Skip to Main Content

  • image Severe acute hypercalcemia can result in cardiac arrhythmias, whereas chronic hypercalcemia can lead to calcium deposition in soft tissues including blood vessels and the kidney.
  • image The correction of hypercalcemia can include multiple pharmacotherapeutic modalities such as hydration, diuretics, bisphosphonates, and steroids, depending on the etiology and acuity of the hypercalcemia.
  • image Hypocalcemia is typically associated with an insidious onset; however, some drugs such as cinacalcet are associated with rapid decreases in serum calcium.
  • image Acute treatment of hypocalcemia requires calcium supplementation whereas chronic management may require other therapies such as vitamin D to maintain serum calcium values.
  • image Hyperphosphatemia occurs most frequently in patients with chronic kidney disease (CKD).
  • image Treatment of nonemergent hyperphosphatemia includes the use of phosphate binders to decrease absorption of phosphorus from the GI tract.
  • image Hypophosphatemia is a relatively common complication among critically ill patients.
  • image Treatment of acute hypophosphatemia usually requires IV supplementation of phosphorous salts.

On completion of this chapter, the reader will be able to:

  1. Identify the most prevalent etiologies of both acute and chronic hypercalcemia.

  2. List the signs and symptoms most commonly associated with hypercalcemia.

  3. Develop appropriate treatment plans for hypercalcemia based on acuity and symptoms manifested.

  4. Distinguish benefits versus risks among therapeutic agents used to treat hypercalcemia.

  5. Recommend appropriate treatment for nephrolithiasis associated with hypercalcemia and hypercalciuria.

  6. Identify the most common manifestations of hypocalcemia.

  7. Explain the pathophysiology of hypocalcemia involving vitamin D and parathyroid hormone.

  8. Formulate a treatment plan for a patient with acute hypocalcemia.

  9. List the most common causes of hyperphosphatemia.

  10. Describe symptoms associated with hyperphosphatemia.

  11. Recommend drug therapy based on duration, efficacy, and adverse effects.

  12. Identify the patient populations that are most likely to develop hypophosphatemia.

  13. Describe the mechanisms by which hypophosphatemia leads to the clinical symptoms manifested.

  14. Identify other concomitant electrolyte disorders that may be present in a patient with hypophosphatemia.

  15. Recommend appropriate phosphorus replacement based on clinical data on acuity of hypophosphatemia and profile of other electrolytes.

Disorders of calcium and phosphorus are common complications of multiple acute and chronic diseases. These disorders are frequently seen in the acute care setting; however, they are also often present in ambulatory patients, usually in a less severe state. The consequences of electrolyte disorders can range from asymptomatic to life-threatening, requiring hospitalization and emergent treatment. The maintenance of fluid and electrolyte homeostasis requires adequate functioning and modulation by multiple hormones on tissues of multiple organ systems.

There are many common drug therapies that can disturb the normal homeostatic mechanisms that maintain calcium and phosphorous balance. In addition, with some drug therapies, toxicity is enhanced when underlying electrolyte disorders are present. Drug-induced disorders typically respond well to discontinuation of the offending agent(s); however, additional therapies are sometimes required to correct the disorder. This chapter reviews the etiology, classification, clinical presentation, and therapy for the most common disorders of calcium and phosphorus homeostasis.

The maintenance of physiologic calcium concentrations in the intracellular and extracellular spaces is vital for the ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.