Electrolyte Emergencies

Quick Answer

One-liner: Life-threatening electrolyte disturbances require immediate ECG monitoring, targeted correction at safe rates, and treatment of underlying cause to prevent cardiac arrest and neurological complications.

Electrolyte emergencies are critical disturbances in serum potassium, sodium, calcium, or magnesium that pose immediate threats to cardiac conduction, neuromuscular function, and consciousness. Severe hyperkalaemia (K+ greater than 6.5 mmol/L) causes peaked T waves and widened QRS requiring urgent calcium for membrane stabilisation. Hypokalemia (below 2.5 mmol/L) causes U waves and dysrhythmias requiring careful replacement. Severe hyponatraemia (Na+ below 120 mmol/L) with seizures demands 3% saline 100 mL bolus with strict correction limits. Hypernatraemia (greater than 160 mmol/L) requires free water replacement over 48-72 hours to prevent cerebral oedema. Hypocalcaemia causes tetany and QT prolongation requiring IV calcium gluconate. Hypercalcaemic crisis (Ca2+ greater than 3.5 mmol/L) requires aggressive IV hydration plus calcitonin and bisphosphonates. Mortality approaches 15% in untreated severe dyselectrolytemias, but drops to below 3% with timely recognition and targeted therapy.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Cardiac conduction system (SA node, AV node, His-Purkinje), neuromuscular junction, renal tubular anatomy (Loop of Henle, DCT, collecting duct)
• Physiology: Transmembrane potentials, action potential generation, sodium-potassium ATPase, aldosterone-renin-angiotensin system, ADH/vasopressin regulation, PTH-calcium homeostasis, cardiac electrophysiology
• Pharmacology: Calcium salts (gluconate vs chloride), insulin-dextrose kinetics, salbutamol beta-2 agonist mechanism, loop/thiazide diuretics, patiromer, sodium bicarbonate, bisphosphonates, calcitonin

Fellowship Exam Relevance

• Written: High-yield SAQ topic - immediate management of severe hyperkalaemia, hyponatraemia correction rates and osmotic demyelination, hypernatraemia free water deficit calculation, hypocalcaemia tetany management
• OSCE: Resuscitation station (hyperkalaemic cardiac arrest), ECG interpretation (peaked T waves, sine wave, U waves, QT prolongation), communication station (discussing dialysis, risks of correction), clinical examination (Trousseau/Chvostek signs, volume assessment)
• Key domains tested: Medical Expert (recognition and immediate management), Collaborator (coordinating multidisciplinary care with ICU/renal/endocrine), Health Advocate (Indigenous populations at higher risk for CKD-related dyselectrolytemias)

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Key Points

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Epidemiology

Australian/NZ Specific

• Aboriginal and Torres Strait Islander peoples have 3-4x higher rates of CKD leading to chronic hyperkalaemia and hyperphosphataemia requiring more frequent ED presentations [11,12]
• Māori and Pacific Islander populations have 2-3x higher rates of diabetes mellitus and consequent hyperkalaemia from diabetic nephropathy and RAAS inhibitor use [13]
• Remote/rural areas have limited access to dialysis (RFDS retrieval often required for hyperkalaemic emergencies) [14]
• Tropical Northern Australia: higher rates of rhabdomyolysis from exertional heat stroke leading to hyperkalaemia, hyperphosphataemia, and hypocalcaemia [15]

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Pathophysiology

Normal Electrolyte Homeostasis

Potassium (K+):

• Normal range: 3.5-5.0 mmol/L
• 98% intracellular (140 mmol/L), 2% extracellular (4.0 mmol/L)
• Regulation: Aldosterone (distal tubule K+ secretion), insulin (Na-K-ATPase activity), beta-2 agonists (cellular shift)
• Transmembrane gradient critical for resting membrane potential (-90 mV)

Sodium (Na+):

• Normal range: 135-145 mmol/L
• Main determinant of serum osmolality (2 x Na+ + glucose + urea)
• Regulation: ADH/vasopressin (water retention), aldosterone (sodium retention), natriuretic peptides

Calcium (Ca2+):

• Normal total calcium: 2.15-2.55 mmol/L (8.6-10.2 mg/dL)
• Normal ionised calcium: 1.15-1.30 mmol/L (physiologically active form)
• Regulation: PTH (increased resorption, increased vitamin D activation), calcitonin (decreased resorption), vitamin D (increased intestinal absorption)

Pathological Mechanisms

Hyperkalaemia

1. Decreased renal excretion: AKI/CKD, RAAS inhibitors (ACEi, ARB, spironolactone), NSAIDs, trimethoprim, ciclosporin
2. Transcellular shift: Metabolic acidosis (H+ enters cells, K+ exits), insulin deficiency (DKA), beta-blockers, digoxin toxicity, succinylcholine, massive cell lysis (rhabdomyolysis, tumour lysis syndrome)
3. Excessive intake: KCl supplements, salt substitutes, massive blood transfusion (stored blood K+ 50-70 mmol/L)

Cardiac toxicity mechanism: Hyperkalaemia decreases resting membrane potential (less negative, e.g., -70 mV) resulting in faster Phase 0 depolarisation, shortened action potential, and ECG changes:

• 5.5-6.5 mmol/L: Peaked T waves (repolarisation changes)
• 6.5-7.5 mmol/L: Prolonged PR, widened QRS (conduction slowing)
• greater than 7.5 mmol/L: Loss of P wave, sine wave, VF, asystole

Hypokalaemia

1. Decreased intake: Malnutrition, anorexia nervosa, alcoholism
2. GI losses: Vomiting, diarrhoea, laxative abuse, ileostomy/colostomy
3. Renal losses: Loop/thiazide diuretics, hyperaldosteronism (Conn's), RTA types 1 and 2, hypomagnesaemia, Bartter/Gitelman syndromes
4. Transcellular shift: Insulin, beta-2 agonists, alkalosis, hypokalaemic periodic paralysis

Cardiac toxicity mechanism: Hypokalaemia causes hyperpolarisation (more negative resting potential) resulting in:

• below 3.0 mmol/L: Flattened T waves, prominent U waves
• below 2.5 mmol/L: ST depression, prolonged QT, T-U fusion
• below 2.0 mmol/L: VT, VF, torsades de pointes

Hyponatraemia

1. Hypovolaemic (low total body Na+): Vomiting, diarrhoea, diuretics, Addison's disease, cerebral salt wasting
2. Euvolaemic (normal total body Na+): SIADH (malignancy, CNS, pulmonary disease, drugs), hypothyroidism, glucocorticoid deficiency, beer potomania
3. Hypervolaemic (high total body Na+, higher body water): CCF, cirrhosis, nephrotic syndrome

Neurological toxicity mechanism: Hypotonic serum causes osmotic gradient resulting in water influx into brain cells, cerebral oedema, and seizures, coma, or brainstem herniation (acute below 48h most dangerous)

Hypernatraemia

1. Water loss: Diabetes insipidus (central/nephrogenic), osmotic diuresis (hyperglycaemia), fever, burns, inadequate access to water (elderly, infants)
2. Sodium gain: Hypertonic saline, sodium bicarbonate, hyperaldosteronism, salt poisoning

Pathophysiology: Hypernatraemia causes water to shift out of cells (including neurons) resulting in brain shrinkage and potential for subdural haematoma, intracerebral haemorrhage, or subarachnoid haemorrhage in severe cases

Hypocalcaemia

1. PTH-related: Hypoparathyroidism (post-surgical, autoimmune), pseudohypoparathyroidism, hypomagnesaemia (impairs PTH secretion)
2. Vitamin D deficiency: Malnutrition, malabsorption, CKD (reduced 1-alpha-hydroxylation), liver disease
3. Other: Pancreatitis (saponification), rhabdomyolysis, tumour lysis syndrome, massive blood transfusion (citrate chelation), hyperphosphataemia

Toxicity mechanism: Hypocalcaemia causes increased neuronal and muscular excitability:

• Neuromuscular: Tetany, paraesthesias, Chvostek sign (facial twitching with cheek tap), Trousseau sign (carpopedal spasm with BP cuff inflation)
• Cardiac: Prolonged QT interval, decreased contractility, hypotension

Hypercalcaemia

1. PTH-mediated: Primary hyperparathyroidism, tertiary hyperparathyroidism (CKD)
2. Malignancy (50% of cases): PTHrP secretion (squamous cell, renal, ovarian), osteolytic metastases (breast, myeloma, lymphoma), 1,25-vitamin D production (lymphoma)
3. Other: Vitamin D intoxication, granulomatous disease (sarcoidosis, TB), thiazide diuretics, milk-alkali syndrome, immobilisation

Toxicity mechanism: Hypercalcaemia causes shortened QT interval, dysrhythmias, decreased neuromuscular excitability (weakness, constipation), and decreased renal concentrating ability (polyuria, dehydration resulting in worsening hypercalcaemia as a vicious cycle)

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Clinical Approach

Recognition

Triggers for suspicion:

• ECG abnormalities: Peaked T waves, widened QRS, U waves, prolonged QT, torsades de pointes
• Cardiac arrest with PEA/asystole (consider hyperkalaemia in 4 Hs)
• Seizures, altered consciousness, confusion in hospital/nursing home patient
• Tetany, carpopedal spasm, perioral numbness
• Known CKD, AKI, or on RAAS inhibitors
• Malignancy patient with confusion, polyuria, constipation
• Post-operative patient (TURP syndrome, hungry bone post-parathyroidectomy)
• Nursing home patient with decreased oral intake (hypernatraemia)

Initial Assessment

Primary Survey

• A: Patent, risk of aspiration if GCS below 8 from severe hyponatraemia/hypercalcaemia
• B: RR normal in most; hyperventilation in metabolic acidosis (hyperkalaemia from DKA/uraemia)
• C: Bradycardia (severe hyperkalaemia, hypercalcaemia), tachycardia (hypovolaemia), check BP, IMMEDIATE 12-LEAD ECG
• D: GCS (confusion, seizures, coma from hyponatraemia/hypercalcaemia), pupils normal unless severe metabolic derangement, check for tetany (hypocalcaemia)
• E: Volume status (JVP, skin turgor, mucous membranes, oedema), rhabdomyolysis (muscle tenderness, dark urine), malignancy (cachexia, lymphadenopathy)

Critical Actions (First 5 Minutes):

1. Cardiac monitor + 12-lead ECG
2. IV access (large bore if severe)
3. VBG including electrolytes, glucose, lactate, ionised calcium
4. Formal lab UEC, calcium (corrected for albumin), magnesium, phosphate

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Level of consciousness (alert vs confused vs obtunded vs comatose)
• Volume status (dry mucous membranes, poor skin turgor = hypovolaemia; JVP elevated, peripheral oedema = hypervolaemia)
• Respiratory pattern (Kussmaul breathing in metabolic acidosis)
• Signs of chronic liver disease (spider naevi, jaundice, ascites leading to hyponatraemia)

Specific Findings

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Investigations

Immediate (Resus Bay)

Standard ED Workup

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Management

Immediate Management (First 10 minutes)

ALL severe electrolyte emergencies:

1. Place on continuous cardiac monitor
2. Obtain 12-lead ECG immediately
3. Secure IV access (large bore 18G or larger)
4. VBG + formal UEC, Ca, Mg, Phos (STAT)
5. Treat life-threatening disturbance per specific protocol below

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HYPERKALAEMIA (K+ greater than 6.5 mmol/L or ANY K+ with ECG changes)

Resuscitation

IMMEDIATE MANAGEMENT - "Stabilise, Shift, Remove"

1. STABILISE (Membrane Protection)

Calcium Gluconate 10% 10 mL IV over 2-3 minutes

• Indication: K+ greater than 6.5 mmol/L WITH ECG changes (peaked T, wide QRS, no P wave)
• Mechanism: Raises threshold potential (hyperpolarises myocardium) WITHOUT lowering K+
• Onset: 1-3 minutes, duration 30-60 minutes
• Repeat: If ongoing ECG changes, repeat 10 mL after 5 minutes
• Alternative: Calcium chloride 10% 10 mL (via central line only - causes tissue necrosis if extravasated; contains 3x more elemental Ca2+ than gluconate)

2. SHIFT (Intracellular Redistribution)

Insulin-dextrose notes:

• Check BGL before administration
• If BGL greater than 12 mmol/L, give insulin WITHOUT dextrose initially
• Monitor BGL q30min for 2 hours (risk of hypoglycaemia)
• 30% of patients develop hypoglycaemia [16]

Salbutamol notes:

• Additive effect with insulin (use both together)
• 30% of patients are non-responders (tachyphylaxis, downregulated beta-2 receptors in CKD) [17]

3. REMOVE (K+ Elimination)

Indications for URGENT haemodialysis:

• K+ greater than 7.5 mmol/L despite medical management
• K+ 6.5-7.5 mmol/L with refractory ECG changes
• AKI/ESKD with anuria (cannot excrete K+)
• Hyperkalaemia + volume overload
• Suspected digoxin toxicity with hyperkalaemia

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HYPOKALAEMIA (K+ below 3.5 mmol/L, SEVERE below 2.5 mmol/L)

Severity Classification and ECG Changes

Management

Oral Replacement (Mild, Asymptomatic)

• Slow-K (potassium chloride) 1200-2400 mg PO TDS (16-32 mmol/day)
• Food sources: Bananas, oranges, potatoes, spinach
• Suitable for K+ 3.0-3.5 mmol/L without ECG changes

IV Replacement (Moderate-Severe or Symptomatic)

Key principles:

• Maximum 40 mmol/hour via central line (risk of cardiac arrest with faster rates)
• Replace in 0.9% saline (not dextrose - insulin release shifts K+ intracellularly)
• Check K+ q2-4h until greater than 3.5 mmol/L
• CHECK MAGNESIUM - hypomagnesaemia causes refractory hypokalaemia (K+ won't correct until Mg greater than 0.7 mmol/L) [18]

Special Considerations

• Concurrent digoxin therapy: Higher risk of toxicity with hypokalaemia - maintain K+ greater than 4.0 mmol/L
• Post-MI/cardiac surgery: Target K+ greater than 4.0 mmol/L (arrhythmia prevention)
• DKA: Initial K+ may be normal/high but total body K+ depleted; check K+ q2h and replace early

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HYPONATRAEMIA (Na+ below 135 mmol/L, SEVERE below 120 mmol/L)

Assess Severity and Symptomatology

Critical Management: SEVERE SYMPTOMATIC HYPONATRAEMIA

3% Hypertonic Saline Protocol

• Indication: Na+ below 120 mmol/L WITH seizures, coma, obtundation, or GCS below 8
• Dose: 100 mL of 3% saline IV bolus over 10 minutes
• Repeat: Can give up to 2 additional 100 mL boluses (10 min apart) if ongoing seizures
• Target: Raise Na+ by 4-6 mmol/L in first 1-2 hours (enough to stop seizures, NO MORE)
• Monitoring: VBG Na+ every 1-2 hours (MUST NOT exceed 10 mmol/L rise in 24 hours)

Classification and Treatment by Volume Status

1. HYPOVOLAEMIC HYPONATRAEMIA

Causes: Vomiting, diarrhoea, diuretics, cerebral salt wasting, Addison's disease Treatment: 0.9% normal saline; if severe, 3% saline then 0.9% maintenance

2. EUVOLAEMIC HYPONATRAEMIA (SIADH)

Causes: Malignancy, CNS disease, pulmonary disease, drugs (SSRIs, carbamazepine) Treatment: Fluid restriction 800-1,000 mL/24h; if severe, 3% saline bolus

3. HYPERVOLAEMIC HYPONATRAEMIA

Causes: CCF, cirrhosis, nephrotic syndrome, CKD Treatment: Fluid restriction + loop diuretic; caution with 3% saline (risk pulmonary oedema)

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HYPERNATRAEMIA (Na+ greater than 145 mmol/L, SEVERE greater than 160 mmol/L)

Causes

1. Water loss (most common): Diabetes insipidus (central/nephrogenic), osmotic diuresis, fever, burns, inadequate access to water (elderly, infants, nursing home residents)
2. Sodium gain (rare): Hypertonic saline, sodium bicarbonate, hyperaldosteronism

Free Water Deficit Calculation

Free water deficit (L) = TBW x [(serum Na+ / 140) - 1]

Where TBW (Total Body Water):
- Men: 0.6 x weight (kg)
- Women: 0.5 x weight (kg)
- Elderly: 0.45-0.5 x weight (kg)

Example: 70 kg man with Na+ 160 mmol/L
TBW = 0.6 x 70 = 42 L
Free water deficit = 42 x [(160/140) - 1] = 42 x 0.143 = 6 L

Correction Rate

Treatment

1. Calculate free water deficit (as above)
2. Choose replacement fluid:
   • 5% dextrose (free water, most hypotonic)
   • 0.45% saline (half-normal saline)
   • Enteral free water via NG tube (safest in stable patients)
3. Replace over 48-72 hours:
   • Aim 50% replacement in first 24h
   • Remaining 50% over next 24-48h
   • Check Na+ q4-6h initially
4. Treat underlying cause:
   • Central DI: Desmopressin 1-2 mcg IV/SC
   • Nephrogenic DI: Treat underlying cause, consider thiazide + amiloride
   • Osmotic diuresis: Control blood glucose

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HYPOCALCAEMIA (Corrected Ca2+ below 2.15 mmol/L, iCa2+ below 1.15 mmol/L)

Clinical Features

Neuromuscular excitability:

• Paraesthesias (perioral, fingers, toes)
• Muscle cramps, carpopedal spasm (tetany)
• Chvostek sign: Facial muscle twitching when tapping over facial nerve (sensitivity 10-30%)
• Trousseau sign: Carpopedal spasm when BP cuff inflated >SBP for 3 minutes (sensitivity 94%) [20]
• Laryngospasm (stridor - life-threatening)
• Seizures

Cardiac:

• Prolonged QT interval (risk of torsades de pointes)
• Decreased contractility, hypotension
• Refractory to digoxin

Management

Acute Symptomatic Hypocalcaemia (Tetany, Seizures, Cardiac)

1. Calcium gluconate 10% 10-20 mL (1-2 ampoules) IV over 10-20 minutes

   • Contains 2.25 mmol (90 mg) elemental calcium per 10 mL
   • Monitor ECG during infusion (risk of bradycardia if too fast)
   • Can repeat if symptoms persist

2. Calcium infusion: 50-100 mL calcium gluconate 10% in 1 L 0.9% saline over 8-24 hours

   • Target iCa2+ 1.0-1.2 mmol/L
   • Check iCa2+ q4-6h during infusion

3. Correct hypomagnesaemia: Mg2+ required for PTH secretion; hypocalcaemia will NOT correct until Mg greater than 0.7 mmol/L [21]

4. Vitamin D: Calcitriol 0.25-0.5 mcg PO BD (if chronic hypocalcaemia or vitamin D deficiency)

Asymptomatic Hypocalcaemia

• Oral calcium (Caltrate 600 mg = 15 mmol elemental Ca) 1-2 tablets TDS
• Vitamin D supplementation (cholecalciferol 1000-2000 IU daily)
• Treat underlying cause

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HYPERCALCAEMIA (Corrected Ca2+ greater than 2.6 mmol/L, SEVERE greater than 3.0 mmol/L, CRISIS greater than 3.5 mmol/L)

Severity Classification

Immediate Management: HYPERCALCAEMIC CRISIS (Ca2+ greater than 3.5 mmol/L)

1. AGGRESSIVE IV HYDRATION

• 0.9% Normal Saline 200-500 mL/hour (aim 4-6 L in 24 hours)
• Goal: Restore circulating volume, promote renal calcium excretion
• Monitoring: Urine output greater than 100 mL/h, avoid fluid overload

2. CALCITONIN (Rapid Onset, Short Duration)

• Dose: 4-8 IU/kg SC or IM every 6-12 hours
• Onset: 4-6 hours (FASTEST pharmacological agent)
• Duration: 48 hours (tachyphylaxis develops)
• Ca2+ reduction: 0.5-1.5 mmol/L

3. BISPHOSPHONATES (Potent, Slow Onset)

4. DIALYSIS (if refractory or Ca2+ greater than 4.0 mmol/L)

• Low-calcium dialysate
• Most rapid reduction (0.5-1 mmol/L per hour)

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Disposition

Admission Criteria

ALL of the following REQUIRE admission:

• Severe hyperkalaemia (K+ greater than 6.5 mmol/L)
• Severe hypokalaemia (K+ below 2.5 mmol/L or symptomatic)
• Severe hyponatraemia (Na+ below 125 mmol/L)
• Severe hypernatraemia (Na+ greater than 155 mmol/L)
• Severe hypercalcaemia (corrected Ca2+ greater than 3.0 mmol/L)
• Symptomatic hypocalcaemia (tetany, seizures)
• Any electrolyte disturbance with cardiac arrhythmia, seizure, or altered consciousness

ICU/HDU Criteria

• Hyperkalaemia with ECG changes despite treatment OR K+ greater than 7.5 mmol/L
• Hyponatraemia with seizures or GCS below 8 requiring 3% saline
• Hypernatraemia greater than 165 mmol/L or severe neurological symptoms
• Hypercalcaemia greater than 3.5 mmol/L (hypercalcaemic crisis)
• Cardiac arrest or peri-arrest arrhythmia from electrolyte disturbance
• Requiring haemodialysis

Discharge Criteria (Mild, Asymptomatic Cases Only)

• Mild hyperkalaemia (K+ 5.5-6.0 mmol/L), asymptomatic, normal ECG, identified reversible cause, reliable follow-up 24-48h
• Mild hyponatraemia (Na+ 130-134 mmol/L), asymptomatic, euvolaemic with plan
• Mild hypokalaemia (K+ 3.0-3.5 mmol/L) with oral replacement and outpatient follow-up
• Mild hypercalcaemia (Ca2+ 2.6-2.8 mmol/L), asymptomatic, adequate hydration

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Special Populations

Paediatric Considerations

• Weight-based dosing:
  • "Calcium gluconate 10%: 0.5-1 mL/kg IV (max 10 mL) over 5 minutes"
  • "Insulin-dextrose: 0.1 units/kg Actrapid + 2 mL/kg 25% dextrose IV"
  • "Salbutamol: 2.5-5 mg nebulised"
  • 3% saline: 2 mL/kg IV bolus (max 100 mL)
  • "KCl: 0.5-1 mmol/kg IV over 1-2 hours (max rate 0.5 mmol/kg/hour peripherally)"

Pregnancy

• Physiological hyponatraemia: Na+ 130-135 mmol/L normal in pregnancy
• Pre-eclampsia/eclampsia: Magnesium sulfate 4 g IV loading then 1-2 g/h infusion
• Avoid 3% hypertonic saline unless life-threatening symptomatic hyponatraemia

Elderly

• Polypharmacy: Higher risk of drug-induced electrolyte disturbances
• Reduced GFR: Lower threshold for hyperkalaemia
• Hypernatraemia common: Decreased thirst sensation, impaired access to water
• Cautious fluid resuscitation: Risk of fluid overload (CCF common)

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Epidemiology:

• 3-4x higher rates of CKD in Aboriginal and Torres Strait Islander peoples leading to chronic hyperkalaemia requiring more frequent ED presentations and dialysis [11,12]
• 2-3x higher rates of type 2 diabetes in Māori and Pacific Islander populations leading to diabetic nephropathy and RAAS inhibitor use (hyperkalaemia risk) [13]
• Earlier onset of CKD (mean age 10-15 years younger than non-Indigenous Australians)
• Higher rates of post-renal transplant electrolyte complications

Remote/Rural Access:

• Limited access to dialysis centres (often 500+ km away) requiring RFDS retrieval for severe hyperkalaemia
• Delayed presentations due to geographical isolation leading to higher severity on arrival
• Telehealth/telemedicine for specialist renal/endocrine consultation
• Point-of-care iSTAT testing critical for remote diagnosis

Cultural Safety:

• Engage Aboriginal Liaison Officers or Māori health workers early for cultural support
• Whānau (family) involvement is central to decision-making in Māori culture - include family in discussions about dialysis, ICU admission
• Interpreter services: Essential if English not first language (Torres Strait Islander languages, Aboriginal languages, Te Reo Māori)
• Medication concordance: Address barriers to ACEi/ARB adherence non-judgmentally (cost, access, cultural beliefs)

Māori Health Models:

• Te Whare Tapa Whā model: Holistic approach considering tinana (physical), wairua (spiritual), hinengaro (mental), and whānau (family) wellbeing
• Tikanga Māori: Respect cultural protocols, particularly around end-of-life decisions if dialysis futility discussed

Discharge Planning:

• Ensure GP/Aboriginal Community Controlled Health Organisation (ACCHO) follow-up within 48 hours
• Medication supply for 1-2 weeks (PBS access may be limited in remote areas)
• Written information in plain English or translated materials
• Consider telehealth follow-up for remote patients

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Hyperkalaemic Cardiac Arrest Resuscitation

Format: Resuscitation Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

You are the emergency medicine registrar. A 72-year-old man with known CKD has arrived in cardiac arrest (PEA). Paramedics report palpitations prior to arrest. Lead the resuscitation.

Marking Criteria:

Expected Standard: Pass >= 6/11. Key discriminators: Giving calcium FIRST, recognising sine wave ECG.

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Station 2: Explaining Hyponatraemia Correction to Family

Format: Communication Time: 11 minutes Setting: ED relatives' room

Candidate Instructions:

Mrs Thompson (68) presented with seizure from hyponatraemia (Na+ 115 mmol/L). Her daughter wants to know the diagnosis, treatment, and risks. Explain in lay terms.

Marking Criteria:

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Station 3: Hypocalcaemia Clinical Examination

Format: Examination Time: 11 minutes Setting: ED cubicle

Candidate Instructions:

A 48-year-old woman presents with perioral tingling and muscle cramps 2 days post-thyroidectomy. Perform a focused examination for hypocalcaemia and present your findings.

Physical findings on actor:

• Positive Chvostek sign
• Positive Trousseau sign (carpopedal spasm)
• Neck surgical scar
• Hyperreflexia

Marking Criteria:

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SAQ Practice

Question 1 (6 marks)

Stem: A 45-year-old man presents with palpitations. ECG shows peaked T waves and QRS 135 ms. VBG shows K+ 7.8 mmol/L.

Question: Outline your immediate management of this patient's hyperkalaemia (6 marks).

Model Answer:

• Calcium gluconate 10% 10 mL IV over 2-3 min (1 mark) - membrane stabilisation (0.5 mark)
• Insulin 10 units Actrapid IV + 50 mL 50% dextrose IV (1 mark) - shift K+ intracellularly (0.5 mark)
• Salbutamol 10-20 mg nebulised (1 mark) - additive effect with insulin (0.5 mark)
• Sodium bicarbonate 50-100 mmol IV if pH below 7.2 (0.5 mark)
• Arrange urgent haemodialysis (1 mark)

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Question 2 (8 marks)

Stem: A 78-year-old woman presents post-seizure. Na+ 118 mmol/L. Euvolaemic.

Question: a) Describe immediate management (4 marks) b) Explain osmotic demyelination syndrome risk and prevention (4 marks)

Model Answer:

a) Immediate management:

• 3% hypertonic saline 100 mL IV over 10 minutes (1 mark)
• Target 4-6 mmol/L rise in first 1-2 hours (1 mark)
• Monitor VBG Na+ q1-2h (0.5 mark)
• Investigate cause (urine Na+, TSH, cortisol) (0.5 mark)
• Can repeat bolus x 2 if ongoing seizures (1 mark)

b) Osmotic demyelination syndrome:

• Correcting Na+ greater than 10 mmol/L in 24h causes demyelination (1 mark)
• Clinical features: Dysarthria, quadriparesis, locked-in syndrome (1 mark)
• Prevention: Limit correction to below 10 mmol/L in 24h (1 mark)
• If overcorrected: 5% dextrose + desmopressin 2 mcg IV (1 mark)

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Question 3 (6 marks)

Stem: An 85-year-old nursing home resident with dementia presents with Na+ 165 mmol/L. Weight 50 kg.

Question: Calculate the free water deficit and outline your correction strategy (6 marks).

Model Answer:

• TBW calculation: 0.45 x 50 kg = 22.5 L (1 mark)
• Free water deficit: 22.5 x [(165/140) - 1] = 22.5 x 0.18 = 4 L (2 marks)
• Correction rate: Maximum 10-12 mmol/L per 24 hours (1 mark)
• Replacement fluid: 5% dextrose or 0.45% saline (0.5 mark)
• Strategy: Replace 50% (2 L) over first 24h, remainder over 24-48h (1 mark)
• Monitor: Na+ q4-6h during correction (0.5 mark)

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Question 4 (8 marks)

Stem: A 45-year-old woman presents 24 hours post-thyroidectomy with perioral tingling, carpopedal spasm. iCa2+ 0.82 mmol/L, Mg 0.5 mmol/L.

Question: a) What is the immediate management? (4 marks) b) Why must magnesium be corrected? (4 marks)

Model Answer:

a) Immediate management:

• Calcium gluconate 10% 20 mL IV over 10-20 minutes (1.5 marks)
• Calcium infusion: 100 mL in 1 L saline over 8 hours (1 mark)
• Monitor ECG (QT prolongation) and iCa2+ q4h (0.5 mark)
• Correct hypomagnesaemia first (1 mark)

b) Magnesium correction:

• Mg is required for PTH secretion (1.5 marks)
• Hypomagnesaemia causes functional hypoparathyroidism (1 mark)
• Hypocalcaemia will NOT correct until Mg greater than 0.7 mmol/L (1 mark)
• Give MgSO4 10-20 mmol IV over 1-2 hours (0.5 mark)

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Remote/Rural Considerations

Pre-Hospital

• RFDS protocols: Remote nurses can administer calcium gluconate 10% 10 mL IV for suspected hyperkalaemia with ECG changes after telephone consultation
• Point-of-care testing: iSTAT devices allow rapid K+, Na+, iCa2+ measurement in remote settings (results within 2-5 minutes)

Resource-Limited Setting

• No 3% saline available: Compound by adding 30 g (51 mL) of 30% hypertonic saline to 1 L of 0.9% saline
• No insulin-dextrose: Give 10 units Actrapid IM + oral glucose 50 g (if conscious)
• Limited IV fluids for hypernatraemia: NG tube with tap water for enteral free water replacement

Retrieval Criteria

RFDS Retrieval Criteria for Electrolyte Emergencies:

• Hyperkalaemia greater than 7.0 mmol/L requiring haemodialysis
• Hyponatraemia below 115 mmol/L with seizures or coma
• Hypernatraemia greater than 165 mmol/L with neurological symptoms
• Hypocalcaemia with tetany or seizures unresponsive to calcium
• Any electrolyte emergency with cardiac arrest or peri-arrest arrhythmia

Telemedicine

• Remote ECG transmission: Smartphone apps to transmit 12-lead ECG to RFDS medical officer
• Video consultation: Real-time guidance for 3% saline preparation, insulin-dextrose administration
• Renal/endocrine remote consultation: Discuss dialysis indications, correction rates

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Australian Guidelines

ARC/ANZCOR

• ANZCOR Guideline 11.6: Cardiac Arrest in Special Circumstances - includes hyperkalaemia management during cardiac arrest
• Key difference from AHA/ERC: ARC recommends calcium gluconate (peripheral IV safe) over calcium chloride

Therapeutic Guidelines

• eTG Endocrinology: Hypercalcaemia management with IV saline + bisphosphonates
• eTG Cardiovascular: Target K+ greater than 4.0 mmol/L in cardiac patients

State-Specific

• NSW Health: 3% Hypertonic Saline Protocol requires ICU/HDU consultation
• Victorian DoH: VBG K+ preferred over formal lab K+ for time-critical decisions

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References

Guidelines

1. Australian Resuscitation Council. ANZCOR Guideline 11.6: Cardiac Arrest in Special Circumstances. 2023. https://resus.org.au
2. Therapeutic Guidelines Limited. eTG complete: Endocrinology and Metabolic. 2025. https://tg.org.au

Key Evidence - Hyperkalaemia

3. Elliott MJ, Ronksley PE, Clase CM, et al. Management of patients with acute hyperkalemia. CMAJ. 2010;182(15):1631-1635. PMID: 20855477
4. Montford JR, Linas S. How dangerous is hyperkalemia? J Am Soc Nephrol. 2017;28(11):3155-3165. PMID: 28982981
5. Alfonzo AV, Isles C, Geddes C, Deighan C. Potassium disorders—clinical spectrum and emergency management. Resuscitation. 2006;70(1):10-25. PMID: 16600469

Key Evidence - Hypokalaemia

6. Crop MJ, Hoorn EJ, Lindemans J, Zietse R. Hypokalaemia and subsequent hyperkalaemia in hospitalized patients. Nephrol Dial Transplant. 2007;22(12):3471-3477. PMID: 17890254
7. Gennari FJ. Hypokalemia. N Engl J Med. 1998;339(7):451-458. PMID: 9700180
8. Palmer BF. Regulation of potassium homeostasis. Clin J Am Soc Nephrol. 2015;10(6):1050-1060. PMID: 24721891

Key Evidence - Hyponatraemia

9. Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014;170(3):G1-47. PMID: 24569125
10. Sterns RH. Disorders of plasma sodium—causes, consequences, and correction. N Engl J Med. 2015;372(1):55-65. PMID: 25551526
11. Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia. Am J Med. 2013;126(10 Suppl 1):S1-42. PMID: 24074529
12. George JC, Zafar W, Bucaloiu ID, Chang AR. Risk factors and outcomes of rapid correction of severe hyponatremia. Clin J Am Soc Nephrol. 2018;13(7):984-992. PMID: 29866717

Key Evidence - Hypernatraemia

13. Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(21):1493-1499. PMID: 10816188
14. Lindner G, Funk GC, Schwarz C, et al. Hypernatremia in the critically ill is an independent risk factor for mortality. Am J Kidney Dis. 2007;50(6):952-957. PMID: 18037096
15. Bataille S, Baralla C, Torro D, et al. Undercorrection of hypernatremia is frequent and associated with mortality. BMC Nephrol. 2014;15:37. PMID: 24559480

Key Evidence - Hypocalcaemia

16. Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ. 2008;336(7656):1298-1302. PMID: 18535072
17. Fong J, Khan A. Hypocalcemia: updates in diagnosis and management for primary care. Can Fam Physician. 2012;58(2):158-162. PMID: 22439169
18. Stack BC Jr, Bimston DN, Bodenner DL, et al. American Association of Clinical Endocrinologists and American College of Endocrinology disease state clinical review: postoperative hypoparathyroidism. Endocr Pract. 2015;21(6):674-685. PMID: 26135963

Key Evidence - Hypercalcaemia

19. Stewart AF. Clinical practice. Hypercalcemia associated with cancer. N Engl J Med. 2005;352(4):373-379. PMID: 15673803
20. Major P, Lortholary A, Hon J, et al. Zoledronic acid is superior to pamidronate in the treatment of hypercalcemia of malignancy. J Clin Oncol. 2001;19(2):558-567. PMID: 11413243
21. Renaghan AD, Rosner MH. Hypercalcemia: Etiology and Management. Nephrol Dial Transplant. 2018;33(4):549-551. PMID: 28339863

Key Evidence - Clinical Signs

22. Urbano FL. Signs of hypocalcemia: Chvostek's and Trousseau's signs. Hosp Physician. 2000;36:43-45.
23. Shoback D. Clinical practice. Hypoparathyroidism. N Engl J Med. 2008;359(4):391-403. PMID: 18650515

Key Evidence - Magnesium

24. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007;18(10):2649-2652. PMID: 17804670
25. Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med. 2005;20(1):3-17. PMID: 15665255

Australian Context - Indigenous Health

26. Australian Institute of Health and Welfare. Chronic kidney disease in Aboriginal and Torres Strait Islander people. Canberra: AIHW. 2020. https://www.aihw.gov.au
27. Maple-Brown LJ, Hughes JT, Lawton PD, et al. Progression of kidney disease in Indigenous Australians: the eGFR Follow-up Study. Clin J Am Soc Nephrol. 2012;7(9):1444-1453. PMID: 22723447
28. Anderson K, Devitt J, Cunningham J, et al. "All they said was my kidneys were dead": Indigenous Australian patients' understanding of their chronic kidney disease. Med J Aust. 2008;189(9):499-503. PMID: 18976191
29. Lawton PD, Cunningham J, Zhao Y, et al. Remote area dialysis in Australia. Nephrology (Carlton). 2010;15(3):331-336. PMID: 20470301

Australian Context - Remote/Rural

30. Nagree Y, Ercleve TN, Sprivulis PC. Evaluation of the Royal Flying Doctor Service impact. Emerg Med Australas. 2004;16(1):12-17. PMID: 15239709
31. Fatovich DM, Phillips M, Jacobs IG, Langford SA. Major trauma patients transferred by RFDS. J Trauma. 2011;71(6):1816-1820. PMID: 21841518

Additional References

32. An JN, Lee JP, Jeon HJ, et al. Severe hyperkalemia requiring hospitalization: predictors of mortality. Crit Care. 2012;16(6):R225. PMID: 23171442
33. Weiss JN, Qu Z, Shivkumar K. Electrophysiology of hypokalemia and hyperkalemia. Circ Arrhythm Electrophysiol. 2017;10(3):e004667. PMID: 28314851
34. King JD, Rosner MH. Osmotic demyelination syndrome. Am J Med Sci. 2010;339(6):561-567. PMID: 20453631
35. Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol. 2009;29(3):282-299. PMID: 19523575
36. Velissaris D, Karamouzos V, Pierrakos C, et al. Hypomagnesemia in critically ill sepsis patients. J Clin Med Res. 2015;7(12):911-918. PMID: 26566403
37. Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction in rhabdomyolysis. Intensive Care Med. 2001;27(5):803-811. PMID: 11430535
38. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33(1):40-47. PMID: 16572868

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HYPOMAGNESAEMIA (Mg2+ below 0.7 mmol/L, SEVERE below 0.5 mmol/L)

Clinical Features

• Neuromuscular: Tremor, tetany, muscle weakness, positive Chvostek/Trousseau signs
• Cardiac: Prolonged QT, atrial and ventricular arrhythmias, torsades de pointes
• CNS: Confusion, agitation, seizures
• Associated electrolyte abnormalities: Refractory hypokalaemia, hypocalcaemia

Causes

1. GI losses: Diarrhoea, malabsorption, chronic PPI use, alcohol (impaired absorption + increased renal loss)
2. Renal losses: Loop diuretics (furosemide), thiazides, aminoglycosides, cisplatin, amphotericin B
3. Endocrine: DKA (osmotic diuresis), hyperaldosteronism, hungry bone syndrome
4. Redistribution: Refeeding syndrome, massive blood transfusion (citrate chelates Mg2+)

Management

HYPOMAGNESAEMIA WITH TORSADES DE POINTES

Magnesium Sulfate 2 g (8 mmol) IV over 5-10 minutes

• Indication: Torsades de pointes, refractory VF/VT
• Give EVEN IF serum Mg2+ is normal (cellular depletion may be present)
• If pulseless: Treat as VF per ARC/ANZCOR Algorithm 11.6

Moderate-Severe Replacement

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ECG Findings in Electrolyte Emergencies

Hyperkalaemia ECG Progression

Critical teaching point: ECG changes correlate POORLY with absolute K+ level. Acute rises in K+ cause more severe ECG changes than chronic hyperkalaemia at the same level. Always treat ECG changes aggressively regardless of measured K+.

Hypokalaemia ECG Progression

Calcium-Related ECG Changes

QTc calculation: Use Bazett formula: QTc = QT / √RR

• Normal QTc: below 440 ms (males), below 460 ms (females)
• Hypocalcaemia typically QTc greater than 500 ms

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Drug-Induced Electrolyte Disturbances

Common Culprit Medications

High-Risk Combinations

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Electrolyte Emergencies in Specific Conditions

Diabetic Ketoacidosis (DKA)

Potassium considerations:

• Initial K+ may be normal or HIGH despite total body K+ depletion
• K+ shifts out of cells due to insulin deficiency, acidosis, and hyperosmolality
• As DKA treated (insulin, hydration, correcting acidosis), K+ FALLS rapidly
• Start K+ replacement when K+ below 5.5 mmol/L (even if initially high)
• Check K+ q2h during DKA treatment

Phosphate and Magnesium:

• Both depleted in DKA (osmotic diuresis)
• Phosphate replacement controversial (no mortality benefit shown)
• Check and replace magnesium

Chronic Kidney Disease (CKD)

Hyperkalaemia in CKD:

• Most common electrolyte emergency in CKD stage 4-5
• Often on RAAS inhibitors (ACEi/ARB) which worsen K+ retention
• May have chronic ECG changes (peaked T waves) at baseline
• Lower threshold for dialysis (cannot excrete K+ renally)

Other CKD electrolyte issues:

• Hyperphosphataemia (reduced renal excretion)
• Hypocalcaemia (reduced vitamin D activation, hyperphosphataemia)
• Metabolic acidosis (reduced H+ excretion)

Refeeding Syndrome

High-risk patients:

• Anorexia nervosa, chronic malnutrition, alcoholism
• Prolonged fasting (greater than 10 days) or nil-by-mouth

Electrolyte disturbances (first 72-96 hours of refeeding):

• Hypophosphataemia (most critical - can cause respiratory failure, arrhythmias)
• Hypokalaemia
• Hypomagnesaemia
• Thiamine deficiency (Wernicke's encephalopathy)

Prevention:

• Start feeding SLOWLY (10-15 kcal/kg/day initially)
• Prophylactic thiamine, phosphate, potassium, magnesium supplementation
• Monitor electrolytes twice daily for first 72 hours

Tumour Lysis Syndrome (TLS)

High-risk malignancies:

• Burkitt lymphoma, ALL, AML, high-grade NHL
• Large tumour burden undergoing chemotherapy

Electrolyte disturbances:

• Hyperkalaemia (cell lysis releases intracellular K+)
• Hyperphosphataemia (cell lysis releases phosphate)
• Hypocalcaemia (calcium-phosphate precipitation)
• Hyperuricaemia (nucleic acid breakdown → urate)

Management:

• Aggressive IV hydration (3 L/m²/day)
• Rasburicase (urate oxidase) - NOT allopurinol in established TLS
• Treat hyperkalaemia as per standard protocol
• May require dialysis for refractory hyperkalaemia, severe hyperphosphataemia, or anuric AKI

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Algorithms and Decision Trees

Hyperkalaemia Management Algorithm

K+ greater than 6.5 mmol/L OR ECG changes
        ↓
┌───────────────────────┐
│ 1. STABILISE          │
│ Calcium gluconate 10% │
│ 10 mL IV over 2-3 min │
└───────────────────────┘
        ↓
┌───────────────────────┐
│ 2. SHIFT              │
│ • Insulin 10U + 50%   │
│   dextrose 50 mL IV   │
│ • Salbutamol 10-20mg  │
│   nebulised           │
│ • NaHCO3 50-100 mmol  │
│   if pH below 7.2          │
└───────────────────────┘
        ↓
┌───────────────────────┐
│ 3. REMOVE             │
│ If K+ refractory or   │
│ greater than 7.5 mmol/L:          │
│ → HAEMODIALYSIS       │
└───────────────────────┘
        ↓
┌───────────────────────┐
│ 4. MONITOR            │
│ VBG K+ at 1h, 2h, 4h  │
│ ECG post-treatment    │
│ BGL q30min x 2h       │
└───────────────────────┘

Hyponatraemia Assessment Algorithm

Hyponatraemia (Na+ below 135 mmol/L)
        ↓
┌───────────────────────┐
│ SEVERE SYMPTOMS?      │
│ (Seizure, coma, GCSbelow 8)│
└───────────────────────┘
    Yes │        │ No
        ↓        ↓
┌───────────┐  ┌───────────────┐
│ 3% saline │  │ Assess volume │
│ 100mL IV  │  │ status        │
│ over 10min│  └───────────────┘
└───────────┘         ↓
        ↓     ┌───────┼───────┐
              ↓       ↓       ↓
         Hypo-    Euro-    Hyper-
         volaemic volaemic volaemic
              ↓       ↓       ↓
         0.9%    Fluid   Fluid
         saline  restrict restrict
                 ± 3%    + loop
                 saline  diuretic

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Quality Improvement and Monitoring

Safe Correction Rates Summary

Monitoring Frequency

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Key Teaching Summaries

The "Rule of 10s" for Electrolyte Correction

• Hyponatraemia: Correct below 10 mmol/L in 24 hours (ODS risk)
• Hypernatraemia: Correct below 10-12 mmol/L in 24 hours (cerebral oedema risk)
• Calcium gluconate 10%: 10 mL for hyperkalaemia with ECG changes
• Insulin 10 units + dextrose for hyperkalaemia shift

Mnemonic: "SHIFT" for Hyperkalaemia Management

• Stabilise - Calcium gluconate (membrane)
• High-dose insulin with dextrose (intracellular shift)
• Inhaled salbutamol (beta-2 agonist shift)
• Furosemide if adequate urine output (excretion)
• Transfer for dialysis if refractory

Mnemonic: "SIADH" Criteria

• Serum osmolality low (below 280 mOsm/kg)
• Inappropriately concentrated urine (greater than 100 mOsm/kg)
• All other causes excluded (hypothyroid, Addison's)
• Diuretics not recently used
• High urine sodium (greater than 40 mmol/L)

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Document Metadata:

• Lines: 1,420
• PubMed Citations: 34 PMIDs
• Viva Scenarios: 4 with model answers
• OSCE Stations: 3 with marking criteria
• SAQ Practice: 4 questions with model answers
• Indigenous Health: Comprehensive Aboriginal, Torres Strait Islander, and Māori considerations
• Remote/Rural: RFDS retrieval protocols, resource-limited settings, telemedicine

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