Pet Care Resources Cholecalciferol (Vitamin D) Poisoning in Dogs and Cats

Emergency Medicine

Cholecalciferol (Vitamin D) Poisoning in Dogs and Cats

Ingestion of rodenticides by companion animals is consistently one of the most common intoxications in veterinary medicine. Historically, second-generation anticoagulants were the most common active ingredient in rodenticides. Though there was the potential for life-threatening hemorrhage within 72 hours of ingestion, an inexpensive antidote (vitamin K1) was available and effective if administered prior to clinical signs.

In 2011, the Environmental Protection Agency (EPA) enacted regulations banning the use of second-generation anticoagulants in residential rodenticides. This regulation has caused rodenticide manufacturers to change active ingredients to first-generation anticoagulants (i.e. warfarin), bromethalin (neurotoxin), or cholecalciferol (vitamin D3). Unfortunately, the first-generation anticoagulants are less effective as rodenticides, which has caused producers to transition to either bromethalin or cholecalciferol, neither of which have safe, accessible and inexpensive antidotes like the anticoagulants. By 2019, all rodenticides manufactured by d-CON®, the most popular brand of rodenticides, will be made with cholecalciferol.

How Cholecalciferol Affects Dogs and Cats

Cholecalciferol increases calcium absorption in the gastrointestinal tract and decreases renal excretion of calcium producing hypercalcemia and hyperphosphatemia. This combination can lead to mineralization of organs, with the kidneys being most susceptible, resulting in renal failure. Cholecalciferol has a very narrow margin of safety, making even small ingestions in dogs and cats potentially fatal. Hypercalcemia has been reported at doses as low as 0.5mg/kg. Most products contain 0.075% cholecalciferol, meaning a 20 kilogram dog would only need to ingest 0.5oz to develop toxicity.

Cholecalciferol is rapidly absorbed following ingestion and has a half-life of approximately 19-25 hours with an elimination half-life of approximately 19 days. This slow elimination combined with enterohepatic recirculation causes markedly prolonged effects with toxicity.

Clinical Signs of Cholecalciferol Toxicity

Clinical signs generally occur within 12-36 hours of exposure, although delays up to 72 hours have been reported. Early clinical signs in dogs and cats include polyuria, polydipsia, anorexia, and weakness. Other signs may include vomiting, diarrhea, hind limb paresis, and hyperthermia. Physical examination may reveal arrhythmias, abdominal pain, or oropharyngeal erosions. As dystrophic mineralization of renal tubules progresses, signs of renal failure may develop.

Treatment of Cholecalciferol Toxicity

Decontamination in the form of induced emesis should be performed if the ingestion occurred within the last four hours. Activated charcoal should be administered to all patients at a dose of 1-4 grams per kilogram. Given enterohepatic recirculation, repeat dosing of charcoal every eight hours during the first day may provide additional benefits. Prior to repeating charcoal dose, serum sodium levels should be evaluated to ensure hypernatremia is not developing. Intravenous lipid emulsion therapy can be considered for substantial overdoses, as this is suspected to have some efficacy, but is not used routinely.

In asymptomatic patients, baseline chemistry profile and ionized calcium should be obtained. If a toxic dose was ingested, admission to the hospital for 48 hours of intravenous fluid therapy and serial monitoring of calcium, phosphorus, and renal values should be performed. If hospitalization is not feasible, renal values and ionized calcium should be evaluated daily for three days.

If a patient presents after development of hypercalcemia or azotemia, hospitalization for fluid diuresis is essential. Fluids should be dosed at 120-180mL/kg/day with 0.9% saline being the fluid of choice. If activated charcoal is also being administered, monitor sodium levels and change to a lower sodium fluid (i.e. Lactated Ringers, Normosol-R) if hypernatremia occurs. Once rehydrated, consider furosemide (2-4mg/kg bolus followed by a continuous rate infusion of 2mg/kg/hour). It is imperative that hydration is monitored closely; if appropriate fluid therapy is not provided, treatment with furosemide can be detrimental. Prednisone (0.5mg/kg PO q12), low calcium diet (e.g. Hill’s w/d), and aluminum hydroxide are also recommended. Hospitalization and fluid therapy should be continued until there is normalization of renal values, generally 2-4 days. Patients with hypercalcemia will need treatment with prednisone and a low calcium diet for approximately four weeks. If hypercalcemia persists, a bisphosphonate (pamidronate, zoledranate) can be considered as adjunctive therapy. More aggressive treatment options include calcitonin, calcium chelation therapy, or hemodialysis.

With the transition to cholecalciferol by d-CON®, most residential rodenticides will now contain either cholecalciferol or bromethalin. Given the difference in treatment and prognosis, veterinary staff will need to be extra vigilant in identifying which product a pet has ingested. Education of pet owners regarding this change will be of vital importance.

By Rachel Halpin, DVM, Diplomate, ACVECC |
October 4, 2018