February 23, 2011 by dailybolusoflr
The two most common etiologies of hypercalcemia in patients seen in the ED are:
· Primary hyperparathyroidism
· 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)
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