Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism
Abstract
UNLABELLED: The purpose of this study was to determine if the relationship between abnormalities in glucose, lactate, and oxygen metabolism were predictive of neurologic outcome after moderate or severe head injury, relative to other known prognostic factors. Serial assessments of the cerebral metabolic rates for glucose, lactate, and oxygen were performed using a modified Kety-Schmidt method. In total, 31 normal control subjects were studied once, and 49 TBI patients (mean age 36+/-16 years, median GCS 7) were studied five times median per patient from postinjury days 0 to 9. Univariate and multivariate analyses were performed. Univariate analysis showed that the 6-month postinjury Glasgow Outcome Scale (GOS) was most strongly associated with the mean cerebral metabolic rate of oxygen (CMRO2) (P = 0.0001), mean arterial lactate level (P = 0.0001), mean arterial glucose (P = 0.0008), mean cerebral blood flow (CBF), (P = 0.002), postresuscitation GCS (P = 0.003), and pupillary status (P = 0.004). Brain lactate uptake was observed in 44% of all metabolic studies, and 76% of patients had at least one episode of brain lactate uptake. By dichotomized GOS, patients achieving a favorable outcome (GOS 4-5) were distinguished from those with an unfavorable outcome (GOS1-3) by having a higher CMRO2 (P = 0.003), a higher rate of abnormal brain lactate uptake relative to arterial lactate levels (P = 0.04), and lesser degrees of blood-brain barrier damage based on CT findings (P = 0.03). CONCLUSIONS: During the first 6 days after moderate or severe TBI, CMRO2 and arterial lactate levels are the strongest predictors of neurologic outcome. However, the frequent occurrence of abnormal brain lactate uptake despite only moderate elevations in arterial lactate levels in the favorable outcome patients suggests the brain's ability to use lactate as a fuel may be another key outcome predictor. Future studies are needed to determine to what degree nonglycolytic energy production from alternative fuels such as lactate occurs after TBI and whether alternative fuel administration is a viable therapy for TBI patients.
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Cerebral ischemia and hypoxia lead to accumulation of lactic acid due to anaerobic glycolysis, increased permeability of membranes, and consecutive edema formation.
“Because cerebral metabolic dysfunction occurs due to head trauma, cerebral ischemia and hypoxia lead to the accumulation of lactic acid due to anaerobic glycolysis, increased permeability of membranes, and consecutive edema formation (117, 118).”
From Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach (2015) · cites this paper as [118]
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- Authors
- Glenn, T. C., Kelly, D. F., Boscardin, W. J., McArthur, D. L., Vespa, P., Oertel, M., Hovda, D. A., Bergsneider, M., Hillered, L., & Martin, N. A.
- Affiliations
- University of California, Los Angeles (US)
- Uppsala University Hospital (SE)
- Corresponding author
- Kelly, Daniel F
- ORCID
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2003-10
- Volume
- 23
- Issue
- 10
- Pages
- 1239-1250
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2028546276
- Cited by
- 296
- References
- 80
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 16 · 2023: 8 · 2022: 10 · 2021: 11 · 2020: 9 · 2019: 11 · 2018: 17 · 2017: 21 · 2016: 8 · 2015: 27 · 2014: 13 · 2013: 16 · 2012: 13
- FWCI
- 5.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (P50NS030308, NS 30308)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Emergency Medicine › Trauma and Emergency Care Studies
- Keywords
- traumatic brain injury, brain energy metabolism, cerebral oxygen consumption, arterial lactate, brain glucose metabolism, prognostic factors, neurological outcome, Glasgow Outcome Scale, Kety-Schmidt method, cerebral blood flow, blood-brain barrier disruption, cerebral hypoxia
- MeSH terms
- Adult, Brain, Brain Injuries, Hypoxia, Brain, Cerebrovascular Circulation, Energy Metabolism, Female, Glucose, Glycolysis, Humans, Hypotension, Intracranial Pressure, Male, Middle Aged, Oxidative Phosphorylation, Oxygen, Predictive Value of Tests, Prognosis, Pupil Disorders, Cohort Studies, Glasgow Coma Scale, Multivariate Analysis, Lactic Acid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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