Neonatal hypoxic-ischaemic encephalopathy
Dr Ayush Goel and Dr Bruno Di Muzio et al.

Diffuse hypoxic-ischaemic brain injury in the neonate results in neonatal hypoxic-ischaemic encephalopathy (HIE).  A closely related condition is periventricular leukomalacia (PVL), which is a white matter disease that affects the periventricular zones in preterm infants.

It is important to remember that neonatal encephalopathy may result from a variety of conditions and hypoxic-ischaemic brain injury is one of then.

Epidemiology

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

Pathophysiology

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.

Clinical presentation

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.

Radiographic features

Ultrasound

Sonography is sensitive for the detection of haemorrhage, periventricular leukomalacia (PVL), and hydrocephalus.

CT

CT is the least sensitive modality for evaluation of HIE because of the high water content in the neonatal brain and high protein content of the cerebrospinal fluid, which result in poor parenchymal contrast resolution.

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 gray matter (deep gray 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 due to ischaemia-induced edema
diffusion-weighted MR imaging performed between 24 hours and 8 days of life is more sensitive for the detection of cytotoxic edema, as it reveals restricted diffusion earlier than the signal intensity abnormalities are evident on conventional T1 or T2 weighted images
Treatment and prognosis

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.