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, M Ross (2005). Cerebral acid-base homeostasis after severe traumatic brain injury. Journal of neurosurgery, 103(4), pp. 597-607. Charlottesville, Va.: American Association of Neurological Surgeons 10.3171/jns.2005.103.4.0597

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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.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurosurgery
UniBE Contributor:	Reinert, Michael
ISSN:	0022-3085
ISBN:	16266040
Publisher:	American Association of Neurological Surgeons
Language:	English
Submitter:	Factscience Import
Date Deposited:	04 Oct 2013 15:02
Last Modified:	05 Dec 2022 14:19
Publisher DOI:	10.3171/jns.2005.103.4.0597
PubMed ID:	16266040
Web of Science ID:	000232385000005
URI:	https://boris.unibe.ch/id/eprint/27032 (FactScience: 101357)