Hyponatremia
Serum sodium under 120 mEq/L may produce seizures. Hyponatremia occurs in neonates with inappropriate antidiuretic hormone secretion syndrome, congenital adrenal hyperplasia, and those receiving hypo-osmolar formula. Inappropriate antidiuretic hormone secretion syndrome should be suspected in a neonate with decreased urinary output and high urinary osmolarity. The immediate treatment of hyponatremic seizures in neonates consists of providing enough sodium in a 10-minute period to elevate the serum sodium level to 125 mEq/L by using 3% normal saline solution (contains 513 mEq of sodium/L). The amount of sodium required is calculated using the following formula:

(125 -?) x (0.6) x (wt kg) = X mEq

where ? represents the patient’s serum sodium, 0.6 is the dilution constant, and X represents the number of mEq needed to correct the sodium level to 125 mEq. Neonates with inappropriate antidiuretic hormone secretion syndrome should also be given furosemide 1 mg/kg intravenously, followed by replacing urinary sodium milliequivalent for milliequivalent with 3% normal saline solution. Neonates with congenital adrenal hyperplasia and neonates receiving diluted formulas do not require furosemide. Antiepileptic drugs should be used if seizures persist after the infusion of 3% normal saline solution or if it is not available.
Central pontine myelinolysis may occur due to rapid correction of hyponatremia. Central pontine myelinolysis should be suspected in a neonate with hyponatremia that in the course of correction of the hyponatremia develops cranial nerve dysfunction and quadriparesis. Magnetic resonance imaging is the study of choice (Figure 42.1).

A	B

Figure 42.1.— Central pontine myelinolysis. [A] MRI of the brain (T1-weighted image) demonstrating a round lesion in the central pontine area. [B] MRI of the brain (T2-weighted image) demonstrating an oval lesion in the central pontine area.

Hypernatremia
Serum sodium above 150 mEq/L may produce seizures. Hypernatremia occurs in neonates who have received excessive sodium orally (by mistakenly trying to sweeten formula with salt) or intravenously (miscalculating the sodium in hyperalimentations or not accounting for the sodium in sodium bicarbonate when it is used to correct acidosis). Signs of dehydration may or may not be present.
The correct treatment of hypernatremic seizures in a neonate is uncertain. Some advocate blood volume correction using 5% albumin followed by forced diuresis (furosemide 1 mg/kg) and replacement of the urine volume with a 10% dextrose solution. Others advocate using D5W 0.2 normal saline solution at 100 to 150 cc/kg per day according to the gestational age of the neonate. After seizures stop, serum sodium should be measured and further correction should aim at decreasing serum sodium by 10 mEq a day. Serum potassium and blood calcium should be monitored carefully. Antiepileptic drugs may be necessary.

Local anesthetic intoxication
Local anesthetic intoxication should be considered as a possible cause of seizures in neonates with scalp puncture wounds. Neonates with local anesthetic intoxication may have fixed and dilated pupils, and absence of extraocular movements during the first 6 hours after the administration of local anesthetic. The usual offenders are mepivacaine and lidocaine. The half-life of these drugs is about 8 to 10 hours. Treatment consists of diuresis with acidification of urine and support of vital signs. Antiepileptic drugs are of questionable value.