Hypercalcemia: Acute treatment


Symptoms: mild to moderate hypercalcemia (11 to 14 mg/100 mL) often has no symptoms, but when levels > 15 mg/100 mL, clinical changes become more common

Hypercalcemia produces changes primarily in the central nervous system (e.g., mental status changes), the gastrointestinal tract (e.g., vomiting), the kidneys (e.g., polyuria, renal calculi, oliguric renal failure), and the heart (e.g., shortened P–R or Q–T interval, possible QRS widening).

Today, hypercalcemia is most commonly diagnosed in asymptomatic patients, whereas clinical features previously were the earliest manifestations.

Etiologies: thiazide diuretic therapy, malignancy (now known as humoral hypercalcemia of malignancy), granulomatous disease (related to increased intestinal absorption of calcium induced by elevated calcitriol levels), vitamin D intoxication, or parathyroid hormone adenoma. Additional causes of hypercalcemia include lithium therapy, thyrotoxicosis, pheochromocytoma, immobilization, vitamin A intoxication, renal failure, and theophylline therapy.

Treatment: diuresis and administration of normal saline to dilute plasma calcium. These primary treatments also are useful because sodium inhibits the renal reabsorption of calcium.

Additional therapies include 1)bisphosphonates (pamidronate is the most commonly used) 2)calcitonin 3)ambulation 4)hemodialysis 5)treatment of the underlying condition.

Certain conditions, including numerous cancer-related hypercalcemias, can be treated with calcium-lowering agents, such as mithramycin and glucocorticoids.

Anesthetic management: avoidance of thiazide diuretics and maintenance of hydration and urine output with sodium-containing fluids. Monitoring the patient by means of electrocardiograms is useful to detect cardiac conduction abnormalities with shortened P–R or Q–T interval, with or without widening of the QRS complex. Patients who have muscle weakness should receive decreased doses of nondepolarizing muscle relaxants.


  • Symptoms (> 15 mg/dL): CNS, heart, GI tract, kidneys
  • Etiologies: thiazides, malignancy, granulomatous disease, parathyroidoma, vitamin D, lithium
  • Treatment: diuresis + normal saline
  • Anesthesia: avoid thiazides; hydrate; potentially decrease NMBDs; vigilance re: EKG


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See Also:

ABA:Hyperparathyroidism – signs