PE19.12 | Neonatal Seizures — Summary & Reflection

KEY TAKEAWAYS

Neonatal seizures occur in 1–5 per 1,000 live births and are most commonly caused by HIE (~50%), followed by metabolic causes (hypoglycemia, hypocalcemia, hyponatraemia — 10–15%), intracranial infections, and haemorrhage/infarction. Clinically, subtle seizures (eye deviation, lip smacking, cycling movements) are the most common type and the most easily missed — they are distinguished from jitteriness by non-suppressibility. Diagnosis requires urgent bedside glucose and electrolytes, EEG/aEEG, cranial ultrasound, and MRI. Management starts with correcting the metabolic cause; the first-line AED is phenobarbitone 20 mg/kg IV, escalating to phenytoin or levetiracetam if seizures persist. Therapeutic hypothermia (33–34°C for 72 hours, within 6 hours of birth) reduces disability in term neonates with moderate-severe HIE.

REFLECT

Return to the opening case: a term neonate after prolonged second stage, Apgar 4/7, with recurring episodes of eye deviation and lip smacking. You now know this is most likely a subtle seizure from HIE. You know the immediate steps — check glucose, start aEEG, prepare phenobarbitone. But reflect on a deeper question: this baby's brain is simultaneously suffering ongoing injury from seizure activity and from the HIE itself. The neuroprotective window for therapeutic hypothermia is closing. How does understanding the pathophysiology — excitotoxicity, secondary energy failure, the 6-hour cooling window — change the urgency with which you act? What would happen to this neonate's outcome if subtle seizures went unrecognised for 3 hours while the team waited for a 'classic' generalised seizure?