Normobaric hyperoxia-induced improvement in cerebral metabolism and reduction in intracranial pressure in patients with severe head injury: A prospective historical cohort-matched study

Christos M. Tolias, Michael Reinert, Rolf Seiler, Charlotte Gilman, Alexander Scharf, Ross Bullock

Research output: Contribution to journalArticle

153 Citations (Scopus)

Abstract

Object. The effect of normobaric hyperoxia (fraction of inspired O 2 [FIO2] concentration 100%) in the treatment of patients with traumatic brain injury (TBI) remains controversial. The aim of this study was to investigate the effects of normobaric hyperoxia on five cerebral metabolic indices, which have putative prognostic significance following TBI in humans. Methods. At two independent neurointensive care units, the authors performed a prospective study of 52 patients with severe TBI who were treated for 24 hours with 100% FIO2, starting within 6 hours of admission. Data for these patients were compared with data for a cohort of 112 patients who were treated in the past; patients in the historical control group matched the patients in our study according to their Glasgow Coma Scale scores after resuscitation and their intracranial pressure within the first 8 hours after admission. Patients were monitored with the aid of intracerebral microdialysis and tissue O2 probes. Normobaric hyperoxia treatment resulted in a significant improvement in biochemical markers in the brain compared with the baseline measures for patients treated in our study (patients acting as their own controls) and also compared with findings from the historical control group. In the dialysate the glucose levels increased (369.02 ± 20.1 μmol/L in the control group and 466.9 ± 20.39 μmol/L in the 100% O 2 group, p = 0.001), whereas the glutamate and lactate levels significantly decreased (p < 0.005). There were also reductions in the lactate/glucose and lactate/pyruvate ratios. Intracranial pressure in the treatment group was reduced significantly both during and after hyperoxia treatment compared with the control groups (15.03 ± 0.8 mm Hg in the control group and 12.13 ± 0.75 mm Hg in the 100% O2 group, p < 0.005) with no changes in cerebral perfusion pressure. Outcomes of the patients in the treatment group improved. Conclusions. The results of the study support the hypothesis that normobaric hyperoxia in patients with severe TBI improves the indices of brain oxidative metabolism. Based on these data further mechanistic studies and a prospective randomized controlled trial are warranted.

Original languageEnglish
Pages (from-to)435-444
Number of pages10
JournalJournal of Neurosurgery
Volume101
Issue number3
StatePublished - Sep 1 2004
Externally publishedYes

Fingerprint

Hyperoxia
Intracranial Pressure
Craniocerebral Trauma
Cohort Studies
Control Groups
Lactic Acid
Cerebrovascular Circulation
Prospective Studies
Therapeutics
Glucose
Glasgow Coma Scale
Dialysis Solutions
Microdialysis
Brain
Pyruvic Acid
Resuscitation
Glutamic Acid
Randomized Controlled Trials
Biomarkers

Keywords

  • Brain metabolism
  • Glucose
  • Head injury
  • Hyperoxia
  • Lactate
  • Microdialysis

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Normobaric hyperoxia-induced improvement in cerebral metabolism and reduction in intracranial pressure in patients with severe head injury : A prospective historical cohort-matched study. / Tolias, Christos M.; Reinert, Michael; Seiler, Rolf; Gilman, Charlotte; Scharf, Alexander; Bullock, Ross.

In: Journal of Neurosurgery, Vol. 101, No. 3, 01.09.2004, p. 435-444.

Research output: Contribution to journalArticle

Tolias, Christos M. ; Reinert, Michael ; Seiler, Rolf ; Gilman, Charlotte ; Scharf, Alexander ; Bullock, Ross. / Normobaric hyperoxia-induced improvement in cerebral metabolism and reduction in intracranial pressure in patients with severe head injury : A prospective historical cohort-matched study. In: Journal of Neurosurgery. 2004 ; Vol. 101, No. 3. pp. 435-444.
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AU - Gilman, Charlotte

AU - Scharf, Alexander

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N2 - Object. The effect of normobaric hyperoxia (fraction of inspired O 2 [FIO2] concentration 100%) in the treatment of patients with traumatic brain injury (TBI) remains controversial. The aim of this study was to investigate the effects of normobaric hyperoxia on five cerebral metabolic indices, which have putative prognostic significance following TBI in humans. Methods. At two independent neurointensive care units, the authors performed a prospective study of 52 patients with severe TBI who were treated for 24 hours with 100% FIO2, starting within 6 hours of admission. Data for these patients were compared with data for a cohort of 112 patients who were treated in the past; patients in the historical control group matched the patients in our study according to their Glasgow Coma Scale scores after resuscitation and their intracranial pressure within the first 8 hours after admission. Patients were monitored with the aid of intracerebral microdialysis and tissue O2 probes. Normobaric hyperoxia treatment resulted in a significant improvement in biochemical markers in the brain compared with the baseline measures for patients treated in our study (patients acting as their own controls) and also compared with findings from the historical control group. In the dialysate the glucose levels increased (369.02 ± 20.1 μmol/L in the control group and 466.9 ± 20.39 μmol/L in the 100% O 2 group, p = 0.001), whereas the glutamate and lactate levels significantly decreased (p < 0.005). There were also reductions in the lactate/glucose and lactate/pyruvate ratios. Intracranial pressure in the treatment group was reduced significantly both during and after hyperoxia treatment compared with the control groups (15.03 ± 0.8 mm Hg in the control group and 12.13 ± 0.75 mm Hg in the 100% O2 group, p < 0.005) with no changes in cerebral perfusion pressure. Outcomes of the patients in the treatment group improved. Conclusions. The results of the study support the hypothesis that normobaric hyperoxia in patients with severe TBI improves the indices of brain oxidative metabolism. Based on these data further mechanistic studies and a prospective randomized controlled trial are warranted.

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