Elderly woman with heart failure, CKD and suspected digoxin toxicity after a new NSAID

Recognise the syndrome first. Nausea, anorexia, confusion and xanthopsia (yellow-tinged vision) with bradycardia in a patient on digoxin is chronic digoxin toxicity until proven otherwise.

Ranked contributors

1. Ibuprofen, started 10 days ago - the timing is the strongest clue. In a patient with heart failure and CKD, NSAID-mediated prostaglandin inhibition causes afferent arteriolar constriction and AKI (creatinine 150 → 210 micromol/L, a ~40% rise). Digoxin is predominantly renally cleared, so its clearance fell at the same time.
2. Digoxin dose - 0.25 mg daily is too high as maintenance for eGFR ~26 mL/min. Reduced clearance plus an unchanged dose produces accumulation over 7–14 days, matching the symptom timeline.
3. Ramipril + spironolactone + new AKI - three insults to potassium handling converge; this, not digoxin alone, is the likeliest driver of the K 6.1 mmol/L.
4. Carvedilol + digoxin - additive AV nodal suppression explains the bradycardia and first-degree block.

Withhold now: digoxin, ibuprofen, spironolactone and ramipril. Hold carvedilol if the bradycardia is symptomatic or HR falls further; continue furosemide only if there is volume overload, with strict fluid balance. Do not simply 'adjust' the digoxin dose while the creatinine is moving - the level will change again once renal function recovers.

Sequence: stabilise membrane → shift potassium → remove potassium → confirm the diagnosis.

1. ECG immediately and continuous monitoring. If there are conduction changes or arrhythmia, give IV calcium gluconate - but note that calcium salts are traditionally avoided in suspected digoxin toxicity, so this is a prescriber-level decision, not an automatic one.
2. Stop all potassium-raising drugs (ramipril, spironolactone) and any potassium-containing fluids or salt substitutes.
3. Shift: insulin 10 units with 25 g glucose IV, plus nebulised salbutamol as adjunct. Consider sodium bicarbonate only if acidotic.
4. Remove: review urine output; a potassium binder may be used, but dialysis is the definitive option if hyperkalaemia is refractory in the setting of AKI.
5. Digoxin-specific antibody fragments are indicated for life-threatening arrhythmia, and are considered at K >5.5–6 mmol/L or high levels in acute toxicity; in this chronic, renally-driven picture the potassium is largely renal/ACE-inhibitor/spironolactone-related, so the priority is stopping those drugs and correcting renal perfusion while the level is pending.
6. Send magnesium, repeat renal function and a digoxin level; hypomagnesaemia and hypercalcaemia both potentiate toxicity. Ask specifically about recent amiodarone, verapamil, diltiazem or macrolide exposure, which would raise digoxin levels further.

Restart only when the creatinine has returned to baseline, K <5.0 mmol/L, and the level is known.

• Digoxin: restart at a reduced maintenance dose (e.g. 0.125 mg daily, or 0.125 mg on alternate days if renal function remains impaired), targeting a trough <0.9–1.0 ng/mL in heart failure. Re-check a level 5–7 days after any dose change - not sooner, as distribution is incomplete.
• Spironolactone: restart cautiously only if K and creatinine are stable, with K checked at 1 week and 4 weeks. Ramipril: restart at a lower dose with the same monitoring.
• Pain strategy: document a clear NSAID-avoidance alert, recommend paracetamol (dose-reduced for age) and topical NSAID or physiotherapy instead. The intervention that caused this admission was a walk-in clinic prescription, so make the allergy/intolerance field explicit so the next prescriber sees it.
• Patient counselling: report nausea, anorexia, confusion, visual changes or a pulse below 60 bpm; understand that digoxin has a narrow therapeutic index and that dehydration or a new illness changes the dose requirement.
• Documentation: record the suspected adverse drug reaction, the prescriber contact, the recommendations made and the monitoring plan; a formal ADR report is appropriate.