Hypercalcaemia in Children
Hypercalcaemia, defined as a serum calcium level above 2.75 mmol/L, is a less common but potentially serious electrolyte disturbance in children. The clinical presentation is often non-specific, so a high index of suspicion is needed, especially in high-risk groups. Management focuses on treating the underlying cause and lowering serum calcium levels to prevent complications like kidney damage and cardiac arrhythmias.
Aetiology
The causes of hypercalcaemia vary depending on the child’s age.
Neonates:
Iatrogenic: Often due to excessive calcium or vitamin D supplementation.
Genetic: Conditions like Williams syndrome, a genetic disorder that can lead to increased calcium absorption, and hypophosphatasia, a rare metabolic bone disease.
Endocrine: Primary congenital hyperparathyroidism.
Skin: Subcutaneous fat necrosis, which can occur after trauma or difficult deliveries, leading to the release of calcium.
Older Children and Adolescents:
Endocrine: The most common cause is primary hyperparathyroidism, often due to a benign parathyroid adenoma.
Malignancy: Cancer, particularly leukaemia and lymphomas, can cause hypercalcaemia through the release of parathyroid hormone-related protein (PTHrP) or bone destruction.
Granulomatous Diseases: Conditions like sarcoidosis and tuberculosis activate vitamin D, leading to increased calcium absorption.
Drugs: Thiazide diuretics can increase calcium reabsorption in the kidneys.
Immobility: Prolonged immobilisation can lead to bone breakdown and a rise in serum calcium.
Clinical Presentation and Investigation
Symptoms of hypercalcaemia are often vague and can be subtle. They can be remembered with the mnemonic “Stones, bones, abdominal groans, and psychic moans.”
Systemic: Lethargy, weakness, and polyuria (frequent urination) and polydipsia (excessive thirst).
Gastrointestinal: Nausea, vomiting, abdominal pain, constipation, and poor appetite.
Renal: High calcium levels can lead to nephrocalcinosis (calcium deposits in the kidneys) and kidney stones.
Neurological: In severe cases, confusion, stupor, or coma may develop.
Cardiac: Hypercalcaemia can shorten the QT interval on an ECG and lead to bradycardia and hypertension.
Management
The management of hypercalcaemia depends on the severity and the underlying cause.
Mild and Asymptomatic: Often managed with a “watch and wait” approach, focusing on identifying and treating the underlying cause.
Moderate to Severe (Symptomatic):
Hydration: The first step is to administer intravenous 0.9% saline. This helps to restore fluid volume and promotes the renal excretion of calcium.
Increased Excretion: Loop diuretics like furosemide can be used in conjunction with hydration to increase urinary calcium excretion, but only after the child is well-hydrated.
Inhibition of Bone Resorption:
Bisphosphonates: These drugs, such as pamidronate or zoledronate, are highly effective and are often used to treat hypercalcaemia due to malignancy. They work by inhibiting bone breakdown.
Calcitonin: This hormone can also be used to lower calcium levels by inhibiting osteoclast activity, but its effect is less pronounced and shorter-lived than bisphosphonates.
Specific Causes:
Hyperparathyroidism: Surgical removal of the parathyroid adenoma is the definitive treatment.
Dialysis: In cases of hypercalcaemia associated with renal failure, peritoneal dialysis or haemodialysis may be needed to remove excess calcium.