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Aspirin toxicity

ffelis

Synonym(s): Salicylates, acetylsalicylic acid, NSAID


Introduction

  • Non-steroidal anti-inflammatory drug Acetyl salicylic acid.
  • Toxicity results following ingestion of products containing aspirin or salicylates.
  • These include some arthritis creams, Pepto-Bismol, Kaopectate liquid and many other products.
  • Signs: vomiting, anorexia, melena, oliguria.
  • Diagnosis: history, clinical signs.
  • Treatment: symptomatic - no specific antidote.
  • Prognosis: depends on amount ingested - good if treated early.

Pathogenesis

Etiology

  • Acetylsalicylic acid Acetyl salicylic acid has been used for its anti-inflammatory, antipyrexic, and analgesic properties for decades.
  • Since 1971, aspirin has been available for use in humans. It is readily absorbed from the stomach and small intestine.
  • Toxicity often occurs due to accidental exposure or inappropriate administration by a well-meaning pet owner. The toxic dose of aspirin in animals varies. In some animals, therapeutic doses can result in GI ulceration.
  • Toxic signs can develop at doses over 25 mg/kg/day.
  • Clinical signs can develop within 4-6 hours after ingestion of a toxic dose.

Predisposing factors

General

  • Animals with underlying renal or hepatic disease are more likely to develop toxicity.
  • Dehydrated animals are also more likely to develop renal damage.
  • Concurrent use with other non-steroidal anti-inflammatories or glucocorticoids also increases the risk of developing aspirin toxicity.

Pathophysiology

  • Aspirin is metabolized by the liver to salicylic acid.
  • Salicylic acid inhibits the cyclo-oxygenase system, which then inhibits the production of prostaglandins responsible for maintaining tissue homeostasis and modulating blood flow.
  • Without the protection of prostaglandins and a direct effect of the drug, gastric ulceration can occur.
  • Renal blood flow can be affected, resulting in renal damage.
  • Salicylic acid irreversibly inhibits thromboxane activity, which inhibits platelet function.
  • Acute massive overdose can directly affect the respiratory center, leading to tachypnea. This leads to a respiratory alkalosis, followed by a metabolic acidosis Acid base imbalance.
  • Acute toxicity can result in hyperthermia due to the ability of aspirin to uncouple oxidative phosphorylation.
  • Hepatic damage can occur.

Timecourse

  • The half-life of aspirin in cats is between 25-40 hours.
  • Clinical signs can develop within 4-6 hours of ingesting a toxic dose.
  • Clinical signs can also develop after days to weeks of therapeutic doses.

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

  • Roder J D (2004) Analgesics. In:Clinical Veterinary Toxicology. (ed) Plumlee K H. Mosby. St. Louis. pp 282-284.
  • Mikiciuk M G (2001) Nonsteroidal Anti-inflammatories. In: Small Animal Toxicology.(eds) Peterson M E and Talcott P A. Saunders. Philadelphia. pp 622-627.
  • Gfeller R W and Messonnier S P (1998) Handbook of Small Animal Toxicology & Poisonings. Mosby. St. Louis. pp 89-93.

Organisation(s)

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