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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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2022-07-01
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Series: | Frontiers in Pediatrics |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fped.2022.925951/full |
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author | Simerdeep K. Dhillon Eleanor R. Gunn Benjamin A. Lear Victoria J. King Christopher A. Lear Guido Wassink Joanne O. Davidson Laura Bennet Alistair J. Gunn |
author_facet | Simerdeep K. Dhillon Eleanor R. Gunn Benjamin A. Lear Victoria J. King Christopher A. Lear Guido Wassink Joanne O. Davidson Laura Bennet Alistair J. Gunn |
author_sort | Simerdeep K. Dhillon |
collection | DOAJ |
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. |
first_indexed | 2024-04-12T08:51:09Z |
format | Article |
id | doaj.art-f50669a6ad1f468395ebf94787cdf834 |
institution | Directory Open Access Journal |
issn | 2296-2360 |
language | English |
last_indexed | 2024-04-12T08:51:09Z |
publishDate | 2022-07-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Pediatrics |
spelling | doaj.art-f50669a6ad1f468395ebf94787cdf8342022-12-22T03:39:34ZengFrontiers Media S.A.Frontiers in Pediatrics2296-23602022-07-011010.3389/fped.2022.925951925951Cerebral Oxygenation and Metabolism After Hypoxia-IschemiaSimerdeep K. DhillonEleanor R. GunnBenjamin A. LearVictoria J. KingChristopher A. LearGuido WassinkJoanne O. DavidsonLaura BennetAlistair J. GunnPerinatal 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.https://www.frontiersin.org/articles/10.3389/fped.2022.925951/fullcerebral blood flowhypoxia-ischemia brainbiomarkersfetal sheepneonatal encephalopathymonitoring |
spellingShingle | Simerdeep K. Dhillon Eleanor R. Gunn Benjamin A. Lear Victoria J. King Christopher A. Lear Guido Wassink Joanne O. Davidson Laura Bennet Alistair J. Gunn Cerebral Oxygenation and Metabolism After Hypoxia-Ischemia Frontiers in Pediatrics cerebral blood flow hypoxia-ischemia brain biomarkers fetal sheep neonatal encephalopathy monitoring |
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 | cerebral blood flow hypoxia-ischemia brain biomarkers fetal sheep neonatal encephalopathy monitoring |
url | https://www.frontiersin.org/articles/10.3389/fped.2022.925951/full |
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