Hypoxic Ischaemic Encephalopathy (HIE)
Why is this topic important?
Hypoxic Ischaemic Encephalopathy (HIE) is one of the most important neonatal neurological emergencies and a major cause of neonatal mortality, cerebral palsy and long-term neurodevelopmental disability worldwide. It is frequently tested in MRCPCH examinations and every paediatrician should understand its pathophysiology, diagnosis, management and follow-up.
Definition
Hypoxic Ischaemic Encephalopathy is a syndrome of disturbed neurological function occurring in the newborn infant due to impaired cerebral blood flow and oxygen delivery before, during or shortly after birth.
It is characterised by:
Altered consciousness
Abnormal tone
Abnormal reflexes
Respiratory dysfunction
Feeding difficulties
Seizures
Key MRCPCH Facts
Most cases occur in term and near-term infants.
Therapeutic hypothermia must be started within 6 hours of birth.
Cooling is continued for 72 hours.
MRI is the gold standard imaging investigation.
Neonatal seizures are common.
Long-term neurodevelopmental follow-up is essential.
Severe HIE is associated with cerebral palsy, epilepsy and cognitive impairment.
Pathophysiology
Primary Hypoxic-Ischaemic Injury
An acute hypoxic event results in:
Reduced oxygen delivery
Reduced cerebral blood flow
Cellular energy failure
ATP depletion
Consequences include:
Failure of cellular ion pumps
Cellular swelling
Neuronal injury
Reperfusion Injury
Following restoration of blood flow:
Free radicals are produced
Inflammatory pathways activated
Excitotoxic neurotransmitters released
Secondary Energy Failure
Occurs approximately 6–48 hours after injury and contributes significantly to neuronal death.
This phase is the target of therapeutic hypothermia.
Risk Factors
Antenatal
Severe maternal hypotension
Placental insufficiency
Maternal haemorrhage
Intrapartum
Placental abruption
Cord prolapse
Uterine rupture
Shoulder dystocia
Severe fetal bradycardia
Postnatal
Severe respiratory failure
Cardiac arrest
Severe shock
Clinical Features
Mild HIE
Irritability
Hyperalertness
Mild hypertonia
Poor feeding
Usually resolves within 24 hours.
Moderate HIE
Lethargy
Hypotonia
Weak suck
Seizures
Reduced spontaneous activity
Severe HIE
Coma
Flaccidity
Absent reflexes
Severe seizures
Respiratory failure
Sarnat Staging
Stage I (Mild)
Hyperalert
Hypertonia
Sympathetic overactivity
Stage II (Moderate)
Lethargy
Hypotonia
Frequent seizures
Stage III (Severe)
Stupor or coma
Flaccidity
Absent reflexes
MRCPCH candidates should know that cooling is usually considered in moderate and severe HIE.
Investigations
Blood Gas
Evidence of perinatal asphyxia:
Severe acidosis
Low pH
High base deficit
Amplitude Integrated EEG (aEEG)
Used to:
Assess cerebral activity
Identify seizures
Assess severity
EEG
Useful when seizures are suspected.
MRI Brain
Gold standard investigation.
Typically performed after therapeutic hypothermia.
Findings may involve:
Basal ganglia
Thalami
Cortex
White matter
Cranial Ultrasound
May identify severe injury but is less sensitive than MRI.
Management
Immediate Stabilisation
Airway
Breathing
Circulation
Glucose control
Therapeutic Hypothermia
Eligibility generally includes:
≥36 weeks gestation
Evidence of perinatal asphyxia
Moderate or severe encephalopathy
Treatment:
Target temperature 33–34°C
Continue for 72 hours
Controlled rewarming
Seizure Management
May include:
Phenobarbital
Levetiracetam
Other anticonvulsants
Supportive Care
Ventilation
Cardiovascular support
Fluid management
Nutritional support
Complications
Short-Term
Seizures
Hypotension
Respiratory failure
Feeding difficulties
Long-Term
Cerebral palsy
Developmental delay
Learning difficulties
Epilepsy
Visual impairment
Hearing impairment
Common Exam Traps
Trap 1
Normal Apgar scores do not completely exclude HIE.
Trap 2
Not every infant with perinatal asphyxia develops HIE.
Trap 3
Cooling must start within 6 hours.
Trap 4
MRI is more sensitive than cranial ultrasound.
Trap 5
Seizures may be subtle in neonates.
One Minute Revision
HIE = brain injury due to hypoxia and ischaemia.
Therapeutic hypothermia within 6 hours.
Cooling for 72 hours.
MRI = gold standard imaging.
Seizures common.
Long-term follow-up essential.
Related Question of the Day
A term infant is born following placental abruption. He requires prolonged resuscitation and develops seizures at 8 hours of age. Which treatment has been shown to reduce mortality and neurodevelopmental disability?
A. Dexamethasone
B. Therapeutic hypothermia
C. Surfactant
D. Ibuprofen
E. Furosemide
Answer
B. Therapeutic hypothermia
Explanation
Therapeutic hypothermia initiated within 6 hours of birth significantly reduces death and neurodevelopmental disability in infants with moderate or severe HIE.
Related Topics
Neonatal Sepsis
Neonatal Hypoglycaemia
Intraventricular Haemorrhage
Neonatal Seizures
Therapeutic Hypothermia
Suggested References
NICE Guidance
BAPM Guidance
RCPCH Guidance
BNF for Children
Nelson Textbook of Pediatrics
Rennie & Roberton's Textbook of Neonatology
Volpe's Neurology of the Newborn
Disclaimer
These notes are intended for MRCPCH revision and educational purposes only. They do not replace local, national or institutional guidelines. Clinical decisions should always be based on current guidance, senior advice and individual patient circumstances.
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