Calcium Disorders in Children

On this page
  1. Direct answer
  2. What you must remember
  3. Working through a fitting neonate
  4. Where students slip
  5. Frequently asked questions
  6. Related topics

Direct answer

Neonatal hypocalcaemia divides cleanly by timing: early hypocalcaemia in the first 72 hours, driven by prematurity, birth asphyxia, maternal diabetes and transient parathyroid suppression; and late hypocalcaemia from the end of the first week onward, driven by hypoparathyroidism (including 22q11 deletion), maternal hypercalcaemia, phosphate loading from whole cow's milk feeds, and vitamin D deficiency. The older child presents with tetany — carpopedal spasm, laryngospasm, stridor, Chvostek and Trousseau signs, or seizures — and the diagnostic fork runs on paired phosphate and parathyroid hormone: low calcium with high phosphate means parathyroid failure or resistance, low calcium with low phosphate means vitamin D deficiency. Symptomatic hypocalcaemia is treated with 10% calcium gluconate, 1-2 mL/kg intravenously, diluted, slow, on cardiac monitoring.

What you must remember

  • Timing framework: early neonatal hypocalcaemia (first 72 hours) — prematurity, asphyxia, infants of diabetic mothers; late neonatal (beyond about day 5-7) — hypoparathyroidism, high-phosphate feeds, maternal hyperparathyroidism, vitamin D deficiency.
  • DiGeorge syndrome (22q11 deletion): hypocalcaemia with hyperphosphataemia, conotruncal heart disease, thymic aplasia with T-cell deficiency, cleft palate — the CATCH-22 mnemonic; low parathyroid hormone with low calcium confirms parathyroid failure.
  • Signs and their limits: Chvostek may be positive in normal neonates; Trousseau (carpal spasm after cuff inflation) is more specific; neonatal seizures justify calcium measurement.
  • Acute dosing: 10% calcium gluconate 1-2 mL/kg (elemental calcium 10-20 mg/kg) diluted in dextrose, given over 10-20 minutes with ECG monitoring — peripheral extravasation causes catastrophic tissue necrosis; oral calcium and vitamin D follow for maintenance.
  • Corrected calcium: add 0.8 mg/dL to the measured total calcium for every 1 g/dL that albumin sits below 4 g/dL; ionised calcium settles all doubt.
  • Pseudohypoparathyroidism: Albright hereditary osteodystrophy — round face, short fourth and fifth metacarpals, subcutaneous ossifications — with high parathyroid hormone and low calcium; the same phenotype with normal calcium is pseudopseudohypoparathyroidism.
  • Hypercalcaemia causes and course: Williams syndrome (elfin facies, supravalvular aortic stenosis), primary hyperparathyroidism, vitamin D intoxication, thiazides, immobilisation and malignancy; treat with saline, loop diuretics once rehydrated, calcitonin and bisphosphonates if refractory.

Working through a fitting neonate

A seven-day-old term infant, fed diluted cow's milk from birth, presents with recurrent multifocal jerks; total calcium is 6.5 mg/dL with phosphate of 9.2 mg/dL. The pathway: secure the airway and control seizures, then give 10% calcium gluconate 2 mL/kg diluted, over 15 minutes, on a monitor through a well-running line — this is late hypocalcaemia, and the high phosphate points to dietary phosphate loading and suppressed parathyroid function. Stop the cow's milk, move to a standard formula or breast milk, start oral calcium and appropriate vitamin D, and measure parathyroid hormone to separate transient neonatal hypoparathyroidism (low) from phosphate-mediated suppression, with magnesium checked because hypomagnesaemia renders hypocalcaemia refractory. The 22q11 question is asked by the heart: a neonate with hypocalcaemia, a conotruncal defect and absent thymic shadow gets a deletion study.

In the older child with tetany, the same physiology runs at larger scale: cuff the arm, confirm the spasm, and let the paired calcium, phosphate, vitamin D and parathyroid hormone panel place the child in the deficient, the hypoparathyroid, or the resistant box before any long-term prescription.

Where students slip

The dosing errors are the scored ones: giving calcium gluconate undiluted or fast (bradycardia, arrest), or extravasating it (necrosis) — examiners pair the dose (1-2 mL/kg of 10% solution) with the safety conditions, and a bare dose answer earns half marks. The second slip is ignoring the calcium-phosphate handshake: a low calcium treated with calcium alone while phosphate stays high fails; the pair, with parathyroid hormone, is the diagnostic triad the viva expects. The third is the sign over-read — Chvostek in a neonate is background noise, and Trousseau carries the specificity. Finally, the corrected-calcium arithmetic (0.8 times 4 minus albumin) appears in near every MCQ set; candidates who skip it call hypoalbuminaemic children hypocalcaemic and treat them unnecessarily.

Frequently asked questions

How is neonatal hypocalcaemia classified by timing?

Early (first 72 hours) from prematurity, asphyxia and maternal diabetes; late (beyond the first week) from hypoparathyroidism, maternal hypercalcaemia, high-phosphate feeds and vitamin D deficiency.

What dose of calcium treats symptomatic hypocalcaemia?

10% calcium gluconate at 1-2 mL/kg (10-20 mg/kg elemental calcium), diluted and infused over 10-20 minutes with continuous ECG monitoring.

What distinguishes hypoparathyroidism from pseudohypoparathyroidism?

Both have low calcium with high phosphate, but parathyroid hormone is low in parathyroid failure and high in pseudohypoparathyroidism, which also shows the Albright hereditary osteodystrophy phenotype.

Which syndrome links hypocalcaemia with heart disease and immune deficiency?

22q11 deletion (DiGeorge) — conotruncal cardiac defects, thymic aplasia with T-cell deficiency, cleft palate and parathyroid failure.

How is symptomatic hypercalcaemia managed?

Aggressive isotonic saline rehydration, then loop diuretics once euvolaemic, with calcitonin for rapid and bisphosphonates for sustained control, and treatment of the underlying cause.

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