Acute salicylate poisoning
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
T39.091A – Poisoning by salicylates, accidental (unintentional), initial encounter
7248001 – Poisoning by salicylate
Differential Diagnosis & Pitfalls
Drug Reaction Data