Salicylate
Pathophysiology
Interference with cellular metabolism (Uncouple oxidative phosphorylation) produces lactic acidosis and generates heat causing anion gap metabolic acidosis, hyperpyrexia, and hypoglycemia
Stimulate respiratory centers to cause hyperventilation causing respiratory alkalosis and increased insensible fluid losses
Salicylate exists more in the uncharged form at an acidic pH and is able to cross the blood-brain barrier causing CNS toxicity
Stimulation of chemoreceptors in the medulla causes nausea and vomiting
Toxic doses:
Aspirin PO: 150 mg/kg or 6.5 grams
Any PO oil of wintergreen exposure
Significant dermal exposures & signs of toxicity
Examples of salicylates : Aspirin, Pepto-Bismol, Ben-gay, and wintergreen oil
Presentation
Early: tinnitus, vertigo, tachypnea (respiratory alkalosis*), GI symptoms,
*Children almost never manifest a respiratory alkalosis and, when significantly poisoned, almost always progress right to acidemia secondary to metabolic acidosis.
Late: metabolic acidosis, hypovolemia, hypokalemia, hypoglycemia
Severe intoxication: fever, AMS, seizures, pulmonary edema
Diagnosis
Consult Poison Control: 1-800-222-1222
Management
References
Juurlink DN, Gosselin S, Kielstein JT, Ghannoum M, Lavergne V, Nolin TD, Hoffman RS; EXTRIP Workgroup. (2015) "Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup." Ann Emerg Med. 266(2):165-81. https://www.extrip-workgroup.org/salicylates