Hypercalcemia intravenous phosphate

Giving intravenous phosphate is probably the fastest and surest way to reduce serum calcium, but it is a hazardous procedure if not done properly. Intravenous phosphate should be used only after other methods of treatment (bisphosphonates, calcitonin, and saline diuresis) have failed to control symptomatic hypercalcemia. Phosphate must be given slowly (50 mmol or 1.5 g elemental phosphorus over 6-8 hours) and the patient switched to oral phosphate (1-2 g/d elemental phosphorus, as one of the salts indicated below) as soon as symptoms of hypercalcemia have cleared. The risks of intravenous phosphate therapy include sudden hypocalcemia, ectopic calcification, acute renal failure, and... 

Not surprisingly, subsequent reports established the danger of utilizing exogenous phosphate to treat hypercalcemia. A 46-year-old woman with multiple myeloma and a calcium of 17.8 mg/ dl was treated with oral and intravenous phosphate and developed acute kidney injury with abrupt cessation of calciuria [40]. A 40-year-old male with squamous cell carcinoma... 

Shackney S, Hasson J. Preciptious Fall In Serum Calcium, Hypotension, and Acute Renal Failure After Intravenous Phosphate Therapy for Hypercalcemia. Ann of Intern Med 1967 5 906-16. 

Finally, intravenous phosphate may rapidly reduce ionized calcium concentrations through the formation of insoluble calcium-phosphate salts. However, intravenous phosphate is extremely hazardous because extraskeletal precipitation of calcium-phosphate may result in metastatic calcification, hypotension, acute renal failure, or death. Therefore intravenous phosphates should be reserved for the extraordinary patient with severe hypercalcemia and concomitant hypophosphatemia. Oral phosphorus is not used chronically for the treatment of hypercalcemia because calcium-phosphate crystals may precipitate in the kidneys or other major organs when the calcium-phosphorus product is > 50 to 60 mg /dL . Serum calcium, phosphorus, and creatinine should be monitored closely. Oral phosphorus treatment is only indicated when there is concomitant hypophosphatemia (<2 mg/dL). 

Oral sodium phosphate lowers plasma Ca concentrations and may offer short-term calcemic control of some patients with primary hyperparathyroidism who are awaiting surgery. However, the risk of precipitating calcium phosphate salts in soft tissues throughout the body is of concern. In light of satisfactory responses to other agents, administration of intravenous sodium phosphate is not recommended as a treatment for hypercalcemia. 

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