Question.

In a young patient symptomatic from aspirin (salicylate) overdose, which one of the following is true?

a. Activated charcoal is ineffective
b. Early symptoms are typically visual disturbance and haematemnesis
c. Mitochondrial oxidative phosphorylation is stimulated
d. Persistent respiratory alkalosis is a poor prognostic sign
e. Salicylate elimination is increased at higher urinary pH

 

 

Answer.

The answer is e. Urine alkalinisation (higher urine pH) enhances salicylate elimination through the kidney.

Explanation.

Salicylates (the active ingredient of aspirin) are markedly harmful in excess. Aspirin tablets often form concretions in the stomach which delay gastric absorption so that multiple doses or delayed administration of activated charcoal are still effective in reducing salicylate absorption.

 

Early features of salicylate overdose include:

  • Tinnitus, dizziness, nausea and vomiting (haematemesis is uncommon)
  • Toxic amounts of salicylates stimulate the respiratory centres and early on give rise to hyperventilation and respiratory alkalosis on the blood gas.

 

Delayed features in moderate and severe toxicity

  • Agitation, pyrexia and sweating. Confusion, convulsions and coma may occur in life threatening overdoses.
  • uncoupling of mitochondrial oxidative phosphorylation, leading to anaerobic respiration and development of metabolic acidosis, a hallmark of serious poisoning.
  • Intracellular glucose depletion and hypokalaemia may also occur

 

Aspirin has a Pk (acid dissociation constant) value of 3.5. Alkalization of urine therefore keeps aspirin in ionized form which inhibits its tubular reabsorption and enhances its elimination in urine.

 

Treatment of salicylate overdose is therefore with activated charcoal, intravenous sodium bicarbonate to alkalinise the urine and in severe poisoning consider haemodialysis – all guided by serial salicylate levels.

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