📋 Key Information Summary
- Normal serum potassium (K⁺) is 3.5–5.0 mmol/L; values outside this range require urgent clinical assessment and serial ECG monitoring.
- Hypokalaemia (K⁺ <3.5 mmol/L) causes characteristic ECG changes including U waves, ST depression, T-wave flattening, and increased risk of torsades de pointes.
- The most common causes of hypokalaemia are diuretic therapy (frusemide, thiazides), gastrointestinal losses (vomiting, diarrhoea), and renal tubular disorders.
- Oral potassium chloride (KCl) is first-line for mild–moderate hypokalaemia; IV KCl is reserved for severe hypokalaemia (K⁺ <2.5 mmol/L), symptomatic patients, or those unable to tolerate oral replacement.
- IV KCl must be administered at ≤20 mmol/hour via infusion pump in normal saline or glucose-free solution; concentrations >40 mmol/L require a central line and cardiac monitoring.
- Hyperkalaemia (K⁺ >5.0 mmol/L) is a medical emergency when K⁺ >6.5 mmol/L or ECG changes are present; it may cause fatal ventricular fibrillation without warning.
- ECG signs of hyperkalaemia progress from peaked T waves → PR prolongation → QRS widening → loss of P waves → sine-wave pattern → asystole/VF.
- The hyperkalaemia emergency protocol prioritises myocardial membrane stabilisation (IV calcium gluconate 10%, 10 mL over 10 min) before potassium-lowering measures.
- Insulin-dextrose (Actrapid 10 units + 50 mL 50% glucose IV over 15–30 min) shifts potassium intracellularly and lowers serum K⁺ by 0.5–1.2 mmol/L within 30–60 minutes.
- Sodium polystyrene sulfonate (Resonium A®) or calcium resonium provides enteral potassium elimination over 1–6 hours; patiromer and sodium zirconium cyclosilicate are newer agents.
- All patients with severe hypokalaemia or hyperkalaemia require continuous cardiac telemetry and serial potassium monitoring every 1–2 hours until stable.
- Aboriginal and Torres Strait Islander peoples experience a higher burden of chronic kidney disease and thus potassium disorders; culturally safe management and remote-area protocols are essential.
Introduction & Australian Epidemiology
Potassium is the principal intracellular cation, with approximately 98% of total body potassium located within cells and only 2% in the extracellular fluid. The narrow normal serum potassium range of 3.5–5.0 mmol/L is tightly regulated by renal excretion, cellular shift mechanisms (primarily insulin- and catecholamine-mediated), and gastrointestinal secretion. Disruptions in potassium homeostasis are common in clinical practice and may be rapidly life-threatening — particularly hyperkalaemia, which can precipitate fatal ventricular fibrillation without preceding warning symptoms.
In Australia, electrolyte disturbances are among the most frequently encountered laboratory abnormalities. Hypokalaemia is identified in approximately 20% of hospitalised patients, while hyperkalaemia affects up to 10% of admissions, with markedly higher prevalence among patients with chronic kidney disease (CKD), heart failure, and those taking renin–angiotensin–aldosterone system (RAAS) inhibitors or potassium-sparing diuretics.
The Australian Institute of Health and Welfare (AIHW) reports that CKD — a leading driver of hyperkalaemia — affects approximately 1 in 10 Australians, with disproportionate burden in Aboriginal and Torres Strait Islander communities. With an ageing population, rising prevalence of diabetes mellitus, and widespread use of RAAS blockade for cardiorenal protection, the clinical significance of potassium disorders in Australian practice continues to grow.
This guideline provides a comprehensive, evidence-based approach to the assessment and management of both hypokalaemia and hyperkalaemia in Australian clinical settings, incorporating PBS-listed therapies, standard emergency protocols, and considerations for special populations.
Hypokalaemia: Causes & ECG Changes
Definition & Severity Classification
Mild
K⁺ 3.0–3.4 mmol/L
Often asymptomatic; may notice mild fatigue, muscle cramps, or constipation.
Setting: Outpatient / GP management
Moderate
K⁺ 2.5–2.9 mmol/L
Muscle weakness (particularly proximal lower limbs), hyporeflexia, ileus, polyuria. ECG changes may appear.
Setting: Hospital admission recommended
Severe
K⁺ <2.5 mmol/L
Flaccid paralysis, respiratory compromise, rhabdomyolysis, cardiac arrhythmias including torsades de pointes.
Setting: ICU / HDU with continuous telemetry
Causes of Hypokalaemia
The differential diagnosis is approached by mechanism: reduced intake, intracellular shift, or increased losses (renal or gastrointestinal).
| Mechanism | Examples | Clinical Clues |
|---|---|---|
| Inadequate intake | Starvation, anorexia nervosa, alcoholism, clay ingestion | Low dietary potassium; often chronic and mild |
| Intracellular shift | Insulin therapy, β₂-agonists (salbutamol), alkalosis, hypothermia, thyrotoxic periodic paralysis | Acute onset; total body K⁺ may be normal |
| Renal losses | Loop diuretics (frusemide), thiazide diuretics, amphotericin B, renal tubular acidosis (Type 1 & 2), hypomagnesaemia, primary hyperaldosteronism, Gitelman syndrome, Bartter syndrome | Spot urine K⁺ >20 mmol/L; metabolic alkalosis often present |
| GI losses | Vomiting, nasogastric drainage, diarrhoea, laxative abuse, villous adenoma | Spot urine K⁺ <20 mmol/L; diarrhoea causes hyperchloraemic metabolic acidosis; vomiting causes metabolic alkalosis |
| Skin losses | Excessive sweating, burns, cystic fibrosis | Usually mild unless extreme |
Hypokalaemia potentiates digoxin toxicity. In patients taking digoxin, even mild hypokalaemia (K⁺ 3.0–3.5 mmol/L) significantly increases the risk of life-threatening arrhythmias. Maintain K⁺ ≥4.0 mmol/L in all digoxin-treated patients.
ECG Changes in Hypokalaemia
ECG changes correlate imperfectly with serum potassium levels but are critical for risk assessment:
- Early: T-wave flattening and U-wave prominence (U wave >T wave in same lead)
- Moderate: ST-segment depression, prolonged QT interval (actually QU interval), T–U fusion
- Severe: Prominent U waves, ventricular ectopy, torsades de pointes (polymorphic VT), ventricular fibrillation
The U wave is the hallmark ECG finding in hypokalaemia — best seen in leads V₂–V₄. Concurrent hypomagnesaemia increases arrhythmia risk independently and must always be checked and corrected.
Hypokalaemia Management (IV/Oral KCl, Treat Cause)
General Principles
- Always identify and treat the underlying cause (e.g., cease offending diuretic, treat diarrhoea, correct hypomagnesaemia).
- Concurrent hypomagnesaemia must be corrected — refractory hypokalaemia will not resolve until magnesium is replete.
- Oral replacement is preferred whenever feasible due to safety and efficacy.
- A 20 mmol oral KCl dose raises serum K⁺ by approximately 0.1–0.2 mmol/L in patients with normal renal function.
- Maximum recommended IV KCl infusion rate: 20 mmol/hour via peripheral line; 40 mmol/hour via central line with continuous telemetry in ICU.
Pharmacotherapy
Potassium Chloride (Slow-K®)
Slow-K® · Span-K® · Chlorvescent® · Oral effervescent tablets
Adult dose
20–40 mmol PO TDS–QDS; effervescent tablets dissolved in water to reduce GI irritation
Paediatric dose
1–2 mmol/kg/day PO divided into 3–4 doses (max 40 mmol/dose)
Route
Oral
Key notes
Take with food and full glass of water; avoid in patients with GI obstruction or dysphagia
Renal adjustment
Use with caution in CKD G4–5; monitor closely
PBS status
✔ PBS General Benefit
Potassium Chloride (IV)
Potassium chloride 0.9% or 10% injection · In normal saline or Plasmalyte
Adult dose
10–20 mmol/hour IV infusion via syringe driver or infusion pump; max 20 mmol/hour via peripheral line
Severe / ICU
Up to 40 mmol/hour via central venous catheter with continuous cardiac monitoring
Paediatric dose
0.2–0.5 mmol/kg/hour IV (max 1 mmol/kg/hour in ICU); cardiac monitoring mandatory
Key safety
NEVER give IV push bolus; NEVER add to glucose/dextrose solutions (worsens hypokalaemia via insulin-mediated shift)
Monitoring
Serial K⁺ every 2–4 hours; continuous ECG telemetry if rate >10 mmol/hour
PBS status
✔ PBS General Benefit (inpatient)
Critical safety warning: IV potassium chloride is a high-alert medication in Australian hospitals. Never administer as an IV bolus — risk of fatal cardiac arrest. Always use an infusion pump. Concentrated KCl (10%) must never be administered via peripheral IV line without dilution. Follow your institution's high-alert medication policy.
Additional Agents for Refractory Hypokalaemia
- Magnesium replacement: Magnesium sulfate 1–2 g IV over 1–2 hours (or 600 mg PO TDS as MgO). Check serum Mg²⁺ — target ≥0.7 mmol/L. Without magnesium repletion, potassium correction will be refractory.
- Spironolactone / Eplerenone: In hyperaldosteronism-mediated hypokalaemia, potassium-sparing diuretics can help maintain K⁺ within normal range.
- Amiloride: 5–10 mg PO daily; useful in Gitelman syndrome and lithium-induced nephrogenic diabetes insipidus with potassium wasting.
Treatment Algorithm
1
Assess severity & symptoms
12-lead ECG, serum K⁺, Mg²⁺, renal function. Determine if patient is symptomatic (weakness, arrhythmia, respiratory compromise).
2
Mild (K⁺ 3.0–3.4) — Oral replacement
KCl 20–40 mmol PO TDS; correct Mg²⁺; review medications; repeat K⁺ in 24–48 hours.
3
Moderate (K⁺ 2.5–2.9) — Oral ± IV
Oral KCl 40 mmol QDS; if unable to tolerate oral or not responding, commence IV KCl 10 mmol/hr. Monitor K⁺ every 4 hours.
4
Severe (K⁺ <2.5) or symptomatic — IV replacement
IV KCl 20 mmol/hr via central line (10 mmol/hr peripheral max if no central access). Continuous telemetry. Correct Mg²⁺ aggressively. Repeat K⁺ every 1–2 hours.
Hyperkalaemia: Causes & ECG Changes
Definition & Severity Classification
Mild
K⁺ 5.1–5.9 mmol/L
Usually asymptomatic; review medications and renal function. Rule out pseudohyperkalaemia (haemolysed sample, prolonged tourniquet, severe thrombocytosis/leucocytosis).
Setting: Outpatient / GP with urgent review
Moderate
K⁺ 6.0–6.4 mmol/L
May present with paraesthesiae, muscle weakness, palpitations. ECG changes may be present. Requires hospital admission.
Setting: Hospital admission, cardiac monitoring
Severe / Emergency
K⁺ ≥6.5 mmol/L or ECG changes at any level
Risk of fatal arrhythmia (VF, asystole). Muscle paralysis, respiratory failure. Treat as medical emergency.
Setting: ED / ICU — immediate intervention
Causes of Hyperkalaemia
| Mechanism | Examples | Clinical Clues |
|---|---|---|
| Reduced renal excretion | CKD (GFR <30), acute kidney injury, Type 4 RTA, potassium-sparing diuretics (spironolactone, amiloride, eplerenone), RAAS inhibitors (ACEi, ARB, direct renin inhibitors), NSAIDs, trimethoprim | Most common cause; check eGFR and medication reconciliation |
| Transcellular shift (out of cells) | Metabolic acidosis, insulin deficiency (DKA), β-blockers (non-selective), digitalis toxicity, succinylcholine, hyperosmolality, tissue necrosis (rhabdomyolysis, burns, tumour lysis syndrome, severe trauma) | Acute rise; total body K⁺ may be normal or low |
| Excessive intake | IV KCl excess, salt substitutes (KCl-based), massive blood transfusion, potassium-rich diet in setting of impaired renal function | Rarely causes hyperkalaemia alone without impaired excretion |
| Pseudohyperkalaemia | Haemolysed sample, prolonged tourniquet/clenching, severe thrombocytosis (>500 × 10⁹/L), severe leucocytosis (>100 × 10⁹/L) | Repeat sample with minimal tourniquet time; plasma K⁺ vs serum K⁺ may help differentiate |
| Adrenal insufficiency | Primary adrenal failure (Addison disease), congenital adrenal hyperplasia, heparin therapy | Hyperkalaemia + hyponatraemia + hypotension is the classic triad |
Drug-induced hyperkalaemia is the most common iatrogenic cause in Australia. The combination of an ACE inhibitor (or ARB) + spironolactone + NSAID ("triple whammy") is a particularly high-risk regimen. Always check renal function and K⁺ within 1–2 weeks of starting or uptitrating RAAS blockade.
ECG Changes in Hyperkalaemia
ECG changes are the most important bedside indicator of hyperkalaemia severity and the need for emergent treatment. Changes progress in a predictable sequence:
K⁺ 5.5–6.5
Peaked T waves — tall, narrow, symmetrically peaked ("tenting") T waves, best seen in leads V₂–V₄ and II.
K⁺ 6.5–7.5
PR prolongation → loss of P waves — first-degree AV block progressing to absent P waves; atrial standstill.
K⁺ 7.0–8.0
QRS widening — progressive QRS complex broadening; may resemble LBBB or RBBB pattern; S waves deepen in lateral leads.
K⁺ >8.0
Sine-wave pattern → VF / asystole — merging of QRS and T wave producing a sinusoidal pattern; imminent cardiac arrest without intervention.
Critical: ECG changes may occur at any serum K⁺ level and do not always correlate with the absolute value. If ECG changes consistent with hyperkalaemia are present — treat as an emergency regardless of the lab value. Conversely, severe hyperkalaemia (K⁺ >7.0 mmol/L) may occasionally present with a near-normal ECG initially.
Hyperkalaemia Emergency Management
The emergency management of hyperkalaemia follows a structured protocol targeting three goals: (1) myocardial membrane stabilisation, (2) intracellular potassium shift, and (3) total body potassium elimination. All three measures should be initiated simultaneously in severe hyperkalaemia.
Immediate Emergency Protocol
1
Resuscitate & monitor
Continuous cardiac telemetry, IV access, 12-lead ECG. Call for senior help. Urgent bloods: K⁺, Ca²⁺, Mg²⁺, renal function, venous blood gas. Alert laboratory to expedite K⁺ result.
2
Membrane stabilisation — Calcium
Calcium gluconate 10% — 10 mL (2.2 mmol Ca²⁺) IV over 10 minutes. Repeat if ECG changes persist after 5 minutes. Use calcium chloride 10% (6.8 mmol Ca²⁺ per 10 mL) only if central line in situ or cardiac arrest. Effect within 1–3 minutes, lasts 30–60 minutes.
3
Intracellular K⁺ shift — Insulin-Dextrose
Actrapid® (regular insulin) 10 units IV bolus + 50 mL of 50% glucose (25 g) IV over 15–30 minutes. Onset 15–30 min; peak effect 30–60 min; lowers K⁺ by 0.5–1.2 mmol/L. Monitor blood glucose hourly for 6 hours — risk of hypoglycaemia.
4
K⁺ elimination — Resonium / Dialysis
Sodium polystyrene sulfonate (Resonium A®) 15–30 g PO (or 30–50 g rectally as retention enema). Onset 1–6 hours; removes ~0.5–1 mmol K⁺ per gram. Consider haemodialysis in refractory hyperkalaemia, oliguric AKI, or CKD G5.
Pharmacotherapy — Emergency Agents
Calcium Gluconate 10%
Calcium gluconate injection 10% · Myocardial membrane stabiliser
Adult dose
10 mL (2.2 mmol Ca²⁺) IV over 10 minutes; repeat ×1 if ECG changes persist at 5 min
Paediatric dose
0.5 mL/kg of 10% solution IV over 5–10 min (max 10 mL); cardiac monitoring
Key notes
Does NOT lower serum K⁺; stabilises cardiac membrane only. Compatible with digitalis — calcium chloride is contraindicated with digoxin toxicity. Effect lasts 30–60 min; repeat if rebound ECG changes.
PBS status
✔ PBS General Benefit
Insulin-Dextrose Infusion
Actrapid® (regular insulin) + 50% glucose · Intracellular K⁺ shift
Adult dose
Actrapid 10 units IV + 50 mL 50% glucose (25 g) IV over 15–30 min
If glucose >14 mmol/L
Omit dextrose; give insulin alone with close glucose monitoring every 30 min
Paediatric dose
Insulin 0.1 units/kg IV + glucose 0.5 g/kg IV; discuss with paediatric endocrinology
Onset / Duration
Onset 15–30 min; peak 30–60 min; duration 4–6 hours; K⁺ rebound common
Monitoring
Blood glucose every 30 min for 2 hours, then hourly for 6 hours. Treat hypoglycaemia (<4 mmol/L) with 50 mL 50% glucose IV
PBS status
✔ PBS General Benefit (inpatient)
Salbutamol (High-Dose Nebulised)
Airomir® / Ventolin® · β₂-agonist · Adjunctive K⁺ shift
Adult dose
10–20 mg nebulised over 15 minutes (via high-output nebuliser)
Effect
Lowers K⁺ by ~0.5 mmol/L; onset 30 min; additive effect with insulin-dextrose
Cautions
Use with caution in ischaemic heart disease, tachyarrhythmias; may cause tachycardia and tremor
PBS status
✔ PBS General Benefit
Sodium Polystyrene Sulfonate (Resonium A®)
Resonium A® · Calcium resonium · Cation-exchange resin
Adult PO dose
15 g PO TDS dissolved in 50–100 mL water; may mix with sorbitol 70% 15 mL to reduce constipation risk
Adult rectal dose
30–50 g as retention enema in 100–200 mL water; retain for 30–60 min
Onset
1–6 hours; removes ~0.5–1 mmol K⁺ per gram of resin
Cautions
Risk of colonic necrosis (especially post-operatively or with sorbitol); avoid in bowel obstruction, post-op, neonates; sodium load in heart failure
PBS status
✔ PBS General Benefit
Newer Potassium-Binding Agents
| Agent | Dose | Onset | PBS Status | Notes |
|---|---|---|---|---|
| Patiromer (Veltassa®) | 8.4 g PO daily | 7 hours | ✘ Not PBS listed | For chronic hyperkalaemia in CKD on RAAS blockade; TGA-approved; separate from other oral medications by 3 hours |
| Sodium Zirconium Cyclosilicate (Lokelma®) | 10 g PO TDS (acute); 5–10 g daily (maintenance) | 1–6 hours | ✘ Not PBS listed | Faster onset than patiromer; TGA-approved; sodium load — use with caution in heart failure |
Definitive Therapy — Haemodialysis
Indications for urgent haemodialysis: Refractory hyperkalaemia (K⁺ not responding to medical therapy), oliguric/anuric acute kidney injury, severe CKD (GFR <15) not yet on dialysis presenting with K⁺ >6.5, concurrent fluid overload or metabolic acidosis requiring dialysis. Intermittent haemodialysis removes potassium more rapidly than peritoneal dialysis or CRRT.
Ongoing Monitoring & Disposition
- Repeat serum K⁺ at 1 hour, 2 hours, and 4 hours post-treatment, then 6–hourly until stable.
- Continuous cardiac telemetry for minimum 6 hours after K⁺ normalisation (rebound hyperkalaemia common).
- Monitor blood glucose every 30 min for 2 hours post insulin-dextrose; maintain glucose >4.0 mmol/L.
- Identify and cease offending medications (ACEi/ARB, spironolactone, NSAIDs, trimethoprim, potassium supplements).
- Treat underlying cause (rhabdomyolysis, DKA, AKI).
Investigations
Essential
Serum Potassium (Lithium Heparin)
MBS Item 66515 (Electrolyte panel). Ensure non-haemolysed sample; avoid prolonged tourniquet. Results within 30–60 min in Australian hospital laboratories.
Essential
12-Lead ECG
Bedside ECG — perform immediately in all suspected potassium disorders. Serial ECGs to track progression or response to therapy.
Essential
Renal Function (eGFR, Creatinine, Urea)
MBS Item 66515. Essential to determine renal potassium handling capacity and guide therapy selection.
Available
Serum Magnesium
MBS Item 66515. Critical in hypokalaemia — refractory hypokalaemia is often due to concurrent hypomagnesaemia.
Available
Venous Blood Gas (VBG)
Rapid point-of-care testing; provides K⁺, pH, bicarbonate, lactate. Useful for urgent assessment while lab results pending.
Available
Spot Urine Potassium & Creatinine
Transtubular K⁺ gradient (TTKG) or urine K⁺/creatinine ratio differentiates renal from GI losses in hypokalaemia.
Available
Serum Calcium, Phosphate, Bicarbonate
MBS Item 66515. Concurrent electrolyte disturbances common; metabolic acidosis/alkalosis influences potassium handling.
Consider Referral
Renin–Aldosterone Ratio
If primary hyperaldosteronism suspected (hypokalaemia + hypertension). Endocrinology referral required. Collect with patient seated, off interfering medications for 4 weeks.
Specialist
Haemodialysis Access Assessment
For refractory hyperkalaemia requiring dialysis. Nephrology team for urgent vascular access or peritoneal dialysis catheter.
Monitoring
| Scenario | K⁺ Monitoring Frequency | ECG Monitoring | Glucose Monitoring |
|---|---|---|---|
| Mild hypokalaemia (outpatient) | Repeat in 24–48 hours | 12-lead ECG at baseline | Not required |
| Moderate–severe hypokalaemia (IV KCl) | Every 2–4 hours during infusion | Continuous telemetry | Not required unless diabetic |
| Mild–moderate hyperkalaemia (no ECG changes) | Every 2–4 hours until <5.5 | Telemetry recommended | Not required unless insulin given |
| Severe hyperkalaemia (emergency treatment) | Every 1 hour for 4 hours, then every 2 hours | Continuous telemetry — minimum 6 hours post-normalisation | Every 30 min for 2 hours post insulin-dextrose; then hourly × 6 hours |
Special Populations
Pregnancy
Physiological changes
Increased GFR and aldosterone in pregnancy lower serum K⁺ by ~0.2–0.3 mmol/L. Mild hypokalaemia (3.2–3.5) is common and usually benign.
Hyperkalaemia management
Calcium gluconate and insulin-dextrose are safe in pregnancy. Avoid sodium polystyrene sulfonate — limited safety data. Avoid patiromer and SZC — not studied in pregnancy.
Medications
ACE inhibitors and ARBs are teratogenic — contraindicated in pregnancy. Spironolactone has anti-androgenic effects — avoid, especially in second/third trimester.
Paediatrics
Hypokalaemia IV replacement
0.2–0.5 mmol/kg/hour via syringe driver (max 1 mmol/kg/hour in ICU). Cardiac monitoring mandatory. Higher risk of cardiac arrhythmias than adults.
Hyperkalaemia in neonates
Non-oliguric hyperkalaemia is common in extremely preterm neonates (<28 weeks). Salbutamol nebuliser (4 μg/kg) is often first-line in NICU settings. Calcium gluconate 0.5 mL/kg of 10% over 5–10 min.
Diarrhoeal illness
Paediatric gastroenteritis is the most common cause of hypokalaemia in children in Australia. ORS with adequate potassium is first-line; IV KCl if severe or unable to tolerate oral.
Elderly
Reduced renal reserve
Age-related decline in GFR increases susceptibility to hyperkalaemia, particularly with RAAS inhibitors and potassium-sparing diuretics.
Polypharmacy
Triple whammy (ACEi + spironolactone + NSAID) is particularly dangerous in elderly patients. Consider medicines review via RACGP-aligned GP management plan.
Diuretic use
Thiazide-induced hypokalaemia is very common. Monitor K⁺ at 1–2 weeks after commencing thiazides and regularly thereafter.
Renal Impairment
CKD G3–4
Increased hyperkalaemia risk with RAAS blockade. Target K⁺ 4.0–5.0 mmol/L. May require dose reduction of RAAS inhibitors rather than cessation to preserve cardiorenal benefits.
CKD G5 / Dialysis
Hyperkalaemia is a leading cause of sudden cardiac death in dialysis patients. Dietary potassium restriction (as per renal dietitian). Adjust dialysate K⁺ concentration (typically 2 mmol/L) for interdialytic hyperkalaemia.
Acute kidney injury
Oliguric AKI rapidly causes hyperkalaemia. Low threshold for haemodialysis if medical management fails or K⁺ >7.0 despite treatment.
Hepatic Impairment
Diuretic-related
Spironolactone (used for ascites) causes hyperkalaemia; frusemide causes hypokalaemia. The combination is used to balance K⁺. Monitor frequently.
Insulin resistance
Advanced liver disease impairs insulin-mediated K⁺ shift, increasing susceptibility to hyperkalaemia. Dose-adjust insulin-dextrose cautiously.
Immunocompromised
Amphotericin B
IV amphotericin B causes renal tubular damage and hypokalaemia. Monitor K⁺ and Mg²⁺ daily. Liposomal formulations (AmBisome®) reduce but do not eliminate nephrotoxicity.
Calcineurin inhibitors
Tacrolimus and cyclosporin cause hyperkalaemia via hypoaldosteronism (Type 4 RTA). Common post-transplant; monitor K⁺ closely.
Tumour lysis syndrome
Acute hyperkalaemia from massive cell lysis — one of the most dangerous complications. Rasburicase, insulin-dextrose, and early dialysis may be required.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
📚 References
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