Birth asphyxia and hypoxic-ischaemic encephalopathy

Overview

Birth asphyxia (perinatal asphyxia) is a lack of oxygen to the baby's organs from failure to start breathing at birth, often after reduced oxygen supply before or during labour. It causes hypoxia (low oxygen), ischaemia (poor blood flow) and acidosis.

It is a major cause of neonatal death and of cerebral palsy and epilepsy in Pakistan, where many births still happen at home without skilled attendants. Most of it is preventable with good obstetric care and prompt resuscitation.

Definition

• Asphyxia: lack of oxygen due to failure to initiate breathing, with acidosis and organ injury.
• Hypoxic-ischaemic encephalopathy (HIE): the brain disturbance (abnormal consciousness, tone, reflexes and seizures) in a term or near-term baby after hypoxia and ischaemia around birth.

The incidence is higher in preterm babies and much higher in developing than developed countries.

Causes and risk factors

Warning signs in labour: fetal bradycardia, late decelerations or loss of variability on CTG, reduced fetal movements, and thick meconium-stained liquor.

Pathophysiology

Breathing pattern

When the fetus or newborn is deprived of oxygen it first breathes rapidly, then enters primary apnoea (responds to stimulation), then gasps, and then enters secondary apnoea, which needs positive pressure ventilation. Because the two kinds of apnoea cannot be told apart at birth, every apnoeic baby is treated as if in secondary apnoea.

What happens in the cells

1. Lack of oxygen switches cells to anaerobic glycolysis: lactate rises and high-energy phosphates (ATP) fall.
2. Energy-dependent ion pumps fail: potassium leaks out; sodium, chloride and calcium flood in.
3. The cells swell (cytotoxic oedema) and release the excitatory neurotransmitter glutamate, which over-stimulates NMDA receptors and drives more calcium entry.
4. Calcium switches on destructive enzymes and reactive oxygen species that kill neurons.
5. After resuscitation, a secondary energy failure follows over the next hours to days (reperfusion injury, inflammation, apoptosis). This delay is the window for therapeutic cooling.

Blood flow changes

At first cerebral blood flow rises, but autoregulation is lost, cardiac output and BP fall, and brain perfusion drops.

Clinical features at birth

• Pale or blue, floppy, apnoeic or gasping, slow heart rate, poor response to stimulation.
• Delayed cry in the history ("did not cry for 15 minutes").
• Meconium staining of skin, cord and nails.

The Apgar score

The score is recorded at 1 minute and again at 5 minutes. Nelson notes that healthy term babies score 8-9; scores of 4-7 need close watching for improvement and a cause.

• Score of 10 is the best possible; a score of 0-3 needs immediate resuscitation.
• The 10-minute (and later) score relates best to death and later neurological damage and shows how well resuscitation worked. Nelson gives a 20% mortality and 5% cerebral palsy rate for a score of 0-3 at 10 minutes, rising to 60% mortality and 57% cerebral palsy if it is still 0-3 at 20 minutes.

Multi-organ effects of asphyxia

The body diverts blood to the brain, heart and adrenals, so other organs suffer first.

Hypoxic-ischaemic encephalopathy: staging

Babies can move from one stage to another over the first 24-72 hours.

Investigations

• Cord or early arterial blood gas: metabolic acidosis (low pH, large base deficit).
• Blood glucose, calcium, magnesium, electrolytes, urea and creatinine, liver enzymes, coagulation screen, full blood count, cultures.
• Amplitude-integrated EEG (aEEG): detects subclinical seizures and helps select babies for cooling and predict outcome.
• Imaging:
  • Diffusion-weighted MRI: the imaging of choice in term HIE (most sensitive and specific), ideally in the first days.
  • Cranial ultrasound: limited value in term HIE but the first choice in preterm babies (IVH, PVL).
  • CT is less sensitive and uses radiation.
• Urine output monitoring; echocardiography if heart failure or pulmonary hypertension.

Management

Prevention

The best management is prevention: good antenatal care, recognition of high-risk pregnancies, monitoring in labour, timely caesarean section, and a skilled person trained in resuscitation at every birth.

At birth

Prompt neonatal resuscitation with effective ventilation (see the newborn resuscitation chapter).

Therapeutic hypothermia (neuroprotection)

• Indicated in term and near-term babies (Nelson: more than 35 weeks) with moderate or severe (stage 2-3) HIE.
• Cool the whole body (or the head selectively) to a core temperature of 33-34°C.
• Start within 6 hours of birth and continue for 72 hours, then rewarm slowly.
• It lowers brain metabolism, glutamate release, inflammation, oxidative damage and apoptosis, and reduces death or major disability.
• It needs a unit able to monitor and ventilate. Where cooling is not available, keep the baby in a thermoneutral environment and avoid overheating, which worsens brain injury.

Supportive care

Neonatal seizures and HIE

• HIE is the commonest cause of seizures in the first day of life (Akbar: about 60% of neonatal seizures).
• Other causes to check: hypoglycaemia, hypocalcaemia, hypomagnesaemia, hyponatraemia, intracranial haemorrhage, meningitis, and (rarely) pyridoxine deficiency.

• Newborns do not have generalised tonic-clonic fits. Subtle seizures (eye deviation, blinking, lip smacking, cycling movements, apnoea) are the commonest type, especially in preterm babies; clonic seizures are more typical of term babies.

Complications and long-term outcome

• Cerebral palsy (spastic quadriplegia, dyskinetic types; spastic diplegia in preterm PVL).
• Epilepsy, microcephaly.
• Intellectual disability, learning problems.
• Visual and hearing impairment.
• Feeding difficulties and failure to thrive.

Prognosis

• Akbar gives an overall mortality of 10-20% for asphyxiated term babies, with neurological sequelae in 20-45% of survivors.
• Outcome depends mostly on the stage of HIE: stage 1 is normal; stage 2 is about 80% normal; stage 3 has about 50% mortality and nearly all survivors are severely disabled.

Poor prognostic features:

• Apgar 0-3 at 20 minutes.
• Stage 3 HIE or long-lasting stage 2.
• Early, frequent or hard-to-control seizures.
• Multi-organ failure, especially oliguria.
• Severely abnormal EEG (burst suppression, isoelectric) and abnormal MRI in the first days.
• Persistent brainstem signs; microcephaly at 3 months.

Quick revision

• Asphyxia = failure to breathe at birth with hypoxia, ischaemia and acidosis.
• Causes: pre-eclampsia, abruption, cord prolapse, obstructed labour, post-maturity, IUGR.
• Apgar: Appearance, Pulse, Grimace, Activity, Respiration; 0-3 needs immediate resuscitation.
• Low Apgar can occur without asphyxia (preterm, maternal drugs, malformations).
• HIE stage 1 hyperalert/dilated pupils/no fits; stage 2 lethargic/constricted pupils/fits; stage 3 coma/flaccid/burst suppression.
• Diffusion MRI is best in term HIE; ultrasound first in preterm.
• Cooling 33-34°C within 6 h for 72 h in stage 2-3.
• Phenobarbitone 20 mg/kg for seizures; no steroids.
• Term: parasagittal injury; preterm: PVL, spastic diplegia.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).

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