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Electroencephalographic (EEG) Stages in Patients With Cerebral Edema Following Cardiac Arrest
David E Horvat1, Julia S Keenan2,3, Caroline Conley2,3
1Department of Neurology, Uniform Services University of the Health Sciences, Bethesda, MD, USA.
Insights
Electroencephalography (EEG) stages in pediatric cerebral edema after cardiac arrest were identified. Early EEG changes may offer therapeutic targets for neuroprotection and reducing brain swelling.
Area of Science:
- Pediatric neurology
- Critical care medicine
- Neurophysiology
Background:
- Cerebral edema is a critical complication following pediatric cardiac arrest.
- Electroencephalography (EEG) monitoring is essential for assessing neurological function in critically ill children.
- Standardized EEG terminology is crucial for consistent interpretation in pediatric intensive care units.
Purpose of the Study:
- To describe and characterize the electroencephalographic (EEG) changes in pediatric patients experiencing cerebral edema subsequent to cardiac arrest.
- To establish distinct EEG stages associated with cerebral edema development and progression in this population.
Main Methods:
- Retrospective study of pediatric patients admitted to the ICU between July 2021 and January 2023.
- Inclusion criteria: cardiac arrest, EEG background changes, and neuroimaging/clinical signs of cerebral edema; exclusion: electrographic seizures.
- Application of American Clinical Neurophysiology Society standardized critical care EEG terminology.
Main Results:
- Nine pediatric patients met the criteria (median age 24 months, 89% male).
- Five common EEG stages were identified: burst suppression/attenuation, epileptiform discharges, discontinuous/burst patterns, gradual voltage suppression, and diffuse suppression.
- Stage durations varied, with one patient showing clinical changes at Stage 3; others presented with fixed, dilated pupils indicating global anoxic injury.
Conclusions:
- This study is the first to describe distinct EEG stages of cerebral edema following pediatric cardiac arrest.
- These identified EEG stages may be applicable to other patient populations with cerebral edema.
- Early stages of EEG changes represent potential therapeutic targets for interventions aimed at lowering intracranial pressure and neuroprotection.
Abstract:
ObjectiveTo describe electroencephalographic (EEG) changes in pediatric patients with cerebral edema after cardiac arrest.MethodsA retrospective study of patients admitted to the pediatric intensive care unit from July 2021 to January 2023. We included patients with cardiac arrest and changes in EEG background with clinical changes and/or neuroimaging consistent with cerebral edema. We excluded patients with electrographic seizures. We applied American Clinical Neurophysiology Society standardized critical care EEG terminology to classify EEG background, noting timing of the change in background classification. Clinical variables included age, sex, and neuroimaging findings and were described with descriptive statistics.ResultsNine patients met inclusion criteria, with median age 24 months (interquartile range 21-49), and 89% were male. There were 5 common EEG stages: stage 1, burst suppression/burst attenuation; stage 2, continuous/discontinuous ± multifocal sporadic epileptiform discharges ± rhythmic or periodic patterns; stage 3, discontinuous/burst suppression/burst attenuation ± rhythmic or periodic patterns; stage 4, gradual voltage suppression; and stage 5, diffuse suppression. The ranges for each stage were as follows: stage 1, 2-10 hours; stage 2, 2.5-15.5 hours; stage 3, 0.5-6.24 hours; and stage 4, 0.5-11 hours. We could not calculate the duration of stage 5 given no uniform time to EEG discontinuation. One patient had a clinical change in stage 3. Remaining patients presented with fixed and dilated pupils with global anoxic injury.ConclusionsEEG stages of cerebral edema have not been described after pediatric cardiac arrest. These stages may be relevant to other patient populations. Early stages may be a therapeutic target for intracranial pressure-lowering medications and/or neuroprotective strategies to minimize sequalae of cerebral edema.
