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. 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.

Automated summary

Perinatal hypoxia-ischemia (HI) is a major cause of mortality and adverse neurodevelopmental outcomes in term and preterm infants. Understanding the timing and progression of brain injury is crucial for guiding treatment. The recovery after HI is associated with specific changes in cerebral perfusion and oxygenation. The changes in cerebral perfusion, including delayed reduction and subsequent hyperperfusion, are related to injury severity and stages of evolution.