Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain.
Level 4 - case-series / case-control
Prospective single-arm interventional study without a control group.
PubMed 24477453 · doi:10.1007/s00134-013-3203-6
What was done
Fifteen consecutive patients with severe traumatic brain injury (TBI) monitored with cerebral microdialysis, brain tissue PO2 (PbtO2), and intracranial pressure (ICP) received a 3-hour intravenous infusion of hypertonic sodium lactate (titrated to systemic lactate ~5 mmol/L). Infusions started at a mean of 33 ± 16 hours post-injury. Effects on microdialysis metabolites (lactate, pyruvate, glucose, glutamate), PbtO2, and ICP were assessed using mixed-effects multilevel regression modeling.
What was found
Sodium lactate infusion significantly elevated cerebral microdialysis lactate (coefficient 0.47 mmol/L, 95% CI 0.31 to 0.63), pyruvate (13.1 μmol/L, 95% CI 8.78 to 17.4), and glucose (0.1 mmol/L, 95% CI 0.04 to 0.16; all p < 0.01). ICP decreased significantly by -0.86 mmHg (95% CI -1.47 to -0.24, p < 0.01), and glutamate showed a non-significant trend toward reduction (-0.95 mmol/L, 95% CI -1.94 to 0.06, p = 0.06). Numerical values for PbtO2 were not reported in the abstract.
Why it matters
Provides direct human evidence that exogenous lactate reaches the injured brain parenchyma and increases cerebral glucose and pyruvate availability, supporting its role as an alternative metabolic substrate and potential osmotic agent after acute TBI.
Limits
The study was very small (n = 15) and lacked a randomized or blinded control group. The protocol evaluated short-term surrogate neurochemical and intracranial pressure metrics rather than long-term clinical or functional neurological recovery. PbtO2 quantitative data were not provided in the abstract.
Cited by
- supports Administering lactate salts can mitigate cerebral swelling and acidosis following traumatic brain injury.