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Management. Metabolic derangements should be managed first. Hypoglycemia
can be corrected by parenteral administration of a 10% dextrose solution (D10):
initial administration should include a bolus of 5 mL/kg followed by continuous
dextrose infusion that can be titrated as needed to maintain euglycemia. Anything
equal to or greater than 25% dextrose solutions should be avoided unless there is
a central line or intraosseous access or a patient is refractory to D10 boluses.
Hypocalcemia should be treated with parenteral infusion of calcium, most often
calcium gluconate; concordant hypomagnesemia should be also corrected, as
calcium levels may not normalize until serum magnesium normalizes. Hyper- or
hyponatremia should generally be correctly slowly to avoid sudden fluid shifts in
the brain. Ongoing seizures caused by hyponatremia will often stop with a simple
normal saline bolus of 20 mL/kg; continued seizures due to hyponatremia
refractory to standard sodium corrections may require administration of
hypertonic saline (3%) at a dose of 4 mL/kg. Given the associated risks of
hypertonic saline administration, 3% saline is ideally given through a central line.
Infants at risk for infection or meningitis should be treated with broad-spectrum
antibiotics as soon as cultures are obtained. The use of antiepileptics is
controversial in that some believe only clinical seizures should be treated, while
others that only seizures confirmed by EEG should be treated. If antiepileptics are
administered, the most common treatment includes phenobarbital and
phenytoin/fosphenytoin. Benzodiazepines are the second most common
medications, but the associated sedative effects and potential for respiratory
depression requires close monitoring of the infant’s cardiorespiratory status. The
decision to treat thrombotic cerebrovascular lesions should be made in
conjunction with a pediatric hematologist. Severe hyperammonemia and other
metabolites due to IEM may require dialysis and should be managed in
conjunction with a metabolic geneticist. Pyridoxine deficiency may respond to
parenteral administration of pyridoxine, but requires continuous EEG monitoring
to assess effectiveness.

Neonatal Encephalopathy

Goals of Treatment
The primary goal of treatment is to identify the encephalopathic newborn, and
provide supportive care while determining the etiology of encephalopathy. Infants
with encephalopathy due to asphyxial events may present in multisystem organ
failure as well autonomic instability secondary to brain injury. In this instance,
goals of treatment include cardiorespiratory stabilization, particularly if there are
signs of autonomic dysfunction, and maintaining thermoneutral environment,