Literature DB >> 22610193

Tight glycemic control increases metabolic distress in traumatic brain injury: a randomized controlled within-subjects trial.

Paul Vespa1, David L McArthur, Nathan Stein, Sung-Cheng Huang, Weber Shao, Maria Filippou, Maria Etchepare, Thomas Glenn, David A Hovda.   

Abstract

OBJECTIVE: To determine the effects of tight glycemic control on brain metabolism after traumatic brain injury using brain positron emission tomography and microdialysis.
DESIGN: Single-center, randomized controlled within-subject crossover observational trial.
SETTING: Academic intensive care unit.
METHODS: We performed a prospective, unblinded randomized controlled within-subject crossover trial of tight (80-110 mg/dL) vs. loose (120-150 mg/dL) glycemic control in patients with severe traumatic brain injury to determine the effects of glycemic control on brain glucose metabolism, as measured by [18F] deoxy-D-glucose brain positron emission tomography. Brain microdialysis was done simultaneously.
MEASUREMENTS AND MAIN RESULTS: Thirteen severely injured traumatic brain injury patients underwent the study between 3 and 8 days (mean 4.8 days) after traumatic brain injury. In ten of these subjects, global brain and gray matter tissues demonstrated higher glucose metabolic rates while glucose was under tight control as compared with loose control (3.2 ± 0.6 vs. 2.4 + 0.4, p = .02 [whole brain] and 3.8 ± 1.4 vs. 2.9 ± 0.8, p = .05 [gray matter]). However, the responses were heterogeneous with pericontusional tissue demonstrating the least state-dependent change. Cerebral microdialysis demonstrated more frequent critical reductions in glucose (p = .02) and elevations of lactate/pyruvate ratio (p = .03) during tight glycemic control.
CONCLUSION: Tight glycemic control results in increased global glucose uptake and an increased cerebral metabolic crisis after traumatic brain injury. The mechanisms leading to the enhancement of metabolic crisis are unclear, but delivery of more glucose through mild hyperglycemia may be necessary after traumatic brain injury.

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Year:  2012        PMID: 22610193     DOI: 10.1097/CCM.0b013e31824e0fcc

Source DB:  PubMed          Journal:  Crit Care Med        ISSN: 0090-3493            Impact factor:   7.598


  38 in total

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Journal:  J Neurotrauma       Date:  2015-09-30       Impact factor: 5.269

3.  Therapeutic intravascular normothermia reduces the burden of metabolic crisis.

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Review 4.  Brain metabolism and severe pediatric traumatic brain injury.

Authors:  Heidi Griffiths; Manu S Goyal; Jose A Pineda
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6.  Influence of Glycemic Control on Endogenous Circulating Ketone Concentrations in Adults Following Traumatic Brain Injury.

Authors:  Stephanie M Wolahan; Mayumi L Prins; David L McArthur; Courtney R Real; David A Hovda; Neil A Martin; Paul M Vespa; Thomas C Glenn
Journal:  Neurocrit Care       Date:  2017-04       Impact factor: 3.210

7.  Glucose administration after traumatic brain injury exerts some benefits and no adverse effects on behavioral and histological outcomes.

Authors:  Katsunori Shijo; Sima Ghavim; Neil G Harris; David A Hovda; Richard L Sutton
Journal:  Brain Res       Date:  2015-04-21       Impact factor: 3.252

8.  Novel Metabolomic Comparison of Arterial and Jugular Venous Blood in Severe Adult Traumatic Brain Injury Patients and the Impact of Pentobarbital Infusion.

Authors:  Stephanie M Wolahan; Elliott Lebby; Howard C Mao; David McArthur; Courtney Real; Paul Vespa; Daniel Braas; Thomas C Glenn
Journal:  J Neurotrauma       Date:  2018-08-13       Impact factor: 5.269

9.  Frequency and impact of intensive care unit complications on moderate-severe traumatic brain injury: early results of the Outcome Prognostication in Traumatic Brain Injury (OPTIMISM) Study.

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Journal:  Neurocrit Care       Date:  2013-06       Impact factor: 3.210

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