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

Handle URI:
http://hdl.handle.net/10754/621433
Title:
Improvement of Neuroenergetics by Hypertonic Lactate Therapy in Patients with Traumatic Brain Injury Is Dependent on Baseline Cerebral Lactate/Pyruvate Ratio
Authors:
Quintard, Hervé; Patet, Camille; Zerlauth, Jean-Baptiste; Suys, Tamarah; Bouzat, Pierre; Pellerin, Luc; Meuli, Reto; Magistretti, Pierre J. ( 0000-0002-6678-320X ) ; Oddo, Mauro
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. Copyright © 2016 Mary Ann Liebert, Inc.
KAUST Department:
Biological and Environmental Sciences and Engineering (BESE) Division
Citation:
Quintard H, Patet C, Zerlauth J-B, Suys T, Bouzat P, et al. (2016) Improvement of Neuroenergetics by Hypertonic Lactate Therapy in Patients with Traumatic Brain Injury Is Dependent on Baseline Cerebral Lactate/Pyruvate Ratio. Journal of Neurotrauma 33: 681–687. Available: http://dx.doi.org/10.1089/neu.2015.4057.
Publisher:
Mary Ann Liebert Inc
Journal:
Journal of Neurotrauma
Issue Date:
30-Sep-2015
DOI:
10.1089/neu.2015.4057
Type:
Article
ISSN:
0897-7151; 1557-9042
Appears in Collections:
Articles; Biological and Environmental Sciences and Engineering (BESE) Division

Full metadata record

DC FieldValue Language
dc.contributor.authorQuintard, Hervéen
dc.contributor.authorPatet, Camilleen
dc.contributor.authorZerlauth, Jean-Baptisteen
dc.contributor.authorSuys, Tamarahen
dc.contributor.authorBouzat, Pierreen
dc.contributor.authorPellerin, Lucen
dc.contributor.authorMeuli, Retoen
dc.contributor.authorMagistretti, Pierre J.en
dc.contributor.authorOddo, Mauroen
dc.date.accessioned2016-11-03T08:29:12Z-
dc.date.available2016-11-03T08:29:12Z-
dc.date.issued2015-09-30en
dc.identifier.citationQuintard H, Patet C, Zerlauth J-B, Suys T, Bouzat P, et al. (2016) Improvement of Neuroenergetics by Hypertonic Lactate Therapy in Patients with Traumatic Brain Injury Is Dependent on Baseline Cerebral Lactate/Pyruvate Ratio. Journal of Neurotrauma 33: 681–687. Available: http://dx.doi.org/10.1089/neu.2015.4057.en
dc.identifier.issn0897-7151en
dc.identifier.issn1557-9042en
dc.identifier.doi10.1089/neu.2015.4057en
dc.identifier.urihttp://hdl.handle.net/10754/621433-
dc.description.abstractEnergy 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. Copyright © 2016 Mary Ann Liebert, Inc.en
dc.publisherMary Ann Liebert Incen
dc.subjectcerebral blood flowen
dc.subjectcerebral microdialysisen
dc.subjecthypertonicen
dc.subjectlactateen
dc.subjecttraumatic brain injuryen
dc.titleImprovement of Neuroenergetics by Hypertonic Lactate Therapy in Patients with Traumatic Brain Injury Is Dependent on Baseline Cerebral Lactate/Pyruvate Ratioen
dc.typeArticleen
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Divisionen
dc.identifier.journalJournal of Neurotraumaen
dc.contributor.institutionDepartment of Intensive Care Medicine, Neuroscience Critical Care Research Group, Lausanne, Switzerlanden
dc.contributor.institutionDepartment of Anesthesia and Intensive Care, Nice University Hospital, Nice, Franceen
dc.contributor.institutionDepartment of Medical Radiology, Lausanne University Hospital, Lausanne, Switzerlanden
dc.contributor.institutionDepartment of Anesthesia and Intensive Care, Grenoble University Hospital, Grenoble, Franceen
dc.contributor.institutionInstitute of Physiology, University of Lausanne, Lausanne, Switzerlanden
dc.contributor.institutionCentre de Neurosciences Psychiatriques, Department of Psychiatry, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne University Hospital, Lausanne, Switzerlanden
dc.contributor.institutionLaboratory of Neuroenergetics and Cellular Dynamics, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerlanden
dc.contributor.institutionDepartment of Intensive Care Medicine, CHUV-University Hospital, Rue du Bugnon 46, BH 08.623, Lausanne, Switzerlanden
kaust.authorMagistretti, Pierre J.en
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