Hypokalaemia and hypomagnesaemia

Definitions and the ageing background. Hypokalaemia = serum K⁺ <3.5 mEq/L (severe <2.5); hypomagnesaemia = serum Mg²⁺ <1.7 mg/dL. Total body potassium is lower in healthy older people, and the potassium-controlling ATPases of the collecting tubule are impaired by ageing — so a given loss produces greater depletion and slower repletion than in the young.

Causes of hypokalaemia in the elderly. Diuretics (loop and thiazide) are by far the commonest; also GI losses (diarrhoea, vomiting, laxative abuse), poor dietary intake and malnutrition, primary or secondary hyperaldosteronism, and drugs — corticosteroids, insulin, β₂-agonists, amphotericin B. Magnesium depletion is an under-recognised cause.

Causes of hypomagnesaemia in the elderly. Chronic proton-pump inhibitor use (the classic geriatric cause), diuretics, alcohol excess, chronic diarrhoea and malabsorption, aminoglycosides, cisplatin, amphotericin, calcineurin inhibitors, and poorly controlled diabetes with osmotic diuresis.

Clinical features. Hypokalaemia — muscle weakness, cramps, constipation and ileus, polyuria (nephrogenic DI), rhabdomyolysis, and ECG changes: flattened T waves, ST depression, prominent U waves, prolonged QU, ventricular ectopy. Hypomagnesaemia — tremor, tetany with positive Trousseau and Chvostek signs, seizures, and torsades de pointes. In older adults, both frequently present atypically as falls, generalised weakness or delirium.

The critical link — correct magnesium first. Magnesium depletion causes refractory hypokalaemia and refractory hypocalcaemia: low intracellular magnesium releases the inhibition of the ROMK channel in the distal nephron, so potassium is wasted in the urine and cannot be corrected until magnesium is replaced. Hypomagnesaemia also impairs PTH secretion and end-organ response.

Management. Replace magnesium first — oral magnesium salts if mild; IV magnesium sulphate 1–2 g for symptomatic disease or torsades. Then potassium: oral KCl is preferred whenever the patient can take it; IV KCl only for severe or symptomatic hypokalaemia, at a maximum of 10 mEq/h peripherally (up to 20 mEq/h centrally with cardiac monitoring), and never in dextrose — dextrose stimulates insulin and drives potassium intracellularly, worsening the deficit. Finally, review and deprescribe the culprit diuretic, laxative or PPI.

Deprescribing, not escalating replacement, is the modern answer to drug-induced hypomagnesaemia. Chronic PPI use is now firmly established as a cause of hypomagnesaemia and of acute interstitial nephritis, and PPIs have accordingly become a major target of deprescribing strategies in older adults. Current guidance in unexplained or recurrent hypomagnesaemia is to stop the PPI rather than keep increasing magnesium supplements. Note also that SGLT2 inhibitors consistently raise serum magnesium, an incidental benefit in the diabetic older patient on a diuretic.