A stable elevation of the serum calcium level reflects an equilibrium between net entry of calcium from gut and bone and exit through the kidney. In some patients, the rate of bone resorption overwhelms this balance, and disequilibrium hypercalcemia results. As the serum calcium level begins to rise, distal renal tubular reabsorption of salt and water is impaired. Volume deficiency, often aggravated by vomiting, leads to increased proximal sodium and calcium reabsorption. Most causes of hypercalcemia can be specifically treated, and it is almost always better to use this approach than to consider chronic pharmacologic efforts to lower the serum calcium level.
Several approaches are available for the emergency management of hypercalcemia.
If the patient is not fully alert and able to drink, every fourth or fifth bottle of fluid should be hypotonic to prevent hypernatremia. In patients with marginal left ventricular function, venous pressures should be monitored with a central venous line to prevent overloading of the heart. Care must also be taken to prevent potassium and magnesium depletion. The drug of choice in treating hypercalcemia is pamidronate, and an effective dose is 45 to 60 mg in a single 24-hour infusion that is started as soon as diuresis has been achieved. Once the calcium level is normal, antitumor therapy may be effective in preventing recurrence of hypercalcemia.