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Mild asymptomatic hypercalcemia requires no specific treatment. The definitive treatment of moderate or severe hypercalcemia depends on the specific diagnosis, but the initial treatment and resuscitation is the same in all cases. Patients with potentially life-threatening manifestations (altered conscious level, bradycardia, short QT interval on electrocardiogram) should be treated immediately as there is a risk of coma and death in these patients.

The mainstay of treatment is rehydration, which should be commenced with 0.9 per cent saline solution intravenously. Intravenous therapy will correct the inevitable dehydration, and the added sodium load reduces calcium reabsorption in the proximal renal tubule. Once the patient is adequately hydrated, forced saline diuresis is initiated, supplemented with intravenous furosemide (frusemide) as required. Furosemide inhibits calcium reabsorption in the distal renal tubules. The aim of therapy is to induce a diuresis of approximately 5 liters over each 24-h period. This therapy must be individualized, and, in patients with cardiovascular or renal failure, fluid management should be guided by invasive monitoring such as a central venous or pulmonary artery flotation catheter. In renal failure, hemodialysis using a low-calcium dialysate is an effective alternative to forced diuresis. In all cases, it is important to monitor serum calcium, electrolyte, magnesium, and phosphate concentrations carefully and to correct any abnormalities. Hypophosphatemia exacerbates hypercalcemia and should be addressed promptly. Other monitoring should include continuous electrocardiography, blood pressure, and neurological observations.

Glucocorticosteroids are useful in hypercalcemia attributable to excess calcium absorption from the gastrointestinal tract, since they antagonize vitamin D. They may be effective in myeloma-associated cytokine release and lymphoma, but high doses may be required (prednisolone 60-100 mg/day). High-dose corticosteroid therapy may be safely stopped abruptly at the end of a course of up to 1 week, but if longer courses are given it is necessary to taper the dose before discontinuation. In the presence of high-dose corticosteroid, it may be necessary to increase the dose of furosemide administered, as salt and water retention is a common effect of high-dose corticosteroids.

Calcitonin inhibits osteoclast function and is effective within 2 h of subcutaneous injection (4 IU/kg every 12 h); a reduction in serum total calcium concentration of 2 mg/dl is typical, although tachyphylaxis develops within days. Calcitonin should be commenced early, and is safe during the rehydration phase of treatment. Calcitonin is not contraindicated in renal failure. Side-effects are benign; flushing, transient nausea, and local hypersensitivity at the injection site may be seen. Calcitonin is ineffective in approximately 25 per cent of patients.

Several other drugs are available which prevent osteoclast resorption of bone and will reduce serum calcium over the short term. They each have a delayed action; serum calcium concentration falls after 2 to 3 days of therapy. These agents include biphosphonates (diphosphonates), plicamycin (mithramycin), and gallium nitrate. Use of these drugs is secondary to rehydration, and they are best prescribed by a physician experienced in their use since some of the agents (particularly plicamycin and gallium nitrate) may induce nephrotoxicity.

Phosphates were previously given routinely to control hypercalcemia, and intravenous preparations may still be given in life-threatening hypercalcemia. Phosphates are not indicated if hyperphosphatemia coexists with hypercalcemia.

Verapamil, a calcium-channel blocker, has been used successfully to control severe cardiovascular manifestations of hypercalcemia (arrhythmia and hypertension) before measures to control serum calcium concentration have taken effect.

Whichever medical therapy is used, the effect is transient. Definitive correction of the underlying pathology should be undertaken once the patient's condition is stabilized.

Whichever medical therapy is used, the effect is transient. Definitive correction of the underlying pathology should be undertaken once the patient's condition is stabilized.


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Chapter References

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