- Despite improvements in packaging, toxic ingestions of aspirin continue to occur.
- Children with aspirin toxicity can rapidly develop metabolic acidosis without a respiratory alkalosis.
- Treatment of mild-to-moderate aspirin overdose consists primarily of supportive management and alkalinization of the urine.
- The decision to treat is predicated on the patient's symptoms.
Acetylsalicylic acid (aspirin, ASA) is easily accessible and is commonly used in suicide attempts. Accidental overdoses continue to occur despite improved packaging. Patients who are acutely poisoned with aspirin generally exhibit less toxicity than patients who receive aspirin chronically, such as individuals taking high doses of aspirin for chronic inflammatory conditions.1 Individuals poisoned from chronic aspirin administration may present with signs consistent with sepsis and/or dementia. Annual data from the 2006 American Association of Poison Control Centers reported more than 17 000 exposures to aspirin alone, with 3600 of these occurring in children younger than 6 years.2
Aspirin is rapidly absorbed from the stomach and small intestine. If taken in large amounts, absorption can be delayed by the formation of concretions. Enteric coated preparations will also have delayed absorption.3
In therapeutic doses, aspirin's metabolism is first-order, but in the overdose setting pharmacokinetics change to zero-order enzyme saturable, in which a small increase in dose will result in a large increase in plasma salicylate level. Thus, there is a very narrow therapeutic range for aspirin when it is used in higher doses.
Ingestions of <150 mg/kg are generally nontoxic.4 With ingestions of 150 to 300 mg/kg mild-to-moderate toxicity occurs, and overdoses of >300 mg/kg can be lethal. It is crucial to know the concentration of the preparation ingested in order to estimate the potential for toxicity. Infant aspirin bottles are limited to 36 tablets of 81 mg each. Oil of wintergreen, on the other hand, contains 100% methyl salicylate and can be lethal in extremely small amounts.
Children have a quicker onset of toxicity from salicylate poisoning and exhibit more severe signs than adults. This can occur in part because salicylate is distributed more rapidly into organs such as the brain, kidney, and lungs. Patients may complain of tinnitus and impaired hearing. Direct stimulation of respiratory centers causes tachypnea, which in turn results in an early respiratory alkalosis. Uncoupling of the Krebs cycle results in anaerobic metabolism and ketonemia causing the characteristic anion gap metabolic acidosis. The acidosis can be exacerbated by hypovolemia as a result of vomiting, increased insensible losses from tachypnea and perspiration, and an osmotic diuresis. Fluid losses are especially severe in young children. In pediatric patients, the onset of metabolic acidosis tends to occur more rapidly than in adults, and a respiratory alkalosis may not occur.
An acidotic environment facilitates salicylate distribution into the brain, where it can cause agitation, delirium, seizures, and coma. Rhabdomyolysis can occur and can cause acute renal failure.
Patients can develop noncardiogenic pulmonary edema, most likely because of a ...