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How do I investigate mild hypokalaemia?

Q - What investigations should be carried out for isolated hypokalaemia in primary care?

A - Always check for diuretics in the drug history or any record of prescriptions, as this requires oral potassium supplementation and makes for a clear distinction between the commonest single cause, and the other minority causes.

Without diuretics, hypokalaemia suggests potassium loss: consider faeces, vomit and urine. Chronic diarrhoea may have a definitive aetiology such as colitis, or may be caused by laxative abuse. Emetic abuse or bulimia are other possibilities.

Laxatives are detectable in a urine sample, where the urine potassium should also be relatively low.

If GI-tract loss is ruled out, urinary loss not caused by diuretics leads to some much rarer causes.

Renal tubular acidosis has the unusual feature of hypokalaemia with low serum bicarbonate: otherwise hypokalaemia is associated with alkalosis.

Conn's syndrome (hyperaldosteronism) and Cushing's syndrome (hypercortisolism) cause hypokalaemia from urinary loss with excess sodium retention. That is ironic as the first-line treatment of the resulting hypertension is often with a diuretic.

Old and cold samples cause artefactual hyperkalaemia as potassium leaks from cells. Transporting samples in hot weather also causes artefactual hypokalaemia.

The effect is thought to be less with serum than with plasma samples. Against an unvarying reference range, mild hypokalaemia will appear to be more common in summer.

Mark Buckley-Sharp is a consultant chemical pathologist, University College London Hospitals

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