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Although this rodenticide was introduced with claims that it was less toxic to nontarget species than to rodents, clinical experience has shown that rodenticides containing cholecalciferol are a significant health threat to dogs and cats. Cholecalciferol produces hypercalcemia, which results in systemic calcification of soft tissue, leading to renal failure, cardiac abnormalities, hypertension, CNS depression, and GI upset.
Signs generally develop within 18–36 hr of ingestion and can include depression, anorexia, polyuria, and polydipsia. As serum calcium concentrations increase, clinical signs become more severe. Serum calcium concentrations >16 mg/dL are not uncommon. GI smooth muscle excitability decreases and is manifest by anorexia, vomiting, and constipation. Hematemesis and hemorrhagic diarrhea may develop as a result of dystrophic calcification of the GI tract and should not lead to a misdiagnosis of anticoagulant rodenticide toxicosis. Loss of renal concentrating ability is a direct result of hypercalcemia. As hypercalcemia persists, mineralization of the kidneys results in progressive renal insufficiency.
Diagnosis is based on history of ingestion, clinical signs, and hypercalcemia (see The Parathyroid Glands and Disorders of Calcium Metabolism: Hypercalcemia in Dogs and Cats). Other causes of hypercalcemia, such as hyperparathyroidism, normal juvenile hypercalcemia, paraneoplastic hypercalcemia, hemoconcentration (hyperproteinemia), and diffuse osteoporosis should be ruled out. Gross lesions associated with hypercalcemia include pitted, mottled kidneys; diffuse hemorrhage of the GI mucosa; and roughened, raised plaques on the great vessels and on the surface of the lungs and abdominal viscera.
Recommended therapy includes gastric evacuation, generally followed by administration of activated charcoal at 2–8 g/kg in a water slurry. Calciuresis is accomplished with 0.9% sodium chloride solution and administration of furosemide (initial bolus of 5 mg/kg, IV, followed by a constant rate IV infusion of 5 mg/kg/hr) and corticosteroids (prednisolone, 1–2 mg/kg, bid). Furosemide and prednisolone should be continued for 2–4 wk, and the serum calcium concentration monitored at 24 hr, 48 hr, and 2 wk after cessation of treatment. Additionally, calcitonin may be used at 4–6 IU/kg, SC, every 2–3 hr, until the serum calcium stabilizes at <12 mg/dL. The IV use of calcium chelators such as Na-EDTA has been used in severe cases, but this use is experimental and requires close monitoring of blood calcium to prevent hypocalcemia. The dose of prednisolone should be tapered if it is administered for >2 wk to prevent acute adrenocortical insufficiency. Continuous peritoneal dialysis may be considered if the animal is in renal failure. A low-calcium diet should be provided in all cases of significant exposure to cholecalciferol rodenticides.
Recently, pamidronate disodium, a specific inhibitor of bone resorption used for the treatment of hypercalcemia of malignancy and Paget's disease in humans, has shown promise in the treatment of cholecalciferol toxicosis in dogs. It is given slowly IV at 1.3–2.0 mg/kg in saline solution over 2–4 hr. Two infusions are given 4 days apart. Pamid-ronate disodium has a long-lasting inhibitory action on bone resorption, thus requiring only limited infusions. Total serum calcium and BUN should be monitored 2 and 4 days after the last infusion.
Last full review/revision March 2012 by Frederick W. Oehme, DVM, PhD
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