Pediatric emergency medicine trisk 642

monitoring, as these medications can quiet clinical seizures despite ongoing
electrical seizures.
Clinical Considerations
Clinical Recognition. Clinical seizures can be focal clonic, multifocal or
migratory clonic, tonic, myoclonic, or subtle. The most common is the subtle
seizure, often presenting with repetitive tongue or lip-smacking movements, eye
deviations, or unusual bicycling or peddling movements. These movements may
be associated with autonomic dysfunction, such as changes in heart rate, blood
pressure, or oxygenation. The converse, autonomic disturbances such as apnea or
bradycardia without associated movement anomalies rarely reflect seizure
activity.
Triage Considerations. Neonates with suspected seizures should be triaged
urgently as prolonged seizures can cause permanent brain injury or progress to
systemic cardiorespiratory compromise.
Clinical Assessment. Often, parents will present to the ED with videos of
repetitive behaviors believed to be seizures. These videos can be very helpful.
Common causes of seizures are summarized in Table 96.4 . Detailed history can
suggest recent asphyxial events or trauma. Prenatal history can identify the
neonate at risk for withdrawal syndromes, and serum or urine toxicology screens
can identify acute intoxication. STAT bedside glucose and sodium testing should
be performed. Serum evaluation should include glucose and electrolytes
(including magnesium, calcium, and phosphorus). Ammonia, lactate, and
pyruvate can identify metabolic derangements as well as suggest certain IEM.
Serum blood gas evaluation may identify recent hypoxic–ischemic injury.
Cultures and viral testing of the blood, urine, and CSF can identify infection.
CNS imaging may include head US, CT, or MRI. Head US can be done through
the anterior fontanelle, and can help identify ventriculomegaly or intraventricular
hemorrhage, but could also suggest cerebral edema when the lateral ventricles are
small. Head CT is the test of choice when there is a concern for trauma or
cerebrovascular lesions. This does expose the neonate to radiation and so should
only be used when there is high suspicion of these lesions. Brain MRI can

identify CNS malformations, abscesses or empyemas (with the use of
gadolinium), asphyxial events (particularly with the use of diffusion-weighted
sequences), certain metabolic derangements and IEM (with magnetic resonance


spectroscopy). These tests require a trained pediatric neuroradiologist because of
the numerous differences between the neonatal and adult brains.


TABLE 96.4
COMMON CAUSES OF NEONATAL SEIZURES
Asphyxia-related events

Metabolic derangements

Cerebrovascular lesions

Infection

Intrapartum stress or infection
Postnatal hypoxia due to trauma or systemic
illness
Hypoglycemia
Hypocalcemia
Hyponatremia/Hypernatremia
Neonatal stroke
Venous thrombosis
Subarachnoid hemorrhage
Subdural hematoma
Congenital infections (e.g., toxoplasmosis,

rubella, cytomegalovirus, herpes simplex
virus)
Viral meningitis or meningoencephalitis (e.g.,
herpes simplex virus, enterovirus,
parvovirus)
Bacterial meningitis

Central nervous system
malformations

Dysgenetic syndromes (e.g.,
holoprosencephaly, lissencephaly)
Chromosomal anomalies (e.g., trisomy 18)
Acquired malformations

Inborn errors of metabolism

Nonketotic hyperglycinemia
Branched-chain aminoacidopathies
Urea cycle defects with hyperammonemia
Adrenoleukodystrophies (e.g., Zellweger
syndrome)
Mitochondrial disorders with elevated lactate
and pyruvate
Pyridoxine deficiency
Prenatal exposure to barbiturates, alcohol,
heroin, cocaine, methadone may seize within
2 days to 6 weeks of age

Drug withdrawal or

intoxication


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,