Hypercalcemia in the Emergency SettingJune 21, 2019

Hypercalcemia in the Emergency Setting

Written by Jennie Gavin, DVM

This article will summarize the most common causes of hypercalcemia as seen in the ER. We will briefly touch on the physiology of calcium and then discuss clinical signs, differentials, diagnostics and treatment.

The Physiology of Calcium

Calcium is stored in the body in the serum and the bone.  In the serum, there is free “active” calcium that makes up approximately 60% of total and protein bound calcium that makes up approximately 40%. Free calcium is measured as ionized or iCa.  Total calcium as read by most chemistry panels is a combination of free and protein bound calcium.

Calcium regulation is complicated and involves interaction of the parathyroid gland, the thyroid gland, the gut and the kidneys.  Sources of calcium include increased GI absorption and release from bone. Excretion is via the kidneys. The main hormones involved in regulation include PTH, calcitriol and calcitonin.

PTH has action including absorption of calcium from the intestines, stimulation of calcium release from bones, decreasing excretion from the kidneys and stimuling calcitriol. Calcitriol is the precursor of Vitamin D which increased GI absorption of calcium.  Calcitonin is released from the thyroid gland following a meal.  It is short lived.

Clinical Signs of Hypercalcemia

Clinical signs of hypercalcemia include PU/PD (due to decreasing ADH sensitivity causing a relative diabetes insipidus state), dehydration, weakness, vomiting, tremors and arrhythmias.  We sometimes have seen urinary tract symptoms as the first sign of hypercalcemia due to the formation of calcium oxalate stones.

Causes of hypercalemia in dogs include:

  1. Neoplasia (lymphoma, anal sac adenocarcinoma, multiple myeloma)
  2. Addisons disease
  3. Primary hyperparathyroidism
  4. Chronic renal disease
  5. Vitamin D toxicosis

Vitamin D toxicity is a problem that we have been seeing with increasing frequency.  This can occur due to exposure to rodenticides (as little as 0.5mg/kg of the current product), high potency Vitamin D supplements, prescription topical products (acute exposure or chronic licking) and inappropriately balanced dog foods as we have recently seen.  Clinical signs of Vit D toxicity usually occur within 12 hours but can be up to 72 hours.  Patients are noted to be anorexic and lethargic and then will progress to PU/PD, vomiting and tremors.  Decontamination is recommended if ingestion is greater than 0.1mg/kg.  Vomiting can be induced if within 4-6 hours, then toxiban should be administered every 8 hours for 48 hours.

If the patient is not hypercalcemic at time of presentation, the patient should be treated with IV fluids and renal values should be monitored every 24 hours for 3-4 days.  If the patient is hypercalcemic, renal values should be continued to be monitored every 24 hours for 7 days after azotemia is resolved, then 3x/week for 2 weeks then 1x/week for another two weeks.

ASPCA poison control is an excellent resource in these cases.

Causes of hypercalcemia in cats include:

  1.  Idiopathic
  2. Chronic renal disease
  3. Neoplasia (lymphoma, SCC)
  4. Primary hyperparathyroidism

Your diagnostic work-up will include baseline bloodwork, imaging and sending out hormone levels. It is very important to remember that the calcium can be falsely elevated in cases of lipemia, hemoconcentration and hemolysis.

The following are diagnostic findings you may encounter:

  1. Chem profile: Azotemia (can be a cause or a result of hyperalcemia), elevated phosphate (found with renal disease, addisons or Vitamin D toxicity), electrolyte abnormalities consistent with Addisons disease or elevated globulins in the case of multiple myeloma
  2. PTH: This hormone should be low in the face of hypercalcemia. It will be normal to elevated with primary hyperparathyroidism or kidney disease.
  3. PTHrp: This is a PTH analogue that is produced by cancer cells. The absence of this finding does not rule out neoplasia.
  4. Vitamin D level: Can be used to confirm Vit D toxicosis
  5. Radiographs / CT / Ultrasound: Used to search for neoplasia or parathyroid tumor
  6. ACTH stim to rule out Addisons disease


Treatment is aimed at primarily decreasing the active calcium in the serum and treating the primary cause once determined.

  • Fluid therapy is the most important first line of treatment.  Dehydration will increase calcium due to decreasing GFR and worsen the clinical signs of hypercalcemia.  IV saline is the classic fluid of choice.  The fluids should be aimed at correcting the level of dehydration over 24 hours in addition to maintenance and covering losses.  Remember that losses are higher than expected because of insensitivity to ADH.
  • Furosemisde is commonly used in the ER setting once a patient has been adequately hydrated. This will help decrease the renal absorption of calcium.  The dosing starts at 2mg/kg IV or IM q 8-12 hours.
  • Glucocorticoids help to reduce serum calcium in several ways including reducing absorption from bone, decreasing GI absorption and increasing renal excretion.  Steroids are usually starting if IV fluids and diuretics are not enough.  **Diagnostics should always be started prior to starting steroids**.
  • Biphosphonates such as pamidronate can be given as an IV infusion every 3-4 weeks.  This drug works by inhibiting osteoclast function and reducing calcium absorption from bone.  There is nephrotoxic potential to these medications – care should be taken to ensure that the patient is not dehydrated prior to use.

As always, the doctors at CDVRH are more than willing to consult regarding a specific case or potential transfer.  Do not hesitate to call us when you feel you would benefit from a consultation!

About the author

Jennie Gavin, DVM

Gavin_JDr. Gavin grew up in neighboring Glenville, NY. She attended Tufts University College of Veterinary Medicine. She then completed an internship in emergency and critical care medicine at the New England Animal Medical Center in West Bridgewater, MA. During her internship, she also rotated through the surgical and internal medicine departments. After practicing as an emergency veterinarian in Massachusetts, she moved back to her home town in 2007 and joined our team.

Jennie’s special areas of interest include the critical care aspect of veterinary medicine, feline medicine, ultrasound, exotics and wildlife. Dr. Gavin is continuously impressed by the strength of the human-animal bond.

She lives with her husband, daughter, and many pets. Dr. Gavin freely admits to being a “crazy cat lady” and also loves beagles!

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