Salicylate (Aspirin) Poisoning

Basics

Analgesics are the most common drugs implicated in human exposures reported to U.S. poison control centers.
Salicylate preparations constitute ~10% of all analgesic poisoning exposures reported to poison control centers.

Ingested drug is absorbed in stomach and proximal intestine.
With therapeutic aspirin dosing, serum levels peak in 1 to 2 hours (standard preparations) or 4 to 6 hours (enteric coated).
After oral overdose, absorption may be prolonged and erratic.
Acetylsalicylate ingestion may produce gastritis and may trigger centrally mediated vomiting.
After overdose, the elimination half-life of salicylate becomes prolonged.
As blood pH falls, the proportion of nonionized salicylate rises, and more salicylate shifts into tissues, including brain.
Toxic salicylate exposures uncouple mitochondrial oxidative phosphorylation and increase oxygen consumption.
Direct stimulation of the medullary respiratory center leads to hyperventilation and respiratory alkalosis.
Multiple metabolic derangements produce a wide anion gap metabolic acidosis.
Dehydration and electrolyte shifts are common.
Low cerebral glucose concentrations may exist despite normal serum glucose concentrations.
Pulmonary and/or cerebral edema may occur.

Aspirin is often marketed in combination with other pharmaceuticals, which may complicate drug overdose situations.
Adolescents frequently overdose on >1 drug preparation.
Therapeutic use of acetylsalicylic acid among children with influenza has been associated with the occurrence of Reye syndrome.

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