Potassium Disorders — Written Clinical Reasoning

Prompt 1 — Severe hyperkalaemia in a complex CKD patient

Question

Summarise this patient's problems, explain the immediate emergency management in the first 30 minutes with specific drugs and doses, identify the cause of the hyperkalaemia, outline the decision about whether and when to dialyse, and describe the subsequent management and monitoring plan including the cardiorenal trade-offs. ^[1]

Case vignette: A 72-year-old man with stage 3b CKD, HFrEF and type 2 diabetes on sacubitril/valsartan, spironolactone and empagliflozin presents with two days of weakness and confusion after gastroenteritis with reduced intake. K+ 7.6 mmol/L with sine-wave ECG (broad QRS, absent P waves) and bradycardia, pH 7.28, bicarbonate 16 mmol/L. ^[1]

Model answer

Problem list (prioritised): ^[1]

1. Severe hyperkalaemia — K+ 7.6 mmol/L — with a pre-terminal ECG (QRS 150 ms, sine-wave morphology) — this is a cardiac emergency with imminent risk of ventricular fibrillation or asystole.
2. Metabolic acidosis — pH 7.28, bicarbonate 16 — a contributing factor to the hyperkalaemia through transcellular shift, and a feature of his CKD.
3. Bradycardia (HR 56) — likely a consequence of the hyperkalaemia acting on the conducting system.
4. Stage 3b CKD with a cardiorenal drug regimen (sacubitril/valsartan, spironolactone, empagliflozin, frusemide, bisoprolol) — the structural and pharmacological substrate for impaired potassium excretion.
5. Recent gastroenteritis with volume depletion and reduced intake — the precipitant, reducing distal sodium delivery and potassium excretion.
6. Heart failure with reduced ejection fraction and ischaemic heart disease — the indication for his mortality-reducing drugs and the context for his cardiovascular risk.
7. Type 2 diabetes on metformin with an acute kidney injury on top of CKD — metformin should be held during acute illness and AKI given the risk of lactic acidosis.
8. Encephalopathy — likely a combination of acidosis, the underlying illness, and the electrolyte disturbance; assess for alternative causes (sepsis, intracranial event). ^[1]

Immediate management in the first 30 minutes — the four pillars: ^[1]

First, secure the patient and confirm the value. ABC assessment, high-flow oxygen if hypoxic, continuous cardiac monitoring, two large-bore cannulae, and an immediate repeat of the potassium as a venous or arterial blood gas to confirm the value and exclude pseudohyperkalaemia (less likely here given the ECG changes, but the discipline matters). I would obtain a group and hold and send full blood count, urea and electrolytes including magnesium, liver function, troponin, and venous lactate. ^[1]

Pillar 1 — Stabilise the myocardium. Given the sine-wave ECG, I give calcium gluconate 10 mL of 10% (2.25 mmol of calcium) intravenously over 2 to 5 minutes, with continuous ECG monitoring, and repeat once after 5 minutes if the ECG changes persist. Calcium raises the threshold for excitation and reverses the membrane effect of hyperkalaemia within 1 to 3 minutes; it does not lower the potassium but buys time. I would re-dose every 30 to 60 minutes if ECG changes recur while awaiting definitive therapy ^[7].

Pillar 2 — Shift potassium into cells. I give 10 units of rapid-acting (soluble) insulin with 25 g of intravenous dextrose (50 mL of 50% dextrose over 15 to 30 minutes, or as a bolus), which stimulates the Na+/K+-ATPase and lowers the potassium by 0.5 to 1.2 mmol/L over 30 to 60 minutes, with effect for 4 to 6 hours. I combine this with salbutamol 10 to 20 mg nebulised, which is additive and lowers the potassium by a further 0.5 to 1.0 mmol/L. Because he is acidaemic, I add sodium bicarbonate 50 mmol of 8.4% intravenously over 15 to 30 minutes, which is effective in this context (bicarbonate is confined to the acidotic patient and not effective as monotherapy in non-acidotic hyperkalaemia). I would check a blood glucose at baseline, at 30 minutes, at 1 hour, then hourly for 4 to 6 hours, because hypoglycaemia is the commonest serious adverse event of insulin-dextrose, occurring in up to 20 percent of patients, sometimes delayed, and a lower-dose insulin regimen (5 units) lowers potassium as effectively with less hypoglycaemia ^[5].

Pillar 3 — Remove potassium. I give frusemide 80 mg intravenously (he has residual renal function and is not described as oliguric) to promote potassium excretion. I start an oral potassium binder — sodium zirconium cyclosilicate 10 g three times daily for the first 48 hours (faster onset than patiromer; HARMONIZE demonstrated a rapid reduction ^[4]) — with a plan to step down to maintenance dosing. I would avoid sodium polystyrene sulfonate (resonium) given the risk of intestinal necrosis, especially if he has any ileus.

Pillar 4 — Address the cause. I hold the sacubitril/valsartan and spironolactone immediately, hold the metformin (AKI risk), and review the empagliflozin (also a contributor to volume depletion and euglycaemic ketoacidosis risk). I correct the volume depletion with cautious isotonic saline (mindful of his heart failure — small boluses, reassess). I treat the acidosis with bicarbonate as above. I reassess his medications once the potassium is controlled. ^[1]

The dialysis decision. The indications for urgent haemodialysis in hyperkalaemia are: refractory hyperkalaemia despite medical therapy, severe hyperkalaemia with ECG changes in a patient with oligoanuria or end-stage CKD, and ongoing potassium release (rhabdomyolysis, tumour lysis). This patient presented with a pre-terminal ECG but has stage 3b CKD (not oligoanuric) and has good urinary output expected with frusemide. I would give the full medical protocol above first, reassess the potassium and ECG at 1 to 2 hours, and call the nephrology team early. If the potassium fails to fall below 6.5, or the ECG fails to improve, or he becomes oliguric, I would proceed to haemodialysis via temporary vascular access. Continuous renal replacement therapy (CVVHDF) would be preferred if he is haemodynamically unstable. I would warn the team of rebound — the insulin-dextrose wears off at 4 to 6 hours, and if the underlying cause persists, the potassium will rise again; ongoing removal (binder, diuretic, dialysis) is essential. ^[1]

Subsequent management and monitoring plan. I would admit him to high dependency with continuous cardiac monitoring. I would recheck the potassium at 1, 2, 4, 6, then 12 hours during the acute phase, watching for rebound. I would monitor the blood glucose hourly for 4 to 6 hours after insulin-dextrose. Once the potassium is below 6.0 and the ECG has normalised, I would start to plan the cardiorenal trade-off: the sacubitril/valsartan, spironolactone, and empagliflozin are each proven to reduce mortality and hospitalisation in HFrEF and CKD, and ceasing them permanently worsens his outcome. The modern approach is to reintroduce the RAAS inhibitor and MRA at a lower dose once the potassium is controlled, maintain the patient on an oral potassium binder (patiromer or SZC) to enable continuation, and monitor the potassium and renal function closely — typically 1 to 2 weeks after reinitiation and dose changes ^[1][3]. The binder is the bridge that allows continuation of mortality-reducing therapy. I would address his diabetes (continue metformin only after the AKI resolves; the empagliflozin is cardiorenal-protective but should be held during acute illness), review his heart failure and volume status, and investigate the precipitant (the gastroenteritis with volume depletion and reduced intake is the trigger superimposed on the drug regimen). I would also arrange a diabetes and heart failure review and ensure he has a sick-day plan for future illness (hold the RAAS inhibitor, SGLT2 inhibitor, and diuretics during acute illness — the "Sick Day Guidance").