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Published on: May 26, 2023
Oxidative Stress and Indicators of Brain Damage Following Pediatric Heart Surgery
Débora Cañizo Vázquez1, Stephanie M Hadley2, Marta Pérez Ordóñez3
1BCNatal-Barcelona Center for Maternal Fetal and Neonatal Medicine, Hospital Sant Joan de Déu-Hospital Clinic, University of Barcelona, 08950 Barcelona, Spain.
Insights
Oxidative stress (OS) biomarkers in infants undergoing heart surgery correlate with brain injury indicators. Elevated OS markers post-surgery are linked to seizures and poorer neurological outcomes, highlighting OS
Area of Science:
- Biomedical Research
- Pediatric Cardiology
- Neuroscience
Background:
- Pediatric cardiac surgery is known to induce oxidative stress (OS).
- Increased OS is linked to adverse neurologic outcomes in neonates with similar brain injury patterns.
- Understanding OS in infants undergoing heart surgery is crucial for predicting neurodevelopmental outcomes.
Purpose of the Study:
- To investigate the relationship between oxidative stress and brain injury in infants undergoing heart surgery.
- To assess OS biomarkers and their correlation with neurologic outcomes in this vulnerable population.
- To identify potential markers for early detection of brain damage.
Main Methods:
- Prospective, observational study including infants (≤6 months) undergoing cardiac surgery.
- Quantification of urine 8-iso-prostaglandin F2α (OS biomarker) and serum S100B protein (brain damage biomarker).
- Analysis of intra-surgery electroencephalography and 24-month neurodevelopmental evaluations (Bayley III/Vineland).
Main Results:
- Post-surgery levels of 8-iso-prostaglandin F2α and S100B protein were significantly elevated.
- Increased S100B levels correlated with elevated 8-iso-prostaglandin F2α levels post-surgery.
- Elevated 8-iso-prostaglandin F2α levels correlated with intra-surgery seizures and abnormal neurological evaluations at 24 months.
Conclusions:
- Post-operative oxidative stress is associated with brain injury indicators in infants undergoing cardiac surgery.
- 8-iso-prostaglandin F2α may serve as a predictive biomarker for neurologic complications.
- Targeting oxidative stress could be a potential strategy to mitigate brain damage in pediatric cardiac surgery patients.
Abstract:
Pediatric cardiac surgery induces an increased oxidative stress (OS) response. Increased OS is associated with poor neurologic outcomes in neonatal populations with similar patterns of brain injury. We investigated OS and brain injury in infants undergoing heart surgery. Patients 6 months or younger, undergoing cardiac surgery with or without cardiopulmonary bypass (CPB), were included in this prospective, observational study. Patients were divided into infant (30 days−6 months) and neonatal (<30 days) groups for analysis. Urine OS biomarker 8-iso-prostaglandin F2α (8-iso-PGF2α) was quantified pre-surgery and at 0 and 24 h post-surgery. A serum brain damage biomarker S100B protein was also measured pre-surgery and at 0 and 72 h post-surgery. Amplitude-integrated electroencephalography during surgery was analyzed. Neuropsychological evaluation using the Bayley III or Vineland test was performed in all patients at 24 months of age. Sixty-two patients were included, 44 of whom underwent follow-up neurologic evaluation. 8-iso-PGF2α and S100B levels were increased after surgery. Postoperative levels of S100B were positively correlated with 8-iso-PGF2α levels 24 h after surgery (rho = 0.5224; p = 0.0261). There was also a correlation between immediate post-surgery levels of 8-iso-PGF2α and intra-surgery seizure burden (rho = 0.4285, p = 0.0205). Patients with an abnormal neurological evaluation had increased levels of S100B 72 h after surgery (p = 0.048). 8-iso-PGF2α levels 24 h after surgery were also related to abnormal neurologic outcomes. Levels of 8-iso-PGF2α following pediatric cardiac surgery are associated with several indicators of brain injury including brain damage biomarkers, intra-operative seizures, and abnormal neurological evaluation at follow-up, suggesting the importance of oxidative stress response in the origin of brain damage in this population.
