Version July 2025
PTH: parathyroid hormone; VLBW: very low birth weight.
* For asymptomatic neonates with early hypocalcemia, dietary management includes early enteral feedings or the addition of calcium to parenteral nutrition for neonates who cannot tolerate enteral feeds. In asymptomatic neonates with late hypocalcemia, hyperphosphatemia is typically due to increased dietary intake of phosphorus; management includes a high calcium, low phosphorus diet and oral calcium supplementation. Other causes of hyperphosphatemia should be addressed (if present), including acute kidney injury, perinatal asphyxia, or therapeutic interventions (eg, phosphate enemas). Serum calcium and phosphate levels usually improve within 1 to 4 days after starting therapy. For asymptomatic neonates with persistent hypocalcemia or those with late hypocalcemia and a normal/low phosphorus level, enteral (or parenteral) nutrition is continued, and additional laboratory testing is obtained.
¶ In neonates with early hypocalcemia due to diabetes in the pregnant parent, hyperphosphatemia may present with low serum magnesium and low PTH.
Δ Hyperparathyroidism in the pregnant parent can rarely lead to early neonatal hypocalcemia by suppressing PTH in the neonate and can be confirmed by measuring the parent's serum calcium and PTH level (if calcium is elevated). Hypoparathyroidism in the neonate can also be caused by DiGeorge (22q11 deletion) syndrome, and genetic testing is warranted for neonates with congenital heart disease or other concerning clinical features.
◊ Elevated creatinine and electrolyte imbalances on the basic metabolic panel are suggestive of acute kidney injury. A low urinary calcium excretion indicates calcium deficiency and is typically found in neonatal hypoparathyroidism; the level can vary depending on the severity of hypocalcemia, dietary calcium intake, and kidney function.
