Aspirin (acetylsalicylic acid, ASA) is the salicylate ester of acetic acid and is a weak acid derived from phenol. Aspirin
reduces pain and inflammation by reducing prostaglandin and thromboxane synthesis through inhibition of cyclooxygenase. At
very high doses, aspirin and other salicylates uncouple oxidative phosphorylation leading to decreased ATP production. Salicylates
also affect platelet aggregation.
Aspirin is rapidly absorbed from the stomach and proximal small intestines in monogastric animals. The rate of absorption
is dependent upon gastric emptying, tablet disintegration rates, and gastric pH. Absorption of large, potentially lethal doses
may be slower than therapeutic doses partly due to the effect of aspirin on gastric emptying. Aspirin is metabolized in the
liver and excreted through the urine. The elimination half-life increases with the dose. In dogs, the half-life at the therapeutic
dose is 8.6 hours. Cats are deficient in glucuronyl transferase and have prolonged excretion of aspirin due to decreased metabolism.
Since aspirin is highly protein bound, it should be used with caution in patients with hypoproteinemia or pre-existing hepatic
or renal disease. Aspirin is contraindicated in patients with bleeding GI ulcers. In dogs, toxicity has been noted at doses
of 100 - 300 mg/kg/day PO for 1 - 4 weeks. Doses of 325 mg twice a day were lethal to cats.
Signs may include vomiting (+/- blood), hyperpnea, respiratory alkalosis, metabolic acidosis, gastric hemorrhage, centrilobular
liver necrosis, and bleeding diathesis. Fever and seizures may be seen due to the uncoupling of oxidative phosphorylation.
Renal insufficiency is uncommon with salicylate toxicoses but could develop secondary to rhabdomyolysis (from seizing) or
The primary goal of treatment is to prevent or treat gastric ulceration, acidosis, hepatopathy, and coagulopathy. Emesis can
be performed in the asymptomatic animal, unless contraindicated. Activated charcoal adsorbs aspirin and repeated doses may
be used with large ingestions. A cathartic should be used, unless the animal is dehydrated or has diarrhea. Peritoneal dialysis
can be effective in removing salicylate. Liver values, glucose, acid base status and electrolytes should be monitored. Maintain
hydration and start GI protectants (sucralfate, H2 blockers, +/- misoprostol, +/- omeprazole) to help manage and/or prevent
gastric ulcers. In the asymptomatic patient, gastric protectants should be continued for 5 - 7 days. Metoclopramide can be
used to control vomiting. Bismuth subsalicylate antacid formulations and corticosteroids are contraindicated.
Alkalinization of the urine results in ion trapping of salicylate in the kidney tubule and increases its secretion. Ion trapping
can have adverse effects, therefore it should be used only in cases where the acid base balance can be monitored. Assisted
ventilation and supplemental oxygen may be required if the animal is comatose. Seizures should be treated with diazepam. Fluids,
whole blood, and electrolytes should be given to control hypotension and hemorrhage, manage acute bleeding ulcers, and correct
electrolyte abnormalities. Acid base imbalances should be corrected. Hyperpyrexia should be treated conservatively as aggressive
cooling (ice baths or cold water enemas) may result in hypothermia.
Prognosis is good if the animal is treated promptly and appropriately. The development of central lobular hepatic necrosis
is considered to have a poor prognosis. With hepatic damage, treatment may need to be continued for weeks.