Subtle findings but grave consequences of hypoxic ischemic encephalopathy

A full-term male neonate, born to a diabetic mother, had a history of perinatal respiratory distress of about 3 minutes due to meconium aspiration. The patient presented at 6 months of age with recurrent episodes of seizures, worsening over the prior few days. He was found to have global development delay, hypertonia, and hyperreflexia.

Magnetic resonance imaging (MRI) performed during the neonatal period showed subtle changes of faint diffusion restriction involving perirolandic region, corpus callosum, and thalami with absent T1 bright signal of posterior limb internal capsule suggestive of severe birth asphyxia. MRI performed recently demonstrated marked cerebral brain atrophy (a sequel to hypoxic-ischemic encephalopathy) with asymmetric bilateral subdural effusions (left more than right) showing few areas of blooming artifacts (blood products).

Hypoxic-ischemic encephalopathy (HIE) when severe can cause significant neurologic disability and mortality. Imaging plays an important role in diagnosis, management plan, follow-up, and predicting prognosis. Duration and severity of insult and timing are important in influencing findings [1]. Our case is a good example of an acute (less than 10 min. duration) severe (profound) event that led to the affection of metabolically active and therefore most susceptible regions of the brain in a term neonate baby namely the basal ganglia-thalami, and corticospinal tract (from perirolandic region to posterior limb internal capsule). Such injury when occurring in a premature baby can have effects on the thalami, cerebellum, and brainstem. Degree of brain maturity, duration of hypoxic-ischemic insult, and severity of such injury, all influence imaging findings. A severe injury in both preterm and term neonates specifically affects deep grey matter, with more frequent perirolandic involvement in the latter age group. Less severe injury results in intraventricular haemorrhages and periventricular white matter injury in preterm neonates, and parasagittal watershed territory infarcts in term neonates. After birth, severe injury results in diffuse grey matter injury, with relative sparing of the perirolandic cortex and the structures supplied by the posterior circulation. Profound injury in older children and adults affects the deep grey matter nuclei, cerebral cortices, hippocampi, and cerebelli. Early imaging findings can be subtle and are often overlooked on conventional imaging in the acute setting and particularly in neonates. Therefore, it is important to know patterns of injury that may be observed while interpreting such or advanced MR imaging. 

Diffusion-weighted imaging (DWI) is sensitive to detect such changes within 24 hours despite normal-appearing conventional T1 and T2W sequences [2]. Abnormalities seen on DWI peak in 3-4 days, therefore, a repeat MRI in 2-4 days may be considered if initial imaging is negative [3]. Following initial resuscitation and stabilization, management of HIE includes hypothermia therapy, adequate ventilation, fluid therapy, glucose monitoring, and treatment of seizures [4]. Subdural collections or effusions may be the result of atrophy, trauma (during seizure activity), or non-accidental injury-related. Radiologists should be aware of subtle changes pertaining to HIE to diagnose this entity promptly and guide clinicians for follow-up and counselling based on the severity of the injury.

Written informed patient consent (from guardians/ parents) for publication has been obtained.