Hyperkalaemia After an Ankle Sprain

This is a hyperkalaemic emergency with ECG changes (peaked T waves, QRS 112 ms) - membrane instability, not the numerical value, dictates urgency. A potassium of 6.3 with a widening QRS can degenerate into a sine wave and ventricular fibrillation within minutes.

1. Cardiac membrane stabilisation: 10 mL of 10% calcium gluconate IV over 5–10 min into a large vein (calcium chloride 10 mL is equivalent in calcium content but far more irritant and must go centrally or via a large peripheral vein). It acts within 1–3 min, lasts only 30–60 min, and does not lower potassium at all - so it must always be followed by a shifting agent. Attach continuous ECG monitoring.
2. Shift potassium intracellularly: 10 units of soluble insulin in 25 g glucose (50 mL of 50% dextrose) IV over 15–30 min. This lowers potassium by 0.5–1.2 mmol/L within 15–30 min. In CKD the hypoglycaemia risk is high and prolonged, so follow with a 10% dextrose infusion at 50–100 mL/h and hourly capillary glucose for at least 6 h.
3. Nebulised salbutamol 10–20 mg as an adjunct, lowering potassium by a further 0.5–1.0 mmol/L; watch for tachycardia, tremor and arrhythmia.
4. Sodium bicarbonate is not routine. His bicarbonate of 17 reflects only mild acidosis, and the sodium and volume load are risky in HFrEF. Reserve it for significant metabolic acidosis or when other measures fail.
5. Remove the source now: stop ibuprofen, spironolactone and sacubitril/valsartan. He is not congested (JVP not raised, weight down 2 kg), so high-dose furosemide is not the priority and risks worsening the AKI.
6. Escalate to nephrology: refractory hyperkalaemia, oliguria or volume overload are indications for dialysis irrespective of the creatinine.
7. Recheck potassium at 1, 2, 4 and 6 h - the insulin effect is transient and rebound is the rule. Also check calcium, magnesium, CK and screen for haemolysis.

Stop permanently: ibuprofen. In a patient with HFrEF, CKD, a RAAS inhibitor and a diuretic, an NSAID completes the 'triple whammy' - afferent arteriolar vasoconstriction on top of efferent blockade - and is contraindicated. Record it as an intolerance so it is not restarted by another prescriber.

Stop temporarily:

• Spironolactone - a major driver of the hyperkalaemia, especially with AKI. Stop now; restart at 25 mg on alternate days only when potassium is <5.0 mmol/L and creatinine has returned towards baseline.
• Sacubitril/valsartan - stop now; restart at the lowest dose (24/26 mg twice daily) once potassium is <5.0, creatinine is stable and he is euvolaemic, then titrate every 2–4 weeks. Do not abandon it: the mortality benefit is substantial and is precisely why he needs a potassium-lowering strategy rather than permanent withdrawal.
• Dapagliflozin - hold under the sick-day rule (reduced intake, AKI); restart once he is eating and drinking. It does not itself cause hyperkalaemia and is long-term renoprotective.

Continue: metoprolol - no bradycardia or shock. Continue statin therapy and other non-contributory drugs.

Furosemide: reassess. He is currently euvolaemic to dry, so a high dose would worsen renal function; continue his usual dose or reduce temporarily, then adjust to dry weight.

Reintroduction rules. Change one drug at a time. Check potassium and creatinine 1 week and 4 weeks after each change and after every titration. Accept a potassium up to 5.5 mmol/L in a stable, monitored patient rather than losing the RAAS inhibitor. If potassium sits between 5.0 and 5.5 and blocks titration, add a potassium binder. Give a normal rather than severely restricted diet, and warn him about salt substitutes (potassium chloride) and over-the-counter 'cold cures' containing NSAIDs.

Evidence. Patiromer and sodium zirconium cyclosilicate both lower serum potassium within hours to days and maintain normokalaemia over weeks (OPAL-HK for patiromer, HARMONIZE for SZC). The clinically meaningful endpoint is not the potassium value itself but whether the binder allows the patient to stay on a RAAS inhibitor or MRA: in the AMBER trial, patiromer with spironolactone in CKD with heart failure produced more persistent spironolactone use with less hyperkalaemia than placebo. That is a surrogate endpoint, however - no trial has shown a reduction in mortality or cardiovascular events.

Caveats to state explicitly. Gastrointestinal effects are common (constipation, diarrhoea); SZC can cause hypokalaemia and oedema; cost and availability limit use; and neither drug is a licence to continue a nephrotoxic agent such as an NSAID. The binder is a means of preserving disease-modifying therapy, not of permitting harmful therapy.

Practical use here. If his potassium stabilises between 5.0 and 5.5 and this prevents reintroduction of sacubitril/valsartan and spironolactone, start a binder, keep the diet normal, and recheck potassium and creatinine at 1–2 weeks. If potassium exceeds 5.5 despite a binder, reduce then stop the MRA before the ARB component.

What to tell the patient. 'The anti-inflammatory tablet your GP gave you for your ankle is what caused this admission. With your heart and kidney function, ibuprofen and similar painkillers can shut the kidneys down and push the potassium up dangerously - it can stop the heart. Use paracetamol for pain. If any doctor suggests an anti-inflammatory in future, tell them you have heart failure and kidney disease.' He should also be warned about potassium-containing salt substitutes and combination cold remedies, and told that the heart failure tablets are being paused, not abandoned.