NEONATAL CONDITIONS
Hypoxic-Ischaemic Encephalopathy
A practical guide for SCN clinical staff · Brain injury from perinatal hypoxia-ischaemia - where therapeutic hypothermia changes the outcome
COOL WITHIN
6 HOURS
The insult
A sentinel event or sustained hypoxia-ischaemia drops cerebral oxygen delivery and blood flow, forcing anaerobic metabolism; lactate rises and pH falls.
Primary energy failure
ATP-dependent pumps fail, cells depolarise, and sodium, calcium and water flood in (cytotoxic oedema) while glutamate spills into the synapses. The worst-affected cells die immediately by necrosis.
Latent phase - the window
With reperfusion, oxidative metabolism partly recovers over about 1-6h. Cells are alive but primed for delayed death - this is the window in which cooling can intervene.
Secondary energy failure
From about 6-48h a second wave hits: mitochondrial failure, glutamate excitotoxicity (NMDA-receptor calcium influx), oxidative free-radical injury, inflammation and apoptosis. Its extent tracks with the eventual outcome.
Selective vulnerability
The injury pattern depends on the insult: acute profound (sentinel) events damage the deep grey matter (basal ganglia, thalamus); prolonged partial hypoxia injures the watershed cortical and white-matter zones.
Why cooling helps
Cooling to 33-34°C lowers the cerebral metabolic rate (~5% per °C) and reduces glutamate release, free radicals, inflammation and apoptosis - blunting the secondary phase.
Tertiary phase
Ongoing inflammation, impaired repair and altered plasticity continue for weeks to months, and shape the final neurodevelopmental picture.
CLINICAL FINDINGS (SARNAT)
- Mild: hyperalert, irritable, normal tone, no seizures
- Moderate: lethargy, hypotonia, weak suck, seizures common
- Severe: stupor or coma, flaccid, absent reflexes, seizures then suppression
- Brainstem signs: abnormal pupils, apnoea, abnormal breathing
- Multi-organ involvement - renal, hepatic, cardiac, coagulation
INVESTIGATIONS
- Cord or early blood gas: metabolic acidosis (pH <7.0, base deficit ≥12)
- aEEG/EEG: background activity and seizures - aids selection for cooling
- Cranial ultrasound early; MRI (day 4-7) for injury pattern and prognosis
- Bloods: FBC, coagulation, LFTs, U&E, glucose, lactate
- Screen for sepsis and metabolic mimics
COMPLICATIONS & RED FLAGS
- Seizures are often subclinical - monitor with aEEG/EEG
- Multi-organ dysfunction - watch fluids, glucose and electrolytes
- Persistent severe encephalopathy or an abnormal MRI predicts poor outcome
- Cooling is for ≥35-36 weeks; outside criteria, discuss with NICU
- Do not let the baby overheat - hyperthermia worsens injury
MRI brain
MRI (typically day 4-7) shows the injury pattern and is the best predictor of outcome. Acute profound injury involves the basal ganglia/thalamus and posterior limb of the internal capsule; partial prolonged injury gives a watershed/cortical pattern. Early cranial ultrasound has low sensitivity.
MANAGEMENT
Recognise it early, start passive cooling at once, avoid hyperthermia, and call NETS/NICU - then support every organ system while the brain recovers.
Recognise & cool
- Assess cooling criteria: gestation, acidosis/resuscitation, encephalopathy +/- aEEG
- Start passive cooling immediately (turn the warmer off), target 33-34°C; servo-controlled cooling in NICU
- Avoid hyperthermia and call NETS/NICU early - cooling within 6h
- Continuous core temperature monitoring
Supportive (multi-organ)
- Ventilation and oxygenation - avoid hypocapnia and hyperoxia
- Fluids (often restricted), glucose, electrolytes, BP and perfusion
- Treat seizures (phenobarbitone first-line); monitor with aEEG/EEG
- Monitor renal, hepatic and coagulation function; treat coagulopathy
Prognosis & family
- MRI day 4-7 plus serial neurological exam guide prognosis
- Arrange structured neurodevelopmental follow-up
- Honest, supportive communication; involve the parents
- Document the timeline of events and resuscitation
- If HIE is suspected, start passive cooling at once (warmer off) and call for senior/NETS help - the window is 6 hours.
- Monitor core temperature continuously and avoid hyperthermia; manage shivering and comfort during cooling.
- Watch closely for seizures (often subtle), support aEEG/EEG monitoring, and protect airway and perfusion.
- Support the family through a frightening time and keep communication consistent.
What are the criteria for therapeutic hypothermia, and why is the 6-hour window so important?
How do you grade encephalopathy at the cot side using Sarnat staging?
Why is hyperthermia harmful, and how do you avoid it during stabilisation and transport?
How does MRI timing inform prognosis and the conversations you have with families?
Take-home message: HIE is brain injury from perinatal hypoxia-ischaemia, presenting as an evolving encephalopathy in a term infant. Therapeutic hypothermia within 6 hours improves outcome, so recognise it early, start passive cooling, avoid hyperthermia, and call NETS/NICU. Care is supportive and multi-organ, with seizure control and MRI-guided prognosis.
For educational purposes only. Always align management to current ANZCOR/NRP guidelines and your local SCN/NICU or NETS protocols.