Hypoxic-Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is one of the most common causes of severe neurologic deficit in children and occurs in up to about 10/1,000 live births. HIE is thought to occur due to insufficient cerebral blood flow in combination with decreased oxygen content, which leads to loss of normal cerebral autoregulation and diffuse brain injury.

Different patterns of injury have been described in preterm (< 36 weeks) and term (> 36 week) neonates and based on severity. They include:

• Mild-to-moderate hypotension in preterm infants: The periventricular regions are most affected. MR shows areas of T1 hyperintensity within larger areas of T2 hyperintensity. Periventricular leukomalacia (cavitation and periventricular cyst formation) develops 2 to 6 weeks later. End-stage periventricular leukomalacia refers to progressive necrosis of the periventricular tissue with ex-vacuo enlargement of the ventricles and manifests on cross sectional imaging as ventriculomegaly with irregular margins of the bodies and trigones of the lateral ventricles, loss of periventricular white matter with increased T2 signal, and thinning of the corpus callosum.
• Severe hypotension in preterm infants: The thalami, brainstem, and cerebellum in are most affected due to their high metabolic activity in the immature brain. Ultrasound shows hyperechogenicity, CT shows hypoattenuation, and DWI shows restricted diffusion in these regions. T2 signal is variable.
• Mild-to-moderate hypotension in term infants (shown above): The intervascular watershed zones between the anterior and middle cerebral arteries and between the middle and posterior cerebral arteries and the border zone are affected. The parasagittal cortex and subcortical white matter demonstrate restricted diffusion.
• Severe hypotension in term infants: The lateral thalami, posterior putamina, hippocampi, brainstem, corticospinal tracts, and the sensorimotor cortex are affected. These areas may be hyperechoic on ultrasound and low attenuation on CT. The CT findings may be subtle, with the hypoattenuation of the basal ganglia and thalami manifesting as isoattenuation compared to adjacent white matter. MRI will show abnormal T1 hyperintensity, variable T2 signal, and restricted diffusion in these areas.

References

Chao CP, Zaleski CG, Patton AC. Neonatal hypoxic-ischemic encephalopathy: multimodality imaging findings. Radiographics. 2006 Oct;26 Suppl 1:S159-72.