Peer-reviewed veterinary case report
Cholecalciferol poisoning in dogs and cats from rodenticide baits
By Peterson, Michael E & Fluegeman, Kerstin·Published in Topics in companion animal medicine·2013·Reid Veterinary Hospital, United States·View original on PubMed →
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Original publication title: Cholecalciferol.
- Species:
- dog
Plain-English summary
A dog was brought to the vet after eating rat poison that contained vitamin D3, which can cause serious health issues. The dog showed signs like weakness, vomiting, and increased thirst. The vet confirmed high calcium levels in the blood and started treatment by making the dog vomit and giving activated charcoal to prevent further absorption of the toxin. They also provided intravenous fluids and medications to lower calcium levels. Fortunately, the dog responded well to the treatment, especially since it was started early before any lasting damage occurred.
People also search for: dog rat poison symptoms · vitamin D3 poisoning in dogs · treatment for high calcium in dogs
Abstract
The primary source of exposure to cholecalciferol in dogs and cats is ingestion of rodenticide baits with vitamin D3 as the active ingredient. Other sources of this toxin are human medications and rarely, contaminated pet food. Although the reported lethal dose 50% for cholecalciferol is 88 mg/kg, deaths have been seen with an individual exposure of 2 mc g/kg in dogs. Clinical signs are induced by profound hypercalcemia affecting multiple body systems. Clinical presentations may include anorexia, depression, muscle weakness, vomiting, polyuria, polydipsia, dehydration, abdominal pain, hematemesis, melena, and bradycardia. Tissue mineralization may develop if calcium × phosphorous product is greater than 60. Serum testing for hypercalcemia, hyperphosphatemia, and decreased serum parathyroid hormone are confirmatory. Initial treatment relies upon decontamination with emesis induction followed by administration of pulse-dose activated charcoal designed to interfere with the extensive enterohepatic recirculation of toxin. Medical management is designed to decrease serum calcium levels by use of intravenous fluid diuresis with administration of furosemide and prednisolone. Biphosphate pamidronate is used to inhibit calcium release from the bone. Phosphate binders aid in decreasing phosphate availability to interact with calcium. The prognosis is better if treatment is instituted early before development of hypercalcemia and hyperphosphatemia enables tissue mineralization to progress.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/23796485/