Hyperkalaemia

Hyperkalaemia is a serum potassium above the reference range, and is one of the few electrolyte abnormalities capable of causing cardiac arrest within minutes.

Severity is conventionally graded as mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L) and severe (≥6.5 mmol/L, or any level with ECG changes), though the rate of rise and the presence of ECG changes matter more than the number alone.

Causes fall into three groups: reduced excretion (acute kidney injury, chronic kidney disease, ACE inhibitors and ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, hypoaldosteronism), transcellular shift (metabolic acidosis, insulin deficiency, beta-blockers, digoxin toxicity, rhabdomyolysis, tumour lysis) and increased intake (supplements, transfusion of stored blood), usually only significant when excretion is already impaired.

Often asymptomatic and detected incidentally on blood tests taken for another reason; when symptoms occur they correlate poorly with the severity of the biochemical derangement, which is why the ECG and potassium level, not symptoms, drive the urgency of treatment.

• Cardiac: palpitations, and the ECG changes described under Diagnosis. The first clinical sign can be cardiac arrest, so the absence of symptoms never excludes danger
• Neuromuscular: weakness, classically ascending and starting in the legs; paraesthesiae; in severe cases, flaccid paralysis that can mimic Guillain-Barré syndrome
• Non-specific: fatigue, nausea

• ECG is the most important immediate investigation and should be obtained before waiting for confirmatory bloods in any patient with suspected hyperkalaemia. The classic progression is: tall, peaked T waves → flattening and loss of P waves → PR prolongation → widening QRS → sine wave pattern → ventricular fibrillation or asystole. However, ECG changes correlate imperfectly with potassium level, and their absence does not make a high potassium safe
• Serum potassium, urea and creatinine, bicarbonate and glucose
• Exclude pseudohyperkalaemia before treating an unexpected result in a well patient with a normal ECG, particularly if there was a difficult venepuncture, a tourniquet held long, fist clenching, or a markedly raised white cell or platelet count
• Venous blood gas gives a rapid potassium result while awaiting the laboratory value, and simultaneously assesses acid-base status
• Review medications systematically, since drug-induced hyperkalaemia is common and frequently multifactorial, an ACE inhibitor plus spironolactone plus an NSAID in a patient with declining renal function is a familiar and preventable combination
• Consider digoxin toxicity, rhabdomyolysis (creatine kinase) and adrenal insufficiency where the picture fits

Treatment follows three sequential aims: protect the heart, shift potassium into cells, then remove it from the body. The first two buy time; only the third actually lowers total body potassium.

1. Cardiac protection:

• Intravenous calcium (calcium gluconate 10% 10–30 mL, or calcium chloride via central access) for any ECG changes or potassium ≥6.5 mmol/L. It does not lower potassium but stabilises the myocardium within minutes. The dose can be repeated if ECG changes persist
• Calcium is given with more caution in digoxin toxicity, though the historical concern about precipitating irreversible cardiac arrest is now considered overstated

2. Shift potassium intracellularly:

• Insulin with glucose: typically 10 units of soluble insulin in 25 g of glucose intravenously, lowering potassium by roughly 0.6–1.0 mmol/L over 15–30 minutes. Hypoglycaemia is the commonest complication and often occurs late, so glucose must be monitored for several hours afterwards and a glucose infusion considered
• Nebulised salbutamol (10–20 mg) as an adjunct, additive to insulin, though tachycardia limits its use in ischaemic heart disease
• Sodium bicarbonate has a limited role, and is reserved for significant metabolic acidosis rather than used routinely

3. Remove potassium:

• Loop diuretics with adequate volume status
• Potassium binders: sodium zirconium cyclosilicate or patiromer, which are effective and better tolerated than older resins and have made outpatient management of chronic hyperkalaemia considerably more feasible
• Haemodialysis is definitive, and is indicated in severe or refractory hyperkalaemia, established kidney failure, or where potassium continues to rise despite medical therapy

Alongside: stop all contributing drugs and potassium supplements, treat the underlying cause, and recheck potassium within 1–2 hours since shifting agents wear off and rebound is common. A patient treated with insulin and salbutamol alone, without removal, will frequently rise again.

Referral: nephrology urgently for refractory hyperkalaemia or where dialysis may be needed; critical care for arrhythmia or haemodynamic instability.