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.
Presenting signs
Depression.
Vomiting .
Melena.
Tachypnea.
Hyperthermia .
Oliguria or polyuria.
Rarely, seizures .
Acute presentation
Depending on the dose, signs of toxicity can develop within 4-6 hours of aspirin ingestion and can include depression, vomiting, anorexia and tachypnea.
Hyperthermia can also occur .
If gastrointestinal ulceration has occurred, hematemesis may be noted.
Geographic incidence
Since aspirin is readily available, toxicities can occur anywhere.
Age predisposition
There is no age predisposition for aspirin toxicity but older and younger cats may be at greater risk for developing GI ulcers and renal damage.
Sex predisposition
None.
Breed predisposition
None.
Public Health considerations
None.
Cost considerations
Cost of therapy will vary depending on the amount ingested and the severity of clinical signs.
Acetylsalicylic 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 .
Acute toxicity can result in hyperthermia due to the ability of aspirin to uncouple oxidative phosphorylation.
Hepatic damage can occur.
Timecourse (incubation, duration)
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.
Acute onset of gastrointestinal signs, changes in respiration, lethargy, oliguria or polyuria.
Client history
Anorexia.
Vomiting .
Melena.
Depression.
Oliguria or polyuria.
Tachypnea.
Clinical signs
Lethargy.
Vomiting .
Anorexia.
Melena.
Hyperthermia .
Tachypnea.
Anemia.
Ataxia.
Oliguria.
Polyuria.
Polydipsia.
Weakness.
Rarely seizures.
Rarely coma.
Confirmation of diagnosis Discriminatory Diagnostic features
History of ingestion with appropriate clinical signs.
Laboratory findings can include hyperglycemia or hypoglycemia , wide anion gap , elevated BUN and creatinine , hyperkalemia or hypokalemia , hypernatremia , metabolic acidosis , anemia , elevated liver enzymes (ALK, AST , ALT ), prolonged clotting times , thrombocyopathia .
Definitive Diagnostic features
Serum can be submitted for salicylic acid levels but this is rarely done.
Induce emesis if ingestion occurred recently (less than 2 hours).
Activated charcoal administration. Use judiciously if gastrointestinal ulceration is present.
IV fluid therapy .
Correct acid base and electrolyte imbalances.
Sodium bicarbonate therapy may be indicated if severe metabolic acidosis is present.
Blood transfusions may be required if profound anemia develops .
Sucralfate (250 to 1000 mg PO every 6 to 8 hours) and famotidine (0.5 to 1 mg/kg IV, SC, PO every 12 to 24 hours) or misoprostol (1 to 5 mcg/kg PO every 8 to 12 hours) to treat gastrointestinal ulceration.
Control seizures with diazepam .
Monitoring
Monitor for seizures , hyperthermia , anemia , and azotemia .
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.
Vetstream contributor(s)
Dawn Ruben DVM, 11719 Castle Ranch Road, De Soto, MO 63020, USA.
Patricia Talcott MS DVM PhD DiplABVT, Department of Food & Toxicology, Holm Research Center, 2222 West Sixth Street, PO Box 442201, University of Idaho, Moscow ID 83844-2201, USA.
