Effect of hyperoxia on regional oxygenation and metabolism after severe traumatic brain injury: preliminary findings.
OBJECTIVE
To determine the effect of normobaric hyperoxia on cerebral metabolism in patients with severe traumatic brain injury.


METHODS
Prospective clinical investigation.


METHODS
Neurosciences critical care unit of a university hospital.


METHODS
Eleven patients with severe traumatic brain injury.


METHODS
Cerebral microdialysis, brain tissue oximetry (PbO2), and oxygen-15 positron emission tomography (15O-PET) were undertaken at normoxia and repeated at hyperoxia (FiO2 increase of between 0.35 and 0.50).


RESULTS
Established models were used to image cerebral blood flow, blood volume, oxygen metabolism, and oxygen extraction fraction. Physiology was characterized in a focal region of interest (surrounding the microdialysis catheter) and correlated with microdialysis and oximetry. Physiology was also characterized in a global region of interest (including the whole brain), and a physiologic region of interest (defined using a critical cerebral metabolic rate of oxygen threshold). Hyperoxia increased mean +/- sd PbO2 from 28 +/- 21 mm Hg to 57 +/- 47 mm Hg (p = .015). Microdialysate lactate and pyruvate were unchanged, but the lactate/pyruvate ratio showed a statistically significant reduction across the study population (34.1 +/- 9.5 vs. 32.5 +/- 9.0, p = .018). However, the magnitude of reduction was small, and its clinical significance doubtful. The focal region of interest and global 15O-PET variables were unchanged. "At-risk" tissue defined by the physiologic region of interest, however, showed a universal increase in cerebral metabolic rate of oxygen from a median (interquartile range) of 23 (22-25) micromol x 100 mL(-1) x min(-1) to 30 (28-36) micromol x 100 mL(-1) x min(-1) (p < .01).


CONCLUSIONS
In severe traumatic brain injury, hyperoxia increases PbO2 with a variable effect on lactate and lactate/pyruvate ratio. Microdialysis does not, however, predict the universal increases in cerebral metabolic rate of oxygen in at-risk tissue, which imply preferential metabolic benefit with hyperoxia.
Nortje
Jurgens
J
University Division of Anaesthesia, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.
Coles
Jonathan P
JP
Timofeev
Ivan
I
Fryer
Tim D
TD
Aigbirhio
Franklin I
FI
Smielewski
Peter
P
Outtrim
Joanne G
JG
Chatfield
Doris A
DA
Pickard
John D
JD
Hutchinson
Peter J
PJ
Gupta
Arun K
AK
Menon
David K
DK
D000293:Adolescent; D000328:Adult; D001930:Brain Injuries / Q000378:metabolism*; D054022:Cerebrum / Q000378:metabolism; D005260:Female; D006801:Humans; D018496:Hyperoxia / Q000378:metabolism*; D007427:Intracranial Pressure; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism; D011446:Prospective Studies; D019289:Pyruvic Acid / Q000378:metabolism
D019344:Lactic Acid; D019289:Pyruvic Acid; D010100:Oxygen