Aspirin & Salicylate poisoning
Aspirin is the commonest cause of salicylate poisoning in the UK. The characteristic biochemical pattern is a mixed acid-base disorder: an early respiratory alkalosis (from central respiratory stimulation) with a later or concurrent high‑anion‑gap metabolic acidosis (from lactic acid, ketones and acidic metabolites).
Early recognition, serial monitoring and timely use of urinary alkalinisation and haemodialysis determine outcome. (RCEM Management of Suspected Poisoning 2025; RCEM-NPIS Antidote Guideline 2023)
Pathophysiology
- Salicylates stimulate the medullary respiratory centre, causing hyperventilation and a primary respiratory alkalosis (often an early sign).
- They uncouple oxidative phosphorylation and inhibit Krebs‑cycle metabolism, reducing ATP production and increasing anaerobic metabolism, lactate and ketone production, and accumulation of acidic metabolites, which produces a high‑anion‑gap metabolic acidosis.
- Renal impairment, dehydration and tissue hypoperfusion worsen metabolic acidosis by reducing drug and acid excretion.
- The net effect is often a combination of low PaCO2 and low HCO3-; patients frequently have simultaneous respiratory alkalosis and metabolic acidosis.
Clinical features
- Early features: hyperventilation, tinnitus/hearing loss, nausea, vomiting and diaphoresis.
- Progressive or severe features: confusion, agitation, seizures, coma, cerebral oedema and pulmonary oedema.
- Systemic effects: fever (hyperpyrexia, more common in children), hypoglycaemia (especially in children) or hyperglycaemia, hypokalaemia (especially during alkalinisation) and coagulopathy.
- Vulnerable groups: young children and older adults (>70 years) are at higher risk of severe toxicity at lower doses.