Hypocalcemic Seizures in Neonates

Infants with seizures caused by hypocalcemia were unusually alert between seizures, which were often multifocal and migration. Early-onset neonatal hypocalcemia occurring during the first 2 or 3 days after birth is observed in infants of diabetic mothers and infants of low birth weight for gestation age and associated with hypoxic-ischemic encephalopathy. The reduced serum calcium in such patients may cause or contribute to the occurrence of convulsion; however, in some infants, correction of calcium deficit does not alleviate the neurological abnormalities. Prematurity may cause more severe and prolonged hypocalcemia in newborns. Hypocalcemia is commonly seen in infants of a diabetic mother, in which case 50% of infants will present within the first few days of life, and the frequency and severity is directly proportional to that of the mother’s diabetes. In these patients hypocalcemia may present early in life and may be prolonged and severe. Neonatal hypocalcemia is rare with pure gestational diabetes.

TABLE 4 — Causes of Neonatal Hypocalcemia
Early neonatal hypocalcemia
Asphyxia, prematurity, infants of diabetic mother
Late neonatal hypocalcemia
Increased dietary phosphate intake
Maternal hyperparathyroidism
Hypomagnesemia (transient and primary)
DiGeorge syndrome

Late-onset neonatal hypocalcemia is less frequent, usually affects full-term infants, and can present as early as day three of life or as late as the end of the second month. Occasionally, however, it is seen in premature infants presenting with a particularly severe and/or unusually long-lasting early neonatal hypocalcemia. The main etiological factor is hypoparathyroidism with inappropriately low serum PTH concentration in the face of hypocalcemia and hyperphosphatemia. Late-onset neonatal hypocalcemia is either asymptomatic or manifests as transient tremors, irritability, and seizures. Maternal hypocalcemia secondary to primary hyperparathyroidism is also a rare cause of depressed neonatal parathyroid function with increased serum calcium levels. [13] Hypocalcemia is also seen in association with hypomagnesemia. Newborns with hypomagnesemia fall into two groups–transient hypomagnesemia and chronic congenital (primary) hypomagnesemia. [14] Both cause a secondary hypocalcemia by impairing parathyroid hormone secretion and perhaps by blunting the end-organ response to parathyroid hormone. [15] Primary hypomagnesemia is a rare disease, with autosomal recessive inheritance caused by an isolated defect in the intestinal transport of magnesium. Serum magnesium levels are very low (less than 0.33 mmol/L).

Functional hypoparathyroidism exists, leading to magnesium-dependent hypocalcemia. Patients have similar symptoms as those seen with hypocalcemia. Treatment in the Emergency Department consists of slow intravenous administration of magnesium sulfate (1.0 to 1.5 mmol/kg) followed by intramuscular injections. Chronic treatment requires oral magnesium lactate, chloride, citrate, or sulfate at a daily dose of 0.5 to 1.5 mmol/kg, depending on the severity of the magnesium deficiency and the digestive tolerance. Successful treatment leads to spontaneous parallel increase in serum PTH, calcium, and serum magnesium. [13] High dietary phosphorus intake causes late-onset hypocalcemia. This occurs in infants receiving cow milk and soy protein formula with high phosphorus contents. A high phosphorus intake and decreased glomerular filtration rate of immature kidneys for phosphorus may result in an increase in serum phosphorus levels and a secondary decrease in serum ionized calcium. [16] Hypocalcemia is also an initial presentation of DiGeorge syndrome. These patients have embryologic defects in the third and fourth pharyngeal pouches resulting in absence of the thymus and parathyroid glands. It is frequently associated with defects of the aortic arch and heart, such as interrupted aortic arch or truncus arteriosus, and less commonly, tetralogy of Fallot and ventricular septal defect. Dysmorphic facial features include hypertelorism, down-slanting palpebral fissures, ear anomalies, and short philtrum. [17]

In this case, the infant had seizures at 2 weeks of age, was not born premature, had no oral intake of infant formula with high phosphorus content, had normal maternal serum calcium levels, had no evidence of dysmorphic features, had normal cardiac examination results, and the CT scan was normal. There was a fairly quick response to oral calcium replacement, which ruled out primary hypomagnesemia. In most instances, hypoparathyroidism is unexplained and is transient, so that within a few days or weeks the serum calcium levels return to normal. In this case, the infant probably had transient idiopathic hypocalcemia.


The infant presented in this case had subtle neonatal seizure secondary to hypocalcemia. Transient idiopathic hypoparathyroidism occurring in the late neonatal period was probably responsible for the hypocalcemia. This infant, because of the brief nature of the seizure, did not require any therapeutic intervention in the ED. Oral calcium was successful in treating hypocalcemia and seizure.


American Journal of Emergency Medicine
Volume 15 Number 7 November 1997
Copyright 1997 W. B. Saunders Company

Brief Reports, Hypocalcemic Seizures in Neonates, DIPAK P. SHETH, MD

From the Division of Emergency Medicine, Tulane University School of Medicine, New Orleans, LA.


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