Exposure to ambient temperatures above the neutral thermal environment results in heat stress and an elevated core temperature. Sweating is uncommon in newborns and may be noted only on the forehead. In response to moderate heat stress, infants may increase their respiratory rate to dissipate heat. Excessive environmental temperatures may result in heatstroke or in hemorrhagic shock encephalopathy syndrome.
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Hypocalcemia is common in sick and premature newborns. Calcium levels are higher in cord blood than in maternal blood because of active placental transfer of calcium to the fetus. Fetal calcium accretion in the third trimester approaches 150 mg/kg/24 hr; fetal bone mineral content doubles between 30 and 40 weeks of gestation. All infants show a slight decline of serum calcium levels after birth, reaching a trough level at 24 to 48 hours, the point at which hypocalcemia usually occurs. Total serum calcium levels of less than 7 mg/dL and ionized calcium levels of less than 3 to 3.5 mg/dL are considered hypocalcemia.
The etiology of hypocalcemia varies with the time of onset and the associated illnesses of the child. Early neonatal hypocalcemia occurs in the first 3 days of life and is often asymptomatic. Transient hypoparathyroidism and a reduced parathyroid response to the usual postnatal decline of serum calcium levels may be responsible for hypocalcemia in premature infants and infants of diabetic mothers. Congenital absences of the parathyroid gland with DiGeorge syndrome is a cause of hypocalcemia. Hypomagnesemia (<1.5 mg/dL) may be seen simultaneously with hypocalcemia, especially in infants of diabetic mothers. Treatment with calcium alone does not relieve symptoms or increase serum calcium levels until hypomagnesemia is also treated. Sodium bicarbonate therapy, phosphate release from cell necrosis, transient hypoparathyroidism, and hypercalcitoninemia may be responsible for early neonatal hypocalcemia associated with asphyxia. Early-onset hypocalcemia associated with asphyxia often occurs with seizures as a result of hypoxic-ischemic encephalopathy
Late neonatal hypocalcemia, or neonatal tetany, often is the result of ingestion of high phosphate–containing milk or the inability to excrete the usual phosphorus in commercial infant formula. Hyperphosphatemia (>8 mg/dL) usually occurs in infants with hypocalcemia after the first week of life. Vitamin D deficiency states and malabsorption also have been associated with late-onset hypocalcemia.
The clinical manifestations of hypocalcemia and hypomagnesemia include apnea, muscle twitching, seizures, laryngospasm, Chvostek sign (facial muscle spasm when the side of the face over the seventh nerve is tapped), and Trousseau sign (carpopedal spasm induced by partial inflation of a blood pressure cuff). The latter two signs are rare in the immediate newborn period.
Neonatal hypocalcemia may be prevented in high-risk neonates by administration of IV or oral calcium supplementation at a rate of 25 to 75 mg/kg/24 hr. Early asymptomatic hypocalcemia of preterm infants and infants of diabetic mothers often resolves spontaneously. Symptomatic hypocalcemia should be treated with 2 to 4 mL/kg of 10% calcium gluconate given intravenously and slowly over 10 to 15 minutes, followed by a continuous infusion of 75 mg/kg/24 hr of elemental calcium. If hypomagnesemia is associated with hypocalcemia, 50% magnesium sulfate, 0.1 mL/kg, should be given by intramuscular injection and repeated every 8 to 12 hours.