Acute salicylate poisoning occurs after toxic ingestion of a salicylate, most commonly acetylsalicylic acid (aspirin). Aspirin toxicity can occur with just 3 g in children and 10-30 g in adults. Other associated medications include salicylic acid (wart removers), methyl salicylate (oil of wintergreen), and bismuth subsalicylate (Pepto-Bismol). One teaspoon of oil of wintergreen contains approximately 7 g of salicylate. Toxicity may occur acutely due to a large ingestion or may be chronic from repeated overmedication for several days.

Aspirin works by inhibiting cyclooxygenase, which decreases levels of prostaglandins and can lead to a metabolic acidosis and respiratory alkalosis. Aspirin is rapidly absorbed in the stomach, and patients with toxic ingestion usually present within a few hours after acute overdose. Patients will exhibit signs of intoxication when serum levels are 40-50 mg/dL.

Common clinical manifestations include hyperpnea, tachypnea, tinnitus, nausea, vomiting, and diarrhea. In severe cases, patients can have hyperthermia, encephalopathy, seizures, pulmonary edema, cerebral edema, fever, sweating, listlessness, incoordination, hallucinations, coma, and cardiovascular collapse. Salicylates can also cause gastrointestinal (GI) hemorrhage, with complications including anemia, melena, epigastric pain, or hematochezia. Absorption and peak concentrations are delayed when ingestion involves delayed release or enteric-coated formulations.

Treatment of salicylate toxicity involves early recognition based on history and examination and acute stabilization of airway, breathing, and circulation (ABC). Serum salicylate concentration is then decreased with activated charcoal, intravenous (IV) sodium bicarbonate, and sometimes hemodialysis.

Related topic: chronic salicylate poisoning