Normobaric hyperoxia is associated with increased cerebral excitotoxicity after severe traumatic brain injury - PubMed (original) (raw)
Normobaric hyperoxia is associated with increased cerebral excitotoxicity after severe traumatic brain injury
Hervé Quintard et al. Neurocrit Care. 2015 Apr.
Abstract
Background: Normobaric oxygen therapy is frequently applied in neurocritical care, however, whether supplemental FiO2 has beneficial cerebral effects is still controversial. We examined in patients with severe traumatic brain injury (TBI) the effect of incremental FiO2 on cerebral excitotoxicity, quantified by cerebral microdialysis (CMD) glutamate.
Methods: This was a retrospective analysis of a database of severe TBI patients monitored with CMD and brain tissue oxygen (PbtO2). The relationship of FiO2--categorized into four separate ranges (<40, 41-60, 61-80, and >80 %)--with CMD glutamate was examined using ANOVA with Tukey's post hoc test.
Results: A total of 1,130 CMD samples from 36 patients--monitored for a median of 4 days--were examined. After adjusting for brain (PbtO2, intracranial pressure, cerebral perfusion pressure, lactate/pyruvate ratio, Marshall CT score) and systemic (PaCO2, PaO2, hemoglobin, APACHE score) covariates, high FiO2 was associated with a progressive increase in CMD glutamate [8.8 (95 % confidence interval 7.4-10.2) µmol/L at FiO2 < 40 % vs. 12.8 (10.9-14.7) µmol/L at 41-60 % FiO2, 19.3 (15.6-23) µmol/L at 61-80 % FiO2, and 22.6 (16.7-28.5) µmol/L at FiO2 > 80 %; multivariate-adjusted p < 0.05]. The threshold of FiO2-related increase in CMD glutamate was lower for samples with normal versus low PbtO2 < 20 mmHg (FiO2 > 40 % vs. FiO2 > 60 %). Hyperoxia (PaO2 > 150 mmHg) was also associated with increased CMD glutamate (adjusted p < 0.001).
Conclusions: Incremental normobaric FiO2 levels were associated with increased cerebral excitotoxicity in patients with severe TBI, independent from PbtO2 and other important cerebral and systemic determinants. These data suggest that supra-normal oxygen may aggravate secondary brain damage after severe TBI.
Similar articles
- 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 CM, Reinert M, Seiler R, Gilman C, Scharf A, Bullock MR. Tolias CM, et al. J Neurosurg. 2004 Sep;101(3):435-44. doi: 10.3171/jns.2004.101.3.0435. J Neurosurg. 2004. PMID: 15352601 - Lung Injury Is a Predictor of Cerebral Hypoxia and Mortality in Traumatic Brain Injury.
Robba C, Asgari S, Gupta A, Badenes R, Sekhon M, Bequiri E, Hutchinson PJ, Pelosi P, Gupta A. Robba C, et al. Front Neurol. 2020 Aug 7;11:771. doi: 10.3389/fneur.2020.00771. eCollection 2020. Front Neurol. 2020. PMID: 32849225 Free PMC article. - High arterial oxygen levels and supplemental oxygen administration in traumatic brain injury: insights from CENTER-TBI and OzENTER-TBI.
Rezoagli E, Petrosino M, Rebora P, Menon DK, Mondello S, Cooper DJ, Maas AIR, Wiegers EJA, Galimberti S, Citerio G; CENTER-TBI, OzENTER-TBI Participants and Investigators. Rezoagli E, et al. Intensive Care Med. 2022 Dec;48(12):1709-1725. doi: 10.1007/s00134-022-06884-x. Epub 2022 Oct 20. Intensive Care Med. 2022. PMID: 36264365 Free PMC article. - A systematic review of cerebral microdialysis and outcomes in TBI: relationships to patient functional outcome, neurophysiologic measures, and tissue outcome.
Zeiler FA, Thelin EP, Helmy A, Czosnyka M, Hutchinson PJA, Menon DK. Zeiler FA, et al. Acta Neurochir (Wien). 2017 Dec;159(12):2245-2273. doi: 10.1007/s00701-017-3338-2. Epub 2017 Oct 7. Acta Neurochir (Wien). 2017. PMID: 28988334 Free PMC article. Review. - [Normobaric hyperoxia therapy for patients with traumatic brain injury].
Francony G, Bouzat P, Picard J, Fevre MC, Gay S, Payen JF. Francony G, et al. Ann Fr Anesth Reanim. 2012 Mar;31(3):224-7. doi: 10.1016/j.annfar.2011.11.009. Epub 2012 Feb 3. Ann Fr Anesth Reanim. 2012. PMID: 22305404 Review. French.
Cited by
- Effect of Early Normobaric Hyperoxia on Blast-Induced Traumatic Brain Injury in Rats.
Li Y, Lv W, Cheng G, Wang S, Liu B, Zhao H, Wang H, Zhang L, Dong C, Zhang J. Li Y, et al. Neurochem Res. 2020 Nov;45(11):2723-2731. doi: 10.1007/s11064-020-03123-x. Epub 2020 Sep 9. Neurochem Res. 2020. PMID: 32902742 - Use a "GHOST-CAP" in acute brain injury.
Taccone FS, De Oliveira Manoel AL, Robba C, Vincent JL. Taccone FS, et al. Crit Care. 2020 Mar 14;24(1):89. doi: 10.1186/s13054-020-2825-7. Crit Care. 2020. PMID: 32171298 Free PMC article. No abstract available. - Early Hyperoxia in Patients with Traumatic Brain Injury Admitted to Intensive Care in Australia and New Zealand: A Retrospective Multicenter Cohort Study.
Ó Briain D, Nickson C, Pilcher DV, Udy AA. Ó Briain D, et al. Neurocrit Care. 2018 Dec;29(3):443-451. doi: 10.1007/s12028-018-0553-5. Neurocrit Care. 2018. PMID: 29949002 - Traumatic Brain Injury and Blood-Brain Barrier (BBB): Underlying Pathophysiological Mechanisms and the Influence of Cigarette Smoking as a Premorbid Condition.
Sivandzade F, Alqahtani F, Cucullo L. Sivandzade F, et al. Int J Mol Sci. 2020 Apr 14;21(8):2721. doi: 10.3390/ijms21082721. Int J Mol Sci. 2020. PMID: 32295258 Free PMC article. Review. - Hyperoxia results in increased aerobic metabolism following acute brain injury.
Ghosh A, Highton D, Kolyva C, Tachtsidis I, Elwell CE, Smith M. Ghosh A, et al. J Cereb Blood Flow Metab. 2017 Aug;37(8):2910-2920. doi: 10.1177/0271678X16679171. Epub 2016 Jan 1. J Cereb Blood Flow Metab. 2017. PMID: 27837190 Free PMC article.
References
- Neurocrit Care. 2011 Jun;14(3):361-9 - PubMed
- J Neurosurg. 2003 May;98(5):952-8 - PubMed
- J Neurosurg. 2004 Sep;101(3):435-44 - PubMed
- Neurocrit Care. 2010 Aug;13(1):47-56 - PubMed
- J Intern Med. 2013 Dec;274(6):505-28 - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical