Hyperkalaemia ladder and acute hyponatraemic seizure

Part A — ECG-unstable hyperkalaemia. Treat immediately; calcium is first because the ECG shows cardiotoxicity.^[1][2]

1. Membrane stabilisation (does not lower K): calcium chloride 10 mL of 10% IV over 2–5 minutes (or calcium gluconate 30 mL of 10% IV). Protects the heart within minutes; re-dose if QRS remains wide.^[1][2]
2. Intracellular shift (temporary): soluble insulin 10 units IV with 50 mL of 50% dextrose (monitor glucose); nebulised salbutamol 10–20 mg; consider sodium bicarbonate IV if significantly acidotic and ventilating adequately.^[1]
3. Removal (definitive): enhance excretion / remove K — loop diuretic if residual renal function and volume allows; potassium binders (e.g. sodium zirconium cyclosilicate / patiromer per availability); urgent dialysis for refractory hyperK, anuria, severe AKI, or ongoing tissue release.^[1]
4. Continuous monitoring; treat cause (AKI, drugs, rhabdo); repeat ECG and K.

Part B — acute symptomatic hyponatraemia with seizure. This is cerebral oedema physiology. Give 3% hypertonic saline 100 mL IV bolus, repeated until seizures stop, aiming for a small controlled rise in Na (4–6 mmol/L) sufficient to stop seizures. Then slower correction. For chronic hyponatraemia, limit correction typically to ≤8 mmol/L in 24 hours (stricter 4–6 mmol/L limits in high osmotic-demyelination risk: chronic alcohol use, malnutrition, hypokalaemia, hypophosphataemia) with frequent Na checks. Do not use fluid restriction alone in a seizing patient — hypertonic saline is the treatment.^{[3][4][5][6][8]}