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J Neurotrauma. 2016 Apr 1;33(7):681-7. doi: 10.1089/neu.2015.4057. Epub 2015 Dec 15.

Improvement of Neuroenergetics by Hypertonic Lactate Therapy in Patients with Traumatic Brain Injury Is Dependent on Baseline Cerebral Lactate/Pyruvate Ratio.

Author information

1
1 Department of Intensive Care Medicine, Neuroscience Critical Care Research Group, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne University Hospital , Lausanne, Switzerland .
2
2 Department of Anesthesia and Intensive Care, Nice University Hospital , Nice, France .
3
3 Department of Medical Radiology, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne University Hospital , Lausanne, Switzerland .
4
4 Department of Anesthesia and Intensive Care, Grenoble University Hospital , Grenoble, France .
5
5 Institute of Physiology, University of Lausanne , Lausanne, Switzerland .
6
6 Division of Biological and Environmental Sciences and Engineering, King Abdullah University of Science and Technology (KAUST) , Thuwal, Kingdom of Saudi Arabia .
7
7 Centre de Neurosciences Psychiatriques, Department of Psychiatry, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne University Hospital , Lausanne, Switzerland .
8
8 Laboratory of Neuroenergetics and Cellular Dynamics, Brain Mind Institute , Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland .

Abstract

Energy dysfunction is associated with worse prognosis after traumatic brain injury (TBI). Recent data suggest that hypertonic sodium lactate infusion (HL) improves energy metabolism after TBI. Here, we specifically examined whether the efficacy of HL (3h infusion, 30-40 μmol/kg/min) in improving brain energetics (using cerebral microdialysis [CMD] glucose as a main therapeutic end-point) was dependent on baseline cerebral metabolic state (assessed by CMD lactate/pyruvate ratio [LPR]) and cerebral blood flow (CBF, measured with perfusion computed tomography [PCT]). Using a prospective cohort of 24 severe TBI patients, we found CMD glucose increase during HL was significant only in the subgroup of patients with elevated CMD LPR >25 (n = 13; +0.13 [95% confidence interval (CI) 0.08-0.19] mmol/L, p < 0.001; vs. +0.04 [-0.05-0.13] in those with normal LPR, p = 0.33, mixed-effects model). In contrast, CMD glucose increase was independent from baseline CBF (coefficient +0.13 [0.04-0.21] mmol/L when global CBF was <32.5 mL/100 g/min vs. +0.09 [0.04-0.14] mmol/L at normal CBF, both p < 0.005) and systemic glucose. Our data suggest that improvement of brain energetics upon HL seems predominantly dependent on baseline cerebral metabolic state and support the concept that CMD LPR - rather than CBF - could be used as a diagnostic indication for systemic lactate supplementation following TBI.

KEYWORDS:

cerebral blood flow; cerebral microdialysis; hypertonic; lactate; traumatic brain injury

PMID:
26421521
PMCID:
PMC4827289
DOI:
10.1089/neu.2015.4057
[Indexed for MEDLINE]
Free PMC Article

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