What is Cholecalciferol poisoning?
Due to EPA regulations that restrict anticoagulant rodenticides, cholecalciferol (vitamin D3) has become increasingly more common as a residential rodenticide. This type of rodenticide is commonly found in soft baits and pellets. Rarely, hard blocks can be found through online sources, agricultural stores, and pest control services. While cholecalciferol may seem like a safer option than anticoagulants, there is no antidote available and the amount in a single block is a severe overdose in nearly all animals.
Vitamin D3 (cholecalciferol) is an essential vitamin that helps regulate calcium and phosphorus within the body. It is typically synthesized by the body when exposed to the sun but is also found naturally in food. High doses of vitamin D3 will result in overactive absorption of calcium and phosphorus from the bones and gastrointestinal (GI) tract and will decrease excretion via kidneys. This causes severe hypercalcemia (elevated calcium levels in blood) and hyperphosphatemia (elevated phosphorus levels in blood).
If left untreated, this condition will lead to mineralization in soft tissues of the kidneys, heart/vasculature, lungs, and stomach. Kidney failure is the most common outcome of untreated cholecalciferol poisoning, but other consequences can include GI ulceration, cardiac arrhythmias, and respiratory distress. Cholecalciferol and its metabolite, calcifediol, persist in the body for weeks, resulting in prolonged treatment needs.
What are the clinical signs of cholecalciferol poisoning?
Serious signs of cholecalciferol poisoning may not be present for several days. Within the first 24 hours, anorexia, vomiting, lethargy, increased thirst, and increased urination occur. As hypercalcemia/hyperphosphatemia develops, these clinical signs persist or worsen, and the patient may develop melena (dark stool due to digested blood) or bloody vomiting.
Hypercalcemia and hyperphosphatemia are seen on bloodwork within 24-72 hours. If hypercalcemia is not controlled, subsequent mineralization will start between 3 and 7 days after exposure. Clinical signs depend on the site of mineralization. The most common site is the kidneys, resulting in elevated kidney values, continued anorexia, vomiting, diarrhea, increased or decreased urine production, and lethargy. More rarely, mineralization in the heart and lungs can result in cardiac arrhythmias and pulmonary hemorrhage, respectively.
How is cholecalciferol poisoning treated?
If a pet has ingested cholecalciferol, immediate decontamination is important to reduce the amount absorbed. Vomiting should be induced as quickly as possible with your veterinarian or under the direction of a veterinarian. Further decontamination includes medical-grade activated charcoal and a drug called cholestyramine, which is a bile acid binding agent. As cholecalciferol is metabolized in the liver, some will be returned to the digestive tract via the bile, prior to being reabsorbed again. Cholestyramine binds to these toxin-bound bile acids and prevents reabsorption.
After decontamination, the next goal is to reduce calcium availability. A low-calcium diet can help decrease the amount of calcium available for absorption from the gut. Steroids can increase excretion of excess calcium via the kidneys and decrease intestinal calcium absorption. If GI signs develop, they are treated symptomatically with antiemetics and antacids.
Serum calcium, phosphorus, and kidney values are monitored daily. Toxicity is not expected if calcium levels remain normal by day 3-4.
Once hypercalcemia develops, the patient is started on intravenous fluids, using saline therapy to promote excretion of calcium and maintain hydration. If the patient is still eating, phosphorous-binding agents can be used to help control hyperphosphatemia. With severe hypercalcemia, a diuretic may be started to help with calcium excretion. The most effective treatment, however, is bisphosphonate drugs. Bisphosphonates (i.e., pamidronate, zolendronate) are given to block calcium resorption from bone. This class of drugs will lower serum calcium levels within 24-48 hours of administration. Repeat dosing is sometimes required as the calcium levels rebound due to continued presence/metabolization of cholecalciferol.
Continue fluid therapy and symptomatic care if kidney damage or other soft tissue mineralization develops. Working closely with your pet’s veterinarian is imperative to successful therapy for cholecalciferol poisoning.
What is the prognosis for cholecalciferol poisoning?
Prognosis is good if treatment is started before the onset of hypercalcemia, but fair to guarded if hypercalcemia is already present. If treatment is started after kidney failure has developed, prognosis is guarded to poor. Mineralization can reabsorb over time but may have caused irreversible damage. Bloody vomiting, cardiac arrhythmias, and lung mineralization are indicators that point to a poor prognosis.
If you suspect or witnessed your pet ingesting cholecalciferol rodenticide, please call Pet Poison Helpline, a 24/7 animal poison control center, at 1-855-764-7661 and take your pet to a veterinarian for treatment.
Pet Poison Helpline, an animal poison control center based out of Minneapolis, MN, is available 24/7 for pet owners and veterinary professionals that require assistance treating a potentially poisoned pet. The staff provides treatment advice for poisoning cases of all species, including dogs, cats, birds, small mammals, large animals, and exotic species. As the most cost-effective option for animal poison control care, Pet Poison Helpline’s per incident fee includes follow-up consultations for the duration of the poison case. Pet Poison Helpline is available in North America by calling 800-213-6680. Additional information can be found online at www.petpoisonhelpline.com.
