Hyperglycemia and Glucose Variability Are Associated with Worse Brain Function and Seizures in Neonatal Encephalopathy: A Prospective Cohort Study.


Journal

The Journal of pediatrics
ISSN: 1097-6833
Titre abrégé: J Pediatr
Pays: United States
ID NLM: 0375410

Informations de publication

Date de publication:
06 2019
Historique:
received: 09 11 2018
revised: 17 01 2019
accepted: 15 02 2019
pubmed: 16 4 2019
medline: 16 4 2020
entrez: 16 4 2019
Statut: ppublish

Résumé

To investigate how glucose abnormalities correlate with brain function on amplitude-integrated electroencephalography (aEEG) in infants with neonatal encephalopathy. Neonates born at full term with encephalopathy were enrolled within 6 hours of birth in a prospective cohort study at a pediatric academic referral hospital. Continuous interstitial glucose monitors and aEEG were placed soon after birth and continued for 3 days. Episodes of hypoglycemia (≤50 mg/dL; ≤2.8 mmol/L) and hyperglycemia (>144 mg/dL; >8.0 mmol/L) were identified. aEEG was classified in 6-hour epochs for 3 domains (background, sleep-wake cycling, electrographic seizures). Generalized estimating equations assessed the relationship of hypo- or hyperglycemia with aEEG findings, adjusting for clinical markers of hypoxia-ischemia (Apgar scores, umbilical artery pH, and base deficit). Forty-five infants (gestational age 39.5 ± 1.4 weeks) were included (24 males). During aEEG monitoring, 16 episodes of hypoglycemia were detected (9 infants, median duration 77.5, maximum 220 minutes) and 18 episodes of hyperglycemia (13 infants, median duration 237.5, maximum 3125 minutes). Epochs of hypoglycemia were not associated with aEEG changes. Compared with epochs of normoglycemia, epochs of hyperglycemia were associated with worse aEEG background scores (B 1.120, 95% CI 0.501-1.738, P < .001), less sleep-wake cycling (B 0.587, 95% CI 0.417-0.757, P < .001) and more electrographic seizures (B 0.433, 95% CI 0.185-0.681, P = .001), after adjusting for hypoxia-ischemia severity. In neonates with encephalopathy, epochs of hyperglycemia were temporally associated with worse global brain function and seizures, even after we adjusted for hypoxia-ischemia severity. Whether hyperglycemia causes neuronal injury or is simply a marker of severe brain injury requires further study.

Identifiants

pubmed: 30982528
pii: S0022-3476(19)30259-8
doi: 10.1016/j.jpeds.2019.02.027
pii:
doi:

Substances chimiques

Blood Glucose 0

Types de publication

Comparative Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

23-32

Subventions

Organisme : CIHR
ID : MOP-133710
Pays : Canada

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Elana F Pinchefsky (EF)

Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada. Electronic address: elana.pinchefsky.hsj@ssss.gouv.qc.ca.

Cecil D Hahn (CD)

Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada.

Daphne Kamino (D)

Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada.

Vann Chau (V)

Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada; BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada.

Rollin Brant (R)

BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada; Department of Statistics, The University of British Columbia, Vancouver, British Columbia, Canada.

Aideen M Moore (AM)

Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada.

Emily W Y Tam (EWY)

Division of Neurology, Department of Paediatrics, The Hospital for Sick Children and the University of Toronto, Toronto, Ontario, Canada; Program in Neurosciences and Mental Health, SickKids Research Institute, Toronto, Ontario, Canada.

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