Asphyxia, in neonates

Hypoxic-ischaemic encephalopathy (HIE) is the result of global rather than focal brain injury. Whereas cerebral infarction results from abnormalities in local vascular circulation, HIE is the consequence of global perfusion or oxygenation disturbance. Some common causes of HIE are severe prolonged hypotension, cardiac arrest with successful resuscitation, profound neonatal asphyxia and carbone monoxide inhalation.

Multicystic encephalomalacia is seen in severe cases.

Asphyxia and infarction are among the common causes of intracranial haemorrhage in nontraumatized term neonates.

Term infants suffering profound perinatal asphyxia show a characteristic sequence of imaging findings. Initial CT scan may be normal or minimally abnormal. Severe generalized cerebral oedema ensues over 24 to 48 hours and is seen as diffusely low density brain, often with a reversal sign. The cerebellum appears hyperdense compared to abnormally low density cerebral hemispheres. Grey-white matter differentiation is lost. Haemorrhagic cortical necrosis with secondary calcifications can often be observed within a few days after the hypoxic-ischaemic insult. Severe atrophic changes are common in surviving infants.

MR scan show high signal on T1-weighted images in the basal ganglia, particularly the posterior lateral lentiform nuclei and ventrolateral thalamus. The midbrain tegmentum and the lateral geniculate nuclei are commonly affected. Thinning of the perirolandic gyri can be seen in surviving infants. Low signal perpiginous perirolandic cortical lesions on T2-weighted sequences reflect haemorrhagic or calcific residua.

GS