Key Facts

Hyperkalaemia is a potentially fatal electrolyte disturbance requiring urgent recognition and management. It is the most dangerous electrolyte abnormality due to its effect on cardiac conduction. Serum potassium >6.5 mmol/L with ECG changes is a medical emergency.

Epidemiology

• Occurs in up to 10% of hospitalised patients
• Prevalence increases significantly with CKD stage 3b-5 (up to 40-50%)
• More common in patients taking RAAS inhibitors (ACE inhibitors, ARBs, spironolactone)
• Leading cause of cardiac arrest in dialysis patients
• Incidence rising due to increased use of RAAS inhibitors and ageing population

Aetiology

• Reduced excretion: AKI, CKD, adrenal insufficiency (Addison disease), hypoaldosteronism, type 4 RTA
• Increased intake: potassium supplements, potassium-containing salt substitutes, massive transfusion
• Transcellular shift: metabolic acidosis, insulin deficiency (DKA), tissue necrosis, rhabdomyolysis, tumour lysis syndrome, burns, suxamethonium
• Drugs: ACE inhibitors, ARBs, spironolactone, eplerenone, amiloride, trimethoprim, NSAIDs, ciclosporin, tacrolimus, heparin
• Pseudohyperkalaemia: haemolysed sample, thrombocytosis (>500 × 10⁹/L), leucocytosis, prolonged tourniquet

Pathophysiology

• Potassium is the major intracellular cation (98% intracellular, 2% extracellular)
• Normal serum K+: 3.5-5.0 mmol/L; tightly regulated by renal excretion and cellular uptake
• Hyperkalaemia reduces the resting membrane potential of cardiac myocytes, increasing excitability initially then reducing conduction velocity
• Progressive depolarisation leads to impaired cardiac conduction, arrhythmias, and ultimately asystole or ventricular fibrillation

Symptoms

• Often asymptomatic until severe
• Muscle weakness (ascending, may mimic Guillain-Barré)
• Paraesthesiae and numbness
• Palpitations
• Nausea and diarrhoea
• Lethargy and fatigue

Signs

• Flaccid paralysis in severe cases
• Bradycardia or irregular pulse
• Hypotension in severe cases
• Reduced or absent tendon reflexes

ECG Changes (Progressive)

• Mild (5.5-6.0 mmol/L): Tall, peaked/tented T waves
• Moderate (6.0-7.0 mmol/L): Prolonged PR interval, flattened P waves, widened QRS
• Severe (>7.0 mmol/L): Sine wave pattern, ventricular fibrillation, asystole

Red Flags

• Any ECG changes with hyperkalaemia → immediate treatment required
• K+ >6.5 mmol/L even without ECG changes → urgent treatment
• Cardiac arrest (PEA/asystole) → consider hyperkalaemia as reversible cause (4 Hs and 4 Ts)

Bedside

• 12-lead ECG: essential – look for tall tented T waves, widened QRS, loss of P waves
• Capillary blood gas: rapid potassium result at bedside (within 1-2 minutes)
• Blood glucose: to guide insulin-dextrose therapy and exclude DKA
• Urine output monitoring: assess for oliguria/anuria

Bloods

• U&Es: potassium, sodium, urea, creatinine – assess renal function
• Venous blood gas: rapid K+ result, pH (acidosis drives K+ out of cells)
• Calcium: may be low (especially in CKD)
• Bicarbonate: low in metabolic acidosis
• CK: if rhabdomyolysis suspected
• Cortisol/short Synacthen test: if adrenal insufficiency suspected
• Digoxin level: if on digoxin (hyperkalaemia potentiates toxicity)

Imaging

• Renal ultrasound: if renal impairment of unclear cause (assess for obstruction)

Special Tests

• Continuous cardiac monitoring: essential during treatment
• Serial potassium measurements: every 1-2 hours during acute management
• Transtubular potassium gradient (TTKG): if cause unclear (low TTKG suggests hypoaldosteronism)

Emergency Management (K+ >6.5 or ECG changes)

Step 1 – Cardioprotection:

• Calcium gluconate 10% 30mL (3 ampoules) IV over 10 minutes – stabilises cardiac membrane; does NOT lower K+. Repeat after 5 minutes if ECG changes persist. Use calcium chloride 10% 10mL via central line if available.

Step 2 – Intracellular K+ shift:

• Insulin (Actrapid) 10 units + 50mL 50% glucose IV over 15-30 minutes – lowers K+ by 0.5-1.2 mmol/L within 15 minutes, lasts 4-6 hours. Monitor BM hourly for 6 hours (risk of hypoglycaemia 15-20%).
• Salbutamol 10-20mg nebulised – additional K+ shift (lowers K+ by ~0.5-1.0 mmol/L). Use with caution in cardiac patients.
• Sodium bicarbonate 1.26% 500mL IV – only if concurrent metabolic acidosis (pH <7.2)

Step 3 – Potassium removal:

• Calcium resonium (calcium polystyrene sulphonate) 15g TDS PO – onset 4-24 hours; can cause constipation/bowel necrosis
• Sodium zirconium cyclosilicate (Lokelma) 10g TDS for 72 hours, then 5-10g OD maintenance – faster onset, better tolerated
• Patiromer 8.4g OD – alternative oral K+ binder
• Haemodialysis: definitive treatment for refractory hyperkalaemia or K+ >7.0 mmol/L with ECG changes

Non-pharmacological

• Dietary potassium restriction (<40-60 mmol/day in CKD)
• Review and stop/reduce causative medications (ACE inhibitors, ARBs, spironolactone, NSAIDs)
• Ensure adequate hydration if pre-renal cause

Pharmacological (Chronic Management)

• Treat underlying cause (e.g., optimise CKD management)
• Sodium zirconium cyclosilicate 5-10g OD or patiromer 8.4-25.2g OD for chronic hyperkalaemia (enables continuation of RAAS inhibitors)
• Fludrocortisone 50-200mcg OD if hypoaldosteronism

Referral Criteria

• Refractory hyperkalaemia despite treatment → urgent nephrology/renal team
• K+ >7.0 mmol/L or haemodynamic instability → ICU
• Recurrent hyperkalaemia with CKD → nephrology for dialysis assessment

• Untreated severe hyperkalaemia (>7.0 mmol/L) carries a mortality rate of >50% from cardiac arrest
• With prompt treatment, >95% of episodes resolve without complications
• Hypoglycaemia complicates insulin-dextrose therapy in 15-20% of cases
• Patients on chronic dialysis have recurrent hyperkalaemia as the leading cause of death between dialysis sessions
• New potassium binders (Lokelma, patiromer) have reduced the need to discontinue RAAS inhibitors by 40-60%

Hyperkalaemia Treatment Algorithm

Drugs Causing Hyperkalaemia