ISSN 2398-2969      

Arsenic toxicity

icanis

Introduction

  • Arsenic is found in insecticides, herbicides and some medications. Some wood preservatives contain arsenicals and ash from burnt wood containing these preservatives can be toxic. The most common source of toxicity in dogs and cats is exposure to ant or roach baits.
  • Arsenic can be found in the pentavalent (usually naturally occurring) and trivalent forms. The trivalent form is up to 10 times more toxic than the pentavalent form.
  • Arsenic exposure most commonly occurs by ingestion and arsenic is readily absorbed from the gastrointestinal tract. Dermal exposure can occur, particularly through non-intact skin, and may result in systemic toxicity.

Pathogenesis

Etiology

  • Arsenic toxicity occurs following ingestion of products containing arsenic or topical exposure to pentavalent or trivalent forms of arsenic.

Predisposing factors

General
  • Weak, elderly, dehydrated or debilitated animals are more susceptible to toxicity, possibly due to reduced renal excretion.
  • Cats are very sensitive to arsenicals and the lethal dose is much lower than in dogs.

Pathophysiology

  • Trivalent arsenicals disrupt cellular respiration by binding sulfhydryl groups to enzymes. This will result in capillary vasodilation and a loss of capillary integrity. Fluid loss and hypovolemia ensue.
  • Actively dividing cells, such as gastrointestinal epithelium, are most affected by arsenic. Fluid will leak from the capillaries into the intestinal mucosa and GI lumen. This results in a reduction of blood volume, hypotension and eventual circulatory collapse.
  • Kidneys, liver, skin and lungs can also be injured.
  • The pentavalent form of arsenic, not a common source of toxicity in dogs and cats, is substituted for phosphate resulting in uncoupling of oxidative phosphorylation. This leads to axonal degeneration and demyelination. It is thought that it also interferes with the metabolism of Vitamin B1 and B6.
  • Pathological: gastrointestinal tract:
    • Submucosal edema, congestion and vesicle development. The GI mucosa may slough.
  • Kidneys:
    • Capillaries within the glomeruli dilate, swell and undergo degeneration. Tubular necrosis and renal fibrosis may develop. Hypotension and dehydration occur which leads to proteinuria Urinalysis: protein and oliguria.
  • Skin:
    • Dermal exposure to arsenical leads to hyperemia, blistering and edema.
  • A single lethal dose of trivalent arsenic is approximately 1-25 mg/kg. Subacute toxicity can occur when animals ingest small amounts over several days.
  • Arsenic is excreted by the kidneys and bile. Excretion in animals that ingest sublethal doses is usually complete within a few days.

Timecourse

  • Peracute death can occur following large exposures. Small exposures can result in morbidity and mortality over several days.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

Other sources of information

  • Neiger R D (2004)Arsenic Toxicosis.In:The 5-Minute Veterinary Consult. (ed) Tilley L P, Smith F W K. Lippincott, Williams & Wilkins. Philadelphia. p 95.
  • Neiger R D (2001)Small Animal Toxicology.(ed) Peterson, Talcott. Saunders. Philadelphia. pp 420-428.
  • Plunkett S (2001)Emergency Procedures for the Small Animal Veterinarian.2nd edition. Saunders. St. Louis. pp 295-298.
  • Gfeller R W & Messonnier S P (1998)Handbook of Small Animal Toxicology & Poisonings. Mosby. St. Louis. pp 85-89.
  • Osweiler G D (1996)Toxicology.Lippincott Williams & Wilkins. Philadelphia. pp181-186.

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