NephrologyTier 1Disease (DEADMAN)

Electrolyte abnormalities - hypo- and hyperkalaemia

Description

Hypokalaemia <3.5 mmol/L, hyperkalaemia >5.0-5.5 mmol/L
Both are true deficit/excess or transcellular shift - the distinction changes management
Hyperkalaemia is the more immediately dangerous direction - arrhythmia and cardiac arrest can occur without warning ECG changes

Hypokalaemia - up to 20% of inpatients, mostly diuretic-related
Hyperkalaemia - ~1-10% of inpatients; strongly associated with CKD and RAAS-inhibitor use

Hypokalaemia

Shift: insulin, beta-agonists, alkalosis, refeeding
Renal loss: diuretics, mineralocorticoid excess, RTA type 1/2, Bartter/Gitelman, Mg2+ depletion (impairs renal K+ conservation)
Extrarenal loss: vomiting, diarrhoea, laxative abuse

Hyperkalaemia

Reduced excretion - AKI/CKD (commonest cause), RAAS inhibitors (ACEi/ARB, spironolactone/MRA), NSAIDs, trimethoprim, type 4 RTA, Addison's
Shift out of cells: acidosis, insulin deficiency, tissue breakdown (rhabdomyolysis, tumour lysis, haemolysis), beta-blockade, digoxin toxicity
Excess intake - usually only causes hyperkalaemia with impaired excretion (salt substitutes, IV replacement error)
Pseudohyperkalaemia - haemolysed sample, prolonged tourniquet, marked thrombocytosis/leucocytosis - repeat before treating an asymptomatic patient

Hypokalaemia

Hyperkalaemia

Always get an ECG immediately - peaked T waves -> widened QRS -> sine wave -> VF/asystole
- ECG changes correlate poorly with K+ level - treat a compatible ECG as an emergency regardless of the number, and do not delay treatment awaiting confirmation of a critical result
VBG (acidosis), UEC (renal function), CK (rhabdomyolysis), review medication list

Hypokalaemia

Oral if K+ >2.5-3.0 and asymptomatic; IV if severe/symptomatic/ECG change
Max peripheral IV rate ~10 mmol/h (up to 20 mmol/h centrally with cardiac monitoring); never IV push
Correct Mg2+ concurrently - hypokalaemia will not correct otherwise

Hyperkalaemia - stabilise, shift, remove

Step	Agent	Effect
1. Stabilise myocardium	IV calcium gluconate 10%	Onset mins, no effect on K+ level - repeat if ECG changes persist
2. Shift K+ intracellularly	Insulin (10 units) + 50 mL 50% dextrose; salbutamol nebulised	Onset ~15-30 min, lasts hours; salbutamol not used as monotherapy
3. Remove K+	Loop diuretic (if adequate renal function), dialysis (severe/refractory/AKI)	Definitive removal
Correct acidosis	Sodium bicarbonate	Adjunct if significant metabolic acidosis present

Monitor glucose after insulin/dextrose - delayed hypoglycaemia is a recognised harm; consider glucose-only if patient already hyperglycaemic
Potassium binders - sodium zirconium cyclosilicate or patiromer - for outpatient/subacute persistent hyperkalaemia (esp. enabling RAASi continuation in CKD/HF), not for acute severe hyperkalaemia (onset hours, not minutes)
Stop/reduce causative drugs where safe; avoid reflexively ceasing RAASi in HF - weigh cardioprotective benefit against hyperkalaemia risk, use binders to allow continuation where possible

Hypokalaemia - rhabdomyolysis, ileus, nephrogenic DI, digoxin toxicity potentiation
Hyperkalaemia - CKD, RAAS-inhibitor use, Addison's disease, tumour lysis syndrome, rhabdomyolysis

Hyperkalaemia can progress from normal ECG to cardiac arrest with little warning - lowest threshold for urgent treatment of any electrolyte emergency
Chronic RAASi-associated hyperkalaemia in CKD/HF - binder therapy now allows most patients to remain on guideline-directed therapy rather than stopping it
Recurrent unexplained hypo/hyperkalaemia - investigate for RTA or mineralocorticoid axis disorder rather than treating repeatedly in isolation

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