Chapter 7.4 — Electrolyte Disorders & Metabolic Bone Disease

This chapter is a consolidated quick-reference for the common neonatal electrolyte disturbances and for metabolic bone disease (osteopenia) of prematurity. It complements the detailed physiology of fluids and sodium/potassium in chapter 7.1 and calcium/magnesium in chapter 4.8, bringing the practical "recognize–interpret–correct" points together in one place, with emphasis on phosphate and bone health, which are otherwise easy to overlook in the growing preterm infant.

• Neonates with electrolyte disturbances and preterm infants at risk of metabolic bone disease.
• Infants on parenteral nutrition, diuretics, or prolonged fluids.
• Cross-references: fluids & electrolytes (7.1), calcium/magnesium (4.8), parenteral nutrition (7.2), and enteral nutrition (7.3).

• Early sodium mostly reflects water balance: high Na = free-water deficit (give water); low Na = fluid excess (restrict water).
• Late hyponatremia in preterm infants usually reflects true sodium depletion → supplement.
• Correct dysnatremia slowly to avoid cerebral edema/osmotic demyelination.

• Hypophosphatemia results from inadequate intake, refeeding (rapid growth in growth-restricted infants), and is central to metabolic bone disease.
• Ensure adequate phosphate in parenteral and enteral nutrition (with calcium); watch for refeeding shifts in IUGR infants.
• Hyperphosphatemia is less common (renal impairment, high phosphate load) and contributes to late hypocalcemia (see 4.8).

• Measure ionized calcium directly. The relationship between total and ionized calcium is not linear, so total calcium is not a reliable predictor. Ionized calcium is relatively higher for any total calcium in a very premature infant (low total protein) or an acidotic one — which means the greatest risk of true hypocalcaemia is in the large, alkalotic baby, the opposite of intuition. Jitteriness and QT prolongation are unreliable indicators.
• Thresholds: in VLBW infants, ionized calcium below 0.8 mmol/L (normal 0.9–1.45). Above 1500 g, below 1.0 mmol/L, though many are asymptomatic between 0.8 and 1.0; a total calcium below 8 mg/dL usually indicates hypocalcaemia. Check ionized calcium at 24 hours and every 12 hours until the infant is on a calcium source with a stable normal value — usually by 48–72 hours.
• Treatment: calcium gluconate 500 mg/kg/day by continuous infusion for maintenance; for a symptomatic infant of any size, calcium gluconate 100 mg/kg or calcium chloride 20 mg/kg over 10–20 minutes with cardiorespiratory monitoring, always followed by the maintenance infusion. Do not give IV calcium for more than 48 hours without phosphorus — and if potassium phosphate comes out of the PN for hyperkalaemia, take the calcium out too unless sodium phosphate replaces it.
• Hypocalcaemic seizures at 3–10 days, above 34 weeks: send total and ionized calcium, phosphorus, magnesium, intact PTH, FISH for 22q deletion and a chest radiograph for the thymic shadow (the last three can wait until stable). Bolus calcium gluconate 100 mg/kg IV over 30 minutes — about 10 mg/kg elemental — then infuse at 1000 mg/kg/day through a central line, or 600 mg/kg/day maximum peripherally because of extravasation risk. Ionized calcium one hour after the bolus, then every 4 hours, easing to 6–8 hourly once above 1.0 with seizures stopped. Seizures commonly persist until the ionized calcium has been above 1.00 for 1–2 hours — EEG, CT, anticonvulsants and neurology are usually unnecessary when the biochemistry is diagnostic. Wean at 1.21–1.30 mmol/L to 250 mg/kg/day and stop once feeds with oral calcium are tolerated. Oral calcium carbonate 30 mg/kg every 6 hours gives roughly 50 mg/kg/day of elemental calcium — high osmolarity, so use caution in VLBW infants, and avoid concurrent H₂ blockers and PPIs, which impair absorption.
• Magnesium: below 1.5 mg/dL suggests deficiency (normal 1.6–2.6), and PTH cannot work without it — hypocalcaemia may be untreatable until magnesium is corrected. Magnesium sulfate 25–50 mg/kg/dose (0.2–0.4 mEq/kg) over at least 2–4 hours twice daily; never as a rapid push. In the seizure protocol, 25 mg/kg over 1 hour repeated every 12 hours until above 1.6 mg/dL — rarely more than two doses.
• Hypercalcaemia: the ceiling is 1.40–1.45 mmol/L. Mild elevation (1.45–1.65) or mild hyperphosphataemia (>9 mg/dL) needs no specific therapy; if it persists, a change of no more than 20% in the calcium-to-phosphorus molar ratio usually corrects it within 48 hours. At ≥1.6 mmol/L, reduce the ratio to about 0.5:1 to 0.8:1. Under no circumstances remove calcium from the PN for an ionized calcium below 1.8 mmol/L, and if it is removed, cut phosphorus by 50% or delete it, for rarely more than 24 hours, checking ionized calcium every 12 hours. Hypercalcaemia has no therapeutic benefit and above 1.6 mmol/L risks tissue calcium deposition, including in the brain.

• Risk factors: prematurity (high needs, low stores), insufficient Ca/P intake, prolonged PN, loop diuretics, corticosteroids, fluid restriction, and chronic kidney disease.
• Birth weight <1500 g: check phosphorus and alkaline phosphatase at about day 35. Above 1500 g, there is no routine nutritional monitoring unless fluid-restricted or slow to reach full feeds.
• Alkaline phosphatase <600 IU/L and phosphorus >4.5 mg/dL, with no clinical concern: no further routine checks unless the clinical course changes.
• Alkaline phosphatase >600 IU/L or phosphorus <4.5 mg/dL: recheck weekly until ALP <600 and P >4.5 when there is clinical suspicion; otherwise every 2 weeks, twice, until stable. Suspicion means an incidental finding on an unrelated film, a fracture, PN for more than 3–4 weeks, or ALP >800.
• Wrist radiograph: if ALP >800 IU/L, or below 800 with clinical suspicion (incidental film finding, fracture, PN for more than 3–4 weeks, P <4.5 mg/dL).
• Infants transferred in after 2–3 months of age, or with risk factors: evaluate within the first week — ALP, phosphorus, 25-OH vitamin D, and a wrist film — and optimize Ca, P and vitamin D with the nutrition team (vitamin D goals in chapter 7.7).
• Human-milk-based fortifier can cause hyperphosphataemia: check phosphorus 3–5 days after PN stops, again a week later if above 8 mg/dL. At above 10 mg/dL, check ionized calcium and creatinine and hold the fortifier from every other feed or all feeds for 1–2 days. Oral calcium is generally not advised here; involve nutrition if the fortifier is off for more than 48 hours.
• Normal numbers do not end the risk: preterm infants stay at risk of osteopenia and rickets for some time and need re-evaluation when new risk factors appear.