Hyperkalemia

Hyperkalaemia is a serum potassium above 5.0–5.5 mEq/L; it is life-threatening above 6.5 mEq/L or with any ECG change.

Total body potassium is lower in the old because of reduced muscle mass and poor dietary intake, so a normal or high serum level may coexist with total-body depletion.

Renal potassium excretion is significantly reduced in ageing, explained by reduced serum aldosterone and reduced tubular responsiveness to aldosterone (hyporeninaemic hypoaldosteronism), plus increased activity of the H+/K+-ATPase pump in the collecting duct.

Reduced GFR with age means that any additional potassium load is poorly handled — the elderly kidney has little reserve.

Drugs are the dominant cause: ACE inhibitors, ARBs, mineralocorticoid receptor antagonists (spironolactone, eplerenone), potassium-sparing diuretics, NSAIDs, trimethoprim/co-trimoxazole, heparin, beta-blockers, digoxin toxicity, calcineurin inhibitors, and potassium supplements.

Renal: acute kidney injury, chronic kidney disease (especially stage 4–5), obstructive uropathy, and type 4 renal tubular acidosis (classically in diabetic nephropathy).

Transcellular shift: metabolic acidosis, insulin deficiency and hyperglycaemia, beta-blockade, rhabdomyolysis, tumour lysis syndrome, massive haemolysis, and suxamethonium.

Endocrine: adrenal insufficiency, isolated hypoaldosteronism.

Dietary/iatrogenic: potassium-based “low-sodium” salt substitutes (increasingly used in India for hypertension), coconut water, banana, citrus, stored blood transfusion.

Pseudohyperkalaemia — haemolysed sample, prolonged tourniquet, fist clenching, marked leucocytosis or thrombocytosis — must be excluded before treatment.

Symptoms are non-specific: muscle weakness, flaccid paralysis, paraesthesiae, palpitations, and sometimes cardiac arrest as the first manifestation.

Progressive ECG sequence: tall peaked T waves → flattened P waves with PR prolongation → widening QRS → sine wave pattern → asystole or ventricular fibrillation.

The ECG is insensitive — a normal ECG does not exclude dangerous hyperkalaemia, and the rate of rise matters as much as the absolute value.

1. Protect the myocardium: 10 mL of 10% calcium gluconate intravenously over 2–5 minutes, repeated if ECG changes persist. Onset is immediate but lasts only 30–60 minutes; use calcium chloride via a central line if severe. Use with great caution in digoxin toxicity.

2. Shift potassium into cells: 10 units of soluble insulin in 25 g of dextrose (50 mL of 50% or 125 mL of 20%) intravenously over 15–30 minutes, plus nebulised salbutamol 10–20 mg. Sodium bicarbonate only if there is significant metabolic acidosis.

3. Remove potassium from the body: loop diuretic with volume repletion, potassium binders, and haemodialysis for severe or refractory hyperkalaemia, oliguric AKI or ESRD.

4. Stop the source: discontinue causative drugs, potassium supplements and salt substitutes; restrict dietary potassium.

5. Monitor: continuous ECG, and repeat potassium at 1, 2, 4 and 6 hours — rebound hyperkalaemia is common once the insulin effect wanes.

Hypoglycaemia after insulin–dextrose is the commonest iatrogenic complication, occurring in up to a fifth of patients — particularly in the elderly, in CKD, and in those not eating; monitor capillary glucose hourly for at least 6 hours.

Long-term management aims to allow continuation of prognostically important RAAS inhibitors rather than stopping them: dietary counselling, correction of metabolic acidosis with sodium bicarbonate, use of loop or thiazide diuretics, and potassium binders.

Sodium polystyrene sulfonate is slow, unpalatable and carries a warning for serious gastrointestinal necrosis, especially with sorbitol — its role is now limited.