Salicylate poisoning: urinary alkalinisation with sodium bicarbonate
Salicylate (the active form of aspirin) is a weak acid, so intravenous sodium bicarbonate makes the urine alkaline and holds the ionised (charged) form in the urine.
Remember
Salicylate is a weak acid, so alkaline urine, made with intravenous sodium bicarbonate, traps the ionised drug in the urine and speeds its excretion; acidifying the urine slows excretion.
Memory aid
an acid is held in alkaline urine, so make the urine alkaline to hold the aspirin in it
It reminds you that an acid drug calls for alkaline urine.
Salicylate (the active form of aspirin) is a weak acid, which means it exists as a mix of a charged form and an uncharged form. In the kidney tubule (where a drug in the fluid can slip back into the blood through the tubule wall), the uncharged form tends to be reabsorbed readily. The charged form is called the ionised form, and it crosses the tubule wall poorly. A weak acid becomes more ionised as its surroundings become more alkaline.
Intravenous sodium bicarbonate raises the urine pH, with a target above 7.5. More salicylate is then ionised, so it is reabsorbed less and is excreted faster. This is ion trapping. It is the standard teaching, though the mechanism has not been fully worked out; clinically, the technique does raise salicylate elimination.
The aim is to change the urine pH, not to force a large urine volume, so saline alone does not do the job. Acidifying the urine would have the opposite effect, because a weak acid is less ionised in acidic urine.
An expert position paper advises considering urinary alkalinisation as first-line treatment (the treatment tried first) when salicylate poisoning is moderately severe and the criteria for haemodialysis (filtering the blood through a machine) are not met. Haemodialysis removes salicylate from the blood directly and is kept for severe poisoning. Other poisons need other methods. Multiple-dose activated charcoal (charcoal that binds drug in the gut) is mainly used for drugs that recirculate between the gut and the liver.
Key facts
- Drug type
- a weak acid such as salicylate is more ionised when the urine is alkaline.
- Target
- urinary pH above 7.5, reached with intravenous sodium bicarbonate.
- Ion trapping
- the ionised form crosses the tubule wall poorly, so more stays in the urine and is excreted.
- Potassium
- alkalinising the urine is harder when serum potassium is low, so potassium is replaced with the bicarbonate.
- Blood gas
- a mixed picture of respiratory alkalosis (overbreathing blows off carbon dioxide) and metabolic acidosis (lactic acid and other acids build up) is typical of salicylate poisoning; early on, the respiratory alkalosis is the main disturbance, and later the metabolic acidosis dominates.
- Haemodialysis
- reserved for severe poisoning, for instance with altered mental status or when standard treatment is failing.
Exam traps
- Acidifying the urine does the opposite of what is needed for a weak acid such as salicylate, because a weak acid is less ionised in acidic urine, so more of it is reabsorbed and less is excreted.
- Forced diuresis (giving large volumes of fluid to push out more urine) with saline alone raises urine flow without raising urine pH, so a weak acid is not trapped in its ionised form.
- Alkalinising the urine does not reduce the binding of salicylate to proteins in the blood, because that binding is determined in the blood, and alkalinisation happens inside the tubule, after filtration.
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