title: Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury.
abstract: OBJECTIVE
  Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2).
  
  
  METHODS
  In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2 was increased to 441+/-88 mm Hg over a period of 6 hours by raising the FiO2 from 35+/-5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4+/-22.1 mm Hg). The mean brain PO2 levels increased in the O2-treated patients up to 359+/-39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period.
  
  
  CONCLUSIONS
  Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.
authors.affiliation: Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0631, USA.
authors.forename: M
authors.initials: M
authors.lastname: Menzel
authors.forename: E M
authors.initials: EM
authors.lastname: Doppenberg
authors.forename: A
authors.initials: A
authors.lastname: Zauner
authors.forename: J
authors.initials: J
authors.lastname: Soukup
authors.forename: M M
authors.initials: MM
authors.lastname: Reinert
authors.forename: R
authors.initials: R
authors.lastname: Bullock
mesh_terms: D000328:Adult; D000368:Aged; D001921:Brain / Q000378:metabolism*; D016022:Case-Control Studies; D006259:Craniocerebral Trauma / Q000378:metabolism* / Q000628:therapy*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D018496:Hyperoxia / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D010100:Oxygen / Q000032:analysis*; D012121:Respiration, Artificial / Q000379:methods*; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D019344:Lactic Acid; D005947:Glucose; D010100:Oxygen