Effect of hyperoxia on cerebral metabolic rate for oxygen measured using positron emission tomography in patients with acute severe head injury.
OBJECTIVE
Recent observations indicate that traumatic brain injury (TBI) may be associated with mitochondrial dysfunction. This, along with growing use of brain tissue PO2 monitors, has led to considerable interest in the potential use of ventilation with 100% oxygen to treat patients who have suffered a TBI. To date, the impact of normobaric hyperoxia has only been evaluated using indirect measures of its impact on brain metabolism. To determine if normobaric hyperoxia improves brain oxygen metabolism following acute TBI, the authors directly measured the cerebral metabolic rate for oxygen (CMRO2) with positron emission tomography before and after ventilation with 100% oxygen.


METHODS
Baseline measurements of arterial and jugular venous blood gases, mean arterial blood pressure, intracranial pressure, cerebral blood flow (CBF), cerebral blood volume, oxygen extraction fraction, and CMRO2 were made at baseline while the patients underwent ventilation with a fraction of inspired oxygen (FiO2) of 0.3 to 0.5. The FiO2 was then increased to 1.0, and 1 hour later all measurements were repeated. Five patients were studied a mean of 17.9 +/- 5.8 hours (range 12-23 hours) after trauma. The median admission Glasgow Coma Scale score was 7 (range 3-9). During ventilation with 100% oxygen, there was a marked rise in PaO2 (from 117 +/- 31 to 371 +/- 99 mm Hg, p < 0.0001) and a small rise in arterial oxygen content (12.7 +/- 4.0 to 13.3 +/- 4.6 vol %, p = 0.03). There were no significant changes in systemic hemodynamic or other blood gas measurements. At the baseline evaluation, bihemispheric CBF was 39 +/- 12 ml/100 g/min and bihemispheric CMRO2 was 1.9 +/- 0.6 ml/ 100 g/min. During hyperoxia there was no significant change in either of these measurements. (Values are given as the mean +/- standard deviation throughout.)


CONCLUSIONS
Normobaric hyperoxia did not improve brain oxygen metabolism. In the absence of outcome data from clinical trials, these preliminary data do not support the use of 100% oxygen in patients with acute TBI, although larger confirmatory studies are needed.
Diringer
Michael N
MN
Department of Neurology, Neurology/Neurosurgery Intensive Care Unit, Barnes-Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110, USA. diringerm@neuro.wustl.edu
Aiyagari
Venkatesh
V
Zazulia
Allyson R
AR
Videen
Tom O
TO
Powers
William J
WJ
D000293:Adolescent; D000328:Adult; D001784:Blood Gas Analysis; D001930:Brain Injuries / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000628:therapy*; D002560:Cerebrovascular Circulation / Q000502:physiology; D015331:Cohort Studies; D005260:Female; D015600:Glasgow Coma Scale; D006801:Humans; D018496:Hyperoxia / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology*; D010102:Oxygen Inhalation Therapy; D049268:Positron-Emission Tomography; D013997:Time Factors