History and Physical
A male infant was born by cesarean section at 40 +2 weeks of gestation for nonreassuring fetal heart tracing. Birth weight was 3530 g. Meconium-stained amniotic fluid, nuchal cord, fetal tachycardia, and maternal chorioamnionitis were present during birth. Prenatal labs were negative for Group B streptococcus, hepatitis B surface antigen, gonorrhea and chlamydia, HIV, and syphilis, and showed immunity to rubella. There was no family history of neurologic disorders or seizures. He required positive pressure ventilation for 2 minutes in the delivery room with Apgar scores of 1, 3, and 5 at 1, 5, and 10 minutes, respectively. He then received supplemental oxygen in the neonatal intensive care unit (NICU) and developed seizures after 6 hours of life. Amplitude integrated EEG showed seizure activity, and blood gas analysis showed metabolic acidosis. Hence, therapeutic hypothermia was started with seizure medications, intubation due to recurrent apnea, and hypoglycemia. Seizures were controlled with administration of phenobarbital, fosphenytoin, midazolam, and levetiracetam.
Diagnostic Workup
Head ultrasound (US) was reported as normal at 2 and 7 days after birth. Brain MRI on day 5 showed global hypoxia-ischemia with cerebral edema. There was diffuse T2 hyperintensity with loss of gray-white matter differentiation, especially involving the left basal ganglia ( Fig. 8.1 ). Diffusion-weighted images demonstrated increasing restricted diffusion with relative sparing of the cerebellum ( Fig. 8.2 ).
Hypoxic-ischemic encephalopathy. Brain MRI, (A) axial and (B) coronal T2 show severe cerebral edema with diffuse T2 hyperintensity and loss of gray-white matter differentiation. There is focal T2 hyperintensity involving the left basal ganglia ( arrow ).
Hypoxic-ischemic encephalopathy. Brain MRI, (A and B) axial DWI, and (C and D) axial ADC show profound restricted diffusion throughout the cortex ( white arrows ), white matter, and deep gray structures. There is relative sparing of the cerebellum ( black arrow ). ADC , Apparent diffusion coefficient; DWI , diffusion-weighted imaging .
Clinical Differential Diagnoses
The differential diagnosis for neonatal seizures includes hypoxic-ischemic encephalopathy (HIE), intracranial hemorrhage, intracranial infection, developmental defects, hypoglycemia, hypocalcemia, metabolic disorders, and epilepsy syndromes. In a prospective cohort of 426 neonates with seizure who underwent continuous EEG, the most common seizure etiologies were HIE in 38%, ischemic stroke in 18%, neonatal-onset epilepsy in 13%, intracranial hemorrhage in 11%, neonatal genetic epilepsy syndrome in 6%, congenital cerebral malformation in 4%, and benign nonfamilial neonatal convulsions in 3%.
Imaging Differential Diagnoses
Hypoxic-ischemic encephalopathy
Neonatal metabolic encephalopathies: organic acidemias, urea cycle defects, and aminoacidemias including maple syrup urine disease
Congenital malformations
Central nervous system infection
Final Diagnosis
Hypoxic-ischemic encephalopathy
Discussion
The incidence of HIE is 2 to 3 per 1000 live-term births in developed countries. The major causes of serious ischemia are intrauterine asphyxia, postnatal cardiac insufficiency, and postnatal circulatory insufficiency. Maternal clinical factors associated with neonatal encephalopathy include obesity, diabetes, fetal growth restriction, hypertension, and clinical chorioamnionitis. Symptoms of neonatal encephalopathy include decreased level of consciousness, abnormality of muscle tone and power, respiratory depression, disturbances of cranial nerve function, and seizures. Low Apgar scores and metabolic acidosis are associated with neurologic dysfunction. Therapeutic hypothermia initiated within the first 6 hours of life is the only treatment proven to reduce the risk of death and neurodevelopmental impairment.
Head US is the most utilized neuroimaging modality in the NICU. However, US is limited in evaluating cerebral injury in HIE. Brain MRI is preferred and is a useful tool to predict neurodevelopmental outcomes. In the first week after birth, diffusion-weighted (DWI) MRI of the brain may assist physicians in making management decisions for infants with HIE. Because pseudonormalization occurs 7 to 8 days after birth, the optimal time for detection of DWI abnormality in the term infant is 2 to 3 days after birth.
Clinical Red Flags
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Decreased level of consciousness
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Abnormality of muscle tone and power
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Respiratory depression
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Disturbances of cranial nerve function
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Seizures
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Low Apgar scores
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Metabolic acidosis
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