Neonatal hypoxic-ischaemic encephalopathy

Neonatal hypoxic-ischaemic encephalopathy (HIE) is the result of a global hypoxic-ischaemic brain injury in a term neonate, usually after asphyxia.

It is important to remember that neonatal encephalopathy may result from a variety of conditions and hypoxic-ischaemic brain injury is the most important of them 1. Consequently, both terms are frequently used as synonyms. 

Hypoxic-ischaemic encephalopathy is one of the most common causes of cerebral palsy and other severe neurological deficits in children, occurring in 2-9 of every 1000 live births.

The encephalopathic neonate may have low Apgar scores at delivery and metabolic acidosis documented in the cord blood. Within the first 24 hours of life, the infant may develop symptoms of apnea and seizures with abnormal electroencephalographic (EEG) results.

The lack of sufficient blood flow, in conjunction with decreased oxygen content in the blood (perinatal asphyxia), leads to loss of normal cerebral autoregulation and diffuse brain injury. The exact nature of the injury depends on the severity of hypotension and the degree of brain maturation. In term infants, myelinated areas are more metabolically active and express more glutamate receptors (NMDA receptors) which make them more vulnerable to HIE due to excitotoxicity.

In term infants blood flow is ventriculofugal and changes are mainly like older children in watershed-border zones; namely parasagittal grey matter and subcortical white matter. Profound HIE in term babies results in thalami and basal ganglia as well as sensorimotor cortex (perirolandic region) injury.

Ultrasound

Sonography is sensitive for the detection of haemorrhage, periventricular leukomalacia (PVL), and hydrocephalus. Resistive index (RI) of the middle cerebral arteries, if correlated with gestational age, can add more information. Severe HIE results in loss of autoregulation and increased RI.

CT

CT is the least sensitive modality for evaluation of HIE because of poor parenchymal contrast resolution in the neonatal brain due to the high water content of the parenchyma and high protein content of the CSF.

MRI

Is the most sensitive and specific imaging technique for examining infants with suspected hypoxic-ischemic brain injury. Conventional sequences can help exclude other causes of encephalopathy such as haemorrhage, cerebral infarction, neoplasms, or congenital malformations.

  • hypoxic-ischemic injury to grey matter (deep grey matter, cortex) demonstrates characteristic T1 hyperintensity and variable T2 intensity, depending on the time at imaging and the dominant underlying pathologic condition, such as haemorrhage or gliosis
  • injury to white matter generally results in T1 hypointensity and T2 hyperintensity particular in posterior limb of internal capsule due to ischaemia-induced oedema
  • diffusion-weighted MR imaging performed between 24 hours and 8 days of life is more sensitive for the detection of cytotoxic oedema, as it reveals restricted diffusion earlier than the signal intensity abnormalities are evident in conventional T1 or T2 weighted images. Pseudonormalisation occurs at the end of the first week

Increased severity of encephalopathy is indicated by the presence of cortical and basal ganglia abnormalities on conventional MR images, on diffusion-weighted MR images, and at MR spectroscopy. Severe EEG abnormalities also portend a poor outcome.

Although term infants with mild encephalopathy generally make a full recovery, 20% of affected infants die in the neonatal period and another 25% develop significant neurologic sequelae. For preterm infants, compared with term infants, the overall prognosis is worse.

Studies estimate a short therapeutic window of 2-6 hours during which interventions may be efficacious in reducing the severity of ultimate brain injury; thus, early identification of a neonate who has sustained a hypoxic-ischaemic insult is a paramount objective for optimal management and treatment.

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Article Information

rID: 12856
Section: Pathology
Synonyms or Alternate Spellings:
  • Neonatal hypoxic-ischemic encephalopathy
  • Hypoxic ischaemic encephalopathy in neonates

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    Case 1: multicystic encephalomalacia
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    Case 2: multicystic encephalomalacia on CT
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    Case 3: ulegyria
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    Case 4: injury to grey matter (thalami and lentiform nuclei)
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    Case 5: moderate insult in a preterm
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