Potassium and Other Electrolyte Disorders — Advanced

Correct answer: Give intravenous calcium to stabilise the myocardium. In life‑threatening hyperkalaemia with ECG evidence of cardiac membrane instability (widened QRS, absent P waves, severe bradyarrhythmia), the immediate priority is membrane stabilisation with IV calcium (calcium gluconate or calcium chloride) because it reduces the risk of ventricular arrhythmia within minutes. After stabilisation, potassium shifting therapies (insulin + dextrose, nebulised β2 agonist) and measures to remove potassium (diuretics if effective, binders for non-urgent situations, or urgent dialysis if refractory or with renal failure) should follow. Sodium bicarbonate is only helpful when hyperkalaemia is accompanied by significant metabolic acidosis and its potassium-lowering effect is unpredictable; it is not first-line for membrane stabilisation. Urgent haemodialysis is definitive in severe or refractory hyperkalaemia, especially in advanced CKD, but it is not the immediate first action when there is ECG change — you must stabilise the myocardium first while organising dialysis.

Correct answer: Repeat the potassium using a plasma (heparinised) or otherwise non‑haemolysed specimen. Marked thrombocytosis or in vitro haemolysis can cause pseudohyperkalaemia when serum (clotted) samples are used because platelets release potassium during clotting. In an asymptomatic patient with a normal ECG and no other reason for hyperkalaemia, the appropriate immediate step is to verify the result with a properly collected plasma sample (or a fresh venous gas) before instituting potentially harmful therapies. Commencing insulin/dextrose, resins, or arranging dialysis is inappropriate without confirming true hyperkalaemia. IV calcium is only indicated when there are ECG changes or clinical instability.

Correct answer: Begin slow IV potassium chloride via a central line with cardiac monitoring. Severe hypokalaemia (<2.5 mmol/L) with neuromuscular weakness and ECG changes is a medical emergency; prompt potassium repletion is required, usually with intravenous potassium chloride. Because large amounts are often necessary and intravenous potassium can cause local irritation and arrhythmia, central access and continuous ECG monitoring are recommended for higher rates/concentrations. Oral therapy is too slow and may be impractical in profound paralysis. Potassium bicarbonate is not indicated unless there is concurrent metabolic acidosis and the potassium formulation should be KCl unless there is a specific reason to choose another salt. Insulin would shift potassium intracellularly and worsen hypokalaemia. Spironolactone is not an acute rescue therapy and would act too slowly.

Correct answer: Commence a potassium-binding agent and reintroduce/continue RAAS inhibitor with monitoring. Contemporary guidelines and expert opinion support using potassium binders (patiromer or sodium zirconium cyclosilicate) to control chronic hyperkalaemia so patients can continue guideline-directed RAAS blockade when clinically indicated, with regular monitoring. Permanently stopping an ACE inhibitor may deprive the patient of renal and cardiovascular benefit. Reducing dietary salt alone is insufficient and delaying reassessment is inappropriate. Oral sodium bicarbonate may help when chronic metabolic acidosis is present but is not the standard approach solely to control RAAS inhibitor–associated hyperkalaemia. Adding a diuretic can lower potassium in some patients, but its effectiveness depends on renal function and volume status and it may cause other problems; a potassium binder is the preferred step to enable continuation of RAASi when available and appropriate.

Correct answer: Despite hyperkalaemia at presentation, total body potassium is usually depleted and potassium replacement is generally required once insulin therapy commences. In DKA, insulin deficiency and acidosis cause potassium to shift out of cells, raising serum potassium despite total body potassium depletion due to osmotic diuresis and urinary losses. When insulin is given and acidosis corrected, potassium moves intracellularly and serum potassium falls, so potassium replacement is commonly necessary to avoid dangerous hypokalaemia. Serum potassium does not reliably reflect total body stores in this context. The other statements are incorrect: total body potassium is typically low, you should not withhold replacement solely because serum potassium is initially high, and DKA is associated with acidosis (not alkalosis) that shifts potassium out of cells.

Correct answer: Administer rasburicase and aggressive IV hydration. In patients at high risk for TLS (high tumour burden, high uric acid), rasburicase rapidly lowers uric acid by converting it to allantoin and, together with aggressive hydration and monitoring, reduces the risk of uric acid nephropathy and associated electrolyte derangements including hyperkalaemia. Allopurinol prevents formation of new uric acid but does not reduce existing uric acid rapidly and is less effective in high-risk TLS. A single dose of IV calcium does not prevent hyperkalaemia and may be harmful if potassium subsequently changes. Sodium polystyrene sulfonate has slow and variable onset and is not a prophylactic substitute for definitive TLS prevention. Withholding chemotherapy is not an appropriate prophylactic strategy; rather TLS risk should be mitigated to enable safe treatment.

Correct answer: Replace magnesium while continuing potassium. Hypomagnesaemia increases renal potassium loss by impairing the normal potassium‑conserving mechanisms; unless magnesium is corrected, hypokalaemia is often refractory to potassium repletion. Therefore magnesium replacement (oral or IV depending on severity) should be undertaken alongside potassium replacement. Increasing potassium alone without correcting magnesium frequently fails. Spironolactone can help potassium retention but is not the immediate primary step when hypomagnesaemia is present; also address the magnesium deficiency. IV calcium does not treat hypomagnesaemia. Switching diuretics may be considered in the long term but is not the immediate corrective measure for refractory hypokalaemia due to low magnesium.

Correct answer: Gitelman syndrome. Gitelman syndrome typically presents in adolescence or adulthood with hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria (low urinary calcium). Blood pressure is usually normal or low. Bartter syndrome classically presents earlier, often with salt wasting and hypercalciuria. Liddle syndrome causes hypertension with suppressed renin and aldosterone and features potassium wasting but without hypomagnesaemia and with hypertension. Primary hyperaldosteronism causes hypertension with suppressed renin and metabolic alkalosis but usually without hypomagnesaemia and often with normal/high urinary calcium. Apparent mineralocorticoid excess also causes hypertension and hypokalaemia; the presence of normal blood pressure and hypomagnesaemia with low urinary calcium points to Gitelman.

Correct answer: Review for reversible contributors and arrange prompt repeat potassium with close monitoring. In a clinically well patient with moderate hyperkalaemia and no ECG changes, immediate steps should focus on identifying and treating reversible causes (other medications such as NSAIDs, potassium supplements, trimethoprim; metabolic acidosis; constipation), dietary counselling, and repeating the potassium promptly to confirm persistence, while planning management (e.g. consider diuretics or potassium binders) rather than reflexively stopping RAAS inhibitors. Immediate dialysis is not indicated without ECG changes or refractory hyperkalaemia. Waiting months is unsafe. Chronic sodium polystyrene sulfonate is not recommended as the first-line long-term strategy because of tolerability and uncertainty about safety; newer binders are preferred. Spironolactone would increase potassium and worsen hyperkalaemia.

Correct answer: Perform urgent haemodialysis. In end-stage kidney disease with severe hyperkalaemia that is refractory or recurrent despite membrane stabilisation and potassium-shifting therapies, urgent haemodialysis is the definitive method to remove potassium quickly and is indicated, particularly when ECG changes persist or recur. Repeating calcium alone is only temporising. Nebulised salbutamol and bicarbonate can be adjuncts but are not definitive when hyperkalaemia rebounds in a dialysis patient. Oral patiromer is for chronic management and has slow onset; it is not appropriate for immediate control of life‑threatening hyperkalaemia. IV magnesium does not treat hyperkalaemia or stabilise the cardiac membrane in this context.