Early neonatal hypocalcemia occurs in the first 24 to 48 hours of life and is observed most frequently in premature infants, sick infants, and infants born of an abnormal labor or pregnancy. The condition can be explained as an exaggeration of the normal postnatal decrease in serum calcium; the fall in serum calcium is inversely proportional to the gestational age of the infant. The serum calcium remains low for a few to several days and then gradually increases, usually reaching normal levels by 1 to 2 weeks of age. The serum inorganic phosphate concentration is usually normal, although it may be elevated in asphyxiated infants and in infants born of diabetic mothers.

It has been suggested that inappropriate parathyroid secretion, parathyroid hormone (PTH) resistance, and/or vitamin D metabolic abnormalities may contribute to the development of this condition, but no single conclusive mechanism has been confirmed. Many premature infants with early neonatal hypocalcemia are asymptomatic, but in others, tetany or convulsions may be present. Symptomatic infants obviously require calcium therapy, but there is no unanimity regarding treatment of hypocalcemic infants who are asymptomatic. The emergency treatment of neonatal hypocalcemia consists of the intravenous administration of 1 mL per minute 10% calcium gluconate, which should not exceed 2.0 mL/kg. This may be repeated three to four times in 24 hours to control the acute symptoms. After the acute symptoms have been controlled, 5.0 mL/kg 10% calcium gluconate may be given with intravenous fluids over a 24-hour period, or calcium supplements may be given orally if feedings are tolerated. Occasionally, hypomagnesemia is concomitantly identified; this can be treated with 0.1 to 0.2 mL/kg of a 50% solution of magnesium sulfate (MgSO₄•7H₂O).

Late neonatal hypocalcemia appears at the end of the first week of life or later, often in full-term infants who have received a high phosphate load, such as that formerly encountered with feedings of evaporated cow’s milk formula or from a phosphate enema.2a Infants with late neonatal hypocalcemia usually have clinical manifestations of tetany or convulsions. Hyperphosphatemia is a prominent feature, and the serum PTH level may be low, reflecting a state of functional hypoparathyroidism in the presence of hypocalcemia. This form of hypocalcemia is seen in infants born to hyperparathyroid mothers and in children with congenital heart disease in the postoperative period.

The emergency treatment of acute tetany or convulsions secondary to hypocalcemia is the same as for early neonatal hypocalcemia. Dietary factors are of importance in the management of late neonatal hypocalcemia; the phosphate load should be diminished, with an increase of the calcium/phosphate ratio of milk feedings to 4:1. The author often uses Similac PM 60/40 (Ross Laboratories, Columbus, Ohio) in this setting. The serum calcium level usually increases when the infants are given such milk feedings; and, after several days to weeks, the serum PTH level gradually rises and the infants can tolerate higher phosphate loads. The pathogenesis of the transient hypoparathyroidism in these infants is unknown.