title: Cerebral acid-base homeostasis after severe traumatic brain injury.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany
authors.forename: Tobias
authors.initials: T
authors.lastname: Clausen
authors.forename: Ahmad
authors.initials: A
authors.lastname: Khaldi
authors.forename: Alois
authors.initials: A
authors.lastname: Zauner
authors.forename: Michael
authors.initials: M
authors.lastname: Reinert
authors.forename: Egon
authors.initials: E
authors.lastname: Doppenberg
authors.forename: Matthias
authors.initials: M
authors.lastname: Menzel
authors.forename: Jens
authors.initials: J
authors.lastname: Soukup
authors.forename: Oscar Luis
authors.initials: OL
authors.lastname: Alves
authors.forename: M Ross
authors.initials: MR
authors.lastname: Bullock
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology*; D000328:Adult; D001923:Brain Chemistry; D001930:Brain Injuries / Q000150:complications*; D002245:Carbon Dioxide / Q000032:analysis; D016923:Cell Death; D005260:Female; D006706:Homeostasis; D006801:Humans; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000032:analysis; D008297:Male; D008875:Middle Aged
chemical_list: D002245:Carbon Dioxide; D019344:Lactic Acid