Daily Bolus of LR: Hypercalcemia

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February 23, 2011 by dailybolusoflr

Hypercalcemia

 

The two most common etiologies of hypercalcemia in patients seen in the ED are:

·         Malignancy

·         Primary hyperparathyroidism

 

Facts:

·         Calcium is absorbed by the small intestine, is excreted by the kidney.

 

·         Hypercalcemia typically results from an excess of PTH or a mimicker of this hormone or an overload of calcium (destruction of bone)

 

·         About 40% of calcium is bound to protein (mainly albumin) and about 50% is in the active ionized form.

o   Corrected total calcium (mg/dL) = (measured total calcium mg/dL) + 0.8 (4.4 – measured albumin g/dL)

 

·         Symptoms:

o   Bones (muscle, join aches)

o   Stones (kidney stones)

o   Moans (constitutional sx: lethargy, weakness, headache)

o   Abdominal Groans (abd pain, n/v, constipation)

o   Psychic Overtones (depression, confusion)

 

·         EKG: most common abnormality found is a shortened QT interval

 

·         Treatment: (Note: these are the most commonly used modalities and not an inclusive list)

o   Initial step is to ensure adequate hydration with normal saline.  This will help to decrease the calcium level due to dilation as well as to help enhance urinary excretion.

§  In patients with renal failure, dialysis may be necessary.

o   A loop diuretic may be used to increase calcium excretion.

o   Bisphosphonate: bind to bone matrix and interfere with osteoclastic activity.  Longer acting but more delayed onset of action than calcitonin.

o   Calcitonin: naturally occurring hormone that inhibits bone resorption as well as increases excretion of calcium.  Shorter acting but more rapid onset of action than the bisphosphonates.

o   Steroids: inhibit vitamin D activity. Slow onset, often used in lymphoma/myeloma related hypercalcemia.

 

 

Hematol Oncol Clin N Am 24 (2010) 553–565

 

 

Linda Regan, MD FACEP

Program Director, Emergency Medicine Residency

Johns Hopkins Medical Institutions

 

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