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Neonatal Encephalopathy Following Fetal Distress
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15
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1976
Year
NeonatologyPediatric HydrocephalusFetal MedicineStage 2Social SciencesChronic HypoxiaBrain InjuryNeurologyNeuropathologyMaternal HealthNewborn MedicineFetal NeurodevelopmentNeurophysiologyPediatricsElectrophysiologyNeuroscienceCentral Nervous SystemFetal ComplicationMedicinePerinatal Asphyxia
Perinatal asphyxia can occur in term neonates without chronic hypoxia, as illustrated by 21 infants over 36 weeks' gestation. The study identified three postanoxic encephalopathy stages—stage 1 (<24 h hyperalertness), stage 2 (obtundation, seizures, and abnormal EEG), and stage 3 (stupor, flaccidity, suppressed brain‑stem function)—and found that prolonged stage 2 or persistent abnormal EEG predicted later neurologic impairment or death.
Twenty-one neonates of over 36 weeks' gestation suffered perinatal asphyxia but not chronic hypoxia. Three clinical stages of postanoxic encephalopathy were distinguished. Stage 1 lasted less than 24 hours and was characterized by hyperalertness, uninhibited Moro and stretch reflexes, sympathetic effects, and a normal electroencephalogram. Stage 2 was marked by obtundation, hypotonia, strong distal flexion, and multifocal seizures. The EEG showed a periodic pattern sometimes preceded by continuous delta activity. Infants in stage 3 were stuporous, flaccid, and brain stem and autonomic functions were suppressed. The EEG was isopotential or had infrequent periodic discharges. Infants who did not enter stage 3 and who had signs of stage 2 for less than five days appeared normal in later infancy. Persistence of stage 2 for more than seven days or failure of the EEG to revert to normal was associated with later neurologic impairment or death.
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