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Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia

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. Understandi...

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Autores principales: Dhillon, Simerdeep K., Gunn, Eleanor R., Lear, Benjamin A., King, Victoria J., Lear, Christopher A., Wassink, Guido, Davidson, Joanne O., Bennet, Laura, Gunn, Alistair J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9314655/
https://www.ncbi.nlm.nih.gov/pubmed/35903161
http://dx.doi.org/10.3389/fped.2022.925951
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author Dhillon, Simerdeep K.
Gunn, Eleanor R.
Lear, Benjamin A.
King, Victoria J.
Lear, Christopher A.
Wassink, Guido
Davidson, Joanne O.
Bennet, Laura
Gunn, Alistair J.
author_facet Dhillon, Simerdeep K.
Gunn, Eleanor R.
Lear, Benjamin A.
King, Victoria J.
Lear, Christopher A.
Wassink, Guido
Davidson, Joanne O.
Bennet, Laura
Gunn, Alistair J.
author_sort Dhillon, Simerdeep K.
collection PubMed
description 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.
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spelling pubmed-93146552022-07-27 Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia Dhillon, Simerdeep K. Gunn, Eleanor R. Lear, Benjamin A. King, Victoria J. Lear, Christopher A. Wassink, Guido Davidson, Joanne O. Bennet, Laura Gunn, Alistair J. Front Pediatr Pediatrics 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. Frontiers Media S.A. 2022-07-12 /pmc/articles/PMC9314655/ /pubmed/35903161 http://dx.doi.org/10.3389/fped.2022.925951 Text en Copyright © 2022 Dhillon, Gunn, Lear, King, Lear, Wassink, Davidson, Bennet and Gunn. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pediatrics
Dhillon, Simerdeep K.
Gunn, Eleanor R.
Lear, Benjamin A.
King, Victoria J.
Lear, Christopher A.
Wassink, Guido
Davidson, Joanne O.
Bennet, Laura
Gunn, Alistair J.
Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia
title Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia
title_full Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia
title_fullStr Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia
title_full_unstemmed Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia
title_short Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia
title_sort cerebral oxygenation and metabolism after hypoxia-ischemia
topic Pediatrics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9314655/
https://www.ncbi.nlm.nih.gov/pubmed/35903161
http://dx.doi.org/10.3389/fped.2022.925951
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