Vitamin D poisoning (cholecalciferol)

Buy now to access the full article, existing subscribers login

Sections available in full article Introduction, Presenting signs, Geographic incidence, Pathogenesis, Pathophysiology, Timecourse (incubation, duration), Diagnosis, Client history, Clinical signs, Diagnostic investigation, Confirmation of diagnosis, Gross autopsy findings, Histopathology findings, Differential diagnosis, Treatment, Initial symptomatic treatment, Standard treatment, Monitoring, Subsequent management, Sequelae, Prognosis, Expected response to treatment, Reasons for treatment failure, Sources, Publications, Vetstream contributor(s),
Contributors Dr Rosalind Dalefield BVSc PhD DipABVT DipABT
Synonyms Cholecalciferol poisoning, calciferol poisoning, calcipotriol poisoning

Introduction

  • Cause : poisoning with vitamin D3 rodenticide or ingestion of poisoned wildlife. Ingestion of human medications containing vitamin D, which are prescribed for a variety of conditions including hypoparathyroidism, osteomalacia, osteoporosis, renal failure, psoriasis, and to prevent recurrence of cancer.
  • Signs : anorexia, vomiting, polydipsia, polyuria, fetid diarrhea.
  • Diagnosis : signs, hypercalcemia.
  • Treatment : detoxification, calcitonin, pamidronate, fluid diuresis, corticosteroids.
  • Prognosis : guarded to poor.

Diagnosis

Clinical signs

  • As listed previously.

Diagnosis

Differential diagnosis

  • Other causes of hypercalcemia (including lymphoma, hyperparathyroidism, acute or chronic renal failure, pheochromocytoma, hypoadrenocorticoidism).
  • Other causes of polydipsia.

Sequelae

Prognosis

  • Guarded to poor. Prognosis is good if treatment is initiated prior to onset of hypercalcemia and calcification of soft tissues, but animals are usually presented too late in the course of toxicosis.
  • Prognosis is grave if hematemesis is present.
  • Animals often deteriorate rapidly and may be dead within a few days.
  • If absorption is minimized and/or if aggressive and prolonged (2-4 weeks) treatment is given, animals may survive.
  • Kidneys, lungs and/or heart may be permanently damaged by mineralization.

Expected response to treatment

  • Calcium levels should fall within hours of effective treatment.

Reasons for treatment failure

  • Animal is presented too late in the course of toxicosis.
  • Severe renal damage prior to treatment.

Sources

Publications

Refereed papers

  • Recent references fromPubMed.
  • Bahri LE (1990).Poisoning in dogs by vitamin D3-containing rodenticides.Comp. Cont. Educ. Pract. Vet.12, 1414-1417.
  • Moore FM, Kudish M, Richter K, Fagella A (1988).Hypercalcaemia associated with rodenticide poisoning in three cats.JAVMA193, 1099-1100.

Other sources of information

  • Rumbeiha W (2006)CholecalciferolIn:Small Animal Toxicology.Eds: M E Peterson and P A Talcott. Philadelphia: W B Saunders. ISBN: 0 7216 7826 2.
  • Rumbeiha W (2001)CholecalciferolIn:Small Animal Toxicology.2nd edn. Eds: M E Peterson and P A Talcott. Elsevier Inc, St Louis. ISBN: 0 7216 0639 3.
  • Osweiler G D (1995)Toxicology.Philadelphia: Williams and Wilkins. ISBN: 0 6830 6664 1.

Sample content only, to unlock the full article login or buy now

Loading...