Hyperkalaemia after a routine antibiotic in heart failure and CKD
A 78-year-old woman with heart failure with reduced ejection fraction (LVEF 32%), stage 3b chronic kidney disease (baseline creatinine 1.5 mg/dL, eGFR 34 mL/min/1.73 m²), type 2 diabetes and knee osteoarthritis presents with three days of nausea, weakness and palpitations. Her medications are sacubitril–valsartan 97/103 mg twice daily, spironolactone 25 mg daily, furosemide 40 mg daily, metformin 1 g twice daily, atorvastatin 40 mg nightly and ibuprofen 400 mg as needed. Two days ago a walk-in clinic prescribed trimethoprim–sulfamethoxazole for cystitis. Blood pressure is 98/60 mmHg, pulse 88, oxygen saturation 96%. The ECG shows peaked T waves and a widened QRS. Potassium 5.9 mmol/L, sodium 133 mmol/L, bicarbonate 18 mmol/L, creatinine 2.1 mg/dL and glucose 9.8 mmol/L. She is alert and her urine output is 20 mL/hour.
1. Outline your immediate management in the first 60 minutes, including drug doses and the order of priorities.
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Treat this as a hyperkalaemic emergency because of the ECG changes, not because of the number alone.
- Stabilise the myocardium first. Give calcium gluconate 10% 10–30 mL IV over 5–10 minutes with continuous ECG monitoring. Onset is 1–3 minutes and it does not lower potassium; repeat after 5 minutes if ECG changes persist.
- Shift potassium intracellularly. Give 10 units of regular insulin with 25 g glucose (50 mL of 50% dextrose) IV. Check capillary glucose every 30–60 minutes for at least 6 hours. Add nebulised salbutamol 10–20 mg. Consider sodium bicarbonate 50 mmol IV only if there is significant metabolic acidosis (bicarbonate is 18 here); it is adjunctive and must not delay definitive removal.
- Remove potassium. Stop spironolactone, sacubitril–valsartan, trimethoprim–sulfamethoxazole, ibuprofen and metformin immediately. Give furosemide 40–80 mg IV, higher if oliguric, and consider a potassium binder, although these work slowly. Ask nephrology about urgent dialysis if potassium does not fall, urine output stays below 0.5 mL/kg/hour, or the ECG does not normalise.
- Recheck potassium and creatinine within 1–2 hours. The glucose of 9.8 mmol/L does not remove the need for dextrose with insulin.
2. Which medications precipitated this episode, and how would you prioritise deprescribing? Include the mechanism for each.
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Several drugs are contributing, and they interact:
- Trimethoprim–sulfamethoxazole: trimethoprim blocks the epithelial sodium channel in the distal nephron, mimicking amiloride and reducing potassium excretion; sulfamethoxazole can also raise creatinine. This is the proximate trigger.
- Spironolactone: a mineralocorticoid receptor antagonist that is now unsafe with an eGFR of 34 and acute kidney injury.
- Sacubitril–valsartan: reduces aldosterone and angiotensin II, and worsens renal function when the patient is volume-depleted.
- Ibuprofen plus furosemide: the NSAID causes afferent arteriolar vasoconstriction and the diuretic causes volume depletion; together with the ARB this is the 'triple whammy' for acute kidney injury.
- Metformin: at an eGFR below 30 and during acute illness, lactic acidosis risk rises; hold it now and review.
Permanent changes: stop ibuprofen (offer topical NSAID or paracetamol), avoid trimethoprim–sulfamethoxazole in future, and document this. For the cystitis, choose an agent guided by culture and renal function; nitrofurantoin is best avoided at eGFR below 30, so fosfomycin single dose or an alternative based on susceptibilities is preferable. Temporary changes: hold spironolactone and sacubitril–valsartan until renal function and potassium recover rather than stopping them forever.
3. When would you restart the heart-failure medications, and what monitoring schedule would you arrange? What would prompt nephrology referral?
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Restart only when potassium is below 5.0 mmol/L, creatinine is returning towards baseline, and the patient is euvolaemic.
- Restart sacubitril–valsartan first at a reduced dose (for example 24/26 mg twice daily), because it is the most prognostically important and can be titrated. Check potassium and creatinine at 1 week and 4 weeks.
- Restart spironolactone at 12.5 mg daily only if potassium is below 5.0 mmol/L and eGFR is above 30, with a potassium check at 1 week and after any dose change.
- Do not restart the NSAID. Use paracetamol and topical diclofenac; if a systemic NSAID is ever considered it should be a short course with monitoring, and not alongside a diuretic plus ARB.
- Give sick-day rules: hold sacubitril–valsartan, diuretic, spironolactone and metformin during vomiting, diarrhoea or dehydration.
- Consider adding an SGLT2 inhibitor once stable, as it reduces heart-failure hospitalisation and slows CKD progression, but only after the acute episode.
- Refer to nephrology if potassium remains above 5.5 mmol/L despite measures, creatinine does not recover, urine output stays low, or dialysis is needed. Arrange heart-failure review and a full medication reconciliation.