Overview
Why Aspirin Overdose Demands a Different Response
A patient with salicylate toxicity may be breathing rapidly and have an alkalemic arterial pH while already developing serious cellular toxicity.
A patient with salicylate toxicity may be breathing rapidly and have an alkalemic arterial pH while already developing serious cellular toxicity. The respiratory alkalosis is not reassurance: salicylate is driving the hyperventilation, while mitochondrial dysfunction is generating metabolic acids at the same time. A falling pH changes the drug's distribution, allowing more non-ionised salicylate to enter the brain. Management therefore has two linked aims: keep the blood mildly alkaline to limit CNS penetration and make the urine alkaline to increase renal elimination. Potassium replacement, appropriate fluid support, glucose treatment for neurological symptoms, and protection of compensatory ventilation are part of the same strategy. A single serum concentration cannot establish safety; delayed absorption, chronic exposure, acid-base status, and the patient's neurological and respiratory condition determine urgency. In Canada, involve the applicable provincial or regional poison centre early and interpret reported concentrations in mmol/L.