Pediatric emergency medicine trisk 2569 2569

avoiding hyperthermia. For neonates encephalopathic immediately after birth,
therapeutic hypothermia initiated within 6 hours of life and continued for 72
hours is now an evidence-proven therapy that should be considered. Parenteral
fluids should be administered to ensure adequate cardiac output. Metabolic
derangements should be addressed in order to maintain serum sodium close to
140 to avoid exacerbations of cerebral edema, and hypoglycemia should be
treated aggressively to avoid secondary neuronal injury. Infants with evidence of
trauma or increased intracranial pressure may need to have emergent
neurosurgical interventions, and coagulation disturbances should be corrected to
try and control intracranial hemorrhage. Acute intoxication and/or IEM may
present with worsening encephalopathy, and in certain circumstances, may
require emergent dialysis to clear the offending metabolite.
CLINICAL PEARLS AND PITFALLS
The neonatal neurologic examination can be challenging due to subtle
changes in mental status in infants with underdeveloped CNSs.
Nonetheless, the neurologic examination can identify infants at high
risk for brain injury and timely interventions, such as hypothermia, can
result in neuroprotection.
In some circumstances, brainstem herniation can occur without bulging
of the anterior fontanelle because of isolated increased pressure in the
posterior fossa.
It is not uncommon for the infant to have waxing and waning of
neurologic signs, and careful documentation and serial evaluations are
important diagnostic and prognostic clues.
Perinatal hypoxia–ischemia is a major cause of neonatal
encephalopathy, however, additional etiologies for late-onset or
progressive encephalopathy must be evaluated.
Current Evidence
Hypoxic–ischemic injury during the perinatal period is the most common
identified cause of neonatal encephalopathy. The pathophysiology of injury
leading to cerebral edema, reperfusion injury, and neuronal cell death can also be

applied to any acute asphyxial event in the neonatal period. Brain injury in
response to such an event continues to evolve over a period of hours to days, and
can account for changes seen in the clinical examination.