential to conclude that cerebral perfusion management, and not PaO2 management, was responsible for the reduction in cerebral hypoxic episodes.
A major difficulty in the analysis of two consecutive series of patients lies in ensuring that the groups are equivalent at baseline and controlling for confounding interventions. General intensive care management has significantly evolved in the past decade and the possibility that co-interventions unrelated to perfusion management were responsible for the reduction in cerebral hypoxic events cannot be ruled out. Furthermore, the non-consecutive nature of recruitment may have resulted in selection bias. As the authors pointed out, it is clear that randomised controlled studies are needed to evaluate properly current monitoring and therapeutic strategies in the management of severe traumatic brain injury. Although expensive and labour intensive, such trials are warranted because of the tremendous burden of this disease on patients and society.
References
Meixensberger J, Jaeger M, Vath A, et al. Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury. J Neurol Neurosurg Psychiatry 2003;74:760–4.
Menzel M, Doppenberg EM, Zauner A, et al. Cerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure. J Neurosurg Anesthesiol 1999;11:240–51.
Longhi L, Valeriani V, Rossi S, et al. Effects of hyperoxia on brain tissue oxygen tension in cerebral focal lesions. Acta Neurochir Suppl 2002;81:315–17.(D Zygun)
Dr D Zygun
University Department of Anaesthesia, University of Cambridge, Box 93, Level 4, E block, Hills Road, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK; dzygun@ucalgary.ca
Keywords: brain tissue oxygen; cerebral perfusion pressure; head injury; outcome
The recent article by Meixensberger and colleagues comparing a brain tissue oxygen guided treatment protocol with a ICP/CPP protocol1 presents insufficient evidence to support the conclusion that PtiO2 guided cerebral perfusion management reduced cerebral hypoxic events following traumatic brain injury. Brain tissue oxygen levels can easily be modified through changes in FiO2.2,3 Although the authors indicated that changes in FiO2 were not used to raise the PtiO2, no data were presented to support this assertion. What was the FiO2 before and after cerebral hypoxic episodes in each group? Furthermore, despite no significant difference in CPP, PtiO2 was significantly higher on days 1, 2, 5, and 6. This could be explained by higher PaO2 levels in the PtiO2 guided group, yet no data on PaO2 were presented. To assess the influence of the PtiO2 guided cerebral perfusion management accurately, the patient’s PaO2 and incidence of systemic hypoxaemia must be known, because of the strong correlation between PaO2 and PtiO2. These data are essential to conclude that cerebral perfusion management, and not PaO2 management, was responsible for the reduction in cerebral hypoxic episodes.
A major difficulty in the analysis of two consecutive series of patients lies in ensuring that the groups are equivalent at baseline and controlling for confounding interventions. General intensive care management has significantly evolved in the past decade and the possibility that co-interventions unrelated to perfusion management were responsible for the reduction in cerebral hypoxic events cannot be ruled out. Furthermore, the non-consecutive nature of recruitment may have resulted in selection bias. As the authors pointed out, it is clear that randomised controlled studies are needed to evaluate properly current monitoring and therapeutic strategies in the management of severe traumatic brain injury. Although expensive and labour intensive, such trials are warranted because of the tremendous burden of this disease on patients and society.
References
Meixensberger J, Jaeger M, Vath A, et al. Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury. J Neurol Neurosurg Psychiatry 2003;74:760–4.
Menzel M, Doppenberg EM, Zauner A, et al. Cerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure. J Neurosurg Anesthesiol 1999;11:240–51.
Longhi L, Valeriani V, Rossi S, et al. Effects of hyperoxia on brain tissue oxygen tension in cerebral focal lesions. Acta Neurochir Suppl 2002;81:315–17.(D Zygun)