1. Identify and treat cause where possible.

2. Carefully monitor haemodynamic variables, urine output, and ECG morphology with frequent estimations of plasma Ca2 + , PO43-, Mg2 + , Na + and K+.

3. Intravascular volume repletion — this inhibits proximal tubular reabsorption of calcium and often lowers the plasma calcium by 0.4-0.6 mmol/l. It should precede diuretics or any other therapy. Either colloid or 0.9% saline should be used, depending on the presence of hypovolaemia-related features.

4. Calciuresis — after adequate intravascular volume repletion, a forced diuresis with furosemide plus 0.9% saline (6-8 l/day) may be attempted. An effect is usually seen within 12 h. Loop diuretics inhibit calcium reabsorption in the ascending limb of the loop of Henle. More aggressive furosemide regimens can be attempted but can potentially result in complications. Thiazides should not be used as tubular reabsorption may be reduced and hypercalcaemia worsened.

5. Dialysis/haemofiltration — may be indicated at an early stage if the patient is in established oligo-anuric renal failure ± fluid overloaded.

6. Steroids can be effective for hypercalcaemia related to haematological cancers (lymphoma, myeloma), vitamin D overdose and sarcoidosis.

7. Calcitonin has the most rapid onset of action with a nadir often reached within 12-24 h. Its action is usually short-lived and rebound hypercalcaemia may occur. It generally does not drop the plasma level more than 0.5 mmol/l.

8. Biphosphonates (e.g. pamidronate) and IV phosphate should only be given after specialist advice is taken in view of their toxicity and potential complications.


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