Conditions · Pediatrics and neonatology
Perinatal asphyxia and hypoxic-ischaemic encephalopathy !
Brain injury in a newborn caused by too little oxygen and blood flow around birth. Cooling treatment can lower the damage.
Updated 2026-11-01
Structures involved
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Why it happens
- Hypoxia, ischemia and reperfusion injury
- Mechanisms of cell injury: ATP, mitochondria, calcium, membranes and DNA
- Watershed areas and the organs most sensitive to ischemia
- Cerebral blood flow, brain metabolism and intracranial pressure
- Glutamate (glutamic acid)
What it is
Perinatal asphyxia is impaired gas exchange around birth leading to hypoxaemia, hypercapnia and metabolic acidosis; hypoxic-ischaemic encephalopathy (HIE) is the resulting brain dysfunction in a term or near-term newborn, with altered consciousness, tone and often seizures.
Who gets it
HIE affects a few per thousand live births in high-income countries and is several times more frequent where obstetric care is limited. Birth asphyxia is one of the leading causes of neonatal death and of cerebral palsy worldwide, and in Latin America remains an important cause of neonatal morbidity.
Causes
- Sentinel events: placental abruption, uterine rupture, cord prolapse, shoulder dystocia
- Prolonged or obstructed labour and abnormal fetal heart rate patterns
- Maternal hypotension, cardiac arrest or severe haemorrhage
- Failure of the newborn to establish breathing at birth
Risk factors
- Pre-eclampsia and maternal diabetes
- Fetal growth restriction and post-term pregnancy
- Chorioamnionitis and maternal fever
- Breech or instrumental delivery
- Limited access to fetal monitoring and skilled birth attendants
Pathophysiology
Reduced oxygen and blood flow to the brain switches neurons to anaerobic metabolism, depleting ATP and causing primary energy failure with cytotoxic oedema and glutamate excitotoxicity. After resuscitation there is a latent phase of some hours followed by secondary energy failure, with free radicals, inflammation and apoptosis; this latent window is the target of therapeutic hypothermia. Acute severe insults injure the deep grey matter (thalamus, basal ganglia) and perirolandic cortex, while prolonged partial insults damage watershed white matter and cortex.
Classification
- Sarnat stage 1 (mild): hyperalert, irritable, normal or increased tone, no seizures
- Sarnat stage 2 (moderate): lethargy, hypotonia, weak suck and reflexes, often seizures
- Sarnat stage 3 (severe): stupor or coma, flaccidity, absent reflexes, brainstem dysfunction
Symptoms and signs
- Low Apgar scores and need for resuscitation at birth
- Altered level of consciousness: from hyperalertness to lethargy or coma
- Abnormal tone (hypotonia or hypertonia) and weak or absent primitive reflexes
- Poor suck and feeding difficulty
- Seizures, usually within the first 24 to 48 hours
- Apnoea or irregular breathing
Diagnosis
- Clinical
- Evidence of a perinatal hypoxic-ischaemic event (sentinel event, low Apgar scores at 5 and 10 minutes, prolonged resuscitation) plus an abnormal neurological examination staged with Sarnat or a similar score; eligibility for cooling is decided within the first 6 hours.
- Tests
- Umbilical cord or early neonatal blood gas with severe metabolic acidosis (low pH, large base deficit) and raised lactate; amplitude-integrated or conventional EEG to grade background and detect seizures; renal, liver and coagulation tests for other organ injury; glucose and electrolytes.
- Imaging
- Brain MRI with diffusion weighting, usually in the first one to two weeks, shows the injury pattern (basal ganglia–thalamus or watershed) and helps predict outcome; cranial ultrasound at the bedside.
Differential diagnosis
- Neonatal stroke or intracranial haemorrhage
- Meningitis or encephalitis and neonatal sepsis
- Inborn errors of metabolism
- Neonatal hypoglycaemia
- Neuromuscular disorders and maternal sedative or opioid effects
Goal of treatment
Start therapeutic hypothermia within 6 hours in eligible infants, keep oxygenation, perfusion, glucose and electrolytes normal, control seizures, and support failing organs to limit secondary brain injury.
Treatment
- Acute
- Neonatal resuscitation following a standard algorithm, then transfer to a unit able to offer cooling; passive cooling may begin while avoiding hyperthermia.
- Procedure
- Therapeutic hypothermia (whole-body cooling to about 33.5 °C for 72 hours followed by slow rewarming) for term or near-term infants with moderate or severe HIE, started within 6 hours of birth.
- Medical
- Anticonvulsants (phenobarbital first line) for clinical or EEG seizures; support of blood pressure, ventilation, fluids and glucose; management of kidney and liver dysfunction and coagulopathy.
- Follow-up
- Nursing care: continuous core temperature during cooling, EEG, heart rate and blood pressure, skin integrity, fluid balance and urine output, glucose, signs of seizures and family support.
- Rehabilitation
- Early developmental follow-up with physiotherapy, occupational and speech therapy; hearing and vision assessment.
Complications
- Cerebral palsy, often dyskinetic or spastic quadriplegic after deep grey matter injury
- Epilepsy
- Intellectual disability and learning difficulties
- Hearing and visual impairment (including cortical visual impairment)
- Acute kidney injury, liver injury, myocardial dysfunction and persistent pulmonary hypertension
- Death in severe cases
Prognosis
Mild HIE usually has a good outcome; moderate HIE carries a substantial risk of death or disability that cooling reduces; severe HIE has high mortality and most survivors have major disability. The MRI pattern and EEG recovery are the best early predictors.
Prevention
- Quality prenatal and intrapartum care with fetal heart rate monitoring
- Timely management of obstetric emergencies
- Training of birth attendants in neonatal resuscitation (for example, Helping Babies Breathe)
Test yourself
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What staging system grades the severity of neonatal hypoxic-ischaemic encephalopathy?
The Sarnat staging (mild, moderate, severe), based on consciousness, tone, reflexes, autonomic function and seizures.
Within what time window should therapeutic hypothermia start for HIE?
Within 6 hours of birth, during the latent phase before secondary energy failure.
Which brain regions are injured by an acute, severe (near-total) asphyxial event at term?
The deep grey matter (thalamus and basal ganglia, especially putamen) and the perirolandic cortex.
What is the first-line anticonvulsant for neonatal seizures?
Phenobarbital.
What cord blood finding supports perinatal asphyxia?
Severe metabolic acidosis: low pH with a large base deficit and raised lactate.
Related conditions
- Epilepsy and seizures
- Placental abruption
- Prematurity and its complications
- Neonatal hypoglycaemia (including infant of a diabetic mother)
- Neonatal sepsis
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Cooling for newborns with hypoxic ischaemic encephalopathy (Cochrane Database of Systematic Reviews, 2013).
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