Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia.

biomarkers cerebral blood flow fetal sheep hypoxia-ischemia brain monitoring neonatal encephalopathy

Journal

Frontiers in pediatrics
ISSN: 2296-2360
Titre abrégé: Front Pediatr
Pays: Switzerland
ID NLM: 101615492

Informations de publication

Date de publication:
2022
Historique:
received: 22 04 2022
accepted: 15 06 2022
entrez: 29 7 2022
pubmed: 30 7 2022
medline: 30 7 2022
Statut: epublish

Résumé

Perinatal hypoxia-ischemia (HI) is still a significant contributor to mortality and adverse neurodevelopmental outcomes in term and preterm infants. HI brain injury evolves over hours to days, and involves complex interactions between the endogenous protective and pathological processes. Understanding the timing of evolution of injury is vital to guide treatment. Post-HI recovery is associated with a typical neurophysiological profile, with stereotypic changes in cerebral perfusion and oxygenation. After the initial recovery, there is a delayed, prolonged reduction in cerebral perfusion related to metabolic suppression, followed by secondary deterioration with hyperperfusion and increased cerebral oxygenation, associated with altered neurovascular coupling and impaired cerebral autoregulation. These changes in cerebral perfusion are associated with the stages of evolution of injury and injury severity. Further, iatrogenic factors can also affect cerebral oxygenation during the early period of deranged metabolism, and improving clinical management may improve neuroprotection. We will review recent evidence that changes in cerebral oxygenation and metabolism after HI may be useful biomarkers of prognosis.

Identifiants

pubmed: 35903161
doi: 10.3389/fped.2022.925951
pmc: PMC9314655
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

925951

Informations de copyright

Copyright © 2022 Dhillon, Gunn, Lear, King, Lear, Wassink, Davidson, Bennet and Gunn.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Simerdeep K Dhillon (SK)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Eleanor R Gunn (ER)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Benjamin A Lear (BA)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Victoria J King (VJ)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Christopher A Lear (CA)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Guido Wassink (G)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Joanne O Davidson (JO)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Laura Bennet (L)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Alistair J Gunn (AJ)

Fetal Physiology and Neuroscience Group, Department of Physiology, The University of Auckland, Auckland, New Zealand.

Classifications MeSH