Cholecalciferol rodenticide toxicity & how to treat it
Dr. Justine Lee, DVM, DACVECC, DABT

Cholecalciferol, the chemical name for vitamin D3, is one of the most deadly– and costly – rodenticides to pets. Ingestion of toxic levels of cholecalciferol can result in severe hypercalcemia and hyperphosphatemia, with secondary acute kidney injury (AKI) developing as a result of dystrophic mineralization to the soft tissue and kidneys. Common sources of Vitamin D3 include over-the-counter (OTC) or prescription vitamins (typically found in a calcium/Vitamin D3 combination), psoriasis creams (in the form of calcipotriene), and rodenticides. With cholecalciferol-containing rodenticides, only a tiny amount of rodenticide needs to be ingested before clinical toxicosis occurs due to a very narrow margin of safety within these products. In dogs, cholecalciferol has an LD50 of 85 mg/kg (based on the rodenticide concentration of 0.075%).1 Doses of Vitamin D3 > 0.1-0.5 mg/kg can result in clinical signs and hypercalcemia, respectively.1

Typically, clinical signs often do not develop for 1-3 days until the patient has already developed clinical signs of AKI.1 That said, renal failure can occur within 12-36 hours following toxic ingestion. Clinical signs and clinicopathologic findings include:

  • PU/PD
  • Weakness
  • Lethargy
  • Anorexia
  • Vomiting
  • Generalized malaise
  • Uremic halitosis
  • Dehydration
  • Hypercalcemia
  • Hyperphosphatemia
  • Azotemia
  • Melena
  • Hemorrhagic diarrhea
  • Death

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Aggressive treatment must be initiated with cholecalciferol toxicosis, due to the narrow margin of safety. Decontamination should include emesis induction, if ingestion was recent and the patient is asymptomatic. As cholecalciferol undergoes enterohepatic recirculation, the administration of multiple doses of activated charcoal (without a cathartic) is warranted q 6 hours X 24 hours.

Additional treatment includes the aggressive use of:

  • IV fluid therapy to promote calciuresis (e.g., 0.9% NaCl)
  • Calcium monitoring
  • Gastrointestinal support (e.g., anti-emetics, H2 blockers, sucralfate, phosphate binders, etc.)
  • The use of medications to increase calciuresis (e.g., prednisone, furosemide) and prevent hypercalcemia (e.g., pamidronate, calcitonin).

Treatment is often expensive, and requires hospitalization for an extended period of time. Most patients are continued on oral furosemide and prednisone for weeks, following discharge from the hospital. Frequent monitoring of renal function and electrolytes is imperative. Calcium, phosphorous, BUN, creatinine, and ionized calcium should be evaluated every 12-24 hours while hospitalized, and then every 2-3 days thereafter for the next 2-4 weeks. This will allow one to assess the ability to titrate the prednisone and furosemide therapy, and to ensure that the patient does not develop secondary ARF [or potentially chronic renal failure (CRF)]. Even with aggressive treatment, CRF may be a secondary sequela. The prognosis for this rodenticide is poor due to the risk of CRF once clinical signs and azotemia develop.

When in doubt, this is a toxicity that you want to consult with ASPCA Animal Poison Control Center for, as you’ll be calling frequently! Alternatively, note that the majority of EPA-products (e.g., rodenticides, pesticides, ant traps, etc.) have a free 800-medical line that is available 24/7 for free advice!

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  1. Do you have any evidence of secondary poisoning with cholecalciferol where a pet ate a rat or mouse that consumed bait?

    • This is called “relay toxicity” and is generally considered very rare in domesticated pet dogs and cats – more common with birds of prey, wildlife, etc. However, it’s not reported as commonly as second generation anticoagulant rodenticides (ACRS).

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