Cerebral acid-base homeostasis after severe traumatic brain injury

Tobias Clausen, Ahmad Khaldi, Alois Zauner, Michael Reinert, Egon Doppenberg, Matthias Menzel, Jens Soukup, Oscar Luis Alves, Ross Bullock

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Object. Brain tissue acidosis is known to mediate neuronal death. Therefore the authors measured the main parameters of cerebral acid-base homeostasis, as well as their interrelations, shortly after severe traumatic brain injury (TBI) in humans. Methods. Brain tissue pH, PCO2, PO2, and/or lactate were measured in 151 patients with severe head injuries, by using a Neurotrend sensor and/or a microdialysis probe. Monitoring was started as soon as possible after the injury and continued for up to 4 days. During the 1st day following the trauma, the brain tissue pH was significantly lower, compared with later time points, in patients who died or remained in a persistent vegetative state. Six hours after the injury, brain tissue PCO2 was significantly higher in patients with a poor outcome compared with patients with a good outcome. Furthermore, significant elevations in cerebral concentrations of lactate were found during the 1st day after the injury, compared with later time points. These increases in lactate were typically more pronounced in patients with a poor outcome. Similar biochemical changes were observed during later hypoxic events. Conclusions. Severe human TBI profoundly disturbs cerebral acid-base homeostasis. The observed pH changes persist for the first 24 hours after the trauma. Brain tissue acidosis is associated with increased tissue PCO2 and lactate concentration; these pathobiochemical changes are more severe in patients who remain in a persistent vegetative state or die. Furthermore, increased brain tissue PCO2 (> 60 mm Hg) appears to be a useful clinical indicator of critical cerebral ischemia, especially when accompanied by increased lactate concentrations.

Original languageEnglish
Pages (from-to)597-607
Number of pages11
JournalJournal of Neurosurgery
Volume103
Issue number4
StatePublished - Oct 1 2005
Externally publishedYes

Fingerprint

Homeostasis
Lactic Acid
Acids
Persistent Vegetative State
Brain
Acidosis
Wounds and Injuries
Microdialysis
Traumatic Brain Injury
Brain Ischemia
Craniocerebral Trauma
Brain Injuries

Keywords

  • Carbon dioxide
  • Cerebral acid-base homeostasis
  • Lactate/ischemia
  • Multimodal monitoring
  • Traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Clausen, T., Khaldi, A., Zauner, A., Reinert, M., Doppenberg, E., Menzel, M., ... Bullock, R. (2005). Cerebral acid-base homeostasis after severe traumatic brain injury. Journal of Neurosurgery, 103(4), 597-607.

Cerebral acid-base homeostasis after severe traumatic brain injury. / Clausen, Tobias; Khaldi, Ahmad; Zauner, Alois; Reinert, Michael; Doppenberg, Egon; Menzel, Matthias; Soukup, Jens; Alves, Oscar Luis; Bullock, Ross.

In: Journal of Neurosurgery, Vol. 103, No. 4, 01.10.2005, p. 597-607.

Research output: Contribution to journalArticle

Clausen, T, Khaldi, A, Zauner, A, Reinert, M, Doppenberg, E, Menzel, M, Soukup, J, Alves, OL & Bullock, R 2005, 'Cerebral acid-base homeostasis after severe traumatic brain injury', Journal of Neurosurgery, vol. 103, no. 4, pp. 597-607.
Clausen T, Khaldi A, Zauner A, Reinert M, Doppenberg E, Menzel M et al. Cerebral acid-base homeostasis after severe traumatic brain injury. Journal of Neurosurgery. 2005 Oct 1;103(4):597-607.
Clausen, Tobias ; Khaldi, Ahmad ; Zauner, Alois ; Reinert, Michael ; Doppenberg, Egon ; Menzel, Matthias ; Soukup, Jens ; Alves, Oscar Luis ; Bullock, Ross. / Cerebral acid-base homeostasis after severe traumatic brain injury. In: Journal of Neurosurgery. 2005 ; Vol. 103, No. 4. pp. 597-607.
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