Investigation and Management of Hypercalcaemia in Children
Investigation and Management of Hypercalcaemia in Children
The management objectives are to establish the underlying cause and to lower the plasma calcium concentration to prevent end organ damage.
Calcium intake should be reduced by minimising calcium concentration in enteral and parenteral feeds and discontinuation of oral calcium supplements and drugs known to cause hypercalcaemia. Weight bearing activity should be increased and, when relevant, withdrawal of sedatives to promote mobility.
Hyperhydration With Intravenous 0.9% Saline and Loop Diuretics The majority of children with symptomatic hypercalcaemia are dehydrated at presentation from reduced fluid intake and the diuretic effect of hypercalcaemia (secondary to hypercalcaemia-induced nephrogenic diabetes insipidus). Inhibiting sodium reabsorption at the proximal convoluted tubule and the loop of Henle will increase urinary calcium excretion. Hyperhydration with 0.9% saline alone is often an effective treatment for hypercalcaemia. A loop diuretic, for example frusemide, may be added to further promote natriuresis and therefore hypercalciuria, but if used long term may increase predisposition to nephrocalcinosis.
Bisphosphonates Bisphosphonates reduce plasma calcium levels by inhibiting osteoclastic bone resorption. Pamidronate (0.5–1.0 mg/kg infusion over 4–6 h) is the drug of choice in children and a reduction in calcium is observed 12–24 h after administration and may last for 2–4 weeks. Ibandronate and clodronate are licensed for use of treatment of hypercalcaemia of malignancy in adults. There may be a sustained period of hypocalcaemia following the initial pamidronate infusion, which may require calcium supplementation.
The use of bisphosphonates in renal failure is a potential concern but must be balanced against the potential for improving renal function by treatment of hypercalcaemia per se. A reduced dose of pamidronate should be given in the presence of renal failure.
Cinacalcet Cinacalcet is a calcimimetic and reduces PTH levels by allosteric activation of the CaSR. In adult practice cinacalcet is used for the treatment of primary hyperparathyroidism and may delay the need for surgical intervention. Its use in children is evolving but it has been used in selected cases for primary hyperparathyroidism, neonatal hyperparathyroidism and in dialysis patients with secondary hyperparathyroidism.
Glucocorticoids Glucocorticoids, usually prednisolone, have been used for conditions when there is extra-renal synthesis of 1,25-dihydroxyvitamin D3, such as granulomatous conditions, tuberculosis, sarcoid and subcutaneous fat necrosis. Glucocorticoids act by inhibiting synthesis of 1,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D.
Parathyroidectomy Parathyroidectomy is required for primary hyperparathyroidism and must be undertaken by an experienced surgeon. The timing of the procedure depends on the degree of hypercalcaemia, evidence of end-organ damage from hypercalcaemia and the underlying cause. Parathyroidectomy for NSHPT is undertaken in the first few weeks of life as long-term medical treatment is ineffective and the skeletal complications of NSHPT are life threatening.
Following parathyroidectomy, replacement with maintenance calcium and vitamin D should be commenced. Immediately following surgery, hypocalcaemia secondary to a 'hungry bone' syndrome may develop despite maintenance treatment. Serial calcium measurements should therefore be taken following surgery and additional calcium supplementation given if appropriate. If severe hypocalcaemia develops, intravenous calcium may be required.
Haemodialysis This intervention is reserved for life-threatening hypercalcaemia resistant to medical therapy. Haemodialysis with a dialysate with a low calcium concentration is used.
Management of Hypercalcaemia
The management objectives are to establish the underlying cause and to lower the plasma calcium concentration to prevent end organ damage.
General Measures
Calcium intake should be reduced by minimising calcium concentration in enteral and parenteral feeds and discontinuation of oral calcium supplements and drugs known to cause hypercalcaemia. Weight bearing activity should be increased and, when relevant, withdrawal of sedatives to promote mobility.
Specific Measures
Hyperhydration With Intravenous 0.9% Saline and Loop Diuretics The majority of children with symptomatic hypercalcaemia are dehydrated at presentation from reduced fluid intake and the diuretic effect of hypercalcaemia (secondary to hypercalcaemia-induced nephrogenic diabetes insipidus). Inhibiting sodium reabsorption at the proximal convoluted tubule and the loop of Henle will increase urinary calcium excretion. Hyperhydration with 0.9% saline alone is often an effective treatment for hypercalcaemia. A loop diuretic, for example frusemide, may be added to further promote natriuresis and therefore hypercalciuria, but if used long term may increase predisposition to nephrocalcinosis.
Bisphosphonates Bisphosphonates reduce plasma calcium levels by inhibiting osteoclastic bone resorption. Pamidronate (0.5–1.0 mg/kg infusion over 4–6 h) is the drug of choice in children and a reduction in calcium is observed 12–24 h after administration and may last for 2–4 weeks. Ibandronate and clodronate are licensed for use of treatment of hypercalcaemia of malignancy in adults. There may be a sustained period of hypocalcaemia following the initial pamidronate infusion, which may require calcium supplementation.
The use of bisphosphonates in renal failure is a potential concern but must be balanced against the potential for improving renal function by treatment of hypercalcaemia per se. A reduced dose of pamidronate should be given in the presence of renal failure.
Cinacalcet Cinacalcet is a calcimimetic and reduces PTH levels by allosteric activation of the CaSR. In adult practice cinacalcet is used for the treatment of primary hyperparathyroidism and may delay the need for surgical intervention. Its use in children is evolving but it has been used in selected cases for primary hyperparathyroidism, neonatal hyperparathyroidism and in dialysis patients with secondary hyperparathyroidism.
Glucocorticoids Glucocorticoids, usually prednisolone, have been used for conditions when there is extra-renal synthesis of 1,25-dihydroxyvitamin D3, such as granulomatous conditions, tuberculosis, sarcoid and subcutaneous fat necrosis. Glucocorticoids act by inhibiting synthesis of 1,25-dihydroxyvitamin D3 from 25-hydroxyvitamin D.
Parathyroidectomy Parathyroidectomy is required for primary hyperparathyroidism and must be undertaken by an experienced surgeon. The timing of the procedure depends on the degree of hypercalcaemia, evidence of end-organ damage from hypercalcaemia and the underlying cause. Parathyroidectomy for NSHPT is undertaken in the first few weeks of life as long-term medical treatment is ineffective and the skeletal complications of NSHPT are life threatening.
Following parathyroidectomy, replacement with maintenance calcium and vitamin D should be commenced. Immediately following surgery, hypocalcaemia secondary to a 'hungry bone' syndrome may develop despite maintenance treatment. Serial calcium measurements should therefore be taken following surgery and additional calcium supplementation given if appropriate. If severe hypocalcaemia develops, intravenous calcium may be required.
Haemodialysis This intervention is reserved for life-threatening hypercalcaemia resistant to medical therapy. Haemodialysis with a dialysate with a low calcium concentration is used.
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